Predictive model for non-malignant portal vein thrombosis associated with cirrhosis based on inflammatory biomarkers

BACKGROUND Portal vein thrombosis(PVT),a complication of liver cirrhosis,is a major public health concern.PVT prediction is the most effective method for PVT diagnosis and treatment.AIM To develop and validate a nomogram and network calculator based on clinical indicators to predict PVT in patients with cirrhosis.METHODS Patients with cirrhosis hospitalized between January 2016 and December 2021 at the First Hospital of Lanzhou University were screened and 643 patients with cirrhosis who met the eligibility criteria were retrieved.Following a 1:1 propensity score matching 572 patients with cirrhosis were screened,and relevant clinical data were collected.PVT risk factors were identified using the least absolute shrinkage and selection operator(LASSO)and multivariate logistic regression analysis.Variance inflation factors and correlation matrix plots were used to analyze multicollinearity among the variables.A nomogram was constructed to predict the probability of PVT based on independent risk factors for PVT,and its predictive performance was verified using a receiver operating characteristic curve(ROC),calibration curves,and decision curve analysis(DCA).Finally,a network calculator was constructed based on the nomograms.RESULTS This study enrolled 286 cirrhosis patients with PVT and 286 without PVT.LASSO analysis revealed 13 variables as strongly associated with PVT occurrence.Multivariate logistic regression analysis revealed nine indicators as independent PVT risk factors,including etiology,ascites,gastroesophageal varices,platelet count,D-dimer,portal vein diameter,portal vein velocity,aspartate transaminase to neutrophil ratio index,and platelet-to-lymphocyte ratio.LASSO and correlation matrix plot results revealed no significant multicollinearity or correlation among the variables.A nomogram was constructed based on the screened independent risk factors.The nomogram had excellent predictive performance,with an area under the ROC curve of 0.821 and 0.829 in the training and testing groups,respectively.Calibration curves and DCA revealed its good clinical performance.Finally,the optimal cutoff value for the total nomogram score was 0.513.The sensitivity and specificity of the optimal cutoff values were 0.822 and 0.706,respectively.CONCLUSION A nomogram for predicting PVT occurrence was successfully developed and validated,and a network calculator was constructed.This can enable clinicians to rapidly and easily identify high PVT risk groups.

Predictors of portal vein thrombosis after splenectomy in patients with cirrhosis

BACKGROUND Portal vein thrombosis(PVT)is a commonthsn complication after splenectomy in patients with cirrhosis.However,the predictors of postoperative PVT are not known.AIM To investigate the predictors of PVT after splenectomy in patient with cirrhosis.METHODS A total of 45 patients with cirrhosis who underwent splenectomy were consecutively enrolled from January 2017 to December 2018.The incidence of PVT at 1 months,3 months,and 12 months after splenectomy in patients with cirrhosis was observed.The hematological indicators,biochemical and coagulation parameters,and imaging features were recorded at baseline and at each observation point.The univariable,multivariable,receiver operating characteristic curve and timedependent curve analyses were performed.RESULTS The cumulative incidence of PVT was 40.0%,46.6%,and 48.9%at 1 months,3 months,and 12 months after splenectomy.Multivariable analysis showed that portal vein diameter(PVD)≥14.5 mm and monthsdel end-stage liver disease(MELD)score>10 were independent predictors of PVT at 1 months,3 months,and 12 months after splenectomy(P<0.05).Time-dependent curve showed that the cumulative incidence of PVT was significantly different between patients with MELD score≤10 and>10(P<0.05).In addition,the cumulative incidence of PVT in the PVD≥14.5 mm group was significantly higher than that in the PVD<14.5 mm group(P<0.05).CONCLUSION Wider PVD and MELD score>10 were independent predictors of PVT at 1 months,3 months,and 12 months after splenectomy in patient with cirrhosis.

