Incidence Of Portal Vein Thrombosis Research Articles

Effects of surgical procedures on the occurrence and development of postoperative portal vein thrombosis in patients with cirrhosis complicated by portal hypertension

ObjectiveWe have compared the influences of three surgical strategies on the occurrence and development of portal vein thrombosis (PVT) in patients with liver cirrhosis complicated by portal hypertension (PHT) in this study. MethodsTotal 116 patients who respectively underwent pericardial devascularization (PCDV) with splenectomy (PDS group: n = 50), selective PCDV (SPD group: n = 28) and splenorenal shunt (SRS) combined with PCDV (combined group: n = 38) were investigated in this study. The incidence of PVT before and after operation was monitored. The incidence of Grade II-IV PVT was used to assess the severity of PVT. The liver function was assessed according to the Child-Pugh classification. ResultsThe incidence and severity of PVT and live function were similar among the three groups before operation (P > 0.05). The incidence of PVT was significantly increased after surgery in each group (P < 0.001), but recovered to the baseline level at six months in combined group (P = 0.629). Besides, the severity of PVT was significantly aggravated in PDS (P < 0.001) and SPD (P = 0.026) groups after operation, but not in combined group (P = 0.525). Patients in combined group showed significantly lower incidence and severity of PVT than those in the other two groups at each follow-up time point (P < 0.05). In addition, the liver function in the combined group was significantly improved compared with the other two groups. ConclusionsSRS combined with PCDV is superior to PCDV with splenectomy and selective PCDV for PHT in liver cirrhotic patients in inhibiting the occurrence and development of postoperative PVT and improving liver function.

Causes and consequences of portal vein thrombosis in 1,243 patients with cirrhosis: results of a longitudinal study.

In cirrhosis, portal vein thrombosis (PVT) could be a cause or a consequence of the progression of liver disease. We analyzed data from a prospective trial of ultrasound screening for hepatocellular carcinoma in order to identify risk factors for and the impact of PVT in patients with cirrhosis. In all, 1,243 adults with cirrhosis without PVT were enrolled from 43 liver units in France and Belgium between June 2000 and March 2006. The mean follow-up was 47 months. Doppler ultrasonography was used to check the portal vein. Progression of liver disease was defined by the development of: ascites, hepatic encephalopathy, variceal bleeding, prothrombin <45%, serum bilirubin >45 μmol/L, albumin <28 g/L, and/or creatinine >115 μmol/L. G20210A prothrombin and factor V gene mutations were assessed in sera stored at three large centers. The 5-year cumulative incidence of PVT was 10.7%. PVT was mostly partial and varied over time. The development of PVT was independently associated with baseline esophageal varices (P = 0.01) and prothrombin time (P = 0.002), but not with disease progression before PVT, or prothrombotic mutations. Disease progression was independently associated with baseline age (hazard ratio [HR] 1.55; 95% confidence interval [CI]: 1.11-2.17), body mass index (HR 1.40; 95% CI: 1.01-1.95), prothrombin time (HR 0.79; 95% CI: 0.70-0.90), serum albumin (HR 0.97; 95% CI: 0.94-0.99), and esophageal varices (HR 1.70; 95% CI: 1.21-2.38) but not with the prior development of PVT (HR 1.32; 95% CI: 0.68-2.65). In patients with cirrhosis, the development of PVT is associated with the severity of liver disease at baseline, but does not follow a recent progression of liver disease. There is no evidence that the development of PVT is responsible for further progression of liver disease.

Central neuraxial blockade for splenectomy in myeloproliferative disease: A word of caution

We describe management of portal vein thrombosis (PVT) in a patient with myeloproliferative disease after splenectomy. This case posed a unique therapeutic challenge in maintaining a fine balance between life-saving thrombolysis and the risk of neuraxial complications due to bleeding. The incidence of PVT after splenectomy in patients with myeloproliferative disorders is high (40%). Anaesthesiologists should be aware of this and avoid central neuraxial blockade in such cases. If post-operative emergency thrombolysis is required in a patient having an epidural catheter in situ, it should be done under close monitoring, weighing the risks and benefits. Fibrinogen levels should be monitored to evaluate the presence of residual thrombolytic effects and to time the catheter removal.

