Etiology and portal vein thrombosis in Budd-Chiari syndrome

AIM： To research the etiology, portal vein thrombosis and other features of Budd-Chiari syndrome （BCS） patients prospectively.
METHODS： A total of 75 patients （40 female, 35 male） who were diagnosed between January 2002 and July 2004 as having BCS were studied prospectively. Findings from on physical examination, ultrasonography, duplex ultrasonography and venography were analyzed. Hemogram and blood chemistry were studied at the time of diagnosis and on each hospital visit. Bone marrow examination and immune phenotyping were performed by a hematologist when necessary. Protein C, S, antithrombin Ⅲ, activated protein C resistance, and anticardiolipin antibodies, antinuclear antibodies, and anti ds-DNA were studied twice. The presence of ascite, esophageal varices, and portal thrombosis were evaluated at admission and on every visit.
RESULTS： At least one etiological factor was determined in 54 （72%） of the patients. The etiology could not be defined in 21 （28%） patients. One etiological factor was found in 39, 2 factors in 14 and 3 factors in 1 patient. The most common cause was the web （16%）, the second was Hydatid disease （11%）, the third was Behcet’s disease （9%）. Portal vein thrombosis was present in 11 patients and at least one etiology was identified in 9 of them （82%）.
CONCLUSION： Behcet’s disease and hydatid disease are more prominent etiological factors in Turkey than in other countries. Patients with web have an excellent response to treatment without signs of portal veinthrombosis while patients having thrombofilic factors more than one are prone to develop portal vein thrombosis with worse clinical outcome.     

原发性骨髓纤维化继发门脉高压症六例分析并文献复习

目的 探讨原发性骨髓纤维化(PMF)继发门脉高压症患者的临床特点.方法 对北京大学第三医院确诊的6例PMF继发门脉高压症患者进行临床分析,并进行文献复习.结果 6例患者中,男、女各3例,年龄(52.8±11.7)岁,临床起病至确诊的中位时间为24个月.门脉高压症相关症状主要包括腹胀、腹部包块、呕血和黑便,体征主要包括脾大(均为中重度肿大)、肝大(以轻中度肿大多见)、移动性浊音阳性和腹壁静脉曲张,而黄疸、肝掌和蜘蛛痣少见.大多数患者的肝功能指标正常.门、脾静脉宽度为(16.0±3.2)、(11.0±3.4)mm,2例合并门静脉或脾静脉血栓.1例患者进行了肝穿刺,显示有髓外造血.5例患者接受了门脉高压症相关药物治疗,脾切除术和食管曲张静脉套扎治疗各1例.结论 PMF继发门脉高压症临床罕见,极易误诊.脾大显著、轻中度肝大、肝功能较好、肝掌和蜘蛛痣等体征少见、肝穿刺显示髓外造血等是其与肝硬化的鉴别要点.     

Portal vein thrombosis associated with factor V Leiden mutation in a woman who underwent exchange transfusion at birth

We report the case of a 18-year-old woman with portal vein thrombosis and chronic hepatitis C virus. Portal vein thrombosis was diagnosed by chance on ultrasound examination during initial hepatitis C virus-positive patient screening. The patient interview revealed a history including exchange transfusion at birth, followed by necrotising ulcerocolitis and septicemia. The investigation of general factors favoring thrombosis showed acquired protein S deficiency and heterozygous factor V Leiden mutation. This case demonstrates the value of systematic investigations for general thrombophilic factors in cases of portal vein thrombosis even when a local cause is found.     

Endoscopic variceal sclerosis does not increase the risk of portal venous thrombosis.

