This document provides an overview of acute and chronic pancreatitis. Regarding acute pancreatitis, it defines the condition, discusses etiology, pathophysiology, clinical features, investigations, management, complications like pseudocyst, and outcomes. It emphasizes that acute pancreatitis is a biochemical diagnosis based on elevated serum amylase and lipase levels. For chronic pancreatitis, it defines the condition as irreversible progressive destruction of pancreatic tissue causing loss of exocrine and endocrine function and pain. Key investigations and treatments are also summarized.

1. Dr.S.Easwaramoorthy
MS FRCS (Eng) FRCS (Glas) FRCS (Edin) FIAGES, FMAS, FALS, FAES
Chairman, ASITN & P Chapter
Vice President, IAGES South Zone
Examiner, RCS of Edinburgh
Consultant Surgeon, Lotus hospital, Erode

2. Pancreatitis
 Learning Objectives
 Acute Pancreatitis
Pathophysiology
Management of acute pancreatitis
Complications of pancreatitis
 Pseudocyst of pancreas
 Chronic Pancreatitis

3. Acute Pancreatitis
 Introduction/ Definition
 Etiology
 Pathophysiology
 Clinical features
 Symptoms
 Signs
 General examination
 Examination of Abdomen
 Inspection/palpation/percussion/Auscultation/PR
 Investigation
 Hematological/biochemical/radiology/Special
 Management
 Outcome
 Summary

4. Acute Pancreatitis:
Definition
 Acute inflammatory process of pancreas
 With variable degree of involvement of
 Regional tissues
 Remote organ systems

5. Acute Pancreatitis:Acute Pancreatitis:
EtiologyEtiology
 Gall stone
 Alcohol
 Metabolic- hypertriglyceridaemia, hypercalcemia
 ERCP, Cardiac surgery, post-operative
 Trauma
 Infection- mumps,coxackie
 Drugs- thiazides,6-MP,estrogen etc
 Tumours

6. Acute Pancreatitis:
Pathophysiology
Release of Mediators
Trigger Mechanism
Acinar Cell Injury
Cell Activation
Consequences
IL1 IL6 IL8 IL10
TNF NO PAF
E.g.: Alcohol, Gall stones
E.g.: Neutrophil, Monocyte

8. Types of Pancreatitis
Acute edematous pancreatitis Acute nectrotizing pancreatitis
Mild acute pancreatitis
Good Prognosis
Severe acute pancreatitis
Poor Prognosis

9. Pancreatitis: Clinical Features
 Typical History
 Severe Upper abdominal pain
radiating to back
 Clinical Findings
 Hypovolumic shock
 Inspection
 Distended
 Grey Turner’s Sign
 Cullen’s Sign
 Palpation
 Tender
 Mild guarding
 No rigidity
 Percussion
 Dull to percuss due to ascites
 Asucultation
 Bowel sounds: often absent
Grey Turner’s Sign
Cullen’s Sign

10. Acute Pancreatitis:Acute Pancreatitis:
Investigations:
 Haemotological:
 FBC
 Leucocytosis
 Biochemical:
 Serum Amylase/Lipase
 Normal values
 Amylase: Up to 80 u/l
 Lipase: Up to 160 u/l
 Blood urea and Sugar
 Liver Function tests
 Calcium
 Radiological:
 Non Invasive
 X ray chest and abdomen
 US abdomen
 CT abdomen
 Invasive
 CT guided biopsy
 ERCP

11. Acute Pancreatitis is aAcute Pancreatitis is a
biochemical diagnosis!biochemical diagnosis!
Serum amylaseSerum amylase
- >- >1000 units is diagnostic1000 units is diagnostic
-starts to rise after 2-12 hrs and normal again by 3-5-starts to rise after 2-12 hrs and normal again by 3-5
daysdays
-Normal in 30% of cases(alcoholics)-Normal in 30% of cases(alcoholics)
Serum amylase level is helpful
For making the diagnosis
But not for assessing the prognosis

12. Acute PancreatitisAcute Pancreatitis
Non-pancreatic causes of hyperamylasaemia
 AAA(leaking)
 Bowel pathology
 Perf DU/Ischemic bowel
 Chronic renal failure
 Diabetic ketoacidosis
 Ectopic gestation
 Salivary gland disease

13. US Scan in Acute
Pancreatitis
Edematous Pancreas
Gall
Stones

14. CT Scan Abdomen
Pancreas
Renal vein
SMA
Splenic v
Aorta
Kidney
Stomach

15. Severity Scoring
 Glasgow Severity scoring
 Ranson’s criteria
 Apache II Criteria
 Balthazar CT criteria
APACHE: Acute physiology and chronic health
evaluation

