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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of 250 consecutive open-heart operations, three cases of late cardiac tamponade were noted following the operation. This led the authors to review the literature pertaining to this complication. Ninety-nine cases were collected. The frequency of late tamponade associated with cardiac surgery was 0.62% and was fatal in 16.2% of those cases. The delay before the tamponade appeared varied from 3 days to 3 months (mean 14.5 +/- 7.8 days). The initial clinical picture is insidious and vague, and this constitutes the danger of late cardiac tamponade. The clinical signs are of the respiratory (dyspnea, chest pain), gastrointestinal (anorexia, vomiting) and central nervous (mental confusion, even coma) systems. Pallor with a drop in hematocrit in patients on anticoagulant therapy suggests occult bleeding. A definitive diagnosis depends on catheterization of the right side and on mono- and bidimensional echocardiography. The authors believe that computerized axial tomography represents an interesting noninvasive and reliable examination technique when it can be used during emergency treatment. Pericardial puncture, which is both a diagnostic and therapeutic technique, was useful in one third of the cases; it produced a false-negative result in 12%. The resulting differential diagnoses are pulmonary embolism, myocardial insufficiency and septic shock. Late cardiac tamponade may be produced by one of two mechanisms: hemopericardium due to overdosage of anticoagulants or an exacerbated form of the post-pericardiotomy syndrome. Emergency treatment is always necessary. Pericardiocentesis is a useful diagnostic aid and provides temporary stabilization preoperatively. A wide surgical approach is always indicated. The mortality in untreated patients is 100%. The frequency of immediate relapse or, occasionally, of delayed relapse is estimated to be 11%; relapse may be lethal.
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PMID:[Late tamponade after heart surgery: a dreadful diagnostic pitfall]. 634 35

In a retrospective study over the years 1978-1982, 729 cases of acute pulmonary embolism were analyzed in relation to history, clinical signs and laboratory findings and the results compared with the findings of the urokinase pulmonary embolism trial. As far as history and clinical symptoms were concerned, breathlessness, chest pain, tachypnea, tachycardia and cyanosis were the dominating features. Among laboratory tests, the radiological and electrocardiographic findings of pulmonary hypertension were of little value. In contrast, arterial hypoxemia and isotope scanning provided the most reliable diagnostic information. The most frequent problem in differential diagnosis was acute myocardial infarction.
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PMID:[Diagnostic problems in acute pulmonary embolism]. 652

Recurrent pulmonary embolism sometimes (3% of hospital autopsies) determines a progressive obstruction of the pulmonary vascular bed, which in turn causes pulmonary arterial hypertension and in time right ventricular hypertrophy and failure. The first stages of this process are characterized by slight pulmonary arterial hypertension at rest and by few and deceiving symptoms which make the diagnosis very difficult. Regarding anatomy, in most cases recurrent thromboembolism obstructs one of the main branches of the pulmonary artery. At the beginning pulmonary embolism usually manifests itself in a spontaneous and atypical manner: paroxysmal dyspnea, tachycardia, lateral chest pain, mild hemoptysis and recurrent fever. The clinical signs of peripheral thrombophlebitis are not very frequent. The chest roentgenogram supplies diagnostic information in 20% of cases, the electrocardiogram in 10%. Very important is the contribution of the analysis of arterial blood gases: hyperventilation, moderate hypoxia associated with shunting, hypocapnia with a widened difference between alveolar and arterial CO2. Pulmonary perfusion scintiphotography shows vast unperfused areas, different to the "plexogenic" appearance in primitive pulmonary arterial hypertension, in about 50% of cases. Pulmonary angiography discloses the exact site and extension of the obstruction in 80-90% of cases. On catheterization pulmonary arterial hypertension results to be inconstant and may appear only during stress. Regarding the evolution of pulmonary embolism, the forms associated with pulmonary arterial hypertension may last several years, although recurrent embolism may shorten its course. When the stage of right ventricular hypertrophy is reached, the evolution is generally rapid (from 1 to 4 years).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pulmonary thromboembolism. 653 60

A retrospective analysis of the postoperative ophthalmic surgical mortality during the 20-year period ending in 1974 at the Jules Stein Eye Institute was performed. Eleven of 17,632 patients died following ophthalmic surgery (0.062%). Frequently, the cause of death was related to pulmonary embolism, myocardial infarction, congestive heart failure, or pneumonia. The postoperative complications were often heralded by complaints referable to the chest, and misdiagnosis was common. A simplified approach to postoperative chest pain based on location is presented.
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PMID:Chest pain in the postoperative ophthalmic patient. 726 18

Three patients with malignant mesothelioma of the pleura presented with unilateral pleural effusion and recurrent horizontal linear opacities on the chest radiograph. Although an initial diagnosis of pulmonary embolism was made in all three patients and two received anticoagulants, it is more likely that the opacities represented plate atelectases due to restriction of basal lung expansion by severe chest pain. It is suggested that the early manifestations of malignant mesothelioma of pleura may be confused with recurrent pulmonary embolism.
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PMID:Pleural mesothelioma presenting as apparent recurrent pulmonary embolism. 730 68

