Advances in the diagnosis and treatment of pulmonary embolism. Pulmonary embolism--how can you mend a broken clot?
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We compared 41 patients with angiographic proof of pulmonary embolism and clinical signs of pulmonary infarction (as evidenced by an infiltrate on x-ray study and pleuritic pain in the area of the embolus) with 24 patients with pulmonary embolism but without infarction. Only 18 of the 41 patients with pulmonary infarction had associated heart disease. Pulmonary infarction was uncommon when emboli obstructed central arteries but frequent when distal arteries were occluded. Follow-up x-ray examination showed that the infiltrates resolved in the patients with pulmonary infarction without heart disease, but persisted when heart disease was present. We suggest that obstruction of distal arteries results in pulmonary hemorrhage owing to an influx of bronchial arterial blood at systemic pressure. Hemorrhage causes symptoms and x-ray changes usually attributed to pulmonary infarction. However, hemorrhage resolves without infarction in patients without, but progresses to infarction in those with, heart disease.
A rare cause of pulmonary embolism and pulmonary artery hypertension in young women is choriocarcinoma growing in the pulmonary artery. This growth is reversible, and the disorder can be cured. We describe three patients with this feature who have been treated with appropriate high-risk chemotherapy and who are now in remission. Contrast-enhanced computed tomography can be used to identify major emboli, and progress of the disease can be monitored by serial ventilation/perfusion scans and measurement of serum human chorionic gonadotropin. Recognition of this rare syndrome is important because of the generally excellent outlook with appropriate treatment.
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CTPA is a highly sensitive and excellent primary method for evaluating patients with symptoms of PE. Ongoing studies will demonstrate the good clinical outcome of patients with negative CTPA results. The ability to visualize the lung parenchyma in addition to the pulmonary vasculature, and the smaller number of nondiagnostic scans, make CT more cost effective than V/Q scans, and CT therefore should be used as a first-line evaluation. MR imaging is a continually developing modality with more imaging options that could make it an invaluable or adjunctive test in the near future.
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Pulmonary embolism is poorly diagnosed and therefore not treated in patients with chronic diseases, whereas it is overdiagnosed in formerly healthy patients. The diagnostic level is not satisfactory even in departments of cardiology. Insufficient use of auxiliary laboratory tests constitutes one of the main reasons for the unsatisfactory state of pulmonary embolism diagnostics. The clinical picture of pulmonary embolism depends on a) the size of pulmonary embolism, b) the previous state of the cardiopulmonary system. A massive pulmonary embolism can lead to a) sudden death, b) shock, c) acute cor pulmonale. The most typical diagnostic sign is suddenly developed or deteriorated dyspnea (present in 94% of patients). The presence of venous thrombosis and the appearance of sudden dyspnea always support the diagnosis very strongly. Dyspnea or tachypnea occur in more than 90% of patients. Dyspnea, tachypnea or deep venous thrombosis occur in 99% of patients with acute pulmonary embolism. Electrocardiographic signs of acute pulmonary embolism were present in 67% of our patients with hemodynamically significant pulmonary embolism. Electrocardiographic signs are most marked in cases in which pulmonary embolism originates suddenly, in patients with a normal cardiopulmonary system, if the pulmonary embolism is extensive and the electrocardiogram is carried out early and repeatedly. The electrocardiographic signs of pulmonary embolism in cardiac patients, however, are not specific and only rarely present. The principal advantages of the chest X-ray are simplicity, safety and low costs. A negative chest X-ray was found only in 16.6% of our patients with pulmonary embolism.(ABSTRACT TRUNCATED AT 250 WORDS)
Pulmonary arteriography is the most reliable technique for evaluation of pulmonary embolism and other vascular abnormalities. A definitive diagnosis of pulmonary embolism is made on the basis of direct angiographic signs of emboli of intravascular filling defect and vessel cut-off sign. To obtain these findings, pulmonary arteriography needs to be performed as soon as possible, and in acutely ill patients who are in shock and under consideration for thrombolytic therapy or emergency embolectomy, the study should be performed on an emergency basis. Digital subtraction pulmonary angiography may be an useful technique for massive pulmonary embolism, but it cannot exclude clinically important peripheral pulmonary embolism. Wedged pulmonary arteriography can demonstrate the direct signs of distal emboli, which are difficult to obtain by main pulmonary artery injection angiogram. In the chronic stage of pulmonary embolism, bronchial arteriogram shows collaterals to pulmonary arteries. This study may be useful in patients with chronic pulmonary embolism, especially when thromboembolectomy is planned.
