For Surgeon

1. PANCREATITIS
LT COL SM SHAHADAT HOSSAIN
MCPS,FCPS(surgery)FCPS(Thoracic surgery)
Adv Trg on Thoracoscopy CNUH, South Korea

2. INTRODUCTION
Pancreatitis is inflammation of the pancreatic parenchyma.
It is divided:
a. Acute: which presents as an emergency.
b. Chronic: which is a prolonged and frequently lifelong
disorder resulting from the development of fibrosis.

3. ACUTE PANCREATITIS
An acute condition presenting with abdominal pain, a
threefold or greater rise in the serum levels of the
pancreatic enzymes in blood and urine, which is usually
reversible.

4. PATHOGENESIS
 Premature activation of pancreatic enzymes > leading to
autodigestion.
 Inflammatory process lead to pancreatic
oedema>haemorrhage >eventually necrosis.

5. PATHOGENESIS
 Inflammatory mediators are released into the circulation,
causing haemodynamic instability> bacteraemia> acute
respiratory distress syndrome > pleural effusions.
 It also causes >gastrointestinal haemorrhage> renal
failure >disseminated intravascular coagulation (DIC).

6. ACUTE PANCREATITIS
Two types:
1.Mild (interstitial oedematous pancreatitis)(90-95%).
 Interstitial oedema of the gland
 Minimal organ dysfunction.

7. ACUTE PANCREATITIS
2.Severe (necrotising pancreatitis)(5–10%):
 Pancreatic necrosis
 Severe systemic inflammatory response
 Multi-organ failure.

8. ACUTE PANCREATITIS
Incidence
 3% of all cases of abdominal pain among patients
admitted to hospital in the UK.
 It may occur at any age, with a peak in young men and
older women.

9. AETIOLOGY
 Gallstones (50-70%)
 Alcoholism (25%)
 Post ERCP
 Abdominal trauma
 Following biliary, upper gastrointestinal or cardiothoracic
surgery
 Ampullary tumour
 Drugs (corticosteroids, azathioprine, asparaginase,
valproic acid)

10. AETIOLOGY
 Hyperparathyroidism
 Hypercalcaemia
 Pancreas divisum
 Autoimmune pancreatitis
 Hereditary pancreatitis
 Viral infections (mumps, coxsackie B)
 Malnutrition
 Scorpion bite
 Idiopathic (5%).

11. CLINICAL FEATURES
Abdominal pain
 Develops quickly, reaching maximum intensity within
minutes rather than hours and persists for hours or days
 which is severe, constant and refractory to usual doses of
analgesics
 usually felt in the epigastrium, radiates towards back
(50%)
 gain relief by sitting or leaning forwards.

12. CLINICAL FEATURES
 Nausea
 Vomiting
 Retching
 Hiccoughs due to gastric distension or irritation of the
diaphragm.

13. ON EXAMIATION
 Patient is gravely ill with profound shock, toxicity and
confusion.
 Tachypnoea; common
 Tachycardia
 Temperature is often normal or even subnormal.

14. ON EXAMIATION
Bleeding into the fascial planes:
 Bluish discolouration of the flanks (grey turner’s sign) or
 Umbilicus (cullen’s sign).
Subcutaneous fat necrosis;
 Red, tender nodules on the skin of the legs.

15. ON EXAMIATION
Abdomen:
 Distended
 Muscle guard
 Rigidity
Chest:
 Pleural effusion(10–20%)

16. DIFFERENTIAL DIAGNOSIS
1. Perforated duodenal ulcer
2. Acute Cholecystitis
3. Mesenteric ischaemia
4. Ruptured aortic aneurysm
5. Intestinal obstruction

17. INVESTIGATIONS
 Serum amylase (Normal value; 200-250 somogyi unit):
Three times of upper limit of the normal (1000).
 Urinary amylase (Normal value;24–400 IU/L).
 S. lipase (Normal value;0–50 units/L).

18. INVESTIGATIONS
 CBC: Leukocytosis
 RBS: High
 Liver function tests: Serum bilirubin, albumin,
prothrombin time, alkaline phosphatase.
 Urea/S.creatinine
 S. electrolytes
 Serum calcium level: low

19. Plain X-ray shows
 ‘Sentinel loop’ of dilated proximal small bowel.
 Distension of transverse colon with collapse of
descending colon (colon cut off sign).
 Air-fluid level in the duodenum.
 Renal halo sign.
 Obliteration of psoas shadow.
 Localized ground glass appearance.

