急性肺栓塞尿激酶静脉溶栓治疗的护理

2002年6月～2004年6月,我院用尿激酶静脉溶栓治疗急性肺栓塞11例,取得良好疗效。出将护理体会报告如下。     

急性肺栓塞溶栓治疗的系统评价设计方案

评价急性肺栓塞溶栓治疗的临床疗效与安全性。通过电子检索Cochrane气道组注册库(来自MEDLINE，EMBASE，CINAHL标准化检索)截止到2003年4月，手检呼吸系统的杂志和会议要。纳入所有采用溶栓治疗并继以肝素治疗或外科干预作比较的临床随机对照试验，排除不同溶栓之间或同一溶栓不同剂量之间比较的临床随机对照试验。两个评价员独立挑选纳入的试验，评价试验的质量及提取数据。     

尿激酶溶栓对急性大面积肺栓塞的疗放

溶栓疗法已被广泛用于治疗危及生命的急性大面积肺栓塞，它可迅速而持续减轻肺血管阻塞和肺动脉高压的作用，溶栓后使得肺血管再通，肺血液灌注恢复，不仅有助于降低急性肺栓塞的病死率厂还可防止再栓塞。但经静脉和经肺动脉溶栓的疗效比较国内未见报道，而国外的报道结果不一致。本试验初步探讨尿激酶经静脉和经肺动脉溶栓治疗肺栓塞疗效的差异。     

尿激酶溶栓加肝素抗凝治疗急性肺栓塞40例疗效观察

目的：观察尿激酶溶栓加肝素抗凝治疗急性肺栓塞的疗效。方法：尿激酶2万U/kg溶栓，待凝血活酶时间或激活的全血凝固时间恢复到基础值的1．5－2．0倍以内，开始给予肝素100mg，静脉滴注，1次／d，用肝素后3天，口服华法令3mg，1次／d，据凝血酶原活动度调整华法令剂量，使PTA维持在30％－40％或PTT在16－20s，持续服用约6个月。结果：溶栓加抗凝治疗者临床症状改善，核素肺灌注扫描总有效率，联用组为60％，单用组为10％，超声心动脉动脉收缩压比较，联用组为60％，单用组为10％，两组比较有显著性差异（P＜0．05），结论：尿激酶溶栓加肝素抗凝是治疗急性肺栓塞的可行方法。     

尿激酶,肝素治疗急性肺栓塞疗效观察

对比观察了联合应用尿激酶和肝素治疗急性肺栓塞（联用组）与单用肝素治疗（单用组）各３０例的治疗效果，结果：联用组放射核素肺扫押显示有效率与临床症关改善率均显著优于单用组（均Ｐ〈０．０１）；两组治疗均无出血并发症，提示联用尿激酶与肝素治疗优于单用肝素者，所用剂量安全。     

溶栓治疗22例急性肺栓塞疗效分析

急性肺栓塞国内并不少见 ,临床上极易误诊、漏诊 ,病死率仅次于肿瘤和心肌梗塞[1 ] 。美国肺栓塞死亡率 15 % ,国内尚无发病率的确切统计。溶栓疗法已广泛用于治疗急性大面积肺栓塞 ,降低了病死率和肺栓塞的复发率。近年来我们采用尿激酶不同剂量与方法进行溶栓治疗 ,现报道如下。一、资料与方法1.病例选择 :均为住院病人 ,诊断条件 ,有典型病史加下列之一者可确诊为肺栓塞 :(1)经选择性肺动脉造影证实肺动脉有阻塞 ,充盈缺损 ,内壁不光滑及截断现象 ;(2 )心脏彩超发现肺动脉血栓、肺动脉高压 ,右心扩大或右室肥厚或典型的心电图改变者 ,且…     

尿激酶溶栓治疗急性肺栓塞的临床护理

急性肺栓塞（APE）是由内源性或外源性栓子堵塞肺动脉或其分支,诱发肺循环出现障碍的一种临床综合征。APE临床表现多样,缺乏特异性,主要为胸部突然剧烈疼痛、咯血、呼吸困难、昏迷等。APE是一种临床急症,容易发生误诊、漏诊。及时溶栓治疗可使阻塞的肺动脉再次畅通,限制肺梗死范围,维持肺功能,降低死亡率。早期采取尿激酶溶栓治疗是目前治疗APE的主要方法,APE患者如能得到及时诊治与护理,病死率可下降2％～3％。本文就尿激酶溶栓治疗APE的护理作一探讨。     

