Surgical creation of portacaval shunts during temporary intestinal arterial and venous occlusion in dogs

OBJECTIVE: To surgically create complete portacaval shunts in dogs during temporary arrest of intestinal arterial and portal venous blood flow. DESIGN: Complete portacaval anastomoses were surgically created, and liver function was evaluated for 14 to 18 weeks after surgery. ANIMALS: 32 adult mixed-breed dogs of either sex. PROCEDURE: Administration of deferoxamine and temporary intestinal arterial occlusion were used to minimize the intestinal cellular damage resulting from the complete, temporary arrest of portal venous blood flow during creation of the portacaval anastomosis. Side-to-side, appositional anastomoses ( > 2 cm diameter) were formed between the portal vein and caudal vena cava. Dogs were observed daily for signs of hepatic encephalopathy, and food intake was recorded. Body weight was recorded weekly. Preprandial plasma ammonia, serum urea nitrogen, and glucose concentrations and sulfobromophthalein retention were measured monthly. The dogs were euthanatized, and necropsy was performed 14 to 18 weeks after surgery. RESULTS: 30 of 32 dogs recovered without complications. Complete portosystemic shunting was documented by increased plasma ammonia concentration, decreased serum urea nitrogen and glucose concentrations, prolonged sulfobromophthalein retention (P < 0.01), and inspection at necropsy. CONCLUSION: This method of providing temporary, complete arrest of portal venous blood flow was helpful in allowing accurate, appositional portacaval anastomoses to be created that remained patent for 14 to 18 weeks. CLINICAL RELEVANCE: This method of providing temporary, complete arrest of portal venous blood flow may prove useful in clinical surgery when temporary arrest of portal blood flow is desired.     

Effects of vena caval banding in experimentally induced multiple portosystemic shunts in dogs

Effects of vena caval banding on portal venous and vena caval hemodynamics were examined in 6 control dogs and in 10 dogs that had undergone attenuation (banding) of the abdominal part of the caudal vena cava and had dimethylnitrosamine-induced multiple portosystemic shunts (PSS). Additionally, indocyanine green (ICG) extraction and clearance after infusion to steady state were used to calculate hepatic plasma flow in these dogs. Sixteen dogs were randomly assigned to 2 groups: control (n = 6) or diseased (n = 10). Diseased dogs were administered dimethylnitrosamine (2 mg/kg, PO, twice weekly) until multiple PSS developed, as assessed by results of clinical laboratory tests, ultrasonography, and hepatic scintigraphy. Shunts were confirmed visually at celiotomy and by contrast portography. Venous pressures (caudal vena caval, portal, and hepatic) were recorded before and after vena caval banding for up to 7 days in dogs from both groups. Peritoneal cavity pressures were recorded in all dogs after closure of the body wall. To determine ICG extraction and clearance, a bolus injection of ICG (0.5 mg/kg, i.v.) was administered, followed by steady-state infusion of 0.097 mg/min. Extractions and clearances of ICG were measured, and from these, hepatic plasma flow rates were determined immediately before and after banding and at 6 hours, 48 hours, and 7 days after banding. The gradient (caudal vena caval pressure within 1 to 2 mm of Hg of portal pressure) between caudal vena cava and portal venous pressures established at banding was maintained after the first hour in both groups. Caudal vena cava pressures established at banding were maintained throughout the study, with the exception of the first hour in diseased dogs. Extraction ratios were higher in control dogs at all times, except at 48 hours. Clearance was higher in control dogs at all times. Hepatic plasma flow did not differ between groups, except immediately after banding, when flow was greater in diseased dogs, and differences were not found over time in either group. This study indicated that vena caval banding in this model of experimentally induced multiple PSS increases and maintains caudal vena cava pressure, relative to portal venous pressure (after the first hour) for 7 days, and that calculated hepatic plasma flow is not persistently improved by vena caval banding.     

