Nutrition in Pancreatic

Diseases

Acute Pancreatitis

Acute Pancreatitis Clinical Patterns Range

Mild
mostly self-limiting

Severe
necrotizing disease with local
and systemic complications

It involves a systemic immuno-inflammatory response to a localized

process of autodigestion of the pancreatic gland with variable
involvement of the peri-pancreatic tissue and remote organ systems

Acute Pancreatitis
MEN
Alcohol Abuse
Most important
underlying conditions

WOMEN
Gallstone

The sentinel acute pancreatitis event (SAPE) hypothesis:

while there is a plethora of etiologic agents or insults which may
injure the pancreas, there is a final common pathway of
inflammation in the disease process termed the sentinel event

Acute Pancreatitis
The sentinel acute pancreatitis event (SAPE)
hypothesis:
while there is a plethora of etiologic agents or
insults which may injure the pancreas, there is a
final common pathway of inflammation in the
disease process termed the sentinel event

Acute Pancreatitis
An early pro-inflammatory process starts with the
stimulation of chemotaxis and migration of neutrophils
into and around the pancreatic acinus, with neutrophil
activation, recruitment, and infiltration.
This is followed by a later pro-fibrotic response that
involves stimulation of stellate cells surrounding the
acinar cells. It is not the initial insult, but the subsequent
sentinel event and its vicious cycle of inflammation that
drives the morbidity and mortality.
As the sentinel event sets up around the acinar cell, two
defects occur which promote further inflammation and
stimulate autolysis or autodigestion the pancreatic
tissue.

Acute Pancreatitis
The first defect is an intra-acinar activation of
pancreatic enzymes in which zymogen are colocalized with lysosomal enzymes like Cathepsin.
The second defect is inhibitioof secretion, in which
the zymogen enzymes are activated, but then
retained within the acinar cell.
This process results in inflammation, edema, an
necrosis of the pancreatic tissue as well as
inflammation and injury of extrapancreatic organs
75-80% has mild, oedematous and about 20-25%
severe necrotizing pancreatitis.

Acute Pancreatitis
The first defect is an intra-acinar activation of
pancreatic enzymes in which zymogen are colocalized with lysosomal enzymes like Cathepsin.
The second defect is inhibitioof secretion, in which
the zymogen enzymes are activated, but then
retained within the acinar cell.
This process results in inflammation, edema, an
necrosis of the pancreatic tissue as well as
inflammation and injury of extrapancreatic organs
75-80% has mild, oedematous and about 20-25%
severe necrotizing pancreatitis.

Acute Pancreatitis
In patients with acute pancreatitis was the
absolute influence of organ failure and infected
pancreatic necrosis on mortality the same. Both
indicate severe disease. If both are present the
relative risk of mortality doubles.
Nutritional support in severe necrotising
pancreatitis is essential because these patients
develop rapidly nutritional deficiencies. This is
even more fatal if patients are already
malnourished at the time of the initial attack.

Outcome predictors
Two factors, the severity of pancreatitis and the
nutritional status can be used to predict the
outcome in acute pancreatitis.

Severity Of Acute Pancreatitis

a score of 3 or more in the Ranson Criteria (Table 1) or a score of 8 or

more in the APACHE II-Score and evidence of organ failure and
intrapancreatic pathological findings (necrosis or interstitial
pancreatitis) (Tab. 2).
This classification is helpful because it also allows the comparison of
different trials and methodologies

Severity Of Acute Pancreatitis

Quantity of
necrotic pancreas

CT grade
Grade A =
0

Normal appearing pancreas

Grade B =
1

Focal or diffuse enlargement

of the pancreas

Grade C =
2

Pancreatic gland
abnormalities accompanied
by mild

Grade D =
3

parapancreatic inflammatory
changes

Grade E=
4

Fluid collection in a single

location, usually within the

<33% = 2
33% - 50% = 4
> 50% = 6

Failure
of pancreatic
parenchyma
enhance(0-6)
during the arterial phase of
Total
score
= CT grade
(0-4) +tonecrosis
intravenous contrast-enhanced CT indicates necrosis, which predicts a
severe attack if more than 30% of the gland is affected.

