Risk stratification of patients with acute symptomatic pulmonary embolism

Patients with acute symptomatic pulmonary embolism (PE) who present with arterial hypotension or shock have a high risk of death (high-risk PE), and treatment guidelines recommend strong consideration of thrombolysis in this setting. For normotensive patients diagnosed with PE, risk stratification should aim to differentiate the group of patients deemed as having a low risk for early complications (all-cause mortality, recurrent venous thromboembolism, and major bleeding) (low-risk PE) from the group of patients at higher risk for PE-related complications (intermediate-high risk PE), so low-risk patients could undergo consideration of early outpatient treatment of PE and intermediate-high risk patients would undergo close observation and consideration of thrombolysis. Clinicians should also use risk stratification and eligibility criteria to identify a third group of patients that should not undergo escalated or home therapy (intermediate-low risk PE). Such patients should initiate standard therapy of PE while in the hospital. Clinical models [e.g., Pulmonary Embolism Severity Index (PESI), simplified PESI (sPESI)] may accurately identify those at low risk of dying shortly after the diagnosis of PE. For identification of intermediate-high risk patients with acute PE, studies have validated predictive models that use a combination of clinical, laboratory and imaging variables.     

Risk stratification of normotensive patients with acute symptomatic pulmonary embolism

Treatment guidelines recommend strong consideration of thrombolysis in patients with acute symptomatic pulmonary embolism (PE) that present with arterial hypotension or shock because of the high risk of death in this setting. For haemodynamically stable patients with PE, the categorization of risk for subgroups may assist with decision-making regarding PE therapy. Clinical models [e.g. Pulmonary Embolism Severity Index (PESI)] may accurately identify those at low risk of overall death in the first 3 months after the diagnosis of PE, and such patients might benefit from an abbreviated hospital stay or outpatient therapy. Though some evidence suggests that a subset of high-risk normotensive patients with PE may have a reasonable risk to benefit ratio for thrombolytic therapy, single markers of right ventricular dysfunction (e.g. echocardiography, spiral computed tomography, or brain natriuretic peptide testing) and myocardial injury (e.g. cardiac troponin T or I testing) have an insufficient positive predictive value for PE-specific mortality to drive decision-making toward such therapy. Recommendations for outpatient treatment or thrombolytic therapy for patients with PE necessitate further development of prognostic models and conduct of clinical trials that assess various treatment strategies.     

Fibrinolysis for acute pulmonary embolism

Acute pulmonary embolism (PE) presents as a constellation of clinical syndromes with a variety of prognostic implications. Patients with acute PE who have normal systemic arterial blood pressure and no evidence of right ventricular (RV) dysfunction have an excellent prognosis with therapeutic anticoagulation alone. Normotensive acute PE patients with evidence of RV dysfunction are categorized as having submassive PE and comprise a population at intermediate risk for adverse events and early mortality. Patients with massive PE present with syncope, systemic arterial hypotension, cardiogenic shock, or cardiac arrest and have the highest risk for short-term mortality and adverse events. The majority of deaths from acute PE are due to RV pressure overload and subsequent RV failure. The goal of fibrinolysis in acute PE is to rapidly reduce RV afterload and avert impending hemodynamic collapse and death. Although generally considered to be a life-saving intervention in massive PE, fibrinolysis remains controversial for submassive PE. Successful administration of fibrinolytic therapy requires weighing benefit versus risk. Major bleeding, in particular intracranial hemorrhage, is the most feared complication of fibrinolysis. Alternatives to fibrinolysis for acute PE, including surgical embolectomy, catheter-assisted embolectomy, and inferior vena cava (IVC) filter insertion, should be considered when contraindications exist or when patients have failed to respond to an initial trial of fibrinolytic therapy. Patients with massive and submassive PE may be best served by rapid triage to specialized centers with experience in the administration of fibrinolytic therapy and the capacity to offer alternative advanced therapies such as surgical and catheter-assisted embolectomy.     

Catheter embolectomy for acute pulmonary embolism

Massive pulmonary embolism (PE) is a life-threatening condition with a high early mortality rate due to acute right ventricular failure and cardiogenic shock. As soon as the diagnosis is suspected, an IV bolus of unfractionated heparin should be administered. In addition to anticoagulation, rapid initiation of systemic thrombolysis is potentially life-saving and therefore is standard therapy. Many patients with massive PE cannot receive thrombolysis because of an increased bleeding risk, such as prior surgery, trauma, or cancer. In these patients, catheter or surgical embolectomy are helpful for rapidly reversing right ventricular failure. Catheter thrombectomy appears to be particularly useful if surgical embolectomy is not available or the patient has contraindications to surgery. Although no controlled clinical trials are available, data from cohort studies indicate that the clinical outcomes after surgical and catheter embolectomy may be comparable.     

