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At least 559 records · Page 31Linked to original sources
PubMed1986

Does large spontaneous portal systemic shunt in cirrhosis protect from the risk of gastroesophageal bleeding?

The risk of gastroesophageal bleeding in cirrhotic patients with massive spontaneous portosystemic shunt (SPSS) has been evaluated variously in the literature. We undertook a retrospective study in a large group of cirrhotic patients admitted to our surgical department to evaluate the incidence of large SPSS and the correlation with current or previous episodes of gastroesophageal hemorrhage. Of 456 patients submitted to splenoportography or celiac-mesenteric angiography, 20 showed evidence on the roentgenograms of large self-established SPSS. They were classified into three groups: (a) splenorenal shunts (three patients); (b) mesenteric-caval shunts (two patients), and (c) large patent umbilical vein (15 patients). Twelve of these 20 patients had one or more episodes of gastrointestinal bleeding, and seven of them were submitted to surgical treatment to prevent recurrent bleeding. No correlation was found between the risk of esophageal hemorrhage and the type of SPSS. We concluded that, despite the presence of massive SPSS, cirrhotic patients have an unpredictable risk of bleeding and they often require surgical treatment to prevent recurrent episodes.

Collateral Circulation↗
PubMed1997

Extrahepatic portal venous obstruction in childhood: etiology, clinical and laboratory findings and prognosis of 34 patients.

Extrahepatic obstruction of the portal vein is a well known cause of portal hypertension in childhood, that causes severe morbidity. We evaluated 34 children (24 boys, 10 girls, age 4.5 months to 12 years, mean 5.5 +/- 3.8 years) with this diagnosis, to define the clinical picture, laboratory changes, diagnostic tools and therapeutic modalities. Gastrointestinal bleeding was the commonest mode of presentation (64.7%), with the second being splenomegaly. The cause of the obstruction could be determined in 38.2% (13/34) of the subjects. At the beginning of the study the main diagnostic procedure was splenoportography although in more recent years pulsed duplex Doppler ultrasonography has been used. The follow up period was median of 5 years (range 1-11 years). The mean number of bleeding episodes was 4.7 +/- 5.9 (range 1-26), while nine patients never bled. There was no mortality. Ten patients underwent surgery, while sclerotherapy was performed on 10. Twenty-one patients received beta-blocker drugs. No difference was found among these therapeutic modalities. It is well established that the major risk for children with extrahepatic portal vein obstruction is gastrointestinal bleeding which is tolerated quite well. Surgery should be indicated only in children where bleeding cannot be controlled by medical means including sclerotherapy.

Child↗
PubMed2006

Is congenital hepatic fibrosis a pure liver disease?

OBJECTIVES: An association between congenital hepatic fibrosis (CHF) and several different conditions is being increasingly recognized. We aimed to investigate, prospectively, these associated disorders and the clinical consequences for patients with CHF. MATERIALS AND METHODS: CHF was diagnosed using liver biopsy, abdominal ultrasound (US), Doppler US, upper endoscopy, and abdominal computed tomography (CT) in 19 patients (13 women, 6 men). CT portography and splenoportography with digital subtraction angiography were performed if indicated. Endoscopic retrograde cholangiopancreatography (ERCP) was performed to investigate the extent of portal vein involvement of the common bile duct if it existed, to remove a stone located in the common bile duct when documented, and to confirm the diagnosis of Caroli's syndrome. Cranial MRI was done when clinical findings suggested brain involvement. RESULTS: The mean age of the patients was 29.47+/-12.06, ranging from 13 to 57. CHF-associated diseases were Caroli's syndrome, polycystic kidney disease, cavernous transformation of the portal vein, Joubert's syndrome, von Meyenburg complex, polydactyly, medullary sponge kidney, and pancreatic duct atrophy. In two cases, cholangiocarcinoma had developed. There was only one case with pure CHF. Portosystemic shunt, TIPS, or splenectomy were performed in some cases to control bleeding from esophageal varices. Papillotomy and stone extraction from the common bile duct were performed in four patients with Caroli's syndrome complicated by cholangitis. Three patients died of complications of CHF. Two patients with Caroli's syndrome underwent liver transplantation. CONCLUSION: In this prospective study, it seems that CHF is not a pure liver disease but rather a multiorgan disorder involving the brain, portal vein, kidneys, and bile ducts. In most cases, the clinical picture includes other organ involvement, rather than purely the liver parenchyma.

