[Show abstract][Hide abstract] ABSTRACT: Twenty-two cholangiograms of adults with congenital dilatation of the common bile duct were studied and analyzed. Diagnosis of this disease was established by endoscopic retrograde cholangiopancreaticography in nine patients, by percutaneous transhepatic cholangiography in two patients, and by operative cholangiography in 11 patients. All patients, except one with Caroli's disease, were classified as type I according to Alonso-Lej. An anomalous junction of the pancreaticobiliary ductal system (AJPBDS) was observed in 15 cases. In nine patients the common bile duct joined the main pancreatic duct, and in the remaining six patients, the pancreatic duct was noted to join the common bile duct. These anomalies are considered to be an important etiologic factor in the development of choledochal dilatation. Total cyst excision and hepaticojejunostomy in a Roux-en-Y fashion is recommended as the procedure of choice in those cases with AJPBDS. This is based on the high incidence of cholangitis and the high propensity to induce malignancy of cystic wall following simple drainage.
[Show abstract][Hide abstract] ABSTRACT: This study is prompted in order to clarify the pathophysiological aspect of the liver in acute obstructive suppurative cholangitis (AOSC). An experimental model of AOSC, was prepared by intracholedochal infusion of endotoxin in dogs with and without obstructive jaundice. In the patients with AOSC, liver function was aggravated remarkably compared with that in the stage of non suppurative cholangitis. A rapid fall of platelet count occurred. Experimentally, after intracholedochal infusion of endotoxin, liver function revealed significant hepatic cellular damage. A considerable increase in the S-OCT level was accompanied by a marked rise in blood ammonia concentration. Liver damage due to obstructive jaundice was further aggravated by endotoxin infusion. The level of serotonin in the liver tissue increased markedly after endotoxin infusion. This was accompanied by a rapid fall of platelet counts. Serotonin is considered to be a factor which may cause an impairment of hepatic microcirculation and then hepatic cellular damages. It may be concluded that AOSC is induced by cholangio-venous reflux of endotoxin. Liver function is impaired remarkably due to increased bile canalicular pressure, to the direct affect of endotoxin on liver cells during the process of cholangio-venous reflux, and to impairment of hepatic microcirculation in endotoxin shock. Liver dysfunction contributes to develop this clinical entity and play an important role to make its outcome fatal.
No preview · Article · Feb 1981 · Gastroenterologia Japonica
[Show abstract][Hide abstract] ABSTRACT: Portopulmonary shunting by splenopneumopexy was devised as a new surgical procedure for treatment of portal hypertension accompanied by Budd-Chiari syndrome. Technique of this procedure is simple and is safely performed. The remarkable portopulmonary shunts were visualized by splenoportography postoperatively. Splenic pulp pressure was reduced to a postoperative mean value of 258.3 mm H2O from a preoperative mean value of 336.8 mm H2O. Hemorrhage from esophageal varices and ascites were well controlled after operation. Postoperative liver function tests were essentially unchanged from the preoperative values. Any respiratory and circulatory complications after this shunting have not been observed so far. It is concluded that portopulmonary shunt by splenopneumopexy is an effective procedure for portal hypertension caused by Budd-Chiari syndrome.