June/July 2020 Issue
Dietary Interventions for Pancreatitis
By Carrie Dennett, MPH, RDN, CD
Today’s Dietitian
Vol. 22, No. 6, P. 24
Nutrition plays a key role in saving lives and preserving quality of life.
Both acute and chronic pancreatitis pose significant burdens to health and the health care system. Acute pancreatitis is one of the most common gastrointestinal reasons for hospital admission in the United States, and chronic pancreatitis significantly impairs quality of life.1 In both acute care and outpatient settings, nutrition is a key factor in treating and managing these conditions.
Pancreatitis is inflammation of the pancreas—a large gland that secretes digestive juices into the small intestine and releases the hormones insulin and glucagon into the bloodstream—that occurs when digestive enzymes start digesting the pancreas itself. Both acute and chronic pancreatitis are serious conditions that can lead to sometimes life-threatening complications.
Acute pancreatitis happens suddenly, most often marked by mild to severe pain in the upper abdomen that may spread to the back, chest, or flanks. The intensity and location of the pain don’t correlate with severity. Fever, nausea, and vomiting also may be present.2
In 40% to 70% of cases, the primary cause is gallstones, which can cause inflammation as they pass through a bile or pancreatic duct and get stuck. Heavy alcohol use—more than 50 g per day for more than five years—accounts for 25% to 35% of cases. Acute pancreatitis also may occur in individuals with triglyceride levels above 1,000 mg/dL or in those with benign or malignant pancreatic tumors, the latter especially when pancreatitis is idiopathic, ie, has no identifiable cause.2
In the United States, more than 270,000 hospital stays each year are due to acute pancreatitis.3,4 Cases are classified as mild, moderate, or severe, and overall mortality ranges from 5% to 30% based on severity.3 With treatment, mild acute pancreatitis generally resolves within several days; however, about 15% to 20% of cases are severe, taking more time to resolve and requiring a longer hospital stay.2
The immune system is thought to play a role in the progression of acute pancreatitis—in some patients, the release of proinflammatory mediators triggered by autodigestion of the pancreas can cause necrotizing pancreatitis and failure of the small intestinal barrier. This allows for bacterial translocation, which in turn can lead to systemic inflammatory response syndrome and multiple organ dysfunction syndrome.5
Recurrent episodes of acute pancreatitis can lead to chronic pancreatitis, which affects about 42 to 73 out of 100,000 US adults,6 resulting in 86,000 yearly hospital stays.7 Although the progression of chronic pancreatitis is variable and may include long periods without symptoms, the condition does worsen over time, leading to permanent damage. Symptoms may include abdominal pain, and when pain is present it may become constant and more severe after eating. Ironically, as the condition progresses, the pain may recede.7
Other symptoms include nausea, vomiting, diarrhea, oily and foul-smelling stools, and weight loss. For acute flare-ups, treatment of chronic pancreatitis is similar to that for acute pancreatitis.7
Persistent abdominal pain, scarring of the pancreas, diabetes, and pancreatic cancer all may be complications of chronic pancreatitis. Maldigestion, malnutrition, and malabsorption also may occur, potentially leading to osteopenia and osteoporosis, which in turn can result in bone fractures.8
Men and black Americans are at higher risk, as are people with a family or personal history of gallstones or a family history of pancreatitis. In addition to heavy alcohol use and high triglycerides, causes can include high blood levels of calcium, genetic disorders of the pancreas, and some medications.8 Having celiac disease increases the risk of chronic pancreatitis—specifically, a subtype known as autoimmune pancreatitis—by about three-fold, and those with inflammatory bowel disease and other autoimmune conditions also have an elevated risk.9
People with cystic fibrosis may have chronic pancreatitis without pain due to pancreatic insufficiency. Environmental toxins, such as ongoing alcohol and tobacco use, contribute to the progression of chronic pancreatitis.7
Diagnosis and Medical Treatment
American College of Gastroenterology recommendations state that a diagnosis of acute pancreatitis is determined by the presence of two of these three criteria: upper abdominal pain, serum amylase and/or lipase greater than three times the upper normal limit, and characteristic findings from abdominal imaging. Serum lipase levels are preferred over serum amylase levels because they remain elevated longer after disease onset.2
Mild cases are defined by the absence of organ failure and/or pancreatic necrosis. Moderately severe cases have local complications, including necrosis, but without persistent organ failure. Severe cases have two distinct phases. The early phase, within the first week, is characterized by systemic inflammatory response syndrome and/or organ failure, with organ failure determining the severity. The second phase is characterized by local complications. Because most patients with severe pancreatitis don’t have organ failure or necrosis at the time of admission, they may be inaccurately diagnosed as having a mild case, which delays necessary treatment.2
