脾切除贲门周围血管离断术治疗470例门静脉高压症疗效分析

目的总结脾切除贲门周围血管离断术治疗不合并肝癌及胆管癌的门静脉高压症患者的疗效。方法对不合并肝癌及胆管癌的门静脉高压症患者行脾切除贲门周围血管离断术并随访470例,其中肝炎后肝硬化436例,占92.8%。结果出血患者424例,手术止血率为99.3%(421/424),围手术期病死率为1.4%(6/424),主要死亡原因是上消化道出血、肝肾功能衰竭;急症及择期手术424例,预防手术46例,预防手术围手术期无死亡。平均随访时间4年,出血患者术后复发出血率为3.2%(15/470),预防手术后无出血,肝性脑病发生率为1.9%(9/470)。结论脾切除贲门周围血管离断术防治门静脉高压症引起的上消化道出血效果好。合理选择手术适应证及手术时机、完全彻底断流、术后早期抗凝及近端脾静脉结扎预防术后肝外门静脉系统血栓形成是提高手术疗效的必要措施。

阻塞性黄疸肝外型门静脉高压症1例诊治经过

病例；男，51岁。因胆总管结石曾行内镜下括约肌切开取石（EST）加鼻胆管引流术（ENBD）。术前腹部CT和磁共振胆胰管造影（MRCP）检查均提示胆管无狭窄，肝、脾形态正常。

食管吻合门奇断流术防治食管静脉曲张破裂出血疗效观察

目的:探讨食管吻合门奇静脉断流术防治门脉高压症食管胃底静脉曲张破裂出血(EGVB)的疗效。方法:回顾性分析20例肝硬化门脉高压症EGVB患者行食管吻合门奇静脉断流术治疗的临床资料和随访结果,判断其疗效。结果:全组病例围手术期恢复顺利,3例出现吻合口中度狭窄,行胃镜下气囊扩张治疗后缓解。无腹腔内出血、食管吻合口漏、肝性脑病、脾静脉血栓、肺感染等并发症发生,无死亡病例。术后3～6月行上消化道造影或胃镜检查显示:16例食道下段、胃底静脉曲张消失,4例尚有轻度的食管静脉曲张;13例术前有门脉高压性胃病的患者中9例术后改善明显,4例无明显改变。结论:食管吻合门奇静脉断流术防治门脉高压症EGVB效果良好,并有效改善门脉高压性胃病,预防再发出血。

肝硬化患者门静脉压力及静脉曲张评估进展

门静脉高压症是一类主要由肝硬化逐步演变而来的疾病,严重威胁人类健康。门静脉压力增高后引起食管胃底静脉曲张,一旦破裂出现上消化道大出血,是导致患者死亡的最常见原因。而我国乙型肝炎发病率很高,很大一部分患者将发展成为门静脉高压症,其中门静脉压力的测定和有无食管胃底静脉曲张的存在对于门静脉高压症的诊断、治疗、手术方式的选择和预后等都极为重要。本文就肝硬化患者门静脉压力及静脉曲张程度的有创以及无创评估的进展做一综述。

TIPS在脾切除治疗门静脉高压症后反复出血病例中的临床应用

目的总结经颈静脉肝内门体静脉分流术(TIPS)治疗未合并肝癌的门静脉高压症患者行脾切除术后反复上消化道出血的疗效。方法对未合并肝癌或胆管癌的门静脉高压症合并上消化道大出血患者行脾切除术后复发出血患者行TIPS术治疗,并随访1～5年(平均3.2年)的资料进行总结与分析。结果 36例脾切除术后再出血者行TIPS术,手术均获成功,围手术期死亡率为2.78%(1/36),死亡原因是肝性脑病。随访期间患者术后再次复发出血率为5.71%(2/35)。结论 TIPS对脾切除治疗门静脉高压症后反复出血病例的效果良好。

