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Clinical Nutrition (2006) 25, 275284


ESPEN Guidelines on Enteral Nutrition: Pancreas$

R. Meiera,, J. Ockengab, M. Pertkiewiczc, A. Papd, N. Milinice, J. MacFief,
DGEM:$$ C. Lo ser, V. Keim

Department of Gastroenterology, Kantonsspital Liestal, Liestal, Switzerland
Department of Gastroenterology, CCM, Charite-Universitatsmedizin Berlin, Berlin, Germany
Department of Nutrition and Surgery, Central Clinical Hospital, Warsaw, Poland
1st. Department of Gastroenterology, MAV Hospital, Budapest, Hungary
Department of Gastroenterology, University Hospital Bezanijska kosa, Belgrade, Serbia-Montenegro
Department of Surgery, Scarborough Hospital, Scarborough, UK

Received 21 January 2006; accepted 21 January 2006

KEYWORDS Summary The two major forms of inflammatory pancreatic diseases, acute and
Guideline; chronic pancreatitis, require different approaches in nutritional management, which
Clinical practice; are presented in the present guideline. This clinical practice guideline gives
Enteral nutrition; evidence-based recommendations for the use of ONS and TF in these patients. It was
Oral nutritional developed by an interdisciplinary expert group in accordance with officially
supplements; accepted standards and is based on all relevant publications since 1985. The
Tube feeding; guideline was discussed and accepted in a consensus conference.
Pancreatitis; In mild acute pancreatitis enteral nutrition (EN) has no positive impact on the
Undernutrition; course of disease and is only recommended in patients who cannot consume normal
Malnutrition food after 57 days. In severe necrotising pancreatitis EN is indicated and should be
supplemented by parenteral nutrition if needed. In the majority of patients
continuous TF with peptide-based formulae is possible. The jejunal route is
recommended if gastric feeding is not tolerated.
In chronic pancreatitis more than 80% of patients can be treated adequately with
normal food supplemented by pancreatic enzymes. 1015% of all patients require
nutritional supplements, and in approximately 5% tube feeding is indicated.
The full version of this article is available at
& 2006 European Society for Clinical Nutrition and Metabolism. All rights reserved.

Abbreviations: EN, enteral nutrition (both oral nutritional supplements and tube feeding); IU, international units; PEG,
percutaneous endoscopic gastrostomy; MCT, medium chain triglycerides; ONS, oral nutritional supplements; TF, tube feeding
For further information on methodology see Schu tz et al.77 For further information on definition of terms see Lochs et al.78
Corresponding author. Tel.: +41 61 9252187; fax: +41 61 9252804.
E-mail address: (R. Meier).
The authors of the DGEM (German Society for Nutritional Medicine) guidelines on enteral nutrition in pancreatitis are
acknowledged for their contribution to this article.

0261-5614/$ - see front matter & 2006 European Society for Clinical Nutrition and Metabolism. All rights reserved.
276 R. Meier et al.

Summary of statements: Acute pancreatitis

Subject Recommendations Grade77 Number

Mild acute Enteral nutrition is unnecessary, if the patient can B 1.3
pancreatitis consume normal food after 57 days.
Enteral nutrition within 57 days has no positive A 1.6
impact on the course of disease and is therefore not
Give tube feeding, if oral nutrition is not possible due C 1.6
to consistent pain for more than 5 days.
Severe Enteral nutrition is indicated if possible. A 1.3
necrotising Enteral nutrition should be supplemented by C 1.3
pancreatitis parenteral nutrition if needed.
In severe acute pancreatitis with complications 1.8
(fistulas, ascites, pseudocysts) tube feeding can be
performed successfully.
Application Tube feeding is possible in the majority of patients but A 1.4
may need to be supplemented by the parenteral
Oral feeding (normal food and/or oral nutritional C 1.10
supplements) can be progressively attempted once
gastric outlet obstruction has resolved, provided it
does not result in pain, and complications are under
control. Tube feeding can be gradually withdrawn as
intake improves.
Severe Use continuous enteral nutrition in all patients who C 1.7
pancreatitis tolerate it.
Route Try the jejunal route if gastric feeding is not C 1.4
In case of surgery for pancreatitis an intraoperative C 1.7
jejunostomy for postoperative tube feeding is
In gastric outlet obstruction the tube tip should be C 1.8
placed distal to the obstruction. If this is impossible,
parenteral nutrition should be given.
Type of formula Peptide-based formulae can be used safely. A 1.5
Standard formulae can be tried if they are tolerated. C 1.5
Grade: Grade of recommendation; Number: refers to statement number within the text.

Summary of statements: Chronic pancreatitis

Subject Recommendations Grade77 Number

General Adequate nutritional therapy as well as pain C 2.4

treatment may have a positive impact on nutritional
status. Caloric intake is increased after an
attenuation of postprandial pain.
ESPEN Guidelines on Enteral Nutrition 277

Indications More than 80% of patients can be treated adequately B 2.4

with normal food supplemented by pancreatic
1015% of all patients require oral nutritional C 2.4
Tube feeding is indicated in approximately 5% of C 2.4
patients with chronic pancreatitis.
Specific Stenosis of duodenum C 2.5
Grade: Grade of recommendation; Number: refers to statement number within the text.

