Which nutrition intervention generally should be the first used with active pancreatitis?
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Diagnosis | Treatment | Auto Islet Transplants | Diet | Prognosis | FAQ Nutrition is a vitally important part of treatment for patients with pancreatitis. The primary goals of nutritional management for chronic pancreatitis are: To best achieve those goals, it is important for pancreatitis patients to eat high protein, nutrient-dense diets that include fruits, vegetables, whole grains, low fat dairy, and other lean protein sources. Abstinence from alcohol and greasy or fried foods is important in helping to prevent malnutrition and pain. Nutritional assessments and dietary modifications are made on an individual basis because
each patient’s condition is unique and requires an individualized plan. Our Pancreatitis Program offers nutritional and gastrointestinal support for those with pancreatitis. Patients with chronic pancreatitis are at high risk for malnutrition due to malabsorption and depletion of nutrients as well as due to increased metabolic activity. Malnutrition
can be further affected by ongoing alcohol abuse and pain after eating. Vitamin deficiency from malabsorption can cause osteoporosis, digestive problems, abdominal pain, and other symptoms. Therefore, patients with chronic pancreatitis must be tested regularly for nutritional deficiencies. Vitamin therapies should be based on these annual blood tests. In general, multivitamins, calcium, iron, folate, vitamin E, vitamin A, vitamin D, and vitamin B12 may be supplemented, depending on the
results of blood work. If you have malnutrition, you may benefit from working with our Registered Dietitian who can guide you towards a personalized diet plan. Chronic pancreatitis also causes the pancreas to gradually lose its ability to function properly, and endocrine function will eventually be lost. This puts patients at risk for type 1 diabetes. Patients should therefore avoid refined sugars and simple carbohydrates. If pancreatic enzymes are prescribed, it is important to take them regularly in order to prevent flare-ups. The healthy pancreas is stimulated to release pancreatic enzymes when undigested food reaches the small intestine. These enzymes join with bile and begin breaking down food in the small intestine. Since your pancreas is not working optimally, you may not be getting the pancreatic enzymes you need to digest your food properly. Taking
enzymes can help to digest your food, thus improving any signs or symptoms of steatorrhea (excess fat in the stool, or fat malabsorption). In turn this will improve your ability to eat better, lowering your risk for malnutrition. If pancreatitis was caused by alcohol use, you should abstain from alcohol. If other causes of acute pancreatitis have been addressed and resolved (such as via gallbladder removal) and the pancreas returned to normal, you should be able to lead a
normal life, but alcohol should still be taken only in moderation (maximum of 1 serving/day). In chronic pancreatitis, there is ongoing inflammation and malabsorption — patients gradually lose digestive function and eventually lose insulin function — so regular use of alcohol is unwise. People with pancreatitis should avoid smoking, as it increases the risk for pancreatic cancer. If you or someone you care for is dealing with a pancreatitis, the
Pancreas Center is here for you. The Pancreatitis Program works with nutritionists to provide helpful diet suggestions that help manage the impact of the disease. Call us at (212) 305-4795 or use our online form to get in touch today. Overview | Causes | Genetics | Symptoms |
Diagnosis | Treatment | Auto Islet Transplants | Diet | Prognosis | FAQ