Clinical outcomes of transcatheter selective superior mesenteric artery urokinase infusion therapy vs transjugular intrahepatic portosystemic shunt in patients with cirrhosis and acute portal vein thrombosis

AIM To compare the outcomes of transcatheter superior mesenteric artery(SMA) urokinase infusion and transjugular intrahepatic portosystemic shunt(TIPS) for acute portal vein thrombosis(PVT) in cirrhosis.METHODS From January 2013 to December 2014, patients with liver cirrhosis and acute symptomatic PVT who met the inclusion criteria were randomly assigned to either an SMA group or a TIPS group. The two groups accepted transcatheter selective SMA urokinase infusion therapyand TIPS, respectively. The total follow-up time was24 mo. The primary outcome measure was the change in portal vein patency status which was evaluated by angio-computed tomography or Doppler ultrasound.Secondary outcomes were rebleeding and hepatic encephalopathy.RESULTS A total of 40 patients were enrolled, with 20 assigned to the SMA group and 20 to the TIPS group. The symptoms of all patients in the two groups improved within 48 h. PVT was improved in 17(85%) patients in the SMA group and 14(70%) patients in the TIPS group. The main portal vein(MPV) thrombosis was significantly reduced in both groups(P < 0.001), and there was no significant difference between them(P= 0.304). In the SMA group, superior mesenteric vein(SMV) thrombosis and splenic vein(SV) thrombosis were significantly reduced(P = 0.048 and P = 0.02),which did not occur in the TIPS group. At 6-, 12-,and 24-mo follow-up, in the SMA group and the TIPS group, the cumulative rates free of the first episode of rebleeding were 80%, 65%, and 45% vs 90%, 80%,and 60%, respectively(P = 0.320); the cumulative rates free of the first episode of hepatic encephalopathy were 85%, 80%, and 65% vs 50%, 40%, and 35%,respectively(P = 0.022).CONCLUSION Transcatheter selective SMA urokinase infusion and TIPS are safe and effective for acute symptomatic PVT in cirrhosis.

Portal vein thrombosis: Etiology and clinical outcome of cirrhosis and malignancy-related non-cirrhotic, non-tumoral extrahepatic portal venous obstruction

The etiology and pathogenesis of portal vein thrombosis are unclear. Portal venous thrombosis presentation differs in cirrhotic and tumor-related versus non-cirrhotic and non-tumoral extrahepatic portal venous obstruction (EHPVO). Non-cirrhotic and non-tumoral EHPVO patients are young and present with well tolerated bleeding. Cirrhosis and tumor-related portal vein thrombosis patients are older and have a grim prognosis. Among the 118 patients with portal vein thrombosis, 15.3% had cirrhosis, 42.4% had liver malignancy (primary or metastatic), 6% had pancreatitis (acute or chronic), 5% had hypercoagulable state and 31.3% had idiopathy, 12% had hypercoagulable state in the EHPVO group.

Nonselective β-blockers may induce development of portal vein thrombosis in cirrhosis

Currently, nonselective &#x003b2;-blockers (NSBBs) are commonly used for the prevention of variceal bleeding in liver cirrhosis. The beneficial effects of NSBBs are primarily attributed to the reduction in cardiac output by blockade of &#x003b2;1 receptors and vasoconstriction of the splanchnic circulation by the blockade of &#x003b2;2 receptors. The prognostic value of occlusive portal vein thrombosis (PVT) in cirrhotic patients has been increasingly recognized. The most important risk factor for the development of PVT in liver cirrhosis is the decreased portal vein inflow velocity. Collectively, we propose that the use of NSBBs potentially increases the development of portal vein thrombosis by reducing portal vein inflow velocity. The hypothesis should be confirmed by prospective cohort studies, in which cirrhotic patients without prior PVT treated with and without NSBBs are enrolled, and the development of PVT during follow-up is compared between the two groups. Additionally, subgroup analyses should be performed according to the dosage of NSBBs and the reduction of portal inflow velocity after use of NSBBs.