Analysis of factors associated with portal vein thrombosis in pediatric living donor liver transplant recipients.

The technique of vascular reconstruction plays a major role in the outcome of living donor liver transplantation (LDLT). An increased use of vascular grafts (VGs) as replacements for sclerotic portal veins has become a standard technique for our group. The aim of this study was to analyze the factors associated with portal vein thrombosis (PVT) in pediatric LDLT. We performed a retrospective analysis of 486 primary pediatric LDLT procedures performed between October 1995 and May 2013. VGs used for portal reconstruction included living donor inferior mesenteric veins, living donor ovarian veins, recipient internal jugular veins, deceased donor iliac arteries, and deceased donor iliac veins. Thirty-four patients (7.0%) developed PVT. The incidence of PVT dropped from 10.1% to 2%; the overall utilization of VGs increased from 3.5% to 37.1%. In a multivariate analysis, only the use of VGs remained an independent risk factor for the occurrence of PVT (hazard ratio = 7.2, 95% confidence interval = 2.8-18.7, P < 0.001). There was no difference in survival rates between patients with PVT and patients without PVT. No patient with PVT underwent retransplantation. In conclusion, the use of VGs was independently associated with the development of PVT. Over time, there was a reduction in the incidence of early PVT in this cohort, and there was a trend toward a reduction in total PVT. The occurrence of isolated PVT in this study was not associated with decreased patient or graft survival.

Portal vein thrombosis in patients with cirrhosis

Portal vein thrombosis (PVT) can be seen in patients with cirrhosis in association with hepatocellular carcinoma or following splenectomy for the treatment of hypersplenism. PVT can also occur spontaneously in patients with cirrhosis; it is this group that is the subject of this discussion. Incidence, Etiology, and Clinical Consequences PVT may be complete, partial, or associated with cavernous transformation of the portal vein (Fig. 1). The thrombi can be in any part of the portal venous system but are seen most commonly in the main portal vein or its intrahepatic branches. The prevalence of PVT varies widely in patients with cirrhosis, ranging from 5% to 26% in different series of patients who were either evaluated for or underwent liver transplantation. Most of these patients had partial PVT, and many were diagnosed at the time of surgery. 1 In a series of 701 hospitalized patients with cirrhosis undergoing Doppler ultrasound, 11.2% were found to have PVT. In 43% of those with PVT, there were no symptoms, whereas 39% had portal hypertensive bleeding and 18% had abdominal pain, usually associated with intestinal ischemia. 2 There were no clear clinical differences between those patients with cirrhosis who did and those who did not have PVT. In one prospective trial of patients with Child class B/C cirrhosis, 6 of 36 patients (16.6%) developed PVT during a 48week period of observation, 3 suggesting many patients with advanced cirrhosis are at significant risk for developing this complication. PVT may progress or resolve spontaneously. In one series of 42 patients, partial PVT progressed in 48%, improved in 45%, and remained the same in 7%. 4 The pathogenesis of PVT in cirrhosis is not clear. Factors thought to play a role include reduced flow in the portal vein as a consequence of increased resistance in the liver, inherited defects in coagulation (such as factor V Leiden or prothrombin mutations), and an imbalance between proand anticoagulant factors that develop in the patient with cirrhosis due to impaired hepatic function. 1,2 Individuals with PVT and abdominal pain frequently have mesenteric ischemia. The impact of PVT of insidious onset on disease progression and complications of cirrhosis is unclear. Patients with PVT tend to have smaller livers and more severe portal hypertension than those without PVT, but it is unclear whether this difference is a consequence of the PVT. Perhaps the most compelling argument for the negative impact of PVT on disease progression is the recent controlled trial in which 70 outpatients with Child class B/ C cirrhosis and no PVT were randomized to enoxaparin (4000 IU/day subcutaneously) or no treatment for 48 weeks. During active treatment, none of the patients receiving enoxaparin developed PVT compared with 17% of controls. In the treated group, the probability of decompensation was significantly reduced, and survival was improved. 3 The most common cause of decompensation was the development of ascites, which was significantly less in treated patients. Seventy percent of those who developed PVT in the control group developed ascites. The incidence of encephalopathy, sepsis, or variceal bleeding did not differ between the two groups. Which factor accounted for the beneficial effects of enoxaparin is unclear. The use of the drug clearly decreased the incidence of PVT, but its use was also associated with significantly fewer bacterial infections. The data suggest that PVT and perhaps microvascular thrombosis play a role in disease progression in patients with cirrhosis and that their prothrombotic state may require some type of treatment. Further studies are required before one can generally recommend anticoagulants in patients with cirrhosis as a preventative therapy. Limited data suggest the presence of asymptomatic PVT in patients with cirrhosis does not affect overall survival, although in some patients it may add to the technical difficulty of liver