16. Acute PancreatitisAcute Pancreatitis
Glasgow Scoring SystemGlasgow Scoring System
 Age >55
 WBC
 AST (SGOT)
 LDH
 Blood sugar
 Urea
 Calcium
 Albumin
 Po2
(3 or more in 48 hrs)

17. Acute Pancreatitis
Mild Acute Pancreatitis
 Minimal Organ
Dysfunction
 Uneventful Recovery
Severe Acute Pancreatitis
 Organ Failure
 Local Complications
 Necrosis: Sterile/infected
 Pseudocyst
 Abscess
Atlanta 1992

18. Summary of Management in
Acute Severe Pancreatitis
Severity Stratification
To ICU
For CT Scan
Predicted Severe DiseasePredicted Mild Disease
To Ward
Tackle the Complications
Diagnosis

19. Multi organ Failure
Organs Affected:
 Pulmonary
 Renal
 Cardio Vascular
 Central Nervous
 GI Tract
 Coagulation System
ARDS

20. Acute PancreatitisAcute Pancreatitis
‘ Management of acute
pancreatitis is
essentially medical’

21. Acute PancreatitisAcute Pancreatitis
Medicalmanagement:
 Fluid replacement to correct the hypovolumia
 Crystalloids/Colloids
 Treatment of hypoxia
 02
 Minimize pancreatic secretion
 Octreotide: doubtful value
 Nutritional support
 Enteral / Parenteral feeding
 Antibiotics
 Imipenum, Pipracillin, Cefuroxime, quinolones
 Treatment of hyperglycemia,hypocalcemia
 Short acting insulin/IV Ca gluconate

22. Acute PancreatitisAcute Pancreatitis
Role of Surgery:
 To remove necrotic pancreas
 Intervention to remove gallstones
 Surgery for late complications:
 Pseudocyst
 Abscess

23. Principles of Surgical Management
of Acute Pancreatitis
Atlanta Classification Treatment
•Edematous pancreatitis(mild AP) Non-surgical
•Necrotizing pancreatitis(severeAP)
a) Sterile necrosis Non-surgical
b) Infected necrosis Debridement
c) Pancreatic abscess Drainage
d) Pseudocyst Drainage

24. Pseudo Cyst of Pancreas
Fluid collection in and around pancreas and not lined by epithelium

25. Pseudocyst
Investigations:
 Ultrasound/CT
 Size and location of cyst
 ERCP/MRCP
 Define ductal disruption

26. Management of Pancreatic
Pseudocysts
Consider:
 Size
 >6cm
 Duration of cyst
 > 6 weeks
 Symptomatic or not

27. Management of Pseudocyst
 Asymptomatic cyst : Observe
 Symptomatic cyst : Drainage
 Cystogastrostomy
Open surgery
Laparoscopic surgery
Endoscopic drainage

28. Laparotomy/Cystogastrostomy

29. Complications of Pseudocyst
 Infection
 Hemorrhage
 Rupture

30. Acute Pancreatitis
Key Messages
 Consider pancreatitis in patients with acute
onset of severe abdominal pain
 Often caused by Alcohol and Gall stones
 Serum amylase for diagnosis
 CT abdomen for severity assessment
 Early aggressive fluid resuscitation

32. Chronic Pancreatitis
‘Irreversible Progressive destruction of pancreatic tissue’
-Loss of Exocrine function : Steatorrhea
-Loss of Endocrine Function : DM
-Pancreatic ductal hypertension: Pain
Causes:
•Alcohol
•Tropical

33. Chronic Pancreatitis
Pathology
 Fibrosis
 Calcification
 Dilatation and
stricture of
pancreatic duct
Clinical Features:
 Pain
 Steatorrhea
 DM

34. Plain x ray abdomen CT abdomen

35. ERCP/MRCP
Stones &
Strictures

36. Dilated PD with calculi

37. Chronic Pancreatitis
Investigation
 Imaging
 X-ray abdomen
 US abdomen
 Endoscopic US
 CT abdomen
 MRCP
 ERCP
 Function tests
 Stool Fat
Treatment:
 Low fat diet
 No alcohol
 Pain killers
 Pancreatic Enzyme
Preparation
 Surgery
 Resection of Pancreas
 Pancreaticojejunostomy

38. Pancreatico Jejunostomy:
Puestow’s Operation