Portal vein thrombosis in cirrhosis: Controversies and latest developments

Portal vein thrombosis(PVT) is encountered in livercirrhosis, particularly in advanced disease. It has been a feared complication of cirrhosis, attributed to significant worsening of liver disease, poorer clinical outcomes and potential inoperability at liver transplantation; also catastrophic events such as acute intestinal ischaemia. Optimal management of PVT has not yet been addressed in any consensus publication.We review current literature on PVT in cirrhosis; its prevalence, pathophysiology, diagnosis, impact on the natural history of cirrhosis and liver transplantation,and management. Studies were identified by a search strategy using MEDLINE and Google Scholar. The incidence of PVT increases with increasing severity of liver disease: less than 1% in well-compensated cirrhosis, 7.4%-16% in advanced cirrhosis. Prevalence in patients undergoing liver transplantation is 5%-16%.PVT frequently regresses instead of uniform thrombus progression. PVT is not associated with increased risk of mortality. Optimal management has not been addressed in any consensus publication. We propose areas for future research to address unresolved clinical questions.

Portal vein thrombosis in cirrhosis: Why a well-known complication is still matter of debate

Portal vein thrombosis(PVT)represents a well-known complication during the natural course of liver cirrhosis(LC),ranging from asymptomatic cases to lifethreating conditions related to portal hypertension and hepatic decompensation.Portal flow stasis,complex acquired hypercoagulable disorders and exogenous factors leading to endothelial dysfunction have emerged as key factors for PVT development.However,PVT occurrence remains unpredictable and many issues regarding its natural history,prognostic significance and treatment are still elusive.In particular although spontaneous resolution or disease stability occur in most cases of PVT,factors predisposing to disease progression or recurrence after spontaneous recanalization are not clarified as yet.Moreover,PVT impact on LC outcome is still debated,as PVT may represent itself a consequence of liver fibrosis and hepatic dysfunction progression.Anticoagulation and transjugular intrahepatic portosystemic shunt are considered safe and effective in this setting and are recommended in selected cases,even if the safer therapeutic option and the optimal therapy duration are still unknown.Nevertheless,their impact on mortality rates should be addressed more extensively.In this review we present the most debated questions regarding PVT,whose answers should come from prospective cohort studies and large sample-size randomized trials.

Portal vein thrombosis in liver cirrhosis

Portal vein thrombosis(PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to:(1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis;(2) describe the principal factors most frequently involved in PVT development; and(3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.

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

BACKGROUND: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.METHODS: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.RESULTS: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).CONCLUSIONS: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.

Therapeutic and clinical aspects of portal vein thrombosis in patients with cirrhosis

Portal vein thrombosis(PVT) is a frequent complication in cirrhosis, particularly in advanced stages of the disease. As for general venous thromboembolism, risk factors for PVT are slow blood flow, vessel wall damage and hypercoagulability, all features of advanced cirrhosis. Actually, the old dogma of a hemorrhagic tendency in cirrhosis has been challenged by new laboratory tools and the clinical evidence that venous thrombosis also occurs in cirrhosis. The impaired hepatic synthesis of both pro- and anticoagulants leads to a rebalanced hemostasis, more liable to be tipped towards thrombosis or even bleeding. Conventional anticoagulant drugs(low molecular weight heparin or vitamin K antagonists) may be used in cirrhosis patients with PVT, particularly in those eligible for liver transplantation, to prevent thrombosis progression thus permitting/facilitating liver transplant. However, several doubts exist on the level of anticoagulation achieved as estimated by coagulation tests, on the efficacy of treatment monitoring and on the correct timing for discontinuation in non-transplant candidates, while in transplant candidates there is expert consensus on continuing anticoagulation until transplantation. The recent introduction of direct acting oral anticoagulant drugs(DOACs) in other clinical settings generates much interest on their possible application in patients with cirrhosis and PVT. However, DOACs were not evaluated yet in patients with liver disease and cannot be recommended for the present time.

Predictive value of D-dimer for portal vein thrombosis after portal hypertension surgery in hepatitis B virus-related cirrhosis

AIM: To evaluate the predictive value of D-dimer as a predictive indicator of portal vein thrombosis (PVT) after portal hypertension surgery in hepatitis B virus-related cirrhosis. METHODS: A prospective study was carried out in 52 patients who had undergone surgery for portal hypertension in hepatitis B virus-related cirrhosis. Changes in perioperative dynamic D-dimer were observed. The sensitivity, specifi city, positive predictive values and negative predictive values of D-dimer were calculated, and ROC curves were analyzed. RESULTS: The D-dimer levels in the group developing postoperative PVT was signifi cantly higher than those in the group not developing PVT (P = 0.001), and the ROC semi-quantitative and qualitative analysis of D-dimer showed a moderate predictive value in PVT (semi- quantitative value Az = 0.794, P = 0.000; qualitative analysis: Az = 0.739, P = 0.001). CONCLUSION: Dynamic monitoring of D-dimer levels in patients with portal hypertension after surgery can help early diagnosis of PVT, as in cases where the D-dimer levels steadily increase and exceed 16 μg/mL, the possibility of PVT is very high.