Association of Abnormal Plasma Bilirubin With Aggressive Hepatocellular Carcinoma Phenotype

Cirrhosis-related abnormal liver function is associated with predisposition to hepatocellular carcinoma (HCC). It features in several HCC classification systems and is an HCC prognostic factor. The aim of the present study was to examine the phenotypic tumor differences in HCC patients with normal or abnormal plasma bilirubin levels. A 2,416-patient HCC cohort was studied and dichotomized into normal and abnormal plasma bilirubin groups. Their HCC characteristics were compared for tumor aggressiveness features, namely, blood alpha-fetoprotein (AFP) levels, tumor size, presence of portal vein thrombosis (PVT) and tumor multifocality. In the total cohort, elevated bilirubin levels were associated with higher AFP levels, increased PVT and multifocality, and lower survival, despite similar tumor sizes. When different tumor size terciles were compared, similar results were found, even among patients with small tumors. A multiple logistic regression model for PVT or tumor multifocality showed increased odds ratios for elevated levels of gamma glutamyl transpeptidase (GGTP), bilirubin, and AFP and for larger tumor sizes. We conclude that HCC patients with abnormal bilirubin levels had worse prognosis than patients with normal bilirubin. They also had an increased incidence of PVT and tumor multifocality, and higher AFP levels, in patients with both small and larger tumors. The results show an association between bilirubin levels and indices of HCC aggressiveness.

Clinical Outcome of Autologous Hematopoietic Stem Cell Infusion via Hepatic Artery or Portal Vein in Patients with End-stage Liver Diseases

To investigate the efficacy of hematopoietic stem cell (HSC) transplantation via the hepatic artery vs. the portal vein for end-stage liver disease (ESLD). Patients with hepatic decompensation were prospectively recruited from September 2010 to September 2012 to receive HSC transplantation via the hepatic artery or the portal vein. Liver function was examined at 3, 6, and 12 months after transplantation. Liver biopsy Results were analyzed using the Knodell score. Eighty patients (58 males and 22 females) were enrolled in the study. The Child-Pugh score was grade B in 69 cases, and grade C in the remaining 11 cases. HSC transplantation was performed via the portal vein in 36 patients and via the hepatic artery in 44 patients. ALT levels decreased while serum albumin levels increased significantly in both groups at 6 and 12 months after HSC transplantation (P<0.05 compared with pre-transplantation levels). Total bilirubin levels decreased significantly in both groups at 3, 6, and 12 months after HSC transplantation (P<0.05 compared with pre-transplantation levels). Additionally, prothrombin time decreased in both groups at 12 months after HSC transplantation (P<0.05 compared with pre-transplantation level). There were no significant differences in ALT, total bilirubin and prothrombin time between the two groups either before or after transplantation. Moreover, Knodell score decreased significantly at 6 and 12 months. Histological examination showed that liver cell edema, degeneration, necrosis, and inflammation were significantly relieved at 3, 6, and 12 months after transplantation. The incidence of portal vein thrombosis, upper gastrointestinal bleeding, and hepatic encephalopathy were 1.25%, 3.75%, and 2.5% respectively. The one-year survival rate was 100%. Autologous HSC transplantation improves liver function and histology in ESLD patients. The administration route of HSC has no significant impact on the efficacy of transplantation.