CT and MRI in detection of intrahepatic portosystemic shunts in patients with liver cirrhosis

OBJECTIVE: Our goal was to determine the prevalence and anatomic location of intrahepatic portosystemic shunts (IPSs) in patients with hepatic cirrhosis as shown by CT and MRI. MATERIALS AND METHODS: We retrospectively reviewed CT and MR scans of 33 cirrhotic patients who had IPSs. In addition, two series of 100 consecutive CT or MR were reviewed to determine the prevalence of IPSs and the percentage of intrahepatic and extrahepatic paraumbilical veins. RESULTS: Intrahepatic portosystemic shunts were divided into three groups according to the intrahepatic course: paraumbilical shunt between the left portal vein and the paraumbilical vein anterior to the liver (n = 29); inferior vena caval shunt between the posterior branch of the right portal vein and the inferior vena cava (n = 2); and miscellaneous (n = 2). Shunts of the paraumbilical type ran through the medial (n = 23), lateral (n = 3), or both medial and lateral (n = 3) segments of the left lobe of the liver. Twenty-five patients had one shunt, and four had more than one. Six cases were also associated with extrahepatic paraumbilical veins. CONCLUSION: Intrahepatic portosystemic shunts, especially the paraumbilical type, were not infrequently visualized in patients with hepatic cirrhosis.     

Ultrasonography of the ureters

Ultrasonography is a rapid, accurate, noninvasive diagnostic test for primary (congenital) and secondary (acquired) portosystemic shunting in dogs and cats. Two-dimensional, gray-scale ultrasonography alone enables diagnosis of most congenital portosystemic shunts and determination of intra- versus extrahepatic location. Use of duplex- and color-flow Doppler ultrasonography aids detection of congenital and acquired extrahepatic portosystemic shunts. The underlying cause of acquired portosystemic shunting is portal hypertension; this may be documented by finding either hepatofugal or reduced velocity hepatopetal portal blood flow by duplex-Doppler. Also, ultrasonography may enable detection of lesions involved in the pathogenesis of portal hypertension, for example, hepatic arterioportal fistula, hepatic parenchymal lesions, and portal vein thrombosis.     

Measurement of collateral circulation blood flow in anesthetized portal hypertensive rats

AIMS: The aim of this study was to develop a technique to measure collateral blood flow in portal hypertensive rats. METHODS: Morphological techniques included inspection, casts and angiographies of portosystemic shunts. The main hemodynamic measurements were splenorenal shunt blood flow (transit time ultrasound method), percentage of portosystemic shunts and regional blood flows (microsphere method). In study 1, a model of esophageal varices was developed by ligating the splenorenal shunt. In study 2, morphological studies of the splenorenal shunt were performed in rats with portal vein ligation. In study 3, the relationship between splenorenal shunt blood flow with percentage of portosystemic shunts was evaluated in dimethylnitrosamine cirrhosis. In study 4, secondary biliary, CCl4 and dimethylnitrosamine cirrhosis were compared. In study 5, rats with portal vein ligation received acute administration of octreotide. In study 6, rats with dimethylnitrosamine cirrhosis received acute administration of vapreotide. RESULTS: Blood flow of para-esophageal varices could not be measured. SRS blood flow was correlated with the mesenteric percentage of portosystemic shunts (r = 0.74, P < 0.05), splenic percentage of portosystemic shunts (r = 0.54, P < 0.05) and estimated portosystemic blood flow (r = 0.91, P < 0.01). Splenorenal shunt blood flow was 6 to 12 times higher in portal hypertensive rats, e.g., in portal vein ligated rats: 2.8 +/- 2.7 vs 0.3 +/- 0.1 mL.min-1 in sham rats (P < 0.01), and was similar in the different cirrhosis models but was higher in portal vein ligated rats than in cirrhotic rats (1.2 +/- 0.7 vs 0.6 +/- 0.6 mL.min-1.100 g-1, P = 0.05). Octreotide significantly decreased splenorenal shunt blood flow: -23 +/- 20% (P < 0.01) vs -6 +/- 8% (not significant) in placebo rats. The variation of splenorenal shunt blood flow after vapreotide was significant but not that of the splenic percentage of portosystemic shunts compared to placebo. CONCLUSIONS: The splenorenal shunt is the main portosystemic shunt in rats. The measurement of splenorenal shunt blood flow is easy, accurate and reproducible and should replace the traditional measurement of the percentage of portosystemic shunts in pharmacological studies.     

