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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary embolism is nearly always a complication of deep venous thrombosis. The evaluation of risk factors for venous thromboembolism not only aids diagnosis but also guides decisions about the intensity of prophylactic measures. As both the extent and chronicity of pulmonary vascular obstruction vary widely, pulmonary embolism can produce widely differing clinical pictures. From the clinical, pathophysiological and therapeutical point of view, it is convenient to classify pulmonary embolism into four types: acute minor embolism (dyspnoea with or without pleuritic pain or haemoptysis), acute massive embolism (hemodynamic instability), subacute massive embolism (mimicking heart failure or indolent pneumonia), and chronic thromboembolic pulmonary hypertension (slowly progressing dyspnoea). This classification is of importance not only for the rational diagnosis and differential diagnosis, but also for the institution of adequate therapy. Because the disease has many nonspecific manifestations but no pathognomonic symptoms or signs, it is impossible to prove the diagnosis of pulmonary embolism alone on the basis of clinical presentation.
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PMID:[Clinical characteristics of pulmonary embolism]. 1121 69

We report the case of a 48-year-old man who was admitted to our emergency department because of a superior vena caval syndrome from which the symptoms occurred only during exercise. His past history included an episode of lower limb deep venous thrombosis. Because an atrio-ventricular partial block was fortuitously evidenced, the patient was submitted to a pacemaker insertion. A few years later, the patient suffered from rapid dyspnea on exercise, associated with facial cyanosis and systemic hypotension. The exploration by phlebography evidenced that the inferior vena cava was completely obstructed. Therefore the venous return from the lower part of the body to right heart was obtained through hypertrophy of the vena azygos. In addition, the presence of cardiac pacing electrodes induced a stenosis at the level of the superior vena cava, just before its entrance into the right atrium. Such a venous network accounted for the occurrence of a chronic superior vena caval syndrome associated with peripheral arterial hypotension during exercise. Treatment consisted of a superior vena caval percutaneous transluminal balloon angioplasty followed by a Wallstent insertion. This procedure led to a correction of all hemodynamic abnormalities responsible for reported pathophysiological limitations to stress.
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PMID:[Clinical case of the month. An unusual presentation of superior vena cava syndrome]. 1124 97

Pulmonary embolism (PE) was believed to be a rare disease and often misdiagnosed in Thailand. Only a few cases of PE in Thai patients have been reported. The purpose of this study was to describe the characteristics of history, physical examination and laboratory investigations in Thai patients with PE. Forty-nine patients diagnosed as PE in Phramongkutklao Hospital between 1994 and 1998 were included in the study. All patients underwent complete history, physical examination and appropriate laboratory studies. The mean age of this patient group was 53 years. Thirty-four per cent of these patients were first suspected of lung embolism while the others were misdiagnosed as congestive heart failure, myocardial infarction, pneumonia or septic shock. The most common syndrome was isolated dyspnea. Interestingly, chronic thromboembolic pulmonary hypertension which is uncommonly found in western countries was diagnosed in 12 per cent of our patients. Dyspnea, pleuritic pain, leg swelling, cough, tachypnea, tachycardia and increased pulmonary component of second heart sound were common symptoms and signs. A high-probability ventilation/perfusion lung scan and deep vein thrombosis were demonstrated in 93 per cent and 55 per cent of our patients, respectively. The mortality rate was 10 per cent.
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PMID:Clinical and laboratory findings in patients with pulmonary embolism in Phramongkutklao Hospital. 1125 85

A 55-year-old man was admitted to our hospital complaining of dyspnea and chest pain. Transthoracic echocardiography showed dilation of the right ventricle. Chest computed tomography with contrast medium showed multiple emboli in the pulmonary arteries. Venography of the lower extremities showed multiple thrombi in the right popliteal vein and the presence of left-sided vena cava. This unusual case of left-sided vena cava was complicated by deep vein thrombosis due to hemostasis. A Greenfield filter was placed in the vena cava proximal to the right renal vein in a right internal jugular vein approach.
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PMID:[Placement of the inferior vena cava filter proximal to the renal vein in a patient with left-sided inferior vena cava complicated by pulmonary embolism: a case report]. 1168 30

