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Front Page : Library : IVECCS 2009 : Nutrition : Nutrition & Pancreatitis Back to Nutrition Back to Table of Contents
Nutrition and Pancreatitis: Changing Paradigms INTERNATIONAL VETERINARY EMERGENCY AND CRITICAL CARE SYMPOSIUM 2009 Daniel L. Chan, DVM, DACVECC, DACVN, MRCVS The Royal Veterinary College, University of London, North Mymms, UK
INTRODUCTION
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Pancreatitis is a common disease affecting both dogs and less so in cats. Acute pancreatitis is more easily recognized in dogs as there appears to be a consistent clinical syndrome, albeit with varying degrees of severity. In cats, pancreatitis is a much more challenging diagnosis to make as some of the clinical signs are quite vague. In both dogs and cats, the underlying cause of pancreatitis is often unclear, but a number of factors have been implicated. In dogs, these include obesity, dietary indiscretion, hyperlipidemia (either idiopathic or dietary), drugs (e.g., phenobarbital and potassium bromide therapy, azathioprine), toxins (zinc, cholinesterase-inhibitor insecticides), pancreatic duct obstruction, trauma, and ischemia/reperfusion injury. In cats, risk factors are not as well described but include concurrent diseases such as Inflammatory Bowel Disease, and hepatobiliary disorders. Clinical findings vary from mild to severe, and may include vomiting, abdominal pain, inappetance, dehydration. In more severe cases, such as animals with necrotizing acute pancreatitis, manifestations of hypovolemia and systemic inflammatory distress syndrome can be seen. Chronic or recurrent pancreatitis may ultimately result in exocrine pancreatic insufficiency and/or diabetes mellitus.
TRADITIONAL APPROACH The traditional approach to acute pancreatitis was based on the premise that one could reduce pancreatic autodigestion by decreasing pancreatic enzyme release. However, the pathogenesis of pancreatitis more likely involves intracellular premature activation of proteolytic enzymes rather than pancreatic stimulation. Avoidance of feeding as a means to decrease pancreatic stimulation may be unwarranted as this could result in malnutrition. Studies have demonstrated that inflamed pancreas actually do not respond to stimuli in the same fashion and do not "autodigest" if stimulated. Avoidance of feeding may be useful as this decreases abdominal pain and vomiting. More important goals for managing patients with pancreatitis should include maintaining or restoring adequate tissue perfusion, and correcting electrolyte and acid-base imbalances. Much has been made of the role of pancreatic enzyme secretion being triggered by several gastrointestinal hormones including gastrin, secretin, and cholecystokinin (CCK); with CCK being the most potent stimulator of pancreatic secretions. The release of CCK is normally triggered by long chain fatty acids, and amino acids. However, as previously mentioned, these events may not be applicable with pancreatitis.
NUTRITIONAL SUPPORT In most cases of mild pancreatitis (e.g., clinical signs resolve with conservative management) dietary intervention may not be required. Unless serum triglycerides are particularly elevated, diets restricted in fat are not always necessary, albeit unlikely to be harmful. The use of high fibre diets in cases of pancreatitis is of questionable rationale, except that most fibre-rich diets are low in fat. The benefit of adding pancreazyme to the food as a way of triggering a negative feedback loop and decrease pancreatic secretion is also unfounded. In cases of severe pancreatitis, where vomiting and abdominal pain is intractable, parenteral feeding may be indicated. Although most animals should have food and water withheld initially in the management of acute pancreatitis, no animals should have food withheld for more than 5 days. Parenteral nutrition (PN) typically involves a mixture of concentrated glucose, amino acids and lipids. For many years PN has been regarded as particularly complicated, very expensive and associated with a high risk of infection and gut atrophy, with subsequent increased the risk of bacterial translocation and sepsis. Based on the data of all studies on PN in animals do not indicate a high risk for infection or sepsis. Even when septic complications are encountered, most of these
