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Nutritional Strategies in Acute Pancreatitis Kim Feltner Advisor: Gilbert Boissonneault University of Kentucky Overview 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 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 ↑ 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 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