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PubMed1992

Long-term follow-up study of adult patients with non-cirrhotic obstruction of the portal system: comparison with cirrhotic patients.

Thirty-two patients with non-cirrhotic portal system obstruction and oesophageal varices of non-malignant etiology were recruited over 13 years. Diagnosis was based on the presence of oesophageal varices at endoscopy, minor alterations in liver function tests and liver histology, a low hepatic venous pressure gradient, and pertinent angiographic patterns. Twenty-three had portal vein thrombosis, nine had splenic vein thrombosis. Twenty-one had idiopathic portal vein obstruction, 11 had secondary obstruction. The outcome was compared with a group of 32 patients with cirrhosis and portal hypertension, matched for age, Child-Pugh class, previous history of gastrointestinal bleeding, and size of oesophageal varices. Patients with non-cirrhotic obstruction of the portal system were followed for up to 171 months (mean 94 months). During follow-up ten patients had gastrointestinal bleeding, and eight died (five of gastrointestinal bleeding). After 6 years of follow-up, the cumulative risk of gastrointestinal bleeding was 24%, the cumulative risk of death was 17%, and the cumulative risk of death from gastrointestinal bleeding was 14%. Cumulative probability of death by any cause and the probability of gastrointestinal bleeding were significantly lower in patients with non-cirrhotic obstruction of the portal system than in patients with cirrhosis comparable for liver function and portal hypertension (p = 0.04 for both). The cumulative probability of death by gastrointestinal bleeding was not significantly different. In conclusion, the prognosis for non-cirrhotic obstruction of the portal system is significantly better than for patients with cirrhosis with comparable levels of liver function impairment and severity of portal hypertension.

Adult↗
PubMed1985

Portal-systemic myelopathy after portacaval shunt surgery.

Portal-systemic myelopathy is a rare complication of surgically created or spontaneous portal-systemic shunts in patients with chronic liver disease. We treated two patients with this entity, both of whom had undergone portacaval shunt operations.

Aged↗
PubMed1980

Hyperglobulinemia in alcoholic cirrhosis. Relationship with portal hypertension and intrahepatic portal-systemic shunting as assessed by Kupffer cell uptake.

The relative importance of portal hypertension and intrahepatic portal-systemic shunting in the pathogenesis of hyperglobulinemia is examined in 31 alcoholic cirrhotic patients and 6 patients with idiopathic portal hypertension. The degree of portal hypertension was evaluated by combined umbilicoportal and hepatic vein catheterization and the intrahepatic portal-systemic hunting was assessed by the Kupffer uptake of [125I]albumin microaggregates during a single passage through the liver. All patients had comparable severe portal hypertension and most had bled from ruptured varices; however, no demonstrable relationship could be found between portal hypertension and hyperglobulinemia. Elevated levels of serum gammaglobulins and immunoglobulins (mainly IgG) were observed only in cirrhotic patients, particularly those with markedly altered Kupffer cell uptake. It is concluded that intrahepatic portal systemic shunting as evaluated by the Kupffer cell uptake is more important than the collateral circulation secondary to portal hypertension in the pathogenesis of hyperglobulinemia in alcoholic cirrhotic patients.

Adult↗
PubMed2001

Influence of esophageal varices and spontaneous portal-systemic shunts on postprandial splanchnic hemodynamics.

OBJECTIVE: The aim of the study was to assess postprandial splanchnic hemodynamic changes in cirrhosis in relation to variceal status. METHODS: In 9 healthy controls and 56 patients with liver cirrhosis, stratified according to variceal status and presence of spontaneous portal-systemic shunts, the portal vein diameter and flow velocity, the congestion index of the portal vein, and the resistive index of the superior mesenteric artery (SMA-RI) were studied by Doppler ultrasound before and 30, 60, and 120 min after the intake of a standard meal. Comparison of postprandial parameters with basal ones was done within each group by paired t test and among groups by ANOVA and Duncan test. RESULTS: Healthy controls and cirrhotic patients without varices showed similar significant splanchnic hemodynamic changes, namely a reduction of SMA-RI (-13% at 30 min) and a consequent increase in portal vein diameter (respectively, +32% and +17% in the two groups) and velocity (+66% and +51%). A significant reduction of SMA-RI was also found in patients with varices, irrespective of the variceal size (range, -7 to -11%), but the expected portal vein dilation and velocity increase were progressively blunted with the increase of variceal size (range, 0-5% for diameter and 5-19% for velocity). Patients with spontaneous portal-systemic shunts showed a response similar to that of patients with large varices. Significant modification of the congestion index of the portal vein did not occur in any group. CONCLUSIONS: Our results show that the hemodynamic response to meal in patients with liver cirrhosis is influenced by the presence and size of esophageal varices and the presence of spontaneous portal-systemic shunts.