1. Acute pancreatitis (AP) tional requirements in such cases by whatever

means are most appropriate.
Preliminary remarks: The management of acute Both specific and non-specific metabolic altera-
pancreatitis (AP) differs according to its severity. tions occur in AP 9 (Ib). Basal metabolic rate
Classified by the Atlanta criteria1 approximately increases due to inflammatory stress and pain,
75% of the patients have mild disease with a leading to enhanced total energy expenditure.9 In
mortality rate below 1%.2 Mortality increases up severe necrotising pancreatitis, 80% of all patients
to 20% if the disease progresses to its severe are catabolic9 (Ib), with high energy expenditure
necrotizing form38 and in the most severe cases and enhanced protein catabolism10 (IIa). The
mortality can rise to 3040%.7,8 Severe AP with its negative nitrogen balance can be as much as
related systemic inflammatory response (SIR) 40 g/day11,12 and can have a deleterious effect on
causes increased metabolic demands and may both nutritional status and disease progression. In
progress to multiorgan disease (MOD). Using ima- one trial, patients with a negative nitrogen balance
ging methods and laboratory parameters, progres- had a ten-fold higher mortality than those with a
sion can be predicted. Until recently, EN, either normal balance.13 This conclusion has to be treated
orally or by tube, was believed to have a negative with caution since no study has been stratified
impact on the progression of the disease due to according to disease severity, and the relation
stimulation of exocrine pancreatic secretion and between nitrogen balance and progression might,
the consequent worsening of the autodigestive therefore, merely reflect the severity of disease.
processes of the pancreas. Even though nutritional Starvation for more than seven days should
deficits are frequent in severe pancreatitis, nutri- always be avoided, since protein and energy
tion as a part of therapy was neglected for a long catabolism induces undernutritionand probably
time. Even now, few nutritional studies in this worsens the prognosis. It has been shown, that as
condition have been published. little as five days of conservative therapy without
nutritional support in previously healthy men
1.1. What influence does acute pancreatitis suffering from severe pancreatitis results in severe
exert on nutritional status and on energy and undernutrition, water retention and decreased
substrate metabolism? muscle function proportional to decreased protein
Mild pancreatitis has little impact on nutritional
Hyperlipidaemia occurs frequently in acute pan-
status or metabolism. In severe necrotising
creatitis.15,16 It is not clear whether this is a
pancreatitis energy expenditure and protein
consequence of disease or due to pathogenic
catabolism are increased (IIa).
factors or a combination of both17 (Ib). The latter
Comment: In mild acute pancreatitis the clinical seems more likely, since serum lipids normalize
course is usually uncomplicated and patients can during recovery from AP. Severe hyperlipidaemia
consume normal food, low in fat (o30% of total itself may be the sole cause of AP. It is a particular
energy intake [vegetable fat are preferred]), with- problem in the most severe cases, reflecting severe
in three to seven days. The disease has little impact disturbances of fat metabolism secondary to sepsis
on nutritional status or on energy and substrate and treatment.
metabolism. It is not clear whether this is also true The enhanced metabolic rate and protein cata-
in the presence of pre-existing undernutrition, bolism necessitate an increased energy intake from
although it is probably important to meet nutri- both fat (30%) and carbohydrates (50%). 1.01.5 g
278 R. Meier et al.

proteins are usually sufficient. Carbohydrates are syndrome (SIRS) was significantly attenuated in all
the favoured source of calories, since administra- enterally fed patients. Sepsis and multiorgan fail-
tion is easy, although hyperglycaemia, secondary to ure as well as incidence of surgery were reduced.
insulin resistance and in some cases islet cell Whereas two patients died in the PN group, no
damage, has to be avoided, placing a limit on the death occurred in the EN group. Major weaknesses
rate of administration of glucose and, in some of this study are the small number of patients with
cases, necessitating the use of insulin10 (IIa). severe pancreatitis and the marked differences in
nutrient intake between the enteral and the
1.2. Does nutritional status influence outcome?
parenteral groups.
Although not investigated in this context, severe A further trial by Powell et al.22 (Ib) could not
undernutrition is likely to affect outcome nega- confirm these findings. They compared early TF in
tively. patients with severe AP to patients without nutri-
tional support. One possible explanation could be
Comment: Since there are no studies addressing
the different patient populations studied. In the
this issue, the question cannot be properly an-
Windsor group the mean APACHE II was 8 in the EN
swered for AP. It has to be considered that under-
group and 9.5 in the PN group.21 In the Powell series
nutrition is a well-known risk factor for more
APACHE II scores were 13 or more.22
complications and higher morbidity in other dis-
In a randomised prospective controlled trial,
eases. It also has to be considered that under-
comparing EN (TF) vs. PN in patients with severe
nutrition is known to occur in 5080% of chronic
pancreatitis Kalfarentzos et al.23 (Ib) scored less
alcoholics and that alcohol is a major aetiological
than half of those studied, but, in the remainder,
factor in acute pancreatitis (3040% of patients).18
mean APACHE II scores were 12.7 in the EN group
Overweight, with a high body mass index is also
and 11.8 in the PN group. EN was well tolerated and
associated with a poorer prognosis.
was associated with fewer septic and other
1.3. Is EN indicated in acute pancreatitis? complications than PN as well as cost were more
than three times less.
In mild acute pancreatitis EN is unnecessary, if
In recent years it has become clear, that PN
the patient can consume normal food after five
related complications have often been the conse-
to seven days (B).
quence of overfeeding or even just catheter
In severe necrotising pancreatitis, EN is in-
sepsis.24 Van den Berghe et al. showed, irrespective
dicated if possible (A). This should be supple-
of the route of nutritional support, that the control
mented by parenteral nutrition if needed (C).
of hyperglycemia with insulin reduced mortality in
Comment: Parenteral nutrition (PN) has been the critically ill patients.25 Hyperglycaemia may occur
standard way of meeting nutritional requirements with EN as well as PN.
since it avoids pancreatic stimulation and improves Several studies in patients with trauma, thermal
nutritional status. A positive benefit has, however, injury and major gastrointestinal surgery have
not yet been confirmed in trials. There are two shown a reduction in septic complication with
investigations in mild to moderate pancreatitis EN26,27 (Ib) which also helps to maintain mucosal
comparing parenteral to no nutritional support19 function and limit absorption of endotoxins and
(Ib) or to TF20 (Ib). In the trial by Sax et al. no cytokines from the gut.28,29 In animals with induced
difference in mortality or complication rate be- pancreatitis, EN prevented bacterial transloca-
tween the two regimens could be demonstrated.19 tion,30 but whether this occurs in patients with AP
Catheter induced septicaemias as well as hypergly- is still unclear.31
caemia occurred significantly more often in the PN Recent evidence has encouraged a much greater
group. McClave et al., in a prospective randomised use of EN than PN in severe acute pancreatitis,
controlled study, compared early EN via a jejunal whenever possible. EN, by down-regulating
tube to PN in patients with mild to moderate splanchnic cytokine production and modulating
pancreatitis.20 Early EN was initiated within 48 h the acute phase response, reduces catabolism and
after admission to hospital. No difference in the preserves protein.21
investigated parameters was found, although PN Abou-Assi et al.32 studied 156 patients with AP
was found to be four times more expensive. All over 12 months. During the first 48 h all patients
patients in both groups survived. were treated with i.v. fluid and analgesics. 87% of
Windsor et al.21 (Ib) compared PN with EN in patients had mild, 10% moderate, and 3% severe
patients with mild to moderate (total peripheral PN disease. Those who improved went on to normal
vs. ONS) and severe pancreatitis (total central PN food as soon as possible. The non-responders
vs. TF). The systemic inflammatory response were randomized to receive nutrients either by a
ESPEN Guidelines on Enteral Nutrition 279

