肺血栓栓塞症的研究进展

肺栓塞(pulmonary embolism,PE)是以各种栓子阻塞肺动脉系统为发病原因的一组疾病或临床综合征的总称[1]。肺血栓栓塞症(pumlonary thromboembolism,PTE)是PE的最常见类型,是指来自静脉系统或右心的血栓阻塞肺动脉或其分支所致疾病,以肺循环和呼吸功能障碍为其主要临床和病理生     

肺血栓栓塞症治疗进展

肺血栓栓塞症（PTE）是来自静脉系统或右心血栓阻塞肺动脉或其分支所导致的疾病,以肺循环和呼吸功能障碍为主要临床特征。PTE 是临床常见危重病症,未经治疗的 PTE 患者病死率为25％～30％［1］。PTE 的治疗策略主要是根据患者危险度分层决定治疗方法［2］,其疗方法主要有抗凝、溶栓、介入与手术治疗等。     

心房颤动合并左心房巨大血栓及肺动脉血栓栓塞症1例并文献复习

<正>1肺栓塞是以各种栓子阻塞肺动脉或其分支为其发病原因的一组疾病或临床综合征的总称,包括肺血栓栓塞症(PTE)、脂肪栓塞综合征、羊水栓塞、空气栓塞、肿瘤栓塞等,其中PTE为肺栓塞的最常见类型。引起PTE的血栓主要来源于下肢的深静脉血栓形成(DVT)。除了下肢静脉血栓外,右心房血栓也是不容忽视的栓子来源,心房纤颤为引起左心房及右心房血栓的常见原因之一,本文通过我科收治的1例心房颤动引起左心房巨大血栓及慢性肺动脉血栓栓塞症1例进行总结,结合文献     

肺血栓栓塞症的病理与病理生理

肺血栓栓塞症 (ｐｕｌｍｏｎａｒｙｔｈｒｏｍｂｏｅｍｂｏｌｉｓｍ ,ＰＴＥ)为来自静脉系统或右心的血栓阻塞肺动脉或其分支所致的疾病 ,以肺循环和呼吸功能障碍为其主要临床和病理生理特征。引起ＰＴＥ的血栓主要来源于深静脉血栓形成 (ｄｅｅｐｖｅｎｏｕｓｔｈｒｏｍｂｏｓｉｓ,ＤＶＴ)。ＰＴＥ与ＤＶＴ共属于静脉血栓栓塞症 (ｖｅｎｏｕｓｔｈｒｏｍｂｏｅｍｂｏｌｉｓｍ ,ＶＴＥ)。一、深静脉血栓形成ＤＶＴ的病理基础是血管内皮损伤、血流淤滞和血液高凝状态。凡可引起以上任一病理基础的临床病理生理改变均可作为独立的危险因素[1] …     

低分子肝素与血栓栓塞性疾病

血栓栓塞性疾病包括动脉粥样硬化血栓性疾病和静脉血栓栓塞性疾病，动脉粥样硬化血栓性疾病涉及冠状动脉、脑动脉和外周动脉；静脉血栓栓塞性疾病(VTE)包括深静脉血栓形成(DVT)和肺栓塞(PE)。血栓栓塞性疾病是各种内在和外在因素导致动脉和静脉血管内血栓形成和(或)栓塞并导致组织和器官功能受损的病理过程。治疗的关键是抗血小板和抗凝治疗。传统的抗凝药物主要是未分离肝素，     

肺血栓栓塞症的介入治疗

肺动脉血栓栓塞症,简称肺栓塞(pulmonaryembolism,PE)是指血栓堵塞了肺动脉主干或分支所引起的肺循环障碍,其原因多与深静脉血栓形成有关.临床表现复杂,重者猝死.由于PE突发率高、易误诊、漏诊等原因,急性大面积PE死亡率极高[1],我国最新统计资料显示PE占全部死因的第四位. 急性PE主要常用的治疗方法有抗凝、全身静脉溶栓、导管肺动脉局部溶栓、导管碎栓和除栓、外科手术取栓等.如果患者伴发心脏骤停、休克、大面积致死性肺栓塞或存在明确的溶栓、外科手术禁忌证,导管介入治疗是替代治疗方案之一.     

