Acute Abdomen: Special emphasis to

ACUTE
PANCREATITIS

PRESENTOR- Dr BIBASWAN CHAKRABARTY

JR2 (UNIT 1 GENERAL SURGERY)NBMCH

MODERATOR-(Prof) Dr SHIB SHANKAR

RAYCHOWDHURY
 DEFINITION
Acute pancreatitis is an acute inflammatory condition of the
pancreas leading to injury or destruction of acinar components and
clinically characterized by abdominal pain and elevated blood
levels of pancreatic enzymes

300000 admissions per year

Mild cases <1% mortality severe cases 10% - 50% mortality
Mortality- bimodal
early<2wks- MODS late>2wks-sepsis
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 PATHOPHYSIOLOGY
Pancreatitis inciting stimuli
Colocalization of lysosome & zymogen
Contact of lysosomal cathepsin B and trypsinogen
Activation into trypsin
Leakage of colocalized organelle
Cytosolic cathepsin B
Apoptosis and necrosis
Inflammatory response(TNFα, IL 1, IL 2, IL 6) P.T.O
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 Recruitment of neutrophils, macrophages

Release of more inflammatory mediators

Increased vascular permeability and direct damage to

microcirculation

pancreatic necrosis

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 ETIOLOGIES
HYPERLIPIDEMIA
10%
30% HYPERCALCEMIA
MISCELLANEOUS IDIOPATHIC 60 – 80% INBORN ERRORS OF METABOLISM
CAUSES GALL CHRONIC RENAL FAILURE ON
DIALYSIS
STONES DRUG INDUCED
& INFECTIONS
ALCOHOL IATROGENIC
ABUSE TRAUMA
AUTOIMMUNE
ANATOMICAL
TUMOURS
GENETIC

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 BILIARY PANCREATITIS
INCIDENCE- 4-8%
F>M (69% vs 31%)
Pathogenesis:
Passage of stones into ampulla
Passage of infected bile under high pressure , into MPD
(COMMON CHANNEL)
Gene associated – ABCB4

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 ALCOHOLIC PANCREATITIS
PEAK AGE – 40-60 Y
M>F
Avg daily consumption- 100-150g/day
Direct effects:
Releasing GP2 and Lithostatinecalculi
Chronic alcoholism - lysosomal Cathepsin B concentration and
enzyme concentration in pancreatic juice
Alcohol metabolites- ROS & FAEEs-destabilisation of zymogens
and lysosomes
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 Clinical manifestation
1)Pain:
Site – epigastric (right upper quadrant,periumbilical)
Onset – acute
Character – constant
Radiation – back
Associated with nausea & vomiting
2)Dehydration, tachycardia, hypotension etc

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 3)PHYSICAL FINDINGS:
Mild acute pancreatitis(AP): upper
abdominal tenderness (-) signs of peritonitis
Severe AP may mimic acute abdominal
emergencies
Cullen sign & Grey Turner signs
Icterus
Decreased breath sounds

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 DIAGNOSIS
• 2/3 + FINDINGS:
1. PAIN consistent with AP
2. >= 3x rise of serum amylase or lipase levels
3. Imaging findings consistent with AP
Lipase more specific than amylase
• Concomitant findings:
Raised TLC, liver enzymes, RBS,

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 Single parameter Biochemical Marker:
C-REACTIVE PROTIEN- Severe AP if <= 48 hrs value- 150mg/L
Marker of severity of disease

HEMATOCRIT- on admission >44% without fall in 24 hrs

Signifies pancreatic necrosis

PROCALCITONIN cut off- 1.8ng/ml

Signifies infection , infected pancreatic necrosis

Others- IL6, IL8 etc

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 IMAGING
• CONTRAST ENHANCED CT: ( best modality )
Indications:
1:assessment of severity, prognostication
2:failure to respond to conservative management
3:determining need of intervention in severe AP
4:diagnostic uncertainty
• ULTRASONOGRAPHY:
Ordered in AP to rule out Gall stones
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 • EUS:
Helpful in detection of persistent choledocholithiasis
Doesn’t worsen pancreatic inflammation
• MRCP:
Not indicated in acute setting
Helps in evaluation of recurrent attacks

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 SEVERITY ASSESSMENT:
RANSON PROGNOSTIC CRITERIA:
By Ranson and colleagues (1974)
Severe AP if 3 or more Ranson Criteria fulfilled

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 CT SEVERITY INDEX:
Balthazar and associates
Using imaging modality (CECT)

Score Mortality Morbidity

0-3 3% 8%
4-6 6% 35%
7-10 17% 92%

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 ATLANTA BISAP SCORE:
CRITERIA:

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 MANAGEMENT
 FLUID RESUSCITATION:
early aggressive resuscitation
AIM: adequate perfusion of pancreatic microvasculature
RATE: 5-10 ml/kg/hr in the first 12-24 hrs
FLUID: Ringer’s Lactate
frequent re-evaluation
urine output- 0.5ml/kg

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  PAIN CONTROL:
IDEAL: parenteral Opiate Analgesia

 NUTRITION:
MILD AP- additional support usually not required
SEVERE AP- catabolism+ ; hence early initiation
enteral>parenteral:
• gut barrier functions
• reduction of gastric colonisation
• parenteral line sepsis
NASOGASTRIC, NASOJEJUNAL>>TPN
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  ANTIBIOTICS:
patients with co-existent cholangitis (pyrexia+icterus)

 ROLE OF early ERCP

limited to subset having AP+biliary sepsis (jaundice+ SIRS)

Cases with AP & jaundice without SIRS observe for 24-48 hrs
ERCP indicated if persistent rise of bilirubin; EUS detects ductal
stones

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 LOCAL COMPLICATIONS:

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 ACUTE FLUID COLLECTIONS: resolves spontaneously
INFECTED ANC:
Sterile ANC usually don’t require any treatment
If evidence of infection + (gas bubbles on CT)
Choices:
Minimally Invasive RetroPeritoneal necrosectomy
Video Assisted Retroperitoneal Drainage
Endoscopic cystogastrostomy
Laparoscopic cystogastrostomy

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 WALLED –OFF PANCREATIC NECROSIS:
Indications for intervention:
1)Infection
2)Nutritional failure
3)Persistent abdominal pain

Management : LAPAROSCOPIC CYSTOGASTROSTOMY

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Thank you