Case Study - Kelly Bodine, RDN, LDN



Case Study: Nutritional Management of Acute Pancreatitis

Kelly Bodine

Dietetic Intern

ARAMARK Healthcare

Distance Learning Dietetic Internship

------ Community Hospital

February 19, 2010

Case Study: Nutritional Management of Acute Pancreatitis

Abstract

Treatment of AP with PN has long been considered the gold standard to allow the pancreas time to rest and heal; however in recent years, research has led to the wide acceptance of EN to produce the most notable and consistent improvement in outcomes for these patients. The findings are significant due to the disadvantages of PN, including high cost, potential dysfunction of the intestinal mucosal barrier and the increased risk of intestinal organ sepsis. Based on the research, nutrition recommendations for patients with AP are as follows: EN is the preferred route of nutrition support to reduce infectious morbidity, hospital LOS, multi-organ failure and mortality, as well as overall cost; EN via the naso-gastric route was safe and tolerated with a non-significant increase in mortality risk; polymeric formulas can be used without no significant increase in infectious complications or mortality and EN should be initiated within 24-48 hours of admission to produce significant outcome benefits.

Disease Description

Pancreatitis, defined as any inflammation of the pancreas, is a serious condition that can occur in either an acute or chronic nature. Acute pancreatitis (AP) has a rapid onset and a limited duration; in 80 percent of the cases, the disease resolves itself without serious complications (1). During 2009, AP was one of the leading reasons for gastrointestinal hospital admissions in the U.S. with 275,000 cases, a greater than 200 percent increase since 1988(2). The large reported increase in AP cases can likely be attributed to the increasing incidence of obesity, which promotes gallstone formation, the most common cause of AP. According to information published on the Center for Disease Control's website, in 2013, almost 35 percent of adults in the U.S. were obese. Another contributing factor to an AP diagnosis is the growing availability and usage of serum pancreatic enzyme testing in hospital ERs (2). The pancreatic enzyme tests can generate a diagnosis of AP at a much earlier and milder stage.

Etiology

Gallstones (38 percent) and alcohol abuse (36 percent) are the most common causes of acute pancreatitis, comprising almost 80 percent of all cases (1). Gallstones, released by the gall bladder, can migrate and create an obstruction in the common bile and/or pancreatic duct. Acute pancreatitis occurs when the gallstone obstruction blocks flow, increasing pancreatic duct pressure and the subsequent hyper-stimulation of digestive enzymes including lipase and amylase (2). Activation of the pancreatic enzymes leads to the auto-digestion of the gland, inflammatory edema and in 5-10 percent of the cases, necrosis (3). A timely cholecystectomy after an episode of AP can eliminate the risk of future attacks.

Alcohol abuse is the second most common cause of AP, however the cause and effect is not clearly understood. Smoking is considered an independent risk factor in the development of AP. Other less prevalent causes of AP include: structural abnormalities, such as pancreas divisum, where the ducts are not properly joined, choledochal cyst, a congenital defect in the bile ducts, sphincter of oddi dysfunction or obstructions caused by tumors or strictures (1).

The risk of developing AP is equally distributed between men and women, however the etiology is different; alcohol-related AP is more common in men and gallstone-related AP is more common in women. AP is generally uncommon for persons younger than 20 years, as a person ages, the risk of developing AP progressively increases (2).

Diagnosis Criteria

According to the Atlanta Classification, the diagnosis of acute pancreatitis requires confirmation of two of the following three aspects: serum lipase and/or amylase values greater than three times the upper limit of normal, acute onset of persistent abdominal pain that radiates to the back or confirmation from a contrast-enhanced computer tomography (CECT), magnetic resonance imaging (MRI) or transabdominal ultrasound (3). The disease state can be further classified in three degrees of severity, mild acute pancreatitis, moderately severe acute pancreatitis and severe acute pancreatitis. The differences in the stages primarily relate to local versus systemic complications and transient or persistent organ failure.

Mild acute pancreatitis is defined by no local or systemic complications and no organ failure; patients usually experience nausea and/or vomiting and radiating pain that worsens immediately following a meal. Discharge generally occurs after a short stay and mortality is rare. Moderate severe AP has local or systemic complications without persistent organ failure and/or organ failure that is resolved in less than 48 hours. With severe AP, single or multiple organ failure is present and is exacerbated by the body's systemic inflammatory stress response; these patients may have a mortality rate as high as 50 percent (3).

