January 2010 Issue

Nutrition Support in Severe Acute Pancreatitis
By Theresa A. Fessler, MS, RD, CNSC
Today’s Dietitian
Vol. 12 No. 1 P. 36

A 50-year-old woman with a history of gallstones is admitted with severe abdominal pain that worsens when she eats. She asks, “How long will I need this feeding tube? When will I be able to eat again?”

A 42-year-old man with a history of alcohol abuse and recent severe abdominal pain with a 15-lb weight loss has been transferred from another hospital where he was receiving parenteral nutrition (PN) for two days. He has a nasogastric tube that is draining 1.5 to 2 L of fluid each day. A CT scan shows pancreatic necrosis and a pseudocyst.

Another patient has been taking enteral nutrition (EN) via the jejunal (J) port of a percutaneous endoscopically placed gastrostomy tube with jejunal feeding extension (PEG J). He has been compliant with the physician’s order for nil per os (npo) except ice chips but has experienced increased severe pain during feeding for which he has been readmitted to the hospital.

For many hospital RDs, these scenarios are familiar and among the most difficult and challenging to manage. When acute pancreatitis does not resolve within a few days, some patients must remain without oral food intake for several weeks—and in some cases, months—until the pancreatitis resolves.

Optimal nutritional care for patients with pancreatitis requires knowledge of the disease process and gastrointestinal (GI) anatomy, recent research on the best methods of nutrition support, and strategies to manage feeding complications. Much of the discussion on nutrition therapy in this article will focus on my experience at the University of Virginia (UVA) Health System.

Background and Review
The pancreas is located behind the stomach and has both exocrine and endocrine functions. Digestive enzymes are produced and stored in inactive precursor form in the acinar cells and are normally activated in the lumen of the intestine by trypsin. Digestive enzymes and a fluid rich in bicarbonate drain from the pancreatic duct, which joins the common bile duct and empties into the duodenum. The endocrine portion, called the Islets of Langerhans, produces the hormones insulin, glucagon, and somatostatin, which are secreted into the bloodstream.1

Pancreatitis is inflammation of the pancreas that may also involve peripancreatic tissues and/or other organs.2 The incidence of acute pancreatitis in Western countries is estimated at 10 to 20 cases per 100,000 people annually. Approximately 80% of these cases result from disease of the biliary tract or alcohol abuse. Biliary causes of pancreatitis are three times more prevalent in women than men while alcohol-related cause is six times more prevalent in men than women. Acute pancreatitis differs from chronic pancreatitis in that the latter involves permanent damage to the exocrine and, in late stages, endocrine parenchyma; the impairment in acute pancreatitis is usually reversible with removal of the underlying cause.3 It is not uncommon for patients with chronic pancreatitis to have repeated episodes of acute pancreatitis, sometimes referred to as acute-on-chronic pancreatitis.3

Pathogenesis, Diagnosis, and Severity
The pathogenesis of pancreatitis is complex and still not completely understood. Pancreatitis starts with injury to the acinar cells due to ischemia, viruses, trauma, alcohol ingestion, or toxins. Obstruction of the pancreatic duct with gallstones or biliary sludge is one cause of ischemic acinar cell injury. Increased pressure in the ducts and accumulation of lipase cause necrosis of fat tissue, leading to inflammation and edema with disruption of local blood flow. After acinar cell injury, inappropriate activation of trypsinogen to trypsin occurs, with subsequent premature activation of digestive enzymes, leading to autodigestion of the gland itself. The pancreas becomes inflamed and in severe cases, the inflammation spreads systemically by the action of cytokines and other proinflammatory mediators.1,3

The initial symptom of acute pancreatitis is usually severe epigastric abdominal pain that can radiate to the back and often involves nausea and vomiting. Diagnosis is generally based on two of three parameters: abdominal pain, elevations in serum amylase and/or lipase greater than or equal to three times the upper limit of normal, and evidence of pancreatitis on CT scan.2 Amylase and lipase may not be elevated at all due to loss of function in the case of underlying chronic pancreatitis with fibrosis.3 Most patients with acute pancreatitis who require hospitalization have a mild course and recover after a short period of time with IV fluids, analgesia, and bowel rest, but 10% to 20% have serious complications.2,4