Portal vein thrombosis after laparoscopic splenectomy during childhood

Portal vein thrombosis (PVT) is a rare but potentially life-threatening complication of laparoscopic splenectomy (LS) and can lead to bowel ischemia or portal hypertension. In childhood, this complication is reported in 5-10% of the cases whereas it can be up to 50% in adult population. Our aim was to evaluate PVT incidence after LS and associated risks factors. A retrospective chart review identified 37 children who underwent elective LS from 2005 to 2013. The main indications were spherocytosis or sickle cell disease. Median age and weight were respectively 7.4years and 25.1kg. Thromboembolic prophylaxis was not routinely given. Duration of surgery was 129min and hospital length of stay 4days. Doppler ultrasound scan (USS) was performed post-operatively in 26 cases. Post-operative course was uneventful in all but one patient. She was a 17year-old girl previously operated for an ovarian tumor with hyperandrogenism. Histopathology revealed a splenic lymphoma. At day 4, a systematic USS showed a PVT extending in the portal branches. Therapeutic low molecular weight heparin was used and then transitioned to fluindione for 3months. Follow-up USS performed at 1 and 4months demonstrated complete resolution of the PVT. PVT after pediatric LS is a rare event in our series. Clinician should be cautious in oncologic cases and if very large spleen or if thrombocythemia >650.10(9)/L is present. If detected early, PVT can be treated efficiently. We therefore recommend a systematic USS during the first postoperative week.

Incidence and Natural Course of Portal Vein Thrombosis in Cirrhosis

To the Editor: We have read with interest the recent article by Maruyama et al. (1) on the incidence and natural course of portal vein thrombosis (PVT) in viral cirrhosis. Despite the interest of the study being the third to report incidence of PVT in cirrhotics, it presents several inconsistencies and drawbacks in design and data analysis. First, reported incidence of PVT included six patients with only splenic vein thrombosis, thus being 36/150, 24%. Moreover, the occurrence of PVT is strangely not equally distributed during the follow-up, with a 12.8% incidence in the first years and about 2% per year during the follow-up. This is in contrast with the current knowledge of a greater prevalence of PVT in patients with more advanced liver disease. Second, patients were recruited for the study during 11 years, and it is stated that Doppler ultrasonography (US) were performed at least every 6–12 months. However, surprisingly, the median number of US per patient was only 4.4, leading to a period of time covered of a maximum of 4 years. Third, correlation of flows at US Doppler at inclusion with occurrence of PVT after years from the initial evaluation is unlikely due to changing hemodynamics in cirrhotic patients overtime. Fourth, it is difficult to understand why patients were tested for prothrombotic disorders at the beginning of the enrollment in the study (in year 1998 the potential role of these alterations in cirrhosis was still not defined). Fifth, US is characterized by diagnostic limitations, especially in extra-hepatic segments of PV or other splanchnic veins. Sixth, worsening of PVT has been described in only 1/23 patients, data very different from previous studies that described progression of PVT in 48–75% of cases at 2 years (2,3). Finally, the way that data on PVT and survival was analyzed does not allow to conclude that PVT does not have an impact on survival. Kaplan–Meyer curve of survival is faulty because the number of patients plotted in the figure is 156 and not 150, and survival was considered from the enrollment in the study. Therefore, for example a patient developing PVT after 7 years of follow-up and dying 1 month after it is considered as being alive for 7 years and 1 month. In conclusion, we believe that the interpretation of the described data is difficult and no recommendations can be drawn according to the results of the present manuscript.

