Obstructive jaundice produces a number of biochemical and physiologic alterations in the biliary tract. Acute cholangitis occurs in an infected, usually obstructed biliary system, at the level of the common bile duct. The most common cause of obstruction is stones. Bacterial reflux from the biliary tract to the systemic circulation is considered to be the primary etiologic factor in bacteremia and the development of sepsis in cholangitis. The main factors in the pathogenesis of acute cholangitis are biliary tract obstruction, elevated intraluminal pressure, and infection of bile. The bile is normally sterile. The route of infection may be ascending, hematogenous or by lymphatics. Bactibilia (presence of bacteria in the biliary tract) increases in the presence of biliary obstruction, particularly partial and in the presence of foreign bodies like stones. Obstruction produces local changes in the host defenses, both in chemotaxis and phagocytosis along with systemic changes. The absence of bile and secretary IgA from the gastrointestinal tract because of biliary obstruction produces changes in the bacterial flora, loss of mucosal integrity, decreased endotoxin inactivation and promotes bacterial overgrowth, portal bacteremia, endotoxemia and increased translocation of endotoxin (LPS) to the liver, resulting in sepsis and also serving to inhibit hepatic macrophage (Kupffer cell) function in these patients. Early intervention in relieving biliary decompression is imperative in restoring normal function of the Kupffer cells in the liver and to prevent functional alterations in the liver because of chronic obstruction and cholestasis and to decrease the postoperative morbidity and mortality.

BACKGROUND The incidence and mode of spread of carcinoma of the gallbladder into the hepatoduodenal ligament have not been well described pathologically for gallbladder carcinoma extending into the subserosa and beyond. METHODS Between 1985 and 2002, 50 consecutive patients with gallbladder carcinoma extending into the subserosa or beyond underwent radical surgery, including extrahepatic bile duct resection. Serial sections of specimens of the resected extrahepatic bile ducts were examined to determine the incidence and the pattern of invasion of the hepatoduodenal ligament from the primary cancer. RESULTS Invasion of the hepatoduodenal ligament was present in 30 of the 50 specimens. Of these, 9 showed direct extramural spread (type I), 4 showed continuous intramural spread (type II), 5 showed distant spread separated from the primary tumor (type III), and 4 showed spread of cancer cells from metastatic lymph nodes (type IV). The remaining 8 patients had more than 1 type: 1 patient had types I + III; 3 had types I + III + IV; and 4 had types III+IV. Invasion of the hepatoduodenal ligament was present in 24 of 44 patients without preoperative obstructive jaundice and in 2 of 13 patients with stage IB disease. Patients with types II, III, and IV spread into the hepatoduodenal ligament had significantly better survival than those with type I spread. CONCLUSIONS Gallbladder carcinoma extending into the subserosa or beyond invades the hepatoduodenal ligament with relatively high frequency. Preoperative diagnosis of this invasion is difficult; therefore, strong consideration should be given to resection of the extrahepatic bile ducts and lymph nodes.

OBJECTIVE To determine the causes of choledochal dilatation in patients with obstructive jaundice. METHODS One hundred and sixty-four patients with obstructive jaundice were investigated by endoscopic retrograde cholangiopancreatography(ERCP), and patients with choledochal dilatation (group I, n=110) were compared with those without choledochal dilatation (group II, n=54). RESULTS The causes of common bile duct dilatation were choledocholith, juxtapapillary duodenal diverticula and congenital dilatation of the common bile duct. The distal common bile duct and its surroundings were abnormal in 104 (94.55%) of the 110 patients and in 13 (24.08%) of the 54 patients (P<0.01). Juxtapapillary duodenal diverticulum accounted for 24.55% in group I, and only in 9.26% in group II (P<0.05). Post-cholecystectomy patients were 13.64% in group I, and only 5.56% in group II. CONCLUSIONS The abnormalities of the distal common bile duct and its surroundings can usually be detected as underlying causes of common bile duct dilatation. ERCP is necessary before cholecystectomy, since it is considered the "gold standard" for the diagnosis of distal common bile duct abnormalities.

Results of 1831 laparoscopic cholecystectomies (LCE) are analyzed. Symptoms of obstructive jaundice were at 170 (9.3%) patients. All these patients underwent endoscopic papillosphincterotomy before LCE for removal of bile hypertension. Conversion to open surgery was necessary in 44 (2.4%) cases. Intraoperative injuries of extrahepatic bile ducts occurred at 5 (0.27%), bleeding--at 10 (0.6%) patients. Postoperative complications were seen at 36 (2.0%) patients including intraabdominal bleeding (4), drainage bile less (8), subhepatic abscess (4), epigastric wound infection (16). There were 2 (0.1%) lethal outcomes. Accurate surgical technique and timely conversion to open surgery prevent complications of LCE.

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