Gradual occlusion of extrahepatic portosystemic shunts in dogs and cats using the ameroid constrictor

Gradual occlusion of the splenic vein, using a specialized device (ameroid constrictor), was evaluated experimentally in three normal beagle dogs. Splenoportograms were used to verify that total occlusion of the splenic vein had occurred in all dogs within 4 to 5 weeks after application of the device. The ameroid constrictor (AC) was also evaluated as a method of gradual vascular occlusion in 12 dogs and two cats with single, extrahepatic, portosystemic shunts (PSS). Serum bile acid (SBA) concentrations were measured and portal scintigraphy (PS) was performed on all 14 animals preoperatively and 10, 20, 30, and 60 days postoperatively. Two dogs (14%) died from portal hypertension in the early postoperative period. One dog and one cat developed multiple acquired PSS, confirmed by mesenteric portography 90 days after the operation. Portal scintigraphy confirmed total occlusion of the primary shunt in the other 10 animals. Shunt fractions (SF), as measured by PS on postoperative days 30 and 60, declined significantly from preoperative values. Significant decreases were noted between preoperative and postoperative values for preprandial SBA on postoperative day 60 and for postprandial SBA on postoperative day 30. SBA concentrations did not correlate with SF. Based on this study, gradual vascular occlusion using the AC is recommended as a method for treatment of single, extrahepatic, PSS.     

Testosterone concentrations, testes weight and morphology of mule drakes (Muscovy drake x Khaki Campbell)

BACKGROUND: Transjugular intrahepatic portosystemic shunts (TIPS) are sometimes used to reduce the risk of variceal bleeding or treat intractable ascites before orthotopic liver transplantation (OLT). TIPS usually do not make OLT more difficult, but rarely, malposition of TIPS can significantly complicate OLT. METHOD and RESULTS: The following report describes a patient in whom an initially well-placed Wallstent migrated to the confluence of the splenic and superior mesenteric veins. During liver transplantation, the portal vein containing the Wallstent was completely resected, and the portal vein was reconstructed with donor iliac vein. After sewing the iliac vein onto the portal remnant, the liver transplant was completed under portosystemic bypass. The patient had an uneventful recovery. CONCLUSIONS: Wallstents can migrate within the portal vein. An interposition graft of donor vein allows full resection of the portal vein containing a migrated stent and facilitates portosystemic bypass and portal anastomosis.     

Vascular reconstruction using left renal vein graft in advanced hepatobiliary malignancy

BACKGROUND/AIMS: In surgical resection for advanced hepatobiliary malignancies involving the portal vein and inferior vena cava, vascular reconstruction is usually required. We utilized left renal vein grafts for vascular reconstruction in cases of these malignancies, and their clinical significance is evaluated in this study. METHODOLOGY: Left renal vein grafts were utilized for reconstruction of the portal vein in four patients and patch repair of the inferior vena cava was performed in two patients with advanced hepatobiliary malignancies. All six patients underwent hepatic resection with vascular resection and reconstruction. Postoperative renal function and graft patency were assessed. RESULTS: Transient slight renal disturbances appeared in some patients, but there was no severe renal dysfunction requiring specific therapy. Graft patency was maintained during the follow-up period in all patients. CONCLUSION: The use of left renal vein grafts as autovein grafts seems appropriate in cases involving reconstruction of the portal vein and in those involving patch repair of the inferior vena cava defect in surgical resection for advanced hepatobiliary malignancies.     