There’s no single test that definitively diagnoses chronic pancreatitis. It’s usually suspected if a patient has upper abdominal pain, ongoing alcohol or tobacco use, a history of acute pancreatitis, and a family history of pancreatitis, and then is confirmed with a CT or MRI scan.7,10 Pancreatic function testing often is used as a complementary measure. Because endoscopic ultrasound is invasive and lacks specificity, it’s only recommended if cross-sectional imaging can’t confirm a diagnosis.10
Management of chronic pancreatitis is based on pain control, treatment of pancreatic insufficiency, and management of complications.11 Pain control through medical or, less frequently, surgical means, is one of the first steps in treating chronic pancreatitis, followed by alcohol and smoking cessation, if applicable.6
If ongoing management with pancreatic enzyme replacement therapy (PERT) and nutrition is insufficient, proton pump inhibitors may be prescribed to help prevent stomach acid from denaturing pancreatic lipase. More than one-half of patients with chronic pancreatitis develop diabetes—known as pancreatatogenic or type 3c diabetes—due to the loss of islet cell mass in the pancreas, which in turn increases the risk of pancreatic cancer. Medical treatment for diabetes secondary to pancreatitis typically involves insulin-sensitizing medications, such as metformin, along with PERT.9
Treatment for mild acute pancreatitis usually comprises a brief stay in the hospital for IV fluids, pain medication, and antibiotics if infectious complications are present—but not prophylactically.2,12 Severe acute pancreatitis requires a longer hospital stay.
Surgical interventions to remove blockages—including gallstones—or treat narrowing of the pancreatic or bile ducts may be necessary in some patients with acute pancreatitis or acute flare-ups of chronic pancreatitis. Some patients require surgical removal of necrotic tissue, and in rarer cases removal of the gallbladder or pancreas.2,13 Due to the complex etiology and varying clinical manifestations of acute pancreatitis, finding pharmaceutical treatment has been challenging.5
Nutritional Treatment for Acute Pancreatitis
What constitutes optimal nutritional support for acute pancreatitis has been under debate for decades. Conventional treatment had been NPO (nothing by mouth) to allow the pancreas to rest—despite a lack of clinical data to support this,2,5 with most guidelines recommending NPO until pain resolves and some delaying oral feeding until pancreatic enzyme levels normalize or inflammation abates.2
However, this contributes to a variety of other problems, including malnutrition and catabolism due to restriction of energy intake at a time when the body’s energy needs have increased.5 In fact, new guidelines presented at the European Society for Clinical Nutrition and Metabolism (ESPEN) Congress last year state that all patients with predicted mild to moderate acute pancreatitis should be screened for nutritional risk, and that patients with predicted severe acute pancreatitis always should be considered to be at nutritional risk.14
Because malnutrition is of particular concern with severe acute pancreatitis, total parenteral nutrition (TPN) has become standard practice to provide nutrition while avoiding stimulation of the pancreas.15 However, this also prevents stimulation of the intestines, and this bowel rest is associated with atrophy of the intestinal mucosa, which worsens small intestinal barrier function in about 60% of patients, leading to potentially serious complications.2,5 Not only does TPN not benefit intestinal health, but there’s risk of infections stemming from the central venous catheter.16
In patients who can’t tolerate oral feedings, enteral nutrition (EN) helps protect the intestinal mucosa and prevents bacterial overgrowth by stimulating gut motility.5,15 A 2010 Cochrane review found that EN was more likely than TPN to reduce systemic infections, multiorgan failure, and death.15 A 2009 systematic review of 11 randomized controlled trials found similar results. However, researchers noted that, while EN resulted in better outcomes than TPN when nutrition support was started within 48 hours of admission, there was no difference between EN and TPN when nutrition was delayed beyond 48 hours. It’s posited that this was due to the impact of delayed nutrition across the board.17
So while EN may produce better outcomes than TPN, it also appears that it’s better to provide EN earlier than later. Several studies have found that starting EN within 48 hours of admission, compared with waiting for more than 48 hours, reduced the rate of major infection and, in some cases, mortality.17-20 This is consistent with recommendations from nutrition societies in the United States and Europe, including the American Society for Parenteral and Enteral Nutrition, ESPEN, and the Journal of Parenteral and Enteral Nutrition.14,21 These guidelines recommend early EN in all patients with severe acute pancreatitis, using TPN only when EN isn’t tolerated or feasible.
