This presentation compares the European Society of Parenteral & Enteral Nutrition (ESPEN) 2002 guidelines and American College of Gastroenterology (ACG) 2013 guidelines regarding nutrition in patients of acute pancreatitis

1. Nutrition in Acute Pancreatitis:
(According to ESPEN guidelines 2002 & ACG guidelines 2013)
Jibran Mohsin
Resident, Surgical Unit I
SIMS/Services Hospital, Lahore

3. Outline
• Introduction
• Pathophysiology
• Energy Requirement
• Energy Supply
• TPN in AP
• Early Enteral feeding
• Conclusions and Recommendations

4. Introduction
• Two major forms of inflammatory pancreatic diseases – acute and chronic
pancreatitis – are different entities which require different nutritional
approaches.
• Despite increasing knowledge in the fields of metabolism, clinical
nutrition, and intervention
– Still a lot of controversy with respect to the optimal approach concerning
treatment regimens.
• It is generally accepted that nutritional management depends on the
underlying pancreatic disease.
• For many years, textbooks have suggested that oral or enteral feeding may
be harmful in acute pancreatitis
– Feeding was thought to stimulate the exocrine pancreatic secretion and
– Consequently autodigestive processes.

5. Introduction
• On the other hand, nutritional deficiencies can occur in
patients with a prolonged and complicated course of an
acute necrotizing pancreatitis.
• 30% of patients with acute pancreatitis are already
malnourished at the time of the initial attack.
• It has also been questioned whether early feeding changes
the outcome in uncomplicated acute pancreatitis.
• Thus far, there is no generally accepted or standardized
approach for handling nutrition in patients with acute
pancreatitis.

6. Introduction
• With this background, ESPEN invited a group
of gastroenterologists, pancreatologists,
intensive care specialists,and nutritionists
– To prepare guidelines and a consensus report on
nutritional strategies in patients with acute
pancreatitis.

7. Pathophysiology
• Approximately 75% of the patients with acute pancreatitis
have a mild disease with a mortality rate well below 1% as
classified by the Atlanta criteria
• Patients with mild disease may be identified early after
symptom onset by the use of a single marker such as
– urinary trypsinogen activation peptide (TAP) , scoring system
such as the Ranson criteria or CT
• The majority of these patients can be managed with
standard supportive measures that do not need special
nutritional treatment;
– most will resume a normal diet within 3–7 days.

8. Pathophysiology
• Malnutrition may, however, aggravate the
course of the disease in acute pancreatitis.
• In order to understand potential hazards and
benefits of various forms of nutritional
support
– it is necessary to analyze the patterns of
pancreatic secretion during acute inflammation.

9. Pathophysiology
• During acute pancreatitis, specific and non-specific metabolic
changes occur.
• Under the influence of inflammatory mediators and pain, BMR may
increase leading to a higher energy consumption
• These changes do not, however, occur in all the patients.
– This emphasizes the importance of direct measurement of energy
expenditure using techniques such as indirect calorimetry when
possible.
• If acute pancreatitis is complicated by sepsis, roughly 80% of the
patients are in a hypermetabolic state with an increase of the
resting energy expenditure (REE)

10. Pathophysiology
• These patients have increased nutrient
requirements because of increased rates of REE
and protein breakdown
• A negative nitrogen balance has been associated
with an adverse clinical outcome.
– Net nitrogen losses are as much as 20–40 g/day in
some patients
– 10-fold increased mortality rate than those with a
positive balance.

11. Pathophysiology
• Protein calories malnutrition can also arise in patients with
acute pancreatitis simply because
– they are subjected to prolonged periods (>10 days) of
inadequate oral intake.
• Deficiencies in certain amino acids may enhance pancreatic
inflammation, leading to a potential vicious circle
• Increased endogenous gluconeogenesis in patients with
acute pancreatitis is a manifestation of the metabolic
response to severe inflammation.
– In common with patients with sepsis or trauma this can only be
partially suppressed with exogenous glucose.

