Incidence Of Portal Vein Thrombosis Research Articles

Clinical analysis of portal vein thrombosis after splenocaval shunt plus devascularization in treatment of portal hypertension

Objective To explore the clinical characteristics of portal vein thrombosis(PVT) after splenocaval shunt plus devascularization in treatment of portal hypertension and find Out ways for its prevention.Methods The formation,diagnosis,treatment of PVT and variceal rehemorrhage in 110 patients with portal hypertension who received splenocaval shunt plus devascularization procedures (Combined Group)and 92 patients subjected to pericardial devascularization operation(PCDV Group) were retrospectively analyzed.Meanwhile,the effect of two procedures on PVT was compared.Results The incidence of PVT was 10.0%in combined group and 22.8%in PCDV group (P<0.05).The rebleeding rate from esophagogastric varices because of PVT in combined group was 3.6%,which was significantly lower than that of 10.8%in PCDV group(P<0.05).Conclusion Splenoeaval shunt plus devascularization is a better choice to decrease the incidence of PVT.The postoperative anti-coagulation therapy in the early stage is important for the prevention of PVT. Key words: Hypertension,portal; Shunt; Thrombosis; Devascularization

Is there a role for anticoagulants in portal vein thrombosis management in cirrhotic patients?

Importance of the field: Portal vein thrombosis (PVT) is one of the principal complications of liver cirrhosis. The estimated prevalence is < 1% in patients with a compensated disease; this increases to 8 – 25% in candidates for liver transplantation. Many determinants may influence PVT clinical presentation and its outcome.Areas covered in this review: We report the actual knowledge regarding management of PVT and analyze the different therapeutic approaches, focusing particularly on the use of anticoagulants and their implications in the complex clinical setting of liver cirrhosis. We also describe the possible available preemptive strategies, as an early prophylactic management based on clinical, biochemical or radiological parameters may in the future reduce PVT incidence and complications, ameliorating patients' outcome.What the reader will gain: The importance of an accurate PVT diagnosis and its implications in PVT management; a description of the different available therapeutic tools, their efficacy and their possible risks in different typologies of patients; the principal elements to choose a correct individualized therapy for PVT patients.Take home message: The challenge for clinicians is the early identification of PVT, in order to prevent frightening complications, such as variceal bleeding or mesenteric infarction, and to provide the best therapeutic management.

Impact of Antithrombin III Concentrates on Portal Vein Thrombosis After Splenectomy in Patients With Liver Cirrhosis and Hypersplenism

The aim of this study was to determine the role of antithrombin III (AT-III) in portal vein thrombosis (PVT) after splenectomy in cirrhotic patients. There is no standard treatment for PVT after splenectomy in liver cirrhosis. A total of 50 consecutive cirrhotic patients who underwent laparoscopic splenectomy for hypersplenism were enrolled into this study. From January 2005 to December 2005, 25 cirrhotic patients received no prophylactic anticoagulation therapy after the operation (AT-III [-] group). From January 2006 to July 2006, 25 cirrhotic patients received prophylactic administration of AT-III concentrates (1500 U/d) on postoperative day (POD) 1, 2, and 3 (AT-III [+] group). In AT-III (-) group, 9 (36.0%) patients developed PVT up to POD 7, and risk factors for PVT were identified as: low platelet counts, low AT-III activity, and increased spleen weight. Although there were no significant differences in the clinical characteristics, including the above risk factors, between the 2 groups, only 1 (4.0%) patient developed PVT on POD 30 in AT-III (+) group, and the incidence of PVT was significantly lower than in AT-III (-) group (P = 0.01). In AT-III (-) group, AT-III activity was significantly decreased from POD 1 to POD 7, as compared with the preoperative level, whereas AT-III concentrates prevented the postoperative decrease in AT-III activity. These results demonstrate that low AT-III activity and further decreases in this activity are associated with PVT after splenectomy in cirrhotic patients, and that treatment with AT-III concentrates is likely to prevent the development of PVT in these patients.

