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

Electrocardiograms of 90 patients with arteriographically documented acute submassive or massive pulmonary embolism and no associated cardiac or pulmonary disease were studied. Patients were derived from the Urokinase-Pulmonary Embolism Trial National Cooperative Study. In massive embolism, the electrocardiogram was normal in 6 per cent (3 of 50) of patients. With submassive embolism, 23 per cent of patients (9 of 40) had a normal electrocardiogram. Since one or more of the traditional manifestations of acute cor pulmonale (S1Q3T3, right bundle branch block, P pulmonale, or right axis deviation) occurred in only 26 per cent of patients, one could not rely exclusively upon these electrocardiographic abnormalities for the diagnosis of pulmonary embolism. The most common electrocardiographic abnormalities were nonspecific T wave changes which occurred in 42 per cent of patients and nonspecific abnormalities (elevation or depression) of the RST segment which occurred in 41 per cent of patients. Left axis deviation occurring in 7 per cent of the patients was as frequent as right axis deviation. Low voltage QRS complexes, previously undescribed in pulmonary embolism, occurred in 6 per cent of patients. None of the patients had atrial flutter or atrial fibrillation, which appears to occur more typically in patients with pulmonary embolism who have preexistent cardiac disease. All of the varieties of electrocardiographic abnormalities disappeared in some of the patients by 2 wk. Inversion of the T wave was the most persistent abnormality. Larger defects on the lung scan or pulmonary arteriogram occurred in patients with various abnormalities on the electrocardiogram than in patients with normal electrocardiograms. The pulmonary arterial mean pressure and/or right ventricular end-diastolic pressure was significantly higher in patients with several varieties of abnormal electrocardiograms, although the partial pressure of oxygen in arterial blood, in general, did not differ from that in patients with normal electrocardiograms. These hemodynamic correlations, made for the first time in patients, suggest that acute ventricular dilatation, possibly in combination with hypoxemia, is a causative factor of the electrocardiographic changes in acute massive or submassive pulmonary embolism.
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PMID:The electrocardiogram in acute pulmonary embolism. 12 74

Fibrinolytic therapy was carried out in 59 patients suffering from a total of 60 deep venous thromboses of the iliac segment (n = 24), the femoropopliteal segment (n = 18), the deep calf veins (n = 2), or the subclavian vein (n = 16). 46 patients received streptokinase (SK), 4 were given urokinase (UK), and 10 were treated with streptokinase followed by urokinase (SK + UK). The duration of fibrinolytic therapy was between 19 and 596 hours (x = 166 +/- 111 hrs). Phlebographic examination was used to determine the location of the thrombotic occlusion as well as to evaluate therapeutic results. To assure sufficient anticoagulatory protection during therapy with streptokinase the dose of streptokinase was either reduced by steps of 20,000 U/hr to a minimum of 40,000 U/hr or heparin was added as a continuous infusion. Urokinase was administered with a mean loading dose of 75,000 IU followed by an average maintenance dose of 40,000 IU/hr; it was always given in combination with heparin. When therapeutic success was graded as complete/partial/no recanalisation, the following results were obtained: thrombotic occlusion up to 1 week old 35%/48%/17%; up to 2 weeks old 57%/14%/29%; 3 or 4 weeks old 12%/38%/50%; older than 4 weeks 13%/37%/50%. The two most common side effects were a fall of the hemoglobin and a rise of body temperature. Treatment with SK had to be interrupted for bleeding in two cases. One patient diet after rupture of the liver and of the spleen following development of subcapsular hematoma in these organs, 3 patients survived pulmonary embolism without major long-term impairment. Considering medical and social aspects (preservation of capability for working in young adults) it appears justified to administer fibrinolytic agents up to a thrombus age of 14 days, in some cases even up to a thrombus age of 28 days. Good results in cases of deep vein thrombosis of the lower limbs are often obtained only when fibrinolytic therapy is extended beyond 96 hours. It should be performed in intensive care units only. Follow-up examinations of the venous drainage capacity up to 2 years after fibrinolytic therapy document the good therapeutic effect that is warrented by streptokinase or urokinase induced complete recanalisation.
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PMID:[Fibrinolytic therapy in deep venous thrombosis of the upper and lower extremity]. 84 72