In this study the risk of thrombosis in the portal venous system was assessed in patients with chronic variceal bleeding undergoing sclerotherapy. Twenty-two patients with cirrhosis were prospectively studied with angiography before initiation of sclerotherapy and at mean (+/- SD) 26 +/- 17-month (range, 8-63 months) follow-up. Sclerotherapy consisted of flexible endoscopy, intravariceal and paravariceal, using sodium morrhuate (1.5%-2%) and sodium tetradecyl sulfate (0.5%-1.5%), to obliteration. The mean number of sessions was 6.5 +/- 2.2 (range, 3-11), with a mean total amount of sclerosant of 62 +/- 25 mL (range, 25-112 mL). No patient developed splenic or portal vein thrombosis as shown by arteriography. The flow patterns of portal perfusion, vessel size, and coronary vein visualization showed no significant change. Only one patient had spontaneous reversal of portal flow. Splenic vein histology, examined in five patients in whom sclerotherapy failed and who required shunt surgery, was not significantly different from that in eight patients who had no prior sclerotherapy. It is concluded that under the conditions of the current study, chronic sclerotherapy did not increase the risk of thrombosis in the portal venous system and did not significantly alter the histology of the portal hypertensive splenic vein.     

Should anticoagulants be administered for portal vein thrombosis associated with acute pancreatitis?

Venous complications in patients with acute pancreatitis typically occur as a form of splenic, portal, or superior mesenteric vein thrombosis and have been detected more frequently in recent reports. Although a well-organized protocol for the treatment of venous thrombosis has not been established, anticoagulation therapy is commonly recommended. A 73-year-old man was diagnosed with acute progressive portal vein thrombosis associated with acute pancreatitis. After one month of anticoagulation therapy, the patient developed severe hematemesis. With endoscopy and an abdominal computed tomography scan, hemorrhages in the pancreatic pseudocyst, which was ruptured into the duodenal bulb, were confirmed. After conservative treatment, the patient was stabilized. While the rupture of a pseudocyst into the surrounding viscera is a well-known phenomenon, spontaneous rupture into the duodenum is rare. Moreover, no reports of upper gastrointestinal bleeding caused by pseudocyst rupture in patients under anticoagulation therapy for venous thrombosis associated with acute pancreatitis have been published. Herein, we report a unique case of massive upper gastrointestinal bleeding due to pancreatic pseudocyst rupture into the duodenum, which developed during anticoagulation therapy for portal vein thrombosis associated with acute pancreatitis.     

Deficiency of protein C in patients with portal vein thrombosis

Portal vein thrombosis has been considered idiopathic in 50% of cases reported in adults. Protein C deficiency is a recently described disorder characterized by a predisposition to develop thromboembolic disease. We report the findings in two patients with portal hypertension and bleeding varices due to portal vein thrombosis in whom a deficiency of protein C was present. Both cases were very similar, with a history of recurrent episodes of systemic thromboembolic disease, mesenteric venous thrombosis that required intestinal resection and upper gastrointestinal bleeding from gastroesophageal varices. Portal hypertension as well as portal vein thrombosis were demonstrated. The hematologic work-up revealed a deficiency of protein C. Both patients were subjected to the Sugiura procedure, and anticoagulation was instituted thereafter. At the time of surgery, a liver biopsy was performed, which was reported as "normal." Two years and 3 months, respectively, after surgery both patients are in good condition. We conclude that protein C deficiency should be investigated in all cases of portal vein thrombosis, especially in those with a history of thromboembolic disease elsewhere.     

Extensive portal and splenic vein thrombosis: differences in hemodynamics and management

BACKGROUND/AIMS: To assess the incidence of extensive portal and splenic vein thrombosis in patients with extrahepatic portal vein obstruction and determine the differences in presentation, portal hemodynamics and management as compared to patients with portal vein thrombosis alone. METHODOLOGY: 118 patients of extrahepatic portal vein obstruction presenting with variceal hemorrhage, having received no definitive treatment prior to presentation were divided into two groups--with portal and splenic vein thrombosis and with portal vein thrombosis, based on ultrasonography and splenoportography. Collateralization patterns on splenoportography were studied. Results of endoscopic variceal sclerotherapy were compared. RESULTS: Portal and splenic vein thrombosis was seen in 39 patients. Collateralization in case of portal and splenic vein thrombosis, in contrast to portal vein thrombosis, was predominantly left sided (74% vs. 9%, p < 0.0001). Fundal gastric varices were seen more often in patients with portal and splenic vein thrombosis (28% vs. 11%, p = 0.02), developing even after variceal obliteration, though obliteration was achieved in fewer sessions. Surgery for control of variceal bleed was performed more in the portal and splenic vein thrombosis group (33% vs. 15%, p = 0.02), especially for gastric varices (28% vs. 9%, p = 0.006). CONCLUSIONS: Portal and splenic vein thrombosis is present in 33% of patients with extrahepatic portal vein obstruction. Hemodynamic patterns differ, accounting for the preponderance of gastric varices on presentation in patients with portal and splenic vein thrombosis and an increased need for surgery.     