肝硬化门脉高压症合并胆囊结石的治疗

目的总结肝硬化门脉高压症合并胆囊结石的外科治疗经验。方法回顾性分析17例肝硬化门脉高压症合并单纯胆囊结石的临床诊治资料。结果10例行断流术并结合治疗胆囊结石组(3例同期手术),5例分期手术,2例并中西利胆排石)与7例单纯断流术组近期肝功能改善率及食道胃底静脉曲张消除率比较无明显差异(P>0.05),远期肝功能改善率明显优于单纯断流术组,分别为71.4%和14.3%(P<0.05),再出血率小于单纯断流术组(P<0.05)。结论肝硬化门脉高压症合并胆囊结石行断流术结合治疗胆囊结石的预后较单纯断流术好,并且只要加强围手术期的处理,同期手术是安全可行的。

门静脉高压治疗现状与展望

门静脉高压症是一种主要因肝脏病变而引起门静脉系统循环异常为主要特点的病症,经过100多年的研究与探索,门静脉高压症的诊断和治疗手段均得到了不断的发展和完善。如非选择性β受体阻断剂和内镜下曲张静脉套扎术对预防有中、重度静脉曲张的患者首次静脉曲张出血均具有各自的优势,气囊阻断经静脉逆行栓塞术对曲张的食管胃底静脉的具有良好疗效,部分性脾栓塞术已成为肝硬化门脉高压脾亢血液病的最主要非手术治疗措施,外科治疗方面联合手术的优势已经逐步体现出来,但门静脉高压症最根本的治疗措施仍是肝移植。但选择何种方式治疗,仍要根据患者肝功能状况及病情变化而定,本文将就门静脉高压治疗现状与展望做一综述。

Effect of endotoxin on portal hemodynamic in rats

AIM: To study the effects of endotoxin on portal hemodynamic of normal and noncirrhotic portal hypertensive rats. METHODS: Normal rats were intraperitoneally injected with 0.1, 0.25, 0.5, 1.0, 2.0, 4.0mg.kg(-1) of lipopolysaccharide(LPS) respectively, portal vein ligation(PVL) and intrahepatic portal occlusion (IPO) rats as well as sham-operated rats were treated with an intraperitoneal injection of 1.0mg.kg(-1) of LPS, the portal vein pressure(PVP), portal venous flow(PVF), inferior vena cava pressure(IVCP) and portal vein resistance(PVR) were detected 4 hours after injection. RESULTS: PVF of the 5 groups of rats accepting intraperitoneal injection of LPS were increased from 14.0 to 18.0, 22.2, 26.2, 34.8, 39.6, 38.8 mL.min(-1) 4 hours after injection of LPS(P【0.01). PVP of the 4 groups of rats accepting more than 0.1mg/kg.b.w of LPS was increased from 1.04 to 1.25, 1.50, 1.80, 1.95, 2.05 kPa(P【0.01). The increments of PVF and PVP were in a dose-dependent manner of LPS. PVR of the 5 groups of rats was decreased from 51 to 42,44,48,45,44,47 kPa.min.L(-1) (P【0.05) and no dose-dependent manner was observed. PVF of PVL, IPO and sham-operated rats increased from 22.6 to 32.8, 22.0 to 28.0, 14.0 to 34.8 mL.min(-1) (P【0.01), and PVP increased from 1.86 to 2.24, 1.74 to 1.95, 1.04 to 1.80 kPa(P【0.01), PVR decreased from 71 to 61, 67 to 61, 52 to 44 kPa.min.L(-1) after intraperitoneal injection of 1mg.kg(-1) of LPS. The increments of PVF and PVP of PVL and IPO rats were significantly less than the sham-operated rats(P【0.01), There was no significant difference between the amounts of PVR decreased in the two groups of PHT model rats and sham-operated rats(P】0.05) after intraperitoneal injection 1mg.kg(-1) of LPS. CONCLUSION: Endotoxin could prompt portal hypertension of the normal and noncirrhotic portal hypertensive rats by increasing portal blood flow mainly.