Pulmonary embolism has been considered uncommon in chronic dialysis patients, but has not been adequately studied in a large population. In the US Renal Data System (USRDS), 76,718 patients presenting with end-stage renal disease (ESRD) between January 1, 1996, and December 31, 1996, were analyzed in an historical cohort study. The outcome was hospitalizations with a primary discharge diagnosis of pulmonary embolism (International Classification of Diseases, Ninth Revision code 415.1x) occurring within 1 year of the first ESRD treatment and excluding those occurring after renal transplantation. For dialysis patients, hospitalization rates for pulmonary embolism were obtained from the hospitalization section of the 1999 USRDS. For the general population, hospitalization rates for pulmonary embolism were obtained from the National Hospital Discharge Survey for 1996. Comorbidities from the Medical Evidence Form (Centers for Medicare and Medicaid Services, previously known as the Health Care Financing Administration; form 2728) were used to generate approximated stratified models of adjusted incidence ratios for pulmonary embolism (comorbidities could not be stratified for the general population). In 1996, the overall incidence rate of pulmonary embolism was 149.90/100,000 dialysis patients compared with 24.62/100,000 persons in the US population, with an age-adjusted incidence ratio of 2.34 in dialysis patients. Younger dialysis patients had the greatest relative risk for pulmonary embolism. The age-adjusted incidence ratio of pulmonary embolism after excluding dialysis patients with known risk factors for pulmonary embolism was 2.11. Ninety-five percent confidence intervals for all age categories in both models were statistically significant. Chronic dialysis patients have high risk for pulmonary embolism, independent of comorbidity.
Pulmonary embolism is a common and often fatal postoperative complication. Dyspnea is the most common clinical manifestation in pulmonary embolism, and other signs are frequently inconsistent and often vague. The chest film and electrocardiogram may be helpful in excluding other cardiorespiratory diseases but they are frequently unreliable in establishing an objective diagnosis of pulmonary embolism. Documentation of a decreased arterial saturation provides suggestive evidence of pulmonary embolism. Lung scanning is a safe, sensitive procedure for the initial evaluation of symtoms suggestive of pulmonary embolism, and pulmonary arteriography may be necessary to confirm the diagnosis in certain patients. Anticoagulation is effective in the prevention and treatment of pulmonary embolism and proves successful in the vast majority of patients. Emboli that are not fatal gradually resolve in the pulmonary circulation. Vena caval interruption is occasionally beneficial in selected patients, especially those with septic emboli and cor pulmonale, but should only be performed when the indications are quite clear. Under certain selected circumstances pulmonary embolectomy may be indicated. Patients with massive embolism occluding more than one-half of the pulmonary arterial system and prooducing a markedly elevated pulmonary arterial pressure and severe hypoxemia may die in acute right heart failure. Intractable shock unresponsive to aggressive medical therapy in these patients represents an indication for pulmonary embolectomy. The hazards of these surgical procedures demand that a definite diagnosis of pulmonary embolism be made and a systematic approach to the diagnosis and treatment should be followed in all patients with the disorder.
Pulmonary embolism can be a catastrophic event leading to early death or serious hemodynamic instability. Thrombolytic therapy, in addition to heparin therapy, may improve the clinical condition and reduce the chance of recurrent pulmonary embolism in some cases. However, the acceptable "time window" for thrombolytic therapy is not well documented, though it has been used successfully as late as 14 days after pulmonary embolism. Successful delayed thrombolytic therapy beyond this "time window" in patients with massive pulmonary embolism has not been reported. We report a case of massive pulmonary embolism in which thrombolytic therapy was delayed more than 1 month after symptom onset. A 56-year-old woman was taken to National Cheng Kung University Hospital because of an episode of recurrent syncope, followed by progressive shortness of breath of 1 month's duration. Hypoxemia and hemodynamic instability were noted on admission. Echocardiography and a lung perfusion scan provided strong evidence of pulmonary embolism. Subsequent pulmonary angiography confirmed the diagnosis of multiple pulmonary emboli. The patient received a standard dose of intravenous tissue plasminogen activator 7 days after admission because of persistent symptoms and hypoxemia. Her clinical condition dramatically improved after treatment. Follow-up imaging studies showed resolution of the emboli. She was discharged in good condition. This case suggests that delayed thrombolytic therapy in patients with massive pulmonary embolism can still be beneficial in selected cases, even if given more than 2 weeks after symptom onset.