When administering EN to pancreatitis patients, a nasojejunal route—delivering nutrition to the jejunum of the small intestine—traditionally has been preferred, as it sharply reduces stimulation of the pancreas while still prompting gut motility.2,5,15 However, nasojejunal tubes are more difficult to place into patients, requiring specialist staff and increasing costs.22 Recent research has found that nasogastric tube feeding appears safe, and the International Association of Pancreatology and the American Pancreatic Association recommend using either method.3
A 2014 systematic review and meta-analysis found that nasogastric feeding was effective in 90% of patients with severe acute pancreatitis, delivering adequate nutrition without increasing incidence of complications such as diarrhea, abdominal distention, or exacerbation of pain.22 A 2020 Cochrane review found that current evidence is insufficient to show advantage or disadvantage to either mode of tube feeding.23
What about oral feeding? A 2014 multicenter trial in the Netherlands randomized patients with severe acute pancreatitis at high risk of complications to receive either EN within 24 hours of admission or an oral diet after 72 hours. Patients assigned to the oral diet received IV fluids for the first 72 hours, and, if an oral diet wasn’t tolerated at 72 hours, it was offered again at 96 hours; if still not tolerated, EN was offered. Researchers found no difference in rates of major infection—pancreatic necrosis, pneumonia, or bacteria in the bloodstream—or death within six months of admission. They also didn’t see differences in the level of inflammatory response16—notable, because lessening of this response has been hypothesized to be a benefit of early feeding by EN.19
The question of when to start oral feeding in patients with mild acute pancreatitis has a clearer answer.24-26 One randomized clinical study found that immediate oral feeding in patients with mild acute pancreatitis quickened recovery with no adverse gastrointestinal effects.26 Another 2007 randomized trial found that a low-fat solid diet was tolerated as well as a clear liquid diet in patients with mild cases but didn’t result in a shortened hospital stay as hypothesized.24 However, a 2010 randomized controlled trial did find that patients initiated on a full solid diet had a shorter length of stay than those started on a clear liquid diet or a soft diet.25
Accordingly, for patients with predicted mild acute pancreatitis, the new ESPEN guidelines as well as American College of Gastroenterology guidelines recommend starting oral feeding with a low-fat solid diet as soon as tolerated, as it may accelerate recovery, with EN preferable to TPN if not tolerated.14,26,27
When EN is the appropriate intervention, which formulation is best? A polymeric with intact protein, carbohydrates, and long-chain fatty acids? An oligomeric—also known as elemental or semielemental—with peptides and free amino acids, monosaccharides, and medium-chain and free fatty acids? A specialized formula with anti-inflammatory immunonutrients such as glutamine and omega-3 fatty acids, or a formula with prebiotics and probiotics?
A 2015 Cochrane review found insufficient evidence to recommend any specific type of EN formulation. Specifically, evidence on the efficacy and safety of immunonutrients was of low or very low quality, and studies looking at probiotics in the treatment of acute pancreatitis had inconsistent—even contradictory—results, especially about safety.28 Accordingly, the International Association of Pancreatology doesn’t recommend the use of probiotics to help reduce infectious complications, in part because there’s significant variation in type and dosage of probiotic supplements. In one randomized controlled trial, using a specific combination or probiotic strains didn’t prevent complications but did increase mortality.3 The bottom line? Provided the formula doesn’t contain probiotics or immunonutrients, the choice between polymeric and oligomeric formulas will be based largely on patient tolerance.
Nutritional Treatment for Chronic Pancreatitis
Chronic pancreatitis requires a different nutritional approach, with ongoing management that includes nutrition, supplemental digestive enzymes, and cessation of tobacco and alcohol use. Malnutrition is common in patients with chronic pancreatitis due to a variety of factors, including the following14,27,29:
• increased energy expenditure coupled with pain-related loss of appetite and/or fear of eating;
• pancreatic enzyme insufficiency;
• delayed gastric emptying; and
• continued alcohol abuse.