18例急性肺栓塞尿激酶溶栓治疗临床观察

目的:观察并总结急性肺栓塞的溶栓治疗疗效.方法:18例急性肺栓塞患者予尿激酶溶栓,以20 kU/kg加入生理氯化钠100mL静脉滴注2小时,根据部分凝血活酶时间回缩至正常对照值的1.5～2.5倍时,皮下注射低分子肝素4 100U,每12小时1次,共7日,停低分子肝素前3日,开始并用华法林3～5 mg/d,连续3～6个月以上,观察疗效.结果:18例中,显效10例,有效4例,无效4例,总有效率78％.病程在14日以内的总有效12例(86％),病程超过14日总有效2例(2/4).结论:急性肺栓塞溶栓治疗安全有效,不良反应少,对于疗程超过14日的患者,溶栓时间窗可适当放宽,积极溶栓治疗.     

尿激酶、肝素治疗急性肺栓塞疗效观察

对比观察了联合应用尿激酶和肝素治疗急性肺栓塞（联用组）与单用肝素治疗（单用组）各30例的治疗效果。结果：联用组放射核素肺扫描显示有效率与临床症状改善率均显著优于单用组（均P＜0．01）；两组治疗均无出血并发症。提示联用尿液酶与肝素治疗优于单用肝素者，所用剂量安全。     

尿激酶静脉溶栓治疗急性脑梗塞疗效观察

目的：急性脑梗塞患者静脉滴注尿激酶(UK)后皮下注射低分子肝素(LMWH)，观察其临床疗效。方法：选择急性脑梗塞患者42例，用100万U尿激酶静脉点滴，6小时后皮下注射LMWH，与常规治疗组的36例急性脑梗塞作随机同期对照研究。结果：治疗组疗效明显高于对照组。结论：静脉滴注尿激酶治疗急性脑梗塞能显著改善患者的临床症状，降低致残率，并未增加脑出血的发生率。     

肺动脉栓塞不同时相的尿激酶溶栓疗效观察的实验研究

目的探讨肺动脉栓塞不同时相的尿激酶溶栓的疗效。方法成功制作11头小型猪肺动脉栓塞实验模型(另1头死于出血性肺梗死),以尿激酶作为溶栓剂,观察在栓塞不同时相(栓塞术后30min、栓塞术后10天、术后30天)的溶栓治疗效果。结果实验小型猪在肺动脉栓塞急性期(3头次)以尿激酶15×104U溶栓治疗后被栓塞肺动脉恢复通畅;亚急性期(3头次)以30×104U尿激酶后得到同样结果;慢性期(3头次)以50×104U尿激酶溶栓后,肺动脉三级分支内的血栓完全溶解,再追加5×104U尿激酶,肺动脉四级分支内血栓明显减少。结论肺动脉栓塞不同时相的尿激酶溶栓治疗均有一定的疗效,急性期和亚急性期较慢性期的疗效好,不同时相的溶栓治疗所需尿激酶剂量随栓塞时间延长而呈递增趋势。     

急性肺栓塞的腔内治疗效果观察

目的 观察急性肺栓塞的腔内治疗效果.方法 选择2009年1月至2011年6月我院收治的急性肺栓塞患者15例,采用经皮导管碎栓术及溶栓术治疗.局部灌注尿激酶,总量50万U;溶栓后给予低分子肝素钠7～10d,口服华法林钠3～6个月.观察临床症状和体征改善情况、并发症、平均肺动脉压（mPAP）与动脉血氧分压（PaO2）的变化,以及肺动脉开通情况.结果 12例肺动脉完全开通,3例部分开通,有效率100％（15/15）.mPAP较术前降低[（40.07±5.97）、（20.00±4.66） mmHg],PaO2明显升高[（50.26±9.30）、（80.49±9.04） mmHg],差异均有统计学意义（t值分别为-1.128和1.246,P均＜0.05）.随访3～6个月,疗效持续,未见复发.结论 急性肺栓塞介入治疗效果显著,安全可行.     