Blood Flow Velocity↗
PubMedDate not supplied

Distal splenorenal shunt vs. portal-systemic shunt: current status of a controlled trial.

A prospective controlled comparison of portal-systemic (PSS) and distal splenorenal shunts (DSRS) in cirrhotic patients who had survived hemorrhage from esophagogastric varices was undertaken 5 yr ago at five hospitals by the Boston-New Haven Collaborative Liver Group. The clinical and endoscopic criteria for massive hemorrhage were satisfied in 155 patients. Thirty-four patients were excluded, primarily because of uncontrolled hemorrhage. Thirty-four were rejected because the were poor operative risks and 21 because they did not satisfy criteria. Thirteen patients refused to participate; the remaining 53 were randomized; 29 to receive PSS and 24, DSRS. The two groups were similar in clinical, laboratory, and manometric characteristics. The DSRS group was older and tended to have had more previous hemorrhages. Followup ranged from 1 to 56 months (mean 21). After PSS, which was performed by 10 different surgeons, 6 patients died during the hospital admission (21%) compared to 2 after DSRS (12%). There were 6 late deaths in the PSS group and 4 in the DSRS group. Portal-systemic encephalopathy occurred in 5 of the 23 survivors of PSS (23%), and in 6 of the 19 who survived DSRS (32%. Two patients in the PSS group bled (9%), 1 after thrombosis and 1 after stenosis of the shunt. Three patients in the DSRS group bled (16%) and all had thrombosis of the shunt. PSS was associated with an unexplained but inordinately high operative mortality. Although the DSRS was accomplished with an acceptably low operative mortality, it was associated with frequent portal-systemic encephalopathy, shunt occlusion, and recurrent hemorrhage. Similar incidences of portal-systemic encephalopathy, shunt occlusion, and recurrent hemorrhage were observed in the PSS group. More patients and longer followup are necessary to determine which of these portal decompressive procedures is superior.

Clinical Trials as Topic↗
PubMed2006

Study of hemodynamic changes in portal systemic shunts and their relation to variceal relapse after endoscopic variceal ligation combined with ethanol sclerotherapy.

BACKGROUND: Among the factors influencing variceal relapse after endoscopic treatment, portal hemodynamic changes, especially in portal systemic shunts, could be the most important factor because hemodynamics are directly related to the development of esophageal varices. We aimed to clarify the influence of endoscopic treatment for esophageal varices on portal systemic shunts as well as its predictive value for variceal relapse. METHODS: Fifty patients who underwent combined endoscopic variceal ligation and injection sclerotherapy were examined with sonography and portography. RESULTS: Decrease of diameter, hepatopetal flow direction in the left gastric vein, or the presence of non-varices portal systemic shunt were sonographic findings related to a low incidence of variceal relapse. The presence of blood flow in and around the esophagus on venograms was highly predictive for variceal relapse. In patients with such venograms, non-varices portal systemic shunts did not develop. CONCLUSIONS: Sonographic assessment of hemodynamic changes in portal systemic shunt could be useful for estimating the results of endoscopic treatment for esophageal varices.

Esophageal and Gastric Varices↗
PubMed1975

Massive spontaneous portal-systemic shunting without varices.