Implementation of laparoscopic splenectomy in children and the incidence of portal vein thrombosis diagnosed by ultrasonography

BackgroundThe aim of this study is to evaluate if symptomatic or asymptomatic PVT, as diagnosed with ultrasonography (US), occurs more often in children after the introduction and implementation of LS compared to open splenectomy. MethodsA retrospective cohort of 76 splenectomized patients for benign hematological disease were analyzed, 24 after open splenectomy (OS) and 52 after LS. ResultsIn six of the OS and 40 after LS a postoperative US was obtained. In two patients after LS, a PVT was seen on US. Both patients were symptomatic and also underwent a laparoscopic cholecystectomy. The length of stay in the hospital was significantly shorter for LS (median 4.5days, range 2–12) compared to OS (median 7days, range 5–12), (P=.00). Median operation time of OS was 65min (range 35–130min) and of LS 170min (range 85–275min) (P=.00). There was no difference in postoperative complications. ConclusionThe risk of developing a PVT after laparoscopic splenectomy seems low, and thus LS is not contraindicated in patients with benign hematological disease. When combining LS and laparoscopic cholecystectomy, prophylactic heparin might be considered.

Risk factors and clinical characteristics of portal vein thrombosis after splenectomy in patients with liver cirrhosis

Portal vein thrombosis (PVT) is a potential lethal complication and may have negative influence on the prognosis after splenectomy in patients with liver cirrhosis. Prevention and timely detection of PVT are quite significant. There is a lack of knowledge about the clinical features and risk factors of PVT. Our study aimed to investigate the risk factors and clinical characteristics of PVT in order to figure out the high-risk individuals. We collected the clinical data of 472 consecutive patients with non-neoplastic liver cirrhosis who had undergone splenectomy from January 2008 to December 2010 in our institution. Clinical and surgical characteristics of patients who developed PVT postoperatively and those who did not develop PVT were compared. Univariate and multivariate analyses of risk factors of PVT were performed. The mortality and rebleeding rate of the patients were also evaluated. Of the 472 patients, 52 were excluded from the study. PVT developed in 71 (71/420, 16.9%) patients. Multivariate analysis revealed that wider preoperative portal vein diameter, postoperative thrombocytosis, prolonged prothrombin time and periesophagogastric devascularization were significantly correlated with PVT development [odds ratio (OR): 5.701, 2.807, 1.850 and 2.090, respectively]. The incidence of PVT in patients who took antiplatelet drugs was not lower than that in those who did not. Follow-up showed that patients in the PVT group had a tendency towards reduced overall survival but it was not statistically significant. Gastrointestinal bleeding occurred more often in the PVT group than that in the non-PVT group (P=0.044). Wider preoperative portal vein diameter, postoperative thrombocytosis, prolonged prothrombin time and periesophagogastric devascularization are independent risk factors of PVT. PVT is related with higher risk of postoperative gastrointestinal hemorrhage but has no significant impact on the overall survival.

A Review of Autologous Islet Transplantation.

Autologous islet transplantation after total or semitotal pancreatectomy aims to preserve insulin secretory function and prevent the onset of diabetes. The major indication for pancreatectomy is chronic pancreatitis with severe abdominal pain, a benign pancreatic tumor, and trauma. The metabolic outcome of autologous islet transplantation is better than that of allogeneic transplantation and depends on the number of transplanted islets. Achieving islet isolation from a fibrous or damaged pancreas is one of the biggest challenges of autologous islet transplantation; a major complication is portal vein thrombosis after crude islet infusion. However, the incidence of portal vein thrombosis has decreased as islet preparation techniques have improved over time.

Hepatic Hematoma After Islet Cell Transplantation

Hepatic Hematoma After Islet Cell Transplantation

De novo Portal Vein Thrombosis in Virus-Related Cirrhosis: Predictive Factors and Long-Term Outcomes