naso-jejunal tube or by PN. 75% of the initially TF was not possible in most (25 out of 26) patients
enrolled patients improved with the oral regimen with severe AP (mean APACHE II 17.2 and mean
and were discharged within four days. 54% of the TF Ranson score 4.3 on admission) most probably due
group (n 26) and 88% of the PN group (n 27) to severe retroperitoneal inflammatory changes.40
received adequate energy intake. The patients in TF is also possible in the presence of ascites and
the TF group were fed for a significantly shorter pancreatic fistulas. Neither intrajejunally delivered
period (mean 6.7 days vs. 10.8 days [PN]), and had glucose, protein nor fat stimulate the exocrine
significantly fewer metabolic and septic complica- pancreas if they are infused alone41 (III). If fat is
tions. Hyperglycemia, requiring insulin therapy, administered, serum triglycerides should be mon-
occurred more frequently in the parenterally fed itored regularly. Values below 1012 mmol/l are
patients. Despite fewer complications with TF, tolerated but serum lipid levels should ideally be
mortality was similar in the two groups. The kept within normal ranges.
authors concluded that hypocaloric TF is safer and
1.5. Which formulae should be used in AP?
less expensive than parenteral feeding and bowel
rest in patients with AP. Jejunal TF may also reduce Peptide-based formulae can be used safely in
the frequency of pain relapses in patients with mild AP (A).
to moderate AP.33 A recent meta-analysis of TPN Standard formulae can be tried if they are
versus TF in patients with acute pancreatitis by tolerated (C).
Marik and Zaloga concluded that TF should be the
Comment: Most trials (human and animal) have
preferred route of nutritional support in patients
been carried out using peptide-based formula,
with AP, because EN was associated with a
which can therefore be recommended for feed-
significantly lower incidence of infections, reduced
ing.4147 Whether standard formulae can be used
rate of surgical interventions and a reduced length
safely or whether immune-modulating formulae
of hospital stay. There were no significant
have an additional impact on the course of the
differences in mortality and non-infectious compli-
disease remains unclear (IV). Today it is common to
start with a standard formula and if this is not
There are no studies comparing TF to oral
tolerated a peptide-based formula is tried.
1.6. How should nutritional support be given to
1.4. Is TF possible in practice and what is the patients with mild pancreatitis?
preferred route of feeding?
In mild pancreatitis EN within five to seven days
TF is possible in the majority of patients with AP has no positive impact on the course of disease
(Ia) but may need to be supplemented by the and is therefore not recommended (A). Oral food
parenteral route (A). intake should be tried as soon as possible.
If gastric feeding is not tolerated the jejunal If oral nutrition is not possible due to con-
route should be tried (C). sistent pain for more than five days, TF should
be given (C).
Comment: Four prospective studies have shown
that jejunal delivery is possible in most patients Comment: In mild pancreatitis fluid and electro-
with AP20,3537 (Ib). Rarely, proximal migration of lytes are initially given parenterally. When pain
the feeding tube and a subsequent pancreatic ceases, oral food intake is initiated.
stimulation can aggravate AP.38 If the jejunal Patients with mild pancreatitis can be fed orally
tube cannot be placed blindly or with the after a short period of starvation if pain has ceased
aid of fluoroscopy, adequate endoscopic placement and amylase and lipase values are decreasing48 (Ib).
is usually feasible. In a recent study,39 naso- Oral refeeding with a diet rich in carbohydrates and
gastric feeding proved safe, since little difference protein and low in fat (o30% of total energy
in pain, analgesic requirements, serum CRP intake) is recommended, but no clinical trials on
concentrations, or clinical outcome was seen this are available. If the diet is well tolerated, oral
between the two methods. It seems, AP could not nutrition can be increased continuously. Specific
have been very severe, if gastric emptying was products do not have to be used.
1.7. How should nutritional support be given to
Although TF appears to have been possible in
patients with severe pancreatitis?
most prospective studies of TF in acute pancreati-
tis, in more general studies, dealing with larger Early EN improves the course of severe pancrea-
patient groups including all treated patients, this titis (III). Continuous EN is therefore recom-
was not the case. Oleynikow et al. reported, that mended in all patients who tolerate it (C).
280 R. Meier et al.

