The Laparoscopic Finding of Pericholedochitis at Cholecystectomy Predicts the Presence of Unsuspected Bile Duct Stones

Abstract

Routine laparoscopic cholangiography and sonography have been recommended for identification of unsuspected bile duct stones in laparoscopic cholecystectomy. The increased prevalence of retained stones seems, however, to confirm that cholangiography has been used rather selectively. The aim of this study was to investigate the kind and extent of a possible correlation between inflammatory changes in the bile duct mucosa and the hepatoduodenal ligament in patients with and without unsuspected bile duct stones. Sixty-eight patients, without symptoms or signs of bile duct stones in their case histories, laboratory findings, and preoperative sonography results, underwent laparoscopic cholecystectomy for symptomatic gallstone disease and diagnostic transcystic cholangiography and cholangioscopy. The initial step at laparoscopy revealed edema of the periductal loose tissue, vascular dilation, and petechiae on the external surface of the distal portion of the extrahepatic bile duct in 47 of 68 patients. Cholangioscopy revealed inflammatory changes in the mucosa of the distal and sphincteric portions of the extrahepatic bile duct in 45 of 47 patients, and unsuspected ductal stones were identified in 41 of these 45 patients. Neither the external surface of the bile duct nor its mucosa exhibited any signs of inflammation in the 21 remaining patients (controls), all of whom showed stone-free bile ducts. Inflammatory changes in the bile duct mucosa, occurring along with unsuspected mobile ductal stones in this study, were reflected on the external surface of the bile duct with a specificity of 87%. The changes in the external surface of the bile duct can be recognized at the initial inspection in laparoscopic cholecystectomy, as in this study, and indicate that more accurate diagnostic procedures to identify unsuspected ductal stones should be used.

Occult pancreaticobiliary reflux in gallbladder cancer and benign gallbladder diseases

“…OPBR was also present in most patients operated on for other benign gallbladder diseases (Table II). These results support previously published findings [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29] and additionally confirm that OPBR could play an important role in the development of biliary pathology and associated symptoms.…”

“…In all eight patients (100%) operated on for chronic acalculous cholecystitis we found significantly (P < 0.001) elevated gallbladder bile amylase and lipase levels compared with their correspondent serum values which were normal (Tables III and IV). The histopathological report revealed nonspecific inflammatory changes, mononuclear infiltration, Rokitansky-Aschoff sinuses and mucosa and gallbladder wall fibrosis, these findings being compatible with chronic cholecystitis, and consistent with previous reports [10][11][12][13][14][15]27,35,36]. Lack of gallbladder stones as well as chronic irritation of the gallbladder mucosa by intermittent or permanent waves of active pancreatic enzymes (amylase and lipase), is supporting evidence for their role as inflammatory agents in the development of chronic cholecystitis, which after some time may lead to malignant degeneration of the gallbladder epithelium [15,16,18].…”

“…There are also reports of SO dysfunction and pancreatic juice reflux in patients with choledochal cysts in whom the SO was found spastic and did not function as a normal sphincter allowing the free reflux of pancreatic juice into the biliary tree [1][2][3]10,11,15,19]. A similar mechanism in addition to SO dyskinesia or stenosis, could explain OPBR in patients with benign biliary pathology and gallbladder cancer [15,16,18,27,[34][35][36]. In all patients enrolled on this study, intraoperative video-cholangiography showed normal flow of contrast into the duodenum, despite the fact that cholangiography did not rule out intermittent SO spasm, the cause of the findings in our patients could be SO dysfunction [28,29,37,38].…”

“…The only plausible explanation for OPBR in patients with normal PBJ is some form of functional disorder of the SO as previously proposed [8][9][10][11][12][13][14][15][20][21][22][30][31][32][33][34][35][36][37]. Two separate categories of SO dysfunction has been recognized based on distinct pathological mechanisms: SO stenosis and SO dyskinesia [27][28][29]31,[36][37][38], SO dyskinesia is characterized by biliary-type pain in absence of any organic diseases in the pancreaticobiliary system related to disorders in the SO cyclic motility [28,29,31,37,38]. Intermittent spasm of the SO not related to the migrating myoelectric complex could be the cause of OPBR.…”

Conservative treatment versus endoscopic sphincterotomy in the initial management of acute cholecystitis in elderly patients at high surgical risk

“…The significant difference between the conservatively treated group and the endoscopic sphincterotomy group in relation to the appearance of biliary sepsis during the work−up period ± 28 % versus 2 % (P < 0.001) ± suggests that the potent proteolytic mixture of bile and pancreatic juice in the main bile duct caused an enzymatic form of cholangitis, facilitating secondary bacterial invasion and possibly infectious cholecystitis [12]. The enzymat− ic cholangitis was also confirmed cholangioscopically during cholecystectomy, with red, fresh, or necrotic plaques being ob− served in the bile duct mucosa [12]. These changes were most prominent distally in the common bile duct and gradually faded in the proximal direction [12], thus providing evidence of a source of inflammation arising from the common channel.…”