The objective of this study is to investigate predictive factors and long-term outcomes of de novo portal vein thrombosis (PVT) in cirrhosis. The incidence and factors predictive of PVT (diagnosed by Doppler ultrasound) and prognosis were examined in 150 patients with virus-related cirrhosis but without PVT at baseline. PVT developed in 28% of patients (42/150), with cumulative incidence of 12.8%, 20%, and 38.7% at 1, 5, and 8-10 years, respectively. The baseline flow volume in the largest collateral vessel was an independent risk factor for thrombosis (hazard ratio, 3.922; 95% confidence intervals, 3.697-4.415; P<0.0001). The cumulative incidence of PVT at 1, 5, and 10 years was significantly higher in patients with the largest collateral vessel velocity >10 cm/s (19.1%, 27%, and 78.4%, respectively) compared with those with velocity ≤10 cm/s (8.6%, 16.3%, and 24.7%, respectively, P=0.0303), and higher in patients with volume >400 ml/min (27.4%, 36.5%, and 74.6%, respectively) compared with those with volume ≤400 ml/min (10.6%, 16.2%, and 28.8%, respectively, P=0.0075). The natural course of thrombosis was improvement in 47.6%, unchanged in 45.2%, and worsened in 7.2%. The diameter and flow volume in the largest collateral vessel at the time of thrombus detection were significantly smaller in the improved patients than the others. The cumulative survival rate was similar between the thrombosis group and non-thrombosis group. Development of collateral vessels was a significant predictive factor for the occurrence of PVT in virus-induced cirrhosis. Spontaneous resolution or unchanged appearance was the most common outcome of thrombosis, which had little influence on prognosis.

Portal Vein Thrombosis: Should Anticoagulation Be Used?

Portal vein thrombosis (PVT) can contribute to significant morbidity and mortality; in patients with cirrhosis, this can make transplant more technically challenging. Additionally, the clot may extend further into the mesenteric and splenic veins, and disturbance of the hepatic blood flow may lead to faster progression of the cirrhosis. Development of PVT is associated with local risk factors, and many patients have associated systemic prothrombotic factors. Anticoagulation in noncirrhotic patients should be initiated at diagnosis, using low-molecular-weight heparin overlapping with vitamin K antagonists. Cirrhotic patients with PVT should be screened for varices and then anticoagulated with low-molecular-weight heparin for at least a 6-month period. All patients should be assessed for triggering factors and tumors, as well as systemic prothrombotic factors. Newer evidence suggests that prophylactic anticoagulation in patients with cirrhosis may have a role in clinical management with decreased incidence of PVT and improved survival; further study is needed.

Portal Vein Thrombosis in Splenectomized Cirrhotic Patient: A Case Report

Purpose: Portal vein thrombosis (PVT) and systemic venous thromboembolism are significantly increased in cirrhotic patients even without hepatocellular carcinoma. The risk of developing such complications is usually associated with advanced cirrhosis. When cirrhosis is mild and compensated, other possible causes of PVT should also be considered. We present a case of PVT in chronic hepatitis C infection with focal cirrhosis and portal hypertension with history of splenectomy. A 47-year-old Caucasian woman presented with chronic hepatitis C, genotype 1. She was treated with pegylated interferon and ribavirin for 48 weeks, but developed viral relapse. She had splenectomy when she was young for unclear reason. Her findings on pathologic examination of the liver biopsy were consistent with focal cirrhosis in mild to moderate chronic hepatitis; the Knodell's histologic activity index (HAI) score was 7-9/22. Her MELD score was 6. An annual esophagogastroduodenoscopy revealed non-bleeding grade II esophageal varices and cardial gastric varices. A computerized tomography scan revealed the sub-occlusive thrombus at the bifurcation of the main portal vein. The workup for hypercoagulable state showed low protein C, protein S, and antithrombin III levels. The inferior vena caval venogram showed thrombotic occlusion in left, right, and common portal vein with a portal systemic pressure gradient of 11 mmHg. Collateralization was present at portal hiatus. The ultrasound guided thrombus removal with interventional thrombolysis was attempted in order to avoid systemic anticoagulation therapy. However, the guidewire failed to pass through the obstructed portal vein. She eventually was evaluated for liver transplantation. This is a case that demonstrates the presence of PVT in a patient with mild compensated cirrhosis (based on both histological and clinical evaluation) without hepatocellular carcinoma. The incidence of PVT in well-compensated cirrhosis is reported between 0.6-16%. An increased frequency is reported in decompensated cirrhosis and in up to 35% of cirrhotic patients with hepatocellular carcinoma. The origin of PVT is multifactorial in most cirrhotic patients. Low serum protein C, protein S, and antithrombin III level secondary to decreased protein synthesis in cirrhosis can contribute to a prothrombotic state. Splenectomy is another possible cause of PVT in this case, since PVT after splenectomy occurs in 6-8%. However, the late onset of presentation makes it a less likely cause since most PVT occurs in days to weeks after splenectomy.