12. Pathophysiology
• Finally, an increase in oxygen extraction by
20–30% indicates
– an enhanced energy consumption or
– a decreased blood supply to vital organs due to
hypovolemia or decreased cardiac performance
during the inflammatory process

13. Pathophysiology
Substrate metabolism in AP
Lipids
• In the injured pancreas, capillary permeability is
increased which facilitates leakage of activated
pancreatic enzymes
– in turn promote local hydrolysis of triglycerides from
chylomicrons
– Which exhibit local toxicity towards capillary
membranes causing further damage to pancreas
Hyperlipidemia Pancreatitis

14. Pathophysiology
• IV lipid does not increase exocrine pancreatic secretion
• Stimulatory effect of lipid administered into the small
intestine depends on the anatomic site of
administration.
– Lipid perfused into the duodenum is a powerful stimulus
for exocrine pancreatic secretion.
– If, however, the same amount of lipid is perfused into the
jejunum, then only a minimal stimulation of exocrine
pancreatic secretion occurs. (true for all forms of jejunal
food administration)

15. Pathophysiology
• This provides a theoretical rationale for jejunal
administration of nutrients in patients with acute
pancreatitis receiving enteral nutrition.
• BUT as per ACG 2013 guidelines there is no
practical significant difference in nasojejunal vs
nasogastric feeding
• No firm evidence to contraindicate the use IV
lipofundin in AP

16. Pathophysiology
Protein and amino acids
• Negative nitrogen balance has been associated with a poor
clinical outcome in severe AP
• Major objective of nutrition in these patients is to minimize
protein losses in order to compensate the increased protein
turnover
• As for lipid administration, jejunal perfusion of elemental
diets containing defined amounts of protein or amino acids
is well tolerated(ACG 2013 no significant effect)

17. Pathophysiology
• Elemental diet preferred over standard diets
containing intact protein, regardless of site of
administration
• Amino acids, when given parenterally, do not
stimulate the exocrine pancreas directly
– stimulate gastric acid secretion which may
stimulate itself in the duodenum, pancreatic
secretion(INDIRECTLY)

18. Pathophysiology
Carbohydrates
• Preferred energy supply in AP
– can be easily supplied
– Protein conserving : prevents gluconeogenesis from
protein degradation
– reduce the potential risk of hyperlipidemia
• physiological maximum to the rate of glucose oxidation
(4 mg/kg/min)
– provision of glucose in excess of this is wasteful both in
terms of lipogenesis and glucose recycling,
– Results in hyperglycemia and hypercapnia

19. Pathophysiology
• IV high doses of glucose
– Doesn’t stimulate pancreatic exocrine secretions
– carries the risk of hyperglycemia as the insulin
response is often impaired.
• Corrected only in part by exogenous insulin
administration and

20. Energy Requirements
• Reduction in the ingestion of food together with an
increased demand in patients with severe pancreatitis
– results in a negative energy balance with the potential of
development of malnutrition
• Patients with acute severe pancreatitis are
hypermetabolic,
– non-suppressible gluconeogenesis despite sufficient
caloric intake,
– an increased ureagenesis and
– an accentuated net protein catabolism

21. Energy Requirement
• More Ranson’s prognostic signs are present
– more excessive is hypermetabolism
• Resting Energy Expenditure is variable in
patients with pancreatitis which range from
77% to 139% of predicted energy expenditure
– Especially high in pancreatitis complicated by
sepsis or multiorgan failure (MOF)

22. Energy supply
• In severely ill patients, neither hypercaloric nor
isocaloric nutritional support can prevent protein
catabolism.
– both enhance the metabolic burden as measured by
energy expenditure, thermogenesis, urea production
rate, glucose and lactate levels
• Hypocaloric energy supply of 15–20 kcal/kg/day
is more suitable during the early catabolic stage
of non-surgical patients with MOF

23. Energy Supply
• Goal of 1.2–1.5 g/kg/day of protein intake is optimal
for most patients with AP
• Attempt to deliver the caloric need by enteral route
– determined by patient tolerance.
– If the enteral supply is inadequate, then the rest should be
given parenterally.
– When enteral nutrition is impossible total parenteral
nutrition should be started.

