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At least 145 records · Page 8Linked to original sources
PubMed1999

[High intensity signal in basal ganglia on T1 weighted images: case report in Manson's Schistosomiasis with portal systemic encephalopathy].

We report a case of mansonic schistosomiasis with portal systemic encephalopathy associated with a high intensity signal in basal ganglia on TI weighted images due to deposition of manganese in tissues related with portal-systemic collateral vessels. A bibliographic review was done focusing the magnetic resonance findings. To the best of our knowledge, these signal changes have not yet been associated with Manson's schistosomiasis.

Adult↗
PubMed1983

Portal-systemic shunting in patients with non-alcoholic liver disease.

Portal systemic shunting for the treatment of bleeding oesophageal varices in non-alcoholic patients is thought to have a better outcome than in patients with alcoholic portal hypertension. In a retrospective study of twenty-five non-alcoholic patients who had undergone portal systemic shunting for the treatment of bleeding oesophageal varices, the perioperative and long term mortality was found to be unacceptably high. Therefore, an analysis was made to define the factors which may have contributed to the high mortality. It was found that the presence of one or more of the following factors contributed to the patient's demise: presence of active liver disease at the time of surgery, previous abdominal surgery, and the performance of shunting as an emergency in order to stop bleeding. It is concluded that in patients having one or more of these risk factors, currently available non-operative means of treating bleeding oesophageal varices should be considered.

Adolescent↗
PubMed1987

Non-invasive evaluation of portal-systemic shunting in man by D-sorbitol bioavailability.

Portal-systemic shunting is an important circulatory abnormality in patients with cirrhosis. This study explores the potential of the natural polyol D-sorbitol as test compound for non-invasive assessment of shunting. Ten normal subjects, 10 patients with cirrhosis and 12 cirrhotics with surgical portacaval shunts were studied after oral and intravenous administration of a 2 g dose of sorbitol. As measured by the H2 breath test, removal from the intestinal lumen was complete in both groups. Bioavailability of sorbitol, calculated as ratio of the areas under the plasma concentration/time curve after p.o. and i.v. administration, was zero in normal subjects, 0.29 +/- 0.15 in cirrhotic patients, and 0.38 +/- 0.11 in patients with portacaval shunts. Calculation of bioavailability on the basis of urinary outputs of sorbitol gave similar results. It is concluded that the bioavailability of sorbitol reflects portal-systemic shunting, although the relatively low figures suggest some degree of sorbitol metabolism by enterocytes.

Adult↗
PubMed2001

Portal-Systemic shunts reduce asialoglycoprotein receptor density in rats.

UNLABELLED: The clinical usefulness of quantitative functional imaging techniques that use asialoglycoprotein receptor (ASGP-R) binding is based on the correlation between ASGP-R density and hepatic functional reserve. Portal-systemic shunting (PSS) is common in patients with cirrhosis and portal hypertension-the same group that is most frequently considered for such imaging. PSS occurs spontaneously through collateral vessels and from the creation of surgical shunts or placement of transjugular intrahepatic portal-systemic shunts (TIPS). Understanding the physiologic relationship between PSS and ASGP-R activity may aid in the interpretation of quantitative clinical imaging. This study was conducted to determine the relationship between PSS and ASGP-R density in the absence of parenchymal disease. METHODS: Sprague-Dawley rats with end-to-side portal-systemic shunts and sham-operated control rats were imaged with 99mTC-diethylenetriaminepentaacetic acid galactosyl-neoglycoalbumin. Pharmacokinetic modeling of the liver and heart time-activity data was used to measure ASGP-R concentration, as well as hepatic plasma volume and flow. RESULTS: The mean ASGP-R density (nmol/g of liver) was significantly decreased in the shunted rats. Blood ammonia was significantly elevated, whereas hepatic plasma flow, alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase levels were unaltered. Liver histology was normal in both groups. CONCLUSION: A significant change in the ASGP-R density occurs with PSS in the absence of parenchymal disease. PSS appears to be an independent variable affecting ASGP-R activity. This could prove clinically important during interpretation of quantitative imaging from patients with varying degrees of PSS based on underlying disease or the presence of a surgical shunt or TIPS device.

Animals↗
PubMed1977

[Clinical picture and therapy of portal-systemic encephalopathy (author's transl)].