Effect of transjugular intrahepatic portosystemic shunt on pulmonary gas exchange in patients with portal hypertension and hepatopulmonary syndrome

AIM: To assess the impact of transjugular intrahepatic portosystemic shunt (TIPS) on pulmonary gas exchange and to evaluate the use of TIPS for the treatment of hepatopulmonary syndrome (HPS).METHODS: Seven patients, three of them with advanced HPS, in whom detailed pulmonary function tests were performed before and after TIPS placementat the University of Alabama Hospital and at the Hospital Clinic, Barcelona, were considered.RESULTS: TIPS patency was confirmed by hemodynamic evaluation. No changes in arterial blood gases were observed in the overall subset of patients. Transient arterial oxygenation improvement was observed in only one HPS patient, early after TIPS, but this was not sustained 4 mo later.CONCLUSION: TIPS neither improved nor worsened pulmonary gas exchange in patients with portal hypertension. This data does not support the use of TIPS as a specific treatment for HPS. However, it does reinforce the view that TIPS can be safely performed for the treatment of other complications of portal hypertension in patients with HPS.

Splenectomy with endoscopic variceal ligation is superior to splenectomy with pericardial devascularization in treatment of portal hypertension

AIM: To investigate the therapeutic efficacy and complications of splenectomy with endoscopic variceal ligation (EVL) and splenectomy with pericardial devascularization (i.e. Hassab’s operation) in patients with portal hypertension. METHODS: A total of 103 patients with liver cirrhosis and portal hypertension were randomly selected to receive either splenectomy with EVL (n = 53, group A) or Hassab’s operation (n = 50, group B). RESULTS: The portal blood flow volume, the presence of portal vein thrombosis, gastric emptying time and free portal venous pressure (FPP) before and after the operation were determined. Patients were followed up for up to 64 mo with an average of 45 mo, and the Dagradi classification of variceal veins and the grading of portal hypertension gastropathy (PHG) were evaluated. It was found that all esophageal varices were occluded or decreased to grade Ⅱ or less in both groups. There was little difference in the recurrence rate of esophageal varices (11.9% vs 13.2%) and the re-bleeding rate (7.1% vs 5.3%) between groups A and B. The incidence of complications and the percentage of patients with severe PHG after the operation were significantly higher in group B (60.0% and 52.0%) than in group A (32.1% and 20.8%, P < 0.05). No patients died of operation-related complications. There was no significant difference in gastric emptying time, FPP and portal blood flow volume between the two groups. CONCLUSION: The results suggest that splenectomy with EVL achieves similar therapeutic efficacy to that of Hassab’s operation in terms of the recurrence rate of esophageal varices and the re-bleeding rate, but theformer results in fewer and milder complications.

A large congenital and solitary intrahepatic arterioportal fistula in an old woman

Arterioportal fistula(APF)is a rare cause of portal hypertension and may lead to death.APF can be congenital,post-traumatic,iatrogenic(transhepatic intervention or biopsy)or related to ruptured hepatic artery aneurysms.Congenital APF is a rare condition even in children.In this case report,we describe a 73-year-old woman diagnosed as APF by ultrasonography,computed tomography,and hepatic artery selective arteriography.The fistula was embolized twice but failed,and she still suffered from alimentary tract hemorrhage.Then,selective arteriography of the hepatic artery was performed again and venae coronaria ventriculi and short gastric vein were embolized.During the 2-year follow-up,the patient remained asymptomatic.We therefore argue that embolization of venae coronaria ventriculi and short gastric vein may be an effective treatment modality for intrahepatic APF with severe upper gastrointestinal bleeding.

Portal hypertension due to portal venous thrombosis:Etiology, clinical outcomes

The thrombophilia in adult life has major implications in the hepatic vessels. The resulting portal vein thrombosis has various outcomes and complications. Esophageal varices, portal gastropathy, ascites, severe hypersplenism and liver failure needing liver transplantation are known well. The newly formed collateral venous circulation showing itself as pseudocholangicarcinoma sign and its possible clinical reflection as cholestasis are also known from a long time. The management strategies for these complications of portal vein thrombosis are not different from their counterpart which is cirrhotic portal hypertension, but the prognosis is unquestionably better in former cases. In this review we present and discuss the portal vein thrombosis, etiology and the resulting dinical pictures. There are controversial issues in nomenclature, management （including anticoagulation problems）, follow up strategies and liver transplantation. In the light of the current knowledge, we discuss some controversial issues in literature and present our experience and our proposals about this group of patients.