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related to catheter infections and overt sepsis resulting from PN has not been reported in any study. Bacterial translocation resulting from gut atrophy is another very difficult phenomenon to clinically demonstrate. Based on the various veterinary studies, the median time of PN administration has been less than 5 days. Studies in people showing detrimental effects of PN (or lack of enteral nutrition) often describe individuals receiving PN for greater than 2 weeks. Although compounding PN solutions requires specialized care and is limited to referral centres, ready-made amino acid/glucose solutions could be used in practice as interim solutions until the animal can tolerate either placement of feeding tubes or start taking food orally. The use of ready-made PN unfortunately only meets a portion of energy requirements when administered at maintenance fluid rates (typically 40% of Resting Energy Requirements) and should not be used for more than 3-5 days. The author formulates PN solutions for dogs and cats with 5-6 grams of protein per 100 kcal, with the remainder of energy requirements provided by fat and dextrose. There is no evidence to suggest that high lipid PN solutions are detrimental in the management of canine or feline pancreatitis. Patients receiving PN do require dedicated intravenous catheters (preferably central catheters) for PN administration. To date, there is no data suggesting that the use of PN in animals with pancreatitis is detrimental when used appropriately. What has been established is that enteral feeding, when possible, is preferred for the treatment of pancreatitis. In people, feeding through naso-jejunal tubes achieves better results compared with patients treated with PN. In experimental canine models, similar benefits have been demonstrated. Based on these findings, most authors recommend enteral feeding over PN. However, there are a few major differences that must be considered in deciding whether to feed dogs and cats with pancreatitis enterally. In people, the standard manner for placement of jejunal tubes is non-invasively and without general anesthesia. This is extremely difficult in animals. A technique for placement of naso-jejunal tubes using fluoroscopy in dogs has been described but has not been widely adopted. Jejunal tubes have also been placed through gastrostomy tubes endoscopically, but this still requires general anesthesia. Virtually all animals with jejunostomy feeding tubes have the tube placed surgically. In many critically ill animals, especially those with hypotension, general anesthesia is relatively contra-indicated unless a surgical indication (e.g., pancreatic abscess, biliary obstruction, peritonitis) exist. Even in these situations, prolongation of general anesthesia for placement of feeding tubes is questionable. In cats acute pancreatitis is not typically associated with vomiting and therefore withholding food is not part of standard care. In cats, placement of feeding tubes such as naso-esophageal or esophagostomy tubes are quite useful. In cases where patients become hypotensive, enteral feeding should be discontinued until adequate pressures are restored. Feeding patients that are cardiovascularly unstable increases rates of complications such as ileus, vomiting, and diarrhea.
ADVANCEMENTS
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NUTRITIONAL SUPPORT
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The acute phase reactant, C-reactive protein (CRP), is produced by the liver and is reliably detected in serum in response to inflammation, infection, or tissue trauma. CRP synthesis is induced by cytokines such as tumor necrosis factor, interleukin-1 and interleukin-6, which are hallmarks of systemic inflammation. CRP is currently the gold standard serum marker for predicting the severity of disease in human acute pancreatitis. The sensitivity and specificity of CRP in predicting pancreatic necrosis have also been reported to be greater than 80%. In dogs, CRP has been evaluated in a variety of conditions, including pancreatitis. While typical endpoints in pancreatitis studies usually evaluate rates of complications, length of hospitalization, and mortality, more recent studies have evaluated surrogate markers of pancreatic necrosis such as CRP, especially in respect to response to therapy. Serial evaluation of CRP provides a novel approach in monitoring patients with pancreatitis, especially in respect to improvement of the condition. An observational study of dogs with naturally-occurring acute pancreatitis documented significant decrease in serum CRP at 5 days after entry into the study, demonstrating clinical feasibility of serially monitoring CRP in dogs with acute pancreatitis. Monitoring CRP serially and relating changes to response to therapy has also been recently evaluated in dogs being treated with IBD, and could become a similarly useful tool in evaluating treatment of pancreatitis in dogs. Developments in the area of critical care nutrition have been particularly exciting, as nutritional therapies have been shown to positively impact outcome beyond simply proving energy and nutrients. Use of specific nutrients in the care of critically ill human patients, including those with