Covering the Cover

Covering the Cover

Hypercoagulability in End-Stage Liver Disease: Prevalence and Its Correlation With Severity of Liver Disease and Portal Vein Thrombosis

Contrary to well-recognized bleeding diathesis in chronic liver disease, thrombotic events can occur in these patients due to reduction or loss of synthesis of anticoagulant proteins. Forty-seven consecutive patients with end-stage liver disease (ESLD) were investigated for activity of protein C, protein S, antithrombin, and factor V Leiden mutation. Forty-two (89.4%) patients had low levels of at least 1 while 33 (70.2%) patients were deficient for all anticoagulant proteins studied. Forty-six (97.9%) patients were negative for factor V Leiden mutation. The deficiencies were more marked in hepatitis C virus-positive patients and patients with model for end-stage liver disease (MELD) score >15. Six (12.8%) patients had portal vein thrombosis (PVT), and all had diminished protein S activity. In conclusions, deficiency of anticoagulant proteins occur in early phase of chronic liver disease. The severity of deficiency is proportional to the severity of liver disease. Despite the high prevalence of hypercoagulability, the incidence of PVT is low. Further studies with larger cohort of patients are needed to support these conclusions and to study other associated factors.

Implications of portal vein thrombosis after splenectomy for patients with idiopathic portal hypertension

Idiopathic portal hypertension (IPH) is considered to be closely related to portal vein thrombosis (PVT). The aim of this study was to clarify the incidence, clinical characteristics, and outcomes of PVT in patients with IPH after splenectomy. We investigated the rates, clinical characteristics, and outcomes of PVT in 18 patients who underwent splenectomy for IPH, during a mean follow-up period of 152 ± 83 months. Seven of the 18 patients (39%) experienced gastrointestinal bleeding, which was from the varices in 4. Eight patients (44%) had PVT, and the mean interval until its detection after splenectomy was 22 ± 41 months. The cumulative gastrointestinal bleeding rates 5, 10, and 15 years after surgery were 24%, 31%, and 41%, respectively. The cumulative survival rates 5, 10, and 15 years after surgery were 94%, 74%, and 65%, respectively. There were no significant differences in the cumulative gastrointestinal bleeding and survival rates between patients with and those without PVT. Despite the high incidence of PVT in IPH patients postsplenectomy, it may not be related to their gastrointestinal bleeding or prognosis.

Outcomes of Liver Transplantation in Candidates With Portal Vein Thrombosis

Objective The objective of the present study was to analyze the incidence of portal vein thrombosis (PVT), comparing morbidity and mortality rates among those affected with and those free of this complication. In the PVT group, we also analyzed mortality related to partial (PPVT) and total (TPVT) thrombosis. Methods We undertook a retrospective study of orthotopic liver transplantations from deceased donors in 617 recipients from January 1991 until October 2008. Recipients were classified according to whether they had PVT. In all cases, we considered age, sex, Model for End-stage Liver Disease score, Child-Pugh score, indication for transplantation, type of thrombosis, surgical technique blood product transfusion, and survival rate. Results There were 48 patients with PVT (7.78%) among 670 transplantations in 617 recipients in our institution. Concerning the type of thrombosis, 28 (58.3%) were partial and 20 (41.7%) total with complete occlusion of the portal vein lumen. Conclusion PVT in liver transplant candidates is a rare event (7.8%) that entails greater difficulty in the procedure, expressed as a longer operative time, greater consumption of blood products, and complex surgical techniques. The prognosis for these patients depends on the type of thrombosis: patients with TPVT showed a higher mortality, whereas those with PPVT had survival rates comparable to those of candidates with a permeable portal vein.