Nutrition in Pancreatitis

Discuss enteral nutrition in pancreatitis?

  • Mild acute Pancreatitis- EN is not indicated if the patient can eat normal food after 5-7 days
  • Severe acute Pancreatitis (AP)
    • Early EN (asap especially in alcoholics) improves the course of acute pancreatitis
    • Continuous EN is recommended, if tolerated. TF is feasible in the majority of the patients with AP. However TF may need to be supplemented with parenteral feeding if the requirements cannot be met enterally
    • NJ feeding can be tried if gastric feeding is not tolerated
    • Try standard formulae first and if not tolerated peptide based formulae can be used.
    • Avoid overfeeding during the acute phase (CH 50%, Fat 30%, protein 1-1.5 gm/kg/day). TG should be monitored regularly. Values below 10–12 mmol/l are tolerated but serum lipid levels should ideally be kept within normal ranges.
  • Chronic Pancreatitis
    • Pancreatic enzymes taken with meals with a normal fat content (30% of total energy intake) are the mainstay of treatment.
    • Whole protein ONS (with pancreatic enzymes) may be used if oral intake is insufficient.   Peptide-based ONS may be tried if whole protein ONS is not tolerated. However, the palatability of peptide supplements is low and compliance is poor.
    • If adequate weight gain cannot be achieved and steatorrhoea is persistent, then medium chain triglycerides (MCT) are useful due to lipase independent absorption of MCT. However MCTs have a lower energy density (8.3 kcal/g), are not very palatable, and may induce side effects such as abdominal pain, nausea and diarrhoea.
    • Jejunal EN with peptide or amino acid based formula (given overnight) is recommended if the patients cannot ingest sufficient calories.  For long-term therapy a percutaneous endoscopic gastrostomy (PEG) with a jejunal tube is probably best.

When is PN indicated in Acute Pancreatitis?

  • PN is only required when EN is contraindicated (like persisting ileus, complex pancreatic fistulae or abdominal compartment syndrome).
  • PN in pts with severe AP (who cannot be fed enterally) PN initiated within the first 24-48 h of hospital admission have an adverse impact on clinical outcomes. So PN should be delayed till after the period of the peak inflammatory response has passed.

How should PN be used in severe AP?

  • Avoid overfeeding- maximum caloric intake should be 30 Kcal/kg/day. This should be reduced to 15-20 kcal/kg/day in case with SIRS or MODS and when the patient is at risk of refeeding syndrome.
  • 50-70% of the total calories should come from glucose.  As in other critically ill patients, glucose oxidation reaches the maximal level at 4mg/kg/min (3-5 gm/kg/day). Exceeding this limit may cause lipogenesis, hypercapnia and hyperglycemia. Tight glucose control (4-6 mmol/l) with insulin therapy appears to be beneficial in critically ill patients.
  • Protein- 1.2-1.5 g/kg/day.  This should be reduced to 1-1.2 g/kg/day in the case of hepatic or renal failure complicating AP.
  • When PN is indicated, parenteral glutamine supplementation (dose > 0.2, usually 0.3-0.4g/kg) should be considered.
  • Glutamine is the most abundant free amino acid in the body and plays a central role in many metabolic processes (interorgan transport of C and N2 skeletons, regulator of acid base balance). In AP, 3 RCT’s showed use of glutamine was associated with a trend towards reduction in overall complications and shorter hospital stay.
  • Lipid emulsions- not more than 1g/kg/day. The use of IV lipids in AP is safe if hypertriglyceridaemia (HTG) is avoided. The lipid infusion should be discontinued if persistent (>72 hrs) HTG occurs (>12 mmol/l)

Discuss the relationship between hypertriglyceridemia and acute pancreatitis?

The relationship between HTG and AP is controversial because it is still unclear whether hyperlipidaemia is a cause or a consequence of AP or a combination of both. The latter seems more likely, since serum lipids normalize spontaneously within 48-72 hours when there is no continuing exogenous source of lipids.

  • The diagnosis of hypertriglyceridaemia-associated pancreatitis is based on lipaemic serum, a serum
  • TG level greater that 12 mmol/L and the presence of chylomicronaemia. The mechanism is poorly understood. Hydrolysis of TG in and around the pancreas by pancreatic lipase secreted by acinar cell leads to accumulation of free fatty acids in high concentrations. Free fatty acids cause activation of pancreatic pro-enzymes, proinflammatory cytokines and free radicals, thus initiating AP.
  • Lipid emulsion should be avoided with PN in HTG associated pancreatitis. The goal is to maintain TG levels within a normal range.
  • If the serum TG level cannot be maintained below 12 mmol/L, drug therapy is indicated. Plasma exchange has been used to lower lipid and pancreatic enzymes levels, and to improve the signs and symptoms of AP.
  • Keeping blood TG levels < 4.6 mmol/L, in patients with previous HTG-associated AP can effectively prevent further episodes of pancreatitis


  1. ESPEN guidelines

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