67例肺血栓栓塞症患者的临床分析

<正> 肺血栓栓塞症(pulmonary thromboembolism,PTE)是指血栓栓子堵塞肺动脉主干和(或)其分支所引起的以肺循环障碍为主要表现的临床病理综合征。为进一步提高PTE的诊断率及治愈率,本研究对我院收治的67例PTE患者进     

肺血栓栓塞症30例诊治体会

肺血栓栓塞症（PTE）为来自静脉系统或右心的血栓阻塞肺动脉或其分支所致的疾病,以肺循环和呼吸功能障碍为其主要特征。2008年3月～2010年10月,我院共收治PTE患者30例。现将其诊治体会分析如下。     

炎症性肠病血栓栓塞机制的研究进展

静脉血栓栓塞(VTE)是炎症性肠病(IBD)公认的肠外表现,发病率和死亡率均较高。IBD血栓栓塞的机制尚不完全清楚,涉及多种获得性和遗传性因素。目前主要指南推荐给予IBD患者机械或药物治疗以预防血栓栓塞,但临床上尚未广泛应用。本文就IBD血栓栓塞的机制作一综述。     

慢性血栓栓塞性肺动脉高压的研究进展

1 概念及流行病学 慢性血栓栓塞性肺动脉高压(claronic throm boembolic pulmonary hypertension,CTEPH)是指肺动脉及其主要分支由于血栓栓塞所导致的血流受阻,长期不能缓解或进行性加重,导致肺动脉高压.CTEPH是肺血栓栓塞症中的一种特殊类型,是血栓不能完全溶解,或者是在深静脉血栓形成反复脱落的基础上继发反复多次栓塞肺动脉、血栓机化,肺动脉内膜慢性炎症并增厚,发展为慢性肺栓塞.CTEPH进一步发展可出现呼吸功能不全和右心衰竭.     

肺动脉血栓内膜剥脱术后再灌注肺水肿的进展

肺血栓栓塞症是一种常见、多发且病死率和致残率高的疾病。大多数急性肺动脉血栓栓塞经及时的溶栓抗凝等治疗和 (或 )自身的纤溶系统能将血栓不同程度地溶解 ,另有0 1%～ 0 2 %的患者因血栓在急性期未能溶解或栓塞反复发生进而发展成慢性栓塞性肺动脉高压。慢性栓塞性肺动脉高压溶栓无效 ,抗凝、扩血管治疗效果不佳 ,其病理过程多呈进行性加重或稳定一段时间后再次加重 ,自然预后差。肺动脉平均压 >3 0ｍｍＨｇ(1ｍｍＨｇ =0 13 3ｋＰａ)的慢性栓塞性肺动脉高压患者 5年生存率为 3 0 % ,肺动脉平均压 >5 0ｍｍＨｇ者仅为 10 %。肺动脉血…     

Chronic pulmonary embolism and pulmonary hypertension

Incomplete resolution of acute pulmonary embolism (PE) is frequently observed after acute PE and may rarely result in chronic thromboembolic pulmonary hypertension (CTEPH). The underlying pathophysiological mechanism is largely unknown. Evidence underlines the concept of a dual pulmonary vascular compartment model consisting of increased pulmonary vascular resistance by both large vessel obstruction and distal small vessel obliteration, the latter initiated by pathological vascular remodeling. Up to 40% of patients with established CTEPH have no prior history of symptomatic venous thromboembolism. CTEPH is associated with a poor prognosis if left untreated. Therefore, the diagnostic approach of CTEPH aims at assessing the location and extent of the embolic obstruction, establishing the operability and prognosis of the patients and ruling out other variations of pulmonary hypertension with distinct indicated treatment. Heart catheterization for invasive pressure measurements and pulmonary catheter angiography is obligatory for the final diagnosis. Pulmonary thromboendarterectomy is the treatment of choice. In certain patients with persistent or recurrent pulmonary hypertension after surgery or with inoperable disease, pharmacotherapy might be beneficial.     

