Outcomes after withholding anticoagulation from patients with suspected acute pulmonary embolism and negative computed tomographic findings: a cohort study

OBJECTIVE: To determine the outcome of withholding anticoagulation from patients with suspected acute pulmonary embolism in whom computed tomographic (CT) findings are interpreted as negative for pulmonary embolism. PATIENTS AND METHODS: This retrospective cohort study included 1512 consecutive patients referred from August 7, 1997, to November 30, 1998, for CT because of clinically suspected acute pulmonary embolism. All patients were examined by electron beam CT, and scanning was performed in a cephalocaudad direction from the top of the aortic arch to the base of the heart with 3-mm collimation, 2-mm table incrementation, and an exposure time of 0.2 second (130 peak kV, 620 mA, and standard reconstruction algorithm). Contrast material was infused at a rate of 3 to 4 mL/s through an antecubital vein with an automated injector. Findings on CT were interpreted as either positive or negative. The main outcome measures were deep venous thrombosis, pulmonary embolism, and vital status within 3 months after the CT scan and the cause of death based on medical record review, mailed patient questionnaires, and telephone interviews. RESULTS: In 1010 patients (67%) CT scans were interpreted as negative for acute pulmonary embolism. Seventeen patients were excluded because they received anticoagulation. Of the remaining 993 patients, deep venous thrombosis or pulmonary embolism developed in 8; 118 patients died, 3 of pulmonary embolism. Nineteen patients were known to be alive, but additional clinical information could not be obtained. The 3-month cumulative incidence of overall deep venous thrombosis or pulmonary embolism was 0.5% (95% confidence interval, 0.1%-1.0%) and of fatal pulmonary embolism, 0.3% (95% confidence interval, 0.0%-0.7%). CONCLUSIONS: The incidence of (1) overall deep venous thrombosis or pulmonary embolism or (2) fatal pulmonary embolism among patients with suspected acute pulmonary embolism, negative CT results, and no other evidence of venous thromboembolism is low. Withholding anticoagulation in these patients appears to be safe.     

心力衰竭并发肺动脉栓塞研究进展

充血性心力衰竭（CHF）在许多临床表现上与肺动脉栓塞相似,而前者易并发后者,两者一旦合并存在,即提示患者预后更为恶劣。该文从发病原因、危险因素、临床表现、诊断与预后、预防及治疗等方面复习近年心力衰竭并发肺动脉栓塞研究进展,以期能在诊断及预防CHF并发肺动脉栓塞等方面提供相关的信息和思路。     

Air travel and venous thromboembolism: minimizing the risk

For those traveling on long flights, the risk of deep vein thrombosis or pulmonary embolism, generally referred to as venous thromboembolism (VTE), is real and dangerous if left unrecognized or untreated. The goal of this publication is to provide an overview of how best to prevent VTE during travel, and how to diagnose and treat it.     

DVT and pulmonary embolism: Part I. Diagnosis

The incidence of venous thromboembolic diseases is increasing as the U.S. population ages. At least one established risk factor is present in approximately 75 percent of patients who develop these diseases. Hospitalized patients and nursing home residents account for one half of all cases of deep venous thrombosis. A well-validated clinical prediction rule can be used for risk stratification of patients with suspected deep venous thrombosis. Used in combination with D-dimer or Doppler ultrasound tests, the prediction rule can reduce the need for contrast venography, as well as the likelihood of false-positive or false-negative test results. The inclusion of helical computed tomographic venography (i.e., a below-the-pelvis component) in pulmonary embolism protocols remains under evaluation. Specific combinations of a clinical prediction rule, ventilation-perfusion scanning, and D-dimer testing can rule out pulmonary embolism without an invasive or expensive investigation. A clinical prediction rule for pulmonary embolism is most helpful when it is used with subsequent evaluations such as ventilation-perfusion scanning, D-dimer testing, or computed tomography. Technologic advances are improving the resolution of helical computed tomography to allow detection of smaller emboli; however, further study is needed to provide definitive evidence supporting the role of this imaging technique in the diagnosis of pulmonary embolism. D-dimer testing is helpful clinically only when the result is negative. A negative D-dimer test can be used in combination with a clinical decision rule, ventilation-perfusion scanning, and/or helical computed tomography to lower the probability of pulmonary embolism to the point that aggressive treatment is not required. Evidence-based algorithms help guide the diagnosis of deep venous thrombosis and pulmonary embolism.     