The severity of acute pancreatitis is determined by the presence of organ failure and/or other complications and by prognostic indicators. Organ failure in severe pancreatitis can include shock/hypotension, pulmonary insufficiency, renal failure, or GI bleeding. Complications include pancreatic necrosis, pseudocyst, and abscess. Indicators of poor prognosis/increased mortality are APACHE II (Acute Physiology and Chronic Health Evaluation II) scores greater than 8 and Ranson criteria greater than or equal to 3. Pancreatic necrosis and organ failure are the most important determinants of severity. Mortality is 2% to 9% for all acute pancreatitis cases, 8% to 39% for necrotizing pancreatitis, and 14% to 62% in cases of infected pancreatic necrosis.2

Nutrition Therapy 
One of the main goals of treatment for acute pancreatitis is to prevent pancreatic stimulation; thus, npo and bowel rest are typically prescribed. Nutrition support is not needed unless complications develop that prevent the advancement of oral diet within about seven days.2,4 In the past, PN was the accepted method of nutrition support; however, in the past 13 years, many studies have shown that EN is safe, effective, and superior to PN in terms of outcomes and cost. EN can preserve GI function and integrity and may play a role in modulation of the systemic stress and immune response.5

The pancreas is stimulated by cephalic, gastric, and intestinal phases of digestion, including vagal stimulation as food empties from the stomach into the duodenum, the release of cholecystokinin from the presence of luminal fat and protein, and the release of secretin in response to acid. The more distal in the GI tract nutrition is infused, the less stimulation of the pancreas by these factors. Thus, EN into the jejunum, beyond the Ligament of Treitz (LOT), is recommended.4,6,7

The Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition guidelines for adult patients who are critically ill, published in 2009 in the Journal of Parenteral and Enteral Nutrition, state that patients with severe acute pancreatitis should have a nasoenteric tube placed and EN initiated as soon as fluid volume resuscitation has been completed. Three meta-analyses using 10 randomized trials show that EN is associated with a reduction in infectious morbidity, length of hospital stay, the need for surgical intervention, multiple organ failure, and mortality as compared with PN use in these patients. EN tolerance may be improved by feeding more distally in the GI tract, such as 40 cm or more, beyond the LOT, and by the use of an elemental formula if standard polymeric formulas are not tolerated. PN should be used if EN is not possible. The European Society for Clinical Nutrition and Metabolism has very similar guidelines.8

Most patients tolerate standard polymeric formulas well9, but in the case of maldigestion, pancreatic enzyme replacement medication can be used with standard formulas, or elemental-type EN formulas that are low fat and/or contain medium-chain triglyceride oil may be used.10 At UVA Health System, pancrealipase powder is mixed with standard polymeric EN formula at 1⁄2 to 1 tsp per can, or 2 to 4 tsp/L. Another option is to crush pancreatic enzyme tablets finely and either administer with water via the feeding tube or mix into the EN formula. The timed-release tablets must not be used in this manner. Elemental EN formulas are much more expensive than polymeric formulas.7 For some patients who do not tolerate standard formula and do not have financial coverage for the enzyme medications, the option of using an elemental formula (if EN cost is covered) may be more affordable.

Patients with severe acute pancreatitis complicated by necrosis or pseudocyst may be sent home from the hospital on an EN regimen, typically with a PEG-J tube, or a surgically placed J feeding tube or percutaneous endoscopically placed J tube may be chosen depending on the individual patient and the facility.  The medical team may decide on a nasojejunal tube if uncertain whether the patient will need EN long term or if endoscopic or surgical tube placement is not possible, safe, or desired by the patient.

Most of our home patients prefer nocturnal-cycled EN to allow them some freedom from the pump during the day. EN formulas with 1.5 kcal/mL are more convenient than those with 1 kcal/mL, as fewer cans and less volume are required. Depending on individual requirements, typical daily regimens include four to six cans of a standard EN formula infused at a rate of 80 to 130 mL/hour for a duration of eight to 12 hours. Water flushes of 120 to 240 mL at a time, for a total of approximately 1 to 1.5 L per day, are given for adequate hydration.