In case of surgery for pancreatitis an intrao- if possible (IIa). The results must be interpreted
perative jejunostomy for postoperative TF is with caution, however, as indirect calorimetry
feasible (C). shows only part of the picture. At best, it evaluates
the patients basic requirements and therefore
Comment: In severe pancreatitis EN should be helps in formulating an appropriate prescription.
initiated as early as possible, particularly when Overfeeding during the acute phase should be
alcoholism, with its associated undernutrition, is avoided. Afterwards the calories can gradually be
the cause18 (Ib). Water, electrolyte and micronu- increased until full requirements are met.
trient requirements must be met by the intrave-
1.8. How is nutritional management affected by
nous route and decreased gradually as the enteral
supply increases. According to expert opinion EN
should be provided over 24 h via a pump assisted In severe AP with complications (fistulas, as-
jejunal tube, but the evidence base for this cites, pseudocysts) TF can be performed suc-
statement is weak. It has also been recommended cessfully. In gastric outlet obstruction the tube
that TF should be supplemented by PN if require- tip should be placed distal to the obstruction. If
ments cannot be met enterally or there are this is impossible, parenteral nutrition should be
contraindications to TF (e.g. prolonged ileus). given (C).
Two recent studies using special formulae have
Comment: Postoperative TF was successful,
been reported. In a small study29 comparing a
in one small study.36 There are no controlled
glutamine rich, multifibre formula with a standard
fibre-containing formula, there was a beneficial studies of feeding AP patients with gastric outlet
obstruction so that no general recommendation can
effect of the glutamine rich formula on the
be given. Nutrition support has to be planned
recovery of IgG, IgM proteins and a shortening of
according to the clinical situation and course of the
the disease. A second study examined the efficacy
of the tube administration of the probiotic lacto-
bacillus plantarum 299v in patients with severe 1.9. Are there contraindications to EN?
AP.49 22 patients received live bacteria with oat-
There are no specific contraindications known
fibre, and 23 patients the same formula with heat-
killed bacteria. In the group with live bacteria, only for EN.
one patient developed a septic pancreatic compli- Comment: Since there are no prospective studies,
cation requiring surgery, compared to the control nutritional therapy is given according to the clinical
group in which seven patients developed such situation. Expert opinion advises that EN should
complications (Po0.023). These observations are always be tried if an adequate intake of normal
interesting but at present it is not possible to food is not possible. In the presence of gastric
recommend this approach on the basis of this small distension, double lumen tubes, allowing simulta-
study. Larger trials are required to confirm these neous feeding into the jejunum and aspiration of
results. gastric contents, have proved to be of value (IV).
Thiamine deficiency and therefore increased Maintenance of mucosal integrity is regarded as
requirements are common, especially in alcoholic important. Although, in humans, changes in muco-
patients. Extra supply by the intravenous route is sal integrity (villous architecture or intestinal
therefore recommended. permeability) have rarely been assessed. Neither
It has been shown in one study50 that patients of these parameters has been shown to be
with severe AP are selenium deficient and therefore associated with bacterial translocation although
benefit from additional selenium supply. These there is some evidence to implicate the gut origin
results should to be confirmed by other studies; of sepsis in acute pancreatitis.51 A low volume
on the other hand, when choosing an EN formula it jejunal delivery of enteral formula, supplemented
is advisable to check whether it contains selenium. by PN should be considered.27,52 In 1990 Kudsk et
The switch from TF to oral nutrition should be al. reported eleven patients in whom needle
early and gradual according to the clinical situation catheter jejunostomy was placed during laparot-
and course of the disease (IV). A general recom- omy for complications of severe pancreatitis, with
mendation is not possible. only one leak around the tube.36 Hernadez-Aranda
Septic complications are important causes of et al. found no differences between groups of
increased resting energy expenditure.10,11 In AP, patients who received postoperative PN or EN via
since the Harris Benedict formula has not proved jejunostomy.53 However, jejunostomies should be
adequate to estimate energy expenditure with placed only, when the risk of leak or tube
accuracy indirect calorimetry should be performed, dislodgement is minimal.
ESPEN Guidelines on Enteral Nutrition 281

