Nutrition in Acute Pancreatitis

Nutrition in Acute Pancreatitis

A 55-year-old previously healthy lady was admitted with pancreatitis secondary to gallstones. Her admission modified Glasgow Score was 4, and CT scan showed approximately 70% necrosis of the pancreas encompassing the neck, body and tail with sparing of the head. She rapidly developed ARDS, AKI and vasoplegia, and subsequently developed abdominal compartment syndrome requiring decompressive laparotomy. Her later complications included intraabdominal collections requiring percutaneous drainage, upper GI bleeding, and staged closure of her laparostomy. She was initially commenced on enteral NG feeding but developed high NG aspirates despite pro-kinetics. Parenteral nutrition (PN) was commenced in combination with a ‘trophic’ enteral feed. Four weeks into her admission her triglyceride level was found to be elevated, necessitating lipid free PN and cessation of propofol. This led to a drop in her triglyceride level.

How should we manage the provision of nutrition in acute pancreatitis?

Akshay Shah
The metabolic response to the stress of critical illness

The metabolic response to stress is a complex process involving neuroendocrine, inflammatory and immune components.
The net effects of the metabolic response are uncontrolled catabolism, insulin resistance, increase gluconeogenesis and lipolysis, stress hyperglycaemia and net loss of lean body mass. Stress hypergylcaemia resets glucose homeostasis, allowing a higher blood glucose diffusion concentration gradient and maximizes cellular glucose uptake in conditions of altered microvascular flow. (2)

Other physiological responses include hyperthermia and an increase in cardiac output, both of which lead to an increase in energy expenditure (EE). EE elevations of 10-15% are frequently seen in patients with severe infection and trauma and the greatest increases are seen in patients with uncontrolled sepsis +/- ARDS and in severe burns. Conversely, sedation, muscle relaxation/paralysis and physical immobilization reduce EE by 15-20%. (3) Therefore, ICU care can have a significant effect on the metabolic response.

The rationale for nutrition in critical illness

Critical care patients are often unable to feed independently by mouth for variable periods of time due to a variety of reasons such as mechanical ventilation, extensive gastrointestinal surgery, and polytrauma. If not nourished, an energy deficit accumulates that eventually contributes to lean tissue wasting, skeletal-muscle wasting and generalized weakness – all of which are associated with adverse outcomes such as increased critical care length of stay, incidence of infections and risk of death.(4) Nutritional status is also a major determinant of the response to critical illness, maintenance of gut and lung function and wound healing.

Nutrition in Acute Pancreatitis
Acute pancreatitis is a common surgical condition that ranges from a systemic inflammatory response syndrome with recovery in a few days to multi-organ dysfunction syndrome and death. Necrotizing pancreatitis is associated with a mortality of 15%.(5)

Cornerstones of management are good supportive care, pain relief, and treatment of infection. Indications for surgery include infected pancreatic necrosis when percutaneous techniques are not an option, abdominal compartment syndrome and severe retroperitoneal haemorrhage.(6)


Exacerbating factors contributing to poor nutritional intake include pain, ileus, and gastric atony. In addition, patients with excessive alcohol consumption often have pre-existing protein-calorie malnutrition (PCM) and micronutrient deficiencies. Therefore, the risk for deteriorating into a net negative energy and protein balance is high. In severe pancreatitis, the negative nitrogen balance can be as high as 40

Traditionally, starvation was regarded as the most appropriate response to treat pancreatitis in order to prevent any stimuli for exocrine pancreatic function – ‘pancreatic rest’. In mild acute pancreatitis, nutritional support is often unnecessary if the patient is able to restart an oral diet after 5-7 days. Parenteral nutrition (PN) used to be the standard way of providing nutritional support in severe pancreatitis as it allowed ‘pancreatic rest’. However, this has never been shown to affect local inflammatory processes or affect patient outcome.(3)

Complications of enteral and parenteral routes are highlighted in Table 1.(9, 18)

Table 1.

• Independent risk factor for ventilator-associated pneumonia
• Oesophageal trauma related to tube insertion
• Risk of misplaced NG tube into the trachea
• Aspiration
• Diarrhoea
• Metabolic – hypergylcaemia, electrolyte abnormalities
• Refeeding syndrome


•Catheter-related sepsis
• Electrolyte disturbances – hypophosphataemia, hypokalaemia and hypomagnesaemia especially in the first 24-48 hours.
• Hyperchloraemic metabolic acidosis
• Rebound hypoglycaemia
• Refeeding syndrome
• Deranged liver function due to hepatic steatosis, intrahepatic cholestasis and biliary sludging.
• Trace element deficiencies.

There is a reasonable body of evidence supporting the use of EN over PN in acute pancreatitis. Meta-analyses (11,12,13) have consistently shown that EN significantly reduces mortality, multi-organ dysfunction, and systemic infection compared to PN.

Nasojejunal (NJ) feeding is thought to be physiologically ideal as nutrients infused into the jejunum have minimal effect on pancreatic exocrine secretion. However, two meta-analyses(10,12) of patients with severe predicted and/or acute pancreatitis showed that nasogastric (NG) feeding was not inferior to NJ feeding with regards to mortality, tracheal aspiration, pain, and meeting energy balance.

Based on current available evidence, enteral feeding via either NG or NJ routes should be considered as first-line for nutritional support in patients with acute pancreatitis. PN should be considered in patients in whom EN feeding cannot be achieved (intestinal obstruction, extensive necrosis, intolerance).

