Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Better, noninvasive, diagnostics, better knowledge of anatomy and of surgical techniques have been responsible for a considerable development of liver surgery during recent years. Primary malignant liver tumours can only be cured by resection. The decision for resectional surgery should be based on different tumor characteristics, of whom the nature of the liver tissue (normal or cirrhotic) in which the tumor develops in of utmost importance. A malignant tumor should be resected with save, tumor-free margins, leaving behind as much normal functional parenchyma as possible. The role of complementary therapies as e.g. chemotherapy, chemo-embolisation and arterial ischemia must be further developed. Liver transplantation will probably play a more important role in the future development of liver cancer treatment. Surgery for benign liver tumors can be restricted most of the time to a limited resection; extended hepatectomies are rarely necessary. The more deliberate use of intraoperative ultrasound and hepatic vascular exclusion as well as the more frequent use of ultrasound dissectors will allow safer liver surgery; this applies especially for the excision of benign solid liver tumors. Because of their degenerative risks, liver adenomas should be excised. Focal nodular hyperplasia and haemangioma remain rare indications for surgery. The low morbidity and mortality of elective liver resections should favour a more widespread use of surgery for the treatment of malignant as well benign liver tumors.
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PMID:[Surgery of benign and malignant primary liver tumors]. 217 70

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant vascular disorder that can involve the liver diffusely in the form of vascular malformations ranging from small telangiectases to discrete arteriovenous malformations. Anatomically, three different patterns of abnormal vascular communications can occur in liver: portal vein to hepatic vein (portovenous), hepatic artery to hepatic vein (arteriovenous) and hepatic artery to portal vein (arterioportal), with the most common being arteriovenous. Only 5 to 8% of patients with these vascular malformations are symptomatic. When symptomatic, patients present with high-output cardiac failure, biliary ischemia (which, when severe, can progress to biliary and hepatic necrosis and lead to acute liver failure), or portal hypertension. Other less common presentations include portosystemic encephalopathy and abdominal angina. Diagnosis is confirmed by Doppler ultrasonography or multidetector computed tomography. The hallmark findings are intrahepatic hypervascularization and an enlarged common hepatic artery. Focal nodular hyperplasia and nodular regenerative hyperplasia are common findings. Symptomatic patients are treated with intensive medical treatment aimed at the predominant clinical presentation. Patients who fail aggressive medical therapy and those with acute biliary/hepatic necrosis should be considered for liver transplantation.
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PMID:Hepatic vascular malformations in hereditary hemorrhagic telangiectasia. 1881 78

Focal nodular hyperplasia (FNH) is a relatively common benign liver tumor with rare indications to surgery. Early after pregnancy, a 35-year-old woman developed right upper quadrant abdominal pain with fever. A large abdominal mass was palpable. Abdominal CT scan showed a 18-cm FNH substituting all liver segments but S6 and S7, compressing middle and left hepatic vein near their origin, displacing and compressing right hepatic vein, with ascites. Surgery consisted of a left hepatectomy extended to S5-S8 and S1. Main technical challenge was the preservation of the right hepatic vein. Intermittent pedicle clamping was performed, associated with hepatic vascular exclusion with preservation of caval flow; total duration of ischemia was 210 min. The postoperative course was uneventful, except for a transient fall in prothrombin time, and the formation of a sub-diaphragmatic serous collection, which was percutaneously drained. The patient is well 25 months after the operation. To our knowledge, this is the second reported case requiring surgery for a FNH causing a Budd-Chiari syndrome. In these peculiar cases a cumbersome operation may be required, maximizing all precautions to perform a risk-free procedure.
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PMID:Giant focal nodular hyperplasia determining Budd-Chiari syndrome: an operative challenge requiring 210 min of liver ischemia. 2192 17