Severe acute pancreatitis

The measurement of concentrations of serum Creactive protein

(CRP) is very useful in clinical practice. CRP concentration has an
independent prognostic value. A peak of more than 210 mg/l on day
2 to 4, or more than 120 mg/l at the end of the first week, is as
predictive as multiple-factor scoring systems (12).
The blood urea nitrogen levels (BUN) were persistently higher
among nonsurvivors than survivors in the first 48 hours of
hospitalisation --> BUN is a new valuble marker for predicting
mortality (13).

Nutritional status

Undernutrition and obesity are often seen in patients with acute

pancreatitis. Both are well-known risk factors for more complications
and higher mortality. Undernutrition is known to occur in 50-80% of
chronic alcoholics and alcohol is a major etiological factor in acute
pancreatitis patients (30-40%).
Patients with biliary pancreatitis have a high tendency to be
overweight. For nutritional support it is therefore necessary to
assess the severity of acute pancreatitis and the nutritional status at
the time of admission and during the course of the disease. Both
factors are necessary to plan nutrition interventions in patients with
acute pancreatitis.

Energy and substrate metabolism during

acute pancreatitis

Specific and non-specific metabolic changes occur during acute

pancreatitis. A variety of proinflammatory cytokines increase the basal
metabolic rate. This can result in increased energy consumption. The
resting energy expenditure varies according to the severity and the duration
of disease. If patients develop sepsis, 80% of them show an elevation in
protein catabolism and an increased nutrient requirement.
A prolonged negative nitrogen balance determines negative clinical
outcome. Whether negative nitrogen balance is the principle factor for
outcome is not clear. The relationship between nitrogen balance and
outcome may only reflect the relationship between nitrogen balance and
severity of disease. There is no study available in which patients were
stratified according to the disease severity.

Metabolism of carbohydrates

Glucose metabolism in acute pancreatitis is determined by the SIRS

response, oxidative stress, and insulin resistance. The resultant
futile fluid cycling and milieu of inflammatory cytokines may cause
an increase in energy demand. Endogenous gluconeogenesis is
increased as a consequence of the metabolic response to the
severe inflammatory process.
Glucose is an important source of energy and can partially
counteract the intrinsic gluconeogenesis from protein degradation.
This can counteract, to a certain degree, the deleterious and
unwanted effect of protein catabolism.

Metabolism of carbohydrates
The maximum rate of glucose oxidation is approximately
4 mg/kg/min. The administration of glucose in excess
can be harmful, and even wasteful, because of
lipogenesis and glucose recycling. Furthermore,
hyperglycemia and hyperkapnia can occur.
Hyperglycemia is a major risk factor for infections and
metabolic complications. Monitoring and blood glucose
control is therefore essential. Evidence glucose
intolerance occurs in the majority of cases (incidence
85%).

Protein metabolism

A negative nitrogen balance is often seen in severe

acute pancreatitis. The protein losses must be minimized
and the increased protein turnover must be
compensated. If acute pancreatitis is complicated by
sepsis, up to 80% of the patients are in a hypermetabolic
state with an increase of the resting energy expenditure.
A negative nitrogen balance is associated with adverse
clinical outcome.
Nitrogen losses are as much as 20-40 g/day in some
patients with acute pancreatitis.

Lipid metabolism

Hyperlipidemia is a common finding in acute pancreatitis.