Correlation of routinely used coagulation parameters and presence of portal vein thrombosis in patients with liver cirrhosis

Portal vein thrombosis (PVT) is a serious complication in patients with liver cirrhosis. In patients with advanced stages of liver cirrhosis plasmatic coagulation and platelet count are often reduced. However, patients with normal coagulation status might carry a high risk for developing PVT. A correlation between coagulation status used in clinical routine and the incidence of PVT in patients with liver cirrhosis has been evaluated in the present retrospective analysis. 88 patients with liver cirrhosis were identified by screening a database. Of these patients, 23 suffered from PVT. Patients were classified according to the Child-Pugh classification. Patients were subdivided into early stages (Child A) and advanced stages (Child B/C) of liver cirrhosis. In patients with Child-Pugh A cirrhosis, there was no difference in activated partial thromboplastin time (apTT), international normalized ratio (INR), and platelet count between the PVT (n = 7) and the control group (n = 35). In contrast, the median apTT and INR were significantly lower in patients with Child B/C cirrhosis and PVT (n = 16) in comparison with patients without PVT (37 s vs 43 s [P = 0.017] and 1.25 vs 1.40 [P = 0.022]), respectively. Platelet count did not differ significantly in patients with advanced liver cirrhosis and PVT from those without PVT. Patients with advanced liver cirrhosis and PVT displayed lower apTT and INR compared with those without PVT. Therefore, patients with advanced liver cirrhosis and almost normal coagulation parameters might be at particular risk of developing PVT. The results suggest that regular monitoring using Doppler-ultrasound should be carried out in these patients, especially when liver transplantation is intended.

Portal Vein Thrombosis After Laparoscopic Splenectomy: The Size of the Risk

Portal vein thrombosis (PVT) after splenectomy is a potentially life-threatening complication. Clinical symptoms may be insidious, and progression can lead to intestinal infarction and portal hypertension. Interest in PVT has increased as a high incidence has been found in the laparoscopic setting. The higher incidence of PVT found in recent prospective studies of laparoscopically operated patients compared with retrospective reports from the 1990s suggests that PVT may have been underreported. Clinical outcome depends on the extension of the thrombus and the underlying disease. Main risk factors may be myeloproliferative diseases requiring splenectomy and splenomegaly, but PVT may occur after splenectomy for any clinical indication. The extent to which laparoscopy is responsible for PVT remains unclear. Laparoscopic surgeons should be aware of the risk of PVT, and it should be suspected in cases with an atypical outcome after laparoscopic splenectomy. Once diagnosed, prompt anticoagulation therapy may resolve the thrombotic event.

Portal vein and systemic thromboses in hepatocellular carcinoma

15048 Background: Hemostatic activation may be important for tumor growth and metastasis. Hepatocellular carcinoma (HCC) is commonly associated with portal vein thrombosis (PVT). Very little is known about factors predictive for PVT in patients with HCC or its correlation with systemic venous thromboembolism (VTE). Methods: We conducted a retrospective chart review of 194 patients diagnosed with HCC at the University of Rochester between 1998 and 2004. The primary endpoints of this study were presence of PVT and any systemic VTE. The secondary endpoint was overall survival calculated from time of diagnosis. Univariate and multivariate logistic regression analyses were conducted to assess the association of PVT with a set of clinical covariates, and the survival curve was estimated using the method of Kaplan-Meier. Results: The mean age of the total population was 60.4 ± 11.9, and one-third of the patients underwent liver transplant. The incidence of PVT in the total population was 31% (60/194) with a higher incidence in the non-transplant group compared to transplanted patients (34% vs. 24%; p= 0.08). In univariate analysis, advanced stage, major vessel involvement, higher MELD score, higher Child-Turcotte-Pugh (CTP) classification, lower serum albumin, elevated serum bilirubin, elevated serum alpha-fetoprotein (AFP) level, and elevated INR were associated with development of PVT (p &lt;0.05 for each). In multivariate analysis CTP class, stage, major vessel involvement, serum albumin, and serum AFP were independently and significantly associated with PVT (p &lt;0.05 for each). The presence of PVT was associated with reduced survival (median survival 4.61 months for those with PVT versus 17.55 months for those without PVT, HR 2.01, p &lt;0.001). The incidence of systemic VTE in the total population was 6.7%, and patients with PVT had a higher rate of systemic VTE compared to patients without PVT (11.5% vs. 4.4%; p 0.044). Conclusions: PVT is common in patients with HCC and is associated with worse outcomes. The correlation between PVT and systemic VTE suggests a common mechanism of hemostatic activation. Advanced stage, higher CTP class, major vessel involvement, and serum albumin and AFP levels are predictive of PVT. Identifying patients at high-risk for PVT and instituting prophylaxis may affect HCC outcomes. No significant financial relationships to disclose.