Colorectal variceal bleeding in patients with extrahepatic portal vein thrombosis and idiopathic portal hypertension.

We report three patients with colonic variceal bleeding secondary to portal hypertension, 0.5% of all cases with hemorrhagic portal hypertension studied by us in the last 16 years. One patient had idiopathic portal hypertension, and the others had extrahepatic portal vein thrombosis. Colonic varices were documented in all three cases by angiogram; large arteriovenous fistulas in the territory of the superior mesenteric artery and between the inferior mesenteric artery and hemorrhoidal veins were demonstrated in one patient. Two patients underwent colonoscopy; colonic varices were seen in only one. Two patients also had bled from esophagogastric varices. One patient underwent descending colon and sigmoid resection after failure to control bleeding with ligation of arterial supply; one patient underwent the Sugiura procedure, plus transanal ligation of hemorrhoids and rectal varices. At 3 months, 2 years, and 4 years of follow-up, the patients were in good general condition without any evidence of rebleeding.     

Successful use of danaparoid in the treatment of portal vein thrombosis that developed in a warfarin-administered hepatitis C virus-related cirrhosis patient

An 84-year-old woman with hepatitis C virus-related cirrhosis, hepatocellular carcinoma and atrial fibrillation, who presented with hematemesis, was initially treated with endoscopic variceal ligation (EVL) for an esophageal varix hemorrhage. However, computed tomography (CT) upon admission had revealed portal vein thrombosis, despite having received warfarin for existing atrial fibrillation. We subsequently initiated a 2-week treatment with danaparoid;warfarin being discontinued in order to reduce the risk of re-hemorrhage. A follow-up CT after treatment revealed complete reduction of the portal vein thrombosis. This is the first successful report of danaparoid use in the treatment of portal vein thrombosis that developed in a patient who had received warfarin.     

Portal vein thrombosis complicating hepatocellular carcinoma. Value of ultrasound-guided fine-needle biopsy of the thrombus in the therapeutic management

Abstract: During a 4-year period portal vein thrombosis was diagnosed in 20 Child class A patients with cirrhosis by means of ultrasound and ultrasound-Doppler study. Seventeen of them showed single or multiple focal liver lesions diagnosed as hepatocellular carcinoma by ultrasound-guided fine-needle biopsy and the remaining three a coarse liver echo-pattern without focal lesions. One patient was found to have developed portal vein thrombosis after the fifth ethanol injection of a single hepatocellular carcinoma lesion 17 mm in diameter. Ultrasound-guided fine-needle biopsy of the thrombus was performed on all the patients: portal vein thrombosis was neoplastic in 13 cases and non-neoplastic in seven cases (five patients with a single lesion; one with two lesions; one with coarse liver echo-pattern). Among the five patients with a single lesion, one had already been treated by percutaneous ethanol injection therapy. There were no complications related to the biopsy procedures. The diagnosis of non-neoplastic thrombosis allowed five new patients to be recruited for percutaneous ethanol injection treatment and allowed it to continue in the patient with portal vein thrombosis occurring after the fifth ethanol injection. The routine use of ultrasound-guided fine-needle biopsy of portal vein thrombosis yields an accurate diagnosis of the nature of the thrombus and can improve the selection for percutaneous ethanol injection treatment of patients with cirrhosis with hepatocellular carcinoma lesions.     

