肝硬化门静脉高压症患者的体位护理

目的探索肝硬化门静脉高压症患者的最佳体位护理。方法采用彩色多普勒流速剖面图技术检测90°坐位、左侧卧位和平卧位的门静脉内径和平均血液流速变化。结果平卧位门静脉内径平均为(10.38±1.78)mm,90°坐位门静脉内径平均为(11.28±1.19)mm,左侧卧位为(11.08±1.69)mm,差异无统计学意义(P>0.05)。平卧位门静脉血液平均流速为(31.08±8.80)cm/s,而90°坐位时门静脉血液平均流速为(37.32±9.14)cm/s,左侧卧位门静脉血液平均流速为(36.34±9.01)cm/s,差异具统计学意义(P<0.01)。结论肝硬化门静脉高压症患者的体位护理应该有别于传统的护理理念,尽可能取90°坐位或左侧卧位。

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。

奥曲肽对婴幼儿肝移植后小体积移植肝相关门静脉高灌注的调节作用

目的探讨奥曲肽在调节婴幼儿肝移植受者小体积移植肝相关门静脉高灌注中的作用。方法2013年12月至2016年8月共有22例婴幼儿受者植入小体积移植肝，小体积移植肝定义为移植肝体积与受者标准肝体积比（GV／SLV）〈0．5，且移植肝重量（GW）〈150g。22例受者中，12例应用奥曲肽治疗（奥曲肽组），术后每日持续静脉输注奥曲肽300gg，用药时间24-96h；余10例为早期移植病例，未给予奥曲肽干预，作为对照组。对比分析术后早期（术后7d内）两组受者门静脉血流量及血清天冬氨酸转氨酶（AST）、胆红素总量（TB）和直接胆红素（DB）等移植肝功能生化指标的变化与差异，并观察两组受者肝动脉闭塞和胆道并发症发生情况。结果奥曲肽组和对照组初始时门静脉血流量分别为（413．43±76．24）和（390．83±107．89）ml·min^-1·100g（P〉0．05），术后第3天分别为（334．90±96．67）和（441．04±117．41）ml·min^-1·100g（P〈0.05），术后第5天分别为（322．20±81．04）和（423．23±100．81）ml·min^-1·100g（P〈0.05）。两组受者术后早期各时间点血清AST、TB和DB水平的差异均无统计学意义（P〉0．05）。奥曲肽组与对照组的肝动脉闭塞发生率分别为33．33％和44．44％，胆道并发症发生率分别为33．33％和11．11％，两组间差异均无统计学意义（P〉0．05）。结论奥曲肽可以降低婴幼儿肝移植受者小体积移植肝相关的门静脉血流量，但对于术后早期移植肝功能及相关并发症的影响还有待于更大样本的研究证实。

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。

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。

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。

Gd-EOB-DTPA增强MRI肝胆期弥漫性门静脉周围高信号的影像表现分型及临床意义

目的探讨钆塞酸二钠(Gd-EOB-DTPA)增强MRI肝胆期(HBP)弥漫性门静脉周围高信号(PHI)的影像表现分型及临床意义。方法回顾接受Gd-EOB-DTPA增强MRI检查者,从中筛选出26例伴有HBP弥漫性PHI的患者。根据HBP与T_(2)WI肝内弥漫性PHI区匹配模式进行分型,比较不同影像分型之间临床及肝功能生化指标[谷丙转氨酶(ALT)、谷草转氨酶(AST)、γ-谷氨酰转肽酶(GGT)、碱性磷酸酶(ALP)、总胆红素(TBil)、直接胆红素(DBil)、白蛋白(ALb)及总蛋白(TP)]的差异性。结果26例患者中,12例HBP与T_(2)WI肝内弥漫性PHI区相匹配(A型),14例HBP与T_(2)WI肝内弥漫性PHI区不相匹配,表现为前者(HBP)位于后者(T_(2)WI)的外围(B型,n=11)或后者无PHI(C型,n=3)。相匹配组主要与活动性肝炎相关,疾病包括戊型肝炎、自身免疫性肝炎、药物性肝损伤;不相匹配组主要与肝硬化等慢性病程相关,疾病包括原发性胆汁性胆管炎、自身免疫性肝炎-原发性胆汁性胆管炎重叠综合征和各种病因的慢性肝炎、肝硬化。A型患者的ALT、AST、GGT、TBil、DBil水平显著高于(B+C)型,差异均有统计学意义(P值均<0.05);ALP、ALb与TP水平稍低于(B+C)型,差异均无统计学意义(P值均>0.05)。ALT、AST、GGT、TBil和DBil预测A型PHI的受试者工作特征曲线下面积均>0.8。结论HBP弥漫性PHI的影像学分型,可能反映肝功能损伤的严重程度,并作为判断疾病处于何种阶段的影像指标之一。

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。

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.

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.

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.

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.

Bile duct ligation in rats: A reliable model of hepatorenal syndrome?

The two most widely used experimental models of advanced liver disease are the administration of carbon tetrachloride, and common bile duct ligation (BDL), however, neither has been systematically evaluated as a model of hepatorenal syndrome (HRS). The BDL model in rats, studied at diverse time points, induced a progressive renal dysfunction without structural changes in the kidney. The authors concluded that BDL is a good model for further studies of HRS and its treatment. However, the renal impairment observed at the acute phase of the BDL model is based on a different pathophysiology than that of HRS. Specifi cally, in acute obstructive jaundice, cholemia predominates over parenchymal liver disease (reversible at this stage without portal hypertension or cirrhosis) and independently induces negative inotropic and chronotropic effects on the heart, impaired sympathetic vasoconstriction response and profound natriuresis and diuresis that might lead to volume depletion. In addition, systemic endotoxemia contributes to the prerenal etiology of renal impairment and promotes direct nephrotoxicity and acute tubular necrosis. On the other hand, the renal failure observed in the chronic BDL model (with development of biliary cirrhosis, portal hypertension and ascites) shares pathophysiological similarities with HRS, but the accordance of the chronic BDL model to the diagnostic criteria of HRS (e.g. absence of spontaneous bacterial peritonitis, no renal function improvement after plasma volume expansion) should have been confirmed. In conclusion, we think that the BDL model is not suitable for the study of the natural history of HRS, but the chronic BDL model might be valid for the study of established HRS and its potential therapies.