[Recurrent pulmonary embolism, pulmonary hypertension and pulmonary heart disease].
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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.
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In 53 patients with possible pulmonary embolism, pulmonary abnormalities of 133Xe ventilation and 99Tcm albumin microsphere perfusion scintigraphy were compared with absence or presence of pulmonary emboli documented by concurrent pulmonary angiography. It was found that patients with combined scintigraphy considered as unlikely for pulmonary embolism (ventilation defect larger than perfusion defect) or indicative of pulmonary embolism (ventilation defect smaller than perfusion defect) provide high diagnostic specificity. Patients with equal ventilation-perfusion abnormalities (possible pulmonary embolism) require further evaluation by pulmonary angiography to ascertain diagnosis. Importantly, diagnostic accuracy, using ventilation-perfusion scintigraphy and the quantified method of evaluation delineated, is preserved in patients with severe congestive heart failure.
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Septic pulmonary embolization occurs when an infected thrombus lodges in the pulmonary arterial tree. Pulmonary abscess, empyema, bronchopleural fistula, shock and death may follow. During the preantibiotic era, septic pulmonary embolization was a dread complication of septic thrombophlebitis occurring in the pelvis and after infections of the head and neck. More recently, the multiplicity of long term indwelling catheters has changed the epidemiologic aspect of this disease, pointing toward iatrogenic causes in many instances. The drug addict, however, remains the person at greatest risk of having septic pulmonary embolization develop. A clinical evaluation seeking drug abuse and related stigmata is extremely helpful in suggesting the proper cause, establishing the presence of right-sided endocarditis and directing appropriate therapy. Staphylococcus aureus is the most common offending organism in all patient populations except for the patient with thermal injury in which gram-negative organisms predominate. Early diagnosis and proper therapy, which includes high doses of parenteral antibiotics and control of the inciting septic focus in all instances, are prerequisites for a favorable outcome.
A 59-year-old man underwent successful repair of a pulmonary arterial aneurysm because of peripheral pulmonary embolization. These lesions are relatively rare; and, to out knowledge, peripheral embolization from such an aneurysm has not been previously reported.
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Lethal pulmonary embolism is associated with hypoxemia and hypocapnia in the vast majority of cases. The easily calculated ventilation corrected oxygen tension was a very sensitive test in patients breathing air. It yielded no normals, four percent mild hypoxemia, and 96 percent moderate to extreme hypoxemia. The alveolar-arterial oxygen tension difference and oxygen ratio were equally sensitive during air breathing. During oxygen inhalation, alveolar-arterial oxygen difference was most sensitive; oxygen ratio was second best; and oxygen saturation was the least sensitive test.
Selective pulmonary arteriography, with superselective magnification views of the lung bases or other areas where abnormalities are shown on perfusion lung scans, performed within 24-48 hours after the onset of symptoms, can effectively rule out clinically significant pulmonary thromboembolism. One hundred and eighty consecutive patients (minimum follow up, six months) with suspected pulmonary embolism and negative pulmonary arteriograms were studied. Not one of the 167 untreated patients died as a result of thromboembolic disease during the acute illness (20 died from unrelated causes), and none of the 147 patients who survived suffered "recurrent embolism" during follow up.
The response of pulmonary arterial pressure to minor degrees of pulmonary embolism was examined in 18 patients with embolic occlusion of less than 25% of the pulmonary vascular bed. Patients with pulmonary embolism were compared to normal controls matched for age and sex and to patients with a variety of acute pulmonary disorders without pulmonary embolism. Patients with pulmonary embolism and patients with other acute pulmonary diseases had significantly higher pulmonary arterial pressures and significantly lower values for arterial oxygen tension (PaO2) than did normal subjects. The degree of pulmonary hypertension correlated with the PaO2. Pulmonary hypertension occurring after minor degrees of pulmonary embolism may be a response to mild arterial hypoxemia.
Pulmonary embolism is an emergency situation. The earlier therapy begins, the more effective it will be. This, however, asks for immediate diagnosis. At present the most effective method of diagnosing and localizing pulmonary embolism is perfusion scintiscan of the lung. It should be completed by chest radiography to exclude peripheral infiltration and/or central lung cancer. Generally, these two procedures ensure optimal diagnosis. In case of additional disease of the pleura, mediastinum and lung parenchyma, further measures may be necessary: especially in chronic obstructive lung disease ventilation perfusion ratio and outwash of xenon might be helpful. Scintiscan of the lung is suited for early diagnosis as well as for follow-up examinations. Only if thrombectomy is planned, pulmonary angiography should be preferred. Scintiscan of the lung with marked particle suspensions ensures a minimum of complications. There is only one incident in 10,000 examinations. According to Quinn (1964) and Felix (1971) pulmonary scintiscan might be harmful in patients with right heart failure. We made no such observation in 4000 cases.
