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Fictitious pancreatitis in choledochal cyst
Insights
Recurrent acute pancreatitis in children can indicate a choledocal cyst. High amylase levels in the cyst fluid, not pancreatic inflammation, explain these symptoms. Surgical excision is recommended.
Area of Science:
- Pediatric Surgery
- Gastroenterology
- Medical Diagnostics
Background:
- Choledochal cysts classically present with abdominal pain, jaundice, and a palpable mass.
- Atypical presentations include cyst rupture, bile peritonitis, pancreatitis, and esophageal varices.
Observation:
- Three pediatric cases presented with recurrent acute pancreatitis and elevated serum amylase.
- Laparotomy revealed no pancreatic inflammation but high amylase levels within the choledochal cyst fluid.
- The cyst wall showed inflammatory reactions.
Findings:
- Elevated serum amylase in these cases was attributed to high amylase concentration within the choledochal cyst.
- These findings support the pancreatic reflux hypothesis for choledochal cyst etiology.
- Cyst excision led to asymptomatic outcomes for all three patients.
Implications:
- Hyperamylasemia should not impede surgical management of suspected choledochal cysts.
- Cyst excision is the definitive treatment, resolving cholangitis and hyperamylasemia.
- Early diagnosis and surgical intervention are crucial for pediatric choledochal cyst management.
Abstract:
The classical presentation of choledocal cyst has been regarded as a triad of abdominal pain, jaundice and a palpable abdominal mass; unusual presentations include rupture of the choledocal cyst with bile peritonitis, pancreatitis and bleeding esophageal varices. We are reporting 3 children presenting clinically as recurrent acute pancreatitis with elevated serum amylase and found to have type I choledocal cyst. Despite elevated serum amylase there was no evidence of pancreatic inflammation at laparotomy. High amylase concentration was found in fluid contained within the cyst. This was probably responsible for the elevated serum amylase and also the inflammatory reaction seen in the wall of the choledocal cyst. These cases support the hypothesis that pancreatic reflux into the bile ducts is the etiological factor in the development of choledocal cyst. Our 3 cases were treated by cyst excision and have remained asymptomatic. The presence of hyperamylasemia should not delay appropriate surgical management. The treatment of choice is cyst excision, since it will eliminate factors contributing to the development of cholangitis and hyperamylasemia.