Adrenomedullin in cirrhotic and non-cirrhotic portal hypertension

AIM:Adrenomedullin (ADM) is a potent vasodilator peptide. ADM and nitric oxide (NO) are produced in vascular endothelial cells.Increased ADM level has been linked to hyperdynamic circulation and arterial vasodilatation in cirrhotic portal hypertension (CPH).The role of ADM in non-cirrhotic portal hypertension (NCPH) is unknown,plasma ADM levels were studied in patients with NCPH,compensated and decompensated cirrhosis in order to determine its contribution to portal hypertension (PH) in these groups. METHODS:There were 4 groups of subjects.Group 1 consisted of 27 patients (F/M:12/15) with NCPH due to portal and/or splenic vein thrombosis (mean age:41±12 years),group 2 consisted of 14 patients (F/M:6/8) with compensated (Child-Pugh A) cirrhosis (mean age:46±4), group 3 consisted of 16 patients (F/M:6/10) with decompensated (Child-Pugh C) cirrhosis (mean age:47±12). Fourteen healthy subjects (F/M:6/8) (mean age:44±8) were used as controls in Group 4.ADM level was measured by ELISA.NO was determined as nitrite/nitrate level by chemoluminescence. RESULTS:ADM level in Group 1 (236±61.4 pg/mL) was significantly higher than that in group 2 (108.4±28.3 pg/mL) and group 4 (84.1±31.5 pg/mL) (both P<0.0001) but was lower than that in Group3 (324±93.7 pg/mL) (P=0.002).NO level in group 1 (27±1.4 μmol/L) was significantly higher than that in group 2 (19.8±2.8 μmol/L) and group 4 (16.9±1.6 μmol/L) but was lower than that in Group 3 (39±3.6 μmol/L) (for all three P<0.0001).A strong correlation was observed between ADM and NO levels (r=0.827,P<0.0001). CONCLUSION:Adrenomedullin and NO levels were high in both non-cirrhotic and cirrhotic portal hypertension and were closely correlated,Adrenomedullin and NO levels increased proportionally with the severity of cirrhosis,and were significantly higher than those in patients with NCPH. Portal hypertension plays an important role in the increase of ADM and NO.Parenchymal damage in cirrhosis may contribute to the increase in these parameters.

Serum omentin and vaspin levels in cirrhotic patients with and without portal vein thrombosis

AIMTo investigate serum omentin and vaspin levels in cirrhotic patients; and to assess the relationship of these levels with hemostatic parameters, metabolic abnormalities, cirrhosis severity and etiology.METHODSFifty-one cirrhotic patients (17 with portal vein thrombosis) were analyzed. Serum omentin and vaspin levels were measured with commercially available direct enzyme-linked immunosorbent assays (ELISAs). To assess platelet activity, the following tests were performed using a MULTIPLATE®PLATELET FUNCTION ANALYZER: (1) an ADP-induced platelet activation test; (2) a cyclooxygenase dependent aggregation test (ASPI test); (3) a von Willebrand factor and glycoprotein Ib-dependent aggregation (using ristocetin) test (RISTO test); and (4) a test for thrombin receptor-activating peptide-6 induced activation of the thrombin receptor, which is sensitive to IIb/IIIa receptor antagonists.RESULTSOmentin, but not vaspin, serum concentrations were significantly decreased in patients with portal vein thrombosis (PVT) (P = 0.01). Prothrombin levels were significantly increased in patients with PVT (P = 0.01). The thrombin receptor activating peptide (TRAP) test results were significantly lower in the PVT group (P = 0.03). No significant differences in adipokines serum levels were found regarding the etiology or severity of liver cirrhosis assessed according to the Child-Pugh or Model of End-Stage Liver Disease (MELD) scores. There was a significant increase in the TRAP (P = 0.03), ASPI (P = 0.001) and RISTO high-test (P = 0.02) results in patients with lower MELD scores. Serum omentin and vaspin levels were significantly down-regulated in patients without insulin resistance (P = 0.03, P = 0.02, respectively). A positive relationship between omentin and vaspin levels were found both when all of the patients were analyzed (r = 0.41, P = 0.01) and among those with PVT (r = 0.94, P < 0.001).CONCLUSIONSerum omentin levels are increased in patients without PVT. Cirrhosis origin and grade do not affect omentin and vaspin levels. The analyzed adipokines do not influence platelet activity.

