血管介入在肝硬化脾功能亢进中的应用研究进展

肝硬化是引起继发性脾功能亢进的常见原因,脾功能亢进常常导致患者外周血细胞降低,当白细胞和血小板严重减少时,患者易发生自发性感染和出血,进而加重病情,增加死亡风险.目前对肝硬化脾功能亢进发生机制尚不十分清楚,亦无脾亢治疗适应症标准和合适推荐方法,临床上脾亢的治疗方式有:脾切除术,血管介入术,局部热消融及脾动脉结扎术等.血管介入术主要涉及经颈静脉肝内门体分流术(transjugular intrahepatic portosystemic shunt,TIPS)和部分脾动脉栓塞术(partial splenic embolization,PSE),其中TIPS是治疗肝硬化门脉高压并发症的有效方法,它能有效降低门脉压力,但能否缓解脾亢仍存在争议;PSE对脾亢有一定程度的缓解;TIPS联合PSE应用,在有效降低门脉高压同时对脾亢也能一定程度缓解.本文就血管介入在肝硬化脾亢应用研究进展进行综述.     

Combination treatment of partial splenic embolization, endoscopic embolization and transjugular retrograde obliteration for complicated gastroesophageal varices

The treatment of complicated gastroesophageal varices with a gastrorenal shunt and portal hypertensive gastropathy has not yet been established. We were able to control a case of complicated large gastroesophageal varices with gastrorenal shunt and portal hypertensive gastropathy using a combination treatment of partial splenic embolization, endoscopic embolization and transjugular retrograde obliteration. We first applied partial splenic embolization to reduce the hyperdynamic cycle of portal hypertension and to treat thrombocytopenia. We secondarily applied endoscopic embolization for the esophageal varices. Transjugular retrograde obliteration was performed for the gastric varices 14 days after endoscopic embolization. The wedged hepatic venous pressure had not changed after transjugular retrograde obliteration. After the combination treatment, the gastroesophageal varices were successfully obliterated, but portal hypertensive gastropathy did not worsen. The platelets count, arterial ketone body ratio and ICGR15 were improved. Partial splenic embolization was useful to protect side effects of endoscopic embolization and transjugular retrograde obliteration. We conclude that the combination treatment of partial splenic embolization, endoscopic embolization and transjugular retrograde obliteration is a rational, effective and safe treatment for complicated gastroesophageal varices with gastrorenal shunt and portal hypertensive gastropathy.     

双介入治疗肝硬化门脉高压和脾功能亢进症

目的 探讨经颈内静脉肝内门体分流术(Transjugular intrahepatic portosystemic shunt,TIPS)和部分脾栓塞术(Partial splenic embolization,PSE)联合治疗肝硬化门脉高压及脾功能亢进症的疗效.方法 30例均为肝硬化门脉高压及脾功能亢进症患者,行TIPS术后再行PSE术.用超声检测门、脾静脉内径、门脉主干血流速度、脾脏长径和厚度;血细胞分析仪检测血象.结果 30例患者TIPS术后的门脉压力较术前降低(P＜0.01).门、脾静脉内径较术前缩小(P＜0.01),门脉主干血流速度较术前增快(P＜0.01);术后3～6月的脾脏长径及厚度、白细胞、血小板及血红蛋白较术前均无明显变化(P＞0.05).30例患者PSE术后的门、脾静脉内径、门脉主干血流速度与TIPS术后的比较无明显变化(P＞0,05);而白细胞、血小板及血红蛋白较TIPS术后明显升高(P＜0.01),脾脏长径和厚度较TIPS术后缩小(P＜0.05).结论 联合TIPS和PSE术治疗,能有效降低肝硬化患者的门脉压力,同时又能缓解脾功能亢进.     

