肝肺综合征非创伤性诊断及相关因素分析

目的　探讨肝肺综合征 (HPS)的临床相关因素和非创伤性诊断。方法　对 74例肝炎肝硬化患者进行B超检查、胸部X线摄片、同步检测血气分析和电解质及肺功能 ,然后计算肺泡气 动脉血氧分压差 [P(A a) O2 ]。结果　P(A a) O2 ≥ 2 .0kPa者发生低氧血症占 6 0 .0 % ( 36 /6 0 ) ,而P(A a) O2 <2 .0kPa者发生低氧血症仅占 7.1% ( 1/14 ) ,两者比较差异有非常显著性 ( χ2 =12 .96 ,P<0 .0 1)。同时低氧血症与患者年龄、病毒感染模式、肝功能Child分级、自发性细菌性腹膜炎、肝性脑病、胸部X线片表现及肺活量等均无明显相关。而P(A a) O2 异常多见于肝功能ChildB、C级和门脉高压患者。结论　仅凭低氧血症和动脉血氧饱和度诊断HPS不确切 ,P(A a) O2 增大≥ 2 .0kPa是非创伤性诊断HPS的有效指标     

肝肺综合征的诊断和治疗

肝肺综合征是指继发于肝脏疾病而发生的肺血管扩张、肺部气体交换障碍、动脉血氧分压下降并出现有关临床表现的综合征。早期发现并及时处理有利于改善预后。除临床症状和体征外，血气分析可见直立性动脉血氧分压下降；超声波、放射性核素及肺血管造影等检查有助于发现肺内扩张的血管。氧疗简便而有效；药物治疗尚无确实效果；肺血管栓塞疗法可能有效；肝移植后大部分病人动脉血氧分压可明显提高，故肝肺综合征有严重低氧血症不再是肝     

肝肺综合征

肝肺综合征是指肝功能不全患者肺血管异常、动脉氧合功能降低及低氧血症等所致的一组临床症状。本文对肝肺综合征的病因、发病机理、临床表现、诊断和治疗进行综述。     

肝肺综合征的诊断及治疗研究进展

肝肺综合征是一种与肝病有关的肺血管扩张所致的临床综合征,以动脉氧合障碍为主要表现,是肝脏疾病的肺部严重并发症.其发病机制复杂,发病隐匿,晚期肝病发病率高,目前临床重视不足,远期预后较差,故临床医生需加强对其认识,早期发现,早期诊治,以便改善预后.此文主要对近年来肝肺综合征的诊断及治疗的最新进展进行综述.     

肝肺综合征

肝肺综合征 (Ｈｅｐａｔｏｐｕｌｍｏｎａｒｙｓｙｎｄｒｏｍｅ ,ＨＰＳ)是指在肝病基础上发生的肺血管异常 ,动脉氧合功能降低 ,临床出现低氧血症的功能性病变。肝病、肺泡 动脉血氧分压差 (ＡａＤＯ2 )上升和肺内血管扩张为该综合征的三大主征。随着原位肝移植(ＯＬＴ)的成功 ,晚期肝病患者的肺血管异常再次受到关注。ＨＰＳ是终末期肝脏病的一种严重肺部并发症 ,因此 ,加强对ＨＰＳ的临床研究 ,寻找有效的预防和治疗方法 ,对降低肝硬化的病死率有重要意义。一、概况ＨＰＳ早在 10 0多年前就已被注意到。 1884年Ｆｌｕｃｋｉｇｅｒ曾报道…     

肺灌注扫描在肝肺综合征诊断中的作用——附3例报告

肝肺综合征(Hepatopulmonary syndrome,HPS)是以肝功能不全,肺泡气-动脉血氧分压差上升和肺内血管扩张为三大主征的综合征。及早诊断HPS并采取相应治疗对改善其预后有很大的帮助。有报道认为99mTc-MAA肺灌注扫描是诊断肝肺综合征的一种方法,并利用99mTc-MAA肺灌注扫描显示肝肺综合征组肺外分流率明显高于肝硬化组和正常对     

23例肝肺综合征临床分析

探讨肝肺综合征(HPS)的临床特点和预后。67例肝硬化患者均应用血气分析仪测定其动脉血氧分压(PaO2),其中Ch ild-Pugh分级A级30例,B级22例,C级15例。67例肝硬化患者中23例合并HPS,发病率为34.3%。其发病率与Ch ild-Pugh分级有关,与A级比较C级HPS,发病率显著增高(P<0.05);门静脉增宽与不宽者、胃底食管静脉曲张与未发现曲张者、有蜘蛛痣与无蜘蛛痣者分别合并有HPS,两者比较均差异有显著性(P<0.05)。23例HPS患者中7例死亡,HPS均不是直接死亡原因。有门脉高压、蜘蛛痣时提示HPS的存在。早期诊断和治疗有助于缓解低氧血症,改善预后。     