Stability of a rat model of prehepatic portal hypertension caused by partial ligation of the portal vein

AIM： To study the stability of portal hypertension （PHT） caused by partial ligation of the portal vein ligation （PVL） in a rat model.METHODS： Thirty male adult Wistar rats were divided into two groups： 10 in Group Ⅰ received a sham operation; and 20 in Group Ⅱreceived partial PVL. Portal vein pressure （PVP） was measured at four time periods： before ligation, 2 wk, 6 wk and 10 wk postsurgery. Portal venography, blood sampling and liver and spleen pathological examinations were conducted at 10 wk after surgery.RESULTS： The PVP was 9.15± 0.58 cmH2O before ligation, and increased to 17.32 ±0.63 cmH2O 2 wk after PVL. By repeat measurement of the PVP in each rat, it was shown to remain elevated for 10 wk. There were no significant differences in the pressure measurements at 2 wk, 6 wk and 10 wk. Varices were found mainly in the mesenteric vein 2 wk after PVL, which were more obvious later, while these manifestations were similar at week 6 and week 10. Portal venography demonstrated the varices and collaterals. There was no significant change in liver pathology. The volume of the spleen was enlarged 2-fold after ligation, and the sinus of the spleen was enlarged due to congestion. Significant sinus endothelial cell proliferation was observed, but no evidence of hypersplenia was found on hemogram and biochemical examination.CONCLUSION： These findings suggest that a satisfactory prehepatic PHT rat model can be obtained by partial ligation of the portal vein, and this PHT rat model was stable for at least 10 wk.

Staging of portal hypertension and portosystemic shunts using dynamic nuclear medicine investigations

AIM： To explore portal hypertension and portosystemic shunts and to stage chronic liver disease （CLD） based on the pathophysiology of portal hemodynamics. METHODS： Per-rectal portal scintigraphy （PRPS） was performed on 312 patients with CLD and liver angioscintigraphy （LAS） on 231 of them. The control group included 25 healthy subjects. We developed a new model of PRPS interpretation by introducing two new parameters, the liver transit time （LTT） and the circu-lation time between right heart and liver （RHLT）. LTT for each lobe was used to evaluate the early portal hypertension. RHLT is useful in cirrhosis to detect liver areas missing portal inflow. We calculated the classical per-rectal portal shunt index （PRSI） at PRPS and the hepatic perfusion index （HPI） at LAS. RESULTS： The normal LTT value was 24 ± 1 s. Abnormal LTT had PPV = 100% for CLD. Twenty-seven noncirrhotic patients had LTT increased up to 35 s （median 27 s）. RHLT （42 ± 1 s） was not related to liver disease. Cirrhosis could be excluded in all patients with PRSI 〈 5% （P 〈 0.01）. PRSI 〉 30% had PPV = 100% for cirrhosis. Based on PRPS and LAS we propose the classification of CLD in 5 hemodynamic stages. Stage 0 is normal （LTT = 24 s, PRSI 〈 5%）. In stage 1, LTT is increased, while PRSI remains normal. In stage 2, LTT is decreased between 16 s and 23 s, whereas PRSI is increased between 5% and 10%. In stage 3, PRSI is increased to 10%-30%, and LTT becomes undetectable by PRPS due to the portosystemic shunts. Stage 4 includes the patients with PRSI 〉 30%. RHLT and HPI were used to subtype stage 4. In our study stage 0 had NPV = 100% for CLD, stage 1 had PPV = 100% for non-cirrhotic CLD, stages 2 and 3 represented the transition from chronic hepatitis to cirrhosis, stage 4 had PPV = 100% for cirrhosis. CONCLUSION： LTT allows the detection of early portal hypertension and of opening of transhepatic shunts. PRSI is useful in CLD with extrahepatic portosystemic shunts. Our hemodynamic model stages the evolution of portal hypertension and portosystemic shunts. It may be of use in the selection of patients for interferon therapy.

