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1. Welcome
To
Morning Session

2. Acute Pancreatitis
Dr.Amitav Biswas
Intern Doctor
Department of Medicine
TMMC&H

3. Definition
 Acute pancreatitis is a inflammation of the
pancreas
pancreatic
causes.
induced by the activation of the
enzymes derived from various

4. Causes
Non- traumatic( 75 %)
Biliary tract diseases
Alcohol
Viral infection(EBV, CMV, mumps)
Drugs(steroid, thiazide, furosemide)
Scorpion bites
Hyperlipidemia
Hyperparathyroidism

5. Continue….
Traumatic (5%)
Operativetrauma
Blunt/penetratingtrauma
Labtest(ERCP/angiography)
Idiopathic(20%)

6. Pathogenesis of acute pancreatitis
Interstitial oedema
Impaired blood flow
Ischaemia
Acinar cell injury
ACTIVATED ENZYMES
Interstitial inflammation
oedema
Gallstone
Chronic alcoholism
Release of intracellular
proenzymes and
lysosomal hydrolases
Activation of enzymes
Delivery of proenzymes to
lysosomal compartment
Intracellular activation of
enzymes
Proteolysis
(proteases)
Fat necrosis
(lipase, phospholipase)
Haemorrhage
(elastase)
ACINAR CELL INJURY
Alcohol, drugs trauma,
ischaemia, viruses
DEFECTIVE INTRACELLULAR
TRANSPORT
Metabolic injury (experimental)
Alcohol, duct obstruction
DUCT OBSTRUCTION

7. Symptoms and signs
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.

8. 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. Cullen sign

10. Grey-Turner sign- discolouration in the flanks

11. Severity
Mild form (interstitial or edematous
pancreatitis)
focal or diffused edema
slight leukocyte infiltration



12.  Moderate : transient organ
failure and/or complications <
48hr
May or may not have
necrosis
Local complications such as
fluid collection is usually seen.

13. Severe form (necrotic or hemorrhagic pancreatitis
)

marked acinar destruction with hemorrhage
extensive leukocyte infiltration
necrosis of parapancreatic fat
grossly an inflammatory tumor-
like mass with diffused hemorrhagic change
secondary infection induces the
formation of abscess or pseudocysts


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

14. Full blood count: neutrophil leucocytosis
Lab investigation
Electrolyte abnormalities include hypokaemia, hypocalcemia
ElevatedLDHinbiliary disease
Glycosuria(10%ofcases)
Bloodsugar:hyperglycaemiainseverecases
Ultrasound look for stonesinbiliary tract diseases.
AbdominalCTscanmay revealphlegmon(inflammatory mass), pseudocyst or
abscess(complications of acute pancreatitis)

15. Lab investigation
Amylase and lipase
Elevated serum amylase and lipase levels, in combination with severe
abdominal pain, often trigger the initial diagnosis of acute
pancreatitis.
Serum lipase rises 4 to 8 hours from the onset of symptoms and
normalizes within 7 to 14 days after treatment.
Marked elevation of serum amylase level during first 24 hours

16. Reasons for false positive elevated serum amylase include salivary gland disease
(elevated salivary amylase) and macroamylasemia.
Ifthelipaselevelisabout2.5 to 3 times thatofAmylase,itis an indication of
pancreatitis due to Alcohol or gallstone
Thedegreeofamylase/lipaseelevationdoes not correlatewith severity of acute
pancreatitis.

17. Ranson Score
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 ALT > 250 IU/L
serum LDH > 350 IU/L At 48 hours

18. Calcium(serumcalcium<2.0mmol/L(<8.0mg/dL)
Hematocritfall>10%
Oxygen(hypoxemiaPO2<60mmHg)
BUNincreasedby1.8ormoremmol/L(5ormoremg/dL)afterIVfluidhydration
Basedeficit(negativebaseexcess)>4mEq/L
Sequestrationoffluids>6L

19. APACHE II score
(Acute Physiology And Chronic Health Evaluation)
Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality
Score 5 to 6 : 40% mortality Score 7 to 8 : 100%
mortality
Hemorrhagic peritoneal fluid
Obesity
Indicators of organ failure
Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min
PO2 <60 mmHg
Oliguria (<50 mL/h) or increasing BUN and creatinine
Serum calcium < 1.90 mmol/L (<8.0 mg/dL)

20. Acute pancreatitis. The pancreas is enlarged (blue arrow) with
indistinct and shaggy margins.
There is peripancreatic fluid (red arrow) and extensive
peripancreatic infiltration of the surrounding fat (black arrow).

21. Acute Pancreatitis
Complications
 Two significant local complications
 Pseudocyst
 Abscess

22. Acute Pancreatitis
Complications
 Pseudocyst
 Cavity surrounding outside of pancreas
filled with necrotic products and liquid
secretions
 Abdominal pain
 Palpable epigastric mass
 Nausea, vomiting, and anorexia
 Elevated serum amylase

23. Acute Pancreatitis
Complications
 Pancreatic abscess
 A large fluid-containing cavity within pancreas
 Results from extensive necrosis
 Upper abdominal pain
 Abdominal mass
 High fever
 Leukocytosis

24. Systemic complications
 ARDS
 Acute renal failure
 Heart failure and cardiac arrhythmia
 Gastrointestinal bleeding
 Septicemia
 Disorders of hemostasis: thrombosis, DIC.
 Disorders of CNS: pancreatic encephalopathy Hyperglycemia
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25. Progression of Disease
 Autodigestion
 Acute Inflammation of Pancreas
 Necrosis of Pancreas
 Digestion of vascular walls

 Thrombus and Hemorrhage
 Death

26. Acute Pancreatitis
Goals of Treatment
 Relief of pain
 Prevention or alleviation of shock
 Decrease respiratory failure
 ↓ of pancreatic secretions
 Maintain Fluid/electrolyte balance

27. Treatment and Nursing Care
1. Pain management
 IV morphine
 Antispasmodic agent
 Positioning – sitting up and leaning
forward

28. Treatment
 2. Prevention of Shock – hemodynamic
 stability
 * Administer Blood, Plasma
expanders, Albumin
 * Ringers Lactate solution

29. Treatment and Nursing Care
 3. Suppress pancreatic enzymes
 * NPO
 * NG suction
 * Antacids, H2 receptor antagonists, antispasmotics
4. Decrease respiratory distress
 * Oxygen; check O2 saturation levels
 * Semi-fowlers position, knees flexed,
position changes

 5. Antibiotics

30. Treatment and Nursing Care
 6. Correction of electrolyte imbalance/
hypocalcemia
 7. Maintain Hydration / Nutrition

31. Treatment and Nursing Care
 Surgical therapy – if related to gallstones
 ERCP
 Endoscopic sphincterotomy
 Laparoscopic cholecystectomy

32.  Follow up care
 Dietary teaching
 High-carbohydrate, low-fat diet
 Abstinence from alcohol,
 Patient/family teaching
 * Signs of infection, high blood
 glucose, steatorrhea

Treatment - Home Care

33. Reference
• Davidson’s Principles and Practice of Medicie 22nd
edition
• Oxford Handbook of Clinical Medicine 10th
edition
• Harrison’s Principles of Internal Medicine 19th
edition
• www.Medscape.com

34. Thank You