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Case Study Report: The Use of Nutrition Support in Pancreatitis
Sara Patton
Dietetic Intern
ARAMARK Healthcare
Distance Learning Dietetic Internship
Paoli Hospital
March 15, 2013
Abstract
Pancreatitis is inflammation of the pancreas and usually begins as a sudden
attack1. Gallstones and alcohol abuse account for more than 80% of reported acute
pancreatitis case, making them the two most common etiological factors. In severely ill
patients, complications may occur such as multiple organ failure and pancreatic
necrosis. In such severe cases, an oral diet is usually not an option 3. The initiation of
nutrition support as standard practice when an oral diet is not feasible is becoming a
more common practice. In the past, the common undisputed plan of care was to put the
pancreas “at rest” by making the patient nil per os (NPO), which means nothing by
mouth 1. By having the patient fasting, the assumption was that the pancreas would not
be stimulated to produce any secretions. However, new studies have found that if the
pancreas was keep at baseline secretions, the patient would have better outcomes and
short length of stays 4. The timing of initiating EN has been thought to be within 48hours
to help reduce incidences of multi-organ failure, pancreatic infectious complications, and
mortality4. The main aim of nutrition support is to help cover the body’s elevated
demands due to protein catabolism and metabolic instability. When providing the
elevated needs via enteral nutrition, it is important to prevent over stimulation of
pancreatic secretions and to keep them at baseline4.
Disease Description
The pancreas is a glandular flattened organ that lies in the upper abdomen behind
the stomach. The pancreas has both exocrine and endocrine function. Endocrine
functions include producing glucagon, insulin and somatostatin. Exocrine functions
include secreting enzymes directly into the intestinal lumen to help in digestion of
macronutrients. Neural and hormonal responses play a major role in the regulation of
exocrine secretions. Some outside factors that influence pancreatic function include the
anticipation, sight and taste of food. In a healthy pancreas, the secretions during a meal
can be divided into three phases: the cephalic phase, gastric phase, and ending with
the intestinal phase1.
Pancreatitis is inflammation of the pancreas and usually begins as a sudden attack1.
Once the pancreas is inflamed, its digestive enzymes, mainly trypsin, attack the tissue
that produces said enzymes 2. Furthermore, once trypsin begins to attack the pancreatic
tissue, it can cause bleeding, tissue damage, and cause blood vessels to swell. It can
be classified as either acute or chronic pancreatitis2. If these attacks continually reoccur,
then it is considered chronic pancreatitis. Mahan, Escott-Stump, and Raymond write
that pancreatitis is “characterized by edema, cellular exudates, and fat necrosis. The
disease can range from mild and self-limiting to severe, with auto digestion, necrosis,
and hemorrhage of pancreatic tissue1”. In 1974, Ranson and colleagues had
distinguished 11 sign and symptoms that have prognosis significance of pancreatitis.
Ranson’s criteria are:

age >55 years

white blood count >1600m3

blood glucose levels >200mg/100mL

lactic deydrogenase >350units/L

aspartate transaminase >250units/L

hematocrit decrease of>10mg/dL

blood urea nitrogen increase of >5mg/dL

arterial PO2 <60mm Hg

base deficit >4mEq/L

fluid sequestration >6000mL

serum calcium level <8mg/mL
These symptoms can be measured within the first 48 hours of admission, and therefore
determine likely outcomes of the patient’s hospitalization. By assessing the clinical
presentations of the patient, the degree of intervention can be obtained (see figure1)3.
Pancreatitis can result from chronic alcoholism, biliary tract disease,
hypertriglyceridemia, hypercalcemia, gallstones, trauma, certain drugs or some viral
infections. Alcohol is thought to contribute to about 60-90% of the development of
chronic pancreatitis2. “Obesity appears to be a risk factor for the development of
pancreatitis and an increased severity1”. Pancreatitis can result from one or multiple
compounding factors. Physical symptoms of pancreatitis can include nausea, vomiting,
abdominal distention, steatorrhea, and continuous or intermittent pain varying in
intensity to sever upper abdominal pain which can radiate to the back. More severe
cases of pancreatitis can be complicated by hypotension, oliguria, dyspnea, and
extensive destruction of pancreatic tissue. The destruction of pancreatic tissue leads to
fibrosis in which enzyme production is diminished.
Evidence-Based Nutrition Recommendations
The main factor in pain felt in acute pancreatitis is related to the secretion
mechanisms of pancreatic enzymes and bile. With many patients who acute
pancreatitis, the intake of normal food is often intolerable. The standard nutrition care in
the past was to put the pancreas “at rest” by making the patient nil per os (NPO), which
means nothing by mouth1. The thought behind this action was to prevent the stimulation
of the pancreas by withholding food. The initiation of nutrition support as a means of
providing proper nutrition during times of pancreatitis is becoming more popular
compared to the “old” standard of pancreatic rest. Enteral nutrition is the overall
preferred method for nutrition support when compared to parenteral. However, the exact
route of enteral feeding is still dependant on more studies4.
Coté GA et al, 2011, in a multicenter controlled study, found that the
pathogenesis of chronic pancreatitis is still unknown. There are several mechanisms
thought to be at work to produce the progression of the disorder, but the main culprit
appears to be chronic inflammation. Historically, alcohol abuse has been the widespread common factor of chronic pancreatitis. However, this article discusses the recent
decline in alcohol use as the stand alone contributory factor in pancreatitis. Although
alcohol still remains as the common etiology of pancreatitis, more and more patients are
presenting with non-alcoholic pancreatitis. New genetic analysis is helping researchers
to find a link between previously unrecognized factors that are contributory to
developing the disease. The interactions between possible “culprit” genes and
environmental dynamics may hold the key to future pancreatitis research 2.
Spanier, et al, 2010, in a literature review of nasogastric feedings in patients with
acute pancreatitis, found that enteral nutrition should be initiated as soon as possible to
influence better outcomes. Gallstones and alcohol abuse account for more than 80% of
reported acute pancreatitis case, making them the two most common etiological factors.
In severely ill patients, complications may occur such as multiple organ failure and
pancreatic necrosis. In such severe cases, an oral diet is usually not an option. The idea
of pancreatic rest disregards the persistence of basal pancreatic secretions. There are
three components of pancreatic secretion: protein enzymes, fluid volume, and
bicarbonate. The protein enzyme output is the main perpetuation of the inflammatory
process, and therefore suppression of protein enzyme output theoretically would be
adequate in putting the pancreas to “rest”. Having the pancreas reduced to baseline
stimulation by using nutrition support can help maintain gut integrity 4.
The use of an elemental, semielemental or polymeric formula is still unclear as to