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acute pancreatitis, is becoming quite common with increasing evidence of their benefits with little risk of complications. Of particular interest are the changes in glutamine metabolism associated with critical illnesses. Despite glutamine efflux from skeletal muscle during critical illness, glutamine consumption exceeds glutamine production, resulting in a marked depletion of plasma and tissue glutamine concentrations. This overall depletion of glutamine has been correlated with increased morbidity and poor survival. Glutamine deprivation leads to cellular energy depletion, attenuation of the gastrointestinal barrier, increased risk of bacterial translocation, disturbed immune-function, along with reduced levels of the antioxidant glutathione. These cellular changes are believed to be key events contributing to organ dysfunction and increased mortality and many of these parameters have been shown to improve upon supplementation with glutamine. The pancreas is also the organ with the highest protein turnover and therefore particularly sensitive to negative nitrogen balance. In vivo studies in animals and humans have demonstrated the highest uptake of intravenously infused 11C-labelled glutamine in the pancreas, suggesting an important role of glutamine in the pancreas. Glutamine supplementation in animals have also resulted in prevention of atrophy of pancreatic acinar cells and improvement in pancreatic exocrine function. As further evidence supporting the importance of glutamine in pancreatitis, animal models of acute necrotizing pancreatitis have demonstrated improved preservation of gastrointestinal integrity and significant reduction in pancreatic necrosis and infection when TPN was supplemented with glutamine. Moreover, human patients with acute pancreatitis treated with glutamine-enriched total parenteral nutrition (TPN) demonstrated significant improvement in CRP, as well as decreased dependence on TPN, reduced infectious complications, improved circulating albumin and lymphocyte counts, and reduced length of hospitalization. Despite these exciting developments, the use of pharmaconutrition in veterinary patients is in its infancy. Previous trials evaluating enteral glutamine in models of enteric injury and radiation therapy have not been successful. It is possible that the dose of glutamine used in these small studies were inadequate to demonstrate a beneficial effect. Additionally, parenteral glutamine, which has not been thus evaluated in veterinary patients, may be more effective than enteral glutamine. On-going trials are evaluating the effect of parenteral glutamine in canine pancreatitis.
SUMMARY Nutritional therapy in animals with acute pancreatitis is focused on ensuring prevention or reversal of malnutrition. Prolonged food deprivation to alleviate pancreatic stimulation is completely unnecessary. Pain and nausea should be aggressively treated and only in patients that cannot tolerate enteral nutrition should PN be instituted. Placement of feeding tubes such as esophagostomy, gastrostomy or jejunostomy tubes should be pursued if at all possible, as enteral feeding is not contraindicated in pancreatitis. In the future, nutritional therapies aimed at improving disease resolution by decreasing pancreatic inflammation may be possible. Currently, parenteral glutamine is being evaluated as a possible aide in the treatment of canine pancreatitis. Other nutrients may also impart beneficial effects. References 1. Holm, JL, Chan DL, Rozanski EA. Acute pancreatitis in dogs. J Vet Emerg Crit Care 2004; 13:201-213. 2. Hess RS, Saunders HM, Van Winkle TJ, et al. Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in dogs with fatal acute pancreatitis: 70 cases (1986-1995). J Am Vet Med Assoc1998; 213: 665-670. 3. Hess R, Kass P, Shofer F, et al. Evaluation of risk factors for fatal acute pancreatitis in dogs. J Am Vet Med Assoc 1999; 214(1): 46-51. 4. Chan DL, Freeman LM, Labato MA, et al. Retrospective evaluation of partial parenteral nutrition in dogs and cats. J Vet Intern Med 2002; 16: 440-5 5. Freeman LM, Labato MA, Rush JE, et al. Nutritional support in pancreatitis: A retrospective study. J Vet Emerg Crit Care 1995;5:32-41 6. Holm JL, Rozanski EA, Freeman LM, et al. C-reactive protein concentration in canine acute pancreatitis. J Vet Emerg Crit Care 2004;14:183-186. 7. Qin HL, Su ZD, Gao Q, et al. Early intrajejunal nutrition: Bacterial translocation and gut barrier function of severe acute pancreatitis in dogs. Hepatobiliary Pancreat Dis Int 2002: 1: 150-4. 8. Qin HL, Su ZD, Hu LD, et al. Parenteral versus early intrajejunal nutrition: effect on pancreatic natural course, entero-hormones release and its efficacy on dogs with acute pancreatitis. World J Gastroenterol 2003; 9: 2270-3.
SPEAKER INFORMATION (click the speaker's name to view other papers and abstracts submitted by this speaker)
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Daniel L. Chan, DVM, DACVECC, DACVN, MRCVS
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