The mechanism of altered lipid metabolism is not entirely
clear. After an acute attack, serum lipid concentration
returns to normal ranges. It is also known that in some
patients with severe hyperlipidemia an acute pancreatitis
can develop.
Evidence of fat intolerance occurs only in 12-15% of
cases

Exocrine pancreatic stimulation by

macronutrients
In general all forms of enteral nutrition can stimulate the
exocrine pancreatic secretion to some extent. Only with
parenteral nutrition this is not the case. For nutritional
intervention the administration of glucose, protein and fat
are necessary, but for long time enteral applications were
considered to be harmful because of the potential
stimulation of the exocrine pancreatic enzyme secretion.
Enteral glucose perfusion into the jejunum is a very weak
stimulus for exocrine pancreatic secretory response.
Jejunal perfusion of elemental diets containing defined
amounts of protein or amino acids are well tolerated and
do not stimulate exocrine pancreatic secretion.

Exocrine pancreatic stimulation by

macronutrients

The only concern of potentially exacerbating acute pancreatitis with

intravenous PN is through the development of hypercalcemia or
hypertriglyceridemia.
Compared to delivery of the same nutrients intravenously, an enteral
infusion results in a greater insulin response, less insulin resistance,
and less hypertriglyceridemia due to the enteroinsular pathway. All
this findings have changed the nutritional concept in acute
pancreatitis.
Nowadays, enteral feeding in the jejunum 20-120cm after the
ligamentum of Treitz is regarded to be safe without major stimulating
of autodigestive processes in the pancreas and maintaining the gut
integrity by modulating the GI-tract systemic immunity.

Energy requirements

Patients with severe acute pancreatitis are hypermetabolic. The

more severe acute pancreatitis is the more excessive is
hypermetabolism. Resting energy expenditure can be variable in
these patients. 77- 158% of the predicted energy expenditure was
reported. If the disease is complicated by sepsis or multiorgan
failure, the resting energy expenditure is significantly increased.
It was shown that in severe acute pancreatitis, the Harris-Benedict
equation is not sensitive enough to estimate the caloric expenditure.
In these cases, indirect calorimetry is recommended to avoid overor underfeeding.

For enteral or parenteral nutrition, 25-35kcal/kgBW/d is

recommended. Overfeeding and hyperglycemia should be avoided.
Blood glucose concentration should not exceed 10 mmol/l. Insulin
treatment is recommended, but the doses should not be higher than
4 to 6 units/h.
The impaired glucose oxidation rate can not be normalized by
insulin administration. Normally, 3-6g/kgBW/d of carbohydrates can
be recommended. The optimal goal of protein supply is between 1.2
to 1.5g/kgBW/d. Lower protein intake should only be given to
patients with renal or severe hepatic failure. Fat can be given up to
1g/kgBW/d, but blood triglyceride levels must be monitored carefully.
Triglycerides are tolerated up to 12 mmol/l.

Enteral or parenteral nutrition

In mild to moderate acute pancreatitis these studies showed no effect on outcome in

these patients.
TPN did not change the course of the disease but TPN was more expensive or
accompanied with an increase in catheterrelated infections and a longer hospital stay.
In the last years it became clear, that these complications were often the consequence of
overfeeding. Recently, the nutritional management shifted from parenteral to enteral
feeding.
Enteral eeding in acute pancreatitis may reduce catabolism and loss of lean body mass
and may modulate the acute phase response with the potential to down regulate
splanchnic cytokine response

Nutritional support in mild to moderate

pancreatitis

There is no evidence that a nutritional support (enteral or parenteral) has a

beneficial effect on clinical outcome in patients with mild acute pancreatitis.
Enteral nutrition is unnecessary, if the patients can consume normal food
after 5 to 7 days (ESPEN Guidelines: Grade B).
Enteral or parenteral nutrition within 5 to 7 days has no positive effect on the
course of the disease and is therefore not recommended (ESPEN
Guidelines: Grade A). Early enteral nutrition support can be of importance in
patients with pre-existing severe malnutrition or in patients when early
refeeding in 5 to 7 days is not possible.