24. Energy Supply
• impaired glucose oxidation rate cannot be
normalized by insulin administration or by
increasing glucose administration.
– Normally, the blood glucose levels should not
exceed 10 mmol/l.
– Insulin doses higher than 4–6 units/h should be
avoided

25. Energy Supply
• Aggressive nutritional support (enteral or
parenteral) is not required for mild-to-
moderate forms of acute pancreatitis (the
majority of patients).

26. TPN in AP
• Standard treatment for providing nutrients to
patients with severe AP if enteral route not
tolerated or not fulfilling the requirements
– avoid stimulation of exocrine pancreatic secretory
responses (‘to put the pancreas at rest’-NO
LONGER RECOMMENDED if enteral tolerated) and
– secondly, to improve the nutritional status

27. TPN in AP
– MERIT: useful as an adjunct in the nutritional
maintenance of the patients.
– DEMERITS:
• catheter-related sepsis and metabolic disturbances
such as hyperglycemia (due to overfeeding )
• prolonged TPN may suppress the immune system,
promote gastrointestinal leakage by a loss of intestinal
mucosal barrier with the potential risk of subsequent
bacterial translocation.

28. Enteral feeding
• presence of complications (pancreatic ascites,
fistula formation or fluid collection) is not a
contraindication to enteral feeding.

29. ESPEN 2002
Nutritional support in mild-to-moderate pancreatitis

30. ACG 2013
• In mild AP
– oral feedings can be started immediately if there is no
nausea/vomiting, and the abdominal pain/tenderness/Ileus has
resolved(amylase return to normal, patient feel hunger)
– Initiation of feeding with a small and slowly increasing low-fat
(low-protein) soft diet appears as safe as a clear liquid diet,
providing more calories
• Stepwise manner increase from clear liquids to soft diet NOT necessary
• In severe AP
– Enteral route is recommended to prevent infectious complications
– Parenteral nutrition should be avoided, unless enteral route is not
available, not tolerated, or not meeting caloric requirements

31. RATIONALE OF EARLY ENTERAL NUTRITION
• The need to place pancreas at rest until complete
resolution of AP no longer seem imperative
– Bowel rest associated with intestinal mucosal atrophy and
bacterial translocation from gut and increased infectious
complications
• Early enteral feeding maintains the gut mucosal barrier,
prevents disruption, and prevents translocation of
bacteria that seed pancreatic necrosis
– Decrease in infectious complications, organ failure and
mortality

32. ………………………………………………..
Rather than using antibiotics to prevent infected necrosis………….start early
enteral feeding to prevent translocation of bacteria
RATIONALE MANAGEMENT
PREVENTION OF STERILE NECROSIS Early aggressive IV hydration
PREVENTION OF INFECTED NECCROSIS Early enteral feeding( NOT antibiotics)
TREATMENT OF INFECTED NECROSIS Antibiotics, drainage, necrosectomy

33. Route of enteral Nutrition
• Traditionally nasojejunal route has been preferred
to avoid the gastric phase of stimulation BUT
– Nasogastric route appears comparable in efficacy and
safety
MERITS OF NASOGASTRIC ROUTE DEMERITS OF NASOGASTRIC ROUTE
NG tube placement is far easier than
nasojejunal tube placement( requiring
interventional radiology or endoscopy, thus
expensive) especially in HDU/ICU setting
Slight increased risk of aspiration
(Can be overcome by placing patient in upright
position and be placed on aspiration
precautions)

34. Recommendations
• Nutrient requirements:
– energy 25–35 kcal/kg BW/day;
– protein 1.2–1.5 g/kg BW/day;
– Carbohydrates 3–6 g/kg BW/day
(BSR <10 mmol/l)
– Lipids up to 2 g/kg BW/day
(TAG <12 mmol/l)

35. THANK YOU