Diagnosing pulmonary embolism: A question of too much choice?

The diagnosis of pulmonary embolism (PE) is difficult with many patients treated without the disease or left untreated without an adequate diagnostic work up. Recent advances in PE diagnosis are reviewed. The use of risk stratification in PE diagnosis is strongly recommended and evidence on how it can best be performed summarized. The Ginsberg/Wells stratification rule is recommended currently as the best validated rule. Computed tomographic pulmonary angiography (CTPA) was found to have quite poor sensitivity and to be poorly validated. It is recommended as adequate as a positive test in moderate/high risk groups and an exclusionary test in low risk groups or where an adequate alternative diagnosis is found. For D‐Dimer tests the only test with adequate sensitivity and validation in management studies is the VIDAS© D‐Dimer. This is in low/intermediate risk groups in the ED population. The Simpli‐Red© test is also reviewed but is too insensitive for most populations. Echocardiography: this is good in compromised patients as it is a bedside test which when negative virtually excludes PE. If positive in the right setting it has a high positive predictive value. A negative echocardiogram predicts a benign clinical course for PE. The rest of the paper details the authors approach to integrating these new techniques with established algorithms and where progress is likely to occur in the next few years. These include improvements in CTPA (plus the addition of CT venography), new point of care D‐Dimer tests, better risk stratification rules and integration of new strategies with artificial neural networks or computerized guidelines.     

Saddle pulmonary embolism is not a sign of high-risk deterioration in non-high-risk patients: A propensity score-matched study

BACKGROUND: There is controversy regarding whether saddle main pulmonary artery (MPA) embolism represents a high risk of deterioration in non-high-risk acute pulmonary embolism (PE) patients. This study aims to address this issue by conducting a propensity score matching (PSM) study. METHODS: A total of 727 non-high-risk acute PE patients were retrospectively evaluated. We evaluated the Bova score and risk stratification to examine the risk of deterioration. Deterioration defined as any adverse event within 30 days after admission. Computed tomographic pulmonary angiography was used to identify the embolism type. All patients were matched into four subgroups by PSM according to age, sex, Bova score, and risk stratification: (1) MPA and non-MPA embolism; (2) non-saddle MPA and non-MPA embolism; (3) saddle MPA and non-saddle MPA embolism; (4) saddle MPA and non-MPA embolism. Correlations were analyzed using Cox regression analysis, and deterioration risk was compared between subgroups using Kaplan-Meier analysis. RESULTS: Cox regression analysis revealed that MPA embolism was correlated with deterioration, regardless of whether saddle MPA embolism was included or excluded. Saddle MPA embolism was not correlated with deterioration, regardless of comparison with non-saddle MPA embolism or non-MPA embolism. Patients with MPA and non-saddle MPA embolism presented a high risk for deterioration (log-rank test=5.23 and 4.70, P=0.022 and 0.030, respetively), while patients with saddle MPA embolism were not at a high risk of deterioration (log-rank test=1.20 and 3.17, P=0.729 and 0.077, respetively). CONCLUSIONS: Saddle MPA embolism is not indicative of a high risk of deterioration in non-high-risk acute PE patients.     

Venous Thromboembolic Events in the Rehabilitation Setting

Venous thromboembolism (VTE) is a disease entity that encompasses both deep venous thrombosis and pulmonary embolism. During the past decade there have been significant advances in the understanding of prophylaxis and treatment of VTE. There is an extensive research base from which conclusions can be drawn, but the heterogeneity within the rehabilitation patient population makes the development of rigid VTE protocols challenging and overwhelming for the busy clinician. Given the prevalence of this condition and its associated morbidity and mortality, we review the evidence for the prevention, identification, and optimal treatment of VTE in the rehabilitation population. Our goal is to highlight studies that have the most clinical applicability for the care of VTE patients from a physiatrist's perspective. At times, information about acute care protocols is included in our discussion because these situations are encountered during the consultation process that identifies patients for rehabilitation needs.     