Portal-hypertensive gastropathy

In the present article we describe updated information concerning the clinical feature of portal-hypertensive gastropathy (PHG), which is characterized by mucosal and submucosal vascular dilatation without inflammation. Although this lesion represents non-variceal bleeding, there is a wide variation of its prevalence. Portal pressure and some humoral factors may play important roles in its pathogenesis. Gastric acid secretory activity is reduced, whereas the gastric mucosal barrier is impaired. With regard to gastric mucosal haemodynamics, whether ‘overflow’ (i.e. active congestion) or ‘stasis’ (i.e. passive congestion) cause gastric mucosal hyperaemia is not known. A severe lesion is a potential source of bleeding, while mild lesions are of little clinical significance and endoscopic variceal obliteration aggravates PHG in some patients. In the treatment of PHG, pharmacological (e.g. propranolol), surgical (e.g. portosystemic shunt) and radiological (e.g. transjugular intrahepatic portosystemic shunt) procedures may be useful in preventing bleeding from PHG.     

Transhepatic catheter-directed thrombolysis for portal vein thrombosis after partial splenic embolization in combination with balloon-occluded retrograde transvenous obliteration of splenorenal shunt

A 66-year-old woman underwent partial splenic embolization (PSE) for hypersplenism with idiopathic portal hypertension (IPH). One week later, contrast-enhanced CT revealed extensive portal vein thrombosis (PVT) and dilated portosystemic shunts. The PVT was not dissolved by the intravenous administration of urokinase. The right portal vein was canulated via the percutaneous transhepatic route under ultrasonic guidance and a 4 Fr. straight catheter was advanced into the portal vein through the thrombus. Transhepatic catheter-directed thrombolysis was performed to dissolve the PVT and a splenorenal shunt was concurrently occluded to increase portal blood flow, using balloon-occluded retrograde transvenous obliteration (BRTO) technique. Subsequent contrast-enhanced CT showed good patency of the portal vein and thrombosed splenorenal shunt. Transhepatic catheter-directed thrombolysis combined with BRTO is feasible and effective for PVT with portosystemic shunts.     

Effect of transjugular intrahepatic portosystemic shunt formation on portal hypertensive gastropathy and gastric circulation

OBJECTIVES: The aim of this study was to investigate the effect of a transjugular intrahepatic portosystemic shunt (TIPS) on portal hypertensive gastropathy (PHG) and gastric hemodynamics. METHODS: A total of 16 patients with cirrhosis and portal hypertensive gastropathy were prospectively studied. Of these, 12 patients underwent TIPS for esophageal varices and four for refractory ascites. Gastric mucosal blood flow (GMBF) was assessed by laser Doppler flowmeter, and total blood flow (TBF) in submucosa and mucosa by near-infrared endoscopy. Portal venous pressure was obtained by a transducer during the TIPS procedure. The severity of portal hypertensive gastropathy was classified as none, mild, or severe. The examinations were performed before and 2 wk after the procedure. RESULTS: TIPS significantly reduced portal venous pressure. PHG improved in all four patients with severe PHG and in five of 12 patients with mild PHG after treatment. Gastric mucosal blood flow increased from 49.0 to 55.6 ml/min/100 g after TIPS. In contrast, TBF decreased from 0.35/s to 0.27/s after treatment. Liver function tests showed no significant changes before and after the procedure. CONCLUSIONS: It is considered that TIPS may have a beneficial effect on PHG at least for a short time. The mechanism by which PHG improves may be closely related to the improvement of the injured gastric perfusion in cirrhotic patients with PHG.     

Treatment of post-shunt portal systemic encephalopathy by embolization of the shunt

Operative ligation of portosystemic shunts is effective in controlling chronic portosystemic encephalopathy (CPSE) but is associated with significant mortality. Review of the records of five patients with CPSE treated with radiologic occlusion procedures showed that these are suitable alternatives to surgery. Three patients had alcoholic cirrhosis, one had hepatic fibrosis from schistosomiasis, and one had post-necrotic cirrhosis. All had CPSE with progressive, severe cerebral impairment refractory to clinical treatment. Four patients had a spontaneous splenorenal shunt, and one had a surgically created mesocaval shunt (MCS). Partial splenic embolization was performed in two patients, direct shunt embolization was performed via percutaneous transhepatic portography in two other patients, and an MCS embolization was performed in one patient through the inferior vena cava. In four patients embolization controlled the CPSE. In the remaining patient it could not be evaluated because of his premature death from intraabdominal bleeding, a late complication of the procedure. Interventional radiologic procedures are effective in the control of CPSE in selected patients.     

