Pancreatitis is an inflammation of the pancreas caused by inappropriate activation of pancreatic enzymes (trypsin, phospholipase, elastase) within and surrounding the pancreas, resulting in autodigestion of pancreatic tissue, edema, and possibly necrosis or hemorrhage. The annual global incidence of acute pancreatitis ranges from 13-45 per 100,000 persons.[1]

About 70%-80% of acute pancreatitis cases result from chronic excessive intake of alcohol or from gallstones.[2] ,[3] The mechanisms behind why these factors lead to pancreatitis are still being elucidated. Less common contributors include severe hypertriglyceridemia, hypercalcemia, mumps, abdominal trauma, cigarette smoking and medications such as azathioprine, ACE inhibitors, valproic acid, thiazides, diuretics, narcotics, hormones and steroids. Pancreatitis also occurs as a transient complication of endoscopic retrograde cholangiopancreatography (ERCP) and may manifest only by elevated amylase and/or lipase levels.

Acute pancreatitis ranges 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. The pain often persists for hours to days, 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.

The clinical syndrome of chronic pancreatitis results from a slowly progressive destruction of pancreatic tissue that occurs over several years due to persistent inflammation and fibrosis. Approximately 45% of all cases result from long-standing alcohol abuse but these numbers vary by gender. Among males, about 60% of cases are due to alcohol while among females less than 30% of cases appear to be due to excess alcohol.[4] Other causes of chronic pancreatitis include 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.

Risk Factors

Up to 30% of acute pancreatitis cases are idiopathic, but multiple risk factors have been identified and include:

Alcohol use. About 10% of chronic alcoholics will develop acute pancreatitis. Alcohol is the leading cause of chronic pancreatitis.

Gallstones. Gallstones are the leading cause of pancreatitis in the United States. Consistent with risk factors for gallstones, women develop gallstone pancreatitis more often than men.

Genetics. Five mutations in cationic trypsinogen have been found in patients with hereditary pancreatitis.[5]

Cigarette use is an independent risk factor for acute and chronic pancreatitis.[3]

Diabetes mellitus, type 2, has been found to significantly increase risk, independent of other demographic risk factors.[6]

Celiac disease has been found to increase the risk of acute pancreatitis significantly.[7]

Hypertriglyceridemia, with serum triglycerides > 1000 mg/dL, increases risk for acute pancreatitis.

Hypercalcemia, from any cause, may increase risk.

Multiple viral infections can lead to pancreatitis including: coxsackie, hepatitis B, cytomegalovirus (CMV), varicella-zoster, herpes simplex, and HIV.

A wide array of medications increase risk and include, but are not limited to, metronidazole, tetracycline, diuretics, 5-ASA, azathioprine, NSAIDs, salicylates, calcium, estrogen.

Diagnosis

A thorough history and examination are vital. Initial laboratory studies include complete blood count (CBC), a complete metabolic panel including calcium and liver function tests, blood alcohol level, amylase, lipase, and lipid panel. A pregnancy test should be obtained in any female of reproductive age. 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.

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) and magnetic resonance cholangiopancreatography (MRCP) will reveal strictures of the common bile duct and pancreatic duct. However, ERCP can also be therapeutic as, if necessary, papillotomy, stricture repair and gallstone retrieval can take place during this procedure.

Treatment

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; 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. Limiting other risk factors is also prudent, such as 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.

Nutritional Considerations

Aside from elevated triglyceride levels, the connections between diet and this disease do not appear to be as straightforward as with other common gastrointestinal ailments. Nevertheless, risk appears to be greater in obese individuals, and following a diet that promotes a healthy weight while including generous amounts of fruits, vegetables, and dietary fiber may help reduce the risk for acute pancreatitis. For individuals with chronic pancreatitis, an imbalance between antioxidant status and oxidative stress appears to be an important factor, and high-dose, antioxidant therapy delivered intravenously appears to be helpful.