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1. IntroductionAdequate fluid and food administration can be a major medical problem in patients with acute pancreatitis. Despite the increasing knowledge from research in the fields of metabolism, clinical nutrition and intervention, there is still much controversy with respect to the optimal nutritional treatment regimens for acute pancreatitis. For many years, textbooks have advocated the concept that oral or enteral feeding is harmful in acute pancreatitis; such feeding was thought to stimulate exocrine pancreatic secretory responses and consequently autodigestive processes. On the other hand, it is known that specific nutritional deficiencies can occur in patients with a prolonged and complicated course of acute necrotizing pancreatitis. About 30% of patients with acute pancreatitis are already malnourished at the time of the initial attack. Also, it has been questioned whether early feeding changes the outcome in uncomplicated, acute pancreatitis. Although there is much more evidence available on which to base rational management in acute pancreatitis, there are still areas of controversy which may depend on variations in experience and on the type of patients being treated. 2. Acute pancreatitis2.1 Physiology and pathophysiology with respect to fluid resuscitationAcute pancreatitis remains a serious illness with a mortality of about 10%. In spite of the fact that approximately 80% of the patients have mild or moderate disease with a mortality rate below 1%, about 20–25% of patients with acute pancreatitis have a severe form of the disease which may result in multiorgan failure and death. The principal pathogenic factor in development of acute pancreatitis is activation of pancreatic enzymes within the pancreas with subsequent autodigestion. This activation leads to various pathophysiological changes from mild inflammation to necrosis (frequently haemorrhagic) and development of peripancreatic infiltration. The pathological findings, which correlate with clinical severity, range from mild oedema to pancreatic necrosis. Secondary infection and splanchnic hypoperfusion can lead to the development of septic complications and subsequent multiorgan failure. The discrimination between acute interstitial-oedematous and necrotizing pancreatitis seems to be the most relevant prognostic criterion. It was supposed previously that the most important diagnostic step was to discriminate between interstitial-oedematous and necrotizing pancreatitis by performing contrast-enhanced CT-scanning. The treatment of mild acute pancreatitis then involved intravenous fluid administration, analgesics, avoidance of oral intake and routine ward observations. The patients with the necrotizing form were advised to be managed in an intensive care unit for close monitoring of vital functions and for more aggressive treatment such as antibiotic therapy, peritoneal lavage or surgical treatment of complications. During the early acute state, however, there is only a narrow limit between mild disease and a transition to severe impairment. Especially at this stage, depletion of intravascular volume due to fluid sequestration, without obvious changes in arterial blood pressure and with additional disturbance of pancreatic and splanchnic microcirculation has been demonstrated. Moreover, according to some studies, pancreatic blood flow decreases by 73% immediately after the onset of acute pancreatitis. The resulting ischaemia is probably responsible for further derangement in acinar cells with subsequent intracellular activation of digestive enzymes by lysosomal hydrolases and for progression of mild pancreatitis to parenchymal necrosis. Another consequence of splanchnic hypoperfusion is intestinal injury with damage to barrier function with subsequent infective complications and development of multiple organ failure. It has been shown repeatedly that early fluid resuscitation can prevent these disturbances. For example, lactated Ringer solution administered intravenously at infusion rates of 6.5 mlkg−1h−1, for 4 h prevented a decrease in pancreatic blood flow in dogs with experimental pancreatitis. 2.2 Early fluid resuscitation in acute pancreatitisHypovolaemia with subsequent splanchnic ischaemia is a very important factor in the pathogenesis and progression of acute pancreatitis. All patients presenting with abdominal pain, high CRP levels and a high amylase should be considered as potentially progressing to severe pancreatitis. The patient should be admitted to a high dependency area and intensive fluid resuscitation should be started without delay according to the following scheme:
2.3 Physiology and pathophysiology with respect to nutritionPatients with mild or moderate form of acute pancreatitis may resume a normal diet within 3–7 days (Table 1). However, malnutrition may aggravate the course of the disease in its severe necrotizing form. Table 1Nutritional treatment of mild and moderate pancreatitis.