The controlled clinical trials of thrombolytic agents in the United States have been carried out in two phases, under the auspices of the National Heart and Lung Institute. Phase I was devoted to the comparison of 12-hour Urokinase (12h-UK) followed by heparin (H) with heparin alone in patients with acute pulmonary embolism (Walsh et al. 1969). The results showed that pateints treated with UK had more rapid and gretaer resolution of pulmonary thromboemboli in the first twenty-four hours of therapy than patients treated with H alone, as assessed by serial pulmonary angiography, hemodynamics and lung scanning (The Urokinase Pulmonary Embolism Trial, 1970, 1973; Hyers et al. 1970). Because of the ralatively small size of the Trial and the low mor tality of treated pulmonary embolism, mortality differences were not sought-nor was one found. Although there was early difference in amount of clot resolution, patients treated with H alone showed similar improvement by two weeks. The phase II Urokinase-Streptokinase Pulmonary Embolism Trial (USPET) was begun to assess the comparative results of UK and Streptokinase (SK) therapy. Because of favorable results obtained with SK in other countries, it was deemed necessary to make this comparison (Browse and James, 1964; Hirsh et al. 1968; Miller et al. 1969, 1971; Chesterman et al. 1969). A third group, 12-hour UK, was added to relate this study (24-hour UK and SK) with the Phase I results which employed only a 12-hour infusion of UK. This Phase II Trial represents the first controlled, randomized study of UK and SK in thromboembolic disorders.
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PMID:The phase II urokinase-streptokinase pulmonary embolism trial: a national cooperative study. 109 16

The use of thrombolytic agents in the treatment of postoperative pulmonary embolism presents a dilemma to the surgeon. On one hand, postoperative pulmonary embolism usually occurs within 2 weeks of surgery. On the other hand, recent surgery is considered a contraindication for the use of thrombolytics. We developed a protocol for treating pulmonary embolism patients who have recently undergone surgery. Urokinase, at a dose of 2,200 U/kg wt, is injected directly into the clot via a catheter positioned in the pulmonary artery. This is followed by continuous infusions of urokinase at 2,200 U/kg wt/hr until the clot is lysed (up to 24 hrs). Simultaneously, heparin is administered peripherally at 500 U/hr. The level of serum fibrinogen is monitored every 6 hours and maintained at no less than 0.2 g/dL to prevent bleeding. Thirteen patients were treated for angiographically proven pulmonary embolism within 14 days of surgery. Complete lysis of every embolus was achieved, and no deaths or bleeding complications occurred. Two patients received inferior vena cava filters, and nine patients no longer needed chronic anticoagulants within 3 months after the embolic event.
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PMID:Thrombolytic therapy for postoperative pulmonary embolism. 155 78

Thrombolysis of acute pulmonary embolism can be accomplished more rapidly and safely with 100 mg of recombinant human tissue-type plasminogen activator (rt-PA) (Activase) than with a conventional dose of urokinase (Abbokinase) given as a 4,400-U/kg bolus dose, followed by 4,400 U/kg per h for 24 h. To determine the effects of a more concentrated urokinase dose administered over a shorter time course, this trial enrolled 90 patients with baseline perfusion lung scans and angiographically documented pulmonary embolism. They were randomized to receive either 100 mg/2 h of rt-PA or a novel dosing regimen of urokinase: 3 million U/2 h with the initial 1 million U given as a bolus injection over 10 min. Both drugs were delivered through a peripheral vein. To assess efficacy after initiation of therapy, repeat pulmonary angiograms at 2 h were performed in 87 patients and then graded in a blinded manner by a panel of six investigators. Of the 42 patients allocated to rt-PA therapy, 79% showed angiographic improvement at 2 h, compared with 67% of the 45 patients randomized to urokinase therapy (95% confidence interval for the difference in these proportions [rt-PA minus urokinase] is -6.6% to 30.4%; p = 0.11). The mean change in perfusion lung scans between baseline and 24 h was similar for both treatments. Three patients (two treated with rt-PA and one with urokinase) had an intracranial hemorrhage, which was fatal in one. The results indicate that a 2-h regimen of rt-PA and a new dosing regimen of urokinase exhibit similar efficacy and safety for treatment of acute pulmonary embolism.
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PMID:Recombinant tissue-type plasminogen activator versus a novel dosing regimen of urokinase in acute pulmonary embolism: a randomized controlled multicenter trial. 160 32

