Pulmonary embolism

It is estimated that 600,000 or more symptomatic episodes of pulmonary embolism occur each year in the United States, and this diagnosis is one that may often be missed. This article provides an appraisal of currently used diagnostic procedures, including laboratory tests, arterial oxygen tension, chest radiography, electrocardiography, lung scanning, and selective pulmonary angiography, and examines the available therapeutic options and their indications.     

Pulmonary embolism

Pulmonary embolism (PE) is a common illness that can cause death and disability. It is difficult to detect because patients present with a wide array of symptoms and signs. The clinical setting can raise suspicion, and certain inherited and acquired risk factors predispose susceptible individuals. D-dimer concentration in blood is the best laboratory screening test, and chest CT has become the most widespread imaging test. Treatment requires rapid and accurate risk stratification before haemodynamic decompensation and the development of cardiogenic shock. Anticoagulation is the foundation of therapy. Right-ventricular dysfunction on echocardiography and higher than normal concentrations of troponin identify high-risk patients who might need escalation of therapy with thrombolysis or embolectomy even if the blood pressure is normal on presentation. When patients are admitted to medical wards or when patients undergo surgery, their physicians should prescribe prophylactic measures to prevent PE. After hospital discharge, prophylaxis should continue for about a month for patients at high risk of thromboembolism.     

Pulmonary embolism

The incidence and mortality of acute pulmonary embolism (PE) remain ill defined, particularly in the setting of the emergency department. However, high-risk groups can be identified based on medical conditions known to predispose patients to venous thrombosis. Recent research into the physiologic regulation of coagulation and thrombolysis reveals that recurrent venous thrombosis and PE may be caused by heritable deficiencies and abnormalities of plasma proteins. To decide among options for evaluation and treatment of patients suspected of PE, physicians combine clinical assessment with patterns observed on radionuclide ventilation-perfusion (V/Q) scans. However, the prevalence of PE among patients with "low probability" V/Q scans suggests that current physician behavior may be imprudent. Heparin anticoagulation continues to be standard therapy for acute PE, but newer clot-specific thrombolytic drugs may offer superior benefits with acceptable complication rates in carefully selected patients.     

Pulmonary embolism in younger adults.

To test the hypothesis that the clinical presentation and outcomes are different when pulmonary embolism occurs in younger (age 18 to 40 years) as compared to older (age greater than 40 years) adults, 40 younger patients were compared with older patients. No risk factors could be identified in 28 percent of the younger group. Normal physical examinations were more common (58 vs 28 percent, p = 0.01) among younger as compared with older adults. Hypoxemia was absent in 29 percent of the younger and 3 percent of the older group (p = 0.004); P(A-a)O2 was significantly lower among younger patients even after controlling for age. Mortality was decreased sevenfold (2.5 vs 18 percent, p = 0.03) among younger patients. These data indicate that pulmonary embolism tends to have a subtle presentation in younger adults. When diagnosed and treated, the mortality rate is substantially less among younger as compared with older patients.     

Pulmonary embolism after pacemaker implantation.

One day after implantation of a permanent pacemaker in an 82-year-old man, transthoracic echocardiography showed a mass in the right ventricle and a small pericardial effusion. Transesophageal echocardiography revealed a mass attached to the pacemaker lead. Subcutaneous administration of enoxaparin was begun, and the patient remained free of symptoms for the duration of his hospital stay Follow-up echocardiography performed before discharge failed to show the right ventricular mass, but a lung perfusion scan revealed multiple bilateral perfusion defects consistent with pulmonary emboli. The patient was discharged on a regimen of enoxaparin for another 30 days. Two years later, he remained asymptomatic.     

Pulmonary embolism: diagnostic algorithms.

In 90% of cases the clinical suspicion of pulmonary embolism (PE) is raised by clinical signs and symptoms, while in only 10% of cases PE is suspected on the basis of electrocardiographic, arterial blood gas analysis or radiological findings. The combination of clinical signs and symptoms and the results of first-level diagnostic tests (electrocardiography, gas analysis and chest X-ray) allows a fairly accurate classification of patients with "clinical suspicion of PE" into three categories of clinical (or pre-test) probability: low, intermediate and high. The clinical diagnosis of PE is very often inaccurate making the use of additional tests, including imaging techniques, mandatory. The choice and the combination (= diagnostic algorithms) of second- and third-level diagnostic tests (D-dimer, venous ultrasound, echocardiography, lung scintigraphy, helical computed tomography and pulmonary angiography) depend primarily on the clinical conditions of patients and their pre-test probability. We propose two diagnostic algorithms: 1) a diagnostic algorithm for patients with clinically suspected PE and critical clinical conditions (unstable patients), 2) a diagnostic algorithm for patients with clinically suspected PE and non-critical clinical conditions (hemodynamically stable patients).