An alternative surgical approach to a difficult case of Mirizzi syndrome: a case report and review of the literature.

Mirizzi syndrome (MS) is an uncommon complication of gallstone disease and occurs in approximately 1% of all patients suffering from cholelithiasis. The syndrome is characterized by extrinsic compression of the common hepatic duct frequently resulting in clinical presentation of intermittent or constant jaundice. Most cases are not identified preoperatively. Surgery is the indicated treatment for patients with MS. We report here a 71-year-old male patient referred to the surgical outpatient department for diffuse upper abdominal pain and mild jaundice (bilirubin rate: 4.2 mg/dL). Ultrasound examination revealed a stone in the cystic duct compressing the common hepatic duct. The patient had a history of gastrectomy for gastric ulcer 30 years ago. MRCP revealed a stone impacted in the cystic duct causing obstruction of the common hepatic duct by extrinsic compression. With these findings the preoperative diagnosis was indicative of MS. At laparotomy a moderately shrunken gallbladder was found embedded in adhesions containing a large stone which was palpable in the common bile duct. The anterior wall of the body of the gallbladder was opened by an incision which extended longitudinally along the gallbladder towards the common bile duct. The stone measuring 3.0 cm in diameter, was then removed setting astride a large communication with the common bile duct. A Roux-en-Y cholecysto-choledocho-jejunostomy was performed. The subhepatic region was drained. The patient had an uneventful recovery. He was discharged eleven days after operation and remained well after a 30-mo follow-up.

Management of HILAR malignant biliary strictures.

OBJECTIVE: To determine the etiology of Hilar malignant biliary strictures and the efficacy of hepaticojejunostomy in it's management with or without segmental liver resection. PATIENTS AND METHODS: A retrospective study of 33 patients was carried out at Civil Hospital & Lyari General Hospital Karachi. They presented with signs and symptoms of mechanical cholestasis. Study was conducted to find the etiology, level of obstruction and the extent of the disease together with approaches to either cure the disease or to relieve the symptoms. Curative resection was attempted where possible in all 33 patients but decision of curative resection or palliative bypass with or without liver resection was made per operatively after accessing the level of obstruction and extent of local, parenchymal or vascular infiltration. RESULT: Of the 33 patients studied, 72.73% (n = 24) had cholangiocarcinoma and 27.27% (n = 9) had gall bladder Ca with local bile duct extension. Four different sites of biliary tree (i) common hepatic duct [CHD], (ii) confluence of common hepatic duct [CCHD], (iii) right and left hepatic duct [R&LHD] separately, and (iv) left hepatic duct [LHD] were anastamosed with jejunum. Normal liver functions with complete relieve from symptoms was achieved where CHD or CCHD was anastamosed whereas only a significant decrease was observed when R&LHD and only LHD were anastamosed with jejunum. CONCLUSION: Surgical resection of the tumor together with biliary decompression using different approaches of hepaticojejunostomy is an effective way of managing malignant Hilar bile duct obstruction as well as significantly decreasing the severity of symptoms in irresectable tumours.

[Functional changes in the biliary system following extrahepatic biliary obstruction]. / Alterazioni funzionali del sistema biliare secondarie ad ostruzione biliare extraepatica.

To assess the potential structural changes of the biliary tree and liver in patients with extrahepatic biliary obstruction, the resected specimens of 20 patients operated for benign biliary stricture were evaluated by means of immunocytochemical and histological methods. Furthermore, liver biopsies were taken for the same purposes. The results showed that in the dilated segment of the hepatic duct proximal to the stricture, innervation was greatly reduced or completely absent with associated advanced morphological and histological changes and high intrabiliary pressure levels. Similar findings were observed in the liver biopsies, too. These biopsies showed advanced morphological and histological changes associated with reduced innervation. By contrast, the nondilated segment of the hepatic duct, distal to the obstruction, showed normal innervation, normal morphology and histology and normal levels of intrabiliary pressure. The present study provides evidence that in cases of extrahepatic biliary obstruction, there are advanced pathological changes in the biliary tree associated with innervation impairment. These structural changes are associated with functional changes in both the liver and the biliary tree. Such functional changes represent a threat to the patient, particularly if major surgery is required. Increased biliary pressure appears to be a major cause of the development of these changes. Biliary drainage, either surgical or endoscopic, is indicated as the only alternative to reduce intrabiliary pressure and to contribute to a reversal of these structural and functional changes.