During acute pancreatitis, specific and non-specific metabolic changes occur. Under the influence of inflammatory stress and pain, the basal metabolic rate increases, leading to higher energy consumption. If acute pancreatitis is complicated by sepsis, roughly 80% of the patients are in a hypermetabolic state with an increase in the metabolic rate of 1.4–1.5 times compared to basal and large nitrogen losses of up to 20–40 g·day−1. The metabolic changes found are similar to those described in the chapters on stress starvation and trauma. The route of administration may be important. Protein or amino acids, when given parenterally, do not stimulate the exocrine pancreas, while the anatomical site of nutrient administration determines the extent of pancreatic stimulation during enteral feeding. Infusion of diets containing defined amounts of protein, peptides, or amino acids into the jejunum is also well tolerated and does not stimulate exocrine pancreatic secretory responses. In contrast, gastric and duodenal administration of proteins stimulates pancreatic secretory responses. Hyperlipidaemia is often seen in acute pancreatitis. High triglyceride levels can be a causal factor in acute pancreatitis, although moderate increases can also be a consequence of the disease. In spite of these facts, an intravenous lipid infusion does not seem to stimulate exocrine pancreatic secretion in the majority of published human studies and does not worsen the disease. It is accepted therefore, that the intravenous infusion of lipid emulsions to a patient with acute pancreatitis is safe if plasma clearance is monitored. If fat is given into the small intestine, the stimulatory effect also depends on the anatomical location of administration. Lipid infused into the duodenum is a powerful stimulus for exocrine pancreatic secretory responses; on the other hand, the same amount of lipid infused into the jejunum, either through an operative jejunostomy or through a nasojejunal feeding tube, exerts only a minimal stimulation of exocrine pancreatic secretion. Moreover, this minimal stimulation is not specific for lipids, but can be observed for all forms of jejunal food administration. Glucose metabolism in acute pancreatitis is characterized by lower glucose tolerance due to decrease in insulin sensitivity and impairment in insulin secretion due to damage to the islets. Intravenous administration of high doses of glucose therefore risks hyperglycaemia. This dysregulation can, however, only be partially corrected by exogenous insulin administration without additional risk for the inflamed pancreas. Enteral glucose administration into the jejunum is the weakest stimulus to exocrine pancreatic responses. 2.4 Consequences for nutritional supportIn the past, increasing interest has developed in defining the role of nutritional support in the management of patients with acute pancreatitis. The most controversial topics include:
Until recently, parenteral nutrition has been the standard way of providing nutrients to patients with acute pancreatitis. The evidence for intravenous feeding is however, not supported by large clinical trials. Although, several clinical studies have been performed using parenteral nutrition, only one of them has been prospective and randomized. In this study, intravenous feeding was compared with no nutritional support. The results demonstrate that intravenous nutrition did not affect the medical outcome. On the other hand, an increase in catheter-related infections was observed in the patients receiving total parenteral nutrition. A second trial comparing early total parenteral nutrition versus late total parenteral nutrition in severe pancreatitis found only a trend to a reduced mortality and the need for surgery when total parenteral nutrition was given early. These data suggest that total parenteral nutrition can be deleterious if not indicated correctly. Besides the increased risk of catheter-related sepsis, severe hyperglycaemia and other metabolic disturbances have been reported. It is clear, therefore, that overfeeding is a major risk factor for complications in patients receiving parenteral nutrition. In recent years, it has also been suggested that total parenteral nutrition may promote increased intestinal permeability and bacterial translocation. Whilst there is more evidence to support this hypothesis in animals there is only tenuous or little evidence in clinical practice. On the other hand, some studies have included a high proportion of patients with mild disease who do not need parenteral nutrition anyway and stand only to suffer from the adverse effects of parenteral nutrition. Patients with severe pancreatitis and rapidly developing malnutrition with prolonged gut dysfunction clearly need parenteral nutrition to prevent the ill effects of malnutrition. Small amounts of enteral nutrition may also be combined with supplementary parenteral nutrition. In contrast, several studies of patients with trauma, thermal injury, and major gastrointestinal surgery have shown that septic complications can be reduced when the patient receives early