导管血栓捣碎与局部溶栓术治疗肺动脉栓塞患者的护理

肺动脉栓塞(Pulmonary Embolish，PE)是内源性或外源性栓子阻塞肺动脉或其分支引起肺循环障碍的临床和病理生理综合征。肺动脉内导管血栓捣碎与局部溶栓术是将造影导管直接送至肺动脉血栓处，先将血栓捣碎后注射溶栓药物达到溶解血栓、改善肺动脉循环的目的。此介入治疗损伤小、疗效好、简便易行。但术后的护理观察是保证PE治疗效     

小剂量阿替普酶联合尿激酶在急性肺栓塞治疗中的临床研究

目的研究小剂量组织型纤溶酶原激活物阿替普酶联合尿激酶治疗急性肺动脉栓塞的临床疗效及安全性。方法将46例急性肺动脉栓塞患者随机分为两组,A组22例,第1天阿替普酶20 mg加尿激酶60万U溶栓,第2~5天尿激酶60万U/d;B组24例,第1天尿激酶首剂40 000 U/kg,30 min内静脉注射,然后120万U溶栓,第2~5天尿激酶60万U/d;观察两组溶栓效果及并发症。结果 A组溶栓显效14例,有效5例,无效3例,总有效率为86.36%;B组溶栓显效9例,有效11例,无效4例,总有效率为83.33%;两组有效率比较差异未见统计学意义(P0.05),但两组显效率比较差异有统计学意义(P0.05);溶栓后第1天两组患者肺动脉压、动脉血氧分压比较差异有统计学意义(P0.05);溶栓后3、5 d两组患者肺动脉收缩压、动脉血氧分压比较差异未见统计学意义(P0.05)。除血尿及置管处渗血,未见严重的不良反应,A组渗血1例,B组血尿2例,两组比较差异未见统计学意义(P0.05)。B组24 h死亡1例,其余患者无死亡。结论溶栓治疗急性肺动脉栓塞有效,早期溶栓可以降低病死率;小剂量阿替普酶结合尿激酶治疗急性肺动脉栓塞安全有效,优于单纯尿激酶治疗。     

瑞替普酶与尿激酶在急性肺栓塞溶栓治疗中的比较研究

目的研究瑞替普酶对急性肺动脉栓塞溶栓治疗的方法、临床疗效及安全性。方法47例符合溶栓治疗的急性肺动脉栓塞患者,其中26例给予瑞替普酶18mg溶栓,21例给予尿激酶100万U溶栓,分别观察溶栓前及溶栓4h后患者的临床表现、螺旋CT肺动脉成像的变化,比较两者的溶栓效果。结果应用瑞替普酶对26例急性肺栓塞患者溶栓后显效13例,有效9例,无效4例,总有效率为84.62%;尿激酶的总有效率为76.19%;溶栓后所有患者未见严重的副作用。结论应用瑞替普酶对急性肺动脉栓塞进行溶栓有较好的临床疗效及安全性,优于尿激酶。     

不同剂量尿激酶治疗急性脑梗死的临床观察

目的观察两种剂量尿激酶对急性脑梗死静脉溶栓的疗效及安全性。方法符合标准的80例急性脑梗死患者随机分成2组:A组接受尿激酶7.5×105U,30min滴完,B组接受尿激酶1.0×106～1.5×106U,30～45min滴完。结果两组治疗后神经功能缺损评分较治疗前均有明显改善,组间比较无显著差异(P>0.05);A组总有效率及显效率分别为82.5%、60.0%;B组分别为87.5%、65.0%(P>0.05)。B组较A组发生出血并发症多。结论小剂量尿激酶静脉溶栓治疗急性脑梗死有效,且更安全。     

小剂量尿激酶超早期溶栓治疗急性脑梗死

目的 探讨小剂量尿激酶静脉溶栓治疗发病6 h内的脑梗死急性期的临床疗效.方法 将入选患者80例随机分为溶栓组和对照组,每组各40例,分别进行临床疗效的全面观察.溶栓组选取发病不超过6 h,年龄在30～70岁,使用20万U尿激酶 生理盐水20ml静脉推注,续以尿激酶20～40万U加入生理盐水250 ml静脉点滴,每日1次,连用5～7 d.结果 溶栓组疗效明显优于对照组,P《0.01差异有统计学意义.结论 小剂量尿激酶超早期溶栓治疗能有效阻止血栓进展,减少再栓塞,有利于神经功能恢复,疗效显著而无明显副作用,比常规治疗起效快,作用强,致残率低且安全可靠,值得推广.     