20. Plain X-ray shows:
Colon cut
of sign
Sentinel,loop

21. (CECT–contrast enhanced CT)-gold standard
To look for
 Oedema
 Altered fat and fascial planes
 Fluid collections, necrosis
 Bowel distension
 Mesenteric oedema and haemorrhage.

22. CECT

23. Ultrasound of abdomen

24. INVESTIGATIONS
• MRI, MRCP—should be done at a later date.
• ERCP is usually not done in acute phase.
• Chest X-ray for effusion and ARDS.
• EUS—to see necrosis, calcifications and to assess CBD.

25. ASSESSMENT OF SEVERITY
 It should be performed in patients at 24 hours, 48 hours
and 7 days after admission.
 Ranson and glasgow scoring systems are specific for
acute pancreatitis.
 Score of 3 or more at 48 hours indicates a severe attack

26. Acute pancreatitis be stratified into 3 groups
1.Mild acute pancreatitis:
• no organ failure
• no local or systemic complications.

27. Severity of acute pancreatitis
2. Moderately severe acute pancreatitis:
 organ failure that resolves within 48 hours
 local or systemic complications without persistent organ
failure.

28. Severity of acute pancreatitis:
3.Severe acute pancreatitis:
• persistent organ failure (>48 hours);
• single organ failure;
• multiple organ failure.

29. RANSON SCORE
On admission
 Age >55 years
 White blood cell count >16 × 109/L
 Blood glucose >1.1 mmol/L (>200 mg/dL)
 LDH >350 units/L
 AST >250 units/L

30. RANSON SCORE
Within 48 hours
 Haematocrit fall of 10% or greater
 Serum calcium <2.0 mmol/L
 Blood urea nitrogen rise >5 mg/dL
 Arterial oxygen saturation (PaO2) <8 kPa (60 mmHg)
 Base deficit >4 mmol/L
 Fluid sequestration >6 litres

31. GLASGOW SCORE
Within 48 hours
 Age >55 years
 White blood cell count >15 × 109/L
 Blood glucose >10 mmol/L
 LDH >350 units/L
 Serum urea >16 mmol/L
 Arterial oxygen saturation (PaO2) <8 kPa (60 mmHg)
 Serum calcium <2.0 mmol/L

32. TREATMENT
1. Conservative, 70–90%.
2. Surgery, 10–30%.
3. Treatment of complications like acute pseudocyst,
abscess, fistula, ARDS, renal failure, MODS.

33. TREATMENT
Mild pancreatitis:
i. Nil per oral.
ii. Intravenous fluid: ringer lactate, normal saline, dextrose
saline.
iii. Pain relief: Inj pethidine 75 mg IM tds.
iv. Antibiotics; Inj Ceftriaxone, meropenem, cefuroxime iv
bd.
v. Inj esomeprazole iv bd.
vi. Anti emetics: Inj ondansetron iv bd.
vii. Monitor vitals.

34. TREATMENT OF SEVERE ACUTE PANCREATITIS
i. Aggressive fluid rehydration: ringer lactate, normal
saline, dextrose saline
ii. Nasogastric drainage
iii. Analgesia-inj Pethidine
iv. Antibiotics: Inj Ceftriaxone/meropenem
v. Supplemental oxygen

35. TREATMENT
vi. Monitor:
• vital signs
• central venous pressure
• urine output (1.5 mL /kg wt/hr).
Vii. Laboratory investigations:
• liver and renal function
• clotting, serum calcium
• blood glucose, blood gases.

36. TREATMENT
viii. Calcium gluconate 10 ml 10% IV 8th hourly
ix. Supportive therapy-
 inotropes
 ventilatory support
 haemofiltration
x. Nutritional support- enteral (nasogastric) feeding

37. COMPLICATIONS OF ACUTE PANCREATITIS
Systemic
Cardiovascular
• Shock
• Arrhythmias
Pulmonary
• ARDS
Renal failure
Haematological
• DIC

38. Systemic complications
Metabolic:
• Hypocalcaemia
• Hyperglycaemia
Gastrointestinal: Ileus
Neurological:
• Visual disturbances
• Confusion, irritability
• Encephalopathy
Miscellaneous:
• Subcutaneous fat necrosis, arthralgia

39. Local complications
 Acute fluid collection
 Sterile pancreatic necrosis
 Infected pancreatic necrosis
 Pancreatic abscess
 Pseudocyst
 Pancreatic ascites
 Pleural effusion
 Portal/splenic vein thrombosis
 Pseudoaneurysm