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|Year : 1986 | Volume
| Issue : 2 | Page : 101-2
Spontaneous bronchobiliary fistula--an unusual complication of acalculous cholecystitis (a case report).
Sekar NN, Chandramohan SM, Kannan KK, Venkataraman MS
|How to cite this article:|
Sekar N N, Chandramohan S M, Kannan K K, Venkataraman M S. Spontaneous bronchobiliary fistula--an unusual complication of acalculous cholecystitis (a case report). J Postgrad Med 1986;32:101
|How to cite this URL:|
Sekar N N, Chandramohan S M, Kannan K K, Venkataraman M S. Spontaneous bronchobiliary fistula--an unusual complication of acalculous cholecystitis (a case report). J Postgrad Med [serial online] 1986 [cited 2022 Jan 24];32:101. Available from: https://www.jpgmonline.com/text.asp?1986/32/2/101/5357
Acute acalculous cholecystitis runs a more fulminant course than calculous cholecystitis and the likelihood of gangrene and perforation of the gall bladder is high. Spontaneous perforation of the bile duct in acalculous cholecystitis is, however, rare in adults. A case of acute acalculous cholecystitis with bronchobiliary fistula following spontaneous perforation of the right hepatic duct is reported here. This complication has not been reported in the English literature so far.
A 35 year old man was admitted with six days' history of acute pain in the right hypochondrium and lower chest, associated with vomiting and fever with rigors for six days. He had been getting attacks of colicky pain in the right hypochondrium for one year prior to this. Examination revealed a toxic patient who was jaundiced and a vague mass was palpable in the right hypochondrium with signs of local peritonitis. There was intercostal tenderness and the liver was just palpable. X-ray of the chest revealed elevated right dome of the diaphragm with basal pleural reaction. At laparotomy, the gall bladder was acutely inflamed, grossly thickened and was adherent to the colon and duodenum. The liver was enlarged and there was evidence of acute cholangitis. No pus was found in the subphrenic spaces. Cholecystectomy could not be done because the tissues were highly inflamed and friable. Hence, cholecystostomy was performed. The gall bladder did not contain bile; its wall was 1.5 cm thick. Post-operatively, the patient continued to have fever and the jaundice intensified. On the second post-operative day, the patient started expectorating bile-stained sputum. X-ray of the chest revealed consolidation of the right lower lobe. Cholecysto-cholangiogram showed a leak from the right hepatic duet forming an abscess in the posteroinferior aspect of the liver which was seen communicating with the right pleural cavity and the bronchus [Fig. 1] and [Fig. 2] E. coli was grown in the bile as well as in the sputum. Bile drainage per cholecystostomy started by the third day and the jaundice gradually came down. The patient became afebrile and the sputum cleared by the tenth day.
The patient was re-explored 5 weeks later and cholecystectomy was performed. A small residual abscess was present deep to the gall bladder bed and was drained. The patient made an uneventful recovery and was discharged after 10 days. Six months later, he was completely asymptomatic.
Perforation of the biliary tree occurs usually after blunt, penetrating or surgical trauma and with obstruction to the bile duct either by a stone or a tumour. Spontaneous perforation of the bile duct can occur without any obvious obstruction to the bile duct but most of these patients have associated gall stone disease. Acute cholecystitis complicating unrelated trauma or surgical procedure has been known to be associated with high incidence of necrosis, gangrene and perforation of the gall bladder. However, spontaneous perforation of the bile duct in acalculous cholecystitis has been reported very infrequently.,  In adults, spontaneous perforation of the bile duct is very uncommon and various causative factors have been proposed. Infected bile, mural thrombosis, ischaemia, activation of reflux pancreatic secretion and infection of the mucous cyst or a diverticulum in the duct wall can lead to weakness and/or necrosis of the duct wall. The bile duct, near its junction with 'the cystic duct, is the site, most susceptible to ischaemia and perforation.
In this patient, cholecystitis and cholangitis were present but no stone or diverticulum was detected in the biliary tree. The cystic duct was very narrow and tortuous and was partially obstructed. Glenn and Mannix have shown that cholecystitis can be induced by partially occluding the cystic duct. In this patient, cholangitis and infected bile could have caused necrosis of a portion of the right hepatic duct which ruptured, possibly due to associated raised intraductal pressure, consequent to spasm of the sphincter of Oddi. This had resulted in a localised abscess in the posteroinferior aspect of the liver deep to the gall bladder. This subsequently had ruptured into the pleura and into the bronchial tree establishing a bronchobiliary fistula. No other case report of spontaneous bronchobiliary fistula complicating acalculous cholecystitis has been found in the English literature.
The high incidence of fatal complications in acute acalculous cholecystitis dictates the need for early surgical intervention. Cholecystectomy should be done whenever possible since cholecystostomy alone, in the presence of patches of necrosis or gangrene may not halt the pathological process. In the presence of perforation of the bile duct, 'T' tube drainage of the bile duct should be established and no attempt should be made to repair the perforation.
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