Impact of portal vein thrombosis on the efficacy of endoscopic variceal band ligation

BackgroundInfluence of portal vein thrombosis on efficacy of endoscopic variceal banding in patients with cirrhosis or extrahepatic portal vein obstruction has never been evaluated. Aim of the study was to assess influence of thrombosis on rate and time to eradication in cirrhosis and extrahepatic portal vein obstruction undergoing banding, compared to cirrhotic patients without thrombosis.MethodsRetrospective analysis of 235 consecutive patients (192 with cirrhosis without thrombosis, 22 cirrhosis and thrombosis and 21 extrahepatic portal vein obstruction) who underwent banding. Banding was performed every 2–3 weeks until eradication; endoscopic follow-up was performed at 1, 3, 6 months, then annually.ResultsEradication was achieved in 233 patients. Median time to eradication in cirrhotic patients with portal vein thrombosis vs. cirrhotic patients without thrombosis was 50.9 days (12–440) vs. 43.4 days (13–489.4); log-rank: 0.04; patients with extrahepatic portal vein obstruction vs. cirrhotic patients without thrombosis 63.9 days (31–321.6) vs. 43.4 days (13.0–489.4); log-rank: 0.008. Thrombosis was shown to be the only risk factor for longer time to eradication.ConclusionsPortal vein thrombosis per se appears to be the cause of a longer time to achieve eradication of varices but, once eradication is achieved, it does not influence their recurrence.     

Comparison between portal vein pressure and wedged hepatic vein pressure in hepatitis B-related cirrhosis

Portal vein pressure and wedged hepatic vein pressure were measured simultaneously in 21 patients with hepatitis B-related cirrhosis of the liver and were compared to pressure measured in six patients with idiopathic portal hypertension. No significant difference in the portal venous pressure gradient was found between patients with cirrhosis and those with idiopathic portal hypertension (17.3 +/- 4.3 mmHg (mean +/- S.D.) vs. 19.7 +/- 3.1 mmHg, P greater than 0.05). However, the difference between the portal and the hepatic venous pressure gradient was significantly smaller in patients with cirrhosis than in idiopathic portal hypertension patients (1.3 +/- 1.7 vs. 10.8 +/- 2.1 mmHg, P less than 0.001). An excellent correlation was found between portal vein pressure and wedged hepatic vein pressure in hepatitis B-related cirrhosis (r = 0.94, P less than 0.001). There was no linear relationship between the portal venous pressure gradient and varix size or bleeding episodes. We concluded that a close agreement existed between portal vein pressure and wedged hepatic vein pressure in hepatitis B-related liver cirrhosis. Therefore, measurement of wedged hepatic vein pressure reliably reflects portal vein pressure in these patients.     

Role of portal and splenic vein shunts and impaired hepatic extraction in the elevated serum bile acids in liver cirrhosis

To study the mechanism for the elevation of serum bile acids in liver cirrhosis, bile acid concentrations were measured in the portal, superior mesenteric, and splenic veins, using percutaneous transhepatic catheterization, and compared with those of peripheral veins in 41 patients with mild to moderately advanced cirrhosis. The demonstrated gradient of bile acid concentration was superior mesenteric vein greater than portal vein greater than peripheral vein nearly equal to splenic vein, suggesting that the superior mesenteric vein is the main route of transport for the intestinally absorbed bile acids. Bile acid concentrations in peripheral vein were correlated with the measured portal and splenic vein shunt indexes. The ursodeoxycholic acid oral tolerance test carried out in 10 patients during portal vein catheterization demonstrated that hepatic extraction of this bile acid was correlated with indocyanine green clearance and that it was inversely correlated with portal vein shunt index. These findings are consistent with the view that distorted hepatic blood flow has a significant role in elevating serum bile acid, at least in patients with moderately advanced liver cirrhosis.     