The effects of transjugular intrahepatic portosystemic shunt on portal hypertensive gastropathy

In addition to variceal bleeding, haematemesis may occur due to haemorrhagic gastritis in patients with portal hypertension. This has been known as portal hypertensive gastropathy (PHG). We have evaluated the effects of the transjugular intrahepatic portosystemic shunt (TIPS) on portal venous pressure (PVP) and endoscopic gastric mucosal changes observed in patients with portal hypertension. We performed TIPS in 12 patients with complications due to portal hypertension as follows: variceal bleeding in nine patients (bleeding from oesophageal varices in seven and gastric varices in two), refractory ascites in three and haemorrhage from severe PHG in one. Endoscopic examinations were performed before and after TIPS for all patients. Changes of PVP and gastric mucosal findings on endoscopy were analysed. Before TIPS, PHG was seen in 10 patients. Portal venous pressure decreased from an average of 25.1 ± 8.8 to 17.1 ± 6.2 mmHg after TIPS ( P < 0.005). On endoscopy, PHG improved in nine of 10 patients. Oesophagogastric varices improved in eight of 11 patients. In one patient with massive haematemesis, haemorrhage from severe PHG completely stopped after TIPS. Because TIPS effectively reduced PVP, this procedure appeared to be effective for the treatment of uncontrollable PHG.     

Portal hypertensive gastropathy with portal thrombosis successfully treated with partial splenic embolization

A 60-year-old man with alcoholic liver cirrhosis was admitted to our hospital with severe anemia and tarry stool. Upper gastrointestinal endoscopy revealed grade 4 esophageal varices without bleeding and severe portal hypertensive gastropathy (PHG) of the fornix of the stomach with oozing. These findings suggested that PHG was the cause of progression of anemia. Abdominal computed tomography demonstrated no enhancement of the main portal vein and its first branches, indicating portal thrombosis and cavernous transformation. The patient underwent partial splenic embolization (PSE) to reduce portal hypertension. Two months after PSE was performed, upper gastrointestinal endoscopy showed improvement of PHG and endoscopic variceal ligation was performed to treat the esophageal varices. Contrast-enhanced CT revealed partial enhancement of the main portal vein indicating improvement of portal thrombosis. One year after PSE, hemoglobin had increased from 6.0 to 11.0 g/dl without blood transfusion. Moreover, albumin level had risen from 2.8 to 3.7 g/dl, cholinesterase from 51 to 150 IU/l, and prothrombin time from 47% to 66%. PSE can be an effective alternative for the management of severe PHG with portal vein thrombosis, and it might also be effective in improving liver function.     

Combination treatment of transjugular retrograde obliteration and endoscopic embolization for portosystemic encephalopathy with esophageal varices

The treatment of chronic portosystemic encephalopathy with esophageal varices has not yet been established. We were able to control a case of chronic portosystemic encephalopathy with esophageal varices using a combination treatment of transjugular retrograde obliteration and endoscopic embolization. A 57-year-old man came to our hospital in a confused, apathetic and tremulous state. The grade of encephalopathy was II. The plasma ammonia level was abnormally elevated to 119 microg/dL, and the ICGR15 was 59%. Endoscopic examination revealed nodular esophageal varices with cherry-red spots. There were no gastric varices. Ultrasonography and CT revealed liver cirrhosis with a splenorenal shunt. We first applied endoscopic embolization for the esophageal varices before transjugular retrograde obliteration. We injected 5% ethanolamine oleate with iopamidol retrogradely into the esophageal varices and their associated blood routes under fluoroscopy and obliterated the palisade vein, the cardiac venous plexus and left gastric vein. Transjugular retrograde obliteration was performed 14 days after endoscopic embolization. Retrograde shunt venography visualized the splenorenal shunt and communicating route to the retroperitoneal vein. There was no communicating route to the azygos vein. After obliteration of the communicating route to the retroperitoneal vein with absolute ethanol, 5% ethanolamine oleate with iopamidol was injected into the splenorenal shunt as far as the root of the posterior gastric vein. After transjugular retrograde obliteration, the encephalopathy improved to grade 0 even without the administration of lactulose and branched-chain amino acid. The plasma ammonia level and ICGR15 were reduced to 62 microg/dL and 26%. We conclude that combination treatment of transjugular retrograde obliteration and endoscopic embolization is a rational, effective and safe treatment for chronic portosystemic encephalopathy complicated with esophageal varices.     