Clinical analysis of surgical treatment of portal hypertension

AIM： To review the experience in surgery for 508 patients with portal hypertension and to explore the selection of reasonable operation under different conditions. METHODS： The data of 508 patients with portal hypertension treated surgically in 1991-2001 in our centers were analyzed. Of the 508 patients, 256 were treated with portaazygous devascularization （PAD）, 167 with portasystemic shunt （PSS）, 62 with selective shunt （SS）, 11 with combined portasystemic shunt and portaazygous devascularization （PSS＋PAD）, 9 with liver transplantation （LT）, 3 with union operation for hepatic carcinoma and portal hypertension （HCC＋PH）. RESULTS： In the 167 patients treated with PSS, free portal pressure （FPP） was significantly higher in the patients with a longer diameter of the anastomotic stoma than in those with a shorter diameter before the operation （P〈0.01）. After the operation, FPP in the former patients markedly decreased compared to the latter ones （P〈0.01）. The incidence rate of hemorrhage in patients treated with PAD, PSS, 55, PSS＋PAD, and HCC＋PH was 21.09% （54/256）, 13.77 （23/167）, 11.29 （7/62）, 36.36% （4/11）, and 100% （3/3）, respectively. The incidence rate of hepatic encephalopathy was 3.91% （10/256）, 9.58% （16/167）, 4.84% （3/62）, 9.09% （1/11）, and 100% （3/3）, respectively while the operative mortality was 5.49% （15/256）, 4.22% （7/167）, 4.84% （3/62）, 9.09% （1/11）, and 66.67% （2/3） respectively. The operative mortality of liver transplantation was 22.22% （2/9）. CONCLUSION： Five kinds of operation in surgical treatment of portal hypertension have their advantages and disadvantages. Therefore, the selection of operation should be based on the actual needs of the patients.

Altered blood-brain barrier permeability in rats with prehepatic portal hypertension turns to normal when portal pressure is lowered

AIM： To study the blood-brain barrier integrity in prehepatic portal hypertensive rats induced by partial portal vein ligation, at 14 and 40 dafer ligation when portal pressure is spontaneously normalized. METHODS： Adult male Wistar rats were divided into four groups： Group Ⅰ： Sham14d, sham operated; Group Ⅱ： PHil, portal vein stenosis, （both groups were used 14 days after surgery）; Group Ⅲ： Sham4od, Sham operated and Group Ⅳ： PH4od Portal vein stenosis （Groups Ⅱ and Ⅳ used 40 d afer surgery）. Plasma ammonia, plasma and cerebrospinal fluid protein and liver enzymes concentrations were determined. Trypan and Evans blue dyes, systemically injected, were investigated in hippocampus to study blood-brain barrier integrity. Portal pressure was periodically recorded. RESULTS： Forty days afer stricture, portal pressure was normalized, plasma ammonia was moderately high, and both dyes were absent in central nervous system parenchyma. All other parameters were reestablished. When portal pressure was normalized and ammonia level was lowered, but not normal, the altered integrity of blood-brain barrier becomes reestablished. CONCLUSION： The impairment of blood-brain barrier and subsequent normalization could be a mechanism involved in hepatic encephalopathy reversibility. Hemodynamic changes and ammonia could trigger blood-brain barrier alterations and its reestablishment.