A 17-year-old boy with chest pain and severe bronchospasm underwent lung imaging to exclude pulmonary embolism. This showed widespread nonsegmental defects in both the ventilation and perfusion scans. A repeat study performed immediately after nebulized bronchodilator administration was normal apart from changes consistent with left lower lobe pneumonia and atelectasis which had subsequently evolved on the chest radiograph. Bronchodilator administration is valuable in improving the accuracy of lung scanning in asthmatic patients by reducing the perfusion and ventilation abnormalities caused by hypoxia-induced vasoconstriction.
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PMID:The value of bronchodilator administration in asthmatic patients before lung imaging. 764 28

We report a case of renal vein thrombosis (RVT) and pulmonary embolism associated with diffuse membranous glomerulonephritis. A 44-year-old Japanese male was referred to the Nephrology Department with heavy proteinuria. Renal biopsy revealed diffuse membranous glomerulonephritis and we administered PSL 30mg/day and dipyridamole 300mg/day. Three weeks later, he was admitted with severe chest pain, dyspnea and massive proteinuria. RVT and pulmonary embolism were detected on CT scan and perfusion lung scan. After a few days of continuous intravenous unfractionated heparin (UFH) therapy, we used 72 U (anti-FXa)/kg of intravenous low-molecular-weight heparin (LMWH) every 12 hours for 10 days. He also received urokinase at the dose of 120,000 U/day for 4 weeks and long-term therapy with warfarin potassium at the dose of 3 mg/day. One month later, the thrombi in the pulmonary arteries and inferior vena cava disappeared on CT scan and perfusion lung scan. LMWHs have a longer biological half-life and a lower bleeding tendency than UFH for an equivalent antithrombotic effect. This case indicates that intermittent intravenous LMWH administration combined with urokinase is effective against RVT and pulmonary embolism without any side effect.
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PMID:[A case of renal vein thrombosis and pulmonary embolism associated with diffuse membranous glomerulonephritis: the usefulness of low-molecular-weight heparin and urokinase therapy]. 769 54

A 23-year-old man was admitted because of an attack of chest pain and dry cough. Chest roentogenogram showed a solitary pulmonary nodule in the left upper lobe. Chest CT showed a nodule and a small pleural effusion on the same side. Pulmonary thrombosis was diagnosed by pulmonary Ventilation/perfusion scintigraphy and pulmonary arteriography. Deep vein thrombosis was not detected except in a distal pulmonary artery. The solitary nodule disappeared spontaneously without thrombolytic therapy. An anticardiolipin antibody (IgG) test was positive. Primary antiphospholipid syndrome was diagnosed, because of the absence of physical findings suggesting other collagen vascular diseases. Patients with antiphospholipid syndrome have a high frequency of pulmonary complications that include pulmonary hypertension and pulmonary embolism. Most of the patients with pulmonary embolism have deep vein thrombosis, and pulmonary vessel thrombosis as seen in the present case is a rare complication.
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PMID:[A case of pulmonary thrombosis associated with primary antiphospholipid syndrome]. 773 Nov 19

Pulmonary embolism (PE) is largely undiagnosed because clinical suspicion is not raised in most instances, and thus, patients with PE go undetected. In this paper, we try to define the role of clinical assessment (including chest radiography, electrocardiogram, arterial blood gas analysis) in making the diagnosis early, accurate, and at low cost, and propose a flow chart to be used in clinical practice. All patients with otherwise unexplained dyspnea or chest pain should be sent for perfusion lung scintigraphy; accordingly, underdetection of PE and mortality of PE should be reduced. If, within 1 h after the clinical suspicion has been raised, the above-mentioned simple and noninvasive examinations are available, they may be employed to reduce the number of unnecessary procedures, without losing patients actually affected by PE. Finally, when diagnostic tools are not promptly available, noninvasive techniques may be employed to identify patients with the highest probability of PE where to start with heparin coverage while waiting for definitive diagnosis.
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PMID:The role of suspicion in the diagnosis of pulmonary embolism. 781 24

The diagnosis of pulmonary embolism (PE) can be accurately made by perfusion lung scan and pulmonary angiography; however, when these diagnostic techniques are not promptly available, simple clinical procedures may be useful to identify patients with high probability PE. To this end, collection of clinical data through a standardized questionnaire and the use of findings from chest radiograph, ECG, and blood gas analysis may raise clinical suspicion and decide on therapeutic management. By reviewing published literature and our own experience, we found that unexplained dyspnea and chest pain are the most frequent symptoms, and sudden onset dyspnea and pleuritic chest pain are the most typical. Chest radiograph is abnormal in more than 80% of patients with PE, showing typical signs such as "sausage-like" descending pulmonary artery, Westermark sign, etc. The ECG may show findings characteristic of PE, such as tachycardia, T wave inversion in V1-V2, and PR displacement. Arterial blood gas data frequently demonstrate hypoxia and hypocapnia, being helpful in suspecting or excluding PE. Recent statistical techniques, such as discriminant or logistic analysis, may be applied to the above clinical assessment to refine and improve the noninvasive diagnosis of PE.
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PMID:Clinical features of pulmonary embolism. Doubts and certainties. 781 25


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