Part of our protocol at the UVA Health System is to check 25(OH) vitamin D levels in patients at risk; if suboptimal, repletion is recommended. In a sample of 78 patients with acute pancreatitis at UVA Hospital, more than 93% had suboptimal (less than 30 ng/mL) levels of 25(OH) vitamin D. Seventy-four percent of the patients in this sample had vitamin D levels less than 20 and 37% had levels less than 10 ng/mL.11

Complications During Enteral Feeding
EN during pancreatitis is not always an easy process. Many patients complain of nausea and a sensation of uncomfortable fullness. Vomiting sometimes also occurs. Pancreatic inflammation and associated swelling can cause functional gastric outlet obstruction due to pressure on the stomach and duodenum. Antinausea medications, if not successful on an as-needed basis, should be administered on a scheduled regimen. The use of a proton pump inhibitor (PPI) medication is helpful in reducing the acidity and volume of gastric fluid produced.7 A PPI in the form of a dissolvable tablet that can be mixed with water and administered via the J tube is easiest to use. If necessary, the volume of the EN can be further limited by using a 2 kcal/mL formula. Avoiding fiber may help alleviate gas production and abdominal bloating10, especially if small-bowel bacterial overgrowth has developed.7 The use of narcotic medication can contribute to constipation. Adequate water is important, as is the use of laxatives or stool softeners, if needed.

For those who are vomiting gastric fluids, the gastric port of a PEG-J tube can be opened to drain and relieve pressure and fluid accumulation (venting) on an intermittent or a continuous basis. If a significant amount of fluid (greater than 500 mL/day) is drained and if the stomach acid is suppressed with PPI medication to a pH greater than or equal to 6, the gastric drainage can be reinfused into the jejunal feeding tube, as is common in my institution, using a syringe or feeding bag.7 This practice may seem unpleasant, but it helps avoid electrolyte imbalances and dehydration. It often helps explaining to patients that under normal conditions, this fluid would remain in the GI tract and be reabsorbed. For patients who refuse, or when it is impractical to reinfuse gastric fluid losses, a saltwater solution can be administered via the J tube to approximate the amount of sodium, chloride, and water lost in gastric fluid. Otherwise, IV fluids would be needed.

While some persistent abdominal pain is normal during pancreatitis, pain that worsens with EN feeding may be a sign that the jejunal feeding tube has migrated out of place, resulting in pancreatic stimulation. The previously described case of the patient who stopped his EN due to increased pain is an example of this. After radiologic evaluation of the tube location, it was apparent that the EN formula was infusing into the duodenum. The patient was able to tolerate EN again after the J tube was replaced with the feeding ports in the jejunum, beyond the LOT. Likewise, if a patient is vomiting and the emesis appears milky, similar in appearance to the EN formula, one can suspect that the J tube may have migrated out of place, allowing the flow of formula into the stomach. The caregiver should evaluate tube position to ensure that the end of it (as well as the feeding ports, which may be on the sides near the end of the tube) is beyond the LOT.7

Diarrhea is another common complaint. Medication regimens should be reviewed, as sorbitol-containing liquids, magnesium or potassium salts, and antibiotics are potential contributors to loose stools. Sometimes there is continued inadvertent use of stool softeners or laxatives. Offending medications should be stopped if possible or substituted with more tolerable forms such as crushed tablets instead of sorbitol-containing liquids. Stool samples should be checked to rule out infectious causes of diarrhea, such as Clostridium difficile. Physicians can prescribe antibiotics for the treatment of intestinal infection or small-bowel bacterial overgrowth. Steatorrhea can occur due to maldigestion and malabsorption and can be identified either by fecal fat testing or the observation of oily or floating stools. (Treatment for this is described earlier in this article.) Antidiarrheal medication may be necessary if no cause of diarrhea is identified and if attempts at resolving it have failed.10

Glucose can be elevated in severe acute pancreatitis due to the stress response1 and, in the case of severe necrotizing pancreatitis, loss of endocrine function.3 In patients with underlying chronic pancreatitis, the production of both insulin and glucagon can diminish3, resulting in a brittle form of diabetes mellitus. Diabetes mellitus should be suspected if the patient has unexplained weight loss or lack of weight gain when he or she has been compliant with an amount of EN determined to be sufficient. Physicians should be notified to check hemoglobin A1C and glucose and order glucose monitoring and appropriate medications if necessary.