Adolescent↗
PubMed1998

Cellophane banding for the gradual attenuation of single extrahepatic portosystemic shunts in eleven dogs.

OBJECTIVE: To evaluate the efficacy and short term effects of a cellophane banding technique for progressive attenuation of canine single extrahepatic portosystemic shunts. DESIGN: A prospective trial of 11 dogs with single congenital extrahepatic shunts. PROCEDURE: Rectal ammonia tolerance testing and routine biochemical tests were performed preoperatively on all dogs. In seven dogs, preoperative abdominal Doppler ultrasonography was also performed. Exploratory laparotomy revealed a single extrahepatic portocaval shunt in each animal, which was attenuated using a cellophane band with an internal diameter of 2 to 3 mm. The abdomen was closed routinely. Follow-up biochemical analysis and abdominal Doppler ultrasonography or splenoportography were performed postoperatively. RESULTS: The shunt was not amenable to total ligation in 11 dogs, based upon reported criteria. All dogs recovered uneventfully from surgery without evidence of portal hypertension, and showed clinical improvement thereafter. Shunt occlusion was deemed to have occurred in 10 dogs based on resolution of biochemical and/or sonographic abnormalities. One dog continued to have sonographic evidence of portosystemic shunting when evaluated 3 weeks after surgery, despite normal ammonia tolerance, but was lost to subsequent follow-up. Two dogs, in which 3 mm cellophane bands were placed, experienced delayed shunt occlusion. CONCLUSION: Cellophane banding is simple to perform, and causes progressive attenuation of single extrahepatic shunts in dogs. Further work is needed to determine the maximum diameter of a cellophane band which will produce total attenuation, and the long-term safety and reliability of the treatment.

Animals↗
PubMed1971

Peritoneoscopic features of intraabdominal vessels in cirrhosis of the liver.

Peritoneoscopy was carried out in 57 cirrhotic patients in order to evaluate the morphological features of intraabdominal veins. These were described either as normal or characterized by minimal, moderate, or marked alterations: accordingly, the patients were classified into four groups. Intrahepatic and intrasplenic pressures were measured in most patients; abnormally elevated values were found in every case, and the higher figures belonged to the subjects with minor involvement of the intraabdominal veins. Superficial collateralization and oesophageal varices appeared unrelated to changes in these veins, whereas splenomegaly was mostly found in patients with normal or slightly altered intraabdominal veins. Percutaneous splenoportography was performed in 16 patients, and venographic appearances did not correlate with peritoneoscopic features of the intraabdominal veins. Ascites, on the other hand, was exclusively present in patients with alterations in these veins. It is suggested that some pathogenetic relationship might exist between changes in intraabdominal veins seen by peritoneoscopy and ascites.

Abdomen↗
PubMed1992

Portal vein stenosis complicating liver transplantation in children: percutaneous transhepatic angioplasty.

Portal vein stenosis complicating orthotopic liver transplantation in children is uncommon. The authors report their early experience with transhepatic portal vein angioplasty in the treatment of portal vein stenosis in this setting. The technique was used in two children (aged 2 and 6 years) who had undergone liver transplantation for biliary atresia 15 and 42 months earlier, respectively. Both patients presented with chronic anemia and intermittent gastrointestinal bleeding. The diagnosis of portal vein stenosis was confirmed at fine-needle splenoportography. Access to the portal venous system was gained by means of a transhepatic approach. Low-profile angioplasty balloon catheters were used to dilate anastomotic strictures of the portal vein in both children. At the end of the procedure, the tract within the liver was occluded with gelatin sponge pledgets. Both procedures were technically successful and caused no complications, and in both patients gastrointestinal bleeding ceased.