A recent meta-analysis consisting of 11 studies containing 775 patients with acute pancreatitis, including those with severe acute pancreatitis, showed that early EN within 48 hours of admission was associated with significant reductions in all-infectious complications, catheter-related septic complications, pancreatic infection, hospital length of stay and mortality.(14)

Another RCT, not included in the above meta-analysis, showed that early EN (within 48 hours) significantly moderated the immune response by reducing the incidence of multi-organ dysfunction syndrome, systemic inflammatory response syndrome, pancreatic infection and ICU length of stay. (15)

Guidelines recommend the use of early (within 48 hours) EN in all patients with acute severe pancreatitis.(16)

Types of feed
There is a wide range of enteral feeds available, which vary widely in composition. They can be broadly divided into:(18)
• Polymeric feeds – contain intact proteins derived from whey, meat, soy and carbohydrates in the form of oligo- and polysaccharides. These require pancreatic enzymes for absorption.
• Elemental feeds – contain defined/ ‘part-digested’ nitrogen sources (amino acids or peptides), fatty acids and glucose which can enable feeding with small bowel absorption is impaired e.g. pancreatic insufficiency.
• Electrolyte variable – sodium and potassium-restricted formulations are available.

Acute pancreatitis
Resting EE in pancreatitis can be increased by 5-20%. Despite the physiologic rationale that elemental feeds may be beneficial in pancreatitis, a large meta-analysis showed that there is no specific type of EN that improves outcomes in pancreatitis.(19) Guidelines recommend that either elemental or polymeric feeds can be used.(20) Polymeric solutions may be preferred as they are cheaper. EN should be provided through a continuous 24-hour pump.(20) Overfeeding in the early stages should be avoided and can results in intestinal distension which can worsen gut ischaemia.(3)
Parenteral nutrition should be administered as in other critical care patients and supplemented with glutamine.(20) If nutritional targets aren’t met solely by EN, a combination approach of PN and EN should be considered. If solely on PN, even minimal amounts of EN – ‘trophic feed’ – should be considered and it may have a beneficial effect on preserving intestinal epithelium, preserving epithelial tight cell junctions and preventing bacterial translocation.(21)
Hyperglycaemia and hypertriglyceridaemia should be monitored for.

Lessons learnt
• Necrotising pancreatitis is a resource-intensive condition to manage in the intensive care unit and is associated with multiple-organ dysfunction
• Nutritional support is one aspect of an aggressive supportive treatment ‘package’ for pancreatitis, which requires a multi-disciplinary approach.
• Critical care interventions have an important role in altering the metabolic response to stress and EE.
• The traditional belief of ‘pancreatic rest’ should be discarded and early EN, with its associated benefits, should be advocated in all patients with severe pancreatitis.
• Calculating energy requirements and achieving target calorific requirements remains a challenge in the critical ill patient.


1. Preiser J-C, Ichai C, Orban J-C, Groeneveld ABJ. Metabolic response to the stress of critical illness. British Journal of Anaesthesia 2014; 113 (6): 945-54.
2. Marik PE, Bellomo R. Stress hypergylcaemia: an essential survival response! Critical Care 2013; 17: 305.
3. – Patient-centered Acute Care Training (PACT) programme.
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6. Werner J, Feuerbach S, Uhl W, Buchler MW. Management of acute pancreatitis: from surgery to interventional intensive care. Gut 2005; 54: 426-36.
7. Lochs H, Valentini L, Schutz T et al. ESPEN Guidelines in adult enteral nutrition. Clinical Nutrition 2006; 25: 177-360.
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10. Chang YS, Fu XQ, Xiao YM, Liu JC. Nasogastric or nasojejunal feeding in predicted severe acute pancreatitis: a meta-analysis. Critical Care 2013; 17 (3): R118.
11. Al-Omran M, Albalawi ZH, Tashkandi MF, Al-Ansary LA. Enteral versus parenteral nutrition for acute pancreatitis. Cochrane Database of Systematic Reviews 2010; 1: CD002837.
12. Olah A, Romics L. Enteral nutrition in acute pancreatitis: A review of the current evidence. World Journal of Gastroenterology 2014; 20 (43): 16123-31.
13. Marik PE, Zaloga GP. Meta-analysis of parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. British Medical Journal 2004; 328: 1407.
14. Li JY, Yu T, Chen GC et al. Enteral nutrition within 48 hours of admission improves clinical outcomes of acute pancreatitis by reducing complications: a meta-analysis. PLoS One 2013; 8: e64926.
15. Sun JK, Mu XW, Li WQ et al. Effects of early enteral nutrition on immune function of severe acute pancreatitis patients. World Journal of Gastroenterology 2013; 19 (6), 917-22.
16. Meier R, Ockenga J, Pertkiewicz M et al. ESPEN Guidelines on Enteral Nutrition: Pancreas. Clinical Nutrition 2006; 25: 275-84.
17. Working Party of the British Association for Parenteral and Enteral Nutrition. Current Perspectives on Enteral Nutrition in Adults. Maidenhead: BAPEN; 1999.
18. Bersten AD, Soni N. Oh’s Intensive Care Manual. 6th Edition.
19. Petrov MS, Loveday BP, Pylypchuk RD et al. Systematic review and meta-analysis of enteral formulations in acute pancreatitis. British Journal of Surgery 2009; 96: 917-22.
20. Working Group of IAP/APA. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology 2013; 13: e1-e15.
21. The National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Initial trophic vs. full enteral feeding in patients with acute lung injury: the EDEN randomized trial. Journal of the American Medical Association 2012; 307: 795-803.


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