Facteurs pronostiques de l’embolie pulmonaire

Risk stratification of patients with pulmonary embolism represents an important step and may help to guide initial therapeutic management. Pulmonary embolism can be stratified into several levels of risk of early death or complications based on the presence of several risk factors. High-risk pulmonary embolism is defined by shock or peripheral signs of hypoperfusion. It is a life-threatening emergency with high short-term mortality (> 25%) requiring specific therapeutic strategy with inotropic agents and fibrinolysis. In patients with normotensive pulmonary embolism, the presence of right ventricular dysfunction on echocardiography and/or myocardial injury, as attested by elevated levels of biomarkers, is associated with an intermediate risk of early death. These patients need close monitoring, while evaluation of fibrinolysis efficacy is currently underway. Patients with normotensive pulmonary embolism and without right ventricular dysfunction or myocardial injury have low risk of death. These patients may be candidates for home treatment. Several scores combining these risk factors have been described.     

Early recognition of pulmonary embolism: the key to lowering mortality

Pulmonary embolism is a major cause of morbidity and mortality in the United States. The majority of deaths from pulmonary embolism occur because an accurate diagnosis was not made. It is imperative for clinicians to have a high level of clinical suspicion of pulmonary embolism when patients present with dyspnea, tachypnea, chest pain, hemoptysis, and cough. If pulmonary embolism is diagnosed and treatment initiated, death and recurrence of embolism are uncommon. Beyond correct diagnosis and treatment, the single most effective strategy that can be employed to decrease the high mortality associated with pulmonary embolism is identification of individuals at risk and the institution of prophylactic measures. This article reviews the incidence, risk factors, assessment, physical examination, laboratory, and diagnostic testing for pulmonary embolism.     

Is thrombolytic therapy effective for pulmonary embolism?

Pulmonary embolism is a disorder that is associated with significant morbidity and mortality. Right-sided heart failure and recurrent pulmonary embolism are the main causes of death associated with pulmonary embolism in the first two weeks after the embolic event. Thrombolysis is a potentially lifesaving therapy when used in conjunction with standard anticoagulation. However, it has significant side effects and must therefore be used with caution. Indications for thrombolysis are not well defined and are thus controversial. The only current absolute indication is massive pulmonary embolism with hypotension. Other potential indications include right heart dysfunction, recurrent pulmonary embolism and the prevention of pulmonary hypertension. However, no evidence exists to show benefit of thrombolytic therapy over standard anticoagulation therapy for recurrent pulmonary embolism, mortality or chronic complications. Bleeding is the most common complication of thrombolysis and may be fatal.     

Surrogate markers for adverse outcomes in normotensive patients with pulmonary embolism

BACKGROUND: Although echocardiography has proven utility in risk stratifying normotensive patients with pulmonary embolism, echocardiography is not always available. OBJECTIVE: Test if a novel panel consisting of pulse oximetry, 12-lead electrocardiography, and serum troponin T would have prognostic equivalence to echocardiography and to examine the prognostic performance of age, previous cardiopulmonary disease, D-dimer, brain natriuretic peptide, and percentage of pulmonary vascular occlusion on chest computed tomography. DESIGN: Prospective cohort study. PATIENTS AND SETTING: Normotensive (systolic blood pressure of >100 mm Hg) emergency department and hospital inpatients with diagnosed pulmonary embolism who underwent cardiologist-interpreted echocardiography and other measurements within 15 hrs of anticoagulation. MEASUREMENTS AND MAIN RESULTS: End points were in-hospital circulatory shock or intubation, or death, recurrent pulmonary embolism, or severe cardiopulmonary disability (defined as echocardiographic evidence of severe right ventricular dysfunction with New York Heart Association class III dyspnea or 6-min walk test of <330 m) at 6-month follow-up. The two-one-sided test tested the hypothesis of equivalence with one-tailed alpha = 0.05 and Delta = 5%. Of 200 patients enrolled, data were complete for 181 (88%); 51 of 181 patients (28%) had an adverse outcome, including in-hospital complication (n = 18), death (n = 11), recurrent pulmonary embolism (n = 2), or cardiopulmonary disability (n = 20). Right ventricular dysfunction on initial echocardiogram was 61% sensitive (95% confidence interval, 46-74%) and 57% specific (48-66%). The panel was 71% sensitive (56-83%) and 62% specific (53-71%). The two-one-sided procedure demonstrated superiority of the panel to echocardiography for both sensitivity and noninferiority for specificity. No other biomarker demonstrated equivalence, noninferiority, or superiority for sensitivity and specificity. CONCLUSION: Normotensive patients with pulmonary embolism have a high rate of severe adverse outcomes during 6-month follow-up. A panel of three widely available tests can be used to risk stratify patients with pulmonary embolism when formal echocardiography is not available.     