Acute Pancreatitis

The role of body weight. The risk for severe acute pancreatitis in obese individuals is 2-3 times greater, compared with normal weight persons. Obesity also significantly increases the risk for multi-system organ failure that often accompanies a severe acute attack of pancreatitis.[8] Gallstones are a risk factor for acute pancreatitis, one that also occurs more frequently in obese persons. Although a diet low in fat and high in fiber has not been shown to reduce the risk for all types of pancreatitis, it is likely to be helpful for the prevention of gallstone-related pancreatitis (see Cholelithiasis and Obesity chapters).

Triglycerides. To reduce triglycerides, a diet restricted in fat and simple carbohydrates is advised, as well as weight loss and abstinence from alcohol.[9] (see Dyslipidemias chapter). The only exception is the therapeutic use of high doses of omega-3 fatty acids, which reduce triglycerides by as much as 50%.[10] Foods with a high glycemic load, particularly sucrose (table sugar) and high fructose corn syrup, also tend to raise triglycerides, and one study found a 60% greater risk for non-gallstone-related acute pancreatitis in persons who consumed diets with the highest glycemic load, compared with the lowest.[11] Patients with triglyceridemia-related pancreatitis may be well-advised to choose carbohydrates that do not raise triglyceride levels; ie, ones that are rich in fiber and have a low glycemic index.[12] In the Multiethnic Cohort study, dietary fiber intake was inversely associated with acute pancreatitis, whether gallstone-related or not.[13]

Fruits and vegetables. A review of modifiable risk factors for pancreatic disease (acute, chronic, and pancreatic cancer) found that consuming the highest amounts of fruit reduced the risk for pancreatic diseases by 27%, while eating the most vegetables reduced risk by nearly 30%, compared to persons consuming the lowest amounts.[14]

Chronic Pancreatitis

Several studies have found an increase in oxidative stress in patients with chronic pancreatitis.[15] One possible contributor is the deficiency of fat-soluble vitamins (A, D, and E) that is common in patients with chronic pancreatitis due to chronic malabsorption.[16]

A known source of this imbalance is the metabolism of xenobiotics, resulting in glutathione depletion and subsequent damage to pancreatic acinar cells.[17] Certain antioxidant defense mechanisms (e.g., glutathione) are compromised in patients with chronic pancreatitis.[16] Melatonin is known to scavenge oxygen and nitrogen radicals and activate antioxidant enzymes such as superoxide dismutase, catalase, and glutathione; consequently, connections have emerged between low melatonin levels and the likelihood of having more severe attacks of pancreatitis.[18]

Several controlled clinical trials with antioxidants in the treatment of chronic pancreatitis have been published. These have indicated that individual antioxidants are ineffective.[17] However, an updated systematic review and meta-analysis found that antioxidant therapy, consisting mainly of combinations of vitamins C, E, beta-carotene, selenium, N-acetylcysteine, and glutamine, significantly reduced the length of hospital stay when compared with controls. Some of these trials utilized intravenous antioxidants, while others provided this in oral form.[19] Other reviews have concluded that antioxidant combinations are effective for pain reduction in patients with chronic pancreatitis,[17] particularly when combined with methionine.[20]

Nutrition support for hospitalized patients

Reviews of controlled clinical trials have concluded that intravenous glutamine[20] or a combination of glutamine and long-chain omega-3 fatty acids[21] significantly reduces the risk of infectious complications, mortality, and length of hospital stay when compared with controls.

Orders

See Basic Diet Orders and Obesity chapters for general recommendations.

What to Tell the Family

There are many risk factors for pancreatitis. Supporting the patient in avoiding these risk factors can decrease the likelihood of future episodes of pancreatitis. Avoiding excessive alcohol use, or abstaining altogether, and adopting a low-fat, high-fiber diet are 2 lifestyle steps that can greatly reduce risk.

Family members can help the patient manage medications, taking care to alert physicians to any that may elevate risk to the pancreas.