The authors report the case of a patient treated by subcutaneous injection of calcium heparin after deep vein thrombosis with floating thrombus and pulmonary embolism. She was readmitted to hospital after 16 days' treatment because of a massive aorto-iliac thrombosis due to heparin-induced thrombocytopenia (platelet count = 29.000). This thrombosis was treated by local injection of Urokinase (total dose = 7.425.000 U) over 93 hours without any major complications. The aorto-iliac circulation was completely restored to normal after treatment. Thrombotic complications secondary to immuno-allergic heparin-induced thrombocytopenia are relatively common because of the widespread use of heparin. From the therapeutic point of view, it is imperative to stop the heparin, which makes surgery very difficult, and the platelet-fibrin composition of these thrombi suggests that local thrombolysis with Urokinase is the treatment of choice in this syndrome.
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PMID:[Treatment of massive arterial thrombosis caused by thrombocytopenia induced by heparin with local thrombolysis]. 210 99

A 19-year-old girl had for four weeks the clinical signs of recurrent pulmonary emboli and deep-vein thrombosis (tachycardia, dyspnoea, right inguinal pain), which had been misdiagnosed. The correct diagnosis was made only after drastic deterioration in her condition following appendicectomy for falsely diagnosed appendicitis. Urokinase infusion (80,000-160,000 IU/h for 11 days) having failed to bring about improvement, much greater than ultra-high much less than thrombolysis with streptokinase was begun (250,000 IU streptokinase over 30 min, followed by 9 million IU over 6 hours). Fatal pulmonary embolism occurred seven hours after the end of the infusion. Autopsy revealed extensive separation of thrombotic material in the pelvic veins. This observation and other reports should serve as a warning against using streptokinase in ultra-high doses if large veins, as those in the pelvis, are involved.
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PMID:[Fatal pulmonary embolism in venous thrombosis of the leg and pelvis during lysis therapy]. 237 66

The importance of the fibrinolytic treatment in deep venous thrombosis, to avoid the mortal pulmonary embolism, among other complications, is commented on. The results in 32 patients, presenting deep venous thrombosis and treated with loco-regional Urokinase, are presented. Author carries out some commentaries about surgical and medical treatment.
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PMID:[Loco-regional fibrinolysis with urokinase in the treatment of deep venous thromboses]. 261 Apr 1

Post-operative thrombo-embolic disease remains a frequent occurrence in spite of advances in their prophylaxis. Evaluation of 60 case-reports of this disease which often includes peripheral manifestations and always pulmonary manifestations, enables to specify the role of the procedure itself (mostly orthopaedic surgery 60%), pelvic surgery 20%, the chronology of events (possibility of early embolism between D1 and D3 and usual occurrence of manifestations between D8 and D18, and the importance of the background, whether investigated or not: deficiencies in anti-thrombin III, protein C and S: 4 cases. The diagnosis is based on clinical signs (non-specific) and the laboratory tests, especially scintigraphy (screening) and angiography, absolutely necessary for the diagnosis and evaluation of the amputation coefficient (Miller index). With a diagnosis of pulmonary embolism, it is always necessary to look for a proximal venous thrombosis. The treatment, calls for heparin (quite seldom), thrombolytics (Urokinase, Plasminogen in our experience), the indication of which must take into consideration the delays and the nature of the previous procedure, and finally surgery (massive forms where thrombolytics are contraindicated). The thrombo-embolic manifestations with thrombogenic thrombopenia secondary to heparin are quite frequent, in a surgical environment (10 cases) and difficult to treat.
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PMID:[Postoperative pulmonary embolism]. 266 1

A new abnormal plasminogen, Frankfurt I, has been identified in the plasma of a 42 year-old male patients who had recurring thromboses, thrombophlebitis and pulmonary embolism since his age of 29. Reduced functional and also slightly reduced antigen plasminogen concentrations were found in both the proposituts and his mother. Plasmin generation rates carried out by Streptokinase and Urokinase were also abnormal. The plasmin generated was very unstable in the absence of stabilizing ligands and/or substrates. Crossed immunoelectrophoresis of the purified Frankfurt I revealed a peak with normal size and shape, but displaced with respect to normal Glu-plasminogen toward the anode. Isoelectric focusing followed by zymography on an agarose-fibrin plate proved this observation but did not indicate a separation of the normal from the abnormal plasminogen molecular species, also, fewer bands were found in the abnormal plasminogen isozyme pattern. Kinetic studies of Frankfurt I Glu-plasminogen and plasmin showed that most of the functional abnormality is related to absence of active sites in half of the molecules.
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PMID:Congenital abnormal plasminogen, Frankfurt I, a cause for recurrent venous thrombosis. 296 86


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