The free portal pressure in awake patients with and without cirrhosis of the liver

ABSTRACT— The free portal pressure was measured by percutaneous transhepatic catheterization of the portal vein in 106 patients with cirrhosis of the liver and in 19 patients without liver disease and with normal portography. Patients with cirrhosis had a median portal pressure of 38 cmH₂O and patients without liver disease had a median portal pressure of 16 cmH₂O. Among the cirrhotic patients the free portal pressure showed no relationship to etiology of cirrhosis, ascites, variceal bleedings or extrahepatic shunting. The median portal pressure was significantly higher in patients with (40 cmH₂O) than without (30 cmH₂O) gastroesophageal varices (p<0.01). The pressure was not related to the size of the varices.     

Comparison of splenoportography and transhepatic portography in the diagnosis of portal vein thrombosis

Accurate diagnosis and localization of thrombosis in the portal venous system is essential for proper surgical treatment. We compared the results of percutaneous transhepatic portography and splenoportography in 66 patients with cirrhosis of the liver. The two methods agreed on absence of thrombosis in 48, and in presence of thrombosis (verified later by surgery/autopsy) in four patients. In 12 patients an apparent thrombosis diagnosed by splenoportography was disproved by transhepatic portography, and vice versa in two patients. Free portal pressure and splenic pulp pressure did not differ significantly irrespective of the 'diagnosis' of thrombosis. We conclude, that transhepatic portography is better than splenoportography in making the diagnosis of thrombosis in the portal venous system although failure to visualize the splenic vein may indicate splenoportography.     

Incidence of portal vein thrombosis in liver cirrhosis. An angiographic study in 708 patients

Portal vein thrombosis was thought to be a common complication of liver cirrhosis in the past. The incidence of angiographically demonstrable portal vein thrombosis was studied in 708 consecutive patients with unequivocal cirrhosis seen in the past 10 yr in whom either transhepatic portography or superior mesenteric arterial portography clearly delineated the major portal vein system. Excluding 2 cases that were thought to be associated with past splenectomy, there were 4 cases of portal vein thrombosis related to cirrhosis, all in a decompensated stage. The calculated incidence of portal vein thrombosis was 0.573% of all cirrhotic patients without splenectomy in the past. They constituted 23.5% of the 17 cases of extrahepatic portal vein obstruction encountered during the same period. There were 78 cases of idiopathic portal hypertension similarly studied angiographically, and the incidence of portal vein thrombosis unrelated to splenectomy was 2.86%. A statistical survey based on 247,728 necropsies recorded in the Japan Autopsy Registries of 1975-1982 showed a 0.05489% incidence of portal vein thrombosis and a 6.58857% incidence of cirrhosis of all types among them, suggesting that portal vein thrombosis is not a common complication of cirrhosis in Japan in recent years.     

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.     

Hepatic venous pressure gradient determination in patients with hepatitis C virus-related and alcoholic cirrhosis

OBJECTIVES: Few data exist regarding the degree of portal hypertension in hepatitis C virus (HCV)-related cirrhosis, as the majority of studies have included mainly patients with alcoholic cirrhosis. This study was aimed at comparing the severity of portal hypertension in patients with HCV-related or alcoholic cirrhosis. METHODS: In total, 59 cirrhotic patients with portal hypertension (HCV-related in 34 cases and alcoholic in 25) underwent main right hepatic vein catheterization, with determination of the wedged and free hepatic venous pressures, and of hepatic venous pressure gradient (HVPG). RESULTS: HVPG values did not differ between the two groups of patients (19.4 +/- 6.0 mmHg vs 18.5 +/- 3.5 mmHg; P = 0.51). The prevalence and degree of oesophageal and gastric varices and portal hypertensive gastropathy did not correlate with the aetiology. Patients with viral cirrhosis had a lower prevalence of previous bleeding than those with alcoholic cirrhosis, despite a similar proportion of large varices in the two groups and similar HVPG levels. In both groups of patients, HVPG did not differ between patients with previous bleeds and those without. CONCLUSIONS: The degree of portal hypertension in cirrhotic patients does not correlate with the cause of the disease. Thus, current statements on the management of portal hypertension, although based upon studies including mainly patients with alcoholic cirrhosis, can be applied also to patients with viral-related cirrhosis.     

