血液透析中静脉压高报警的原因与处理

目的分析血液透析中静脉压高报警的原因,并提出处理措施。方法选取我院2016年9月至2018年9月在透析过程中发生过静脉压增高的100例患者作为研究对象,回顾性分析当时的处理情况,得出原因,总结处理措施。结果100例患者中共出现439次静脉压高报警,其中静脉穿刺处血肿132次(30.1%),静脉回路受阻因素79次(18.0%),患者静脉狭窄、硬化因素88次(20.0%),患者血流量大但静脉血管过细、血管弹性差76次(17.3%),凝血因素64次(14.6%)。结论在血透透析过程中,护理人员应密切监测各项数据,出现静脉压高报警时及时查明原因并进行有效处理,才能保证患者的血液透析效果。

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.

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.

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.

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.

Laparoscopic and open splenectomy and azygoportal disconnection for portal hypertension

AIM： To compare the outcomes of laparoscopic and open splenectomy and azygoportal devascularization for portal hypertension. METHODS： From June 2006 to March 2009, laparoscopic splenectomy and azygoportal disconnection （LSD） were performed on 28 patients with cirrhosis, bleeding due to portal hypertension, and secondary hypersplenism. Success was achieved in 26 patients. Demographic, intraoperative, and postoperative variables of the patients were compared. RESULTS： Success of laparoscopic splenectomy and azygoportal disconnection was achieved in all but two patients （7.14%） who required open splenectomy and azygoportal devascularization （OSD）. The operation time was significantly longer in patients undergoing LSD than in those undergoing OSD （235 ± 36 min vs 178 ± 47 rain, P 〈 0.05）. The estimated intraoperative blood loss was much more in patients receiving OSD than in those receiving LSD （420 ± 50 mL vs 200 ± 30 mL, P 〈 0.01）. The proportion of patients undergoing laparoscopic and open splenectomy and azygoportal disconnection who received transfusion of packed red blood cells during or after the operation was 23.08% and 38.46%, respectively （P 〈 0.05）. The time of first oral intake was faster in patients after LSD than in those after OSD （1.5 ± 0.7 d vs 3.5 ± 1.6 d, P 〈 0.05）. The hospital stay of patients after LSD was shorter than that of patients after OSD （6.5 ± 2.3 d vs 11.7 ± 4.5 d, P 〈 0.05）. The pain requiring medication was less severe in patients after LSD than in those after OSD （7.69% vs 73.08%, P 〈 0.001）. The overall complication rate was lower in patients after LSD than in those after OSD （19.23% vs 42.31%, P 〈 0.05）.CONCLUSION： Laparoscopic splenectomy and azygoportal disconnection are the feasible, effective, and safe surgical procedure, and are advantageous over minimally invasive surgery for bleeding portal hypertension and hypersplenism.

Splenic arteriovenous fistula and sudden onset of portal hypertension as complications of a ruptured splenic artery aneurysm: Successful treatment with transcatheter arterial embolization. A case study and review of the literature

Splenic arteriovenous fistula （SAVF） accounts for an unusual but well-documented treatable cause of portal hypertension. A case of a 50-year-old multiparous female who developed suddenly portal hypertension due to SAVF formation is presented. The patient suffered from repeated episodes of haematemesis and melaena during the past twelve days and thus was emergently admitted to hospital for management. Clinical and laboratory investigations established the diagnosis of portal hypertension in the absence of liver parenchymal disease. Endoscopy revealed multiple esophageal bleeding varices. Abdominal computed tomography （CT） and transfemoral celiac arteriography documented the presence of a tortuous and aneurysmatic splenic artery and premature filling of an enlarged splenic vein, findings highly suggestive of an SAVF. The aforementioned vascular abnormality was successfully treated with percutaneous transcatheter embolization. Neither recurrence nor other complications were observed.

Sildenafil does not influence hepatic venous pressure gradient in patients with cirrhosis

AIM： To investigate if sildenafil increases splanchnic blood flow and changes the hepatic venous pressure gradient （HVPG） in patients with cirrhosis. Phosphodiesterase type-5 inhibitors are valuable in the treatment of erectile dysfunction and pulmonary hypertension in patients with end-stage liver disease. However, the effect of phosphodiesterase type-5 inhibitors on splanchnic blood flow and portal hypertension remains essentially unknown. METHODS： Ten patients with biopsy proven cirrhosis （five females/five males, mean age 54：1：8 years） and an HVPG above 12 mmHg were studied after informed consent. Measurement of splanchnic blood flow and the HVPG during liver vein catheterization were done before and 80 min after oral administration of 50 mg sildenafil. Blood flow was estimated by use of indocyanine green clearance technique and Fick＇s principle, with correction for non-steady state. RESULTS： The plasma concentration of sildenafil was 222 ± 136 ng/mL 80 min after administration. Mean arterial blood pressure decreased from 77 ±7 mmHg to 66 ± 12 mmHg, P = 0.003, while the splanchnicblood flow and oxygen consumption remained unchanged at 1.14 ± 0.71 L/min and 2.3 ± 0.6 mmol/ min, respectively. Also the HVPG remained unchanged （18 ± 2 mmHg vs 16 ± 2 mmHg） with individual changes ranging from -8 mmHg to ±2 mmHg. In seven patients, HVPG decreased and in three it increased. CONCLUSION： In spite of arterial blood pressure decreases 80 min after administration of the phosphodiesterase type-5 inhibitor sildenafil, the present study could not demonstrate any clinical relevant influence on splanichnic blood flow, oxygen consumption or the HVPG.