急性肺血栓栓塞的溶栓治疗

急性肺血栓栓塞 (ＡＰＥ)的溶栓治疗始于 30年前。长期以来 ,人们一直在探求能够提高疗效、降低出血风险的药物和治疗方法。随着优质溶栓药物的开发及溶栓方案、给药途径的改进 ,ＡＰＥ的溶栓治疗已取得了长足的进展。现有溶栓剂主要有链激酶 (ＳＫ)、尿激酶 (ＵＫ)、重组组织型纤溶酶原激活剂 (ｒｔ -ＰＡ) ,均为纤溶酶原激活剂 ,是具有启动 -放大纤溶系统的有效药物。它通过激活纤溶酶原而溶解血栓 ,使其降解成可溶性肽类。目前新一代溶栓剂如 :重组组织型纤溶酶原激活剂ｔ -ＰＡ缺失突变体 (ｒ -ＰＡ)、ＴＮＫ -组织型纤溶酶原激活剂 (Ｔ…     

依诺肝素联合阿司匹林治疗急性肺血栓栓塞并发腹膜后巨大血肿一例

患者女,77岁.因"反复活动后气促4个月,加重2 d"于2007年5月10日入院.6年前因"肺肿瘤"行左上肺叶肿瘤剔除术.4个月前曾受凉后出现胸闷、咳嗽、咯痰,痰量多,色白稀,活动后气促,间伴有夜间呼吸困难,但无咯粉红色泡沫痰.于当地卫生所就诊予抗感染化痰药物治疗效果欠佳,遂转我院就诊.起病后无突发胸痛、咯血,无非对称性下肢水肿.入院体格检查:体温37.5℃,血压114/70 mm Hg(1 mm Hg=0.133.kPa),呼吸22次/min,颈静脉无怒张,桶状胸,双肺呼吸音粗,双肺底可闻及少量细湿哕音和干哕音,心率111次/min,房颤,各瓣膜区未闻及杂音,双下肢对称性水肿(±).     

Spiral computed tomography for acute pulmonary embolism

There is still considerable debate about the optimal diagnostic imaging modality for acute pulmonary embolism. If imaging is deemed necessary from an initial clinical evaluation such as d-dimer testing, options include nuclear medicine scanning, catheter pulmonary angiography, and spiral CT. In many institutions, spiral CT is becoming established as the first-line imaging test in daily clinical practice. With spiral CT, thrombus is directly visualized, and both mediastinal and parenchymal structures are evaluated, which may provide important alternative or additional diagnoses. However, limitations for the accurate diagnosis of small peripheral emboli, with a reported miss rate of up to 30% with single-slice spiral CT so far, have prevented the unanimous embrace of spiral CT as the new standard of reference for imaging pulmonary embolism. The clinical significance of the detection and treatment of isolated peripheral pulmonary emboli is uncertain. Evidence is accumulating that it is safe practice to withhold anticoagulation in patients with suspected pulmonary embolism on the basis of a negative spiral CT study. Remaining concerns about the accuracy of spiral CT for pulmonary embolism detection may be overcome by the introduction of multidetector-row spiral CT. This widely available technology has improved visualization of peripheral pulmonary arteries and detection of small emboli. The most recent generation of multidetector-row spiral CT scanners appears to outperform competing imaging modalities for the accurate detection of central and peripheral pulmonary embolism. In this review, we assess the current role and future potential of CT in the diagnostic algorithm of acute pulmonary embolism.     

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.     

Hypoxemia in acute pulmonary embolism

Most patients with severe, acute pulmonary embolism (PE) have arterial hypoxemia. To further define the respective roles of ventilation to perfusion (VA/Q) mismatch and intrapulmonary shunt in the mechanism of hypoxemia, we used both right heart catheterization and the six inert gas elimination technique in seven patients with severe, acute PE (mean vascular obstruction, 55 percent) and hypoxemia (mean PaO2, 67 +/- 11 mm Hg). None had previous cardiopulmonary disease, and all were studied within the first ten days of initial symptoms. Increased calculated venous admixture (mean QVA/QT 16.6 +/- 5.1 percent) was present in all patients. The relative contributions of VA/Q mismatching and shunt to this venous admixture varied, however, according to pulmonary radiographic abnormalities and the time elapsed from initial symptoms to the gas exchange study. Although all patients had some degree of VA/Q mismatch, the two patients studied early (ie, less than 48 hours following acute PE) had normal chest x-ray film findings and no significant shunt; VA/Q mismatching accounted for most of the hypoxemia. In the others a shunt (3 to 17 percent of cardiac output) was recorded along with radiographic evidence of atelectasis or infiltrates and accounted for most of the venous admixture in one. In all patients, a low mixed venous oxygen tension (27 +/- 5 mm Hg) additionally contributed to the hypoxemia. Our findings suggest that the initial hypoxemia of acute PE is caused by an altered distribution of ventilation to perfusion. Intrapulmonary shunting contributes significantly to hypoxemia only when atelectasis or another cause of lung volume loss develops.