Splenogastrorenal shunt in portal hypertension: a little known entity. Study of 6 cases and review of the literature

The authors report 6 cases of portal hypertension with gastrorenal shunt. This shunt did not arise from the left gastric vein, but from the splenic vein. Portal hypertension was related to alcoholic cirrhosis in 3 cases, to extensive portal thrombosis in 2 cases, and to nodular regenerative hyperplasia of the liver in one case. A gastrointestinal hemorrhage revealed portal hypertension and the liver disease in the 3 cases of alcoholic cirrhosis and complicated the course of the disease in the other cases. Hemorrhage was either massive and life-threatening or often recurred. It was related to a rupture of fundic varices in all cases. The fundic varices were not associated with esophageal varices in the 3 cases of cirrhosis. The degree of portal hypertension was above 20 mm Hg, as assessed by the portohepatic gradient (one case), or the pressure gradient between a tributary portal system vein and the inferior vena cava during laparotomy (5 cases). Definitive control of hemorrhage could not be achieved by endoscopic variceal sclerotherapy (2 cases) or percutaneous transhepatic embolization (one case). Portacaval shunt or splenectomy was performed in 5 cases. These findings suggest that spontaneous splenogastrorenal shunt is a clinical and hemodynamic entity which requires specific treatment when associated with gastric variceal bleeding.     

Splenic artery embolization for variceal hemorrhage following blocked distal splenorenal shunt

A blocked distal splenorenal shunt presents with torrential bleeding from gastric varices. Reoperation in the presence of portal hypertension in an unstable patient is difficult. Two patients with a blocked distal splenorenal shunt were subjected to splenic artery embolization. This stopped variceal bleeding from gastric varices resulting from the congested spleen due to thrombosis of the splenic vein. The procedure was successful in stopping the acute bleed in both patients. There were no serious complications or recurrent variceal bleeding and the varices were collapsed at one year on follow-up endoscopy. Splenic artery embolization is a safe and effective minimally invasive treatment for patients with bleeding from a blocked distal splenorenal shunt.     

Portal hypertension and gastrointestinal bleeding:Diagnosis,prevention and management

Bleeding from esophageal varices is a life threatening complication of portal hypertension.Primary prevention of bleeding in patients at risk for a first bleeding episode is therefore a major goal.Medical prophylaxis consists of non-selective beta-blockers like propranolol or carvedilol.Variceal endoscopic band ligation is equally effective but procedure related morbidity is a drawback of the method.Therapy of acute bleeding is based on three strategies:vasopressor drugs like terlipressin,antibiotics and endoscopic therapy.In refractory bleeding,self-expandable stents offer an option for bridging to definite treatments like transjugular intrahepatic portosystemic shunt(TIPS).Treatment of bleeding from gastric varices depends on vasopressor drugs and on injection of varices with cyanoacrylate.Strategies for primary or secondary prevention are based on non-selective beta-blockers but data from large clinical trials is lacking.Therapy of refractory bleeding relies on shuntprocedures like TIPS.Bleeding from ectopic varices,portal hypertensive gastropathy and gastric antral vascular ectasia-syndrome is less common.Possible medical and endoscopic treatment options are discussed.     

Prevention of variceal recurrence, bleeding, and death in cirrhosis patients with hypersplenism, especially those with severe thrombocytopenia