Angioplasty, Balloon↗
PubMed1990

Heterotopic auxiliary liver transplantation with portal flow. Gradual development of the collateral circulation.

One of the causes of auxiliary liver transplantation failure is the inter-liver competition between the host liver and the graft for the hepatotrophic factors of the portal blood. We have developed an experimental model of heterotopic partial (30%) liver isotransplant using Wistar rats so as to study this competition. Splenoportography and dissection demonstrate the existence of collateral circulation. The collaterals at 90 days post-transplant (PT) consisted of veins from the portal vein to the host liver (PR), paraesophageal veins (PE) and splenorenal veins (SR). At 60 days P.T., PR and SR veins but not PE ones appeared, and at 30 days P.T., there were only PR veins. Graft atrophy at 90 days P.T. was associated with a severe degree of bile duct proliferation. The gradual development of portal hypertension causes porto-systemic collateral circulation and the graft loses the portal hepatotrophic factors. The late development of the portal hypertension and the biliary proliferation could be caused by the hepatic arterial ischemia in this experimental model. Thus, as has been described in the orthotopic liver transplantation, the heterotopic one might require a double vascularization, both portal and arterial.

Animals↗
PubMed1979

Extrahepatic portal hypertension due to congenital obstruction of the portal vein and associated gross hepatic lobulation.

A 10-233k old girl presented with splenomegaly and recurrent hematemesis from esophageal varices. Splenoportography revealed a dilated extrahepatic portion of the portal vein with nonvisualization of its intrahepatic tributaries. The child died following an episode of hematemesis and was found to have a dilated portal vein which ended blindly. In addition, there was abnormal lobulation of the inferior surface of the liver which was not cirrhotic. The portal vascular anomaly, which presumably was responsible for the portal hypertension, was probably due to failure of communication between the embryonic vitelline veins or to atresia of the portal vein secondary to pressure from the abnormal hepatic lobulation in utero. It would appear that congenital factors may be significant in the etiology and pathogenesis of some cases of extrahepatic portal hypertension in early life and recognition of such developmental anomalies is of importantance in management.

Female↗
PubMed1981

Cholangio carcinoma treated by liver split and resection.

A case of cholangiocarcinoma at the liver hilum presenting with jaundice is described. Pre-operative transhepatic cholangiography, hepatic arteriography and splenoportography led to liver split, with successful resection of tumour and triple hepatico-jejunostomy. Despite tumour recurrence eight months of palliation were achieved. Current methods of treating the condition are discussed.

Adenoma, Bile Duct↗
PubMed1982

Recanalized umbilical vein in portal hypertension.

Experience with splenoportography suggests that patency of the umbilical vein occurs in about 9% of the patients with portal hypertension. A widely patent umbilical vein might serve as a decompressive portosystemic shunt. Percutaneous transhepatic portography was performed in 107 patients with cirrhosis of the liver and portal hypertension. A patent umbilical vein was found in 28 patients (26%). This finding significantly paralleled the number and size of other collateral veins, apart from gastroesophageal varices. No significant relation was found between umbilical vein patency and portal pressure, extrahepatic shunting, variceal bleeding, or ascites. It is concluded that a large patent umbilical vein does not effectively relieve portal hypertension, prevent gastroesophageal varices, or protect against variceal bleeding or ascites.

Adult↗
PubMed1989

Ultrasonographic diagnosis of portal vein cavernous transformation in children.