Case report: portal vein thrombosis associated with hereditary protein C deficiency: a report of two cases

Protein C deficiency is one of the causes of curable or preventable portal vein thrombosis. We report two patients of portal vein thrombosis associated with hereditary protein C deficiency. The first patient presented with continuous right upper quadrant pain and high fever. The abdominal sonography revealed normal liver parenchyma but portal vein and superior mesenteric vein thrombosis. Based on a 55% (normal 70-140%) plasma protein C level, he was diagnosed as having protein C deficiency. A trace of his family history showed that his elder brother also had protein C deficiency with a 50% plasma C level. Both patients received anticoagulant therapy. The younger brother showed good response. Unfortunately, the elder one suffered from recurrent episodes of variceal bleeding and received a life-saving splenectomy and devascularization. We herein remind clinicians that early screening and therapy are helpful in preventing late complications of protein C deficiency with portal vein thrombosis.     

Comparison of Fondaparinux and Low-Molecular-Weight Heparin in the Treatment of Portal Vein Thrombosis in Cirrhosis

BackgroundPortal vein thrombosis is the most common thrombotic complication in cirrhosis. About 60% of anticoagulated patients can achieve recanalization. Despite fondaparinux (FPX) theoretical advantages, data are lacking about safety and efficacy for treatment of portal vein thrombosis in cirrhosis.MethodsCirrhotic patients with portal vein thrombosis treated with FPX or low-molecular-weight heparin (LMWH) were retrospectively included. The extension of thrombosis at baseline and its evolution during anticoagulant treatment were evaluated. Patients were treated with LMWH or FPX at therapeutic dosage and reduction was considered in selected cases.ResultsThere were 124 patients included. Main portal vein branch, splenic, and superior mesenteric veins were involved in 84%, 13%, and 36% of cases, respectively. Forty-one patients (33%) were treated with FPX and 83 (67%) with LMWH. The probability of resolution of thrombosis at 36 months was significantly higher in patients treated with FPX than in those treated with LMWH (77% vs 51%; P = .001), particularly when prescribed at reduced dose. With multivariate analysis, the treatment with FPX (hazard ratio 2.38; P = .002) and use of a full dose (hazard ratio 1.78; P = .035) were independent predictors of portal vein full recanalization. Bleeding rate was higher in patients treated with FPX than in those treated with LMWH (27% vs 13%; P = .06).ConclusionsFPX appears to be more effective than LMWH in the treatment of portal vein thrombosis when used at reduced dose, also in complete thrombosis. FPX should be considered among possible treatments for portal vein thrombosis in cirrhosis.     

Risk of Venous Thromboembolism in Patients Infected with HIV: A Cohort Study

Introduction Human immunodeficiency virus (HIV) patients are at risk of developing thrombosis than general population. There are several intersecting mechanisms associated with HIV infection and antiviral therapy that are emerging, which may lead to vasculopathy and hypercoagulability in these patients.Methods We analyzed the HIV patients who followed up with our Vascular Medicine outpatient clinic with venous thromboembolism (VTE) over the past 3 years and followed them prospectively. The patients included were those who had minimum, regular follow-up of 3 months, with a Doppler scan in the beginning and last follow-up. Patients were analyzed for age, gender, race, site of thrombosis, coagulation factors, lipid panel, type of antiretroviral treatment, past or present history of infections or malignancy, CD4 absolute and helper cell counts at the beginning of thrombosis, response to treatment and outcome. Patients with HIV with arterial thrombosis were excluded.Results A total of eight patients were analyzed. The mean age was 49.87 years (range, 38-58 years). All were male patients with six patients having lower limb thrombosis, one patient with upper limb thrombosis related to peripheral inserted central catheter (PICC), and one patient had pulmonary embolism with no deep vein thrombosis. Most common venous thrombosis was popliteal vein thrombosis, followed by common femoral, superficial femoral and external iliac thrombosis. Two patients had deficiency of protein S, two had high homocysteine levels, one had deficiency of antithrombin 3, and one had increase in anticardiolipin Immunoglobulin antibody. All patients were taking nucleoside and nonnucleoside inhibitors but only two patients were taking protease inhibitors. There was history of lymphoma in one and nonsmall cell lung carcinoma in one patient. Three patients had past history of tuberculosis and one of these patients also had pneumocystis carinii pneumonia. The mean absolute CD4 counts were 383.25 cells/UL (range, 103-908 cells/UL) and helper CD4 counts were 22.5 cells/UL (range, 12-45 cells/UL). All were anticoagulated with warfarin or enoxaparin. There was complete resolution of deep vein thrombosis in two patients (one with PICC line thrombosis in 3 months and other with popliteal vein thrombosis in 1 year). There was extension of clot in one patient and no resolution in others. Seven patients are still alive and on regular follow-up.Conclusion Thrombosis in HIV patients is seen more commonly in middle aged, community ambulant male patients. Left lower limb involvement with involvement of popliteal vein is most common. Deficiency of protein S and hyperhomocystenaemia were noted in these patients. Most of these patients did not respond to therapeutic anticoagulation, but the extension of the thrombosis was prevented in majority of cases.     