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.     

Direct transhepatic assessment of hepatic vein pressure and direction of flow using a thin needle in patients with cirrhosis and Budd-Chiari syndrome. An effective alternative to hepatic vein catheterization

Portal pressure can be accurately measured transhepatically with a Chiba needle. Since 1980, we have used transhepatic hepatic vein pressures as our zero reference for transhepatic portal pressure measurements. To validate the latter technique, we performed hepatic vein catheterization and transhepatic hepatic vein puncture in 11 patients undergoing portal pressure measurement. Transhepatic hepatic vein puncture was simple, providing pressures as reproducible as those obtained by hepatic vein and inferior vena cava catheterization. These pressures were minimally higher than simultaneous free hepatic vein and inferior vena caval pressures, possibly reflecting the more proximal location of the small hepatic vein radicles often entered by this technique. Transhepatic hepatic vein puncture is an accurate way to determine hepatic vein pressure and, combined with transhepatic portal vein pressure measurement, completely obviates the need for venous catheterization for portal pressure determination. Transhepatic hepatic vein pressure was also measured in 3 patients with Budd-Chiari syndrome. In these patients, transhepatic hepatic vein pressure was elevated and equaled or exceeded portal vein pressure. Abnormal venous collaterals were identified in all patients. Transhepatic portal pressure studies are also an appropriate way to evaluate patients suspected of having hepatic outflow obstruction.     

双导丝一步穿刺法及经皮肝穿刺门静脉造影在TIPS中的应用

目的探讨双导丝一步穿刺法及经皮肝穿刺门静脉造影在TIPS中的操作方法及应用价值。方法采用双导丝一步穿刺法及经皮肝穿刺门静脉造影法,对21例肝硬化并食管胃底静脉曲张破裂出血患者行TIPS术。结果 21例患者均成功实施TIPS手术,手术时间(152.41±50.38)min,手术穿刺针数(2.50±1.54)针,结果显示改良TIPS术可显著降低门静脉压力,改善肝功能,手术成功率100%,病死率5%。结论采用双导丝一步穿刺法及经皮肝穿刺门静脉造影的方法行TIPS术,能降低手术难度,值得临床推广应用。     

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.     

Acute portal vein thrombosis due to chronic relapsing pancreatitis: a fistula between a pancreatic pseudocyst and the splenic vein

Portal vein thrombosis (PVT) is a relatively common complication in patients with liver cirrhosis, but several other causes might play an important role in PVT pathogenesis. We present a case of alcoholic chronic pancreatitis complicated by acute extensive PVT. The patient was managed conservatively with danaparoid sodium at first, but the thrombosis gradually extended. We then tried radiological intervention using the direct transhepatic and transjugular intrahepatic postsystemic shunt approaches. Although we were able to successfully catheterize the percutaneous transhepatic portal vein (PTP), we could not achieve recanalization of the portal vein. Therefore, PTP catheterization and systemic intravenous infusion of urokinase and heparin was performed to prevent further progression of the thrombosis and cavernous transformation was finally achieved. Computed tomography (CT) and magnetic resonance cholangiopancreatography revealed a pancreatic stone which had possibly induced dilatation of the tail duct and formation of a pancreatic pseudocyst and caused intractable pancreatitis. We performed endoscopic retrograde cholangiopancreatography and placed a stent in the pancreatic duct, which completely cured the pancreatitis. Retrospectively, the previous CT with curved multi-planar reconstruction was reviewed and a fistula was detected between the pancreatic pseudocyst and splenic vein. We concluded that the etiology of the PVT was not only inflammatory extension from pancreatitis but also a fistula between the pancreatic duct and the splenic vein.     