胸腹腔镜术后下肢静脉血栓形成及肺动脉栓塞

目的研究胸腹腔镜术后下肢深静脉血栓形成及肺动脉栓塞的发生原因及防治方法。方法回顾总结2001年3月-2003年6月收治的胸腹腔镜术后8例，胸腔镜术后4例下肢深静脉血栓形成及其中2例肺动脉栓塞的病人资料。结果12例病人诊为深静脉血栓形成后均予卧床休息，抬高患肢，使用肝素、尿激酶抗凝、溶栓。2例肺栓塞行2h溶栓，1例发生肺栓塞后出现心跳、呼吸骤停，予心肺复苏、溶栓抢救成功。全组病例均痊愈出院。结论胸腹腔镜术后下肢深静脉血栓形成有一定的发病率，要尽早抗凝、溶栓治疗，其中部分病人可能发生大面积肺动脉栓塞，要及时予以大剂量尿激酶溶栓，才能挽救病人生命。高危病人术前可植入腔静脉滤器防治致死性肺动脉栓塞。     

肾动脉栓塞所致急腹症的诊断及治疗

目的 探讨肾动脉栓塞引发急腹症的早期诊断和治疗方案.方法 大连市中心医院于2007-01～2007-05期间收治的由于肾动脉栓塞引起的急腹症患者3例,均合并有房颤病史.2例行数字减影肾动脉造影确诊为肾动脉主干栓塞,采用尿激酶局部灌注疗法溶栓和血栓抽吸术治疗;1例因肠梗阻、腹膜炎行剖腹探查术,术中发现肾动脉分支栓塞,术后采用尿激酶溶栓、抗凝、祛聚治疗.结果 3例患者均在腹痛发生后12 h内确诊,2例肾动脉主干栓塞患者经积极的溶栓、取栓治疗后再通,肾血流供应恢复,腹痛症状消失,肾功能正常;1例肾动脉分支栓塞患者溶栓治疗后腹痛症状消失.结论 数字减影肾动脉造影是肾动脉栓塞早期诊断最直接可靠的方法,早期尿激酶局部灌注疗法溶栓、血栓抽吸术取栓和抗凝、祛聚等治疗是尽快恢复肾动脉栓塞患者肾脏血流灌注的有效方法.     

纤溶酶联合抗凝治疗急性次大面积肺血栓栓塞症的有效性及安全性研究

目的 观察纤溶酶联合抗凝治疗急性次大面积肺血栓栓塞症的有效性和安全性.方法 选择经CT肺动脉造影(CTPA)或肺动脉造影和心脏超声心动图明确诊断急性次大面积肺血栓栓塞症的患者,随机分为常规抗凝治疗组、纤溶酶治疗组、尿激酶溶栓组,分别予以单纯抗凝、纤溶酶联合抗凝及尿激酶溶栓抗凝治疗,观察治疗10 d后的右心功能及出血副作用的发生率.结果 三组治疗前后右心功能比较均差异有统计学意义(P＜0.05).纤溶酶治疗组及尿激酶溶栓组与常规抗凝治疗组右心功能相比差异均有统计学意义(P＜0.05),而纤溶酶治疗组与尿激酶溶栓组之间相比差异无统计学意义(P＞0.05).常规抗凝治疗组出血副作用与纤溶酶治疗组比较差异无统计学意义 (P＞0.05),而常规抗凝和纤溶酶治疗组与尿激酶溶栓组相比差异均有统计学意义 (P＜0.05),尿激酶溶栓组有更多出血危险性.结论 纤溶酶联合抗凝治疗急性次大面积肺血栓栓塞症是一种安全、有效的方法.     

