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Pancreatitis –
Acute and
Chronic
By Radhika D Prabhu
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.
Pancreatitis
Pancreatitis is a potentially serious disorder characterized by inflammation of the pancreas
that may cause autodigestion of the organ by its own enzymes.
Acute
Presents as an acute
abdomen condition
Chronic
Prolonged & frequently
lifelong disorder
Development of fibrosis
within the pancreas
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%.
Etiology (IGETSMASHED)
 I : Idiopathic
 G: Gallstone
 E: Ethanol ( Alcohol)
 T: Trauma
 S: Steroids
 M: Mumps.
 A: Autoimmune.
 S: Scorpion stings / spider bites
 H: Hyperlipidemia
 E: ERCP ( Endoscopic retrogade cholangio pancreatography)
 D: Drugs: Thiazide,
Azathioprine.
Less common Causes
 Infection
 Hereditary Pancreatitis
 Hypercalcemia
 Tumors
Pathophysiology
P
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)
 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
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
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
Medical Nutrition Therapy
 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
 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.
Figure 1 Management for mild acute pancreatitis
Assessment of severity of acute pancreatitis
mild to moderate
fasting (2-5 days)
• analgesics
• i.v. fluid/electrolytes
no pain, enzymes ↓
refeeding (3-7 days)
• diet rich in CH
• diet moderate in
protein/fat
normal diet
Figure 2 Management for severe acute pancreatitis
Assessment of severity of acute
pancreatitis
severe
early continuous enteral nutrition
(naso-jejunal tube)
• elemental diet or
• polymeric diet or
• immune-enhancing diet
enteral nutrition is not
possible
nutritional goal not reached
add parenteral nutrition
• all in one or single
component solutions
(CH, protein (AS), fat)
• TPN
and
• continuous small amount
of an enteral diet
(10-30 ml/h) perfused to
the jejunum
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
• 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.
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
 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.
Etiology
 Alcohol, 70%
 Idiopathic (including tropical), 20%
 Other, 10%
Hereditary
Hyperparathyroidism
Hypertriglyceridemia
Autoimmune pancreatitis
Obstruction
Trauma
Pathophysiology
 Stone and duct obstruction theory
 Necrosis–fibrosis hypothesis
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
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.
Reference:
 Earnest Alexander, Nutritional Management in Acute and Chronic Pancreatitis, Pharmacotherapy Self-
Assessment Program, 5th 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/
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Pancreatitis - etiology, pathophysiology and nutrition

  • 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.
  • 4.
  • 5.
  • 6. Pancreatitis Pancreatitis is a potentially serious disorder characterized by inflammation of the pancreas that may cause autodigestion of the organ by its own enzymes. Acute Presents as an acute abdomen condition Chronic Prolonged & frequently lifelong disorder Development of fibrosis within the pancreas
  • 7. 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%.
  • 8. Etiology (IGETSMASHED)  I : Idiopathic  G: Gallstone  E: Ethanol ( Alcohol)  T: Trauma  S: Steroids  M: Mumps.  A: Autoimmune.  S: Scorpion stings / spider bites  H: Hyperlipidemia  E: ERCP ( Endoscopic retrogade cholangio pancreatography)  D: Drugs: Thiazide, Azathioprine.
  • 9. Less common Causes  Infection  Hereditary Pancreatitis  Hypercalcemia  Tumors
  • 11. P
  • 12.
  • 13.
  • 14.
  • 15.
  • 16.
  • 17.
  • 18. 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)
  • 19.
  • 20.  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
  • 21. 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
  • 22. 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
  • 24.  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
  • 25.  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.
  • 26. Figure 1 Management for mild acute pancreatitis Assessment of severity of acute pancreatitis mild to moderate fasting (2-5 days) • analgesics • i.v. fluid/electrolytes no pain, enzymes ↓ refeeding (3-7 days) • diet rich in CH • diet moderate in protein/fat normal diet
  • 27. Figure 2 Management for severe acute pancreatitis Assessment of severity of acute pancreatitis severe early continuous enteral nutrition (naso-jejunal tube) • elemental diet or • polymeric diet or • immune-enhancing diet enteral nutrition is not possible nutritional goal not reached add parenteral nutrition • all in one or single component solutions (CH, protein (AS), fat) • TPN and • continuous small amount of an enteral diet (10-30 ml/h) perfused to the jejunum
  • 28. 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
  • 29. • 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.
  • 30. 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
  • 31.  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.
  • 32. Etiology  Alcohol, 70%  Idiopathic (including tropical), 20%  Other, 10% Hereditary Hyperparathyroidism Hypertriglyceridemia Autoimmune pancreatitis Obstruction Trauma
  • 33.
  • 34. Pathophysiology  Stone and duct obstruction theory  Necrosis–fibrosis hypothesis
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  • 36.
  • 37. 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
  • 38. 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.
  • 39. Reference:  Earnest Alexander, Nutritional Management in Acute and Chronic Pancreatitis, Pharmacotherapy Self- Assessment Program, 5th 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/