Using umbilical vein portal phlebography, a group of patients, often with previously unsuspected liver disease or portal hypertension, have been identified with massive spontaneous portal-systemic shunts. In all cases, the collateral circulation was a single large vessel. The splenoadrenorenal, umbilical vein, or inferior mesenteric vein routes were the common pathways. These natural shunts were functional and effective in the alleviation of portal hypertension without evidence of esophageal varices or other collaterals. Portal flow was usually retrograde, perhaps contributing to the small atrophic liver seen in all patients. Six such patients were seen in the last 40 studied. This phenomenon may be more common than suspected in the cirrhotic population and account in part for differences in natural history, complications, and results of surgical therapy.

Adolescent↗
PubMedDate not supplied

Distal splenorenal vs. portal-systemic shunts after hemorrhage from varices: a randomized controlled trial.

Between 1975 and 1983, 303 cirrhotic patients with endoscopically proven major variceal hemorrhage were admitted to the participating hospitals of the Boston-New Haven Collaborative Liver Group. Of these, 274 were evaluated for admission to a prospective, randomized controlled trial comparing portal-systemic shunts with distal splenorenal shunts. The criteria for inclusion were as follows: (i) a portohepatic pressure gradient greater than or equal to 12 mmHg; (ii) angiographic evidence of antegrade portal venous flow; (iii) angiographic demonstration that the inferior vena cava and portal, splenic and left renal veins were anatomically suitable for either a portal-systemic or distal splenorenal shunt, and (iv) the patient was a reasonable operative risk. Eighty-one patients from the six participating hospitals fulfilled the criteria and consented to participate. Thirty-eight patients were randomly assigned to have portal-systemic shunt and 43 to have distal splenorenal shunt. After a follow-up period of 11 years (mean = 3.5 years for all patients), survival was found to be similar in the two groups of patients. The 30-day operative mortality was 13% for the portal-systemic shunt group and 9% for the distal splenorenal shunt patients. Late mortality was 55% for the portal-systemic shunt and 37% for the distal splenorenal shunt group. Total mortality was 68% for the portal-systemic shunt and 46% for the distal splenorenal shunt group. None of these differences is statistically significant. In those patients who survived greater than 30 days after surgery, recurrent variceal hemorrhage occurred in four (12%) in the portal-systemic shunt group compared to seven in the distal splenorenal shunt group (18%) (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Comparison of a modified Sugiura procedure with portal systemic shunt for prevention of recurrent variceal bleeding in cirrhosis.

BACKGROUND: There is no agreement on the management of patients with cirrhosis and recurrent variceal bleeding after failure of medical or endoscopic treatments or both. Portal systemic shunts are highly effective in preventing rebleeding but are associated with a high incidence of chronic encephalopathy. This study compared the results of a slightly modified Sugiura procedure (esophageal transection plus esophagogastric devascularization plus splenectomy) with those of nonselective portal systemic shunts in patients with previous variceal bleeding. METHODS: Fifty-four patients were included in this randomized controlled study between January 1984 and April 1989. The major end point was chronic encephalopathy. Secondary end points were recurrent variceal bleeding, survival, ascites, and hepatocellular carcinoma. RESULTS: Twenty-seven patients were assigned to each group. The rate of chronic encephalopathy was significantly (p = 0.002) lower after modified Sugiura procedure than after portal systemic shunt. Recurrent variceal bleeding was more frequent after modified Sugiura procedure than after portal systemic shunt, but the difference is not significant. One-, two-, and three-year survival rates were 93%, 81%, and 67%, respectively, in the modified Sugiura group and 78%, 66%, and 39%, respectively, in the portal systemic shunt group (p = 0.044). CONCLUSIONS: These results suggest that the modified Sugiura procedure is better overall than the nonselective portal systemic shunt in the management of patients with cirrhosis and recurrent variceal bleeding. Although the rebleeding rate is higher after the modified Sugiura procedure, this does not seem to affect mortality in these patients.

Carcinoma, Hepatocellular↗
PubMed1984

Renal response of fowl to hypertonic saline infusion into the renal portal system.