Trauma to the colon in civilian surgery

An unusual congenital portosystemic shunt was identified in one dog and two cats with clinical signs and laboratory evidence of hepatic dysfunction. In all the animals, the abnormal vessel arose from the portal system between the left medial and quadrate liver lobes and travelled within the falciform fat, exiting the abdomen through the caudal ventral left diaphragm. The intrathoracic course of these vessels was not established. The anatomical location of this anomalous vessel may have hindered attempts at ultrasonographic identification since it was not visualised before surgery in any of the animals. In addition, while the anatomical location of the vessel may facilitate rapid identification and surgical attenuation, it could predispose the vessel to trauma during the coeliotomy approach. It is hypothesised that this form of portosystemic communication results from failure of a portion of the left umbilical vein to degenerate during embryogenesis. This is in contrast to other forms of congenital extrahepatic portosystemic shunt that are presumed to be developmental errors resulting in an abnormal communication between the embryonic vitelline and cardinal venous systems. The prognosis for animals with the vascular anomaly reported here is probably similar to that for animals with other forms of congenital portosystemic shunt.     

Chlorpyrifos elicits mitotic abnormalities and apoptosis in neuroepithelium of cultured rat embryos

Case records of 27 dogs with medically managed congenital portosystemic shunts were reviewed. Fourteen were followed up by telephone questionnaires to the owners. Age, breed, sex, clinical signs and blood results were similar to previous studies. Weight and quality of life were stable or improved on treatment in all cases. Total serum protein concentration and alanine aminotransferase and alkaline phosphatase activities fell significantly during treatment. Fourteen dogs were euthanased, four were lost to follow-up and nine remained alive. Mean survival time for the dogs euthanased was 9.9 months. Mean follow-up period for the dogs still alive was 56.9 months and all had survived more than 36 months from diagnosis. Surviving dogs with intrahepatic shunts had a significantly shorter follow-up period than dogs with extrahepatic shunts. Two prognostic indicators were identified, age at initial signs and blood urea concentration on presentation, both correlating with survival time. It was demonstrated that a significant proportion of dogs with portosystemic shunts managed medically have a good prognosis.     

Doppler US of helical flow in the portal vein

In helical portal venous blood flow, the usual laminar flow in the portal vein is replaced by a spiral. This changes the color Doppler ultrasound (US) appearance to one of alternating or parallel red and blue bands. Duplex US may appear to show hepatopetal, hepatofugal, or simultaneous bidirectional flow depending on placement of the cursor within the helix. Helical portal venous flow is unusual in normal individuals (2.2% of 135 patients). Its presence should prompt further scrutiny for signs of liver disease, particularly portosystemic shunts, as in 20% of 41 patients who subsequently underwent liver transplantation. It is a normal finding immediately after liver transplantation (43% of 35 patients) and transjugular intrahepatic portosystemic shunt (TIPS) creation (28% of 36 patients). In both liver transplant and TIPS recipients, helical flow is usually transient. Its persistence long after transplantation in association with a prolonged increase in portal venous velocity is a useful sign of portal vein stenosis. Helical flow may also occur in cases of neoplastic invasion or displacement of the portal vein.     

Successful repair of total anomalous pulmonary venous connection and incomplete endocardial cushion defect associated with left isomerism

Successful repair of a 8-month-old girl with polysplenia was reported. The cardiovascular anomalies were TAPVC (II b), incomplete ECD, interruption of inferior vena cava with hemiazygos continuation, bilateral superior vena cava, and left superior vena cava draining into the coronary sinus. Cardiopulmonary bypass was established with ascending aortic perfusion and caval cannulation. A left superior vena cava was directly cannulated after establishing partial bypass. In this case the left pulmonary vein drained into the right atrium near the orifice of the coronary sinus, so the atrial septal flap was made and sutured between the orifice of the left pulmonary vein and the coronary sinus in order to avoid late pulmonary vein obstruction. Then, atrium was separated by an intraatrial baffle which was sutured to the atrial septal flap. Recently, it becomes possible to surgical repair of polysplenia syndrome according to the advancements of the diagnostic methods, cardiopulmonary bypass, and the technique of the open heart surgery.     