1.10. How and when can patients be weaned result. In the early stages of the disease digestion
from TF? of fat is more affected than that of carbohydrate
and protein57,58 (IIa) and results in steatorrhoea,
Oral feeding (normal food and/or ONS) can be although, as function deteriorates, and lipase and
progressively attempted once gastric outlet trypsin secretion decline further, azotorrhoea may
obstruction has resolved, provided it does not also develop.
result in pain, and provided that complications In 3050% of patients with a chronic pancreatitis,
are under control. TF can be gradually with- enhanced resting energy expenditure occurs.59
drawn as intake improves (C). Deficiencies in vitamins A, D, E and K60,61 result
Comment: There are currently only two studies from steatorrhoea. Specific deficiencies in Ca, Mg,
study investigating initiation of an oral diet.33,48 In Zn, thiamine and folic acid have also been reported
the study of Levy et al., 21% of patients experienced (IIa).
pain relapse on the first and second day of 2.2. Does nutritional status affect outcome?
refeeding. Serum lipase concentration43  the
upper limit of the normal range and higher The degree of undernutrition probably corre-
Balthazars CT scores at the onset of refeeding were lates with complications and has a negative
identified as risk factors for pain relapse48 (IIa). impact on outcome (IV).
Comment: There are no specific studies investigat-
ing this issue.
2. Chronic pancreatitis
2.3. What are the goals of nutritional therapy?
Preliminary remarks: Alcohol is the etiological The main goal is to influence malabsorption and
factor in 6070% of patients with chronic pancreatitis. prevent undernutrition.
Other causes of chronic pancreatitis are much less
Comment: Late in the course of chronic pancrea-
common (pancreatic duct obstruction, pancreas
titis, weight loss is often seen, due to a reduced
divisum, hereditary or tropical pancreatitis). Between
calorie intake (pain, persistent alcohol intake) and
15% and 35% of patients have no apparent underlying
malabsorption of macronutrients. Undernutrition
diseases (idiopathic chronic pancreatitis).54
is, therefore, common in patients with chronic
The morphological changes include oedema,
pancreatitis and its severity is one of the major
acute inflammation and necrosis, superimposed
factors predicting complications and outcome.
on the background of chronic changes that include
fibrosis, calcification, inflammation, and loss of 2.4. What are the treatment options?
exocrine tissue.55,56 During the course of chronic
More than 80% of patients can be treated
pancreatitis, enzyme secretion is gradually de-
adequately with normal food supplemented by
creased, resulting in maldigestion with steator-
pancreatic enzymes (B).
rhea, and azotorrhea when more than 90% of
pancreatic tissue is destroyed. At this stage of the 1015% of all patients require ONS (C).
disease, diabetes will also develop due to the loss TF is indicated in approximately 5% of
of insulin producing beta cells in the pancreas. patients with chronic pancreatitis (C).
Adequate nutritional therapy as well as pain
2.1. How does chronic pancreatitis influence
treatment may have a positive impact on
nutritional status and metabolism?
nutritional status. Caloric intake is increased
Protein energy undernutrition occurs frequently after an attenuation of postprandial pain (C).
in the terminal phase of chronic pancreatitis,
Comment: The standard therapeutic measures in
partly due to pain induced anorexia and con-
chronic pancreatitis include abstinence from alco-
tinuing alcohol abuse.
hol and pain control (IIa). With these measures,
3050% of patients with chronic pancreatitis
improvement in nutritional status can generally be
have increased resting energy expenditure.
achieved. If analgesics are required, they should be
Comment: Abdominal pain, malabsorption and consumed before the meal, since a reduction in
diabetes mellitus are complications, which have a postprandial pain results in an increased food
negative impact on nutritional status in chronic intake. Whether alcohol abstinence improves out-
pancreatitis. If exocrine (lipase and trypsin) and come is difficult to say, since data are controver-
endocrine pancreatic function are reduced by more sial.54 Exocrine pancreatic insufficiency is manifest
than 90%, maldigestion and diabetes mellitus by steatorrhoea (faecal fat excretion47 g/day).
282 R. Meier et al.

