Splenic vein aneurysm: is it a surgical indication?
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Splenic vein aneurysms are rare and are usually caused by portal hypertension. Symptoms are unusual, but may include rupture or abdominal pain. Diagnosis can usually be made either by means of duplex ultrasonography or computed tomography scanning. Treatment varies from noninvasive follow-up to aneurysm excision. We report an expanding splenic vein aneurysm in a young woman with abdominal and back pain and no history of portal hypertension. She was treated with aneurysm excision and splenectomy. (+info)
Results of surgical treatment (modified Sugiura-Futagawa operation) of portal hypertension associated to complete splenomesoportal thrombosis and cirrhosis.
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BACKGROUND: Hemorrhagic portal hypertension, secondary to both intrahepatic and extrahepatic portal hypertension, is an uncommon entity. In this condition, the extrahepatic and the intrahepatic obstruction of the portal vein, due to chronic liver disease, produce a more severe form of hemorrhagic portal hypertension that is more difficult to control. The results of surgical treatment (modified Sugiura-Futagawa operation) in this subset of patients is analyzed. METHODS: Among 714 patients with a history of hemorrhagic portal hypertension, 14 cases were found with histologically proven liver cirrhosis and complete splenomesoportal thrombosis demonstrated by means of preoperative angiography. Patients with incomplete (partial) splenomesoportal thrombosis were excluded. There were nine males and 5 females with a mean age of 51 years. Alcoholic cirrhosis was demonstrated in 50% of the cases, post hepatitic cirrhosis in 28%, primary biliary cirrhosis in 7%, and cryptogenic cirrhosis in 14%. There were nine Child-Pugh A and 5 B cases. All cases were treated by means of our modified Sugiura-Futagawa procedure. RESULTS: Bleeding recurrence from esophagogastric varices was shown in one case, colonic varices in one case and hypertensive gastropathy in another of the survivors. Post operative encephalopathy was shown in 3 of the cases. The thirty-six month survival rate was 30% (Kaplan-Meier). CONCLUSIONS: The combination of intrahepatic plus extrahepatic portal hypertension has a worse prognosis. Treatment options are limited (sclerotherapy and/or devascularization), because shunt surgery, TIPS and liver transplantation have a very restricted role and postoperative outcome is poor. (+info)
Intractable oesophageal variceal bleeding caused by splenic arteriovenous fistula: treatment by transcatheter arterial embolization.
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We describe a rare case of splenic arteriovenous fistula and venous aneurysm which developed after splenectomy in a 40-year-old woman who presented with epigastralgia, watery diarrhoea, repeated haematemesis and melaena caused by hyperkinetic status of the portal system and bleeding of oesophageal varices. It was diagnosed by computed tomography and angiography, and obliterated with giant Gianturco steel coils. (+info)
Growth stimulation of human bone marrow cells in agar culture by vascular cells.
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Human vascular cells are capable of stimulating granulopoiesis in agar culture of human bone marrow cells. This effect was obtained by including vein fragments in the culture or by using endothelial cells separated from the vein of human umbilical cords as feeder cells. Furthermore, the stimulatory capacity of conditioned medium obtained from cord veins was found to be highly active in comparison to that obtained from peripheral leukocytes. Endothelial cells within the bond marrow cavity are suggested as a local source of factors regulating granulopoiesis in humans in addition to the monocyte. (+info)
Portosystemic shunting in patients with primary biliary cirrhosis: a good risk disease.
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Five patients with primary biliary cirrhosis underwent portosystemic shunting for the control of variceal bleeding. Three procedures were emergencies and two were elective. There was no operative mortality; all patients were followed until the present or until death. One patient is alive 4 years and another, 2 years postoperatively. One patient died 4 years after operation and another died 16 months postoperatively. Another patient survived for 8 years following her shunt and eventually died as a result of a cerebrovascular accident. This group of patients is compared to a larger group undergoing portosystemic shunting because of portal hypertension secondary to other forms of liver disease. The absence of operative mortality and the fact that several of these patients had moderately long postoperative survival despite apparently poor liver function suggest that the usual criteria for the assessment of operative risk are not valid in primary biliary cirrhosis. (+info)
Aspects of treatment. The anatomical basis for portal decompressive surgery.
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Definitive surgical techniques used in the treatment of portal hypertension all aim to achieve portal venous decompression. The historic development of the various procedures currently employed provides a broad repertoire of surgical operations. Each of the procedures merits consideration and may be specifically indicated in a given situation. Description of the operative steps emphasizes the importance of the anatomical relationships of the various structures. (+info)
Pancreatic adenocarcinoma presenting as sinistral portal hypertension: an unusual presentation of pancreatic cancer.
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A rare syndrome, sinistral (left-sided) portal hypertension resulting from splenic vein thrombosis secondary to pancreatic adenocarcinoma of the tail is presented here. Pancreatic cancer is notorious for presenting with vague and nonspecific symptoms, including but not exclusively weight loss, abdominal pain, and anorexia with or without jaundice. However, physicians should be aware that in the presence of splenic vein thrombosis, this finding alone puts pancreatic cancer high on the differential diagnosis. (+info)
Influence of adrenaline on the dissemination of antibody-producing cells from the spleen.
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Plaque-forming cells (PFC) and rosette-forming cells (RFC) were quantificated in splenic venous and splenic arterial blood and in spleen suspensions of guinea-pigs during a secondary immune response to sheep red blood cells (SRBC). The splenic veno-arterial differences in content of PFC and RFC were determined, indicating whether there had been a release of such cells from the spleen into the blood. The effect of an intracardial injection of adrenaline on the release of immune lymphocytes was investigated. In immunized control animals a splenic release of antigen-binding and antibody-forming cells was found, the release being restricted to the peak of the immune response in the spleen. However, after exogenous adrenaline a considerably increased release of both antigen-binding and antibody-forming cells occurred during a longer period of the immune response. Thus, adrenaline caused an enormous release of PFC from the spleen into the blood on day 4 of the secondary immune response, resulting in a diminished number of PFC remaining in the spleen after the treatment. A physiological significance of an adrenaline-induced dissemination of immune lymphocytes in the body during an immune response to a severe infectious disease is suggested. (+info)