The clinical syndrome of portal-systemic encephalopathy is caused by far advanced cirrhosis of the liver in most cases; it is characterized by increasing drowsiness, disturbances of mentation, flapping tremor and hyperreflexia. An early diagnosis can be established by testing writing and drawing abilities. Increased occurrence of spider nevi, a dry, deep red tongue, and hemorrhagic lesions of skin and mucous membranes are symptoms of incipient hepatic insufficiency. The syndrome is initiated in most cases by excessive intake of protein or alcohol, by intestinal bleeding, by diuretics, or by intercurrent infections. Therapy has to include elimination of causes, reduced intake of protein, enemas with acetate buffer solution and oral medication with lactulose, bifidum milk, and certain amino acids in order to lower hyperammoniemia; in serious cases neomycin has to be given. At the same time a normalization of fluid and electrolyte balance has to be achieved; replacement of potassium is especially important, when hypokalemia and alcalosis are present. In general prognosis of portal-systemic encephalopathy however is serious, depending primarily upon the fact, whether or not sufficient functional hepatic parenchyma is present.

Acetates↗
PubMed1975

Urinary and serum octopamine in patients with portal-systemic encephalopathy.

Urinary excretion and serum concentrations of octopamine were studied in seventeen controls, thirty-three patients with portal-systemic encephalopathy, and thirteen patients with liver disease without encephalopathy. No differences were detected between control subjects and patients without encephalopathy. Urinary excretion and serum concentrations of octopamine were significantly higher in patients with encephalopathy compared with those without encephalopathy. The presence and grade of portal-systemic encephalopathy seemed to correlate more closely with the serum-octopamine concentrations than with urinary octopamine excretion. It is postulated that octopamine may be involved in the pathogenesis of portal-systemic encephalopathy.

Adolescent↗
PubMedDate not supplied

Portal system thrombosis: a complication of long-term residence at extreme altitude.

BACKGROUND: With induction of the Indian Army to heights over 5,000 meters above sea level, complications of long-term stay at extreme altitude have come to light. We describe our experience with patients developing portal system thrombosis. METHODS: Clinical data were collected over 2 years on patients hospitalized for thrombotic complications from high-altitude (HAA) and non-high altitude (non-HAA) areas. Site of thrombosis was confirmed by imaging or at surgery. Patients were investigated for conditions that predispose to venous thrombosis. RESULTS: Ten cases of portal system thrombosis were seen during the period; of these, 9 (mean age 28 [SD 3.9] years; all men) were from HAA. Mean duration of residence in HAA was 12.4 (4.9) months; two were smokers and six drank 7-22 g alcohol/day at least 5 times a week. The first symptom was abdominal pain; this was later complicated by gastrointestinal bleeding (n=5), fever (7), vomiting (7), and weight loss (5). Average time between onset of first symptom and reaching a tertiary-care hospital was 9.5 (4.7) days. Clinical examination showed ascites (8 cases), splenomegaly (7), and hepatomegaly (6). Mean hemoglobin level at admission was 15.8 (3.4) g/dL. Ascites was hemorrhagic; five cases also had large splenic hematoma. The site of thrombosis was splenic vein (7 cases), portal vein (6), and superior (4) and inferior (1) mesenteric vein. None of 5 patients investigated had any prothrombotic condition. Endoscopic/ sonographic evidence of development of collaterals appeared as early as 12-20 days after onset of symptoms. CONCLUSION: Residence in HAA for extended periods is a risk factor for development of portal system thrombosis. Persistent pain in abdomen in such individuals should raise the possibility of portal system thrombosis.

Adult↗
PubMed1992

Obliteration of portal systemic shunts as therapy for hepatic encephalopathy in patients with non-cirrhotic portal hypertension.

The effects of obliteration of portal systemic shunts (PSS) in 5 patients with non-cirrhotic hepatic encephalopathy is reported. All patients had a history of disturbance of consciousness for several years, and examinations revealed large PSS, most of which connecting the left gastric vein to the left renal vein. After the obliteration of PSS, portal vein pressure elevated, the shunt ratio of the portal blood flow decreased, the indocyanine green disappearance rate increased, and serum albumin increased. Blood ammonia (NH3) decreased significantly accompanied by disappearance of hepatic encephalopathy. This treatment may open a way to improve the quality of life in patients with large PSS without severe hepatic injury.

Aged↗
PubMed1986

Results of portal systemic shunts in Budd-Chiari syndrome.

