Poster Presentation 6th Australian Health and Medical Research Congress 2012

Falciform ligament abscess from left sided portal pyaemia following malignant obstructive cholangitis (#420)

Leigh R Warren 1 , Manju D Chandrasegaram 1 , Dan Madigan 2 , Eu L Neo 1 , Chris S Worthley 1
  1. Hepatobiliary Unit, Royal Adelaide Hospital, Adelaide, SA, Australia
  2. Department of Radiology, Royal Adelaide Hospital, Adelaide, SA, Australia

Background: 

Abscess formation of the falciform ligament is incredibly rare and perplexing when encountered for the first time. It has been reported to occur in the setting of cholecystitis and cholangitis but the pathophysiology is poorly understood.

Case Presentation:

We present a 73-year old gentleman with this rare condition, in the setting of cholangitis from an obstructive ampullary carcinoma. He was referred from a country hospital with progressive jaundice, anorexia and nausea. Prior to transfer, he deteriorated with cholangitis, dehydration and renal failure. On arrival, his abdomen was exquisitely tender along the course of the falciform ligament. His blood tests revealed an elevated bilirubin of 291 umol/L, creatinine of 347 mmol/L and white cell count of 14.9 x 109/L, . His Ca 19.9 was markedly elevated at 35,000 kU/L. 

Imaging and intervention:

A non-contrast CT demonstrated gross biliary dilatation and a collection tracking along the path of the falciform ligament to the umbilicus. He was commenced on intravenous antibiotics and underwent an urgent endoscopic retrograde cholangiopancreatogram (ERCP) and biliary stent drainage. Cholangiogram revealed a grossly dilated biliary tree, with abrupt transition at the ampulla, which on biopsy confirmed an obstructing ampullary carcinoma.

Following ERCP, his jaundice and abdominal tenderness settled. Subsequent contrast CT revealed left portal venous thrombosis. He was treated with antibiotics and was optimised for an elective pancreaticoduodenectomy.

Operative findings:

At operation, we encountered abscess transformation of the falciform ligament. We drained copious amounts of pus and necrotic material. Part of the round ligament was resected along the undersurface of the liver. On histology, there was prominent histiocytic inflammation with granular acellular eosinophilic components. He recovered slowly but uneventfully.

We present his operative images and radiographic findings, as we may have uncovered key events that may explain the pathophysiology behind this rare complication. 

Conclusion:

We hypothesise that cholangitis, with secondary portal pyaemia and tracking of this via the remnant left umbilical vein, can cause infectious seeding of the falciform ligament, with consequent abscess formation.

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