Signs & Symptoms

An episode of AP causes steady, boring upper abdominal pain that radiates through to the back in approximately 50 percent of patients. Pain is rarely experienced in the lower abdominal region. When gallstones are the source, the pain usually develops suddenly, as compared to alcoholic-related AP where the pain develops over a couple of days. The pain in typically persistent and coughing, deep breathing and sudden movement can magnify it. Nausea and vomiting are common side effects.

With an attack of AP, the patient can appear ill and sweaty with a pulse rate between 100 to 140 beats per minute. Upper abdominal distention occurs in 20 percent of the cases, the abdomen may be tender and the stool is typically negative for occult blood (4).

Evidenced-Based Nutrition Recommendations for Acute Pancreatitis

Acute pancreatitis is traditionally treated with bowel rest, somatostatin or analogues to inhibit pancreatin activity, antibiotics and IV fluids. In a clinical setting, nutrition support for AP has traditionally been treated with parenteral nutrition (PN), rather than enteral nutrition (EN), to allow the pancreas to rest and prevent the stimulation of pancreatin secretion, which could cause further inflammation. Recent research has identified the use of EN produces the most notable and consistent improvement in AP outcomes over the past ten years.

Yi, Ge, Zhao, Lei, Zhou, Chen, Zhu and Xia completed a meta-analysis to compare the resulting outcomes of the use of PN and EN in patients with severe acute pancreatitis. The meta-analysis included eight randomized controlled trials including 381 patients, of which 184, or 48 percent of the patients were treated with EN. The significant factors that were considered when assessing patient outcomes included mortality, hospital LOS, complications from infection, organ failure and need for surgical intervention. These factors were considered because patients with severe AP have a mortality rate of 10-40 percent, long hospital stays (average one month), higher incidence of multi-organ failure (16-33 percent), surgical intervention and infection. Based on the meta-analysis, EN was concluded to be significantly superior to PN in controlling the following outcomes: mortality (p=0.001, 95%CI, 0.37), infectious complications (p-0.004, 95%CI, 0.46), organ failure (p=0.02, 95%CI, 0.44) and surgical intervention (p=0.003, 95%CI, 0.41) (5).

Treatment of severe AP with PN has long been considered the gold standard to allow the pancreas to rest and heal, however this form of nutrition support also has disadvantages including high cost, potential dysfunction of the intestinal mucosal barrier and the increased risk of intestinal organ sepsis. This study puts forth the conclusion that EN should be used to treat AP; pancreatic stimulation and the stress response can be managed so the likelihood of mortality, multi-organ failure and infections can be reduced.

Petrov completed a comprehensive review article of multiple meta-analyses to determine the role of EN in treating AP, optimal route of EN delivery and the optimal EN formulation. Petrov's review of eight meta-analyses comprising 379 patients concluded EN was statistically superior to PN when treating severe AP. The studies concluded that PN was more expensive, increased the risk of catheter-related sepsis and might lead to electrolyte and metabolic disorder and gut barrier dysfunction. A review of the studies revealed a 200 percent reduction in infectious complications and 250 percent decrease in morality risk in patients with severe AP who receive EN. The conclusions are supported by evidence-based analysis, but a limitation to the results is that the exact mechanism of the benefits is not clear. Petrov concludes that further investigation should be completed to determine the exact mechanism that causes EN to be more beneficial than PN with these patients.

Petrov next addressed the optimal route for EN delivery in patients with severe AP, nasogastric or nasojejunal. Placement of a nasojejunal tube relates to the traditional belief that severe AP should be treated by allowing the pancreas to rest; a concept that remained unchallenged for decades. Petrov completed a meta-analysis review of five randomized controlled trials of patients receiving EN via a nasogastric tube versus the traditional nasojejunal method of nutrition delivery. The studies included 157 patients with AP; the etiology of their disease state was 52 percent biliary, 23 percent alcohol and 25 percent other.

The results of the analysis concluded that use of the nasogastric tube provided a non-significant change in mortality risk (p=0.28), a non-significant increase in the incidence of diarrhea (p=0.47) and a non-significant increase in intolerance to feeding (p=0.57). Overall the meta-analysis concluded use of nasogastric tubes for EN feeding was safe, tolerated with a non-significant increase in mortality risk.