High dose vitamin K3 infusion in advanced hepatocellular carcinoma

BACKGROUND AND AIM: The survival of patients with unresectable advanced hepatocellular carcinoma (HCC) with portal vein thrombosis is dismal. Current therapeutic options have limited efficacy. Vitamin K has been shown to have antitumor effect on HCC cells both in cell lines and patients with advanced HCC. The aim of this study was to assess the clinical efficacy of high dose vitamin K3 in the treatment of advanced HCC with portal vein thrombosis. METHODS: Forty-two consecutive patients with advanced HCC (Stage C according to BCLC staging system) with portal vein thrombosis were randomized into two groups: (i) high dose vitamin K3 (n = 23); and (ii) placebo (n = 19). The vitamin K3 was administered by i.v. infusion of 50 mg/day with daily increase of dose by 50 mg for 6 days, followed by 20 mg i.m. twice daily for 2 weeks. RESULTS: Of the 23 patients treated with vitamin K, one (4.3%) achieved complete response and three (13%) partial response, for a total of four (17.4%) objective responders overall. The overall mean survival was 8.9 +/- 8.8 months (median: 6; range 1-37 months) in the vitamin K group and 6.8 +/- 5.3 months (median: 5; range 1.5-21 months) in the placebo group (P = 0.552). The mean duration of survival was longer in patients in the vitamin K group who achieved objective response (22.5 +/- 12.2; median: 21; range 11-37 months) as compared to patients not achieving objective response (6.1 +/- 4.6; median: 5; range 1-16 months) (P = 0.0.002). Portal vein thrombosis resolved with complete patency in one (4.35%) patient. CONCLUSIONS: Treatment with high dose vitamin K produces objective response in 17% patients with improved survival in patients achieving objective response; however, it does not affect the overall survival.     

Symptomatic thrombotic events among Egyptian patients with systemic lupus erythematosus: special consideration for renal vein thrombosis