With a reduced fat diet (0.5 g/kgBW/day), partial The role of enzyme products to manage pain is
symptom control is possible (IIa). Pancreatic en- controversial.75,76
zymes taken with meals with a normal fat content EN is indicated if the patients cannot ingest
(30% of total energy intake) are the mainstay of sufficient calories (in pain or pyloro-duodeno-
treatment. stenosis due to an enlarged pancreatic head or
Glucose intolerance occurs in 4090% of all cases pseudocyst formation, if weight loss continues
with severe pancreatic insufficiency (IIa). In 2030% despite apparently adequate normal food, in the
of all patients manifest diabetes occurs, associated presence of acute complications (acute pancreati-
with impaired glucagon release.6264 Glucagon tis or fistulas), or prior to surgery. It is recom-
secretion is also reduced in type 1 diabetes after mended that EN be delivered via a jejunal tube
a few years, impairing counter-regulation and (IV). For long-term therapy a percutaneous endo-
making patients more susceptible to hypoglycaemia scopic gastrostomy (PEG) with a jejunal tube is
during insulin treatment. probably best. A peptide or amino acid based
Normal food is sufficient in most cases, but, if formula is recommended, given overnight (IV).
calorie intake is low, whole protein ONS and There are no long term studies available showing
pancreatic enzymes can be provided. If they are the efficacy of this approach which is based on
not well tolerated, one should try peptide-based clinical experience.
ONS, which are probably more efficient than whole- PN is only indicated when EN is not possible e.g.
protein ONS (III). The palatability of peptide in severe stenosis of the duodenum prior to surgery.
supplements is low and compliance is poor. There are no published data on patients fed
Reduction in steatorrhoea and an adequate intravenously for a longer period.
intake of energy are the most important principles
2.5. Are there specific contraindications to
of nutrition therapy in chronic pancreatitis.
normal food or EN (ONS & TF) in chronic
Treatment of exocrine pancreatic insufficiency
starts with nutritional counselling as well as
substitution of pancreatic enzymes.65 Frequent Except for stenosis of the duodenum, there are
small meals are important in order to achieve an no contraindications to normal food or EN (C).
adequate intake. The diet should be rich in
Comment: There are no data available concerning
carbohydrates and protein, although carbohydrate
this topic.
intake can cause problems with intercurrent
diabetes. A protein intake of 1.01.5 g/kg is
sufficient and is well tolerated. 30% of calories
can initially be given as fat, which is well tolerated, References
especially in the case of vegetable fat.
If adequate weight gain cannot be achieved and 1. Bradley EL. Members of the Atlanta International Sympo-
steatorrhoea is persistent, then medium chain sium. A clinically based classification system for acute
triglycerides (MCT) can be administered38,66 (III). pancreatitis: summary of the International Symposium on
Due to lipase independent absorption MCT can be Acute Pancreatitis, Atlanta, GA, September 11 through 13,
1992. Arch Surg 1993;128:58690.
recommended. MCTs however, have a lower energy 2. Winslet MC, Hall C, London NJM, Neoptolemos JP. Relation-
density (8.3 kcal/g), are not very palatable, and ship of diagnostic serum amylase to aetiology and prognosis
may induce side effects such as abdominal pain, in acute pancreatitis. Gut 1992;33:9826.
nausea and diarrhoea. The diet should be low in 3. Bradley EL. Indications for surgery in necrotizing pancrea-
fibre, since fibres absorb enzymes and lead to a titis: a millennium review. J Pancreas 2000;1:13.
4. Ashley SW, Perez A, Pierce EA, et al. Necrotizing pancrea-
reduced intake of nutrients. Fat-soluble vitamins titis. Ann Surg 2001;234:57280.
(vitamin A, D, E, K) as well as other micronutrients 5. Buchler MW, Gloor B, Muller CA, Friess H, Seiler CA, Uhl W.
should be supplemented if clinical deficit is Acute necrotizing pancreatitis: treatment strategy accord-
apparent.62 ing to the status of infection. Ann Surg 2000;232:61926.
6. Slavin J, Ghaneh P, Sutton R, et al. Management of
A lot of enzyme supplements are available that
necrotizing pancreatitis. World J Gastroenterol 2001;7:
differ in enzyme content and pharmacological 47681.
preparation.6769 An adequate intake of enzyme 7. Flint R, Windsor J, Bonham M. Trends in the management of
products is crucial67,7072 (Ib). In cases of thera- severe acute pancreatitis: interventions and outcome. ANZ J
peutic resistance despite an adequate diet, good Surg 2004;74:33542.
compliance, correct pharmacological preparation 8. Karsenti D, Bourlier P, Dorval E, et al. Morbidity and
mortality of acute pancreatitis. Prospective study in a
and dosage of enzyme supplements, then H2- French university hospital. Presse Med 2002;31:72734.
antagonists or proton-pump-inhibitors can be 9. Shaw JH, Wolfe RR. Glucose, fatty acid, and urea kinetics in
added.70,73,74 patients with severe pancreatitis. The response to substrate
ESPEN Guidelines on Enteral Nutrition 283