The avian kidney has a dual blood supply: one arising from the renal arteries and the other from the renal portal system. In anesthetized pullets (Gallus gallus) two major shunt pathways bypassing the kidney were occluded to ensure the venous blood returning from the leg suffuses the peritubular sites before it enters the systemic circulation. Urine was collected from the ureteral orifices. When 5% NaCl (2.0 ml X kg-1 X h-1) was infused for 20 min into the renal portal system, urine flow and urinary NaCl concentrations and excretion rates increased immediately in the infused side. Infusion of 5% NaCl into the systemic circulation produced no natriuresis. Infusion of 10% NaCl (4.0 ml X kg-1 X h-1), into either the systemic or renal portal route, caused a prolonged antidiuresis. Plasma renin activity (PRA) decreased after portal infusion of 5% NaCl and after both portal and systemic infusion of 10% NaCl. These results suggest that 1) infusion of hypertonic saline into the renal portal system produces local renal effects and 2) increases in tubular or peritubular NaCl levels may suppress PRA.

Animals↗
PubMed2005

Long-term results of partial splenic artery embolization as supplemental treatment for portal-systemic encephalopathy.

OBJECTIVES: To present long-term results of angiographic partial splenic artery embolization (PSE) as a supplemental treatment of portal-systemic encephalopathy. METHODS: Twenty-five patients with portal-systemic encephalopathy were divided into two groups: 14 patients underwent transportal obliteration and/or balloon-occluded retrograde transvenous obliteration (BRTO) of portal-systemic shunts (PSS), followed by PSE (PSE(+) group), and 11 patients underwent only transportal obliteration and/or BRTO of PSS (PSE(-) group). RESULTS: Portal venous pressures pretreatment was similar to posttreatment in the PSE(+) group, but lower than posttreatment in the PSE(-) group. Serum ammonia levels were higher at pretreatment than at 1 wk posttreatment in both groups, but the levels in the two groups were similar at pretreatment, 1 wk, 3 months, 3 yr, 4 yr, and 5 yr posttreatment. However, serum ammonia levels were lower in the PSE(+) group than in the PSE(-) group 6 months, 9 months, 1 yr, and 2 yr posttreatment. Grades of encephalopathy were higher at pretreatment than at 1 wk posttreatment in both groups, but the levels in the two groups were similar at pretreatment, 1 wk, 2 yr, 3 yr, 4 yr, and 5 yr posttreatment. However, grades of encephalopathy were lower in the PSE(+) group than in the PSE(-) group 3 months, 6 months, 9 months, and 1 yr posttreatment. CONCLUSIONS: Obliteration of PSS followed by PSE benefit patients with portal-systemic encephalopathy.

Adult↗
PubMed1981

Topographical appearance of adenohypophysial cells with special reference to the development of the portal system.

To determine whether or not the portal vessels play any essential role on the cytogenesis of adenohypophysis through the mediation of hypothalamic neurohormones, chronological and topographical relations between the portal system and adenohypophysial cells have been studied in fetal rats aged from 14.5 to 18.5, by vascular infusion with India ink and by immunohistochemistry. On day 14.5 the intraglandular fossa (Atwell's recess) receives several blood vessels (primitive portal vessels) from the subtuberal capillary plexus and a pair of fine branches from the internal carotid arteries: those blood vessels anastomose within the recess. On day 15.5 the recess becomes narrow but the vasculature extends posteriorly into the growing anterior wall of the rathke's pouch, in which they sprout short branches showing terminal dilations. Immunoreactive ACTH cells first appear in the ventral-middle portion of the pars distalis, where the vascular sproutings are not evident. On day 16.5 the intraglandular blood vessels spread through the pars distalis and connect occasionally with extraglandular venous system suggesting the initiation of the hypophysial portal circulation. TSH cells first appear sporadically in the posterior part of the pars distalis, where blood vessels are still scarce and very occasional cells abut on te sinusoids. On day 17.5, the recess becomes indistinct and pituitary acquires the mature shape. The intraglandular vasculature of the portal system makes a dense meshwork in the adenohypophysis except the pars intermedia. LH cells appear first in the ventral region of the anterior half of the adenohypophysis, where occasional cells appear abutting on the sinusoids. The conclusion is that the portal blood supply, which might convey hypothalamic neurohormones, is not essential or initial cytogenesis of the adenohypophysial cells studied here.