尿激酶溶栓治疗人工血管动静脉内瘘急性血栓形成

目的总结尿激酶溶栓治疗人工血管动静脉内瘘急性血栓形成的方法及经验。方法采用人工血管动脉端输液针局部穿刺,尿激酶微量泵持续灌注溶栓作为首选措施治疗人工血管动静脉内瘘急性血栓形成。结果共观察人工血管动静脉内瘘急性血栓形成20例,男性6例,女性14例,平均年龄(61.42±13.30)岁。人工血管动静脉内瘘建立时间1月～8年。急性血栓形成病程1h～6d。溶栓成功14例,溶栓失败6例,成功率70%。平均溶栓时间为(10.73±5.94)h,平均尿激酶溶栓剂量为(81.75±40.01)万U。溶栓成功率与静脉流出道状态显著相关。结论尿激酶直接注射溶栓治疗简便、安全、有效,使进一步球囊扩张成为可能,并减少临时血液透析插管及手术重建及其相关并发症,可作为人工血管内瘘血栓形成的首选方法。     

Cerebral infarction following thrombolysis for massive pulmonary embolism

A 29-year-old male developed a fatal stroke 6 h after successful thrombolysis for massive pulmonary embolism. Autopsy showed thrombus protruding through a patent foramen ovale (PFO). A strand of thrombus extended from the aortic arch into the left common carotid artery. The brain showed extensive infarction of the left fronto-parietal area. Thrombolysis caused initial disintegration of the embolism. It is likely that thrombolysis caused fragments of clot to later break lose and embolise into the cerebral circulation. We discuss the need for risk stratification in patients who present with massive pulmonary embolism and PFO.     

Mortality risk assessment and the role of thrombolysis in pulmonary embolism

Acute venous thromboembolism remains a frequent disease, with an incidence ranging between 23 and 69 cases per 100,000 population per year. Of these patients, approximately one-third present with clinical symptoms of acute pulmonary embolism (PE) and two-thirds with deep venous thrombosis (DVT). Recent registries and cohort studies suggest that approximately 10% of all patients with acute PE die during the first 1 to 3 months after diagnosis. Overall, 1% of all patients admitted to hospitals die of acute PE, and 10% of all hospital deaths are PE-related. These facts emphasize the need to better implement our knowledge on the pathophysiology of the disease, recognize the determinants of death or major adverse events in the early phase of acute PE, and most importantly, identify those patients who necessitate prompt medical, surgical, or interventional treatment to restore the patency of the pulmonary vasculature.     

Factor Xa inhibition and sPESI failure in intermediate-high-risk pulmonary embolism

We report the case of a 61-year-old man who presented at the Emergency Department (ED), complaining of sudden-onset dyspnea and chest pain after a long flight from Tokyo to Houston. Considering his clinical stability and sPESI 0, enoxaparin 1?mg/kg BID was started for 24?h, and the patient was then considered for early discharge with apixaban 10?mg BID. Direct-factor Xa inhibition did not improve extensive thrombus burden and right ventricular dysfunction despite D-dimer measurement reduction. Because of the treatment failure, we considered thrombolysis. Currently, recommendations to use thrombolysis in patients under non-vitamin K antagonist oral anticoagulants (NOACs) do not exist. Hence, the one dose of apixaban was stopped, and 12?h later, we performed successful thrombolysis. A systematic review from 2007 to 2017 did not identify any cases related to NOACs failure to reduce thrombus burdens in patients with PE and persistent right ventricular dysfunction. We also did not find any evidence of cases that reported strategies for urgent thrombolysis in PE patients on NOACs. To the best of our knowledge, apixaban's failure to reduce thrombus burden, persistent right ventricular dysfunction, and a NOACs-thrombolysis bridge in patients with PE on apixaban has not been previously described. Both the bedside risk stratification and the therapeutic failures should alert clinicians in the ED to the potential limitations of low-molecular-weight heparin, NOACs therapy, and sPESI in the setting of intermediate-high-risk PE.     

Volumetric capnography as a bedside monitoring of thrombolysis in major pulmonary embolism

Objective To describe the use of volumetric capnography, a plot of expired CO₂ concentration against expired volume, in monitoring fibrinolytic treatment of major pulmonary embolism.Design and setting Two case reports in the emergency department of a teaching hospital.Patients Two conscious and spontaneously breathing patients (69- and 31-year-old women) with major pulmonary embolism requiring thrombolysis. Decision for thrombolysis was based on the association of right ventricular afterload on echocardiography, with respiratory failure and hypotension in the first patient, and dyspnea and hemodynamically stable parameters in the second one.Interventions Successive capnographic measurements were performed before, during, and after thrombolysis. Curves of volumetric capnography were obtained from a sidestream gas monitor with flow sensor and an arterial blood gas analysis for CO₂ partial pressure.Measurements and results We calculated late deadspace fraction, previously suggested as the most effective capnographic parameter in the diagnosis of pulmonary embolism. Late deadspace fraction decreased in the two patients, respectively, from 64.4% to 1.1% and from 25.6% to 5.7% after thrombolysis, with a concomitant disappearance of right heart dysfunction signs on echocardiography.Conclusions Volumetric capnography can monitor thrombolysis in major pulmonary embolism. Differences between volumetric capnography technology and the more traditional arterial to end-tidal CO₂ gradient are important to take into account for clinical application.     

