Year: 2019
Type: editorial
Abstract: There has been much debate in clinical practice about the delivery of nutrition in patients who have active inflammatory disease of the pancreas. Due to the incredible complexity of this disease process, issues in the management of pancreatitis involve virtually all aspects of clinical nutrition and tax the skill set of the nutrition specialist. Beginning with nutrition assessment, the determination of nutrition risk plays a key role in the direction nutrition therapy will take in these patients. A patient with mild to moderate pancreatitis will be managed much differently than the patient with severe disease.1 Patients with mild or moderate risk can often be managed on the standard hospital unit, supported by fluid resuscitation and analgesia, and encouraged to eat orally when tolerance permits.2 Those patients with severe pancreatitis require a higher level of care in the intensive care unit and more often need aggressive nutrition therapy via an enteral access device with provision of an enteral formulation. The unpredictability of whether nutrition risk will worsen or improve over the early phases of critical illness necessitates close monitoring. Recent literature has focused on gastrointestinal dysfunction and feeding intolerance, which is common in patients with severe pancreatitis and may be caused by ileus, intestinal ischemia, enlarging pseudocyst impinging on the duodenal C-loop, or gut wall edema.3 Proper fluid management with early aggressive volume resuscitation over the first 12 hours followed by more conservative goal-directed therapy can help limit the consequences of third spacing of fluid that is so often associated with acute severe pancreatitis. Aggressive early enteral feeding helps attenuate the ileus, decrease the chances for bowel wall edema, reduce intra-abdominal pressure, and prevent abdominal compartment syndrome.4 Route selection, whether it be oral, parenteral nutrition (PN), or enteral nutrition (EN), can be difficult with acute pancreatitis. While current guidelines recommend a standard polymeric formula, this decision is not straightforward, and extenuating circumstances might warrant alternative formulas.5 Several small randomized trials in the past have suggested improvement in outcomes from use of an arginine/fish oil immune-enhancing formula.6-8 While a signal of benefit was too weak to be captured by meta-analysis,9 further studies might be required before ruling out this treatment option. In an environment of exocrine pancreatic insufficiency (EPI) with reduced intraluminal pancreatic enzymes,10 absorption may be enhanced by switching to a formula with small peptides and medium-chain triglycerides or use of an enteral in-line lipase cartridge, arguably a better strategy than adding pancreatic enzymes delivered by the tube. Depending on the severity of the ileus, there are some patients who will require PN. Monitoring tolerance to enteral feeding is more complex in severe acute pancreatitis vs milder forms of pancreatitis. As for any critically ill patient, clinicians must watch for hypoactive bowel sounds, abdominal distention, and failure to pass stool and gas, and any other signs of ileus and intestinal dysmotility which may limit advancement of feeding. Patients with pancreatitis, however, have the added dynamic of whether the EN is stimulating an inflamed pancreas. In this respect, clinicians must determine whether the enteral feeding is increasing output of pancreatic enzymes alone, increasing symptoms of nausea, vomiting, and abdominal pain, or at worst exacerbating the systemic inflammatory response syndrome (SIRS). Use of probiotics should be considered for any critically ill patient, but such a strategy is very controversial in severe acute pancreatitis. A well-designed multicenter trial showed increased morbidity with aggressive use of fiber and probiotics delivered directly into the small bowel.11 However, 5 other trials included in a meta-analysis showed improvement in outcomes from use of probiotics in severe acute pancreatitis, suggesting a benefit value from a more conservative approach.12 Critical decisions like this highlight the importance of the clinical nutrition specialist involved in the management of the patient with pancreatitis. Pancreatitis as a disease process is the consummate example of the role the gut plays in attenuating or exacerbating disease severity.13 Auto-regulatory defects in the local and systemic circulation lead to a classic model of ischemia/reperfusion injury, which raises the level of oxidative stress and injures the intestinal mucosa.14 This process contributes to intestinal failure and is responsible for necrosis within the gland. EN stimulates blood flow to the splanchnic circulation, and may help prevent these complications. Breakdown of gut integrity may lead to increased permeability, bacterial translocation, and seeding of pancreatic necrosis. Immune dysregulation and “gut sepsis” has been documented in severe acute pancreatitis, and is clearly caused by breakdown of gut defenses and a change in the cross-talk immune signaling between the epithelium and the intraluminal bacteria.15 This phenomenon is likely worsened by failure or inability to provide early EN. Thinning of the mucus layer leads to penetration of the intestinal mucosa and its autodigestion by pancreatic enzymes. These enzymes are then transported into the intestinal lymphatics creating toxic lymph, which ultimately passes into the systemic circulation causing multiple organ failure at distant sites.13 Conversion of a commensal microbiome to a virulent pathobiome contributes further to multiple organ failure and worsens clinical outcomes through loss of biodiversity and antibiotic resistance. Many aspects of routine management in pancreatitis worsen these changes through provision of opioid narcotic agents which stimulate virulence, antibiotic prophylaxis which reduces biodiversity, and feeding by PN which creates an absence of luminal nutrients in the area of greatest microbial burden (i.e., the colon).13 Designing a nutrition regimen that supports gut barrier defense and the microbiome with soluble prebiotic fiber, use of probiotics, and provision of an enteral formulation helps prevent these complications and promotes a pattern of recovery and homeostasis for the patient.16, 17 The current supplement highlights many issues the clinical nutrition specialist deals with in patients with pancreas disorders. There are articles that deal with nutrition management of both acute and chronic pancreatitis. The nutrition strategies used in these patients is significantly different and can challenge clinicians. Building on these articles is a discussion of some of the pathophysiological factors that can worsen acute pancreatitis and theorizes how we can develop novel therapies. The final two articles focus on two specific disease states; pancreatic insufficiency in children and non-alcoholic fatty pancreatic disease (NAFPD). We would like to thank Alcresta for their financial support of the supplement. We would also like to thank the staffs of Nutrition in Clinical Practice and Wiley without who this publication would not have been possible. We hope the readers of Nutrition in Clinical Practice enjoy this special supplement. Financial disclosure: Financial support for the publication of this supplement in which this article appears was provided by Alcresta Therapeutics, Inc.
Source: Nutrition in Clinical Practice
DOI: 10.1002/ncp.10402
Authors: Ryan T. Hurt, Stephen A. McClave
Institution: University of Louisville
Language: English
Subfield: Nutrition and Dietetics
Field: Nursing
Domain: Health Sciences
Open Access status: bronze
Funder: University of Louisville
OpenAlex ID: W4232299662