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Transcript
Nutritional Strategies
in Acute Pancreatitis
Kim Feltner
Advisor: Gilbert Boissonneault
University of Kentucky
Overview
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Occurrence and Disease significance
Pathophysiology
Signs and Symptoms
Diagnosis
Treatment Methods
Pancreatitis
 Incidence ranges from 1-5 cases per 10,000
people each year
 In 85-90% of patients, will subside in 3-7 days
 Most common causes
 Alcohol, gallstones
 Others
 Hypertriglyceridemia, viral infections (mumps or
hepatitis), scorpion bites, some drugs such as
valproic acid, sulfonamides, and thiazide diuretics
and others
Pathophysiology
 Autodigestion
 Activation of proteolytic enzymes
trypsinogen, chymotrypsin, and trypsin
occurs in the pancreas instead of activation
in the intestinal lumen
 These activated proteolytic enzymes digest
pancreatic and peripancreatic tissue
 More enzymes become activated causing
digestion of cellular membranes that cause
proteolysis, edema, and interstitial
hemorrhage
Pathophysiology
 Proteases are packaged in precursor form
and there are also protease inhibitors in the
acinar cell and in the pancreatic secretions
preventing autodigestion from occurring
 Death of the acinar cells releases enzymes
and begins autodigestion
 Death of acinar cells caused by:
 Duct obstruction or reflux of bile or duodenal
contents into pancreas
 Certain drugs or alcohol
Symptoms
 Abdominal pain
 Steady and boring located epigastrically may
radiate to back, chest, flanks, or lower
abdomen
 N/V
Signs
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Low-Grade Fever
Tachycardia
Hypotension
Diminished or absent bowel sounds
Pain may be relieved by bending forward
(patient may be curled up)
Signs
 Turner’s Sign
 Discoloration of the
flanks reflecting tissue
catabolism of hemoglobin
 May indicate severe
necrotizing pancreatitis
From Forbes CD, Jackson WF: Color Atlas and Text of
Clinical Medicine, 3rd ed. London, Mosby, 2003.
Signs
 Cullen’s sign 
 Faint blue
discoloration
around the umbilicus
 Result of
hemoperitoneum
http://content.nejm.org.ezproxy.uky.edu/cgi/content/full/340/2/149
Diagnosis
 CT scan may confirm clinical impression
of pancreatitis
 Sometimes 3 days after dx to identify
necrotizing pancreatitis
 CT of abdomen may show gallstones
 ERCP if gallstones suspected
 Usually not used after first attack unless
cholangitis or jaundice
Lab Abnormalities
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↑ Serum amylase
↑ Lipase parallel with amylase
Hyperglycemia
Hypocalcemia
Leukocytosis
↑ CRP  suggests pancreatic necrosis
and also causes ↓ albumin
Severity Assessment
Ranson’s Criteria
 Admission
 Initial 48 hours
 Age > 55yrs
 WBC > 16,000/mm3
 ↓ Hematocrit > 10%
 ↑ BUN > 5 mg/dL
 Blood Glucose >200mg/dL
 Serum calcium < 8mg/dL
 Arterial Po2 < 60mmHg
 Serum LDH > 350
IU/L
 Serum AST > 250 U/L
0-2 criteria  1% mortality
3-4 criteria  16%mortality
5-6 criteria  40% mortality
7-8 criteria 100% mortality
 Base deficit > 4 mEq/L
 Est. fluid
sequestration > 6 L
Development indicates
worsening prognosis
Treatment
 Narcotics for pain
 IV fluids for hydration
 Normally kept NPO to avoid stimulation
of pancreas until free of pain and N/V
 If pancreatitis does not subside within a
few days
 Total Parenteral Nutrition (TPN)
 Enteral nutrition
Nutritional Strategies
 NPO
 Nothing by mouth
 Fluids replenished by IV
 Reduces stimulation of the pancreas to prevent
worsening of the disease state
 Mild cases may begin oral intake within 3-4 days
 Gastric decompression
 Nasogastric tube suction to remove the acidic
stomach contents and prevent them from reaching
the jejunum
 Recent studies have really shown no benefit to this
therapy
Nutritional Strategies
 Total Parenteral Nutrition (TPN)
 Placement of Central Venous Catheter in order
to provide complete nutrition (internal jugular,
subclavian)
 May be required if an ileus is present or if
patient has been NPO for 7-10 days
 Very invasive, should not be used very early in
pancreatitis
 High risk of catheter related infections and
sepsis
Nutritional Strategies
 Enteral Nutrition
 Naso-gastric feeding usually preferred
(inexpensive and easier-no radiology or
endoscopy)
 Distal to the ligament of treitz produce no
change in complications, mortality, or length of
hospital stay
 Enteral feeding has been shown to improve the
systemic inflammatory response
What Next?
 After free of pain, N/V, bowel sounds return
 Begin with clear liquid diet
 Very few calories (Enlive is a supplement to clear liquids to
provide more calories)
 Low residue food in liquid form to minimize amt of food to be
digested in the intestines
 Next step up to full liquid diet
 All liquids added so some protein and fat are available
 Next step up to small meals, low fat, low cholesterol,
low triglyceride
 May need to provide counseling to patient to avoid
recurrent attacks
 Avoid alcohol, eat small meals
References
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Arend W.P., Ausiello D., Goldman L., editors. Cecil Textbook of Medicine. 22nd ed.
Philadelphia: W. B. Saunders; 2004. 779-884.
Conn's Current Therapy 2004. 56th ed. Philadelphia: W. B. Saunders; 2004. 563-573.
Fauci B., Hauser K., Jameson L., editors. Principles of Internal Medicine. 15th ed. Vol. 2.
New York: McGraw Hill; 2001. 2249-2257.
Green II H.L., Noble J., et al, editors. Textbook of Primary Care Medicine. 3rd ed. St. Louis:
Mosby; 2001. 1792-1803.
Heinrich S., Shafer M., Rousson V., Clavien P. Evidence-based treatment of acute
pancreatitis: a look at established paradigms. Annals of Surgery. 2005 Feb;243(2):154168.
Marik P.E., Zaloga G.P. Meta-analysis of parenteral nutrition versus enteral nutrition in
patients with acute pancreatitis. British Medical Journal (2004):1-6.
Mcphee S. J., Papadakis M.A, Tierney, Jr L.M., editors. Current Medical Diagnosis and
Treatment. Los Altos: California: Lange Medical Publications; 2005. 671-676.
Radenkovic D., Johnson C. Nutritional support in acute pancreatitis. Nutritonal in Clinical
Care. 2004; 7(3):98-103.
Raimondo M., Scolapio J.S. What route to feed patients with severe acute pancreatitis:
vein, jejunum, or stomach? The American Journal of Gastroenterology. 2005
Feb;100(2):440
Retally C.A., Skarda S., Garza M.A, Schenker S. The usefulness of laboratory tests in the
early assessment of the severity of acute pancreatitis. Critical Reviews in Clinical
Laboratory Science. 2003; 40(2):117-149
Questions