infusion and total parenteral nutrition. Ann Surg 1986; functional changes in humans. J Parenter Enteral Nutr
204:66572. 1995;19:45360.
10. Dickerson RN, Vehe KL, Mullen JL, Feurer ID. Resting energy 29. Hallay J, Kova
cs G, Szatmari K, et al. Early jejunal nutrition and
expenditure in patients with pancreatitis. Crit Care Med changes in the immunological parameters of patients with acute
1991;19:48490. pancreatitis. Hepato-Gastroenterology 2001;48:148892.
11. Bouffard YH, Delafosse BX, Annat GJ, Viale JP, Bertrand OM, 30. Kotani J, Usami M, Nomura H, et al. Enteral nutrition prevents
Motin JP. Energy expenditure during severe acute pancrea- bacterial translocation but does not improve survival during
titis. J Parenter Enteral Nutr 1989;13:269. acute pancreatitis. Arch Surg 1999;134:28792.
12. Feller JH, Brown RA, Toussaint GP, Thompson AG. Changing 31. MacFie J. Enteral versus parenteral nutrition: the signifi-
methods in the treatment of severe pancreatitis. Am J Surg cance of bacterial translocation and gut-barrier function.
1974;127:196201. Nutrition 2000;16:60611.
13. Sitzmann JV, Steinborn PA, Zinner MJ, Cameron JL. Total 32. Abou-Assi S, Craig K, OKeefe SJD. Hypocaloric jejunal
parenteral nutrition and alternate energy substrates in feeding is better than total parenteral nutrition in acute
treatment of severe acute pancreatitis. Surg Gynecol Obstet pancreatitis: results of a randomized comparative study. Am
1989;168:3117. J Gastroenterol 2002;97:225562.
14. Hill GL. Body composition research: Implication for the 33. Pandey SK, Ahuja V, Joshi YK, Sharma MP. A randomized trial
practice of clinical nutrition. J Parenter Enteral Nutr of oral refeeding compared with jejunal tube refeeding in
1992;16:197218. acute pancreatitis. Indian J Gastroent 2004;23:5361.
15. Cameron JL, Capuzzi DM, Zuidema GD, Margolis S. Acute 34. Marik PE, Zaloga GP. Meta-analysis of parenteral versus
pancreatitis with hyperlipemia. Evidence for a persistent enteral nutrition in patients with acute pancreatitis. BMJ
defect in lipid metabolism. Am J Med 1974;56:4827. 2004;328:140712.
16. Cameron JL, Capuzzi DM, Zuidema GD, Margolis S. Acute 35. Cravo M, Camilo ME, Marques A, Pinto Correia J. Early tube
pancreatitis with hyperlipemia: the incidence of lipid feeding in acute pancreatitis: A prospective study. Clin Nutr
abnormalities in acute pancreatitis. Ann Surg 1973;177: 1989:A8A14.
4839. 36. Kudsk KA, Campbell SM, OBrien T, Fuller R. Postoperative
17. Greenberger NJ. Pancreatitis and hyperlipemia. N Engl J jejunal feedings following complicated pancreatitis. Nutr
Med 1973;289:5867. Clin Pract 1990;5:147.
18. Robin AP, Campbell R, Palani CK, Liu K, Donahue PE, Nyhus 37. Nakad A, Piessevaux H, Marot JC, et al. Is early enteral
LM. Total parenteral nutrition during acute pancreatitis: nutrition in acute pancreatitis dangerous? About 20 patients
clinical experience with 156 patients. World J Surg 1990;14: fed by an endoscopically placed nasogastrojejunal tube.
5729. Pancreas 1998;17:18793.
19. Sax HC, Warner BW, Talamini MA, et al. Early total 38. Scolapio JS, Malhi-Chowla N, Ukleja A. Nutrition supple-
parenteral nutrition in acute pancreatitis: lack of beneficial mentation in patients with acute and chronic pancreatitis.
effects. Am J Surg 1987;153:11724. Gastroentrol Clin North Am 1999;28:695707.
20. McClave SA, Greene LM, Snider HL, et al. Comparison 39. Eatcock FC, Brombacher GD, Steven A, Imrie CW, McKay CJ,
of the safety of early enteral vs parenteral nutrition in Carter R. Nasogastric feeding in severe acute pancreatitis
mild acute pancreatitis. J Parenter Enteral Nutr 1997;21: may be practical and safe. Int J Pancreatol 2000;28:239.
1420. 40. Oleynikow D, Cook C, Sellers B, Mone M, Barton R.
21. Windsor AC, Kanwar S, Li AG, et al. Compared with Decreased mortality from Necrotizing Pancreatitis. Am J
parenteral nutrition, enteral feeding attenuates the acute Surg 1998;17:64853.
phase response and improves disease severity in acute 41. Stabile BE, Debas HT. Intravenous versus intraduodenal
pancreatitis. Gut 1998;42:4315. amino acids, fats, and glucose as stimulants of pancreatic
22. Powell JJ, Murchison JT, Fearon KC, Ross JA, Siriwardena AK. secretion. Surg Forum 1981;32:2246.
Randomized controlled trial of the effect of early enteral 42. Neviackas JA, Kerstein MD. Pancreatic enzyme response with
nutrition on markers of the inflammatory response in an elemental diet. Surg Gynecol Obstet 1976;142:714.
predicted severe acute pancreatitis. Br J Surg 2000;87: 43. McArdle AH, Echave W, Brown RA, Thompson AG. Effect of
137581. elemental diet on pancreatic secretion. Am J Surg 1974;
23. Kalfarentzos F, Kehagias J, Mead N, Kokkinis K, Gogos CA. 128:6902.
Enteral nutrition is superior to parenteral nutrition in severe 44. Cassim MM, Allardyce DB. Pancreatic secretion in response
acute pancreatitis: results of a randomized prospective to jejunal feeding of elemental diet. Ann Surg 1974;180:
trial. Br J Surg 1997;84:16659. 22831.
24. Nordenstrom J, Thorne A. Benefits and complications of 45. Grant JP, Davey-McCrae J, Snyder PJ. Effect of enteral
parenteral nutritional support. Eur J Clin Nutr 1994;48: nutrition on human pancreatic secretions. J Parenter
5317. Enteral Nutr 1987;11:3024.
25. Van den Berghe G, Wouters P, Weekers F, et al. Intensive 46. Vison N, Hecketsweiler P, Butel J, Bernier JJ. Effect of
insulin therapy in critically ill patients. N Engl J Med 2001; continuous jejunal perfusion of elemental and complex
345:135967. nutritional solutions on pancreatic enzyme secretion in
26. Trice S, Melnik G, Page CP. Complications and costs of early human subjects. Gut 1978;19:1948.
postoperative parenteral versus enteral nutrition in trauma 47. Ragins H, Levenson SM, Signer R, Stamford W, Seifter E.
patients. Nutr Clin Pract 1997;12:1149. Intrajejunal administration of an elemental diet at neutral
27. Heyland DK, Novak F, Drover JW, Jain M, Su X, Suchner U. pH avoids pancreatic stimulation. Studies in dog and man.
Should immunonutrition become routine in critically ill Am J Surg 1973;126:60614.
patiens? A systematic review of the evidence. JAMA 2001; 48. Levy P, Heresbach D, Pariente EA, et al. Frequency and risk
286:94453. factors of recurrent pain during refeeding in patients with
28. Buchman AL, Moukarzel AA, Bhuta S, et al. Parenteral acute pancreatitis: a multivariate multicentre prospective
nutrition is associated with intestinal morphologic and study of 116 patients. Gut 1997;40:2626.
284 R. Meier et al.