Pulmonary embolism

Pulmonary embolism is a commonly suspected but underdiagnosed condition of clinical significance. Preventable deaths continue to occur. We begin this article with an overview of prognosis, clinical evidence, signs and symptoms, and risk factors, followed by an in-depth evaluation of diagnostic techniques and treatment modalities. The greatest improvement in mortality from pulmonary embolism is likely to come from improved and aggressive prevention and prophylaxis by the critical care team.     

Incidence and risk factors for pulmonary embolism in the postpartum period

Summary. Background: Pregnancy and the postpartum period are times of hypercoagulability, increasing the risk of pulmonary embolism. Better quantification of risk factors can help target women who are most likely to benefit from postpartum thromboprophylaxis with heparin. Objectives: To determine the incidence rate and timing of postpartum pulmonary embolism, and assess perinatal risk factors predictive of the event. Patients/Methods: Antenatal, delivery and postpartum admission records of a cohort of 510 889 pregnancies were analysed. Pulmonary embolism was identified from ICD‐10 codes at delivery, transfer or upon readmission at any time in the postpartum period. Results: Pulmonary embolism occurred in 375 women and was most common postpartum. The rate of postpartum pulmonary embolism without an antecedent thrombotic event was 0.45 per 1000 births. By the end of 4 weeks postpartum, the weekly rate approached the background rate of pulmonary embolism in the population. Although the Caesarean section rate rose significantly throughout the study period, and pulmonary embolism was more common following abdominal birth, the rate of pulmonary embolism following Caesarean birth fell. Regression modelling demonstrated that stillbirth (adjusted odds ratio [aOR] =5.97), lupus (aOR = 8.83) and transfusion of a coagulation product (aOR = 8.84) were most strongly associated with pulmonary embolism postpartum. Conclusions: Pulmonary embolism most commonly occurs up to 4 weeks postpartum and following abdominal birth. Despite this the absolute event rate is low and a broadly inclusive risk factor approach to the use of pharmacological thromboprophylaxis will require many women to be exposed to heparin to prevent an embolic event.     

Should thrombolysis be contraindicated in patients with cerebral arteriovenous malformations?

OBJECTIVES: To report the successful and uncomplicated use of systemic thrombolysis for massive pulmonary embolism in a patient with a known cerebral arteriovenous malformation and to suggest that the presence of an unruptured arteriovenous malformation or aneurysm should not be considered an absolute contraindication to systemic thrombolysis. DESIGN: Case report. SETTING: A 16-bed adult neurologic/medical intensive care unit in a university hospital. PATIENTS: A patient developed a massive pulmonary embolism the morning after elective cerebral embolization of a large unruptured cerebral arteriovenous malformation. INTERVENTION: Radial artery catheterization, arterial blood gas measurements, mechanical ventilation, vasopressors, pulmonary perfusion scan, echocardiogram, head computed tomography, heparin therapy, and systemic recombinant tissue plasminogen activator therapy. MEASUREMENT AND MAIN RESULTS: The patient required emergent mechanical ventilation and vasopressor support for respiratory and hemodynamic failure. Echocardiogram showed acute right heart failure, and pulmonary perfusion scan demonstrated massive pulmonary embolism. Despite intravenous heparin therapy, the patient had worsening hypotension and acidosis and we therefore treated with recombinant tissue plasminogen activator. Within the next day the patient was weaned from vasopressor support and extubated. Neurologic examination remained normal, and follow-up head computed tomography revealed no evidence of intracranial hemorrhage. CONCLUSION: Known arteriovenous malformations or aneurysms are considered a contraindication to thrombolysis, although the true risk of thrombolysis-precipitated intracranial hemorrhage is unknown. We believe that this risk is low in the setting of a previously unruptured arteriovenous malformation or aneurysm. The decision to use systemic thrombolysis in a patient with a known vascular malformation should be individualized.     

Microscopic pulmonary tumor embolism causing subacute cor pulmonale: a difficult antemortem diagnosis.

Microscopic pulmonary tumor embolism is difficult to diagnose. The most common initial clinical symptom is subacute progressive dyspnea, and the initial laboratory evaluation typically shows hypoxemia in a patient with clear lung fields on a chest roentgenogram. Another distinguishing feature may be hepatic abnormalities. In general, pulmonary angiography discloses no evidence of emboli, but multiple subsegmental peripheral perfusion defects are noted on ventilation-perfusion lung scans. The diagnosis of microscopic pulmonary tumor embolism can be confirmed by open-lung or transbronchial lung biopsy or by microvascular pulmonary cytology, a less invasive procedure that could be performed at the time of pulmonary angiography. Herein we describe two patients with unsuspected microscopic pulmonary tumor embolism that eventuated in subacute cor pulmonale and death. These cases illustrate the characteristic findings of this entity and emphasize the need for early diagnosis.     