enteral feeding. Today, early enteral nutrition is considered an important mode of acute therapy in critically ill patients, not only to reduce catabolism and loss of lean body mass, but also to modulate the acute phase response and preserve visceral protein metabolism with the potential to downregulate the splanchnic cytokine response. In the most severe cases the consequences of a combination of prolonged fasting and catabolism can lead to a rapid decrease in body protein stores. About 20–25% weight gain due to water retention, 60% decrease in respiratory muscle function and loss of about 20% of body protein stores in 5 days has been shown. If such therapy is continued over the next 5–6 days and patient needs surgery for septic complications the next scenario is pulmonary insufficiency, requiring respirator therapy etc. In these cases one should start parenteral nutrition with small amounts of enteral nutrition into the jejunum as soon as acute shock is controlled. These patients also usually need surgery because of septic complications. Parenteral nutrition has no influence on the course of the disease, but prevents starvation, minimizes tissue loss and preserves function, thereby reducing the risks of surgery or the risk of dying from starvation if GI failure is prolonged. Several prospective randomized clinical trials have been performed comparing early enteral with parenteral nutrition in patients with acute pancreatitis. McClave and co-workers randomized patients either to total parenteral nutritional or total enteral nutrition by a nasojejunal tube in a subset of patients with mild to moderate acute pancreatitis. This study has shown that enteral feeding in mild to moderate acute pancreatitis is possible, but the outcome revealed no statistical differences in the two groups. On the other hand, patients on intravenous feeding had significantly higher glucose concentrations during the early days and the costs were significantly higher. Kalfarentzos and co-workers performed a prospective randomized trial in patients with severe acute pancreatitis. The patients were treated either enterally or intravenously within 48 hours of admission. In this study also, enteral feeding was well tolerated without adverse effects on the course of the disease. More importantly, patients who received enteral feeding experienced fewer septic complications and fewer total complications compared to those receiving total parenteral nutrition. The costs of nutritional support were also significantly higher in patients receiving intravenous nutrition. In a study by Windsor and co-workers, parenteral feeding was compared to enteral feeding and they were able to show that enteral nutrition attenuates the acute phase response in acute pancreatitis and improves disease severity and clinical outcome despite the fact that the pancreatic injuries were virtually unchanged on CT scan. Another recently published study could not confirm these data on the inflammatory response in patients with severe acute pancreatitis. Abou-Assi and co-workers showed recently that hypocaloric enteral feeding seems to be safer and less expensive than parenteral feeding and bowel rest in patients with acute pancreatitis. Unfortunately only 3% of the studied patients had severe pancreatitis. The implications of these studies are contrary to current recommendations:
2.5 RecommendationsConsidering the experiences, mentioned above, together we suggest the following nutritional regimens for mild to moderate (Table 1) and severe pancreatitis (Table 2, Table 3), together with subsequent recommendations:
Table 3Recommended dosages of nutrients in severe acute pancreatitis.
a Overfeeding should be avoided, especially in obese patients possibly according to measured REE (indirect calorimetry).
2.6 Chronic pancreatitisDuring the course of chronic pancreatitis enzyme secretion is decreased, resulting in maldigestion with steatorrhoea and azotorrhoea. Deficiencies of fat-soluble vitamins are the consequence of steatorrhoea. Pain and glucose intolerance are further factors, interfering with nutritional support. Insufficient pancreatic enzyme secretion and pain are the essential causes of malnutrition and weight loss. Dietary modification, pancreatic enzyme supplements and fat-soluble vitamins are the cornerstones of nutritional management of chronic pancreatitis. It has been suggested, that with these recommendations pain reduction can be achieved by influencing a CCK-feedback mechanism. With an adequate dietary regimen, together with enzyme preparations, in mild to moderate but not in severe disease, some pain relief has been found. Enzyme supplements are indicated when maldigestion with steatorrhoea are present. Normally 25,000–50,000 U Lipase per a main meal is necessary. The exact amount differs widely among patients. When weight loss is evident, a high caloric intake is necessary with a diet consisting principally of carbohydrate and protein. To reach the necessary caloric goal, fat must also be given. Generally, fat (50–100 gd−1) is well tolerated especially when rich in vegetable fat. Medium chain triglycerides (MCT) may be used to increase fat absorption. However, their use is often limited because they are unpalatable and because of bloating. 