Use of PN
PN should be used only when the GI tract is not functional, when EN has been tried unsuccessfully, or when enteral access is not possible. Some situations in which EN feeding is not used include abdominal ascites or abnormal anatomy precluding feeding tube placement, prolonged ileus, bowel perforation or obstruction, a high-output enterocutaneous fistula that is too far into the GI tract to allow EN feeding distal to it, and uncommon situations of worsened severe pain during jejunal feeding. IV lipid emulsions should be avoided if serum triglyceride levels are greater than 400 mg/dL.4

Advancement of Oral Diet
During nutrition support with EN or PN, patients often experience hunger and the desire to eat orally. Oral diet advancement can begin when the gastroenterologist has determined that the pancreatitis has resolved. There is no experimental evidence on what type of diet to use, but it makes sense to start with low-fat foods.2 Our practice is to advise patients to start with clear liquids and soft, bland foods and then progress as tolerated while avoiding fried or greasy foods.7 When tolerance of an oral diet is established after acute pancreatitis, there are no diet restrictions given except avoidance of alcohol for alcohol-induced pancreatitis. For patients with ongoing pancreatic insufficiency due to chronic pancreatitis or pancreatic necrosis, some dietary restrictions and/or digestive enzyme medication may be needed due to ongoing pancreatic insufficiency.2

Conclusion
Nutritional care for patients with severe acute pancreatitis is challenging due to the nature of the disease process and the pain and GI symptoms that patients endure. Physician support of EN for these patients is important for success. RDs can make a significant impact in the management of EN and successful outcomes for patients with severe acute pancreatitis.

— Theresa A. Fessler, MS, RD, CNSC, is a nutrition support specialist at the University of Virginia health system in Charlottesville and a freelance writer. She has been a registered dietitian for more than 20 years and has specialized in nutrition support for 17 years.

 

To view diagrams of the pancreas, visit the following Web sites:
• Arizona Transplant Associates, PC: www.arizonatransplant.com/healthtopics/pancreas.html

• National Digestive Diseases Information Clearinghouse: http://digestive.niddk.nih.gov/ddiseases/pubs/dictionary/pages/images/gallstones.jpg

• National Pancreas Foundation: www.pancreasfoundation.org/learn/pancreas.shtml

 

Ligament of Treitz: A band of smooth muscle that extends from the junction of the duodenum and jejunum to the left crus of the diaphragm, described in 1857 by Wenzel Treitz, an Austrian professor of anatomy and pathology.
— Source: Merriam-Webster’s Medical Dictionary

 

References
1. Khokhar AS, Seidner DL. The pathophysiology of pancreatitis. Nutr Clin Pract. 2004;19(1):5-15.

2. Banks PA, Freeman ML; Practice Parameters Committee of the American College of Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol. 2006;101(10):2379-2400.

3. Hruben RH, Iacobuzio-Donahue C. Chapter 19: The pancreas. In: Kumar V, Abbas AK, Fausto N, Aster J. Robbins and Cotran Pathologic Basis of Disease, Professional Edition, 8th ed. Saunders; 2009.

4. Russell MK. Acute pancreatitis: A review of pathophysiology and nutrition management. Nutr Clin Pract. 2004;19(1):16-24.

5. McClave SA, Chang WK, Dhaliwal R, Heyland DK. Nutrition support in acute pancreatitis: A systematic review of the literature. JPEN J Parenter Enteral Nutr. 2006;30(2):143-156.