Nine patients with Budd-Chiari syndrome (BCS) were treated by a portal systemic shunt. One had thrombosis of the superior mesenteric vein (SMV) and another had complete obstruction of the retrohepatic inferior vena cava (IVC). All other patients had a marked stenosis of the retrohepatic IVC with caval pressure ranging from 12 to 24 mmHg (mean: 17 mmHg). Seven patients had an interposition mesocaval shunt using an autologous jugular vein. The patient with a thrombosed SMV had a portoatrial shunt. The patient with an obstructed IVC had a cavoatrial shunt after an erroneous portacaval shunt had failed to relieve ascites. There were no operative deaths and no major postoperative complications. One patient died 19 months after operation of acute leukemia complicating polycythemia rubra vera. All other patients were alive and well 8 months to 6 years after operation. None of them had encephalopathy. These results suggest several comments: Portal systemic shunts are a good treatment for BCS and have a low operative risk. The mesocaval shunt is an efficient procedure, even when there is stenosis of the IVC with high caval pressure; shunts to the right atrium should be performed only in the case of complete obstruction or inaccessibility of the IVC. The long-term prognosis is excellent, except in patients with potential malignancies. Therefore, portal systemic shunts should be indicated early in patients with symptomatic BCS.

Adolescent↗
PubMed2005

[Changes in intrahepatic portal systemic shunt flow in a rat model of acute intrahepatic presinusoidal portal hypertension].

OBJECTIVES: To investigate the changes in intrahepatic portal systemic shunt flow (IHSF) and their relationship with microspheres induced acute portal hypertension. METHODS: Following acute intrahepatic presinusoidal obstruction by intraportal injection of 15 microm diameter microspheres in male Wistar rats, functional hepatic blood flow (FHBF) and IHSF were determined by hepatic sorbitol uptake methods. The percentage of large shunts of diameter > 15 microm were estimated by intraportal injection of 51Cr labeled 15 mum diameter microspheres. RESULTS: In normal control rats, hepatic sorbitol uptake was 97.9%+/-0.5% and IHSF was negligible, with FHBF equaling total hepatic blood flow [(2.52 +/- 0.23) ml/min x 100 g body weight-1]. Microsphere injection decreased sorbitol uptake to 12.8% +/- 4.3% and further to 4.1% +/- 0.7% when followed by hepatic arterial ligation. In the latter two groups, IHSF (1.46 +/- 0.15 and 1.16 +/- 0.19 ml/min x 100 g body weight-1, respectively) was not significantly different from portal venous flow [(1.36 +/- 0.20) and (1.20 +/- 0.20) ml/min x 100 g body weight-1, respectively; t = 2.013 and t = 2.116]. Portal venous flow remained at 70% of basal values and portal venous pressure only increased by 50% from baseline. 51Cr labeled microsphere shunt fraction through large shunts (> 15 microm) was less than 1.0%. CONCLUSION: Intrahepatic portasystemic shunts in the normal rat liver predominantly have diameters less than 15 microm and, when activated by intraportal injection of microspheres, they divert up to 70% of portal venous blood flow away from hepatic sinusoids and thereby they reduce acute increases in portal venous pressure.

Animals↗
PubMed2000

Abnormalities of the fetal central veins and umbilico-portal system: prenatal ultrasonographic diagnosis and proposed classification.

OBJECTIVES: Anomalies of the fetal venous system are poorly documented and their pathogenesis is not well understood. The present study was undertaken to review the spectrum of fetal central veins and umbilico-portal system anomalies, and to propose a classification system. METHODS: A 7-year restrospective survey was conducted. RESULTS: Nineteen fetuses showed abnormal connection between central veins and the fetal heart. Three fetuses showed abnormal connections of the cardinal veins, two of which had interruption of the inferior vena cava, and one had isolated persistent left superior vena cava. Anomalies of pulmonary veins were seen in four fetuses: in two with asplenia syndrome, a vertical confluent pulmonary artery was observed. In a further two cases total anomalous pulmonary venous connections were found. Abnormalities of the umbilical vein (UV) were seen in 10 cases; seven had persistent right UV, and three had a spectrum of anomalies: One had abnormal connections of the UV to the left iliac vein associated with agenesis of the ductus venosus (DV) and hydrops fetalis. One case showed in utero occlusion of the DV by echogenic foci that resulted in a persistent left proximal UV and porto-systemic shunt. One case had obliteration of the DV secondary to in utero fetal hepatic fibrosis. Abnormalities of the vitelline veins or portal system were demonstrated in two cases. One had a left porto-systemic shunt which resolved spontaneously at 3 months of age, and one had secondary partial occlusion of the left portal system with liver echogenicities and direct communication of the UV with the right atrium. None of the 19 cases had an abnormal karyotype or evidence of in utero infection. CONCLUSIONS: Detection of various fetal vein anomalies in utero is feasible. The anomalies vary according to embryologic precursors or etiology. Two major mechanisms seem to be involved in the genesis of fetal vein anomalies: in most cases primary maldevelopment of the venous system occurs, while in the minority secondary anomalies from possible thromboembolic events or systemic disease may play a role.

Abnormalities, Multiple↗
PubMed2004

Hemodialysis-related portal-systemic encephalopathy.