Transarterial Chemoembolization in a Patient With Recurrent Hepatocellular Carcinoma and Portal Vein Thrombosis

Primary hepatocellular carcinoma (HCC) accounts for more than 5% of all cancers in the world, and causes between 250,000 and one million deaths globally each year. The incidence of portal vein thrombosis in HCC patients is around 8%. These patients are regarded as unsuitable for chemoembolization, especially if there is portal vein occlusion. The authors describe a patient with HCC and partial portal vein thrombosis who successfully underwent transarterial chemoembolization.

ALIMENTARY TRACT PERFORATION AFTER LIVER TRANSPLANTATION IN CHILDREN.

A229 Alimentary tract perforation is well-recognized devastating entity that complicates up to 20 % of pediatric liver transplantation (LTx). Aims of the study are to assess the incidence, risk factors, treatment and outcome of alimentary tract perforation after pediatric LTx. Methods: 198 LTx in 182 patients were performed since 1990 to 2003 in our institution. There were 46 living related LTx, nine combined liver and kidney, and one liver and bowel transplantation. Patients older than 18 years old, and those who died before one month after LTx were excluded from further analysis. Children were classified into two groups: with (group I – 10) and without perforation (group II – 146). Age, body weight, UNOS status, previous surgery, duration of hepatectomy and unhepatic phase, blood transfusion during transplantation were retrospectively analyzed. The incidence of portal vein thrombosis, bacterial, fungal, and CMV infections, intensive steroid therapy because of acute rejection were assessed during the first posttransplant month. Results were statistically analyzed using Mann-Whitney, chi2, and t- test. Results: Alimentary tract perforations were diagnosed in 10 children (6,4%), including two who reperforated. Age of patients was between 7 months and 17 years. Indication for LTx in 8 children was biliary atresia, liver fibrosis - 1, cirrhosis of unknown etiology - 1. In three children perforations occurred after retransplantation. The interval between transplantation and perforation was from 6 to 22 days. Perforations were localized in: colon - 6 cases, jejunum - 5, duodenum - 3, stomach – 1. Two children developed recurrent perforations, one of them multifocal. The surgery of perforations consisted of: simple suture in 13 cases, resection and primary anastomosis – 1, ileostomy - 1. One patient died on 5th day after perforation and on 20th day after retransplantation due to multiorgan failure. The follow up of remaining nine patients is between 4 and 147 months. The incidence of perforation was higher (p < 0.05) after pretransplant laparotomy (especially Kasai procedure), and after retransplantation. Patients who perforated required more blood transfusions during LTx (p < 0.05). Between LTx and alimentary tract perforation they developed more frequently (p < 0.05) sever bacterial bowel infections in comparison to non-perforated group. There was no significant differences regarding: age, body weight, UNOS status, portal vein thrombosis, intensive steroid therapy, fungal infection, bacterial sepsis and CMV infection. The duration of hepatectomy and unhepatic phase were longer (not significantly) in the group of alimentary tract perforation. Conclusions: Alimentary tract perforations after pediatric LTx are related to pretransplant surgery (especially Kasai procedure), retransplantation, greater blood transfusions during LTx, and severe bacterial postransplant bowel infections. The mortality of alimentary tract perforation after pediatric LTx is low.

Portal Vein Thrombosis following Splenectomy: Identification of Risk Factors

Portal vein thrombosis (PVT) following splenectomy is a potentially life-threatening complication, and the true incidence of PVT in splenectomized patients is unknown. The objective of this study was to determine the incidence of symptomatic PVT after splenectomy. The hospital database was searched to identify cases of PVT associated with splenectomy from January 1990 to May 2002. Six hundred eighty-eight patients underwent splenectomy during this period, 321 of them for hematologic diseases. Eleven of the 688 patients had PVT associated with splenectomy, and the charts of these patients were reviewed. Six patients developed PVT after splenectomy. Five had hematologic diseases. Symptoms were abdominal pain (6), ileus (5), fever (3), or diarrhea (2). Diagnosis was confirmed by computed tomography (CT) (4), duplex ultrasonography (1), and magnetic resonance imaging (1). The indications for splenectomy included hemolytic anemia (3), thalassemia (1), and myelofibrosis (1). One patient had an incidental splenectomy during gastrectomy. There were four laparoscopic and two open splenectomies. The median interval between splenectomy and diagnosis of PVT was 40 days (range, 13-741). One patient died of pulmonary embolism. Five of six patients with postsplenectomy PVT had splenomegaly and hemolysis. We conclude that the risk of PVT is higher in patients with hematologic conditions associated with splenomegaly and hemolysis.