Low levels of pancreatic lipase can reduce absorption of dietary fat and fat-soluble nutrients (vitamins A, D, E, K)—causing bloating, diarrhea, or fatty stools, leading to further avoidance of fat and interfering with adequate energy intake. Insufficient levels of pancreatic protease can lead to both protein malnutrition and vitamin B12 deficiency, and chronic inflammation can interfere with the body’s use of protein.30
Patients with chronic pancreatitis—even those without heavy alcohol use—are more likely to have micronutrient deficiencies than those without the disease. Markers of bone turnover and formation also are lower,30 and specific deficiencies of calcium, magnesium, zinc, thiamine, and folic acid have been reported.27 PERT helps minimize deficiencies, but some patients will need to take supplemental forms of micronutrients impacted by this condition.27,30
Long-standing advice to limit dietary fat no longer is recommended, largely because it decreases secretion of pancreatic enzymes and can make supplemental pancreatic enzymes less effective. In addition, restricting dietary fat can mask the onset of fat malabsorption, which presents as fat in the stool (steatorrhea)31 and increases the risk of exacerbating weight loss and deficiencies of fat-soluble vitamins.9
ESPEN recommends high-protein, high-calorie foods consumed in five to six small meals per day, while avoiding diets very high in fiber, as fiber can absorb or block the action of pancreatic lipase, leading to reduced nutrient intake. There’s no need to restrict dietary fat unless steatorrhea can’t be controlled.14,32 Protein intake of 1 to 1.5 g/kg generally is sufficient and well tolerated. In more than 80% of cases, food supplemented by pancreatic enzymes before every meal and snack is adequate, while 10% to 15% require oral nutritional supplements—whole protein based if tolerated, peptide based if not—and 5% need EN. Patients at risk of unintended weight loss may supplement with medium-chain triglyceride (MCT) oil, which is absorbed directly into the bloodstream without need for pancreatic enzymes.27 MCT oil is found in coconut and palm kernel oils, as well as in supplemental form.
Final Thoughts
While medical, and sometimes surgical, interventions are important in treating and managing acute and chronic pancreatitis, nutrition also plays a critical role in preventing complications and preserving quality of life.
— Carrie Dennett, MPH, RDN, CD, is the nutrition columnist for The Seattle Times, owner of Nutrition By Carrie, and author of Healthy for Your Life: A Holistic Guide to Optimal Wellness.
References
1. Yadav D, Lowenfels AB. The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology. 2013;144(6):1252-1261.
2. Tenner S, Baillie J, DeWitt J, Vege SS; American College of Gastroenterology. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol. 2013;108(9):1400-1415.
3. Working Group IAP/APA Acute Pancreatitis Guidelines. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology. 2013;13(4 Suppl 2):e1-e15.
4. Forsmark CE, Vege SS, Wilcox CM. Acute pancreatitis. N Engl J Med. 2016;375(20):1972-1981.
5. Pan LL, Li J, Shamoon M, Bhatia M, Sun J. Recent advances on nutrition in treatment of acute pancreatitis. Front Immunol. 2017;8:762.
6. Singh VK, Yadav D, Garg PK. Diagnosis and management of chronic pancreatitis: a review. JAMA. 2019;322(24):2422-2434.
7. Ketwaroo GA, Freedman SD, Sheth SG. Approach to patients with suspected chronic pancreatitis: a comprehensive review. Pancreas. 2015;44(2):173-180.
8. Definitions & facts for pancreatitis. National Institute of Diabetes and Digestive and Kidney Diseases website. https://www.niddk.nih.gov/health-information/digestive-diseases/pancreatitis/definition-facts. Updated November 2017.
9. Pham A, Forsmark C. Chronic pancreatitis: review and update of etiology, risk factors, and management. F1000Res. 2018;7:F1000 Faculty Rev-607.
10. Gardner TB, Adler DG, Forsmark CE, Sauer BG, Taylor JR, Whitcomb DC. ACG clinical guideline: chronic pancreatitis. Am J Gastroenterol. 2020;115(3):322-339.
11. Jalal M, Campbell JA, Hopper AD. Practical guide to the management of chronic pancreatitis. Frontline Gastroenterol. 2019;10(3):253-260.
12. Crockett SD, Wani S, Gardner TB, Falck-Ytter Y, Barkun AN; American Gastroenterological Association Institute Clinical Guidelines Committee. American Gastroenterological Association institute guideline on initial management of acute pancreatitis. Gastroenterology. 2018;154(4):1096-1101.