肝硬化合并门静脉血栓形成的临床特点

目的分析肝硬化患者合并门静脉血栓形成(PVT)的临床特点及危险因素,了解该类患者药物性预防措施是否有效.方法 2008年1月至2011年3月各种原因的肝硬化住院患者共339例,将其分为两组,分别为肝硬化合并有门静脉血栓形成组及未合并有门静脉血栓组.记录患者年龄、性别、凝血酶原时间(PT)、总胆红素、白蛋白、肝硬化的病因...     

门静脉穿刺造影改良经颈静脉肝内门体分流术治疗门静脉高压上消化道出血

目的探讨经颈静脉肝内门体分流术(TIPS)的改良方法,提高其穿刺准确性和安全性,拓宽TIPS治疗适应证。方法在B超引导下经皮经肝穿刺门静脉右支,成功后引入带金标导管进行门静脉造影、测压、栓塞胃冠状静脉,然后将金标置于门静脉靶穿刺点,引导Rups-100穿刺门静脉,进行门静脉正、侧位造影,确保门静脉穿刺点在距离分叉2 cm以上。有门静脉血栓者用10F鞘管吸出,陈旧血栓用支架旷置。球囊扩张肝实质分流道,置入支架,造影测压。结果20例肝硬化门静脉高压上消化道出血患者用改良TIPS方法治疗均获得成功,上消化道出血即刻得到控制;20例患者共穿刺37针,平均(1.85±0.67) 针;门静脉压力由(30.5±1.1)mm Hg降至(16.9±0.9)mm Hg,治疗前后门静脉压力差异有统计学意义(P<0.05)。4例间接门静脉造影未见显影放弃TIPS治疗的患者,经改良TIPS治疗后也获得成功。20例患者共放置25枚支架,未出现一例与TIPS操作有关的并发症。结论直接门静脉穿刺造影金标定位引导TIPS 操作,可提高TIPS穿刺准确性和安全性,进一步拓宽了TIPS治疗适应证,有利于TIPS技术进一步推广。     

Long-term follow-up study of adult patients with non-cirrhotic obstruction of the portal system: comparison with cirrhotic patients.

Thirty-two patients with non-cirrhotic portal system obstruction and oesophageal varices of non-malignant etiology were recruited over 13 years. Diagnosis was based on the presence of oesophageal varices at endoscopy, minor alterations in liver function tests and liver histology, a low hepatic venous pressure gradient, and pertinent angiographic patterns. Twenty-three had portal vein thrombosis, nine had splenic vein thrombosis. Twenty-one had idiopathic portal vein obstruction, 11 had secondary obstruction. The outcome was compared with a group of 32 patients with cirrhosis and portal hypertension, matched for age, Child-Pugh class, previous history of gastrointestinal bleeding, and size of oesophageal varices. Patients with non-cirrhotic obstruction of the portal system were followed for up to 171 months (mean 94 months). During follow-up ten patients had gastrointestinal bleeding, and eight died (five of gastrointestinal bleeding). After 6 years of follow-up, the cumulative risk of gastrointestinal bleeding was 24%, the cumulative risk of death was 17%, and the cumulative risk of death from gastrointestinal bleeding was 14%. Cumulative probability of death by any cause and the probability of gastrointestinal bleeding were significantly lower in patients with non-cirrhotic obstruction of the portal system than in patients with cirrhosis comparable for liver function and portal hypertension (p = 0.04 for both). The cumulative probability of death by gastrointestinal bleeding was not significantly different. In conclusion, the prognosis for non-cirrhotic obstruction of the portal system is significantly better than for patients with cirrhosis with comparable levels of liver function impairment and severity of portal hypertension.     

