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• W4297930688 abstract "Prevention of deep venous thrombosis is fundamental in the prevention of pulmonary embolism. Deep venous thrombosis is common after all surgical procedures, but the frequency differs, as does the effectiveness of various methods of prevention. Low-dose heparin, low molecular weight heparin, graduated compression elastic stockings, intermittent pneumatic compression, and oral anticoagulants have a role in the prevention of deep venous thrombosis, depending on the risks of deep venous thrombosis and their demonstrated effectiveness (or lack of effectiveness) in the particular circumstance. The optimal method of prophylaxis is specific to the predisposing condition.Heparin continues to be a mainstay of anticoagulant therapy. Major bleeding is rare in patients treated with low doses of heparin to prevent deep venous thrombosis. With therapeutic doses, however, major bleeding occurs in about 5% of patients.The optimal dose of warfarin and the method of evaluating the anticoagulant effect of warfarin have undergone modifications in recent years. It is now recognized that the prothrombin time ratio depends on the activity of the thromboplastin used for measuring the prothrombin time. An International Normalized Ratio, which relates to a standardized thromboplastin, has been developed, thus avoiding differences of the prothrombin time ratio that occur from batch to batch of thromboplastin reagent from the same manufacturer and that occur with different thromboplastin reagents from different animal sources and different manufacturers.The bedside diagnosis of pulmonary embolism is useful in helping a physician determine the extent to which diagnostic tests should be pursued. A sound bedside impression also contributes strongly to the formulation of a noninvasive diagnosis of pulmonary embolism. The clinical manifestations of pulmonary embolism form a recognizable constellation of findings that often lead to a correct diagnosis or exclusion of pulmonary embolism.Important clues to the diagnosis of pulmonary embolism relate to the initial syndrome. The presentation of pulmonary embolism is most often in the form of the pulmonary hemorrhage—pulmonary infarction syndrome. The next most common presentation is unexplained dyspnea, unaccompanied by pulmonary hemorrhage or infarction. Least common, but most severe, is the syndrome of circulatory collapse. Immobilization, usually caused by surgery, is the most frequent predisposing factor. Most patients with clinically recognizable pulmonary embolism have dyspnea or tachypnea. Dyspnea or tachypnea or pleuritic pain occurs in nearly all patients who have clinically apparent pulmonary embolism (97%). Ordinary tests such as the electrocardiogram and chest radiograph are helpful if the physician is attentive to nonspecific abnormalities. These abnormalities include atelectasis or parenchymal abnormalities or elevation of the diaphragm on the chest radiograph and nonspecific ST segment or T wave changes on the electrocardiogram. The PaO2 is helpful if it is low. D-dimers may help exclude pulmonary embolism if they are normal.The combination of ventilation/perfusion lung scans, when read according to the criteria in the Prospective Investigation of Pulmonary Embolism Diagnosis study, were indicative of pulmonary embolism in 87% of patients when the ventilation/perfusion scan was read as “high probability” and was indicative of pulmonary embolism in 14% when it was “low probability.” Prior clinical assessment, in combination with the ventilation/perfusion scan probability, strengthened the diagnostic validity of the ventilation/perfusion scan. A concordant high-likelihood clinical assessment with a high-probability ventilation/perfusion scan interpretation was indicative of pulmonary embolism in 96% of patients. A concordant “unlikely” clinical assessment with a low-probability interpretation of the ventilation/perfusion scan was indicative of pulmonary embolism in only 4%.The predictive value of pulmonary embolism can be determined on the basis of the number of mismatched segmental perfusion defects. This shows a numerical probability of pulmonary embolism and eliminates qualitative impressions, which may be misleading. The number of mismatched defects indicative of pulmonary embolism depends on the presence of prior cardiopulmonary disease. Fewer mismatched defects are required to make a diagnosis of pulmonary embolism in a patient with no prior cardiopulmonary disease than in a patient with prior cardiopulmonary disease. Further stratification according to prior clinical assessment enhances the ability to achieve an accurate predictive value for each category of patients.Pulmonary angiography is the definitive diagnostic test for pulmonary embolism. Angiography, however, is associated with risk (1.3% major complications), discomfort, and expense. Because of inaccuracy of the noninvasive diagnosis of pulmonary embolism, the concept of diagnosis and treatment of deep venous thrombosis has been introduced as an alternative. This alternative is based on the recognition that pulmonary embolism is a complication of deep venous thrombosis and part of the spectrum of thromboembolic disease. The concept that pulmonary embolism is a complication of deep venous thrombosis has been recognized for many years. Whether management and prognosis are the same has been questioned. The preponderance of evidence supports the validity of striving to diagnose “thromboembolic disease” if the diagnosis of pulmonary embolism is not readily apparent from noninvasive studies. Strategies of diagnosis, developed on this basis, spare many patients the necessity of pulmonary angiography. If a clinical suspicion of pulmonary embolism exists, and noninvasive tests show deep venous thrombosis, it is reasonable to treat “thromboembolic disease” with anticoagulants.Recommended therapy for deep venous thrombosis and for pulmonary embolism is heparin (activated partial thromboplastin time 1.5 to 2.5 times control) followed by warfarin (International Normalized Ratio of 2.0 to 3.0). Transvenous inferior vena cava occlusion is indicated if there is a contraindication to anticoagulants, a continuing predisposition to deep venous thrombosis, or recurrent pulmonary embolism on full-dose anticoagulants. Some recommend prophylactic vena caval filters for high-risk patients, including those with extensive or progressive deep venous thrombosis, severe pulmonary hypertension, or cor pulmonale, or those who have undergone pulmonary embolectomy.Thrombolytic therapy for pulmonary embolism is indicated if the patient is hypotensive or hypoxic on high levels of oxygen or in the presence of right ventricular failure caused by the pulmonary embolism. Currently, thrombolytic therapy is not recommended for the routine treatment of pulmonary embolism. Open pulmonary embolectomy is rarely, if ever, indicated. Transvenous pulmonary embolectomy has shown potential, and catheter tip fragmentation may be a forthcoming mode of therapy." @default.
• W4297930688 created "2022-10-01" @default.
• W4297930688 date "1994-09-01" @default.
• W4297930688 modified "2023-10-18" @default.
• W4297930688 title "Acute pulmonary embolism" @default.
• W4297930688 doi "https://doi.org/10.1016/0011-5029(94)90017-5" @default.
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