Simultaneous portal vein thrombosis and splenic vein thrombosis in a COVID-19 patient:A case report and review of literature

BACKGROUND It is well-described that the coronavirus disease 2019(COVID-19)infection is associated with an increased risk of thrombotic complications.While there have been many cases of pulmonary emboli and deep vein thrombosis in these patients,reports of COVID-19 associated portal vein thrombosis(PVT)have been uncommon.We present a unique case of concomitant PVT and splenic artery thrombosis in a COVID-19 patient.CASE SUMMARY A 77-year-old-male with no history of liver disease presented with three days of left-sided abdominal pain.One week earlier,the patient was diagnosed with mildly symptomatic COVID-19 and was treated with nirmatrelvir/ritonavir.Physical exam revealed mild right and left lower quadrant tenderness,but was otherwise unremarkable.Significant laboratory findings included white blood cell count 12.5 K/μL,total bilirubin 1.6 mg/dL,aminoaspartate transferase 40 U/L,and alanine aminotransferase 61 U/L.Computed tomography of the abdomen and pelvis revealed acute PVT with thrombus extending from the distal portion of the main portal vein into the right and left branches.Also noted was a thrombus within the distal portion of the splenic artery with resulting splenic infarct.Hypercoagulable workup including prothrombin gene analysis,factor V Leiden,cardiolipin antibody,and JAK2 mutation were all negative.Anticoagulation with enoxaparin was initiated,and the patient’s pain improved.He was discharged on apixaban.CONCLUSION It is quite uncommon for PVT to present simultaneously with an arterial thrombotic occlusion,as in the case of our patient.Unusual thrombotic manifestations are classically linked to hypercoagulable states including malignancy and hereditary and autoimmune disorders.Viral infections such as Epstein-Barr virus,cytomegalovirus,viral hepatitis,and COVID-19 have all been found to increase the risk of splanchnic venous occlusions,including PVT.In our patient,prompt abdominal imaging led to early detection of thrombus,early treatment,and an excellent outcome.This case is unique in that it is the second known case within the literature of simultaneous PVT and splenic artery thrombosis in a COVID-19 patient.

Treatment of portal vein thrombosis in cirrhosis with anticoagulation-more than meets the eye?

Portal vein thrombosis(PVT)is a common complication in patients with advanced chronic liver disease(i.e.,cirrhosis).In contrast to other thrombotic diseases,PVT in patients with cirrhosis is frequently asymptomatic and discovered incidentally during routine imaging procedures.There is ongoing debate on whether all patients with PVT require treatment as it is unclear whether PVT is a relatively innocent bystander or whether PVT worsens disease progression(1).Treatment may be required in patients with>50%occlusion of the portal vein who are transplant candidates to avoid thrombosis progression that may hinder a future liver transplantation or cause progression of portal hypertension(2).Current treatment consists of therapeutic anticoagulation with vitamin K antagonists,heparins,or direct oral anticoagulants.Although anticoagulant therapy for cirrhotic PVT is relatively safe,the efficacy is modest,with meta-analyses demonstrating recanalization of the portal vein in~30-40%of patients without anticoagulation,and~60-70%with anticoagulation(3,4).