Anticardiolipin antibodies in chronic hepatitis B and chronic hepatitis D infection, and hepatitis B-related hepatocellular carcinoma. Relationship with portal vein thrombosis.

To assess the presence of anticardiolipin antibodies (ACAs) in patients with chronic hepatitis B virus (HBV) infection, chronic hepatitis D virus (HDV) infection and HBV-related hepatocellular carcinoma (HCC) and to associate this with the incidence of portal vein thrombosis (PVT) in HCC patients. Sixty-five cirrhotic patients with HBV-related HCC, 28 naive patients with chronic HBV infection and 14 naive patients with chronic HDV infection were enrolled prospectively in the study. Thirty-two healthy blood donors were used as controls. The ACAs (immunoglobulin G and immunoglobulin M) were measured using an enzyme-linked immunosorbent assay system. Statistical analysis used non-parametric methodology (chi-squared test, Student t-test and Fisher exact test, P value<0.05). Eleven of the 65 patients with HCC (16.9%) showed a positive ACA titre and 22 of the patients (34%) had PVT. Of these patients, eight (36%) had a positive ACA titre. In contrast, from the 43 patients without PVT, only three (11%) showed a positive titre. From the 28 HBV patients, six (21.5%) had a positive ACA titre, and six out of 14 (42.8%) HDV patients also showed a positive ACA titre. Three of the six ACA positive HBV patients presented an extrahepatic manifestation of the disease. One out of 32 control patients (3%) had positive ACAs. Both chronic HBV and chronic HDV infections are potent stimulants for the production of ACAs. The presence of ACAs in a great proportion of HBV-cirrhosis-related HCC patients with PVT suggests their possible participation in thrombotic mechanisms and in the hypercoagulable state that occurs in advanced liver disease and HCC.

Liver transplantation in patients with portal vein thrombosis.

The aim of this study is to analyze the incidence, risk factors, management, and follow-up of patients with portal vein thrombosis (PVT) undergoing primary orthotopic liver transplantation (OLT). Four hundred fifteen OLTs were performed in 391 patients. In 62 patients, partial (group 1; n = 48) or complete (group 2; n = 14) PVT was found at the time of surgery. Portal flow was reestablished by venous thrombectomy. In this study, we compare 62 primary OLTs performed in patients with PVT at the time of OLT with a group of 329 primary OLTs performed in patients without PVT (group 3) and analyze the incidence of PVT, use of diagnostic methods, surgical management, and outcome. We found no significant differences among the 3 groups for length of surgery, cold and warm ischemic times, and postoperative stay in the intensive care unit. With the piggyback technique, groups 1 and 2 had greater blood losses and required more blood transfusions than group 3. The early reoperation rate was greater in group 2. The incidence of rethrombosis was 4.8% (group 1, 2%; group 2, 14.3%). Reexploration and thrombectomy (2 patients) and retransplantation (1 patient) had a 100% mortality rate. In particular, the mortality rate of patients with complete PVT with extension into the splanchnic veins is high (33%). Three-month and 4-year patient survival rates were statistically similar in the 3 groups. The presence of PVT at the time of OLT is not a contraindication for OLT. However, if PVT extends into the splanchnic veins, the outcome is guarded.

The role of natural anticoagulant deficiencies and factor V Leiden in the development of idiopathic portal vein thrombosis.

One of the causes of portal hypertension is portal vein thrombosis (PVT). The aim of this study was to determine whether natural anticoagulant deficiencies, activated protein C resistance (APCR), and factor V Leiden play a role in the development of PVT, leading to cavernous transformation of the portal vein (CTPV). Twenty-three patients with idiopathic CTPV (group 1) seen at Hacettepe University Hospital during the past 12 years were identified and prospectively studied. These 23 patients underwent a detailed hematological evaluation including measurement of protein S, protein C, antithrombin III, activated protein C resistance (APCR), and factor V Leiden gene mutation. Additionally, all patients were tested for anticardiolipin antibodies (ACA), IgG, IgM, and lupus anticoagulant (LA). Natural anticoagulants and APCR were measured using available commercial kits, and factor V Leiden mutation (R506Q) was detected by Mnl I digestion of an amplified factor V DNA fragment. All parameters were measured at least 6 months after the diagnosis of CTPV was established. No patient was on anticoagulant or antiaggregant treatment while tested. The findings in these 23 patients were compared with those in 20 healthy control subjects (group 2), in whom all tests mentioned above were also performed. In 23 patients (group 1), who had no recognizable factor for portal vein thrombosis, considerably natural anticoagulant deficiencies and factor V Leiden mutation positivity were found when we compare them to those healthy controls (group 2). The protein C levels of six patients (26%), the protein S levels of 10 patients (43.5%), and the antithrombin III levels of five patients (26%) were lower than in control subjects. Two patients were found to have combined protein S and antithrombin III deficiency, and one had combined protein S and C deficiency and APCR. APCR was detected in seven of the 23 patients, and six of these seven patients were found to have R506Q factor V Leiden mutations. In group 1, ACA IgG levels were higher in four patients (17%) and ACA IgM level was higher in one (4%) compared with the control group. LA was positive in only one patient in group 1. Natural anticoagulant deficiencies and factor V Leiden mutation are strongly associated with PVT. The natural anticoagulant deficiencies and APCR (almost totally caused by R506Q mutation) produce a favorable medium for thrombus generation. PVT seems to be related to the natural anticoagulant deficiencies and factor V Leiden R506Q mutation. A combination of these defects increases the incidence of PVT and these factors should be evaluated carefully in patients with idiopathic CTPV.