急诊重症肺血栓栓塞症12例临床分析

目的 重点探讨重症急性肺栓塞的急诊诊治思路.方法 收集2001-01至今在我科确诊并进行急诊静脉溶栓的急性肺栓塞患者12例,其中男女各6例,平均年龄57.8岁.分别就其临床特征、辅助检查、溶栓治疗及预后等方面进行回顾性分析.结果 ①呼吸困难、胸闷或喘憋是肺栓塞患者最常见的主诉;②下肢深静脉血栓仍是肺栓塞栓子的主要来源;③心电图、血气分析和D-二聚体是急诊筛查肺栓塞的首选手段,而螺旋CT肺血管成像是急诊确诊肺栓塞的首选检查;④静脉溶栓是急诊肺栓塞的一个重要治疗手段,且安全性很好.在实际应用中需要综合考虑患者的临床情况和影像学表现.结论 急诊肺栓塞在诊治方面具有其自身特点,急诊静脉溶栓的选择需要综合考虑患者的临床情况和影像学表现.     

超声心动图急性肺栓塞溶栓治疗的评估

目的应用超声心动图技术观察急性肺栓塞患者溶栓抗凝治疗前后肺动脉栓子、右心结构及收缩功能的改变。方法前瞻性非随机对照研究,对2002年12月至2006年4月间经肺动脉CT或肺血管造影证实的30例急性肺栓塞患者行溶栓治疗,应用经胸超声心动图观察治疗前、治疗后24～30h、1个月的肺动脉栓子、主肺动脉及其分支内径、右房室内径,右室前壁运动幅度、右室舒张末期容积、右室射血分数,三尖瓣返流、肺动脉收缩压等指标。结果30例急性肺动脉栓塞患者溶栓治疗24～30h后右房室结构明显改善,表现为右房长径及横径、右室前后径及横径、主肺及右肺动脉内径、右室舒张末期容积与治疗前比较明显回缩(P<0.01),右室前壁运动幅度、右室射血分数有所增加(P<0.01),肺动脉收缩压明显下降(P<0.01);治疗后1个月后右房室大小、主肺及右肺动脉内径、右室舒张末期容积、右室前壁运动幅度及肺动脉收缩压等仍有恢复(P<0.05或P<0.01)。5例患者主肺动脉和/或右、左肺动脉内检出栓子,溶栓后栓子逐渐消失。结论超声心动图可动态、实时、无创评价急性肺动脉栓塞溶栓治疗效果,尤对血栓的溶解、右房室结构、右室超负荷及肺动脉高压的变化有独到的价值。     

52例急性肺栓塞临床分析

目的 探讨急性肺栓塞的早期临床特征、危险因素以及正确的诊断程序.方法 对我院2004年1月至2005年12月收治的52例急性肺栓塞患者的发病情况、辅助检查以及易患因素进行评估分析.结果 呼吸困难及气促、胸痛、咯血、晕厥等为急性肺栓塞最典型的早期表现,而胸痛、咯血、呼吸困难三者同时出现占11.5%.检测D-二聚体＞500μg/L者为100%,血气分析显示低氧血症占94.2%,心电图呈典型SⅠQⅢTⅢ(Ⅰ导联出现S波、Ⅲ导联出现Q波及T波)占13.6%,超声心动图显示肺动脉高压占82.5%,右心室扩大占38.5%.初诊确诊率为82.7%.下肢深静脉血栓、慢性心、肾疾病、恶性肿瘤以及围手术期患者均是肺栓塞的高危人群.结论 急性肺栓塞早期多数无特异性临床表现,对于有高危因素的患者,排除其他原因的呼吸困难、胸痛、咯血等表现后,特别是对有晕厥史者,应及早床旁进行肺栓塞的相关检查,提高初诊确诊率,以防误诊和漏诊.