2.7 Dietary recommendations6–8 meals/day together with enzyme supplements are recommended. It is crucial to supply an adequate amount of calories (2500–3000 kcald−1). In malnourished patients even higher amounts are necessary. In the early phase of the disease without steatorrhoea a diet rich in carbohydrates, 70–100 gd−1 fat and 1–1.5–2 gkg−1d−1 proteins is recommended. These nutritional recommendations can be difficult to follow if overt diabetes due to endocrine insufficiency is present. Insulin treatment to control blood glucose levels is often necessary. Fat intake has to be reduced to 50–70 gd−1 if steatorrhoea is present. In some cases MCT (80–120 gd−1) can be tried. Fat-soluble vitamins must be given if specific deficits are documented. Antioxidants (e.g. Selenium, Vitamin C, E and l-Methionin) can be given. However, the beneficial effects are controversial. 2.8 Enteral and parenteral nutrition in chronic pancreatitisWhen a patient is not able to eat (pain or pyloroduodenostenosis, due to an enlarged pancreatic head or pseudocyst formation), enteral nutrition should be instituted, using a tube introduced beyond the stenosis into the jejunum. Polymeric formulae can be used, and are usually well tolerated. Only a minority of patients need oligomeric formulae. TPN must be instituted when gastric emptying is blocked or the patient needs gastric decompression and when a double lumen tube cannot be introduced in the jejunum. In rare cases a laparoscopically inserted needle catheter jejunostomy can be used in such patients. As patients with chronic pancreatitis often suffer not only from protein energy malnutrition but multiple electrolyte, mineral and micronutrient deficiencies, these should be corrected. 3. SummaryThe past clinical emphasis on the need for »gut rest« in order to decrease pancreatic stimulation has to be revised. The nutritional management of patients with acute pancreatitis is now guided by five main principles:
Fluid resuscitation is necessary in any form of acute pancreatitis. Aggressive nutritional enteral or parenteral support is not required for mild to moderate forms of acute pancreatitis. The use of early enteral feeding in patients with severe disease can decrease the incidence of nosocomial infections, the duration of the systemic inflammatory response and the overall disease severity. Therefore if tolerated, early enteral nutrition is strongly recommended in these patients. However, when the nutritional goal cannot be achieved by using enteral nutrition, parenteral nutrition must be instituted. This can be combined with small amounts of enteral nutrition. The use of lipid emulsion in TPN was shown to be safe without aggravation of the disease. Dietary recommendations, pancreatic enzyme supplements and fat-soluble vitamins are the cornerstones of the nutritional management of chronic pancreatitis. The diet should consist of carbohydrate and protein, but to reach the caloric goal fat must be given. 50–100 gd−1 is often tolerated. However, if steatorrhoea is present a reduction to 50–70 gd−1 is necessary. MCT can also be tried in this situation. Only a minority of patients need enteral or parenteral nutrition. Conflict of interestThere is no conflict of interest. Article InfoPublication HistoryPublished online: August 25, 2009 Accepted: June 4, 2009 Received: June 4, 2009 IdentificationDOI: https://doi.org/10.1016/j.eclnm.2009.06.014 Copyright© 2009 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Inc. All rights reserved. ScienceDirectAccess this article on ScienceDirect
Related ArticlesWhat is the first line treatment for pancreatitis?Treatment strategies for acute pancreatitis include fasting and short-term intravenous feeding, fluid therapy, and pain management with narcotics for severe pain or nonsteroidal anti-inflammatories for milder cases.
What is the nutrition management for pancreatitis?To best achieve those goals, it is important for pancreatitis patients to eat high protein, nutrient-dense diets that include fruits, vegetables, whole grains, low fat dairy, and other lean protein sources. Abstinence from alcohol and greasy or fried foods is important in helping to prevent malnutrition and pain.
What is the most important intervention for acute pancreatitis?Core tip: Acute pancreatitis is a frequent and potentially life-threatening disease. Therapy is currently mostly symptomatic with fluid resuscitation, pain management, and early oral feeding. Vigorous fluid resuscitation remains a cornerstone of early management of acute pancreatitis.
When should nutritional support be started in patients with acute pancreatitis?Regarding optimal timing of starting nutrition, ESPEN guidelines recommend starting nutrition within 24–72 h of admission. According to AGA, early feeding is not successful in all AP patients due to pain, vomiting, or ileus, and feeding may need to be delayed beyond 24 h in some cases [27,29,30].
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