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 hypersplenisrn 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.

Hyperammonemia,brain edema and blood-brain barrier alterations in prehepatic portal hypertensive rats and paracetamol intoxication

AIM:To study the blood-brain barrier integrity,brain edema, animal behavior and ammonia plasma levels in prehepatic portal hypertensive rats with and without acute liver intoxication. METHODS:Adults male Wistar rats were divided into four groups.Group Ⅰ:sham operation;Ⅱ:Prehepatic portal hypertension,produced by partial portal vein ligation;Ⅲ: Acetaminophen intoxication and Ⅳ:Prehepatic portal hypertension plus acetaminophen.Acetaminophen was administered to produce acute hepatic injury.Portal pressure,liver serum enzymes and ammonia plasma levels were determined.Brain cortex water content was registered and trypan blue was utilized to study blood brain barrier integrity.Reflexes and behavioral tests were recorded. RESULTS:Portal hypertension was significantly elevated in groups Ⅱ and Ⅳ.Uver enzymes and ammonia plasma levels were increased in groups Ⅱ,Ⅲ and Ⅳ.Prehepatic portal hypertension (group Ⅱ),acetaminophen intoxication (group Ⅲ) and both (group Ⅳ) had changes in the blood brain-barrier integrity (trypan blue) and hyperammonemia.Cortical edema was present in rats with acute hepatic injury in groups Ⅲ and Ⅳ.Behavioral test (rota rod) was altered in group Ⅳ. CONCLUSION:These results suggest the possibility of another pathway for cortical edema production because blood brain barrier was altered (vasogenic) and hyperammonemia was registered (oltotoxic).Group Ⅳ,with behavioral altered test,can be considered as a model for study at an early stage of portal-systemic encephalopathy.

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.

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.

Intraoperative pulmonary hypertension occurred in an asymptomatic patient with pre-existent liver cirrhotic and portal hypertension

Portopulmonary hypertension(PPH) is clinically defined as the development of pulmonary arterial hypertension complicated by portal hypertension,with or without advanced hepatic disease.Physical signs may be absent in mild to moderate PPH and only appear in a hyperdynamic circulatory state.Similar signs of advanced liver disease can be observed in severe PPH,with ascites and lower extremity edema.Pulmonary hypertension is usually diagnosed after anesthetic induction during liver transplantation(LT).We present intraoperative pulmonary hypertension in a 41-year-old male patient with hepatic cirrhosis.Since this patient had no preoperation laboratory data supporting the diagnosises of pulmonary hypertension and was asymptomatic for a number of years,it was necessary to send him to the intensive care unit after operation.Further study should be focued on the diagnosis and treatment of pulmonary arterial hypertension in order to reduce its mortality.

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.

Nitroglycerine effects on portal vein mechanics and oxidative stress in portal hypertension

AIM:Тo examine the effects of nitroglycerine on portal vein haemodynamics and oxidative stress in patients with portal hypertension.METHODS:Thirty healthy controls and 39 patients with clinically verified portal hypertension and increasedvascular resistance participated in the study.Liver di-ameters,portal diameters and portal flow velocities were recorded using color flow imaging/pulsed Doppler detection.Cross-section area,portal flow and index of vascular resistance were calculated.In collected blood samples,superoxide anion radical (O 2-),hydrogen per-oxide (H 2 O 2),index of lipid peroxidation (measured as TBARS) and nitric oxide (NO) as a marker of endothelial response (measured as nitrite-NO 2-) were determined.Time-dependent analysis was performed at basal state and in 10th and 15th min after nitroglycerine (sublingual 0.5 mg) administration.RESULTS:Oxidative stress parameters changed sig-nificantly during the study.H 2 O 2 decreased at the end of study,probably via O 2-mediated disassembling in Haber Weiss and Fenton reaction;O 2-increased signifi-cantly probably due to increased diameter and tension and decreased shear rate level.Consequently O 2-and H 2 O 2 degradation products,like hydroxyl radical,initi-ated lipid peroxidation.Increased blood flow was to some extent lower in patients than in controls due to double paradoxes,flow velocity decreased,shear rate decreased significantly indicating non Newtonian char-acteristics of portal blood flow.CONCLUSION:This pilot study could be a starting point for further investigation and possible implemen-tation of some antioxidants in the treatment of portal hypertension.