Single muscle fibre analyses in 2 brothers with succinate dehydrogenase deficiency

Thrombosis of the access site and occlusion of the inferior vena cava after placement of an inferior vena caval filter are known complications of caval interruption. 30 patients were evaluated with colour-coded Doppler sonography 4 to 66 months (average 2.5 years) after percutaneous placement of either a Günther filter, a Bird's Nest filter or a Simon-Nitinol filter. One right internal jugular vein had post-thrombotic alterations. One inferior vena cava was found to be occluded 15 months after Simon-Nitinol filter placement. The long-term occlusion rates of access site and inferior vena cava after percutaneous filter introduction are low. These two factors need not be considered if implantation of a caval filter is contemplated.     

Orthotopic transplantation of a partial hepatic autograft in dogs

The purpose of this study was to investigate the availability of an orthotopic transplantation of partial hepatic autograft in dogs as a means of surgical training. Male mongrel dogs weighting 10-15 kg were used. The left lobe of the liver was harvested while preserving the left branches of the portal vein, hepatic artery and bile duct, and the left hepatic vein. The remnant liver was removed while preserving the inferior vena cava using a veno-venous bypass. Orthotopic transplantation of the autograft was performed while anastomosing the left hepatic vein to the inferior vena cava, portal and arterial reconstruction, and external biliary drainage. Thirteen out of 29 dogs survived more than 48 h after transplantation. However, 6 out of 13 dogs were sacrificed after developing bile peritonitis due to a dislodgement of the biliary catheter, and only two dogs were able to survive for 7 days after transplantation. The arterial ketone body ratio recovered to 1.0 within 1 h after reperfusion, and the ratio of the dogs that survived for more than 48 h remained above 1.0 until sacrifice. Orthotopic transplantation of a partial hepatic autograft is a useful and simple procedure to train surgeons for partial liver transplantation.     

Creation of transjugular intrahepatic portosystemic shunts with the wallstent endoprosthesis: results in 100 patients

One hundred patients underwent transjugular intrahepatic portosystemic shunt (TIPS) creation for variceal bleeding (n = 94), intractable ascites (n = 3), hepatorenal syndrome (n = 2), and preoperative portal decompression (n = 1). Shunts were completed in 96 patients. Portal vein pressure was reduced from 34.5 mm Hg +/- 7.6 (standard deviation) to 24.5 mm Hg +/- 6.2; the residual portal vein-hepatic vein gradient was 10.4 mm Hg +/- 0.9. Acute variceal bleeding was controlled in 29 of 30 patients. Of the 96 patients who underwent successful TIPS creation, 26 have died and 22 have undergone liver transplantation; the remaining 48 patients have survived an average of 7.6 months. Variceal bleeding recurred in 10 patients. Fifteen patients developed shunt stenosis (n = 6) or occlusion (n = 9). Patency was reestablished in eight of the nine occluded shunts. Seventeen patients developed new or worsened encephalopathy. The authors conclude that TIPS creation is an effective and reliable means of lowering portal pressure and controlling variceal bleeding, particularly in patients with acute variceal bleeding unresponsive to sclerotherapy and patients with chronic variceal bleeding before liver transplantation.     

Heterotopic liver transplantation in rats: effect of intrahepatic islet isografts and split portal blood flow on liver integrity after auxiliary liver isotransplantation