Nutritional support in severe acute

pancreatitis

In patients with severe pancreatitis, who have complications or need for

surgery, early nutritional support is needed to take advantage of window of
opportunity by which EN can favorably alter patient outcome. In severe
necrotizing pancreatitis, enteral nutrition is indicated first if possible (ESPEN
Guidelines: Grade A, ASPEN/SCCM Guidelines: Grade C).
In the last decade, the nutritional strategy in acute pancreatitis has changed.
The nutritional management has shifted from parenteral to enteral nutrition.
Enteral feeding in acute pancreatitis have shown to reduce catabolism and
loss of lean body mass, modulation of the acute phase response, with the
potential to down regulate the splanchnic cytokine response. Furthermore,
enteral nutrition has been shown in many studies to be safe and well
tolerated.

Nutritional support in severe acute

pancreatitis

Severe Acute
pancreatitis

nutritional goal not reached

Add parenteral nutrition

all in one or single
component
solutions?
(CH, protein (AS), fat)

Early continuous enteral nutrition

(naso-jejunal tube) elemental diet or polymeric diet or
immune-enhancing diet

Enteral nutrition is not possible

PN after 5 days
if EN is unable to use, add supplemental PN to
hypocaloric EN after 7 days if it is unable to reach the
goal calories by EN alone
and
continuous small amount of an
enteral diet (10-30 ml/h) perfused to the
jejunum

Route of feeding

The route of nutrient delivery (parenteral/enteral) should be determined by

patients tolerance. Tube feeding is possible in the majority of patients, but
some patients need a combination with parenteral nutrition (ESPEN
Guideline: Grade A). Placing a jejunal feeding tube distally to the ligament
of Treitz can easily be performed. The tubes are placed either with
fluoroscopic help or more and more with the endoscope. Another way is also
to use self-propelling nasojejunal feeding tubes. Normally, jejunal tubes are
well tolerated.
Early initiation of distal jejunal feeding was associated with reduced mortality
in patients with severe acute pancreatitis. The early achievement of the
feeding goals was also associated with a shorter length in the ICU. Rarely,
proximal migration of the feeding tube and subsequent pancreatic
stimulation can aggravate acute pancreatitis. Partial ileus is not a
contraindication for enteral feeding because these patients frequently
tolerate continuous low-volume jejunal nutrients.

Which enteral and parenteral formula

should be used in acute pancreatitis

Most studies have been done using peptide-based formulae. The

use of peptide-based formulae showed beneficial effects (ESPEN
Guidelines: Grade A).
Nowadays in most institutions polymeric formula are used although
only few data are concluded that a polymeric formula compared to a
(semi)elemental formula show no significant higher risk of feeding
intolerance, infectious complication or mortality in acute pancreatitis
patients. In addition the polymeric formulas are less expensive

 They found a significant benefit for the early

supplementation of glutamine. They showed a reduction
of the presence and duration of organ failure, the
incidence of infection, the need for surgery, and mortality.
The supplementation of n-3 fatty acids alone in
moderately severe acute pancreatitis significantly
lowered the length of hospital stay, and the need of
nutritional therapy. The overall complication rate was not
different

Gastral versus jejunal feeding

Wheather the jejunal feeding is absolutely necessary is not completely clear.

Minimizing stimulation of the exocrine pancreatic secretion would support
the jejunal feeding route. It is, however, controversial whether stimulation of
pancreatic secretion is important for the outcome in this disease.
Four randomized studies comparing naso-gastric versus naso-jeunal
feeding or naso-gastric versus TPN in severe acute pancreatitis were
published. In these studies, naso-gastric feeding was as safe as nasojejunal feeding;
little difference were documented between the two methods with respect to pain,
analgesic requirements, nutritional intolerances, serum CRP concentration, or
mortality
Compared to parenteral nutrition there were significantly more complications in the
first 3 days in the naso-gastric group, but there was a better control of blood glucose
levels.