Development of portal vein thrombosis complicating idiopathic portal hypertension. A case report

A 58-yr-old woman with biopsy-proven idiopathic portal hypertension presented with ascites and pretibial pitting edema. On admission, ultrasonic Doppler flowmetry demonstrated hepatopetal flow of a markedly reduced velocity in the portal vein, hepatofugal flow in the splenic vein, and a large spontaneous splenorenal shunt. The patient spontaneously developed hepatic encephalopathy 1 mo later. Percutaneous transhepatic portography demonstrated mural thrombi at the porta hepatis after the catheter had penetrated the mural thrombi without resistance; there was also a long retention of contrast medium in the portal vein. 99mTc-Macroaggregated albumin instilled into the superior mesenteric vein was caught in the lungs, and no activity entered the liver. Measurements of ammonia and immunoreactive insulin clearly indicated that superior mesenteric venous blood was shunted through the splenic vein and the splenorenal shunt. Subsequent ultrasonic examination with Doppler flowmetry suggested further growth of the thrombi and lack of blood flow in the portal vein. Although the procedure of percutaneous transhepatic catheterization could have contributed to the growth of thrombi, it is more likely that the thrombosis in the portal vein was a sequela to idiopathic portal hypertension, and was growing at the time of catheterization. This case may be of significance in the understanding of the relationship between idiopathic portal hypertension and extrahepatic portal obstruction.     

Hemodynamic effects of nifedipine on hepatic venous pressure gradient in patients with portal hypertension

The effect of Nifedipine on hepatic venous pressure gradient (HVPG) was determined in 10 patients with portal hypertension due to cirrhosis of the liver, and in 7 control subjects, by hepatic vein catheterization. Twenty min. after sublingual application of 10 mg Nifedipine, patients and controls showed significant hemodynamic changes in the systemic circulation. In contrast, HVPG after Nifedipine was not statistically different from the basal values--neither in patients with portal hypertension (p = 16.6 +/- 5.2 mmHg vs 17.9 +/- 5.3 mmHg) nor in the control subjects (p = 2.9 +/- 1.1 mmHg vs. 1.0 mmHg). We conclude that calcium entry blockade by Nifedipine is not effective in acutely reducing portal venous pressure.     

Propranolol and haemodynamic response in cirrhosis.

In the present study, we compared cirrhotic patients who had a decrease in the hepatic venous pressure gradient after propranolol intake to patients without a decrease. Twenty patients with cirrhosis and oesophageal varices were investigated during hepatic vein catheterization before and 90 min after an oral dose of 80 mg propranolol. The hepatic venous pressure gradient decreased by 12.6% (19.0 +/- 4.7 to 16.3 +/- 3.6 mm Hg, p less than 0.05). Eight (40%) out of 20 patients had a decrease of less than 10% in protal pressure (non-responders). Responders had a higher baseline cardiac index than non-responders (3.79 +/- 0.74 vs. 2.83 +/- 0.53 1.min-1.m-2; p less than 0.01). No difference in the effect of propranolol on portal pressure was observed between patients with or without ascites, or between Child-Turcotte A, B, and C class patients. Our results suggest that cirrhotic patients who respond to oral propranolol with a decrease in portal pressure are more hyperdynamic than those without a significant fall in portal pressure.     

肝硬化患者门静脉血栓形成危险因素的Logistic回归分析

目的研究肝硬化患者门静脉血栓（PVT）形成的相关危险因素。方法回顾性分析我院消化内科2007—2008年确诊的肝硬化患者80例,其中19例肝硬化PVT患者作为血栓组,61例肝硬化非血栓患者作为对照组,收集相关临床资料,对可能影响PVT形成的因素进行单因素分析和Logistic回归模型分析。结果Logistic回归模型分析结果显示,血浆D-二聚体、门静脉宽度（MPV）、血小板（PLT）是肝硬化患者PVT形成的独立危险因素（P值分别为0.003、0.012、0.036）。结论肝硬化患者应注意监测血浆D-二聚体、门静脉宽度、血小板等指标,以便早期预防和发现PVT的形成。