BACKGROUND/AIMS: We investigated the impact of different treatments on the prognosis of cirrhosis patients with esophageal varices and thrombocytopenia. METHODOLOGY: This prospective study enrolled 52 cirrhosis patients with esophageal varices and hypersplenism (platelet count < 50,000/mm3). In 26 patients, endoscopic variceal ligation plus partial splenic embolization were performed, while endoscopic variceal ligation alone was done in 26 patients. Endoscopic variceal ligation was repeated until complete eradication of varices was achieved. Partial splenic embolization was performed using the Seldinger method and embolic material was injected until a 60% to 80% reduction of splenic blood flow was achieved. The primary endpoints during the follow-up period included recurrence of varices, variceal bleeding, and death. RESULTS: Comparison of endoscopic variceal ligation plus partial splenic embolization with endoscopic variceal ligation alone by multivariate analysis showed a relative risk ratio of 0.390 (95% CI [0.178-0.854]; p = 0.024) for new varices, 0.191 (95% CI [0.047-0.780]; p = 0.021) for variceal bleeding, and 0.193 (95% CI [0.053-0.699]; p = 0.012) for death. CONCLUSIONS: These results suggest that endoscopic variceal ligation plus partial splenic embolization can prevent variceal recurrence, bleeding, and death in cirrhosis patients with esophageal varices and thrombocytopenia.     

Partial splenic embolization.

Partial splenic embolization (PSE) is a non-surgical procedure developed to treat hypersplenism as a result of hepatic disease and thus avoid the disadvantages of splenectomy. A femoral artery approach is used for selective catheterization of the splenic artery. Generally, the catheter tip is placed as distally as possible in an intrasplenic artery. After an injection of antibiotics and steroids, embolization is achieved by injecting 2-mm gelatin sponge cubes suspended in a saline solution containing antibiotics. PSE can benefit patients with thrombocytopenia, esophagogastric varices, portal hypertensive gastropathy, encephalopathy, liver dysfunction, splenic aneurysm, and splenic trauma. The contraindications of PSE include secondary splenomegaly and hypersplenism in patients with terminal-stage underlying disease; pyrexia or severe infections are associated with a high risk of splenic abscess after PSE. Complications of PSE include daily intermittent fever, abdominal pain, nausea and vomiting, abdominal fullness, appetite loss, and postembolization syndrome. Decreased portal-vein flow and a rapid increase in the platelet count after excessive embolization may cause portal-vein or splenic-vein thrombosis.     

Gastric antral vascular ectasia in cirrhotic patients: absence of relation with portal hypertension

BACKGROUND: Portal hypertensive gastropathy and gastric antral vascular ectasia (GAVE) are increasingly recognised as separate entities. The pathogenic role of portal hypertension for the development of GAVE is still controversial. AIMS: To evaluate the effects of portal decompression on chronic bleeding related to GAVE in cirrhotic patients. METHODS: Eight patients with cirrhosis and chronic blood loss related to GAVE were included. GAVE was defined endoscopically and histologically. RESULTS: All patients had severe portal hypertension (mean portocaval gradient (PCG) 26 mm Hg) and chronic low grade bleeding. Seven patients underwent transjugular intrahepatic portosystemic shunt (TIPS) and one had an end to side portacaval shunt. Rebleeding occurred in seven patients. In these, TIPS was found to be occluded after 15 days in one patient; in the other six, the shunt was patent and the PCG was below 12 mm Hg in five. In the responder, PCG was 16 mm Hg. Antrectomy was performed in four non-responders; surgery was uneventful, and they did not rebleed after surgery, but two died 11 and 30 days postoperatively from multiorgan failure. In one patient, TIPS did not control GAVE related bleeding despite a notable decrease in PCG. This patient underwent liver transplantation 14 months after TIPS; two months after transplantation, bleeding had stopped and the endoscopic appearance of the antrum had normalised. CONCLUSIONS: Results suggest that GAVE is not directly related to portal hypertension, but is influenced by the presence of liver dysfunction. Antrectomy is a therapeutic option when chronic bleeding becomes a significant problem but carries a risk of postoperative mortality.     

脾动脉栓塞治疗肝硬化继发脾脏功能亢进的临床效果观察

目的 探讨脾动脉栓塞术（PSE）治疗肝硬化继发脾脏功能亢进的临床效果.方法 选取我院肝硬化继发脾脏功能亢进患者80例,其中研究组48例,行脾动脉栓塞术;对照组32例,行脾脏切除术,比较两组患者的出血量、住院时间、术后恢复、并发症等.结果 与对照组比较,研究组患者的住院时间缩短、出血量减少,差异有统计学意义（P＜0.05）;两组患者术后不良反应比较,差异无统计学意义（P ＞0.05）;PSE后脾局部梗死后门静脉内径减小,与对照组比较差异无统计学意义（P＞0.05）.结论 PSE治疗肝硬化继发脾脏功能亢进临床效果显著,微创易恢复,门静脉宽度变窄,门脉压力降低.     