Animals↗
PubMed1999

Sleep disorders and portal-systemic encephalopathy following transjugular intrahepatic portosystemic stent shunt in patients with liver cirrhosis. Relation to plasma tryptophan.

Neuropsychiatric symptoms due to any type of dysfunction and/or portal-systemic shunting are summarized as hepatic encephalopathy (HE). HE in the presence of liver cirrhosis and/or portal-systemic shunting has been termed portal-systemic encephalopathy (PSE). PSE is most frequent among the HE syndromes and is almost exclusively seen in patients with advanced cirrhosis and portal hypertension. Portal-systemic shunting either spontaneous due to portal hypertension, following surgical portocaval anastomosis, or subsequent to transjugular intrahepatic portosystemic stent-shunt (TIPSS) is regarded as the primary causative condition for PSE, not hepatic dysfunction per se. PSE may be considered as a disorder of multiple neurotransmitter systems among which derangements of the serotonergic system have been documented most consistently. Incipient PSE is frequently paralleled by the occurrence of sleep disorders, however, their relation to PSE remains unclear. We observed a transient increase of sleep disorders post-TIPSS, which were only in part correlated to other symptoms of PSE. Among the biochemical parameters studied only an association between arterial ammonia levels and sleep disorders became apparent, whereas no significant relation was observed for peripheral tryptophan.

Adult↗
PubMed2004

Standard planes for ultrasonographic examination of the portal system in dogs.

A scanning protocol for the systematic ultrasonographic examination of the portal system in dogs was developed. Seven planes were used to image the portal system. With the dogs in left lateral recumbency, 3 transverse planes obtained via the right intercostal spaces were used to visualize the portal vein and right portal branch, and a longitudinal plane obtained with the transducer caudal to the last right rib was used to visualize the portal bifurcation. With the dogs in dorsal recumbency, a longitudinal plane was used as an alternative method of visualizing the portal vein and its bifurcation. Finally, with the dogs in right lateral recumbency, longitudinal planes obtained with the transducer in the left flank were used to visualize the hepatic artery, the left renal vein, and the left testicular or ovarian vein. To diagnose or rule out portosystemic shunting, the right portal branch, the left testicular or ovarian vein, the portal vein immediately caudal to the portal bifurcation, and the portal vein at the level of the celiac artery should be examined with this scanning protocol.

Animals↗
PubMed1997

New aspects on etiology, biochemistry, and therapy of portal systemic encephalopathy: a critical survey.

There is scientific agreement that portal systemic encephalopathy (PSE) is caused morphologically by portal systemic shunts and biochemically by constituents of the portal venous blood. Ammonium has a key role in the pathogenesis of PSE. Direct correlations with the degree of PSE have been established exclusively with glutamine, i.e. the terminal product of the peripheral detoxification of ammonium. In PSE, ammonium is probably responsible for damage to astrocytic and neuronal cells. Ammonium's toxic effect is due to the intracerebral glutamine synthesis. After several metabolic steps, which will be discussed in detail, brain cell damage is caused directly or indirectly (exitotoxically) by energy deficiency. Hyperammonemia and PSE are each well defined though different forms of disturbance. Therefore, ammonium is not the sole decisive factor in the pathogenesis of PSE. We performed a detailed and critical analysis of all studies on amino acid therapy of PSE, especially those that were randomized and controlled. This analysis revealed a close and direct correlation between qualitative and quantitative dosages of amino acids on one hand, and parallel improvements of amino acid imbalance (essentially associated with PSE) and degree of PSE on the other. A close and direct dose/efficacy correlation must be assumed. Disturbed plasmatic amino acid homeostasis and cerebral monoaminergic neurotransmission are probably important pathogenic factors of PSE. A fundamental cofactor in the efficacy of each adequate amino acid therapy might be a substantial decrease of endogenous ammonium production. Physiologic benzodiazepines may also have an important function in the pathogenesis of PSE: not so, however, the glutamate-ergic and GABA-ergic neurotransmission, which are disturbed principally in PSE. In close correlation to pathogenesis, established and proposed therapies of PSE are critically discussed.

