Nutrition Management in Acute Pancreatitis
Vol. 28, Issue 4 (December 2023)
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Andrea Kulyk, MD, FRCPC
Advance Nutrition Support Fellow
University of Alberta
Edmonton, Alberta, Canada |
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Donald Duerksen, MD, FRCPC
Associate Professor of Medicine
Section Head Gastroenterology
University of Manitoba
Winnipeg, Manitoba, Canada |
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Introduction
Acute pancreatitis (AP) is an inflammatory-mediated condition of the pancreas with varying degrees of severity. Diagnosis of acute pancreatitis requires two of three features: (1) typical abdominal pain; (2) elevation of serum lipase or amylase at least three times above upper limit of normal; and (3) characteristic findings on imaging (computed tomography (CT), magnetic resonance imaging (MRI), or transabdominal ultrasonography (US)). Given the escalating incidence of AP and elevated mortality rates in those with moderate to severe pancreatitis, there has been increasing attention to optimizing management strategies.1, 2 At present, there are no pharmacologic therapies effective at reducing pancreatic inflammation. The management of acute pancreatitis focuses on supportive care, in which nutrition optimization plays a critical role. One of the more recent advances in the management of acute pancreatitis relates to the role of enteral nutrition (EN) in improving the outcome of acute pancreatitis.
Pathogenesis of acute pancreatitis and potential mechanism of benefit of enteral nutrition
The pathogenesis of AP involves upregulation of proinflammatory cytokines, reactive oxygen species and catabolic stress.3 As part of the inflammatory response, metabolic demand increases resulting in a catabolic state, particularly in those with severe AP. In addition, reduction in intestinal blood flow can lead to increased mucosal permeability, thus becoming a mechanism for increased bacterial translocation and infectious complications.4
The traditional nutrition management of acute pancreatitis focused on “resting” the gastrointestinal tract and pancreas. The intent was to diminish liberation of activated pancreatic enzymes and the resulting tissue destruction and local inflammatory response. However, since then, there is accumulating evidence that use of the gastrointestinal tract is not only safe and well tolerated but associated with improved outcomes compared to supporting nutrition with parenteral nutrition (PN). The mechanism of this benefit of enteral nutrition could relate to maintaining the integrity of the gut mucosal barrier, stimulating intestinal motility, improving splanchnic blood flow, and preventing bacterial overgrowth and translocation.
Nutrition management
Nutritional management has evolved over the past several decades as more evidence has accumulated regarding optimal mode, timing, and composition of nutrition therapy.
Mode of nutrition support: enteral versus parenteral nutrition
In response to the hypothesis that EN would be tolerated and could improve outcomes in acute pancreatitis, a number of randomized control trials (RCT’s) have compared EN (with defined liquid formulae) to PN in mild and severe AP. 12 RCT’s and 11 systematic reviews have demonstrated EN is well tolerated, and improved outcomes include multi-organ failure, local complications, and mortality.5 Furthermore, PN subjects patients to the additional risks of venous thrombosis and central line-associated bloodstream infection. As such, priority should be given to EN, with PN as a second-line therapy if enteral is either not tolerated or not feasible.6
Based on the aforementioned data, both the American Gastroenterology Association (AGA) and European Society of Parenteral and Enteral Nutrition (ESPEN) have recommended patients with AP who are unable to feed orally should be started on EN, as opposed to PN.
Timing of nutrition support: early versus delayed feeds
Historically, oral feeds were not initiated until abdominal pain and electrolytes normalized, with patients being kept nil per os (nothing by mouth), allowing the pancreas to “rest.” As discussed above, the rationale for this strategy was that by reducing stimulation of pancreatic proteolytic enzyme secretion, there would be a reduction in pancreatic autodigestion and inflammation.7 However, there is no supportive data to this effect, and in fact, enzyme secretion may be “stunted” in AP.3, 7, 8
Subsequent studies have shown that early EN within 24-72 hours is both feasible and safe. A meta-analysis comparing early versus delayed EN in critically ill patients showed a significant difference in both mortality and infectious complications favouring early EN, however, studies focusing only on those with AP showed no difference in outcomes, apart from an increased rate of intervention for necrosis in the fasting group.9, 10 It is purported that timely administration of enteral feeds, “maintains gut function, mitigates dysfunction, and restores normal gut function,” giving rise to the concept of “gut rousing.”11
The most recent evidence examining feeding early (within 24-48 hours) shows disparate results. An RCT comparing early (within 24 hours) nasoenteric feeding to oral diet (at 72 hours) did not show a significant difference in either infection or mortality.12 These results may be due too many patients in this study not having severe or necrotizing AP. In contrast, a meta-analysis demonstrated mortality benefit when EN was started within 24 hours, compared to 24-72 hours.13 Despite some heterogeneity of results, current guidelines suggest EN be ideally initiated within 24 hours of admission, but no later than 72 hours.5
Mode of nutrition support: nasogastric versus nasojejunal feeds
With increasing evidence to avoid bowel rest and use the gastrointestinal tract in AP, debate has grown as to whether nasojejunal (NJ) feeds had superior outcomes to nasogastric (NG). The mechanistic rationale was to administer EN distal to the mid-jejunum, thus avoiding stimulating pancreatic enzyme secretion. Three RCT’s have shown no difference with respect to tolerance, complications, or mortality when comparing NG to NJ feeding for AP. A Cochrane and technical review addressed this question and demonstrated no difference in mortality, organ failure, infection rate, or exacerbation of pain, however, results were insufficient to draw conclusions as to whether one was superior to the other.10, 14 At present, either NG or NJ routes can be utilized for enteral feeding, however, NG is more readily available, can be inserted at the bedside, and thus is preferred in many institutions. It is estimated at least 15% of patients with severe AP will be intolerant of nasogastric feeding and will require a trial of NJ feeding.