21例肝肺综合征临床分析

肝肺综合征（hepatopulmonary syndrome，HPS）指慢性肝功能不全患者因肺内血管扩张而出现严重低氧血症，是各种慢性肝脏疾病终末期的一种严重并发症，预后差。HPS近年来引起广泛重视，其三联征为肝功能不全、肺血管扩张和低氧血型引。我院2003年5月至2008年5月对收治61例肝硬化患者进行血气分析等检测发现21例HPS,     

肝肺综合征的临床特点及诊断

目的探讨肝肺综合征(HPS)的临床特点及诊断方法,提高对其认识.方法回顾性分析我院1986年1月～2003年12月确诊的13例患者的临床资料.结果除1例为慢性酒精性肝损害基础上的急性药物性肝炎外,12例均为肝硬化患者,据Child-Pugh分级标准,肝功能B级和C级者11例(84.60%);平均动脉血氧分压(PaO2)为6.94±1.5 kPa,10例中9例直立位缺氧大于10%.临床主要表现为呼吸困难(100%)、紫绀(100%)、杵状指(84.6%)、肝掌(84.6%)、面部毛细血管扩张(84.6%)、蜘蛛痣(69.2%).9例行肺功能检查患者中8例为弥散功能障碍.所有患者均经99mTc标记的人血白蛋白聚合颗粒(99mTc-MAA)首次通过肺灌注显像确诊,测定肺内分流率为22%～57%.11例同时计算吸入100%氧气时动静脉分流占总血流量百分比(Qs/Qt)的结果为10.9%～27.4%,均小于前者所得.结论肝肺综合征的发生与肝功能不全和门脉高压症都有关系,同时有门静脉高压、紫绀、杵状指、蜘蛛痣或面部毛细血管扩张时应考虑该诊断.直立位缺氧(>10%)为典型表现,99mTc-MAA首次通过肺灌注显像是有效的诊断方法,所测定的肺内分流率大于Qs/Qt.     

肝肺综合征19例临床分析

肝肺综合征(hepatopulmonary syndrone，HPS)是指由肝脏疾病导致肺血管异常，动脉氧合功能降低和低氧血症等一系列临床表现的综合征。本文通过19例肝硬化患者临床分析，探讨其发生机制、诊断和治疗。     

The diagnosis and treatment of hepatopulmonary syndrome

Few prognostic indicators and outcomes reported for patients who have hepatopulmonary syndrome can be consistently reproduced between institutions. The lack of practice recommendations based upon consistent and predictable outcomes creates uncertainty for physicians trying to make the best patient choices. With the scarcity of donor organs, these issues are of particular importance when transplantation in considered as a treatment option. Much uncertainty arises from the basic tasks of making an accurate diagnosis in patients who have symptoms suggestive of hepatopulmonary syndrome. This article focuses on problems that underlie diagnostic accuracy and uses this information to appraise critically outcomes literature.     

对肝肺综合征诊治的76例临床分析

目的:探讨肝肺综合征(HPS)的临床特点及诊断方法,提高对其认识。方法:回顾性分析76例HPS患者的临床资料,并与无HPS的133例肝硬化患者在肺功能、血气分析等方面进行比较。结果:在HPS组中除4例为慢性酒精性肝损害基础上的急性药物性肝炎外,72例均为肝硬化患者。临床表现为呼吸困难、紫绀、杵状指及蜘蛛痣。据Child-Pugh分级标准,肝功能B级和C级者59例(77.6%),平均PaO2为(79.93±11.29)mm Hg(1 mm Hg=0.133 kPa),对照组为(92.48±13.53)mm Hg,2组比较有统计学意义(P0.01)。HPS组中76例中有48例直立性缺氧10%(63.1%)。不同门静脉内径、有无蜘蛛痣、不同肝功能分级的PaO2和SaO2值比较,均有统计学意义(P0.01)。影像学检查结果示肺内血管扩张。结论:肝肺综合征的发生与肝功能不全有明显的关系,该病患者常有呼吸困难、紫绀、杵状指、蜘蛛痣及直立性缺氧等典型表现,患者低氧血症发生率高,而肺功能存在弥散功能障碍,肺血管有明显的扩张。     

