Pancreatic Ascites

  • – 75% cases occur in alcohol induced chronic pancreatitis
  • – <1% CP patients develop pancreatic ascites
  • – 80% cases – leakage arise from a pseudocyst communicating with a ductal disruption
  • – Majority of the patients have pancreatic pseudocyst. The site of ductal disruption seldom demonstrated by noninvasive imaging
  • – Intra-abdominal pancreatic enzymes are inactive and do not causes painful ascites

Causes:

  • – Disruption of the pancreatic duct
  • – Leakage from pseudocyst
  • – Complication of acute/chronic pancreatitis
  • – Blunt abdominal trauma with duct disruption

When to suspect in acute pancreatitis?

  • – Gradual increase in abdominal girth with persistently elevated S. amylase

When to suspect in chronic pancreatitis?

  • – Increasing abdominal girth, weight loss, pain due to ductal disruption

 Ascitic fluid aspiration:

  • – Amylase is markedly raised (often>10,000u/ml)
  • – Ascitic fluid protein, albumin high
  • – SAAg <1.1 g/dl
  • – Total protein >2.5 g/dl

Management of pancreatic ascites:

  • Initial management
  •          – Bowel rest
  •          – Parenteral nutrition
  •          – Octreotide
  •      Response to conservative therapy may be successful in > 25% cases
  • 2) Definitive treatment
  •         – Depends on degree and location of ductal disruption
  •                  • ERCP
  •                  • Surgery:
  •                            ◊ Partial pancreatic resection
  •                            ◊ Cystogastrostomy
  •                            ◊ Cystojejunostomy
  •         – Endoscopic transpapillary pancreatic duct stenting
  •         – Stenting done across the ductal disruption in highly specialized centre. Resolution ascites   occur in 80% cases by endoscopic treatment

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