Diagnosis and prognosis of acute pulmonary embolism: focus on serum troponins

Pulmonary embolism is a common disease associated with high mortality. Death due to pulmonary embolism occurs mainly before hospital admission or in the first hours of the hospital stay. Prompt diagnosis and prognostic stratification and more intensive treatment in patients with estimated high risk for adverse outcomes have the potential to reduce mortality due to pulmonary embolism. Significant advances have recently been made in the risk stratification for adverse outcomes in patients with pulmonary embolism and normal blood pressure. In these patients, right ventricle overload assessed by echocardiography and probably by helical computerized tomography is a predictor of in-hospital mortality. Serum troponin is rapidly available in the emergency room, and has a critical role in the management of patients with acute coronary syndromes. The role of serum troponin in patients with pulmonary embolism has been explored recently: it seems to be marginal in diagnosis while it can significantly contribute to prognostic stratification. Elevated serum levels of troponins are associated with right ventricular overload and adverse in-hospital outcomes in patients with pulmonary embolism and normal blood pressure.     

Searching the literature for evidence

Nurses are expected to use evidence‐based knowledge when planning and caring for patients and their families. For nurses who practice evidence‐based care, knowing how to effectively search the literature for evidence is an important skill. The objectives of this article are to provide an overview of key sources of evidence and offer instruction on how to do an effective MEDLINE search in PubMed and how to critically review research articles. A sample literature search is performed using the example case study question, “How effective are compression stockings in preventing deep vein thrombosis or pulmonary embolism for thrombotic stroke patients who are on an oral anticoagulant regimen?”     

Pulmonary embolism. Guide to diagnosis, treatment, and prevention

While more remains to be learned about the natural history of deep vein thrombosis and pulmonary embolism, better information is now available on which to base decisions about diagnosis and treatment. Several retrospective and prospective studies have placed the value of lung scanning, venography, and pulmonary angiography in better perspective. Newer diagnostic techniques for deep vein thrombosis, such as 125I-labeled fibrinogen scanning and impedance plethysmography, are valuable and should be more widely used. Other diagnostic techniques for pulmonary embolism, such as computed tomography and nuclear magnetic resonance imaging, may be of value but are still untested. More effective therapies are now available. Moderate-dose subcutaneous heparin and lower-dose warfarin for long-term therapy of deep vein thrombosis are attractive alternatives to standard warfarin therapy. Thrombolytic therapy has not replaced standard intravenous heparin therapy, although it should be considered in treatment of a massive pulmonary embolus. Perhaps most important, prevention of deep vein thrombosis in most patients at high risk is possible with minidose heparin therapy or intermittent pneumatic compression. One of these methods of prophylaxis should be used in all high-risk patients as the only current effective way to decrease the mortality of pulmonary embolism.     

中危（次大面积）急性肺栓塞患者是否需要溶栓治疗

中危（次大面积）急性肺栓塞患者是否需要溶栓治疗已经争论了很多年。中危肺栓塞患者具有较高的死亡风险。因此,有人建议给予中危肺栓塞患者溶栓治疗,溶栓治疗可以更快地溶解血栓,从而降低中危肺栓塞患者的病死率。但也有研究表明,与单纯抗凝治疗比较,溶栓治疗不能进一步降低中危急性肺栓塞患者的病死率和复发率,且并发出血率较高。该文就中危急性肺栓塞溶栓治疗的有效性及安全性作一综述。     

A novel regional right ventricular wall-motion abnormality observed in a case of acute pulmonary embolism (reverse McConnell sign).

Among various echocardiographic parameters for diagnosis of pulmonary embolism, an abnormal regional contraction pattern of the right ventricular free wall consisting of normokinesia of the apical segment and akinesia of the midfree wall with persistence of abnormal wall motion at the base has proved to be fairly specific for pulmonary embolism. This echocardiographic abnormality has been termed "McConnell sign." We describe the case of a patient with acute pulmonary embolism who developed reversible akinesia of the apex and right ventricular midfree wall, a finding we would like to term "reverse McConnell sign."