尿激酶溶栓治疗血液透析患者动静脉内瘘血栓形成的观察及护理

目的探讨尿激酶溶栓对血液透析患者动静脉内瘘血栓形成的疗效及护理。方法注射尿激酶(5～50)×103U(平均21.6±13.1)×103U对动静脉内瘘血栓行局部溶栓。治疗前后均行血管彩色超声检查,测定肝肾功能、凝血酶原时间(PT)及血浆纤维蛋白原(Fib),并监测血压,观察不良反应发生情况。结果48例患者共行50次溶栓治疗,成功43例次(86%),瘘管在注射尿激酶(47.3±62.8)min后通畅。治疗后患者肝肾功能、PT、Fib及血压与治疗前比较无显著差异。无1例患者发生出血及栓塞并发症,3例患者用药后出现一过性发热。结论尿激酶溶解透析通路血栓操作简单,创伤小,成功率较高,不良反应少,有较高的临床应用价值。但对于女性患者、血栓较为陈旧及存在血栓性静脉炎等情况疗效可能不理想。     

急性肺血栓栓塞症溶栓疗效评价

目的应用多层螺旋CT肺动脉造影评价急性肺血栓栓塞症(PTE)尿激酶溶栓治疗前后血栓的变化。方法总结分析18例急性PTE患者临床表现,溶栓前后实验室检查及心脏超声的变化,应用多层螺旋CT计数溶栓前后血栓累及肺段数量。结果本组患者以胸闷、气短为主诉就诊,院前误诊率(88.9%,16/18),3例(16.7%)曾出现晕厥,经溶栓治疗后临床症状明显缓解;心脏超声显示溶栓后右房、右室直径明显缩小(P<0.05);多层螺旋CT肺动脉造影显示血栓累及肺段数量溶栓后明显减少(P<0.001);其中6例患者血栓完全消失,溶栓治疗前与治疗后的血栓累及肺段数量有相关性(r=0.742,P<0.001)。结论尿激酶溶栓方案对于PTE安全有效,多层螺旋CT肺动脉造影能够明确显示溶栓治疗前后血栓的变化,可作为评价治疗效果的重要客观检查。     

经导管动脉注射玻璃酸酶联合尿激酶溶栓治疗眼动脉栓塞兔模型

目的 观察经导管动脉注射玻璃酸酶联合尿激酶溶栓治疗兔眼动脉栓塞的价值。方法 将27只健康新西兰大白兔随机分A、B、C 3组,每组9只,以微导管超选择至兔眼动脉,注射透明质酸,建立兔眼动脉栓塞模型;建模30 min后,经超选择性动脉插管,分别对A、B及C组兔眼动脉注射尿激酶、玻璃酸酶及玻璃酸酶联合尿激酶,并行眼动脉造影观察各组溶栓情况,观察玻璃酸酶联合尿激酶溶栓治疗兔眼动脉栓塞的价值。结果 建立兔眼动脉栓塞模型耗时12~57 min,平均（23.04±10.05） min。溶栓后10 min,A、B及C组兔眼动脉开通率分别为11.11%（1/9）、22.22%（2/9）及44.44%（4/9）;溶栓30 min后各组开通率分别为11.11%（1/9）、22.22%（2/9）及55.56%（5/9）,组间两两比较差异均无统计学意义（P均>0.05）,但B及C组眼动脉未能开通的兔眼球周围血运较溶栓前明显改善。结论 经导管注射玻璃酸酶联合尿激酶溶栓可用于治疗兔眼动脉栓塞。     

Thrombolysis for pulmonary embolism

More than 10 years ago, thrombolytic therapy with urokinase and streptokinase for pulmonary embolism was found to have considerable advantages over standard heparin therapy. After the introduction of alteplase, a recombinant tissue plasminogen activator, further studies confirmed this benefit. However, thrombolytic therapy for pulmonary embolism has not gained universal acceptance, even though it now has U.S. Food and Drug Administration approval. Clear advantages of thrombolytic therapy over conventional heparin therapy are improved pulmonary capillary blood volume, accelerated clot lysis and accelerated pulmonary perfusion. Earlier reversal of right-sided heart failure, a lower incidence of recurrent pulmonary embolism, a reduced risk of chronic pulmonary hypertension and reduced mortality have been claimed as advantages, but these have not been adequately proved. A recent survey suggests that about half of all patients with pulmonary embolism are potential candidates for thrombolytic therapy. In a subset of patients with hemodynamic compromise, thrombolysis has definite advantages over heparin therapy.     

介入溶栓治疗胸腔镜下肺癌根治术后高危肺栓塞的经验分析

目的 探讨不同介入溶栓方式治疗胸腔镜下肺癌根治术后高危肺栓塞(PE)的价值.方法 选取2018年就诊于河南大学第一附属医院的3例胸腔镜下肺癌根治术后发生高危PE的患者作为研究对象,其中1例接受单纯静脉溶栓治疗,1例接受单纯动脉介入溶栓治疗,1例接受静脉肺动脉联合介入溶栓治疗,分析3例患者住院治疗方式、溶栓治疗效果和术后...     