Umbilical venous catheterization and the risk of portal vein thrombosis

Portal vein thrombosis has been associated with umbilical venous catheterization. We studied the incidence of portal vein thrombosis associated with umbilical venous catheterization with the catheter tip not in the portal venous system. Appropriate placement of an umbilical venous catheter in sick neonates is associated with a low risk of portal vein thrombosis (actual incidence, 1.3%). (J Pediatr 1997;131:760-2)

A High Incidence of Native Portal Vein Thrombosis in Veterans Undergoing Liver Transplantation

The incidence of native portal vein thrombosis (PVT) in liver transplant recipients has been reported to range from 2.1 to 13.8%. We have identified an inordinately high incidence of PVT in a consecutive series of U.S. veterans receiving liver transplants. Between October 1989 and February 1994, 88 consecutive U.S. veterans received 99 orthotopic liver transplants under primary Tacrolimus (Prograf, formerly FK506) based immunosuppression. A number of clinical features were examined in an effort to identify risk factors for PVT and outcome was compared to patients without PVT. Native PVT was present in 23/88 (26%) patients. All of these patients were male U.S. veterans with a mean age of 47 years. When compared to the 65 patients without PVT, we found no significant difference with respect to underlying liver disease, age, Childs–Pugh score (mean = 12), UNOS status as defined prior to April 1995 (95% UNOS 3 or 4), previous abdominal surgery, or liver volume. Median blood loss for patients with PVT (21 units of packed red blood cells) was greater than for those without PVT (14 units,P= 0.04). Portal thrombectomy was performed in 11 patients, 11 patients required mesoportal jump grafts, and 1 patient had an interposition graft. Standard veno–venous bypass was used in 10 patients with single bypass utilized for the remainder. Actuarial patient survival for all patients at 1, 2, and 4 years was 88, 85, and 79%, respectively. There was no significant difference in patients with or without PVT. Patients with PVT had poorer graft survival than patients without PVT (86% vs 65%, 1 year; 81% vs 65%, 2 years; 81% vs 61%, 4 years;P= 0.03); however, this was not related to technical problems with the portal venous inflow. PVT occurred in 26% of U.S. veterans undergoing liver transplantation. These patients had significantly higher operative blood loss and poorer graft survival. The high incidence of postnecrotic cirrhosis in a predominantly male group of patients with advanced disease, as is evident by the high mean Childs–Pugh score and UNOS status, perhaps accounts for our observations.

Portal vein thrombosis following endoscopic variceal sclerotherapy

The association between portal vein thrombosis (PVT) and prior endoscopic variceal sclerotherapy has been suggested but remains unproven. The aim of this study was to compare the incidence of PVT in patients who had received sclerotherapy for esophageal variceal hemorrhage to a control group of cirrhotic patients with portal hypertension who had not received sclerotherapy. Doppler ultrasound was used to assess PVT in 48 patients (group 1) who had received sclerotherapy for variceal hemorrhage as well as in 52 patients (group 3) with cirrhosis and portal hypertension who had not received sclerotherapy. Assessment of PVT was made at the time of surgery in 24 patients (group 2) who had received sclerotherapy for variceal hemorrhage, failed therapy, and had portacaval shunt surgery or received liver transplantation for liver failure. One patient had splenectomy for symptoms related to a massively enlarged spleen. The incidence of PVT in group 1 was 10%, in group 2 was 13%, and in group 3 was 10%. The incidence of PVT in the three groups was not significantly different statistically. In this controlled study of patients with cirrhosis and portal hypertension, sclerotherapy does not increase the incidence of PVT.