对肝肺综合征诊治的探讨

目的提高对肝肺综合征（ＨＰＳ）的认识。方法回顾性分析了６例ＨＰＳ的临床资料，所有患者均经动态肺灌注显像检查。结果６例ＨＰＳ的病因均为肝炎后肝硬化。除有肝病的临床表现外，还有进行性呼吸困难、紫绀（６／６）、杵状指（５／６）和低氧血症，平均动脉血氧分压为６．８７ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ），动脉血氧饱和度为８５．２％。此外，还有立位性缺氧或平卧呼吸。６例患者经动态肺灌注显像均异常，有肺内血管扩张。结论有门脉高压、皮下蜘蛛痣和杵状指体征时，提示ＨＰＳ的存在。早期诊断和治疗有助于缓解低氧血症，改善患者的预后。     

肝肺综合征的诊断与治疗

肝硬化患者肺血管异常越来越受到重视,因为这是影响肝移植患者生存率的重要临床因素.当肺内血管扩张影响到动脉氧合时就可认为存在肝肺综合征(HPS),它可发生在任何年龄阶段的肝病患者中[1].HPS由三部分组成:肝病、肺血管扩张、动脉氧合缺陷.     

经颈静脉肝内门体静脉分流术治疗肝肺综合征

我们采用经颈静脉肝内门体静脉分流术（ＴＩＰＳ）治疗了３例肝肺综合症（ＨＰＳ）患者，现报道如下。 １．资料与方法：（１）临床资料：３例ＨＰＳ患者，为肝炎后肝硬化，均为男性，年龄４５－５２岁．慢性肝炎病史 １０－１５年。１例于１０年前行脾切除术；３例患者均有呕血便血史，术前胃镜检查食道静脉曲张中到重度；活动性肝硬化２例，静止性肝硬化１例。Ｃｈｉｌｄ分级Ａ级１例，Ｂ级２例。３例患者均排除支气管肺部疾病，超声心动及心电图检查正常。３例符合ＨＰＳ的诊断标准［１］， 低氧血症经血气分析、动脉血氧分压（ＰａＯ２…     

Cirrhosis and hepatopulmonary syndrome

Hepatopulmonary syndrome(HPS)is characterized as a triad:liver disease,intrapulmonary vascular dilatation and arterial hypoxemia.HPS is reported to be present in 4%to 32%of adult patients with end-stage liver disease and in 9%-20%of children.The pathogenesis of HPS has not been clearly identified.Portal hypertension causes impairment in the perfusion of the bowel and increases the enteral translocation of Gram(-)bacteria and endotoxins.This stimulates the release of vasoactive mediators,such as tumor necrosis factor-alpha,heme oxygenase-derived carbon monoxide and nitric oxide.Genetic alterations have not been associated with this syndrome yet;however,cytokines and chemokines have been suggested to play a role.Recently,it was reported that cumulated monocytes lead to the activation of vascular endothelial growth factor-dependent signaling pathways and pulmonary angiogenesis,which plays an important role in HPS pathogenesis.At present,the most effective and only radical treatment is a liver transplant(LT).Cirrhotic patients who are on the waiting list for an LT have a shorter survival period if they develop HPS.Therefore,it is suggested that all cirrhotic cases should be followed closely for HPS and they should have priority in the waiting list.     

Portopulmonary hypertension and hepatopulmonary syndrome

The clinically and pathophysiologically distinct entities of portopulmonary hypertension and hepatopulmonary syndrome occur in a substantial proportion of patients who have advanced liver disease of different causes. These disorders are notoriously underdiagnosed, but they have a substantial impact on survival and require focused treatment. Abnormal intrapulmonary vascular dilatation, the hallmark of hepatopulmonary syndrome, can cause profound hypoxaemia that can be very difficult to treat. By contrast, portopulmonary hypertension results from excessive pulmonary vasoconstriction and vascular remodelling that eventually leads to right-heart failure. Insights into the pathogeneses of these syndromes have led to novel therapeutic approaches. However, in severely affected patients, effective treatment remains a difficult task. In selected patients, liver transplantation represents the only treatment option, but the decision to do isolated liver transplantation is particularly challenging in patients who have severe pulmonary disease involvement. Data from several centres have contributed to provide criteria that allow improved prediction of which patients may, or may not, benefit from liver transplantation alone.     

The hepatopulmonary syndrome

The hepatopulmonary syndrome occurs in subjects with chronic liver disease and/or portal hypertension who develop intrapulmonary vasodilation resulting in arterial deoxygenation. Clinical and basic science studies investigating the pathophysiology of HPS are presented. A diagnostic algorithm is provided using contrast echocardiography, the lung perfusion scan, and pulmonary angiography. Medical therapy and experience with liver transplantation are reviewed.