Role of PGI_2 in the formation and maintenance of hyperdynamic circulatory state of portal hypertensive rats

AIM: To investigate the role of prostacyclin (PGI2) and nitric oxide (NO) in the development and maintenance of hyperdynamic circulatory state of chronic portal hypertensive rats. METHODS: Ninety male Sprague-Dawley rats were divided into three groups: intrahepatic portal hypertension (IHPH) group by injection of CCI4, prehepatic portal hypertension (PHPH) group by partial stenosis of the portal vein and sham-operation control (SO) group. One week after the models were made, animals in each group were subdivided into 4 groups: saline controlled group (n = 23), Nω-nitro-L-arginine (L-NNA)group (n = 21) group, indomethacin (INDO) group (n = 22) and high-dose heparin group (n = 24). The rats were administrated 1mL of saline, L-NNA (3.3 mg/kg-d) and INDO (5 mg/kg·d) respectively through gastric tubes for one week/then heparin (200 IU/Kg/min) was given to rats by intravenous injection for an hour. Splanchnic and systemic hemodynamics were measured using radioactive microsphere techniques. The serum nitrate/nitrite(NO2-/NO3-) levels as a marker of production of NO were assessed by a colorimetric method, and concentration of 6-keto-PGF1α, a stable hydrolytic product of PGI2, was determined by radioimmunoassay. RESULTS: The concentrations of plasma 6-keto-PGFla (pg/mL) and serum NO2-/NO3- (μmol/L) in IHPH rats (1123.85±153.64, 73.34±4.31) and PHPH rats (891.88±83.11, 75.21±6.89) were significantly higher than those in SO rats (725.53±105.54, 58.79±8.47) (P<0.05). Compared with SO rats, total peripheral vascular resistance (TPR) and spanchnic vascular resistance (SVR) decreased but cardiac index (CI) and portal venous inflow (PVI) increased obviously in IHPH and PHPH rats (P<0.05). L-NNA and indomethacin could decrease the concentrations of plasma 6-keto-PGFla and serum NO2/7NO3-in IHPH and PHPH rats (P<0.05) .Meanwhile, CI, FPP and PVI lowered but MAP, TPR and SVR increased(P<0.05). After deduction of the action of NO, there was no significant correlation between plasma PGI2 level and hemodynamic parameters such as CI, TPR, PVI and SVR. However, after deduction of the action of PGI2, NO still correlated highly with the hemodynamic parameters, indicating that there was a close correlation between NO and the hemodynamic parameters. After administration of high-dose heparin, plasma 6-keto- concentrations in IHPH, PHPH and SO rats were significantly higher than those in rats administrated vehicle (P<0.05). On the contrary, levels of serum NO2-/NO3- in IHPH, PHPH and SO rats were significantly lower than those in rats administrated Vehicle (P<0.05). Compared with those rats administrated vehicle, the hemodynamic parameters of portal hypertensive rats, such as CI and PVI, declined significantly after administration of high-dose heparin (P<0.05), while TPR and SVR increased significantly (P<0.05). CONCLUSION: It is NO rather than PGI2 that is a mediator in the formation and maintenance of hyperdynamic circulatory state of chronic portal hypertensive rats.

Right liver lobe/albumin ratio:Contribution to non-invasive assessment of portal hypertension

AIM： To study the value of biochemical and ultrasonographic parameters in prediction of presence and size of esophageal varices.METHODS： The study includes selected cirrhotic patients who underwent a complete biochemical workup, upper digestive endoscopic and ultrasonographic examinations. Albumin/right liver lobe diameter and platelet count/spleen diameter ratios were calculated. The correlation between calculated ratio and the presence and degree of esophageal varices was evaluated.RESULTS： Ninety-four subjects （62 males, 32 females）, with a mean age of 52.32 ± 13.60 years, were studied. Child-Pugh class A accounted for 42.6%, class 13 37.2%, whereas class C 20.2%. Esophageal varices （OE） were not demonstrated by upper digestive endoscopy in 24.5%, while OE grade Iwas found in 22.3% patients, grade Ⅱ in 33.0%, grade m in 16.0%, and grade iV in 4.3%. The mean value of right liver lobe diameter/ albumin ratio was 5.51± 1.82 （range from 2.76 to 11.44）, while the mean platelet count/spleen diameter ratio was 1017.75 ± 729.36 （range from 117.39 to 3362.50）, respectively. Statistically significant correlation was proved by Spearman＇s test between OE grade and calculated ratios. The P values were 0.481 and -0.686, respectively.CONCLUSION： The right liver lobe diameter/albumin and platelet count/spleen diameter ratios are noninvasive parameters providing accurate information pertinent to determination of presence of esophageal varices, and their grading in patients with liver cirrhosis.