BACKGROUND: Auxiliary heterotopic liver grafts atrophy in the absence of portal venous inflow; evidence suggests that an islet-derived hepatotrophic factor may exist in the portal drainage. Here we examine the effects of intrahepatic islet isografts in maintaining hepatocyte integrity in Wistar Furth rats with one of several types of arterialized auxiliary liver isografts. METHODS: In type 1 procedures the auxiliary liver was interposed into the recipient infrarenal vena cava and perfused through the graft portal vein with caval blood. In type 2 procedures the donor infrahepatic vena cava was anastomosed end-to-side to the recipient vena cava and the recipient portal vein was diverted to the graft portal vein. Both types of auxiliary grafts were arterialized; bile duct drainage was through the duodenum. Syngeneic islets were isolated and embolized into the portal veins of one half of the donor type 1 or native type 2 livers (1500 to 1700 islets). Finally, we performed six type 3 procedures in which a type 2 procedure was performed except that the portal blood flow was split so that the portal vein receiving the splenic, gastric, pancreatic, and duodenal drainage supplied the native liver and that the common mesenteric vein supplied the auxiliary graft with equivalent portal blood flow. Atrophy in heterotopic and native livers were compared for the three models after 3 months. RESULTS: Intrahepatic islets in type 1 auxiliary liver isografts without portal venous inflow did not prevent graft atrophy. Conversely, native livers deprived of portal venous inflow in our type 2 procedures, regardless of the presence of intrahepatic islet isografts, atrophied relative to auxiliary liver grafts in which portal venous inflow was provided by diverting the recipient's portal vein to the graft. In type 3 recipients atrophy was greater in the native livers than in the grafts. CONCLUSIONS: The results of our study suggest that islet-derived factors are not sufficient to prevent hepatocellular atrophy in auxiliary rat liver transplantation models and that a potent hepatotrophic factor may exist in the venous drainage of the bowel distal to the duodenum.     

Mechanical thrombectomy in acute and subacute thrombosis with use of the Amplatz device: arterial and venous applications

PURPOSE: To perform a feasibility study of the Amplatz Thrombectomy Device (ATD) in a variety of vascular territories with acute or subacute thrombosis. MATERIALS AND METHODS: Thirteen patients (mean age, 44.6 years) with multiple risk factors who had acute/subacute thrombosis of the inferior vena cava (IVC) and iliac veins (n = 3), superior vena cava (SVC) and/or subclavian veins (n = 3), lower extremity polytetrafluoroethylene (PTFE) graft (n = 2), iliac artery (n = 2), portal vein and transjugular intrahepatic portosystemic shunt (TIPS) (n = 2), and an IVC to pulmonary artery Fontan conduit (n = 1), were treated by means of mechanical thrombectomy with use of the ATD. Thrombolysis failed to recanalize the vessels when used before thrombectomy for 12-34 hours in three patients, and was contraindicated in three other patients. Thrombolysis was used as a complement to the ATD procedure in five patients. RESULTS: Technical success was achieved in 11 patients, and procedure success was achieved in 10 patients. Failure was observed in the remaining three patients. One patient with a PTFE graft was successfully declotted but thrombosis occurred 2 weeks later, requiring surgery. The other patient with a PTFE graft did not improve and needed surgery to declot and treat the distal anastomosis and distal circulation. The two patients with an occluded iliac artery underwent successful declotting but rethrombosis occurred in one shortly after the procedure requiring thrombolytic therapy. One patient with TIPS thrombosis improved and another patient with a thrombosed portal vein did not improve after thrombectomy. CONCLUSION: The ATD is useful for recanalization of acute/subacute clotted native vessels and grafts. The application of the device is broad, and although declotting can be achieved in most cases, long-term success may be limited by anatomical and technical problems of the grafts and multifactorial clinical problems of severely sick patients, as was the case in the series. The use of additional thrombolytic therapy may be necessary in a number of patients.     