The authors encountered a case of portal-systemic venous shunt newly diagnosed after initiation of hemodialysis. A 68-year-old Japanese woman began hemodialysis because of symptoms of uremia including loss of appetite and pulmonary edema. Loss of consciousness occurred suddenly after her ninth session of hemodialysis. No hepatic functional abnormality was found other than hyperammonemia (314 microg/dL [184 micromol/L]). Loss of consciousness subsequently occurred often after hemodialysis. Color Doppler ultrasonography and magnetic resonance angiography depicted a large shunt between the left gastric vein and left renal vein resulting in portal flow entering the systemic circulation via the renal vein. Because the shunt was large, ligation of it was performed surgically. Results of histologic examination of a liver biopsy specimen obtained intraoperatively were normal. The patient became well postoperatively. This patient's encephalopathy appeared to be caused by the flow of ammonia-rich portal venous blood into the systemic circulation via the large shunt owing to a decrease in intravenous pressure after rapid hemodialysis. Portal-systemic shunt encephalopathy should be recognized as a "new" neuropsychiatric disorder characteristic of patients undergoing hemodialysis.

Aged↗
PubMed2003

MyWelch: building an information portal system in a medical library environment.

MyWelch is a medical library portal system that users can use to create customized web sites that reflect their research needs and personal interests. In the MyWelch environment, faculty and students are empowered to take a greater role in identifying their needs and determining their requirements in the electronic environment. The portal system also facilitates interaction among library users and staff.

Baltimore↗
PubMed1981

Semi-elective portal systemic shunts for variceal bleeding.

Between June 1977 and November 1980, we performed portal systemic shunt operations on eight patients for esophageal bleeding secondary to portal venous hypertension. One patient had operation as an emergency and the other seven semi-electively during the same hospitalization as admission. The patient operated upon as an emergency was the only hospital death. Life table analysis on this small group of patients indicates that semi-elective portal systemic shunt surgery after hemodynamic stabilization, nutritional support, and improvement of hepatic function is a viable alternative to emergency operation that can be done effectively in a community hospital.

Adult↗
PubMed1994

Treatment of bleeding esophagogastric varices due to extrahepatic portal hypertension: results of portal-systemic shunts during 35 years.

From 1958 to 1990, elective therapeutic portal-systemic shunt (PSS) procedures were performed for recurrent bleeding esophagogastric varices in 162 children and adults with extrahepatic portal hypertension (EHPH) resulting from portal vein thrombosis (PVT). The onset of EHPH was in childhood for at least 74% of patients. Of the 162 patients, 147 were eligible for and received 5 years of follow-up (100%), and 117 were eligible for and received 10 years of follow-up (100%). The longest follow-up was 35 years. The cause of PVT was unknown in 68%, neonatal omphalitis in 12%, umbilical vein catheterization in 8%, peritonitis in 6%, trauma in 4%, and thrombotic coagulopathy in 2%. The number of variceal bleeding episodes ranged from 2 to 18 (mean, 5.6). None of the patients had clinical, biochemical, or liver biopsy evidence of liver disease. Esophageal varices were demonstrated by endoscopy, and/or contrast x-rays, and/or angiography in all patients. Visceral angiography was always used to demonstrate the extent of portal obstruction and the veins available for shunting. Before referral, the following procedures had failed: endoscopic sclerotherapy (68 patients), splenectomy alone (32 patients), central splenorenal shunt with splenectomy (10 patients), transesophageal varix ligation (12 patients). Three types of PSS were used: (1) central side-to-side splenorenal without splenectomy (75 patients, 46%); (2) central end-to-side splenorenal with splenectomy (34 patients, 21%); and (3) mesocaval (end-to-side cavomesenteric) (53 patients, 33%). PSS reduced the mean corrected portal pressure from 292 to 28 mm saline. All patients survived the procedure and left the hospital (100%). The actuarial survival rate for 5 years is 99%, and for 10 years is 96%. Three of the 6 deaths were unrelated to EHPH or PSS. Shunt patency for up to 35 years was demonstrated in 98% of patients by angiography and/or ultrasonography. In four patients (2%), all of whom had end-to-side splenorenal shunts, shunt thrombosis and rebleeding developed 3, 4, 4, and 6 years (respectively) after PSS. There were the only patients who experienced rebleeding. A diligent and repeated effort was made to detect portal-systemic encephalopathy (PSE), and no instance of PSE was found during 3 to 35 years of follow-up. Liver function and morphology remained normal, and hypersplenism was corrected in all patients. Quality of life was good in 98% of patients, and 5 years after PSS 96% were gainfully employed, engaged in full-time homemaking, or attending school.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