Percutaneous portal venoplasty and stenting for anastomotic stenosis after liver transplantation

AIM:To review percutaneous transhepatic portal venoplasty and stenting(PTPVS)for portal vein anastomotic stenosis(PVAS)after liver transplantation (LT). METHODS:From April 2004 to June 2008,16 of 18 consecutive patients(11 male and 5 female;aged 17-66 years,mean age 40.4 years)underwent PTPVS for PVAS.PVAS occurred 2-10 mo after LT(mean 5.0 mo). Three asymptomatic patients were detected on routine screening color Doppler ultrasonography(CDUS). Fifteen patients who also had typical clinical signs of portal hypertension(PHT)were identified by contrastenhanced computerized tomography(CT)or magnetic resonance imaging.All procedures were performed under local anesthesia.If there was a PVAS<75%, the portal pressure was measured.Portal venoplasty was performed with an undersized balloon and slowly inflated.All stents were deployed immediately following the predilation.Follow-ups,including clinical course, stenosis recurrence and stent patency which were evaluated by CDUS and CT,were performed. RESULTS:Technical success was achieved in all patients.No procedure-related complications occurred. Liver function was normalized gradually and the symptoms of PHT also improved following PTPVS.In 2 of 3 asymptomatic patients,portal venoplasty and stenting were not performed because of pressure gradients<5 mmHg.They were observed with periodic CDUS or CT.PTPVS was performed in 16 patients.In 2 patients,the mean pressure gradients decreased from 15.5 mmHg to 3.0 mmHg.In the remaining 14 patients,a pressure gradient was not obtained because of>75%stenosis and typical clinical signs of PHT.In a 51-year-old woman,who suffered from massive ascites and severe bilateral lower limb edema after secondary LT,PVAS complicated hepatic vein stenosis and inferior vena cava(IVC)stenosis. Before PTPVS,a self-expandable and a balloonexpandable metallic stent were deployed in the IVC and right hepatic vein respectively.The ascites and edema resolved gradually after treatment.The portosystemic collateral vessels resulting from PHT were visualized in 14 patients.Gastroesophageal varices became invisible on poststenting portography in 9 patients.In a 28-yearold man with hepatic encephalopathy,a pre-existing meso-caval shunt was detected due to visualization of IVC on portography.After stenting,contrast agents flowed mainly into IVC via the shunt and little flowed into the portal vein.A covered stent was deployed into the superior mesenteric vein to occlude the shunt. Portal hepatopetal flow was restored and the IVC became invisible.The patient recovered from hepatic encephalopathy.A balloon-expandable Palmaz stent was deployed into hepatic artery for anastomotic stenosis before PTPVS.Percutaneous transhepatic internal-external biliary drainage was performed in 2 patients with obstructive jaundice.Portal venous patency was maintained for 3.3-56.6 mo(mean 33.0 mo) and all patients remained asymptomatic.CONCLUSION:With technical refinements,early detection and prompt treatment of complications,and advances in immunotherapy,excellent results can be achieved in LT.

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.

Portal hypertensive colopathy is associated with portal hypertension severity in cirrhotic patients

AIM： To assess the prevalence of portal hypertension （PH） related colorectal lesions in liver transplant candidates, and to evaluate its association with the severity of PH. METHODS： Between October 2004 and December 2005, colonoscopy was performed in 92 cirrhotic liver transplant candidates. We described the lesions resulting from colorectal PH and their association with the grade of PH in 77 patients who underwent measurement of hepatic venous pressure gradient （HVPG）. RESULTS： Mean age was 55 years and 80.7% of patients were men. The main etiology of cirrhosis wasalcoholism （45.5%）. Portal hypertensive colopathy （PHC） was found in 23.9%, colonic varices in 7.6% and polyps in 38% of patients （adenomatous type 65.2%）. One asymptomatic patient had a well-differentiated adenocarcinoma. The manifestations of colorectal PH were not associated with the etiology of liver disease or with the Child-Pugh grade. Ninety percent of patients with colopathy presented with gastroesophageal varices （GEV）, and 27.5% of patients with GEV presented with colopathy （P = 0.12）. A relationship between higher values of HVPG and presence of colopathy was observed （19.9：1：6.2 mmHg vs 16.8 ± 5.4 mmHg, P = 0.045）, but not with the grade of colopathy （P = 0.13）. Preneoplastic polyps and neoplasm （P = 0.02） and spontaneous bacterial peritonitis （P = 0.006） were more prevalent in patients with colopathy. We did not observe any association between previous β-blocker therapy and the presence of colorectal portal hypertensive vasculopathy. CONCLUSION： PHC is common in cirrhotic liver transplant candidates and is associated with higher portal pressure.