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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 can produce severe cardiopulmonary dysfunction characterized by pulmonary artery hypertension, right ventricular failure, and hypoxemia. The search for the source of a pulmonary embolus, by exploration of the veins of the lower limbs and the inferior vena cava should be systematically carried out in all cases of pulmonary embolus which are not immediately life-threatening to the patient. The treatment of deep vein thrombosis associated with pulmonary embolism with thrombolytic agents has been proposed and utilized for approximately 20 years. Although superior results have been claimed with thrombolytic agents, the use of this type of treatment remains limited to massive or sub-massive pulmonary embolism. Fibrinolytic agents with high specificity for fibrin in the thrombi and little systemic activation of the fibrinolytic system have been developed and tested in preliminary clinical trials of patients with acute pulmonary embolism. The largest published experience available has been with recombinant tissue plasminogen activator (rtPA). The acylated streptokinase-plasminogen complex (APSAC) and pro-urokinase also gave promising results. All these agents were accompanied by unexpectedly high incidence of systemic activation of the fibrinolytic system and by hemorrhagic complications with frequencies similar to those that follows the use of first generation products (urokinase and streptokinase). Hence, their superior clinical efficacy must be clearly proven before they are substituted for a more widely available and less expensive drug, such as streptokinase.
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PMID:Pathogenesis and management of acute pulmonary embolism. 251 49

The clinical and echocardiographic features of right atrial thrombi were examined in 9 patients, 5 men and 4 women aged 16 to 86 years. The 2D echocardiographic diagnosis was confirmed at autopsy (4 cases) or by the association of severe recurrent pulmonary embolism (5 cases). Three patients had associated ischaemic heart disease and on patient had dilated cardiomyopathy. The clinical presentation was: acute cor pulmonale (5 cases including 2 patients which biventricular myocardial infarction), chronic post-embolic cor pulmonale (1 case), tricuspid valve obstruction (1 case), general ill health with pyrexia (1 case) and heparin-induced thrombocytopenia (1 case). Predisposing factors included: absence of anticoagulent therapy (7 cases), previous supraventricular arrhythmias (2 cases) and right ventricular failure (6 cases, including 2 of right ventricular infarction). In 2 patients the thrombi were relatively immobile and had a wide base of implantation on the interatrial septum; in 1 patient, multiple thrombi were observed lining the right heart cavities from the inferior vena cava to the pulmonary infundibulum. In the other 6 patients, the thrombi were very mobile with a visible pedicule of implantation (2 cases) or totally free (4 cases). The variable polylobulated appearances, completely irregular whirling motion and intermittent prolapse into the tricuspid valve were characteristic features of the latter 4 cases. They disappeared spontaneously (2 cases) or after fibrinolytic therapy (2 cases) in under 36 hours. Three patients were operated with one postoperative death. The global hospital mortality was 22%. The present occasional detection of right atrial thrombosis will certainly become more common if patients with pulmonary embolism, right ventricular infarction or deep venous thrombosis are systematically examined by 2D echocardiography in the acute phase of their illness.
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PMID:[Clinical, echocardiographic and evolutive aspects of right atrial thrombosis]. 308 12

A 39-years-old male patient with chronic venous insufficiency, deep venous thrombosis and recurrent pulmonary embolism in the past medical history. After syncopal event was diagnosed of bilateral chronic pulmonary embolism, pulmonary hypertension and right ventricular failure. Fibrinolytic treatment was no effective therapeutic modality. Under cardiopulmonary bypass, bilateral pulmonary thromboendarterectomy with extension into lobe arteries, plus insertion of caval filter was performed. We present our experience with this case and a review of the literature.
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PMID:[Bilateral pulmonary thromboendarterectomy in chronic pulmonary thromboembolism. A case report and review of the literature]. 748 Oct 40