References

  1. Yadav D, Lowenfels AB: The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology 144:1252, 2013  [PMID:23622135]
  2. Gullo L et al: Acute pancreatitis in five European countries: etiology and mortality. Pancreas 24:223, 2002  [PMID:11893928]
  3. Frey CF et al: The incidence and case-fatality rates of acute biliary, alcoholic, and idiopathic pancreatitis in California, 1994-2001. Pancreas 33:336, 2006  [PMID:17079936]
  4. Coté GA et al: Alcohol and smoking as risk factors in an epidemiology study of patients with chronic pancreatitis. Clin Gastroenterol Hepatol 9:266, 2011  [PMID:21029787]
  5. Hirota M, Ohmuraya M, Baba H: Genetic background of pancreatitis. Postgrad Med J 82:775, 2006  [PMID:17148697]
  6. Girman CJ, Kou TD, Cai B, et al. Patients with type 2 diabetes mellitus have higher risk for acute pancreatitis compared with those without diabetes. Diabetes Obes Metabol . 2010; 12 :766–771.
  7. Sadr-Azodi O et al: Patients with celiac disease have an increased risk for pancreatitis. Clin Gastroenterol Hepatol 10:1136, 2012  [PMID:22801059]
  8. Acharya C, Navina S, Singh VP: Role of pancreatic fat in the outcomes of pancreatitis. Pancreatology 14:403, 2014 Sep-Oct  [PMID:25278311]
  9. Scherer J et al: Issues in hypertriglyceridemic pancreatitis: an update. J Clin Gastroenterol 48:195, 2014  [PMID:24172179]
  10. Tatachar A et al: Over-the-counter fish oil use in a county hospital: Medication use evaluation and efficacy analysis. J Clin Lipidol 9:326, 2015 May-Jun  [PMID:26073390]
  11. Oskarsson V et al: High dietary glycemic load increases the risk of non-gallstone-related acute pancreatitis: a prospective cohort study. Clin Gastroenterol Hepatol 12:676, 2014  [PMID:24100113]
  12. Riccardi G, Rivellese AA: Dietary treatment of the metabolic syndrome--the optimal diet. Br J Nutr 83 Suppl 1:S143, 2000  [PMID:10889805]
  13. Setiawan VW et al: Dietary Factors Reduce Risk of Acute Pancreatitis in a Large Multiethnic Cohort. Clin Gastroenterol Hepatol 15:257, 2017  [PMID:27609706]
  14. Alsamarrai A et al: Factors that affect risk for pancreatic disease in the general population: a systematic review and meta-analysis of prospective cohort studies. Clin Gastroenterol Hepatol 12:1635, 2014  [PMID:24509242]
  15. Cai GH et al: Antioxidant therapy for pain relief in patients with chronic pancreatitis: systematic review and meta-analysis. Pain Physician 16:521, 2013 Nov-Dec  [PMID:24284838]
  16. Martínez-Moneo E et al: Deficiency of fat-soluble vitamins in chronic pancreatitis: A systematic review and meta-analysis. Pancreatology 16:988, 2016 Nov - Dec  [PMID:27681502]
  17. Siriwardena AK: Reappraisal of xenobiotic-induced, oxidative stress-mediated cellular injury in chronic pancreatitis: a systematic review. World J Gastroenterol 20:3033, 2014  [PMID:24659895]
  18. Belyaev O et al: Protective role of endogenous melatonin in the early course of human acute pancreatitis. J Pineal Res 50:71, 2011  [PMID:20964708]
  19. Gooshe M et al: Antioxidant therapy in acute, chronic and post-endoscopic retrograde cholangiopancreatography pancreatitis: An updated systematic review and meta-analysis. World J Gastroenterol 21:9189, 2015  [PMID:26290647]
  20. Yong L et al: Efficacy of Glutamine-Enriched Nutrition Support for Patients With Severe Acute Pancreatitis: A Meta-Analysis. JPEN J Parenter Enteral Nutr 40:83, 2016  [PMID:25655622]
  21. Jafari T, Feizi A, Askari G, Fallah AA. Parenteral immunonutrition in patients with acute pancreatitis : a systematic review and meta-analysis. Clin Nutr . 2015;3435-3443.
  22. Talukdar R, Murthy HV, Reddy DN: Role of methionine containing antioxidant combination in the management of pain in chronic pancreatitis: a systematic review and meta-analysis. Pancreatology 15:136, 2015 Mar-Apr  [PMID:25648074]

Last updated: November 28, 2017

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TY - ELEC T1 - Pancreatitis ID - 1342009 Y1 - 2017/11/28/ PB - Nutrition Guide for Clinicians UR - https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342009/all/Pancreatitis ER -