The advantage of gastric feeding is to facilitate delivery of EN,

reduce time to initiation of feeding, and minimize chances for ileus
and intolerance. The limitations of jejunal feeding are the need for
expertise in tube placement below the ligament of Treitz. There is
little harm and no real downside from this strategy of gastric feeding,
as evidence of intolerance can be ameliorated by adjustments in
level of infusion and content of formula.

Oral refeeding

There are only few data available on oral

refeeding. Oral feeding with normal food and/or
oral supplements can be progressively
attempted once gastric outlet obstruction has
resolved, provided it does not result in pain, and
if complications are under control. Tube feeding
can be gradually withdrawn as intake improves
with several meals given during the day.

Nutritional support in patients after

pancreatic surgery
Postoperative feeding with a needle catheter
jejunostomy was successful in several small studies.
Hernandez-Aranda et al found no difference between
groups of patients who received postoperative parenteral
nutrition or enteral nutrition via jejunostomy.
Furthermore, in patientsundergoing surgery for severe
acute pancreatitis, needle catheter jejunostomy for
longterm enteral nutrition was safely applied with no
nutritional risk.
In general, in these patients, nutritional support has to be
planned before the operation according to the clinical
situation and the course of the disease

Summary

75-80% of patients with acute pancreatitis have mild to moderate

disease and do not need specific nutritional support. Early oral
refeeding can be started within a few days if the patients have no
pain and GI-disturbances. The best time and the best composition of
the diet are not clear. There is no evidence that a specific enteral or
parenteral nutrition is of benefit in patients with mild to moderate
pancreatitis. There are no data available to give a nutritional
recommendation in patients with severe pre-existing malnutrition or
overweight. Patients with severe disease, complications or the need
for surgery require early nutritional support.

In patients with severe pancreatitis, an enteral jejunal approach

should be established, but parenteral nutrition is an alternative
method, when enteral nutrition is insufficient. For the future, more
aggressive use of pharmaconutrition may be employed to modulate
epigenetics and activate the bodys own antioxidant response
elements to reduce oxidative stress.

Several factors have to be clarified: The optimal timing of nutritional

therapy, the optimal feeding side (oral, gastric, jejunal or TPN), the
optimal nutrient formulation, semi-elemental diet, polymeric diet,
immune-enhancing diet, pre- and probiotics). Furthermore, in new
studies a clear stratification of the patients according to their
nutritional status on admission should be performed.

Chronic Pancreatitis

Pancreatic physiology

The exocrine response of the exocrine pancreas is time dependent (Fig. 2)

and related to several factors (Fig.3). The exocrine pancreas consists
mostly of acinar, but additionally of centroacinar and duct cells. Whereas the
acinar cells synthesize > 10 digestive enzymes, the duct cells are
responsible for generation of bicarbonate, which is necessary to neutralize
gastric acid and to raise the pH in the duodenum to obtain an optimal
alkaline milieu for the pancreatic enzymes as well as for the jejunal digestive
brush border enzymes.
The vagus nerve and the hormones secretin and cholecystokinin (CCK) are
responsible for stimulation of the exocrine pancreas. The pancreatic
enzymes digest starch (amylase), lipids (lipase), and protein (trypsin and
other proteolytic enzymes). The most important stimulus for pancreatic
secretion is the presence of nutrients in the duodenal lumen.

Pancreatic physiology

Pancreatic physiology
The quantity and the composition of nutrients in the duodenal lumen influences
the pancreatic secretory response