The aim of this work was to evaluate the efficiency, sensitivity, and specificity of ultrasonographic findings in the diagnosis of portal vein cavernous transformation and secondary splanchnic hypertension in children. Twenty patients with esophageal varices on endoscopic sclerotherapy, with ages ranging from 1 to 15 years (mean of 7.5), were compared with 20 age-matched normal asymptomatic controls. In 17 cases, diagnosis was confirmed by splenoportography. Ultrasonographic portal vein features, respiratory variations in splenic and superior mesenteric veins, lesser omentum to aorta diameter ratio and spleen size, as well as the presence of vessels in the lesser omentum and of spontaneous anastomoses, were analyzed in both groups. The efficiency of ultrasonography to establish a diagnosis of portal vein cavernous transformation reached 100%. Splenic and superior mesenteric vein respiratory variation was negligible in patients and inspiration versus expiration diameter differences ranged from 1 to 4 mm (mean of 2.4) in controls (p less than .001). Mean lesser omentum to aorta ratio was 2.07 in patients versus .9 in controls (p less than .001). Splenomegaly was found in all but two cases; lesser omentum vessels were visualized in nine cases; whereas five presented spontaneous splenorenal anastomoses and gallbladder varices were observed in five patients. Thus, ultrasonography allowed portal vein cavernous transformation to be diagnosed throughout; portal hypertension was also detected. It may be concluded that ultrasonography, either alone or associated with endoscopy, provides a reliable method for portal vein cavernous transformation diagnosis. Angiography should be reserved for preoperative or controlled hemodynamic studies.

Child↗
PubMedDate not supplied

An experimental model of liver damage and portal hypertension induced by a single dose of monocrotaline.

BACKGROUND/AIMS: Hepatic cirrhosis accompanied by portal hypertension is a common cause of death in human beings. The aim of the present study was to develop an experimental model of hepatic portal hypertension associated with liver damage. METHODOLOGY: To develop liver damage in rats, we used the toxic alkaloid monocrotaline. Two groups of male Wistar rats were used. Group 1 was injected with a single dose of monocrotaline (60 mg/kg of body weight) intraperitoneally. Group 2 was injected with an equal volume of saline solution. After 44 days, the animals underwent the following tests: splenoportography and measurement of portal pressure, hepatic serum biochemical tests, and light and electron microscopy. RESULTS: Group 1 showed a significant increase in splenic pressure, superior and inferior collateral circulation, and an increase in portal vein diameter. Serious alterations were detected in hepatic serum markers. Light microscopy showed different degrees of hepatocyte damage, varying from edema to focal necrosis. Ultrastructural changes were of membrane disruption, mitochondrial and nuclear alterations. CONCLUSIONS: The present experimental model could be useful in establishing the pathophysiological changes associated with portal hypertension due to liver damage.

Animals↗
PubMedDate not supplied

[Portal vein thrombosis in children: clinical and laboratory study of 26 cases].

Portal vein thrombosis represents one of the most frequent causes of portal hypertension in childhood. The aim of the present study was to describe the clinical and laboratorial characteristics of portal vein thrombosis in pediatric patient. We studied 26 children with diagnosis of portal vein thrombosis through splenoportography (two patients) and ultrasound scan (24 patients) which ages varied from 2 months to 11 years and 4 months (median-5 years and 3 months). Data of the patient history, physical and laboratories examination were used to a retrospective study which was done through medical record analysis. The main complaint of the examination was hematemesis, which was found in 57.6%. In 26.9% a possible risk factor for portal vein thrombosis was found [catheterization of the umbilical vein (four), sepsis (two), omphalitis (one)]. Splenomegaly was present in all cases and the associated illness to portal vein thrombosis were: hepatoportal sclerosis (three), cytomegalovirus infection (two), blastomycosis (two), virus C (two), virus B (one) and virus A (one). The time between the first bleeding and the examination at University of Campinas Hospital, in Campinas, SP, Brazil, varied from 0.23 months to 54 months with a median of 12 months. Only 11.5% of patients underwent the endoscopy with sclerotherapy before going to University of Campinas Hospital. Aminotransferases' activities were considered normal in 20 patients. We could conclude that: 1. The most frequent initial symptom was hematemesis. 2. The known risk factors for portal vein thrombosis were present in about 1/3 of the cases. 3. Laboratorial exams usually indicated absence of hepatocitic lesions. 4. The efforts towards sending the patient to a reference center were late with a delayed diagnostic and with delayed effective therapeutic conduct. 5. In about 50% of the cases there was PVT associated with other hepatic diseases.