OBJECTIVE: To evaluate the prevalence of symptomatic thrombotic events among Egyptian patients with systemic lupus erythematosus (SLE), and to evaluate the frequency and the risk factors associated with renal vein thrombosis in those patients. METHODS: Fifty-four patients with SLE, 51 (94.4%) females, were involved in this study. All of them were submitted for abdominal sonography, chest X-ray, echocardiography, and Doppler of renal, abdominal and lower limb veins, with examination of data on clinical and laboratory profile. Abdominal CT, brain MRI, MRI both hips, CT chest and pulmonary scintigraphy were used when needed. RESULTS: Sixteen patients (29.6%) were diagnosed with symptomatic thrombotic events. Eight patients had more than one type of thrombosis. Two patients (3.7%) were diagnosed by Doppler as having renal vein thrombosis (RVT). This was confirmed by abdominal CT. One of them presented with nephrotic syndrome, graded by renal biopsy as World Health Organization (WHO) class V, and had positive anticardiolipin antibodies (ACL). The other patient had RVT and inferior vena cava (IVC) thrombosis, nephrotic syndrome, positive ACL, and died before renal biopsy was performed. Both of them were without history of peripheral thrombotic events. One patient was diagnosed with IVC thrombosis, lupus nephritis grade II, positive ACL, and diagnosed by abdominal CT. One patient was diagnosed with portal vein thrombosis and had positive ACL. One patient with retinal vessel thrombosis and positive ACL. Four patients had deep vein thrombosis (DVT). Recurrent miscarriages were reported in 4 patients (7.4%), skin ulcerations in 3 (5.6%), avascular necrosis of the hips in 4 (7.4%), stroke in 1 (1.9%), and pulmonary hypertension in 2 patients (3.7%). CONCLUSION: Sixteen SLE patients (29.6%) were diagnosed with symptomatic thrombotic events. RVT was detected in 2 patients representing 3.7% of all patients, and 12.5% of patients with thrombosis. Both patients with RVT presented with nephrotic syndrome.     

Case reports of portal vein thrombosis and bile duct stenosis after stereotactic body radiation therapy for hepatocellular carcinoma

The aim of this study was to evaluate portal vein and bile duct toxicity after stereotactic body radiation therapy (SBRT) for hepatocellular carcinoma (HCC). We retrospectively reviewed 63 patients who were administrated SBRT once for HCC. The prescribed doses were from 48 Gy in four fractions to 60 Gy in eight fractions. Portal vein thrombosis and bile duct stenosis were evaluated. The dose received by 2% of the volume (D₂) of the portal vein and bile duct was calculated. Portal vein thrombosis was observed in three patients (4.8%). Common points of these patients were Child–Pugh class B and D₂ of the portal vein 40 Gy or more (BED₃ ≥200 Gy). Bile duct stenosis was observed in one patient (1.6%). The patient had a history of cholangiocarcinoma and left hepatic lobectomy. Portal vein thrombosis may be necessary to be considered when SBRT for HCC is administrated to patients in higher Child–Pugh class with higher D₂ of the portal vein.     

Splanchnic vein thrombosis in severe acute pancreatitis: a 2-year, single-institution experience

ObjectivesThis study aimed to determine current practice in the management and outcome of splanchnic vein thrombosis complicating acute pancreatitis (AP).MethodsAn audit of prospectively collected data for all patients presenting with AP was conducted. Patients with splanchnic vein thrombosis were grouped according to vessel involvement and whether or not systemic anticoagulation was administered.ResultsOf 127 consecutive patients admitted with AP, 20 had splanchnic venous thrombosis; in all cases the thrombosis was associated with a severe attack of AP. Involvement of the splenic vein (SV), portal vein (PV) and superior mesenteric vein (SMV) was observed in 14, 10 and three patients, respectively. Involvement of more than one vessel was observed in six patients (SV and PV in four patients; SMV and SV in one patient; all three veins in one patient). Thromboses were colocalized with collections in 19 patients. Only four patients received systemic anticoagulation. Resolution of thrombosis was observed in six patients over a median of 77 days. No significant differences were observed in recanalization rates following anticoagulation (P= 0.076). No complications associated with systemic anticoagulation occurred. One patient developed liver failure associated with progressive PV thrombosis and one patient died.ConclusionsSplanchnic vein thrombosis is a relatively common observation in severe AP and is associated with pancreatic necrosis and peripancreatic collections. Recanalization is observed in almost a third of patients, irrespective of whether or not they receive systemic anticoagulation.     