The Incidence of Portal Vein Thrombosis At Liver Transplantation

The incidence of portal vein thrombosis was examined in 885 patients who received orthotopic liver transplantations for various end-stage liver diseases between 1989 and 1990. The thrombosis was classified into four grades. Grade 1 was thrombosis of intrahepatic portal vein branches, grade 2 was thrombosis of the right or left portal branch or at the bifurcation, grade 3 was partial obstruction of the portal vein trunk, and grade 4 was complete obstruction of the portal vein trunk. Among the 849 patients without previous portosystemic shunt, 14 patients (1.6%) had grade 1, 27 patients (3.2%) had grade 2, 27 patients (3.2%) had grade 3 and 49 patients (5.8%) had grade 4 portal vein thrombosis. The incidence of portal vein thrombosis was highest (34.8%) in the patients with hepatic malignancy in the cirrhotic liver, followed by those with Budd-Chiari syndrome (22.2%) and postnecrotic cirrhosis of various causes (15.7%). The patients with encephalopathy, ascites, variceal bleeding, previous splenectomy and small liver had significantly higher incidences of portal vein thrombosis than the others. The total incidence of portal vein thrombosis among the 36 patients with previous portosystemic shunt was 38.9%, which was significantly higher than that (13.8%) of those without shunt.

The incidence of portal vein thrombosis at liver transplantation

The incidence of portal vein thrombosis was examined in 885 patients who received orthotopic liver transplantations for various end-stage liver diseases between 1989 and 1990. The thrombosis was classified into four grades. Grade 1 was thrombosis of intrahepatic portal vein branches, grade 2 was thrombosis of the right or left portal branch or at the bifurcation, grade 3 was partial obstruction of the portal vein trunk, and grade 4 was complete obstruction of the portal vein trunk. Among the 849 patients without previous portosystemic shunt, 14 patients (1.6%) had grade 1, 27 patients (3.2%) had grade 2, 27 patients (3.2%) had grade 3 and 49 patients (5.8%) had grade 4 portal vein thrombosis. The incidence of portal vein thrombosis was highest (34.8%) in the patients with hepatic malignancy in the cirrhotic liver, followed by those with Budd-Chiari syndrome (22.2%) and postnecrotic cirrhosis of various causes (15.7%). The patients with encephalopathy, ascites, variceal bleeding, previous splenectomy and small liver had significantly higher incidences of portal vein thrombosis than the others. The total incidence of portal vein thrombosis among the 36 patients with previous portosystemic shunt was 38.9%, which was significantly higher than that (13.8%) of those without shunt. (HEPATOLOGY 1992;16;1195–1198.)

The Significance of Portal Vein Thrombosis After Distal Splenorenal Shunt

The aims of this study were to determine the incidence of portal vein thrombosis after the distal splenorenal shunt, to identify any predictive factors, and to assess the clinical significance of this complication. Preoperative and postoperative angiograms and clinical evaluation were reviewed in 124 patients who underwent distal splenorenal shunts. Total and partial portal vein thrombosis were seen on 13 (10.5%) and 22 (17.7%) postoperative angiograms, respectively. The only preoperative variable correlating with development of portal vein thrombosis was portal venous perfusion, which was significantly lower in patients with than in those without portal vein thrombosis. In six of 10 patients with postoperative pancreatitis, portal vein thrombosis developed. The frequency of early postoperative complications was significantly greater in patients with total portal vein thrombosis than in those with partial or no thrombosis. Long-term follow-up has shown no significant effects of portal vein thrombosis on late ascites, encephalopathy, or survival.

Incidence of Portal Vein Thrombosis Complicating Liver Metastasis as Detected by Duplex Ultrasound

Incidence of Portal Vein Thrombosis Complicating Liver Metastasis as Detected by Duplex Ultrasound

Incidence of portal vein thrombosis complicating liver metastasis as detected by duplex ultrasound.

In a prospective study of 100 patients with liver metastasis using real-time ultrasound, 8 patients (8%) were found to have portal vein thrombosis (PVT). Sixty seven of these patients, which included all with PVT, also underwent duplex examination. Pulsed Doppler showed absent flow in 4 of 8 patients, indicating complete obstruction. The other 4 showed different degrees of flow suggesting incomplete obstruction or collateral formation. We conclude that PVT complicating liver metastasis is not a rare finding.