Budd-Chiari syndrome: a common complication of Beh?et's disease

OBJECTIVE: The Budd-Chiari syndrome is characterized by venous outflow obstruction of the liver, usually occurring as a consequence of thrombosis of the hepatic veins. Vasculitis is a major component of Beh?et's syndrome. The aim of this study was to determine the incidence of hepatic vein thrombosis in patients with Beh?et's disease and to estimate the effect of this entity upon the clinical features and course of Beh?et's syndrome. METHODS: During an 8-yr period from 1985 to 1994, from a total of 493 patients with Beh?et's disease seen at Hacettepe University Hospital, the incidence and effect of hepatic vein thrombosis on the clinical course of Beh?et's syndrome was investigated. The hepatic vein thrombosis in each case was documented by hepatic venography and confirmed by digital subtraction angiography, computed tomography, ultrasonography, and liver biopsy. Coagulation parameters including protein C, protein S, and anti-thrombin III levels were easured in each case. The survival of cases with Beh?et's syndrome complicated by Budd-Chiari syndrome and the effect of the Budd-Chiari syndrome on the survival of individuals with Beh?et's syndrome were determined using the Kaplan-Meier technique. RESULTS: Of the 493 cases of Beh?et's syndrome, 53 (10.8%) were found to have one or more large vessel thrombosis. Of these 53 patients, 14 (26.4%) had hepatic vein thrombosis. Of these 14 patients, 8 had an additional inferior vena cava thrombosis and 4 had portal vein as well as total inferior vena cava thrombosis. Only two patients with isolated hepatic vein thrombosis were identified. These two patients and two additional patients with hepatic vein thrombosis plus thrombosis of the hepatic portion of the inferior vena cava are currently alive. Of the 10 patients with total inferior vena cava and hepatic vein thrombosis (4 also had portal vein thrombosis), all 10 died with a mean survival of 10.3 months. During the same time period, 37 patients obtained from a total of 1494 patients with clinical evidence of either portal hypertension, hepatic venous outflow obstruction or inferior vena caval obstruction without Beh?et's syndrome were found to have a Budd-Chiari syndrome. Of these 37 patients, 19 (51%) had an identifiable underlying disorder responsible for their hepatic vein thrombosis. CONCLUSION: Based upon this experience, it appears as if Budd-Chiari syndrome is a relatively frequent complication of Beh?et's disease. When individuals with Beh?et's syndrome have BCS, concurrent thrombosis of the portal vein and inferior vena cava are often found, if the patency of these vessels is assessed. The clinical course of patients with Beh?et's syndrome complicated by Budd-Chiari syndrome is poor. The extent of the vascular thrombosis within the inferior vena cava rather than the presence of the hepatic vein thrombosis per se is the major determinant of survival.     

Nodular regenerative hyperplasia of the liver in hematologic disorders: a possible response to obliterative portal venopathy. A morphometric study of nine cases with an hypothesis on the pathogenesis

Nodular regenerative hyperplasia was found in nine patients who had hematological disease including polycythemia vera, agnogenic myeloid metaplasia, primary thrombocythemia, rheumatoid arthritis with thrombocytosis, multiple myeloma, and erythrocytosis associated with polycystic renal disease. Portal hypertension was suspected in three and features of hypersplenism were present in four. 2. Nodular regenerative hyperplasia occurred in livers which had widespread obliteration of portal vein radicals (obliterative portal venopathy). Morphometric analysis indicated that the portal vein lesions were predominately located in veins up to 0.2 mm in diameter and were significantly more frequent than similar lesions occurring in elderly persons. 3. The following pathogenesis of nodular regenerative hyperplasia is proposed: Thrombi, perhaps largely composed of platelet aggregates formed in the portal venous circulation or spleen, embolize to the liver and results in obliterative vascular lesions. Atrophy and regenerative nodule formation occur in response to the interruption of the portal blood supply.     

Identification of dipeptidyl peptidase IV as the antigen of a monoclonal anti-prostasome antibody

Two patients with previous distal splenorenal shunts (DSRSs) performed 6 years earlier underwent liver transplantation (LT). A preoperative selective mesenteric artery angiogram showed collateral veins draining mesenteric venous flow into the shunt. Intraoperative flow measurements were performed to assess the steal of portal venous flow by the shunt and determine the need for shunt occlusion. Portal vein, hepatic artery, and shunt flows were measured by ultrasound transit-time flow probes in the native liver and after graft implantation with and without temporary shunt occlusion. Hemodynamic studies showed that long-standing DSRSs are high-flow shunts that steal portal flow. After graft implantation, DSRS flows remained high. Occlusion of the shunts produced an increase in portal vein flow at an amount similar to those of splenorenal shunt. Thus, the flow measurements showed persistent steal by the shunts after graft implantation and, therefore, the DSRSs were occluded but splenectomy was not performed. We conclude that the decision to occlude a DSRS should be based on the demonstration of steal of portal flow by the shunt and reversibility once the shunt is occluded. Splenectomy is not required when the DSRS is occluded.