which would have the better outcome. The idea in using an elemental and semielemental formula is that they would require less digestion and therefore cause less
pancreatic secretions. The timing of initiating EN has been thought to be within 48hours
to help reduce incidences of multi-organ failure, pancreatic infectious complications, and
mortality. One study discussed in the article cites the initiation of EN within 36 hours
when compared to after 36hours in the ICU population and found that earlier initiation
helped to reduce the length of stay in the hospital. Overall, once a patient is unable to
consume sufficient oral intake within 5-7days or is predicted to not be able to meet
estimated needs, nutrition support should begin. Enteral nutrition is preferred over total
parenteral nutrition, and TPN should only be used if EN cannot be tolerated 4.
Ioannidis, et all, 2008, in a series of controlled clinical studies on the
effectiveness of enteral nutrition, shows that enteral nutrition should be the preferred
route in patients with acute pancreatitis. Approximately 75% of patients diagnosed with
mild acute pancreatitis have a mortality rate below 1% and is increased up to 20% if the
disease progresses to a severe necrotizing form. Acute malnutrition is often observed
and can lead to further complications. The main aim of nutrition support is to help cover
the body’s elevated demands due to protein catabolism and metabolic instability. When
providing the elevated needs via enteral nutrition, it is important to prevent over
stimulation of pancreatic secretions and to keep them at baseline. Parenteral nutrition
support can increase complications in patients’ with pancreatitis due to uncontrolled
hyperglycemia and infection. Another downfall to using parenteral nutrition as a first line
of support is that parenteral nutrition is more expensive than enteral. Only patients’ with
severe pancreatitis that cannot tolerate enteral nutrition support should be considered
for parenteral 5.
Mirtallo, et all 2012, in a systematic review and evaluation of published literature
provides an evidence based review for nutrition support of pancreatitis. After evaluating
different trials and studies of patients’ with pancreatitis, the base energy requirements
were found to range from 25-35kcal/kg/d and energy expenditure stayed around
25kcal/kg/d regardless of whether the patient has acute, chronic or sepsis with
pancreatitis. Concerning patients’ on parenteral and enteral nutrition, it was found that
patients receiving parenteral were better able to meet the higher caloric goals. However,
the patients also had higher incidences of hyperglycemia. These findings still beg to
question whether or not patient outcomes would be improved from delivery of fewer
calories and the need to reconsider the volume or dose of feedings. The current
guidelines in place for nutrition therapy in patients with pancreatitis have been assessed
to be universally applicable6.
Case Presentation
The patient is a 53 year old Caucasian male who came to the emergency room
after experiencing significant abdominal pain and vomiting earlier that afternoon. The
symptoms began earlier that day acutely after eating lunch. The pain began to radiate
towards his back and is not relieved with any change in position or fasting. The patient
was begun on dilaudid in the ER, which did help the pain a little.
NCP: Assessment:
Client History: The patient is a 53 year old male whom does not have many
issues with medical problems. His past medical history does include hypertension,
hyperlipidemia, kidney stones, non-alcoholic fatty liver disease, and possible
hypertriglyceridemia. The patient was once told that his liver enzymes were elevated
when he was trying to give blood, in which he discovered that he had non-alcoholic fatty
liver disease. His family history is non-contributory. The patient does not smoke, drinks
socially, and has no history of illicit drug use.
Food/Nutrition-Related History: The patient has recently lost about 44 pound
intentionally over the last 4 months by restricting his diet and aggressively adhering to a
workout regimen. The patient had restricted his diet to about 1200kcals/day. The patient
stated that he was “getting too big” and therefore decided to lose weight. The patient
reported wanting to get healthier. The patient denied any chewing/swallowing difficulties
and any food allergies.
Nutritionally pertinent medications were:

lovenox: anticoagulant. May cause nausea, vomiting, abdominal pain, GI
bleeding, constipation, black tarry stool7

dilaudid: analgesic, antitussive, narcotic.Helps relieve moderate to severe pain.
May cause anorexia, decrease wt, increased thirst, dehydration, nausea,
vomiting 7

primaxin: antibiotic. May cause taste changes, nausea, vomiting, abdominal pain,
diarrhea, dyspenia 7

ativan: anti-anxiety. Limit caffeine and grapefruit. May cause dry mouth, nausea,
vomiting, diarrhea, constipation, anorexia

7
protonix: proton pump inhibitor, antigerd. May cause decrease acid secretions,
increased gastric pH, nausea, diarrhea 7
Nutrition-Focused Physical Findings: Upon admission, the patient had a blood
pressure of 123/73, heart rate of 55 and temperature of 97.5 degrees Fahrenheit.
The patient presented awake and oriented x3 but with a mildly anxious affect. The
patient reported no appetite and was currently nauseous. The patient is capable of
self care and self feeding. There was significant tenderness to the epigastric area in
his abdomen, with mild palpitations. There were no apparent signs of muscle and or
fat wasting. The patient was presenting with the classic signs of pancreatitis.
Anthropometric Measurements:
Height: 70in
Weight: 87.5kg
Usual Body weight: 107.4kg
% weight change: 18.62% in 4 months
IBW: 75.20kg
%IBW: 115%
BMI 27.58. overweight per standards 8
Calculations for the above measurements can be found in table 1.
Biochemical Data/Medical Tests:
The nutritionally relevant biochemical data collected on the pt are described in table 2.
Medical tests performed/findings:
CT ABD and Pelvis with Contrast (2/08/13). Findings: Acute pancreatitis, mild
hypoenhancement of body and tail of pancrease relative to the head, likely
secondary to sever edema. Early pancreatic necrosis possible. Irregular fundus
of gallbladder. Nonobstructive left renal calculi
MRI Abdomen without Contrast(2/08/13): Findings: Cholelithiasis, extensive
peripancreatic edema. Small amount upper abdominal ascites. Trace bilateral
pleural effusions.
CT Abdomen with IV Contrast (2/11/13): Findings New moderate right and small
pleural effusions. Severe pancreatitis with evidence of necrosis in portions of the
body and tail. Wall thickening of small bowel loops in vicinity of pancreas.
Abdomen Survey/KUB (2/12/13): Dobhoff Tube placement. Feeding tube in place
with its tip in the right upper part, likely overlying distal body of the stomach.
Nutrition Needs:
Calories: 2175kcals (using 25kcals/kg actual body weight)
Protein: 130.5-174gm Protein (using 1.5-2.0grams/kg actual body weight)
Fluid: 2175-2610mL (using 25-30mL/kg actual body weight)
Calculations explained in table 3 8.
Nutrition Status Classification: In compliance with ARAMARK’s nutrition status
classification, the patient is classified at moderate nutrition risk due to vomiting (3
points), low albumin (3 points), diagnosis of acute pancreatitis (3 points). Table 4
explains the nutrition status classification and the point system 9.
Diagnosis-Related Group: In accordance to ARAMARK’s diagnosis-related group, the
patient falls into the category of Unspecified PCM (Protein Calorie Malnutrition) due to
his reported inadequate protein and/or calorie intake for > 7 days, and his albumin
levels < 3.5 (patient’s albumin level: 2.4) 9
NCP: Diagnosis:
Inadequate Oral Intake (NI-2.1) related to decreased ability to consume sufficient
energy/food-nutrition-related knowledge deficit concerning appropriate oral food intake
as evidenced by weight loss, nausea/vomiting, reported insufficient intake of energy
when compared to requirements, and sever acute pain 10. (See Table 5).
The patient reported very low PO intake prior to admission due to his abdominal pain.
Furthermore, the patient had been restricting his diet to 1200kcals/day, which is below
is estimated daily requirements.
NCP: Intervention:
Meidcal Intervention:
Antibiotic stopped- no detection of infection was present.
CT ABD and Pelvis with Contrast (2/08/13). Findings: Acute pancreatitis, mild
hypoenhancement of body and tail of pancrease relative to the head, likely
secondary to sever edema. Early pancreatic necrosis possible. Irregular fundus
of gallbladder. Nonobstructive left renal calculi
MRI Abdomen without Contrast(2/08/13): Findings: Cholelithiasis, extensive
peripancreatic edema. Small amount upper abdominal ascites. Trace bilateral
pleural effusions.
CT Abdomen with IV Contrast (2/11/13): Findings New moderate right and small
pleural effusions. Severe pancreatitis with evidence of necrosis in portions of the
body and tail. Wall thickening of small bowel loops in vicinity of pancreas.
Abdomen Survey/KUB (2/12/13): Dobhoff Tube placement. Feeding tube in place
with its tip in the right upper part, likely overlying distal body of the stomach.
Nutrition Intervention: Enteral Nutrition (ND-2.1) 10: recommend start tube feeding of
Peptamen AF @15mL/hrx 24hr, increase by 10mL/hr until goal of 75mL/hr x 24hr is
reached. Recommend flush 125mL H2O every 4 hours. Peptamen AF is an elemental
formula which may be easier on the patient to digest. Once the tube feeding is at the
goal rate of 75mL/hr it will provide 1800mL total volume, 2160kcals, 137grams protein,
99 grams fat, 1460mL water. Total water flushes will provide 750mL water for a total of
2210mL water. (see Table 6 for calculations).
NCP: Monitoring and Evaluation:
Enteral Nutrition Intake (FH-1.3.1) 10.
Begin Enteral nutrition infusion on 2/12/13 using Peptamen AF at a rate beginning at
15mL/hr, increasing by 10mL/hr until goal of 75mL/hr x 24hr with water flushes of
125mL every 4 hours. Monitor Enteral nutrition initiation and rate advancement.
Follow-up: On 2/13/13 the patient was receiving the goal rate of 75mL/hr of the tube
feeding. The patient did not report and nausea or vomiting, no abdominal distention,
and no aspiration. The patient appeared to be tolerating his tube feeding at goal rate.
As of 2/15/13, the Dobhoff tube was removed and advanced to a clear liquid, then a
low-fat diet, both of which he tolerated. Patient reported minimal abdominal discomfort
and was tolerating orals for over 24 hours. The patient was discharged to home on
2/16/13.
Patients’ discharge plan is as follows:

Follow up with PCP in 1 week with CBC and CMP and to discuss with GI as well
as PCP regarding resuming back on Simvastatin as well as low-dose Aspirin.
Avoid Tylenol products and NSAIDs.

Ambulate as tolerated

GI follow-up as recommended

Not to drive while on pain medications
Conclusion
Many patients admitted to the hospital with acute or chronic pancreatitis are often
unable to consume an oral diet. The pain associated from eating often brings an overall
aversion to food. Having pancreatitis can increase the nutrient needs of the body due to
inflammation, possible infection, and multi-organ failure. The increased demand on the
body is hard to reach when the patients do not want to eat. Therefore, the initiation of
nutrition support is becoming a standard practice when the patient is predicted to be
NPO for an extended period of time, or if the patient already presents as malnourished.
Enteral nutrition support helps give the pancreas a “rest” but encourages base-line
pancreatic secretions.
The patient was taken off the tube feeding after three days and started on an oral
diet. After 24 hours of monitoring, the patient was tolerating his diet, and was ready to
go home. The patient was discharged on a low-fat diet. The patient was scheduled for
several gastroenterology follow-ups to monitor pancreatic function.
Appendix
Figure 13:
Table 1: Anthropometric Calculations
Height
Weight
Usual Body Weight
% Weight change
Ideal Body Weight (IBW)
% Ideal Body Weight (%IBW)
Body Mass Index (BMI)
70 inches
192.4lbs /2.2kg = 87.5kg
236.25lbs/2.2kg= 107.4kg
(236.25lbs-192.4lbs)/236.25lbs x 100=
18.62%
106lbs for first 5 feet, 6 lbs for every inch
over.
6 x10in = 60lbs. 106 +60= 166lbs.
166/2.2kg= 75.20kg
236.25lbs / 192.4lbs= 115%
[192.4lbs / (70in)² ] x 703= 27.58
Table 2 Biochemical Data
RBC
WBC Count
Creatinin
Sodium
Potassium
Chloride
136-144
3.6-5.1
98-
Count
4.54.5-5.8
10.8K/UL
mEq/L
mEq/L
Glucose
BUN
e
Albumin
70-99mg/dL
8-20mg/dL
0.8-
3.4-5.0g/dL
109mEq/L
K/UL
1.3mg/dL
2/07
15.5 (H)
5.38
141
4.2
106
141(H)
23(H)
1.1
5.0
2/08
12.1(H)
4.91
141
4.0
110(H)
130(H)
23(H)
0.9
3.9
2/09
14.8(H)
4.67
144
3.7
115(H)
101(H)
18
0.7(L)
3.2(L)
2/10
12.4(H)
4.45(L)
144
3.7
115(H)
114(H)
18
0.7(L)
3.2(L)
2/11
9.9
3.90(L)
143
3.9
114(H)
102(H)
19
0.6(L)
2.9(L)
2/12
9.9
3.94(L)
144
3.5(L)
113(H)
98
16
0.5(L)
142
3.6
112(H)
109(H)
16
0.5(L)
141
3.4(L)
110(H)
123(H)
13
0.5(L)
2.6(L)
Within
normal
limits
Low:
Vomiting,
diarrhea,
laxatives
High:
Dehydratio
n, diarrhea,
decreased
kidney
function
High:
medications
, stress,
illness
High: kidney
damage,
kidney
stones,
dehydration
Low:
decrease
d kidney
function
Low: nephritic
syndrome,
acute/chronic
inflammation
2/13
2/14
Rationale
9.9
3.96(L)
High:
stress,
certain
medications
, infection
Low:
Blood
loss,
kidney
function
Table 3: Nutrition Calculations:
Calories
Protein
Fluid
25kcals/kg x 87.5kg
1.5-2.0 grams/kg x 87.5kg
25-30mL/kg x 87.5kg
2175kcals
130.5-174gm
2175-2610mL