Liver histological, portal flow and plasmatic nitric oxide alterations caused by biliary obstruction and drainage in rats.

PURPOSE: To evaluate liver alterations caused by biliary obstruction and drainage. METHODS: Thirty-nine male Wistar rats were randomly distributed in 4 groups: BO (n=18) bile duct ligation for 20 days, with a periodic evaluation of liver histological alterations, Doppler echography portal flow and measurements of NO and malondialdehyde (MDA); BO/DB (n=13) bile duct occlusion for 20 days followed by biliary drainage by choledochoduodenal anastomosis, 5 days follow-up, same BO group parameters evaluations; group CED (n=4) sham operation and portal flow evaluation trough 20 days; CHB (n=4) sham operation, with hepatic biopsy on 25th day and followed-up trough 25 days, by the same parameters of group BO, with exception of portal flow. Direct bilirubin (DB) and alkaline phosphatase (AP) were evaluated in the group BO, BO/DB and CHB. RESULTS: The bile duct ligation led to an increase of DB and AP, development of liver histological alterations, reduction of portal flow and increase of plasmatic NO and of MDA levels. The bile duct clearing resulted in a reduction of DB, AP, NO, MDA histological alterations and increase of portal flow. CONCLUSION: The biliary occlusion resulted in cholestasis and portal flow reduction, besides the increase of plasmatic NO and of hepatic MDA levels, and histological liver alterations, with a tendency of normalization after the bile duct clearing.

[The pathomorphology of the liver after unilateral hepatic duct obstruction with laboratory-chemical observations of the course in the dog]. / Untersuchungen zur Pathomorphologie der Leber nach unilateralem Hepatikusverschluss mit laborchemischer Verlaufsbeobachtung beim Hund.

UNLABELLED: In an experimental study the morphological and functional changes of the liver with unilateral hepatic duct obstruction were investigated over a period of 13 months. In 4 series different parts of the liver were excluded of the bile drainage by hepatic duct ligation after cholecystectomy (group I = 25%, group II = 50%, group III 75%, group IV = 100% of the liver, series V = control group was cholecystectomy only. The clinical outcome, biochemical parameters, liver biopsy were examined regularly. Bacteriologic investigation of the bile and hepatic flow measurement were performed at the beginning and at the end of the study. RESULTS: The clinical symptoms were discrete and the biochemical parameters showed a typical course. After 6 weeks, atrophy of the excluded liver with contralateral compensatoric hypertrophy was found. The microscopic correlation was the secondary sclerosing cholangitis (SSC). After 6 weeks, a concentric periductal fibrosis was to be observed in the periportal area. After 12 weeks, bile duct vanishing with persistence of the arteries and veins was found. After 36-48 weeks, biliary cirrhosis and total destruction of the liver parenchyma was found respectively. Simultaneously a chronic disturbance of the hepatic perfusion was seen. It was caused by a perivenous fibrosis of the terminal vein with obliteration of the lumen by endangiitic proliferations and cavernous transformation. The genesis of SSC seemed not be be influenced by bile contamination. The ligated as well as the unligated bile ducts were infected in 20-50% only. There was no difference in the liver specimens with sterile or contaminated bile. The hepatic flow measurement showed a reduction of the portal blood flow and a rise of the arterial flow depending on the amount of the excluded liver. A better understanding of the pathophysiological sequelae of the unilateral hepatic duct obstruction suggests that the drainage by surgical or radiological methods may not invariably be necessary.

Lesions of the segmental and lobar hepatic ducts.