Application of ultrasonography-elastography score to suspect porto-sinusoidal vascular disease in patients with portal vein thrombosis

Background:Porto-sinusoidal vascular disease(PSVD)and portal vein thrombosis(PVT)are causes of portal hypertension characterized respectively by an intrahepatic and a pre-hepatic obstacle to the flow in the portal system.As PVT may be a consequence of PSVD,in PVT patients at presentation,a pre-existing PSVD should be suspected.In these patients the identification of an underlying PSVD would have relevant implication regarding follow-up and therapeutic management,but it could be challenging.In this setting ultrasonography may be valuable in differential diagnosis.The aim of the study was to use ultrasonography to identify parameters to discriminate between PSVD and“pure”PVT and then to suspect PVT secondary to a pre-existing PSVD.Methods:Fifty-three patients with histologically proven PSVD and forty-eight patients affected by chronic PVT were enrolled and submitted to abdominal ultrasonography with elastography by acoustic radiation force impulse(ARFI).Results:ARFI was higher and superior mesenteric vein(SMV)diameter was wider in PSVD patients than in PVT patients.Thus,a prognostic score was obtained as linear combinations of the two parameters with a good discrimination capacity between PSVD and PVT(the area under the curve=0.780;95%confidence interval:0.690-0.869).Conclusions:A score based on ARFI and SMV diameter may be useful to suspect an underlying PSVD in patients with PVT and to identify a subgroup of patients to be submitted to liver biopsy.

Current concepts in the management of non-cirrhotic non-malignant portal vein thrombosis

Non-cirrhotic non-malignant portal vein thrombosis(NCPVT)is an uncommon condition characterised by thrombosis of the portal vein,with or without extension into other mesenteric veins,in the absence of cirrhosis or intra-abdominal malignancy.Complications can include intestinal infarction,variceal bleeding and portal biliopathy.In this article,we address current concepts in the management of NCPVT including identification of risk factors,classification and treatment,and review the latest evidence on medical and interventional management options.

Portal vein thrombosis:Insight into physiopathology,diagnosis,and treatment

Portal vein thrombosis (PVT) is a relatively common complication in patients with liver cirrhosis, but might also occur in absence of an overt liver disease. Several causes, either local or systemic, might play an important role in PVT pathogenesis. Frequently, more than one risk factor could be identified; however, occasionally no single factor is discernable. Clinical examination, laboratory investigations, and imaging are helpful to provide a quick diagnosis, as prompt treatment might greatly affect a patient's outcome. In this review, we analyze the physiopathological mechanisms of PVT development, together with the hemodynamic and functional alterations related to this condition. Moreover, we describe the principal factors most frequently involved in PVT development and the recent knowledge concerning diagnostic and therapeutic procedures. Finally, we analyze the implications of PVT in the setting of liver transplantation and its possible influence on patients' future prognoses.

What we should know about portal vein thrombosis in cirrhotic patients:A changing perspective

Portal vein thrombosis(PVT) is one of the most common complications occurring during the natural course of liver cirrhosis.Even though PVT is often asymptomatic,the worsening of liver function,an unexpected episode of gastrointestinal bleeding or ascitic decompensation may be landmarks of PVT development.Beyond these clinical manifestations,it is debated whether PVT really has an impact on liver cirrhosis natural history or rather represents only one of its consequences.Probably PVT development should not only be considered as a matter of impaired blood flow or pro-coagulation tendency.On one hand,PVT seems a consequence of the worsening in portal vein outflow due to the increased hepatic resistance in cirrhotic livers.On the other hand,vascular microthrombosis secondary to necroinflammation may cause liver ischemia and infarction,with loss of hepatic tissue(parenchymal extinction) which is replaced by fibrotic tissue.Therefore,PVT might also be considered as the overt manifestation of the liver fibrosing process evolution and anticoagulant therapy may thus have microscopic indirect effects also on the progression of liver disease.At present,a connection between PVT development and the progression of liver fibrosis/cirrhosis has not yet been demonstrated.Nevertheless,it is not clear if PVT development may worsen cirrhotic patients' outcome by itself.Some authors tried to assess liver transplant benefit in PVT cirrhotic patients but data are contrasting.In this review,we will try to answer these questions,providing a critical analysis of data reported in literature.