Table 4: ARAMARK Classification6 :
Nutrition Status Classification
Points
Normal (Status 1)
0-5
Mildly Compromised (Status 2)
6-7
Moderately Compromised (Status 3)
8-11
Severely Compromised (Status 4)
 12
Nutrition Status Classification
Time Frames for Reassessment/Followup
Normal (Status 1)
5-7 days
Mildly Compromised (Status 2)
4-6 days
Moderately Compromised (Status 3)
3-5 days
Severely Compromised (Status 4)
1-4 days
Table 5: Diagnosis Terminology/PES Statement
Nutrition Diagnosis Terminology / PES Statements
Doma Nutrition
Relat Etiology
As
Signs and/or Symptoms
in
Diagnosis
ed to
eviden
Terminolog
ced by
y
Intak (NI-2.1)
Relat decreased
As
weight loss,
e
Inadequate ed to ability to
eviden nausea/vomiting,
Oral Intake
consume
ced by reported insufficient
sufficient
intake of energy when
energy/foodcompared to
nutritionrequirements, and sever
related
acute pain
knowledge
deficit
concerning
appropriate
oral food
intake
Peptamen AF Nutrition Information (courtesy of Nestle Healthcare Nutrition
Product Guide)
Table 6: Tube Feeding Calculations:
Total Volume (mL)
75mL x 24hrs= 1800mL (1.8 Liters)
Total Calories (kcals)
1800mL x 1.2kcals/mL= 2160kcals
Total Protein (grams)
1.8L x 76grams protein/L= 136grams
Total Fat (grams)
1.8 Lx 54.8grams fat/L= 99grams
Free Water (mL)
1.8L x 811mL= 1460mL
Water Flushes
125 x 6= 750mL
Total Water
1460mL + 750mL= 2210mL
Works Cited
1. Escott-Stump S, Mahan KL, Raymond JL. Krause’s Food and the Nutrition Care
Process, 13th ed. St. Louis: Elsevier Inc.; 2012.
2. Coté GA, Yadav D, Slivka A, et al. Alcohol and Smoking as Risk Factors in an
Epidemiology Study of Patients With Chronic Pancreatitis. Clinical
Gastroenterology and Hepatology. 2011;9(3): 266-273
3. Curtis CS, Kudsk KA. Nutrition Support in Pancreatitis. Surgical Clinics. 2007;
97(6): 1403-14215
4. Spanier BWM, Bruno MJ, Mathus-Vliegen EMH. Enteral Nutrition and Acute
Pancreatitis: A Review. Gastroenterology Research and Practice. 2011;vol
2011:1-9. doi:10.1155/2011/857949
5. Ioannidisi O, Lavrentieva A, Botsiosi D. Nutrition Support in Acute Pancreatitis.
Journal of the Pancreas. 2008; 9(4): 375-390
6. Mirtallo JM, Forbes A, McClave ST, Jensen GL, Waltzberg DL, Davies AR.
International Consensus Guidelines for Nutrition Therapy in Pancreatitis.
Journals of Parenteral and Enteral Nutrition. 2012;36(3): 284-291.
doi:10.1177/01486071 12440823
7. Crowe JP, Pronsky ZM, Food Medication InteractionsTM , 17th ed. Birchrunville:
Food-Medications Interactions; 2012
8. Width M, Reinhard T. The Clinical Dietitian’s Essential Pocket Guide. Baltimore:
Lippincott Williams & Wilkins; 2009.
9. ARAMARK Healthcare. Assessment and education policy #2: Nutrition status
classification worksheet. Patient Food Services: Policies and Procedures,
Volume IV; 2010
10. American Dietetic Association. International Nutrition Terminology (IDNT)
Reference Manual: Standardized Language for the Nutrition Care Process.
Chicago, IL; 2011.