核素肺灌注显像对血压正常伴右室功能不全的急性肺栓塞症溶栓疗效的评价

目的：运用核素肺灌注显像对血压正常伴右室功能不全的急性肺栓塞患者溶栓治疗前后肺血流灌注进行观察和定量分析．为临床疗效评价提供准确和直观的客观依据。方法：36例急性肺栓塞患者分为溶栓组和抗凝组。在治疗前后均行肺灌注显像。应用半定量法计算全肺灌注缺损百分数（percentage of pulmonary defect score，PPDs）和灌注改善百分数（percentage of pulmonary improve score，PPIs）。治疗前、治疗后7～10d及25—30d的PPDs分别记为PPDsD0、PPDsD10和PPDsD30。各组PPDsD0与PPDsD30之差、PPDsD0与PPDsD10之差、PPDsD10与PPDsD30之差分别记为PPIs、PPIsI1、PPIsI2。结果：溶栓组、抗凝组PPDs在治疗后均随时间显著降低（P〈0．001）；溶栓组PPIsI1明显大于抗凝组；两组PPIsI2无明显差异。在整个观察期间（治疗后1个月），溶栓组PPIs明显大于抗凝组。结论：溶栓治疗较单抗凝治疗能够更加迅速而持续地改善肺栓塞患者的肺血流灌注，应用肺灌注显像可以准确地评价患者治疗前后的肺血流变化     

Successful treatment of massive pulmonary embolism with recombinant tissue type plasminogen activator (rt-PA) in a pregnant woman with intact gravidity and preterm labour

We report a patient with massive pulmonary embolism and circulatory shock during pregnancy (31 st gestational week) and preterm labour who has been successfully treated with recombinant tissue type plasminogen activator. Thrombolysis was performed using 10 mg·h^–1 over 4 h followed by 2 mg·h^–1 for 1 h 30 min resulting in complete resolution of cardio-respiratory symptoms. Except for slight bleeding from one puncture site no complications occurred. At 48 h after the end of thrombolytic therapy the patient was delivered spontaneously of a male preterm healthy infant. The relevance of this new thrombolytic agent in the treatment of massive life-threatening pulmonary embolism during pregnancy is discussed.     

Bolus injection of thrombolytic agents during cardiopulmonary resuscitation for massive pulmonary embolism

Thrombolytic therapy has proved to be efficacious in the treatment of massive and fulminant pulmonary embolism (PE), but thrombolysis has been considered as contraindicated during cardiopulmonary resuscitation (CPR). This review on the administration of thrombolytic agents in patients who have suffered massive PE necessitating CPR summarises 14 anecdotal reports and three case series involving 34 patients. The case series revealed an overall initial survival rate of 55–100% following bolus administration of thrombolytic agents. In general, bleeding complications were managed conservatively. The establishment of the diagnosis may be feasible using echocardiography or bedside angiography during CPR. However, therapeutic measures should be taken without delay; the patient's history and the clinical picture may thus be the only diagnostic criteria. Even where myocardial infarction is misinterpreted as PE during CPR, bolus injection of a thrombolytic agent can be an appropriate therapeutic option. An alternative may be mechanical catheter fragmentation of the thrombus with subsequent local thrombolysis. Surgery may be restricted to hospitals with ready access to extracorporeal circulation. We conclude that early administration of thrombolytic agents during PE necessitating CPR may help to reduce mortality. We favour the administration of urokinase (2– to 3 000 000-U bolus) or rt-PA.     

建立及评价适于血流储备分数CT成像模拟的小型猪慢性冠状动脉狭窄模型

目的 建立适于血流储备分数CT成像（FFR_CT）模拟研究的小型猪慢性冠状动脉狭窄模型,并评价其可靠性。方法 巴马小型猪16头,开胸于冠状动脉前降支近或中段放置Ameroid缩窄环。建模后第2周进行冠状动脉CTA监测其狭窄程度;末次冠状动脉CTA检查2日内进行冠脉造影验证狭窄程度,并测血流储备分数（FFR）。基于冠状动脉CTA图像建立计算流体力学模型,获得FFR_CT值,并与FFR值进行比较,验证模型可靠性。结果 10头小型猪成功建模,共完成CTA检查24次,图像质量均达到诊断要求。术后第2周,前降支轻微狭窄,术后第3周9头实验猪狭窄>50%,术后第4周其余1头狭窄>50%。冠状动脉CTA示狭窄程度与冠状动脉造影结果一致。FFR_CT值与实测FFR值差异无统计学意义（t=-1.13,P=0.29）。结论 应用Ameroid环置入巴马小型猪冠状动脉左前降支近段或中段,并定期采用CTA监测,可有效建立适用于基于冠状动脉CTA图像无创性血流动力学模拟研究的慢性冠状动脉狭窄模型。     