49. Olah A, Belagyi T, Issekutz A, et al. Randomized clinical trial 66. Caliari S, Benini L, Sembenini C, Gregori B, Carnielli V,
of specific lactobacillus and fibre supplement to early Vantini I. Medium-chain triglyceride absorption in patients
enteral nutrition in patients with acute pancreatitis. Br J with pancreatic insufficiency. Scand J Gastroenterol
Surg 2002;89:11037. 1996;31:904.
50. Kuklinski B, Zimmermann T, Schweder R. Decreasing 67. DiMagno EP, Malagelada JR, Go VL, Moertel CG. Fate of
mortality in acute pancreatitis with sodium selen: Clinical orally ingested enzymes in pancreatic insufficiency. Com-
results of 4 years antioxidant therapy. Med Klin 1995; parison of two dosage schedules. N Engl J Med 1977;
90(Suppl. 1):3641. 296:131822.
51. McNaught CE, Woodcock NP, Mitchell CJ, Rowley G, 68. Graham DY. Enzyme replacement therapy of exocrine
Johnstone D, Macfie J. Gastric colonization, intestinal pancreatic insufficiency in man. Relations between
permeability and septic morbidity in acute pancreatitis. in vitro enzyme activities and in vivo potency in commercial
Pancreatology 2002;2:4638. pancreatic extracts. N Engl J Med 1977;296:
52. Trice S, Melnik G, Page CP. Complications and costs of early 13147.
postoperative parenteral versus enteral nutrition in trauma 69. Whitehead AM. Study to compare the enzyme activity, acid
patients. Nutr Clin Pract 1997;12:1149. resistance and dissolution characteristics of currently avail-
53. Hernandez-Aranda JC, Gallo-Chico B, Ramirez-Barba EJ. able pancreatic enzyme preparations. Pharm Weekbl Sci
Nutritional support in severe acute pancreatitis. Controlled 1988;10:126.
clinical trial. Nutr Hospital 1996;11:1606. 70. Regan PT, Malagelada JR, DiMagno EP, Glanzman SL, Go VL.
54. Steer ML, Waxman I, Freedman S. Chronic pancreatitis. N Comparative effects of antacids, cimetidine and enteric
Engl J Med 1995;332:148290. coating on the therapeutic response to oral enzymes in
55. Singer MV, Gyr KE, Sarles H. Revised classification of severe pancreatic insufficiency. N Engl J Med 1977;297:
pancreatitis: report of the Second International Symposium 8548.
on the Classification of Pancreatitis in Marseille, France, 71. Suzuki A, Mizumoto A, Sarr MG, DiMagno EP. Bacterial lipase
March 2830, 1984. Gastroenterology 1985;89:6835. and high-fat diets in canine exocrine pancreatic insuffi-
56. Samer M, Cotton PB. Classification of pancreatitis. Gut ciency: a new therapy of steatorrhea? Gastroenterology
1984;25:7569. 1997;112:204855.
57. DiMagno EP, Go VL, Summerskill WH. Relations between 72. Malesci A, Mariani A, Mezzi G, Bocchia P, Basilico M. New
pancreatic enzyme ouputs and malabsorption in severe enteric-coated high-lipase pancreatic extract in the treat-
pancreatic insufficiency. N Engl J Med 1973;288:8135. ment of pancreatic steatorrhea. J Clin Gastroenterol 1994;
58. DiMagno EP, Layer P. Human exocrine pankreatic enzyme 18:325.
secretion. In: Go VL, editor. The pancreas. Biology, 73. Taubin HL, Spiro HM. Nutritional aspects of chronic
pathobiology, and disease. New York: Raven Press; 1993. pancreatitis. Am J Clin Nutr 1973;26:36773.
p. 275300. 74. Heijerman HG, Lamers CB, Bakker W. Omeprazole enhances
59. Hebuterne X, Hastier P, Peroux JL, Zeboudj N, Delmont JP, the efficacy of pancreatin (pancrease) in cystic fibrosis. Ann
Rampal P. Resting energy expenditure in patients with Intern Med 1991;114:2001.
alcoholic chronic pancreatitis. Dig Dis Sci 1996;41:5339. 75. Halgreen H, Pedersen NT, Worning H. Symptomatic effect of
60. DiMagno EP, Clain JE, Layer P. Chronic pancreatitis. In: Go pancreatic enzyme therapy in patients with chronic pan-
VL, editor. The pancreas. Biology, pathobiology, and creatitis. Scand J Gastroenterol 1986;21:1048.
disease. New York: Raven Press; 1993. p. 665706. 76. Ramo OJ, Puolakkainen PA, Seppala K, Schroder TM. Self-
61. Twersky Y, Bank S. Nutritional deficiencies in chronic administration of enzyme substitution in the treatment of
pancreatitis. Gastroenterol Clin North Am 1989;18:54365. exocrine pancreatic insufficiency. Scand J Gastroenterol
62. Havala T, Shronts E, Cerra F. Nutritional support in acute 1989;24:68892.
pancreatitis. Gastroenterol Clin North Am 1989;18:52542. 77. Schutz T, Herbst B, Koller M. Methodology for the develop-
63. Holt S. Chronic pancreatitis. South Med J 1993;86:2017. ment of the ESPEN Guidelines on Enteral Nutrition. Clin Nutr
64. Latifi R, McIntosh JK, Dudrick SJ. Nutritional management of 2006;25(2):2039.
acute and chronic pancreatitis. Surg Clin North Am 78. Lochs H, Allison SP, Meier R, Pirlich M, Kondrup J, Schneider
1991;71:57995. St., van den Berghe G, Pichard C. Introductory to the ESPEN
65. DiMagno EP. Medical treatment of pancreatic insufficiency. Guidelines on Enteral Nutrition: Terminology, Definitions and
Mayo Clin Proc 1979;54:43542. General Topics. Clin Nutr 2006;25(2):1806.