Pulmonary embolism, a major complication of thromboembolic disease, remains an important cause of mortality, both in surgical and medical practice. In recent literature, one finds two different currents: the first one asserts that pulmonary embolism is overdiagnosed and, therefore, "overtreated" with iatrogenic hemorrhagic complications, when other authors assert that pulmonary embolism is underdiagnosed and "undertreated". It is obvious that clinical diagnosis of non massive, acute pulmonary embolism remains difficult and that the classical triad pleuritic chest pain, hemoptysis and signs of deep venous thrombosis is not frequently found. The clinician should be attentive to the different symptoms and clinical signs which might arouse a suspicion of pulmonary embolism. A large range of investigations is available to confirm the clinical diagnosis. In deep venous thrombosis preceding or accompanying pulmonary embolism, treatment should be instituted at the first signs of venous attack. A precise diagnosis will secondarily be confirmed by phlebography. Any delay in effective early treatment of thromboembolic disease will increase the risk of pulmonary embolism and of the mortality inherent in this dreadful complication.
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.
PULMONARY EMBOLISM OCCURS IN THREE FORMS: (1) Asymptomatic "silent" embolization of lungs; (2) pulmonary infarction; and (3) massive pulmonary embolization leading to acute cor pulmonale. The commonest source of emboli are veins of the lower extremities and of the pelvic organs. The prevention and the treatment of pulmonary embolism overlap, for except for the heroic procedure of pulmonary embolectomy, treatment is equivalent to the prevention of further emboli. The diagnosis may be easy in typical cases and very difficult in others.
Pulmonary embolism is a common medical problem whose incidence is likely to increase in our aging population. Although it is life-threatening, effective therapy exists. The treatment is not, however, without significant complications. Thus, accurate diagnosis is important. Unfortunately, the clinical manifestations of pulmonary embolism are nonspecific. Furthermore, in many patients the symptoms of an acute embolism are superimposed on underlying chronic heart or lung disease. Thus, a high index of suspicion is needed to identify pulmonary emboli. Laboratory parameters, including arterial oxygen tensions and electrocardiography, are as nonspecific as the clinical signs. They may be more useful in excluding another process than in diagnosing pulmonary embolism. The first radiologic examination is the chest radiograph, but the clinical symptoms are frequently out of proportion to the findings on the chest films. Classic manifestations of pulmonary embolism on the chest radiograph include a wedge-shaped peripheral opacity and a segmental or lobar diminution in vascularity with prominent central arteries. However, these findings are not commonly seen and, even when present, are not specific. Even less specific findings include cardiomegaly, pulmonary infiltrate, elevation of a hemidiaphragm, and pleural effusion. Many patients with pulmonary embolism may have a normal chest radiograph. The chest radiograph is essential, however, for two purposes. First, it may identify another cause of the patient's symptoms, such as a rib fracture, dissecting aortic aneurysm, or pneumothorax. Second, a chest radiograph is essential to interpretation of the radionuclide V/Q scan. The perfusion scan accurately reflects the perfusion of the lung. However, a perfusion defect may result from a variety of etiologies. Any process such as vascular stenosis or compression by tumor may restrict blood flow. In addition, areas of the lung that are not well ventilated will be poorly perfused. Thus, a ventilation scan and a chest radiograph are essential to optimal interpretation of the perfusion scan. Ventilation/perfusion scans are interpreted as degrees of probability of pulmonary embolism. Emboli are not present in patients with a normal V/Q scan. An embolus is unlikely (10%-15%) among patients with a low-probability V/Q scan. However, small emboli that are nonocclusive may be present, and pulmonary arteriography may be used to further evaluate patients with a high clinical suspicion of pulmonary embolus.(ABSTRACT TRUNCATED AT 400 WORDS)