13. Treatment for pancreatitis. National Institute of Diabetes and Digestive and Kidney Diseases website. https://www.niddk.nih.gov/health-information/digestive-diseases/pancreatitis/treatment. Updated November 2017.
14. Bezmarević M; European Society for Clinical Nutrition and Metabolism. ESPEN guidelines on nutritional support in pancreatic diseases (acute and chronic pancreatitis). http://www.espen.org/presfile/Bezmarevic_2019.pdf. Published 2019.
15. Al-Omran M, Albalawi ZH, Tashkandi MF, Al-Ansary LA. Enteral versus parenteral nutrition for acute pancreatitis. Cochrane Database Syst Rev. 2010;(1):CD002837.
16. Bakker OJ, van Brunschot S, van Santvoort HC, et al. Early versus on-demand nasoenteric tube feeding in acute pancreatitis. N Engl J Med. 2014;371(21):1983-1993.
17. Petrov MS, Pylypchuk RD, Uchugina AF. A systematic review on the timing of artificial nutrition in acute pancreatitis. Br J Nutr. 2009;101(6):787-793.
18. Li JY, Yu T, Chen GC, et al. Enteral nutrition within 48 hours of admission improves clinical outcomes of acute pancreatitis by reducing complications: a meta-analysis. PLoS One. 2013;8(6):e64926.
19. Sun JK, Mu XW, Li WQ, Tong ZH, Li J, Zheng SY. Effects of early enteral nutrition on immune function of severe acute pancreatitis patients. World J Gastroenterol. 2013;19(6):917-922.
20. Wereszczynska-Siemiatkowska U, Swidnicka-Siergiejko A, Siemiatkowski A, Dabrowski A. Early enteral nutrition is superior to delayed enteral nutrition for the prevention of infected necrosis and mortality in acute pancreatitis. Pancreas. 2013;42(4):640-646.
21. Mirtallo JM, Forbes A, McClave SA, Jensen GL, Waitzberg DL, Davies AR. International consensus guidelines for nutrition therapy in pancreatitis. JPEN J Parenter Enteral Nutr. 2012;36(3):284-291.
22. Nally DM, Kelly EG, Clarke M, Ridgway P. Nasogastric nutrition is efficacious in severe acute pancreatitis: a systematic review and meta-analysis. Br J Nutr. 2014;112(11):1769-1778.
23. Dutta AK, Goel A, Kirubakaran R, Chacko A, Tharyan P. Nasogastric versus nasojejunal tube feeding for severe acute pancreatitis. Cochrane Database Syst Rev. 2020;(3):CD010582.
24. Jacobson BC, Vander Vliet MB, Hughes MD, Maurer R, McManus K, Banks PA. A prospective, randomized trial of clear liquids versus low-fat solid diet as the initial meal in mild acute pancreatitis. Clin Gastroenterol Hepatol. 2007;5(8):946-951.
25. Moraes JM, Felga GE, Chebli LA, et al. A full solid diet as the initial meal in mild acute pancreatitis is safe and result in a shorter length of hospitalization: results from a prospective, randomized, controlled, double-blind clinical trial. J Clin Gastroenterol. 2010;44(7):517-522.
26. Eckerwall GE, Tingstedt BB, Bergenzaun PE, Andersson RG. Immediate oral feeding in patients with mild acute pancreatitis is safe and may accelerate recovery — a randomized clinical study. Clin Nutr. 2007;26(6):758-763.
27. Meier R, Ockenga J, Pertkiewicz M, et al. ESPEN guidelines on enteral nutrition: pancreas. Clin Nutr. 2006;25(2):275-284.
28. Poropat G, Giljaca V, Hauser G, Štimac D. Enteral nutrition formulations for acute pancreatitis. Cochrane Database Syst Rev. 2015;(3):CD010605.
29. O’Brien SJ, Omer E. Chronic pancreatitis and nutrition therapy. Nutr Clin Pract. 2019;34 Suppl 1:S13-S26.
30. Greer JB, Greer P, Sandhu BS, et al. Nutrition and inflammatory biomarkers in chronic pancreatitis patients. Nutr Clin Pract. 2019;34(3):387-399.
31. Domínguez-Muñoz JE, Phillips M. Nutritional therapy in chronic pancreatitis. Gastroenterol Clin North Am. 2018;47(1):95-106.
32. Arvanitakis M, Ockenga J, Bezmarevic M, et al. ESPEN guideline on clinical nutrition in acute and chronic pancreatitis. Clin Nutr. 2020;39(3):612-631.