Treatment of portal vein tumor thrombus using ¹²5Iodine seed implantation brachytherapy

We reported two cases of liver metastasis with portal vein tumor thrombus that developed after liver transplantation for hepatocellular carcinoma (HCC). Both the patients were women aged 43 and 55 years, who had liver metastasis and portal vein tumor thrombus formation after liver transplantations for HCC. For the treatment of portal vein tumor thrombus, (125)I seeds were implanted into the hepatic tissue under the guidance of preoperative computed tomography (CT) images with a total radiation dose of 130 Gy. Enhanced spiral CT scan was performed for evaluation of the liver at 12 and 16 wk after treatment. Thereafter, upper abdominal CT examination was performed every 2-3 mo. No severe complications associated with the (125)I seeds were seen in these two patients. The upper abdominal CT images (obtained after 3 and 4 mo of treatment) showed that the thrombosis reactions were complete reaction and restoration of the patency of the partially obstructed portal vein with partial obstruction. In the case with complete obstruction of the portal vein, the thrombosis was resolved completely, but blood flow could not be restored. After this treatment, one of the patients is still alive, while the other died within 6 mo after the treatment due to lung metastasis complicated with lung infection, leading to respiratory failure.     

CEUS： A new imaging approach for postoperative vascular complications after right-lobe LDLT

AIM： To investigate contrast-enhanced ultrasound （CEUS） for early diagnosis of postoperative vascular complications after right-lobe living donor liver transplantation （RLDLT）. METHODS： The ultrasonography results of 172 patients who underwent RLDLT in West China Hospital, Sichuan University from January 2005 to June 2008 were analyzed retrospectively. Among these 172 patients, 16 patients＇ hepatic artery flow and two patients＇ portal vein flow was not observed by Doppler ultrasound, and 10 patients＇ bridging vein flow was not shown by Doppler ultrasound and there was a regional inhomogeneous echo in the liver parenchyma upon 2D ultrasound. Thus, CEUS examination was performed in these 28 patients. RESULTS： Among the 16 patients without hepatic artery flow at Doppler ultrasound, CEUS showed nine cases of slender hepatic artery, six of hepatic arterial thrombosis that was confirmed by digital subtraction angiography and/or surgery, and one of hepatic arterial occlusion with formation of lateral branches. Among the two patients without portal vein flow at Doppler ultrasound, CEUS showed one case of hematoma compression and one of portal vein thrombosis,and both were confirmed by surgery. Among the 10 patients without bridging vein flow and with liver parenchyma inhomogeneous echo, CEUS showed regionally poor perfusion in the inhomogeneous area, two of which were confirmed by enhanced computed tomography （CT）, but no more additional information about bridging vein flow was provided by enhanced CT. CONCLUSION： CEUS may be a new approach for early diagnosis of postoperative vascular complications after RLDLT, and it can be performed at the bedside.     

肝硬化门静脉血栓无创性预测模型的研究

目的建立由血清指标和腹部B超组成的无创性诊断模型来预测肝硬化患者门静脉血栓（PVT）的形成。方法回顾性分析我院消化内科2007年1月～2010年1月确诊的肝硬化患者280例,随机抽取166例作为模型组,84例作为验证组,均行腹部螺旋CT增强扫描以了解有无门静脉血栓形成。记录患者肝硬化病因、年龄、性别以及入院后腹部B超和实验室常用指标,包括血常规、生化、凝血酶原时间、门静脉内径、脾脏厚度等参数。在模型组,对指标依次行单因素分析和多因素Logistic回归分析,筛选出相应的独立预测因子,在此基础上构建肝硬化门静脉血栓的指数模型,最后在独立的验证组中检验模型的诊断效率。结果模型组建立了一个由血浆D-二聚体、门静脉内径（MPV）、血小板（PLT）三项指标组成的综合指数模型（PVT index）。受试者工作曲线（ROC）分析显示PVT index值为7.2时,其预测肝硬化门静脉血栓形成的ROC曲线下面积（AUC）为0.864（0.753,0.946）,诊断敏感性为82.1%,特异性为86.7%,阳性预测值为93.53%,阴性预测值为64.58%,诊断精确性为81.77%。将PVT index以同样标准应用于验证组,ROC曲线下面积为0.886（0.785,0.962）,诊断精确性为82.16%。结论由血浆D-二聚体、门静脉内径、血小板等指标构建的无创性预测模型有助于早期预防和发现PVT的形成。