急性肺栓塞性肺高压局部溶栓和全身溶栓的比较

目的研究经导管肺动脉局部溶栓与外周静脉全身溶栓在急性肺栓塞性肺动脉高压治疗中的作用。方法20只小猪自体血栓注入建立急性肺栓塞性肺动脉高压模型。随机分成两组:经导管肺动脉局部溶栓(A组10只),外周静脉全身溶栓(B组10只)。溶栓前、溶栓后2h测肺动脉压,肺动脉收缩压(PASP),心率(HR),心输出量(CI),血气分析(PaO2、PaCO2、pH),纤溶酶_抗纤溶酶复合物(PAP),DD二聚体(DD),一氧化氮(NO)。结果两组肺动脉压、CI、PaO2、PaCO2、PAP、DD、NO均较治疗前有显著变化(P<0.05),A组的肺动脉压、PaO2、PaCO2、PAP的变化较全身溶栓组B组的变化更显著(P<0.05)。结论肺栓塞治疗中局部溶栓的疗效优于全身溶栓。     

Treatment of acute pulmonary embolism by a low molecular weight heparin fraction. A preliminary study

We evaluated the antithrombotic efficacy of the low molecular weight heparin (LMWH) fraction PK 10169 in nine consecutive patients with acute pulmonary embolism documented by pulmonary angioscan and angiography. Therapy with PK 10169 was initiated by an i.v. bolus of 0.5 mg/kg, followed by a continuous intravenous infusion during the first 10 days; the drug was then given subcutaneously twice daily during the following 15 days. The dosage of PK 10169 was adjusted by daily measurements of anti-Xa and anti-IIa activities using amidolytic methods. For a dosage ranging from 1.4 to 4.1 mg/kg per day during the i.v. period and from 0.7 to 3.5 mg/kg per day during the s.c. period, the anti-Xa activity ranged from 4 to 8.7 PK U/ml and from 4.5 to 7.2 PK U/ml respectively. Clinical improvement was observed in all the patients and was consistent with progressive reperfusion evaluated by successive angioscans. No recurrence of pulmonary embolism occurred. No deleterious hemorrhagic side-effects were observed, even in two patients at high risk of bleeding. In this pilot study, the LMWH fraction PK 10169 proved to be an effective anticoagulant therapy during the first three weeks after pulmonary embolism in man.     

Resolution of Experimental Pulmonary Emboli with Heparin and Streptokinase in Different Dosage Regimens

Thrombolytic agents may be useful in acute pulmonary embolism, but their optimal dosage remains uncertain. We have examined the relative efficacy of heparin and different doses of streptokinase, either alone or in combination, in acute experimental pulmonary embolism. A standardized massive embolus of autologous blood clot incorporating canine [(125)I]-fibrinogen was given to 40 dogs; the degree of resolution after 24 h was quantitated by measuring the radioactivity in the lungs and was compared with detailed postmortem observations.The amount of residual embolus was 49% in control animals, 28% after heparin (200 U/kg loading dose and 800 U/kg/24 h maintenance dose), and 6% after high dose streptokinase (250,000 U loading dose and 100,000 U/h maintenance dose); it was 31% after low dose streptokinase (25,000 U loading dose and 10,000 U/h maintenance dose), 7% after low dose streptokinase with heparin, 14% after very low dose streptokinase (5,000 U/h without a loading dose) with heparin, and 9% after short course streptokinase (250,000 U loading dose and no maintenance dose) with heparin.The combination of heparin and low doses or brief courses of streptokinase appeared to be synergistic and produced as much resolution as did standard high dose streptokinase alone. The enhanced resolution of pulmonary emboli in heparin-treated animals may have been due to the prevention by heparin of further deposition of fibrin on the embolus. It appears that dosage regimens of thrombolytic therapy other than those in current use may be worthy of clinical examination.