A young man with a history of deep vein thrombosis and pulmonary embolism 11 years ago presented again with acute pulmonary embolism and was treated initially with intravenous heparin at our institution. Five days later he had another massive bout of pulmonary embolism causing hypotension. Pulmonary angiography confirmed the presence of thrombi in both pulmonary arteries, with complete obstruction of the left pulmonary artery. He was treated successfully by emergency pulmonary embolectomy. Blood investigations later confirmed the diagnosis of protein S deficiency and he was started on warfarin therapy for life. Massive pulmonary embolism should be treated aggressively. Thrombolytic therapy accelerates clot lysis, reduces pulmonary pressures, restores pulmonary capillary volume and reverses right heart failure faster than heparin alone. There is also a trend towards decreased mortality with thrombolysis. In the presence of shock, the patient should be resuscitated and if facilities for emergency embolectomy are available, surgery is a viable alternative to thrombolysis, especially if the clot burden is massive. In young patients with recurrent venous thromboembolism in the absence of obvious predisposing factors, it is important to exclude inherited plasma protein deficiencies of protein S, protein C, antithrombin III, plasminogen and fibrinogen.
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PMID:Massive acute pulmonary embolism in protein S deficiency--a case report. 794 58

Pulmonary embolism (PE) and deep vein thrombosis are common causes of illness and death. The pharmacological approach to pulmonary embolism includes the use of anticoagulants, unfractionated heparin for the acute phase, and oral anticoagulants for prophylaxis. In massive PE, the use of thrombolytic agents is suggested to reduce systemic hypotension and right ventricular failure and increase cardiac output. Thrombolytic agents act on pulmonary vascular obstruction. In clinical practice, thrombolytic therapy is recommended in case of massive embolism with haemodynamic failure. Recent studies suggest the use of thrombolytic drugs in patients with normal systemic blood pressure who show right ventricular dysfunction at echocardiographic examination. A large randomised trial on lytic agents in submassive PE is therefore needed. Anticoagulants were primarily indicated for prevention of recurrences. Due to the development of low molecular weight heparin, the role of anticoagulants needs to be re-evaluated.
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PMID:Pharmacotherapy of pulmonary embolism. 1247 69

Massive pulmonary embolism (PE) is surprisingly common and is not necessarily heralded by dramatic symptoms or signs. The death rate from PE remains high, and the most common cause of mortality is recurrent PE, not cancer. Prevention of recurrent embolism with intensive anticoagulation remains the foundation of therapy. The Food and Drug Administration has approved use of the low molecular weight heparin enoxaparin for inpatient treatment of deep venous thrombosis (DVT) with or without PE as a "bridge'' to warfarin. However, in patients with massive PE, anticoagulation alone often does not suffice to prevent death or disability from chronic pulmonary hypertension. Impending hemodynamic instability due to massive PE and its attendant ominous prognosis can be detected by rapid identification of moderate or severe right ventricular failure (usually easily with transthoracic echocardiography). Successful treatment of overt cardiogenic shock, manifested by systemic arterial hypotension and tachycardia, is far more difficult than implementing a strategy that champions early intervention after the onset of right ventricular failure. Among patients with massive PE, thrombolysis and embolectomy (often performed in the interventional angiography laboratory) are being used with increasing skill and improved outcomes. Intensive pharmacologic therapy and mechanical support devices portend a new era of improved intensive and multidisciplinary management of these gravely ill patients.
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PMID:The approach to massive pulmonary embolism. 1608 64

Pulmonary thromboendarterectomy (PTE) is a complicated surgical procedure that is an effective treatment in reducing pulmonary artery pressure and pulmonary vascular resistance for chronic thromboembolic pulmonary hypertension. Chronic thromboembolic pulmonary hypertension usually results from incomplete lysis of a large organized thrombus in the main pulmonary artery and secondary branches, leading to pulmonary hypertension, right ventricular failure, and subsequent death because of heart failure. Between March 1997 and April 2005, 30 PTE operations were performed in Fuwai Hospital, Beijing, China. They were 24 men and 6 women, with an average age of 45.7 +/- 11.4 years and average disease history of 48 +/- 12.6 months. Twelve of them were in New York Heart Association (NYHA) class 4, and 18 were in class 3. Seventeen cases were found with deep venous thrombosis (DVT), and inferior vena cava filters were implanted before surgery. The mean systolic pulmonary pressure was 91.4 +/- 22.4 mmHg, mean pressure of arterial oxygen (PaO2) was 56.2 +/- 8.6 mmHg, mean cardiac index (CI) was 1.64 +/- 0.47 L/min/m2, and mean saturation of arterial oxygen (SaO2) was 0.90 +/- 0.05. All operations were performed using the PTE procedure under deep hypothermia and intermittent circulation arrest. Perfusion management consisted of myocardial, cerebral protection, lung protection, and deep hypothermia with multiple periods of circulatory arrest and reperfusion at hypothermia, ultrafiltration, and cell-saving techniques. One patient died of infective shock post-operatively. Four cases experienced complications of the central nervous system. The mean cardiopulmonary bypass time was 191.1 +/- 34.4 minutes, the mean aortic clamping time was 95.1 +/- 27.8 minutes, and mean circulation arrest time was 47.7 +/- 12.9 minutes. Improvement of hemodynamic status occurred immediately after surgery. Mean pulmonary artery pressure decreased from 91.4 +/- 22.4 to 48.3 +/- 10.7 mmHg, and CI increased from 1.64 +/- 0.47 to 2.58 +/- 0.51 L/min/ m2. PaO2 increased from 56.2 +/- 8.6 to 88.9 +/- 6.0 mmHg and SaO2 increased from 0.90 +/- 0.05 to 0.97 +/- 0.01. Twenty-six cases were followed for 36.8 months: 22 in NYHA class 1, 3 in class 2, and 1 in class 3. PTE is an effective treatment for chronic thromboembolic pulmonary hypertension. The key to success is to adopt synthesized measures to protect the vital organ under deep hypothermic circulatory arrest (DHCA) from ischemia and reperfusion injury. Appropriate patient selection, perioperative management, improved techniques, and experience can optimize outcome.
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PMID:Perfusion techniques for pulmonary thromboendarterectomy under deep hypothermia circulatory arrest: a case series. 1731