Retrograde pulmonary perfusion improves results in pulmonary embolectomy for massive pulmonary embolism

Mortality rates for pulmonary embolectomy in patients with acute massive pulmonary embolism have decreased in recent years. However, they still range from 30% to 45% when the surgery is performed on critically ill patients, and the rates reach 60% in patients who have experienced cardiac arrest before the procedure. The causes of death in these patients are generally attributed to right heart failure due to persistent pulmonary hypertension, intractable pulmonary edema, and massive parenchymal and intrabronchial hemorrhage. Clinical and experimental findings indicate that venous air embolism causes severe or even lethal damage to the pulmonary microvasculature and the lung parenchyma consequent to the release of endothelium-derived cytokines. These findings are similar to those observed when severely compromised patients undergo pulmonary embolectomy-air entrapped in the pulmonary artery during embolectomy can lead to fatal outcomes.Besides enabling the removal of residual thrombotic material from the peripheral branches of the pulmonary artery, retrograde pulmonary perfusion fills the pulmonary artery with blood and prevents pulmonary air embolism. In this retrospective study, we analyzed a series of 21 consecutive critically ill patients in whom we applied retrograde pulmonary perfusion while performing standard pulmonary embolectomy. No patient died or experienced major postoperative complications. We believe that the use of retrograde pulmonary perfusion decreases morbidity and mortality rates associated with pulmonary embolectomy in critically ill patients.     

Residual pulmonary thromboemboli after acute pulmonary embolism

BackgroundAfter an acute pulmonary embolism (PE), the complete resolution of thromboemboli may not be routinely achieved. The rate of persistence may depend on the time and the diagnostic technique used for evaluation.Patients and methodsPatients were diagnosed with acute PE by means of computed tomography angiography (CTA). While they were receiving anticoagulant therapy, a second CTA was used to explore the rate of persistence of residual thromboemboli. During the initial episode, the plasma levels of Troponin I and natriuretic peptide, patient demographics, and hemodynamic and gas exchange data were evaluated as risk factors for persistence of pulmonary thromboemboli.ResultsIn this study 166 patients were diagnosed. A second CTA was not made in 46 (28%) patients for different reasons. In 120 (72%) patients a second CTA was made 4.5 [SD2.34] months after the initial episode (range 2–12 months). Complete clearance of thrombi occurred in 89 (74%, 95% CI 65–81) patients. Residual thrombi remained in 31 (26%, 95% CI 18–34) patients. In 6%, 13% and 81% of the patients the size of the residual thrombi was greater, similar to and smaller than initially diagnosed, respectively.The risk factors for residual thrombi included the thrombotic burden (OR 1.95), the alveolar to arterial difference of oxygen (OR 1.64), and the clinical antecedents of venous thromboembolic disease (OR 0.65).ConclusionsAfter 4.5 months of anticoagulant therapy, residual pulmonary thromboemboli persisted in 26% of the patients. The risk factors for residual thromboemboli include a greater initial thrombotic burden, a deeper gas exchange disturbation and a history of previous venous thromboembolism.     

Balloon-occlusion pulmonary cineangiography for diagnosing pulmonary embolism

For the angiographic diagnosis of pulmonary embolism (PE) we performed balloon-occlusion pulmonary cineangiography in ten consecutive patients. The technical aspects of the balloon-occlusion cineangiographic technique are reviewed, and its complementary role in the diagnosis of PE are outlined and illustrated with several examples.     

Ruptured pulmonary artery aneurysm mimicking pulmonary embolism

Aneurysms of the pulmonary artery are very rare pathological vascular conditions. Peripheral pulmonary aneurysms have been reported only in a few cases. The causes of these aneurysms include extensive degenerative changes, traumas, infection and congenital malformations. Because of the imminent danger of rupture, surgical treatment should always be preferred. The following case report demonstrates one of a multitude of possible misdiagnoses for rupture of a pulmonary aneurysm.     

Cavitating pulmonary infarcts revealing thromboembolic pulmonary hypertension

Several etiologies are involved in the pathogenesis of cavitating pulmonary disease including neoplastic, infectious or inflammatory processes. Another is pulmonary infarction associated with venous thromboembolism. The lung cavities tend to be located peripherally and are the result of pulmonary embolism. We report the case of a woman with chronic thromboembolic pulmonary hypertension (CTEPH), associated with familial thrombophilia, revealed by cavitating pulmonary infarcts. CTEPH is sometimes diagnosed during an episode of recurrent pulmonary embolism following previously unnoticed lesions. Thrombophilias such as isolated elevated factor VIII are risk factors for CTEPH.