Despite reports to the contrary, unobstructed drainage of 50% of an otherwise normal liver through either the right or left uninfected hepatic duct is adequate to restore normal liver function, even if the obstructed lobe remains in place. An undrained liver lobe, if present, may require no further treatment. As long as it is completely obstructed and uninfected, it will undergo a progressive asymptomatic atrophy. Cholangitis invariably develops behind a partial lobar ductal obstruction, producing jaundice, pruritus, and fever. Unless unobstructed, uninfected biliary flow can be achieved through a segmental or lobar duct, it is better that the duct be completely obstructed and the affected liver parenchyma allowed to atrophy, provided there is normal biliary flow from the residual 50% of liver. This concept is important in the management of injured anomalous segmental or lobar hepatic duct and in the palliative treatment of bile duct carcinoma. Localized intrahepatic infections communicating with abnormal biliary ducts will require hepatic resection of the infected parenchyma and ducts for cure. The abnormality may be saccular dilatation of the intrahepatic ductal system with abscess formation or intrahepatic abscess associated with stenosis of the ductal system from trauma to the duct, to the duct and liver, or to retained intrahepatic stones. Diffusely situated intrahepatic abscesses secondary to ductal abnormalities can be treated with systemic antibiotics, local drainage of a dmoninant abscess, and efforts to improve biliary drainage.

Liver histological, portal flow and plasmatic nitric oxide alterations caused by biliary obstruction and drainage in rats / Alterações histológicas, do fluxo portal e do óxido nítrico plasmático em ratos submetidos à obstrução/desobstrução biliar

PURPOSE: To evaluate liver alterations caused by biliary obstruction and drainage. METHODS: Thirty-nine male Wistar rats were randomly distributed in 4 groups: BO (n=18) bile duct ligation for 20 days, with a periodic evaluation of liver histological alterations, Doppler echography portal flow and measurements of NO and malondialdehyde (MDA); BO/DB (n=13) bile duct occlusion for 20 days followed by biliary drainage by choledochoduodenal anastomosis, 5 days follow-up, same BO group parameters evaluations; group CED (n=4) sham operation and portal flow evaluation trough 20 days; CHB (n=4) sham operation, with hepatic biopsy on 25th day and followed-up trough 25 days, by the same parameters of group BO, with exception of portal flow. Direct bilirubin (DB) and alkaline phosphatase (AP) were evaluated in the group BO, BO/DB and CHB. RESULTS: The bile duct ligation led to an increase of DB and AP, development of liver histological alterations, reduction of portal flow and increase of plasmatic NO and of MDA levels. The bile duct clearing resulted in a reduction of DB, AP, NO, MDA histological alterations and increase of portal flow. CONCLUSION: The biliary occlusion resulted in cholestasis and portal flow reduction, besides the increase of plasmatic NO and of hepatic MDA levels, and histological liver alterations, with a tendency of normalization after the bile duct clearing.

OBJETIVO: Avaliar alterações hepáticas resultantes do processo de obstrução/desobstrução biliar. MÉTODOS: Trinta e nove ratos Wistar foram distribuídos aleatoriamente em 4 grupos: OB (n=18), oclusão biliar, seguimento de 20 dias, avaliação das alterações histológicas hepáticas, do fluxo portal e dosagens de NO e de malondialdeído (MDA); grupo OB/DB (n=13) oclusão biliar por 20 dias seguida de desobstrução biliar por anastomose colédoco-duodenal, seguimento por 5 dias e avaliação dos mesmos parâmetros do grupo BO; grupo CED (n=4) operação simulada, avaliação do fluxo portal e seguimento por 25 dias; grupo CHB (n=4) operação simulada com biópsia hepática no 25º dia, e seguido por 25 dias com avaliação periódica dos mesmos parâmetros do grupo BO, com exceção da ecografia Doppler. Nos grupos BO, OB/DB e CHB foram avaliadas também a bilirrubina direta (BD) e a fosfatase alcalina (FA). RESULTADOS: A oclusão do colédoco causou aumento da BD e da FA, desenvolvimento de alterações hepáticas, redução do fluxo portal, com aumentos do NO plasmático e do MDA. A desobstrução biliar resultou na redução da BD, da FA, das alterações hepáticas, aumento do fluxo portal e redução do NO e do MDA. CONCLUSÃO: A obstrução biliar resultou em colestase, alterações histológicas hepáticas, diminuição do fluxo portal, aumentos do NO plasmático e MDA hepático, com tendência à normalização após a desobstrução biliar.