[Interventions for benign biliary strictures]. / Interventionen bei benignen Gallengangstenosen.

Due to their potential for serious consequences, even including biliary liver cirrhosis, benign biliary strictures pose a considerable diagnostic and therapeutic challenge. In addition to inflammatory disease or an acute liver injury, iatrogenically caused biliary strictures following hepatobiliary surgery represent in 95% of cases the main cause for all benign entities. The diagnosis should be determined noninvasively with magnetic resonance cholangiopancreaticography (MRCP). Invasive techniques such as ERCP or percutaneous transhepatic cholangiography (PTC) should be reserved for unclear cases and first performed before the scheduled intervention. Depending on the site and cause of the stricture, surgical and interventional procedures are employed in the treatment of biliary strictures. The best results are obtained in short-segment strictures of the main bile duct. Interventional methods such as balloon dilation and/or stent application with concomitant drain insertion achieve patency rates of up to 75% after 5 and 55% after 12 years with a total complication rate of 5-8%. Due to the fact that most of the cases involve cicatricial fibroses, predisposition for recurrence of biliary strictures after interventional therapy can be very high, ranging up to 66% depending on the localization.

Recurrent deep venous thrombosis caused by congenital interruption of the inferior vena cava and heterozygous factor V Leiden mutation.

A case of a 44-year-old patient with recurrent deep venous thrombosis (DVT) caused by congenital dysgenesis of the inferior vena cava (IVC) in coincidence with heterozygous factor V Leiden mutation is presented. The IVC malformation was a fortuitous finding because the vascular malformation of the collateral draining thoracic veins were suspected to be a malignant mass in chest X-ray. This vascular abnormality is a rare finding but recent epidemiological research suggests that there may be an association between the congenital absence of the IVC and DVT. In our case, the patient is even at higher risk combining the malformation probably affecting venous blood flow and the hypercoagulabilic state by heterozygous presence of the factor V Leidenmutation.

Restoration of liver function and portosystemic pressure gradient after TIPSS and late TIPSS occlusion.

TIPSS (transjugular intrahepatic portosystemic shunt) may be indicated to control bleeding from esophageal and gastric varicose veins, to reduce ascites, and to treat patients with Budd-Chiari syndrome and veno-occlusive disease. Numerous measures to improve the safety and methodology of the procedure have helped to increase the technical and clinical success. Follow-up of TIPSS patients has revealed shunt stenosis to occur more often in patients with preserved liver function (Child A, Child B). In addition, the extent of liver cirrhosis is the main factor that determines prognosis in the long term. Little is known about the effects of TIPSS with respect to portosystemic hemodynamics. This report deals with a cirrhotic patient who stopped drinking 7 months prior to admission. He received TIPSS to control ascites and recurrent esophageal bleeding. Two years later remarkable hypertrophy of the left liver lobe and shunt occlusion was observed. The portosystemic pressure gradient dropped from 24 mmHg before TIPSS to 11 mmHg and remained stable after shunt occlusion. The Child's B cirrhosis prior to TIPSS turned into Child's A cirrhosis and remained stable during the follow-up period of 32 months. This indicates that liver function of TIPSS patients may recover due to hypertrophy of the remaining non-cirrhotic liver tissue. In addition the hepatic hemodynamics may return to normal. In conclusion, TIPSS cannot cure cirrhosis but its progress may be halted if the cause can be removed. This may result in a normal portosystemic gradient, leading consequently to shunt occlusion.