Evidence-based analysis leads to the wide acceptance of the benefits of enteral nutrition for patients with AP; the next key question to be addressed is the optimal EN formulation. EN formulas can generally be classified as elemental, polymeric or immune enhancing. Elemental formulas have historically been favored with AP patients because of easier intestinal absorption and better tolerance, however these formulas are 3-7 times more expensive than polymeric formula. Petrov reviewed 20 randomized controlled trials with 1070 patients with AP and concluded the use of elemental formulas provided a non-significant increase in infectious complications (p=0.482) and mortality (p=0.741) when compared to polymeric formulas.

The Nutrition Support guidelines published by ASPEN are consistent with the previous findings. According to guideline K-1, patients with AP should have a nasoenteric tube placed and EN initiated as soon as fluid volume resuscitation is complete. (G) The guideline refers to three meta-analyses that concluded the use of EN vs. PN reduces infectious morbidity, hospital length-of-stay (LOS), multi-organ failure and mortality. EN should be initiated within 24-48 hours of admission to produce significant outcome benefits. Guideline K-3 states patients with severe AP can be fed via the gastric or jejunal route, with no significant differences.

Treatment of AP with PN has long been considered the gold standard to allow the pancreas time to rest and heal; however in recent years, research has led to the wide acceptance of EN to produce the most notable and consistent improvement in outcomes for these patients. The findings are significant due to the disadvantages of PN, including high cost, potential dysfunction of the intestinal mucosal barrier and the increased risk of intestinal organ sepsis. Based on the research, nutrition recommendations for patients with AP are as follows: EN is the preferred route of nutrition support to reduce infectious morbidity, hospital LOS, multi-organ failure and mortality, as well as overall cost; EN via the naso-gastric route was safe and tolerated with a non-significant increase in mortality risk; polymeric formulas can be used without no significant increase in infectious complications or mortality and EN should be initiated within 24-48 hours of admission to produce significant outcome benefits.

References

1. Wang GJ, Bao CF, Wei D, Want C, Ding SQ. Acute Pancreatitis: Etiology and common pathogenesis. World J Gastroenterol. 2009;15(12):1427-1430.

2. Yadav D, Lowenfels A. The Epidemiology of Pancreatitis and Pancreatic Cancer. Gastroenterology. 2013;144(6):1252-1261.

3. Banks P, Bollen T, Dervenis C, Gooszen H, Johnson C, Sarr M, et al. Classification of acute pancreatitis - 2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62:102-111.

4. Freedman S. Acute Pancreatitis. The Merck Manual. Available at: pancreatitis.html. Accessed February-March 2015.

5. Yi F, Ge L, Zhao J, Lei Y, Zhou F, Chen Z, etal. Meta-analysis: Total Parenteral Nutrition Versus Total Enteral Nutrition in Predicted Severe Acute Pancreatitis. Intern Med. 2012;51:523-530.

6. Petrov M. Nutrition, Inflammation and Acute Pancreatitis. ISRN Inflammation. 2013:2013;1-17.

7. McClave S, Martindale R, Vanek V, McCarthy M, Roberts P, Taylor B, etal. Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JParenter Enteral Nutr. 2009;33:277-308.

8. Banks P, Conwell D, Toskes P. The Management of Acute and Chronic Pancreatitis. Gastroenterol Hepatol. 2010;6:1-16.

9. Hasse JM, Matarese LE. Medical Nutrition Therapy for Hepatobiliary and Pancreatic Disorders. In: Mahan LK, Escott-Stump S, Raymond J. Krause’s Food & the Nutrition Care Process, 13th Edition. St. Louis, Mo: Saunders Elesiver; 2012:667-673.

10. Testoni, PA. Acute recurrent pancreatitis: Etiopathogenesis, diagnosis and treatment. World J Gastroenterol. 2014;(45):16891-16901.

11. Academy of Nutrition and Dietetics. Nutrition Terminology Reference Manual. 2014. Available at: . Accessed February - March 2015.

12. Pronsky Z, Crowe J. Food Medication Interactions, 17th Edition. Birchrunville, PA:Food Medication Interactions; 2012.

13. . 2015. Available at: . Accessed February-March 2015.

14. ARAMARK Healthcare. Continuous Nutrition Monitoring: Assessment and Education #2: Nutrition Care Priority Points: Adults. Patient Food Services: Policies and Procedures, Volume IV; 2014.

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