Primary pulmonary hypertension (PPH) is a condition characterized by sustained elevation of pulmonary artery pressure (PAP) without demonstrable cause. The most common symptom at presentation is dyspnea. Other complaints include fatigue, chest pain, syncope, leg edema, and palpitations. Right heart catheterization is diagnostic, showing a mean PAP >25 mmHg at rest and >30 mmHg during exercise, with a normal pulmonary capillary wedge pressure. In the National Institutes of Health-PPH registry, the median survival period was 2.8 years. Treatment is aimed at lowering PAP, increasing cardiac output, and decreasing in situ thrombosis. Vasodilators have been used with some success in the treatment of PPH. They include prostacyclin, calcium-channel blockers, nitric oxide and adenosine. Anticoagulation has also been advised for the prevention of deep vein thrombosis, pulmonary embolism, and in situ thromboses of the lungs. New drug treatments under investigation include L-arginine, plasma endothelin-I, and bosentan. Use of oxygen, digoxin, and diuretics for symptomatic relief have also been recommended. Patients with severe PPH refractory to medical management should be considered for surgery.
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PMID:Primary pulmonary hypertension. 1172 93

XR 5000 is one of a series of tricyclic carboxamide-based cytotoxic agents. It binds to DNA by intercalation and stimulates DNA cleavage by inhibition of both topoisomerase I and II, thus possibly overcoming the resistance resulting from downregulation of either enzyme. Twenty patients with advanced or metastatic colorectal cancer, unpretreated for metastatic disease, received XR 5000 at the dose of 3010 mg/m(2) in a 120-h central intravenous (i.v.) infusion every 3 weeks. Response was evaluated every two cycles. No complete (CR) or partial responses (PR) were observed in eligible patients (response rate, 0 of 19, 0%; 95% confidence interval (CI): 0-18%). 5 patients had stable disease, which lasted from 79 to 157 days. Haematological toxicity was low, since only one grade 4 neutropenia and two grade 3 anaemia were observed. Other treatment-related grade 3-4 toxicities were: deep venous thrombosis (2 cases), liver toxicity, diarrhoea, anorexia, dyspnoea, chest pain, infection (1 case each). Despite the good toxicity profile, these results do not support further trials with XR 5000 in metastatic colorectal cancer.
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PMID:Phase II study of XR 5000, an inhibitor of topoisomerases I and II, in advanced colorectal cancer. 1175 Aug 42

Upper extremity deep venous thromboembolism has become increasingly common due to the use of subclavian venous access. However, forearm deep venous thrombosis is rare. We report a case of chronic pulmonary thromboembolism originating from left forearm deep venous thrombosis. A 66-year-old woman was admitted to our hospital because of dyspnea, which had worsened over the previous 2 months. Echocardiography showed severe right ventricular enlargement and pulmonary hypertension. Perfusion lung scintigraphy revealed multisegmental perfusion defects. No likely factors responsible for hypercoagulability were found. The patient had a history of left radial fracture and had been treated with external fixation. Venography of the upper and lower extremities revealed total occlusion of the deep veins of the left forearm with collateral vessels, but no evidence of other upper or lower extremity venous thrombosis.
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PMID:[Chronic pulmonary thromboembolism originating from left forearm deep vein thrombosis: a case report]. 1187 34

BACKGROUND. Mortality in pulmonary thromboembolism (PTE) decreases considerable when it is diagnosed early. The suspicion based on clinical and complementary data is essential for an early diagnosis. METHODS. Retrospective review of the clinical features in patients diagnosed of PTE in an Internal Medicine department from January 1993 to December 1999. RESULTS. A total of 117 patients with PTE were identified. The median age was 68.8 years. Sixty-six patients (56.4%) had one or more risk factors for PTE. The most common risk factor was immobilization (37.6%). Dyspnea was the most common symptom (74.4%) and tachypnea the most common sign (66.7%). Fever/low grade fever and leukocytosis were present in 16.2% and 31.6% of patients, respectively. Respiratory failure, alkalosis and hypocapnia were present in 44.4%, 38.5% and 47% of patients, respectively. An alveolar-arterial oxygen gradient > 20 mmHg was demonstrated in 96.6% of patients. Chest radiographs and electrocardiograms were normal in 52.1% and 23.9% of patients, respectively. A vein echo-duplex of the lower limbs demonstrated deep vein thrombosis (DVT) in 52.1% of patients. The hospital mortality rate was 6.8%. CONCLUSIONS. PTE still affects older patients mainly and frequently known risk factors are not detected. The presence of fever/low grade fever and/or leukocytosis does not rule out PTE. Both chest radiographs and electrocardiograms may be normal. Not demonstrating DVT in the lower limbs by the vein echo-duplex does not rule out PTE. The hospital mortality rate has not decreased considerably in the last few years.
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PMID:[The current clinical spectrum of pulmonary thromboembolism]. 1199 39