Incidence and clinical presentation of portal vein thrombosis in cirrhotic patients

BACKGROUND: Portal vein thrombosis (PVT) is due to many risk factors, but its pathogenesis is still not clearly understood. To identify the risk factors for PVT, we analyzed the clinical characteristics and complications associated with PVT in cir-rhotic patients. METHODS: We studied patients with liver cirrhosis who were admitted to our unit from April 2009 to December 2014. The patients were divided into the PVT and non-PVT groups, and were compared by variables including gender, age, the etiology of cirrhosis, stage of cirrhosis, complications, imaging, and treatment. RESULTS: PVT was found in 45 (9.8%) of 461 cirrhotic pa-tients admitted to our hospital. Most patients (45.9%) had hepatitis B virus (HBV)-related cirrhosis, with a similar dis-tribution of etiologies between the groups. However, there was no positive relationship between PVT and etiologies of cirrhosis. Most patients (71.5%) were in the stage of hepatic decompensation. No statistically signiifcant differences were found in complications including esophageal varices, ascites, and hepatic encephalopathy between the groups. However, there was a signiifcant positive correlation between hepatocel-lular carcinoma (HCC) and PVT (P<0.01). In 30 patients with PVT, thrombosis occurred in the portal vein and/or portal branches, 37.8% were diagnosed on ultrasound. CONCLUSIONS: The incidence of PVT was 9.8%, mainly in patients with HBV-related cirrhosis. The development of PVT was associated with the severity of liver disease and HCC.

Portal vein thrombosis in cirrhotic patients-it is always the small pieces that make the big picture

Portal vein thrombosis(PVT) is a frequent and serious complication in patients with liver cirrhosis(LC). Recently, a new classification of PVT was proposed, although the functional component was not completed included. The status of liver disease(compensated/decompensated) should be added to this classification. Reduced portal flow velocity and the acquired hypercoagulable status associated with LC are the main risk factors for PVT development, although endothelial dysfunction may play an important role that needs to be further evaluated. The European Association for the Study of the Liver and the American Association for the Study of Liver Disease recommend that the anticoagulant treatment should be consider in cirrhotic patients with PVT. Low molecular weight heparin and vitamin K antagonists proved their efficacy and relatively safety in PVT treatment, although in addition to recanalization rates, more complex endpoints such as mortality and decompensation rate should be evaluated. The new oral anticoagulant therapies offers the advantage of oral administration in the absence of laboratory monitoring, however, there are a few reports regarding their use in cirrhotic patients, most of them referring to compensated isolated cases. Transjugular intrahepatic portosystemic shunt could be an alternative if thrombosis progresses despite anticoagulatant therapy and/or when PVT is associated with portal hypertension complications. The aim of this editorial is to discuss the different aspects of pathophysiology, clinical relevance, diagnosis and management of PVT in patients with LC.

Embolization of splenorenal shunt associated to portal vein thrombosis and hepatic encephalopathy

Hepatic encephalopathy(HE)is a cognitive disturbance characterized by neuropsychiatric alterations.It occurs in acute and chronic hepatic disease and also in patients with portosystemic shunts.The presence of these portosystemic shunts allows the passage of nitrogenous substances from the intestines through systemic veins without liver depuration.Therefore,the embolization of these shunts has been performed tocontrol HE manifestations,but the presence of portal vein thrombosis is considered a contraindication.In this presentation we show a cirrhotic patient with severe HE and portal vein thrombosis who was submitted to embolization of a large portosystemic shunt.Case report:a 57 years-old cirrhotic patient who had been hospitalized many times for persistent HE and hepatic coma,even without precipitant factors.She had a wide portosystemic shunt and also portal vein thrombosis.The abdominal angiography confirmed the splenorenal shunt and showed other shunts.The larger shunt was embolized through placement of microcoils,and the patient had no recurrence of overt HE.There was a little increase of esophageal and gastric varices,but no endoscopic treatment was needed.Since portosystemic shunts are frequent causes of recurrent HE in cirrhotic patients,portal vein thrombosis should be considered a relative contraindication to perform a shunt embolization.However,in particular cases with many shunts and severe HE,we found that one of these shunts can be safely embolized and this procedure can be sufficient to obtain a good HE recovery.In conclusion,we reported a case of persistent HE due to a wide portosystemic shunt associated with portal vein thrombosis.As the patient had other shunts,she was successfully treated by embolization of the larger shunt.