Flight-related deep vein thrombosis (DVT) is well recognized. Reduced venous return occurs during immobility. This alteration in venous hemodynamics may contribute to DVT development. A prototype design of an in-flight exercise device to stimulate ambulatory bloodflow while seated has been developed, consisting of a foot pedal attached to a base by a hinge mechanism. Four devices of differing resistance were evaluated. Calf muscle pump function was assessed by air plethysmography in 10 healthy volunteers. Ejection volume fraction and RVF were determined in the standing position (control values) and were compared with those achieved by depression of the 4 devices while seated. Similar EVF and RVF values were achieved by the control and 2 of the devices. Plantar flexion against a predetermined resistance can effectively activate the calf muscle pump while seated and may reduce the incidence of flight-related DVT.
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PMID:The Tromped: a solution for flight-related deep vein thrombosis? 1831 25

Patients with heart failure (HF) are particularly vulnerable to the development of venous thromboembolism (VTE) and its related complications of pulmonary embolism and right ventricular failure. To improve our understanding of the clinical characteristics, prophylaxis, and initial management of patients with HF and deep vein thrombosis (DVT), we compared 685 patients with a history of HF with 3,890 patients without HF in a prospective registry of 5,451 consecutive patients with ultrasound-confirmed DVT. We excluded 876 patients for whom data regarding HF status were incomplete. Patients with HF had an increased frequency of co-morbid conditions such as neurologic disease including stroke (33% vs 26%, p = 0.0002), acute lung disease including pneumonia (31% vs 15%, p <0.0001), and acute coronary syndrome (11% vs 4%, p <0.0001) contributing to a higher medical acuity than in patients without HF. Furthermore, patients with HF were more likely to have VTE risk factors of immobilization (53% vs 42%, p <0.0001), acute infection (33% vs 27%, p = 0.01), and chronic obstructive pulmonary disease (29% vs 12%, p <0.0001). Patients with and without HF and DVT had a high frequency of recent hospitalization (48% vs 47%, p = 0.96). Fewer than 12 of patients with HF (46%) who subsequently developed DVT received any VTE prophylaxis. In conclusion, the combination of higher medical acuity, increased frequency of VTE risk factors, and low rate of VTE prophylaxis presents a "triple threat" to patients with HF.
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PMID:Heart failure in patients with deep vein thrombosis. 1835 31

Massive pulmonary embolism (PE) is a cardiovascular emergency due to a substantial obstruction of the pulmonary vascular bed, resulting in rapid right heart failure with a potentially fatal outcome.We present the case of a 50-year-old woman with massive PE and recent trans-sphenoid surgery because of pituitary adenoma. An occluding embolus, arising from deep venous thrombosis of the lower limbs, was demonstrated in the right pulmonary artery with selective angiography and treated with selective loco-regional infusion of low-dose tenecteplase. To the best of our knowledge, this is the first case of selective administration of low-dose tenecteplase in the pulmonary artery with successful resolution of PE without the need for adjunctive interventional procedures.
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PMID:[Massive pulmonary embolism treated with selective infusion of tenecteplase]. 2189 24


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