Treatment of bleeding from portal hypertensive gastropathy by portacaval shunt

Portal hypertensive gastropathy is a vascular disorder of the gastric mucosa distinguished by ectasia of the mucosal capillaries and submucosal veins without inflammation. During 1988 to 1993,12 patients with biopsy-proven cirrhosis (10 alcoholic, 2 posthepatitic) were evaluated and treated prospectively by portacaval shunt for active bleeding from severe portal hypertensive gastropathy. Eleven patients had been hospitalized for bleeding three to nine times previously, and one was bleeding uncontrollably for the first time. Requirement for blood transfusions ranged from 11 to 39 units cumulatively, of which 8 to 30 units were required specifically to replace blood lost from portal hypertensive gastropathy. Admission findings were ascites in 9 patients, jaundice in 8, severe muscle wasting in 10, hyperdynamic state in 9. Child's risk class was C in 7, B in 4, A in 1. Ten of the 12 patients had previously received repetitive endoscopic sclerotherapy for esophageal varices, which has been reported to precipitate portal hypertensive gastropathy. Eight patients had failed propranolol therapy for bleeding. Portacaval shunt was performed emergently in 11 patients and electively in 1, and permanently stopped bleeding in all by reducing the mean portal vein—inferior vena cava pressure gradient from 251 to 16 mm saline. There were no operative deaths, and two unrelated late deaths after 13 and 24 months. During 1 to 6.75 years of follow-up, all shunts remained patent by ultrasonography, the gastric mucosa reverted to normal on serial endoscopy, and there was no gastrointestinal bleeding. Recurrent portal-systemic encephalopathy developed in only 8% of patients. Quality of life was generally good. It is concluded that portacaval shunt provides definitive treatment of bleeding portal hypertensive gastropathy by eliminating the underlying cause, and makes possible prolonged survival with an acceptable quality of life.     

Therapeutic effects of endoscopic variceal ligation combined with partial splenic embolization for portal hypertension

AIM: To evaluate the feasibility of a new strategy of endoscopic variceal ligation combined with partial splenic embolization (EVL-PSE) for patients with cirrhosis and portal hypertension. METHODS: From May 1999 to May 2002, 41 cases with cirrhosis and portal hypertension underwent EVL-PSE. Hemodynamics of the main portal vein (MPV), the left gastric vein (LGV) and azygos vein, including maximum velocity, flow rate and vein diameter, were assessed by Doppler ultrasonography. RESULTS: One case died from pulmonary artery embolism. One case complicated with splenic abscess was successfully managed by laparotomy. The esophageal varices and hypersplenism were well controlled after EVL-PSE in other patients. After EVL-PSE, the flow rate and velocity of MPV was significantly reduced (P<0.05), as well as the flow rate of the LGV and azygos vein. During the follow-up, no recurrent bleeding was found. CONCLUSION: Being more convenient and less invasive, EVL-PSE is hopeful to be a proper intervention strategy for portal hypertensive patients with impaired hepatic function or those intolerant to shunting or devascularization surgery.     

Arterioportal Fistula: A Role for Pre-TIPSS Arteriography and Hepatic Venous Pressure Measurements

A 70-yr-old male presented with massive upper gastrointestinal bleeding secondary to esophageal varices. Because the bleeding was not controlled by sclerotherapy or vasopressin and nitroglycerin, the patient was evaluated for a transjugular intrahepatic portosystemic shunt. Preprocedure arteriography was performed because the etiology of the portal hypertension was uncertain. The arteriogram revealed a hepatic artery to portal vein fistula. Hepatic venous pressure measurements documented an elevated hepatic venous pressure gradient, which diminished dramatically upon embolization of the fistula. Rebleeding from the varices was associated with reestablishment of the fistula via collaterals and elevation of the hepatic venous pressure gradient. The case is presented to establish a role for arteriography prior to transjugular intrahepatic portosystemic shunting, especially in patients with unexplained portal hypertension, and to establish the potential value of hepatic venous pressure measurements in the treatment of arterioportal fistulas.