Amino Acids↗
PubMedDate not supplied

Disappearance of hepatic encephalopathy and improvement of liver function after surgical treatment of portal-systemic shunt in a patient with liver cirrhosis.

Large portal-systemic shunts in cirrhotic patients often cause recurrent hepatic encephalopathy and might promote liver dysfunction because of the reduced portal blood flow. We report a case of liver cirrhosis in which hepatic encephalopathy disappeared and liver function improved together with an increase of hepatopetal portal blood flow and liver volume after shunt resection. A 70-year-old woman with liver cirrhosis was admitted because of recurrent disorientation. Serum ammonia levels ranged from 174 to 321 micrograms/dL. Computed tomography demonstrated an atrophic liver and a large shunt. Portography disclosed that this shunt originated from the superior mesenteric vein and flowed into the inferior vena cava, common iliac vein and ovarian vein. Portal blood flow was poor because of the deviation into this shunt. After the surgical resection of the shunt, ammonia levels were normalized and hepatic encephalopathy no longer occurred. Portography and computed tomography after surgery demonstrated that hepatopetal portal blood flow evidently improved and the liver volume increased (before 369; after 574 cm3). Two years after surgery, hepaplastin test and serum albumin level improved from 41 to 76% and from 2.7 to 3.4 g/dL, respectively. This case supports the effectiveness of shunt resection for hepatic encephalopathy and the deteriorated liver function in cirrhotic patients with large portal-systemic shunt.

Adult↗
PubMed2000

Portal-systemic encephalopathy in non-cirrhotic patients: classification of clinical types, diagnosis and treatment.

Hepatic encephalopathy is suspected in non-cirrhotic cases of encephalopathy because the symptoms are accompanied by hyperammonaemia. However, the cause of the large portal-systemic shunt formation observed in these cases is not clear, as cirrhosis and portal hypertension are absent. The frequency of such cases reported in the literature is increasing with progress and spread of abdominal imaging diagnostic techniques. Some cases have been misdiagnosed as psychiatric diseases (dementia, depression and others) and consequently patients have been hospitalized in psychiatric institutions or geriatric facilities. Some paediatric cases have also been misdiagnosed. Therefore, the importance of accurate diagnosis of this disease should be strongly emphasized. Some paediatric cases have also been misdiagnosed. When psychoneurological symptoms are suggestive of hepatic encephalopathy but objective and subjective symptoms or abnormal values of liver function tests are not sufficiently indicative of liver cirrhosis, portal-systemic encephalopathy should be suspected. Abnormal angiograms of the portal vein, superior mesenteric vein or splenic vein are conclusive evidence of portal-systemic encephalopathy. Transrectal portal scintigraphy also provides information useful for detection of shunts and a quantitative estimation of shunt index. We classified the disease into five types based on whether the shunt is formed inside or outside the liver. Type I (intrahepatic type) designates cases in which shunts are located between the portal and systemic veins. Type II designates a type of intra/extrahepatic shunt that originates from the umbilical part of the portal vein and serpentines in the liver, then leaves the liver. Type III (extrahepatic type) occurs most frequently. Type IV (extrahepatic) is accompanied by shunts similar to those in type III, but hepatic pathology presents as idiopathic portal hypertension. Type V (extrahepatic) represents the congenital absence of the portal vein, where the superior mesenteric vein joins the intrahepatic inferior vena cava or the left renal vein. The prevalence of each type in our country was examined by a nationwide investigation. In addition to the conventional diet or drug treatments, obliteration by less invasive interventional radiology using a metallic coil and ethanol has recently been used more frequently than surgical occlusion of shunts. Shunt-preserving disconnection of portal and systemic circulation and partial splenic artery embolization are also performed. International investigation of the disease status and establishment of diagnostic and therapeutic methods for the disease are awaited and investigation of long-term prognosis after therapy is also necessary.

Diagnosis, Differential↗