Pathophysiology of chronic
pancreatitis
Due to the loss of acinar and duct cells (Fig. 4) the secretory capacity of the
exocrine pancreas decreases. The large physiological reserve of the
pancreas is the reason why clinical signs of fat maldigestion occur late in the
course of CP, typically when 80 % of the secretory capacity of the pancreas
has been lost. Fat maldigestion (steatorrhoea; > 10 g of stool fat per 24
hours) is the major problem in these patients.
Steatorrhoea is caused by
(i) reduced pancreatic bicarbonate secretion leading to more rapid and complete
inactivation of lipase in the acidic duodenum;
(ii) further impairment of lipid absorption by bile acid denaturation within the
acidic duodenum;
(iii) rapid degradation of lipase in the small intestine lumen due to its greater
vulnerability to proteolysis thereby reducing the period of lipase activity;
(iv) limited capacity of extrapancreatic lipase (gastric);
(v) no compensating triglyceride-digesting enzymes in the intestinal brush border.
Because fat is the major source of energy, fat maldigestion creates a high risk of
protein-energy malnutrition, but also causes micronutrient and vitamin deficiency

Creatorrhoea (excess nitrogen losses in the stool: >2.5 g of stool nitrogen

per 24 hours) only occurs when trypsin output is less than 10% of normal.
The problem with nitrogen balance studies is the difficulty of separating the
contribution to stool nitrogen loss of ingested protein, compared with that
from proteins secreted into the GI tract and that derived from bacteria.

The effect of enzyme supplementation on protein maldigestion has therefore

not been well characterized. As well as the increased risk of malnutrition, the
increased stool volume and fat content cause abdominal symptoms such as
pain, fullness, distension, diarrhoea, meteorism, and flatulence. Twenty to
25 % of cases with exocrine pancreatic insufficiency may also have the
complication of bacterial overgrowth, which can further contribute to
diarrhoea and other GI symptoms.

Clinical features of chronic

pancreatitis

The cardinal symptom of CP is

pain, which can present either as
repeated mild or moderate attacks
or as persistent and intractable
abdominal and back pain. The
median latency between onset of
first symptoms and signs of
maldigestion is about 89 years in
alcoholic chronic pancreatitis and
more than 15 years in idiopathic
non-alcoholic pancreatitis. In a
minority of patients the clinical
signs of exocrine pancreatic
precede the other features of the
condition.

Nutritional status in CP
Body weight and body composition
Weight loss occurs in those patients with maldigestion and in those with
reduced food intake due to pancreatic pain. Although, weight loss is a
frequent symptom in CP, only limited data on nutritional status in CP
patients are available. Patients with symptomatic CP have a lower body
mass index, reduced lean body mass and fat mass compared to healthy
controls.
Malnutrition is associated with higher morbidity (e.g. higher incidence of
postoperative complications after surgery for chronic pancreatitis).
Therefore, those patients with malnutrition should be identified and treated.
Nutritional assessment is easy to perform. Weight loss over time, body
mass index, anthropometry and some laboratory values are useful
parameters. Furthermore, nutritional screening scores, e.g. subjective global
assessment (SGA), the ESPEN nutritional risk score (ESPEN-NRS; see
www.espen.org/) are available for detecting those patients with nutritional
deficiencies who are at risk of developing complications.

Metabolic situation
In patients with chronic pancreatitis, resting energy expenditure is increased
by 3050%. The loss of endocrine function in the late state of the disease
also leads to glucose intolerance and eventually to frank diabetes. Glucose
intolerance occurs in 4090% of all cases with severe chronic pancreatitis
during the course of disease. In 2030% of all patients insulin-dependent
diabetes develops. This is also associated with impaired glucagon release
and reduced counter-regulatory capacity in the event of insulin induced
hypoglycaemia.
Minerals, Micronutrients and Vitamins
Circulating levels of minerals, micronutrients and vitamins are reduced in CP
patients with fat maldigestion: this includes magnesium, calcium, essential
fatty acids, and vitamin A, D, E, and K. In particular, vitamin D and calcium
deficiencies are associated with an increased risk of osteomalacia and
osteoporosis.