Pulmonary Embolism (PE) poses an important diagnostic problem in patients with chronic obstructive pulmonary disease (COPD). Indeed PE may aggravate the already precarious respiratory state of these fragile patients. Moreover, these two conditions share common symptoms: dyspnoea, wheezing, pleural pain, haemoptysis, palpitations and signs of right cardiac insufficiency. In two studies, one retrospective and the other prospective, we investigated the incidence of PE in patients with non-infective exacerbations of their COPD. The retrospective study was carried out over two years and involved 50 COPD patients with non-infective respiratory exacerbations. In this population, 10 patients out of 50 (20%) had a documented PE. No predictive factor was identified. The prospective study was conducted over one year and COPD patients admitted to hospital with exacerbations were included in the study if they had a positive D-dimer blood test and no evidence of acute respiratory infection. 31 patients were studied with Doppler ultra-sound examination of the legs and a lung perfusion scan. The presence or absence of PE was determined and the two groups were compared. 9 patients out of 31 (29%) had a documented PE. Six of these nine patients had a deep venous thrombosis (DVT). Two predictive factors of PE were identified: existence of a DVT and a significant fall in PaO(2) from baseline state (DeltaPaO(2) > 22 mmHg). We conclude that PE is a frequent (20 to 30%) of non-infective respiratory decompensation in COPD patients. Faced with an unexplained respiratory exacerbation in these patients, a lung perfusion scan should be routinely undertaken to rule out a PE when the D-dimers are positive.
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PMID:[Pulmonary embolism and sibilant types of chronic obstructive pulmonary disease decompensations]. 1241 52

Deep vein thrombosis (DVT) and pulmonary embolism (PE) are distinct but related aspects of the same dynamic disease process known as venous thromboembolism (VTE). An estimated 200,000 new cases occur in the United States every year, including 94,000 with PE, resulting in an incidence of 23 per 100,000 patients per year-cases. Without treatment, pulmonary embolism is associated with a mortality rate of approximately 30%, causing nearly 50,000 deaths per year. Moreover, based on post-mortem studies, two-thirds of the patients with pulmonary emboli remain undiagnosed. Clinically, PE may present as (1) isolated dyspnea, (2) pleuritic pain and/or hemoptysis, and (3) circulatory collapse. However, clinical history and examination can be notoriously misleading in reaching a diagnosis. A number of acquired etiologic risk factors (predispositions) are associated with a tendency to develop VTE. These include increasing age, immobilization, surgery, trauma, hospital or nursing home confinement, malignancy, neurologic disease with extremity paresis, as well as certain types of oral contraception and hormone replacement therapy. In addition, a variety of genetic risk factors, such as factor V Leiden, protein S or C deficiency have also been identified. However, in at least half of the instances, no predisposing factors can be identified (idiopathic PE). In the majority of cases thromboemboli originate in the deep veins of the calf or pelvis. The pathogenic conditions for VTE comprise a triad of factors and include (1) venous stasis, (2) hypercoagulable states, and (3) vascular endothelium injury. Occlusion of pulmonary arteries has variable and transient clinical and pathophysiologic consequences, involving both mechanical and reflex effects of vascular occlusion with a consecutive perfusion defect as well as the release of vasoactive and other inflammatory mediators. The objectives of this article are to present an overview of the etiologic and pathogenic factors promoting VTE as well as the pathophysiologic and inflammatory processes following PE.
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PMID:Principle mechanisms underlying venous thromboembolism: epidemiology, risk factors, pathophysiology and pathogenesis. 1258 87


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