Acute Pancreatitis

2. Definition
 A discrete episode of pancreatic cellular
injury & inflammation with:
 Abdominal pain, nausea, vomiting
 Elevated serum amylase & lipase
 Radiographic evidence of pancreatic
inflammation, oedema or necrosis

3. Epidemiology
 Incidence
 5 – 30 cases / 100000 population
 Increasing incidence due to increase in
cholelithiasis associated with increasing
prevalence of obesity

4. Aetiology
 Gallstones & alcohol account for 70 –
80% of all cases
 In 10% cause unknown

5. Common causes
 Gallstones
 Drugs & toxins
○ Ethanol, methanol
○ Tobacco
○ Azathioprine, 6MPU, didanosine, pentamidine,
○ Scorpion venom
○ Organophosphate insecticides
 Trauma
○ Post ERCP, blunt trauma, post-op
 Metabolic
○ Hyperlipidaemia, hypercalcaemia
 Pancreatic duct obstruction
 Infections
○ CMV, mumps, rubella Coxsackie B, ascaris
 Others
○ Autoimmune, genetic
70 - 80% cases: gall stones &
alcohol

6. Pathophysiology
Trypsinogen Trypsin
Activation of
other digestive
enzymes
Pancreatic damage by
necrosis, apoptosis,
autophagy
Damage to surrounding fat
& structures, loss of fluid
into retroperitoneal spaces
Release of inflammatory
cytokines & digestive
enzymes into systemic
circulation
SIRS, hypotension,
ARF, ARDS

7. Clinical Features
 Symptoms
 Pain abdomen
○ Epigastric, radiating to back, reaches maximum
intensity in 30 – 60 min, persists for days, steady
 Nausea
 Vomiting
 Signs
 Tachycardia
 Tachypnoea, dyspnoea, hypotension, altered
sensorium

8.  P/A
 Distended
 Tenderness in epigastric region
guarding, rebound tenderness
 Diminished bowel sounds
 Grey-Turner & Cullen signs
 Others
 Icterus
 Dull percussion noted in lower lung fields

9. Laboratory Diagnosis
 Indicator tests
 Serum lipase
 Serum amylase
 Prognostic tests
 Leukocytosis (>15000/mm3)
 Haemoconcentration
 Raised BUN (>45mg/dL)
 CRP (>150 mg/L)
 Other
 Blood sugar (>180 mg/dL), corrected ser
calcium (<8 mg/dL), ALT (> 200U/L), LDH
(>600U/L), ser albumin (<3.2g/dL)
Glasgow criteria for prognosis
in acute pancreatitis

10. Imaging
 Utility
 Diagnosis
 Aetiology
 Prognosis
 Modalities
 USG
 CT
○ for first attack, severe disease with systemic
complications, failure to improve or when diagnosis not
clear
 MRI + MRCP
 EUS
 ERCP

11.  USG
 Pancreatic enlargement, oedema, associated
periancreatic fluid collections
 Gall stones, dilated CBD
 CT
 More accurate than USG
 Contrast study helps estimate volume of necrotic &
viable tissue
 Excludes other intra-abdominal mimics of pancreatitis
 Gall stones missed
 Assessment of severity & prognostication

12. Treatment
 General Supportive Care
 NPO
 Pain control – narcotic analgesics IV
 Aggressive volume repletion
 Early enteral nutrition
 No role for prophylactic antibiotics
 Minimizing HAI by high quality nursing care,
attention & care of lines & catheters
 Urgent ERCP & biliary sphincterotomy
 Interval cholecystectomy
Establish diagnosis &
severity
Early resuscitation
Detect & treat complications
Treat underlying cause

13. Complications
 Systemic complications
 Hypotension & shock
 ARDS
 ARF
 DIC
 Hypocalcaemia
 Hyperglycaemia
 Hypertriglyceridaemia
 Encephalopathy/ coma

14.  GI Bleeding
 Stress ulceration
 Pseudoaneurysm
 Local
 Pancreatic necrosis (sterile / infected)
 Acute fluid collection
 Pseudocyst
 Duodenal & biliary obstruction

15. Prognosis
 80% recover quickly without serious
complications
 Mortality due to
 MOSF secondary to pancreatitis or HAI
 Rate 2 – 20%