Child↗
PubMed1975

[Hemobilia (author's transl)].

Hemobilia is a syndrome caused by hemorrhage into the biliary ducts. It is characterized by colicky pains, jaundice, and intestinal bleeding; a correct diagnosis of this syndrome is made rather rarely. The most common cause is trauma; inflammatory or tumorous disease of the liver and bile duct system, bile stones and aneurysms of the hepatic artery are rarer causes. The diagnosis can be established and the arterio-biliary fistula localized by selective arteriography. A case is described, which shows, that, in addition, duodenoscopy with retrograde cholangiography is of diagnostic value. Other helpful diagnostic procedures are: splenoportography, liver scanning, and intraoperative cholangiography. Therapy must be surgical exclusively; palliative operations lead to high rates of relapses and letality. Best results are achieved by ligature of the hepatic artery in cases of central, or by partial resection of the liver in cases of peripheral localization of the fistula.

Accidents, Traffic↗
PubMed1975

Surgery and prognosis of prehepatic portal hypertension.

Results of surgical treatment of prehepatic portal hypertension during the past 15 years were assessed, in addition to routine clinical and laboratory studies, by splenoportography and control mesenteric-venography. One patient survived 14 years. Control angiography of the portal system proved to be most important in assessing the results of surgical treatment, recognizing the cause of late failures and evaluating the course of the disease. All splenectomized patients with general PPH experienced recurrences of hemorrhage which required reoperation. Direct operation on the varices is a favorable procedure, particularly when done as an emergency procedure. Following surgery, early angiographic examination, especially by mesenteric-venography, is mandatory. In cases with poor portal circulation through the liver and massive passage of blood through the varices, PSA should be performed without delay. Portosystemic anastomosis is a selective procedure. Without angiographic study it is contraindicated as an emergency procedure, especially in splenectomized patients.

Adolescent↗
PubMed1992

Portal vein thrombosis following sclerotherapy.

We present the case of a woman with idiopathic portal hypertension who underwent sclerotherapy for bleeding esophageal varices. She had a rebleed 27 months after complete eradication of esophageal varices. Endoscopy showed bleeding gastric varices. Ultrasonography, and later splenoportography, revealed a large thrombus in the right branch of the portal vein causing gross dilation of the portal and splenic vein. A proximal splenorenal shunt was done to decompress the portal system and hence gastric varices. Repeat endoscopy 4 weeks after surgery revealed complete disappearance of the gastric varices, while ultrasonography at 38 weeks showed marked decompression of the portal system with complete disappearance of the thrombus from the right branch of the portal vein. No new thrombus formation was seen.

Adult↗
PubMed2004

Isolated gastric varices due to focal splenic vein stenosis.

Left-sided portal hypertension due to splenic vein stenosis is a very rare disease. We report a case of this condition in a 21-year-old woman who suffered from a first episode of tarry stool passage with fresh blood vomiting. Panendoscopy showed isolated gastric varices while sonography showed a normal liver but the presence of splenomegaly with prominent collateral circulations. Further imaging studies, including abdominal computed tomography, splenoportography and percutaneous transhepatic portography, revealed a focal stenotic proximal splenic vein resulting in left-sided portal hypertension. The collateral circulation ran from the short gastric veins via the left gastric veins into the main portal vein. The intraportal venous pressure was within normal limits. Splenectomy was performed and near normal wedge liver biopsy pathology confirmed non-cirrhotic extrahepatic portal hypertension. The patient had no further variceal bleeding after surgery.

Adult↗