6. Krenitsky J, Makola D, Parrish CR. Parenteral nutrition in pancreatitis is passe: But are we ready for gastric feeding? A critical evaluation of the literature—Part 1. Pract Gastroenterol. 2007;31(9):92-112.

7. Krenitsky J, Makola D, Parrish CR. Parenteral nutrition in pancreatitis is passe: But are we ready for gastric feeding? A practical guide to jejunal feeding: Revenge of the cyst—Part II. Pract Gastroenterol. 2007;31(10):54-72.

8. Meier R, Ockenga J, Pertkiewicz M, et al. ESPEN guidelines on enteral nutrition: Pancreas. Clin Nutr. 2006;25(2):275-284.

9. Petrov MS, Loveday BP, Pylypchuk RD, et al. Systematic review and meta-analysis of enteral nutrition formulations in acute pancreatitis. Brit J Surg. 2009;96(11):1243-1252.

10. Malone AM, Seres DS, Lord L. Chapter 13: Complications of enteral nutrition. In: The A.S.P.E.N. Nutrition Support Core Curriculum: A Case-Based Approach—the Adult Patient. Silver Spring, Md.: American Society for Parenteral and Enteral Nutrition; 2007.

11. Parrish CR, Krenitsky J, Stauffer C, et al. Preliminary results of vitamin D status in patients admitted to a tertiary care center with pancreatitis. Abstract. Nutr Clin Pract. 2009;24(1):138-139.

 

Causes of Acute Pancreatitis3

Common
Gallstones
Alcoholism

Less Common
Blunt abdominal trauma
Injury during surgery or during endoscopic retrograde cholangiopancreatography
Infections (including mumps)
Various drugs
Ischemic injury (shock, embolism, vasculitis)
Metabolic disorders such as hypertriglyceridemia, hyperparathyroidism, and hypercalcemia
Obstruction of the pancreatic duct system (tumors, biliary sludge, parasites, or congenital cystic dilatation of common bile duct)
Genetic abnormalities
Idiopathic

 

Definitions2,3

Pancreatic pseudocyst: A collection of pancreatic secretions enclosed by a nonepithelialized wall composed of granulation and fibrous tissue that occurs as a result of pancreatic trauma or pancreatitis. It can be inside or outside of the pancreas and can range in size from 2 to 30 cm in diameter.
Pancreatic necrosis: An area within the pancreas that contains nonviable pancreatic tissue with variable amounts of pancreatic fluid, typically associated with fat necrosis.
Pancreatic abscess: A pseudocyst that has become infected, or a necrotic area that has liquefied and become infected.

 

Scoring Systems Used in Determining Severity of Acute Pancreatitis4

APACHE II (Acute Physiology and Chronic Health Evaluation II) scores go as high as 71 and are based on 12 parameters: temperature, blood pressure, heart rate, respiratory rate, oxygenation (P O2), arterial pH, serum sodium, potassium, creatinine, hematocrit (Hct), white cell count (WBC), and modified Glasgow Coma Scale (GCS) score. Points are also assigned for increasing age and for the presence of chronic organ insufficiency.

Modified GCS score criteria: age greater than 55; elevated WBC, glucose, lactate dehydrogenase (LDH), and blood urea nitrogen (BUN); and decreased levels of albumin, calcium, and P O2

Ranson criteria: age greater than 55; elevated WBC, blood levels of glucose, LDH, and aspartamine transaminase upon hospital admission; and, after 48 hours of admission, decrease in Hct, increase in BUN, low calcium levels, low P O2, base deficit, and presence of fluid collections

 

Average Electrolyte Content of Gastric Fluid (mEq/L)

Sodium
(Na)

Potassium
(K)

Chloride
(Cl)

Hydrogen ion
(H+)

Bicarbonate
(HCO3)

60

10

130

60

0

— Source: Adapted from Chapter 3: Maintenance and replacement requirements. In: Beaty L, Pemberton DK. Treatment of Water, Electrolyte, and Acid-Base Disorders in the Surgical Patient. New York: McGraw Hill; 1994.

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