Pulmonary profusion scintigraphy is a simple, noninvasive and low-cost method for identifying acute pulmonary embolism. Although the method is highly sensitive, it is relatively non-specific, so that final assessment must include history, clinical findings and plain roentgenography of the thorax. Pulmonary scintigraphy is indicated whenever acute pulmonary embolism is suspected, on account of the therapeutic consequences resulting therefrom, in all cases where clinical findings and basic diagnosis cannot definitely establish the disease. It must not, however, be considered as an alternative to angiography of the pulmonary artery; as a matter of fact, it should be employed early and frequently in view of the high percentage of undiagnosed embolism of the lungs during the patients' lifetime.
Pulmonary thromboembolism is a widespread problem and is an important cause of death in patients with a variety of medical and surgical conditions. There have been few significant advances in the understanding of the aetiology beyond additional evidence confirming the importance of Virchow's triad. An impressive list of epidemiological associations has been compiled, however. Some knowledge of the natural progression of the disease is required as an aid in the understanding of the application of the therapeutic and prophylactic measures available in the management of pulmonary embolism. It would seem that at least two-thirds of pulmonary emboli are non-fatal, and in these cases the natural resolution, even of comparatively large embolic masses, is very efficient in patients without pre-existing cardiopulmonary disease. Diagnosis may prove difficult and most ancillary investigations are of questionable value. On the other hand, pulmonary radio-isotope scanning is far more specific and pulmonary angiography is a comparatively simple and complication-free diagnostic procedure. Prophylaxis is a real and practical aim, especially following surgery or myocardial infarction. In these groups widespread clinical trials of prophylactic measures have been made possible by the objective radio-iosotope screening techniques. Mechanical means of preventing venous stasis and anticoagulation appear effective. In addition, low-dose subcutaneous heparin seems to be as useful as heparin in conventional dosage. Apart from conventional supportive therapy, there are three major approaches to the treatment of pulmonary embolism. Heparin remains the mainstay, particularly in the less severe cases, hopefully preventing propogation of thrombosis and recurrence of embolism, thus allowing resolution to take place. Thrombolytic therapy with streptokinase or urokinase is capable of producing far more rapid dissolution of pulmonary emboli with consequent theoretical advantages over heparin. No reduction in mortality has been shown using thrombolytic therapy. Patients who fail to respond satisfactorily to acute resuscitative measures may require pulmonary embolectomy.
The diagnosis of pulmonary embolism is generally established when the patient has characteristic pulmonary perfusion abnormalities in the setting of an appropriate clinical history and with no concurrent cardiopulmonary disease on chest x-ray film. The initial evaluation, including positive pulmonary perfusion scan, of four young black women suggested the diagnosis of pulmonary emboli. A syndrome of respiratory tract viral infection then developed, and further evaluation by angiography and perfusion scans contradicted the diagnoses of pulmonary emboli. Each patient had substantial convalescent-phase complement-fixation titers to influenza A. Thus, if reliance is placed in pulmonary perfusion scans, an erroneous diagnosis of pulmonary emboli may be made for patients with influenza A.
The frequency of clinical and sub-clinical postoperative pulmonary embolism, demonstrated by combined pulmonary ventilation-perfusion scanning, and the prophylactic effect of low-dose heparin, were assessed in a randomised double-blind study in 43 patients aged over 40 years. Pulmonary embolism was demonstrated using combined ventilation-perfusion scanning in 4 out of 43 patients (9%). The incidence was 1 out of 19 patients in the heparin-treated group and 3 out of 24 patients in the placebo group. This difference was not significant. If post-operative perfusion scanning alone had been utilised for diagnosing pulmonary embolism, the frequency of pulmonary emboli would have been 33%, with 21% in the heparin group and 46% in the placebo group. This difference is not significant. It is concluded that perfusion scanning over-estimates the frequency of post-operative pulmonary embolism. The use of the more specific combined ventilation-perfusion scanning shows that asymptomatic postoperative pulmonary embolism does occur, but that the frequency is considerably lower than indicated by perfusion scanning alone. Combined ventilations-perfusion scanning must be performed in studies assessing the effects of various treatment regimes on the frequency of pulmonary embolism postoperatively. The small number of patients included in the study do not permit any conclusions concerning any prophylactic effect of low-dose heparin against pulmonary embolism.