Pancreatitis - etiology, pathophysiology and nutrition

This includes nutritional management of the disease

1. Pancreatitis – Acute and Chronic By Radhika D Prabhu

2. The Pancreas The pancreas is a gland located in the upper posterior abdomen. It is located behind the stomach and is surrounded by other organs, including the spleen, liver and small intestine. The pancreas is about 6 inches (15.24 centimeters ) long, oblong and flat.

3. Acute Pancreatitis Acute pancreatitis is the result of an inflammatory process involving the pancreas caused by the release of activated pancreatic enzymes . In addition to the pancreas, this disorder can also affect surrounding organs, as well as cause a systemic reaction. In mild pancreatitis, inflammation is confined to the pancreas. Patients do not have organ failure or systemic or local complications. The mortality rate is < 5%. In severe pancreatitis, there is persistent single or multiorgan failure (after about 48 h). Most patients have one or more local complications. The mortality rate is > 30%.

4. Etiology (IGETSMASHED ) I : Idiopathic G : Gallstone E : Ethanol ( Alcohol) T: Trauma S: Steroid s M: Mumps. A: A utoimmune . S: Scorpion stings / spider bites H: Hyperlipidemia E: ERCP ( Endoscopic retrogade cholangio pancreatography ) D: Drugs: Thiazide , Azathioprine .

5. Less common Causes Infection Hereditary Pancreatitis Hypercalcemia Tumors

6. Pathophysiology

7. P

8. Signs and Symptoms The most common symptoms and signs include: Severe epigastric pain radiating to the back, relieved by leaning forward Nausea , vomiting, diarrhea and loss of appetite Fever/chills Hemodynamic instability, including shock In severe case may present with tenderness, guarding, rebound. Signs which are less common, and indicate severe disease, include: Grey-Turner's sign (hemorrhagic discoloration of the flanks) Cullen's sign (hemorrhagic discoloration of the umbilicus)

9. Serum amylase; It stays 48-72h then become normal. Serum lipase; (diagnostic test) It elevated for 7-14 days. Other: -WBC (15000-30000). -LDH>500 U/dl - Glucose. - Albumin. - Ca in serum. - AST.Bilurbin,Alkaline Ph. - ABG show Hypoxia. INVESTIGATIONS

10. RANSON CRITERIA Predicting the severity of acute pancreatitis At admission  age in years > 55 years  white blood cell count > 16000 cells/mm3  blood glucose > 11  mmol /L (> 200 mg/ dL )  serum AST > 250 IU/L  serum LDH > 350 IU/L

11. At 48 hours  Calcium (serum calcium < 2.0  mmol /L (< 8.0 mg/ dL )  Hematocrit fall > 10%  Oxygen (hypoxemia PO2 < 60 mmHg)  BUN increased by 1.8 or more mmol /L (5 or more mg/ dL ) after IV fluid hydration  Base deficit (negative base excess) > 4 mEq /L  Sequestration of fluids > 6 L

12. Medical Nutrition Therapy

13. The nutritional management is based on the pre-existing nutritional status and severity of the disease as given below Group Condition Nutritional Support I Good nutritional status and mild pancreatitis Oral diet with less fat II Poor Nutritional status and mild pancreatitis Parenteral/ Enteral Support III Good/Poor nutritional status and severe pancreatitis Parenteral /Enteral Support

14. Energy and Protein Patients with severe acute pancreatitis are hypermetabolic which may be further complicated by sepsis or multiorgan failure. Usually energy requirements in severe acute pancreatitis are 15-20kcal/kg body weight/day with a total protein intake of 1.2 – 1.5 g/kg body weight/day or 15-20 percent of total energy Fats Severe hyperlipidemia occurs in patients with acute pancreatitis , the mechanism for which is not very clear. Total lipids may be given upto 2g/kg body weight /day or 20-30 percent of total energy depending upon the serum triglyceride concentration.

15. Which formula should be used in acute pancreatitis? Standard polymeric formula and, if this is not tolerated, a peptide-based formula is tried. Several published trials have also used formulae containing immune modulating substrates (glutamine, arginine, n-3 polyunsaturated fatty acids) or pre- and probiotics

16. In mild pancreatitis , patients should be on intravenous (IV) fluids till the pain is controlled . Oral feeding can commence thereafter. The patient should be given small amounts of carbohydrate-protein diet and gradually increased over 3-6 days with careful supplementation of fat . After 7 days , a normal diet can be given. In severe acute pancreatitis , enteral feeding ( nasojejunal or nasogastric) must be started as early as possible. Semi elemental diets at 1 kcal/ml may be started . TPN is used when enteral feeds aggravate pain , ascites etc. Lipid emulsions can be used safely if the serum triglyceride levels remain below 400mg/dl . Once the condition improves , the patient can be shifted to enteral and the oral feeds.

17. Chronic Pancreatitis Chronic pancreatitis is persistent inflammation of the pancreas that results in permanent structural damage with fibrosis and ductal strictures, followed by a decline in exocrine and endocrine function.  Chronic pancreatitis can be broadly classified into 3 forms: Chronic calcifying pancreatitis Chronic obstructive pancreatitis Chronic autoimmune pancreatitis

18. Chronic calcifying pancreatitis is the most common form and is characterized by calcification of the pancreatic parenchyma, formation of intraductal stones, or both. Chronic obstructive pancreatitis results from partial or complete obstruction of the pancreatic duct. Chronic autoimmune pancreatitis is a unique form that often responds to glucocorticoids .

19. Etiology Alcohol, 70% Idiopathic (including tropical), 20% Other , 10%    Hereditary    Hyperparathyroidism    Hypertriglyceridemia    Autoimmune pancreatitis    Obstruction    Trauma

20. Pathophysiology S tone and duct obstruction theory   N ecrosis–fibrosis hypothesis  

21. Symptoms About 10 to 15% of patients have no pain and present with symptoms of malabsorption. Other symptoms include the following: Nausea Vomiting Weight loss Diarrhea Oily or fatty stools Clay- colored or pale stools

22. Nutritional Management Nutritional status of these patients can be improved by providing good dietary counselling. These patients do not require any supplementary food . To promote weight gain the level of fat in the diet must be maximised without increasing steatorrhoea or pain. If there is malabsorption , a low fat diet (20-30 g/day) along with supplementation with medium chain triglycerides is recommended . If there is endocrine involvement of the pancreas , a diabetic diet is recommended.

23. Reference: Earnest Alexander, Nutritional Management in Acute and Chronic Pancreatitis, Pharmacotherapy Self-Assessment Program, 5 th Edition. Orestis Ioannidis , Athina Lavrentieva , Dimitrios Botsios , Nutrition Support in Acute Pancreatitis , JOP.J Pancreas(Online) 2008;9(4):375-390 Textbook of Nutrition and Dietetics,Second Edition, Kumud Khanna, Sharda Gupta, Santosh Jain Passi , Rama Seth, Ranjana Mahna , Seema Puri . Websites: http://www.msdmanuals.com/professional/gastrointestinal-disorders/pancreatitis/chronic-pancreatitis http://epomedicine.com/clinical-cases/acute-pancreatitis-case-discussion/