Type of enteral nutrition: elemental versus polymeric formulae
The type of EN initially provided should be dependent on the absorptive capabilities of the digestive tract; those without evidence of malabsorption and a functioning gastrointestinal tract should be started on polymeric formulas. While initial studies with enteral feeding in AP were performed using elemental enteral formulae, subsequent studies have shown equivalent results with polymeric formulae. Polymeric formulae also have the advantage of being cheaper that elemental or semi-elemental formulae. While polymeric formulae would therefore be considered the enteral formula of choice, if there is concern of malabsorption, which may occur in severe pancreatic necrosis, or if there is altered gastrointestinal anatomy, elemental or partially hydrolyzed formulas should be given.
Management based on severity
Mild AP
Many AP cases are mild. Given that up to 80% can be successfully transitioned to an oral diet within a week of admission, the role of synthetic enteral and parenteral in mild AP is limited.3, 15 Adjunct supportive therapies such as antiemetics, prokinetics, and antidiarrheals can be considered to enhance enteral tolerance.3 It is also recommended to offer oral feeding as soon as clinically tolerated, and independent of serum lipase concentrations in patients with predicted mild AP.5
Severe AP
Severe AP poses specific challenges for nutrition optimization. Severity of emesis, ability to tolerate feeding by mouth, level of alertness, respiratory status, and gut dysfunction may all be altered, limiting the options in providing nutrition. Furthermore, a hypermetabolic, inflammatory state can predispose to rapid nutritional deterioration, and puts patients at high nutritional risk, highlighting the importance of addressing nutrition early in the disease course once severe AP has been predicted.3, 5
As discussed above, early EN is the preferred nutrition management strategy in most patients with severe AP, with PN reserved as a second-line therapy if EN is either not tolerated or not feasible.6
Pancreatic enzyme replacement should be considered in those with necrotizing pancreatitis and those with a prolonged disease course, especially in the presence of significant diarrhea, steatorrhea, weight loss, and other objective evidence of fat malabsorption.5 pH-sensitive enteric coated microspheres are the preparation of choice.5
Special diets and nutrients
Various diets have been studied in AP. These diets include clear fluids, low-fat, normal fat, liquid/soft/solid consistencies, and escalating/initial full diet. Overall, there appears to be supportive evidence in starting patients on any of the above diets as their initial meal for refeeding. In fact, one study demonstrated initially starting with a full solid diet in mild AP was well tolerated, did not result in significant abdominal pain relapse, and resulted in shorter length of hospital stay.16 If patients are reporting early satiety and post-prandial fullness, a low-fat diet can be considered to reduce the amount of delayed gastric emptying from dietary fat.
Additives to enteral nutrition such as arginine, glutamine, and omega-3 fatty acids are being investigated as having a potential immunogenic role in severe AP, however, there is currently insufficient evidence to support its routine use in severe AP.3 Similarly, given the gut dysbiosis seen in persons with AP, probiotics have been explored as a potential immunotherapy.8 Unfortunately, there are a limited number of studies exploring probiotics, and the multi-centre RCT (PROPATRIA trial) demonstrated higher mortality in the enteral probiotic group.17 Currently, the prophylactic use of probiotics is not recommended.5
A number of nutritional deficiencies and derangements are often seen in the setting of AP including, but not limited to: protein calorie malnutrition, malabsorption due to pancreatic exocrine insufficiency, and deficiencies in vitamins B12, A and D, folic acid, and zinc.5 Supplementation with vitamins and micronutrients should be considered, particularly in those that have a prolonged course, or demonstrate objective deficiency.
Citations:
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