Pain treatment
Analgesics. Anti-inflammatory, non-narcotic (and therefore non-addicting) pain
medicines are tried first. If these provide no relief, narcotics or morphine
may be given in addition to relieve sudden episodes of inflammation. The
risk of becoming depended is low in chronic pain. Note also that nonsteroidal anti-inflammatory drugs may themselves cause pancreatitis.
Tricyclic antidepressants. These medications are synergistic with other pain
medication, particularly in those patients in whom pain and depression coexist. .
Pancreatic enzyme supplements. A time limited trial of pancreatic enzyme
supplementation can be tried, but if no pain relief has been observed after 4
weeks, the enzymes should be stopped, unless exocrine deficiency is also
present.
Acid reducers. H2-receptor-blocking medicines and proton pump inhibitors may
be given along with enzymes to reduce the production of stomach acid,
which can stimulate the pancreas. But again, if this is not successful after 4
weeks, the acid reducer can be stopped.

ERCP. Patients with an obstructed pancreatic duct or pancreatic stones may

profit from an endoscopic retrograde cholangiopancreatography (ERCP)
with stone extraction or placement of a stent in a narrowed pancreatic duct.
Coeliac plexus nerve block. An injection of alcohol or corticosteroids into the
retroperitoneal nerves (plexus) may provide temporary relief.
Surgery. Pancreatic surgery (Whipple procedure or duodenum preserving
pancreatic head resection) is the last treatment option for pain in CP
patients. Those patients, in particular, who have had benefit from
endoscopic procedures or have a pseudo-inflammatory mass of the
pancreas, seem to benefit from surgery. It has to be noted, however that
surgery also has some peri- and postoperative side effects.

Diet recommendations

A normal diet should be the target goal in CP patients. In general,

patients should maintain a diet with high energy (35 kcal/kg/24
hours), high protein (1.0 to 1.5 g/kg/24 hours), rich in carbohydrates,
and with moderate amounts of fat (0.7 to 1.0 g/kg/24 hours). A
reduction in oral fat intake or the replacement of dietary fat with
medium chain triglycerides (MCT) risks a reduction in energy intake
and therefore, a negative energy balance. This treatment option
should, therefore, only be considered if adequate enzyme
supplementation and exclusion of bacterial overgrowth has not led
to relief of maldigestion and its accompanying symptom

 Fat soluble vitamins (A, D, E, K), and vitamin B12, as

well as other micronutrients and minerals should be
replaced as clinically indicated. This means that those
patients with signs of persistent maldigestion should
automatically receive multivitamin and trace element
supplements, although neither this nor the effect of
MCTs have been proved in clinical trials. In CP,
antioxidant capacity is decreased and oxidative stress
seems to be a factor promoting CP. This has been
considered as a rationale for interventions with
antioxidants like selenium or vitamin C or E.

Enteral feeding

From clinical experience, enteral

feeding via a gastric or jejunal tube is
seldom necessary except during acute
episodes of pancreatitis.
As in acute pancreatitis, experience
suggests that the optimal method of
feeding may be via the jejunal route.
But enteral sip feeding has the
potential, in patients with severe
malnutrition, to improve energy and
protein intake

In long-term enteral support, this can be maintained either by a percutaneous

endoscopic gastrostomy with jejunal extension or by a direct percutaneous
endoscopic jejunostomy. Parenteral nutrition (PN) is only indicated if enteral
nutrition is not possible. There are no specific considerations with regard to
PN in patients with CP.

Summary

Malnutrition is a frequent feature in patients with CP, with

maldigestion and pain being the two major risk factors for its
development. Nutritional therapy should always be considered as an
integral part of the overall multimodal medical and surgical therapy
of chronic pancreatitis.
A low fat diet is often prescribed, but carries the risk of reduced total
energy intake, thereby worsening the degree of malnutrition. This
approach can, therefore, only be recommended in those patients in
whom pain control and enzyme supplementation fail to resolve the
gastrointestinal symptoms. Sip or enteral tube feeding are options
for patients not responding to medical therapy or for those
undergoing surgery.

TerimaKasih