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

A case of double right and left intraventricular thrombosis diagnosed by 2D echocardiography is reported in a 20 year old man with nephrotic syndrome with eosinophilia and hypercoagulability, admitted as an emergency for a staphylococcal septicaemia in shock and anuria. Anticoagulation with heparin did not prevent two episodes of pulmonary embolism. Complete dissolution of the thrombi was obtained by peripheral administration of fibrinolytic therapy (urokinase and plasminogen). The authors discuss the differential diagnosis of echocardiographic appearances of biventricular masses and possible causes of these thrombi are suggested.
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PMID:[Biventricular thrombosis in nephrotic syndrome with hypercoagulability and hypereosinophilia]. 392 Sep 99

The case of a young man hospitalised for bilateral lower limb deep vein thrombosis is reported. None of the usual causes were found after systematic wide-ranging investigation. The only abnormality on admission was a spontaneous increase in the cephalin-kaolin time to 65 seconds compared to a control time of 40 seconds. Measurements of the clotting factors showed a moderate and isolated deficiency in factor XII (30 p. 100), also present in a brother (50 p. 100) and a sister (42.5 p. 100). Fibrinolytic therapy was administered : an initial course of Streptokinase was followed by extension of a left femoral vein thrombosis and pulmonary embolism. Two courses of Urokinase were given with an eight day interval without significantly improving the venous circulation. This case is an example of thrombogenic disease due to a deficiency of a clotting factor resulting in non-activation of physiological fibrinolysis.
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PMID:[Thrombophlebitis and pulmonary embolism in congenital factor XII deficiency]. 392 76

This study assessed the long-term effects of thrombolytic treatment in patients with acute massive pulmonary embolism (PE). Seven patients with PE that followed deep-vein thrombosis underwent pulmonary angiography and pressure measurements before and 6 +/- 3 days (mean +/- SD) and 15 +/- 4 months after treatment with intrapulmonary infusions of urokinase (average dose 1724 U/kg X hr) and heparin (average dose 17 U/kg X hr). Treatment was guided by daily measurements of pulmonary arterial (PA) pressure and was continued until PA pressure had normalized (average of 6 days). Late after treatment patients returned for pulmonary angiographic examination, right heart catheterization at rest and during bicycle exercise, and phlebography of the deep veins of both legs. Pulmonary angiograms showed massive obstruction before therapy (Walsh index 15 +/- 2 points of a maximum of 18 points), which was improved 6 days (3 +/- 3 points) and 15 months (1 +/- 2 points) after therapy. Mean PA pressure declined from 37 +/- 9 to 13 +/- 3 mm Hg after 6 days and to 15 +/- 3 mm Hg after 15 months. No recurrence of PE was observed. In six of seven patients at rest and during bicycle exercise (up to 100 W) in the supine position mean PA pressure and total pulmonary resistance remained within normal limits. Over the short term all patients showed clinical signs of deep-vein thrombosis; 15 months later four patients had normal deep veins, but three patients had still phlebographic signs of old thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sustained improvement of pulmonary hemodynamics in patients at rest and during exercise after thrombolytic treatment of massive pulmonary embolism. 396 12

To evaluate the role of selective intra-arterial low-dose thrombolytic therapy (SILDT) as an alternative to the surgical management of acute arterial occlusion, the hospital records of 40 patients who underwent 43 SILDT treatments with either streptokinase (36) or urokinase (7) between December 1979 and March 1984 were reviewed. Twenty-eight patients underwent 30 treatments (group 1) for native arterial occlusion and 12 patients underwent 13 treatments (group 2) for prosthetic or autogenous graft occlusions. Therapy was deemed successful if subsequent surgical therapy was obviated. In group 1, SILDT was successful in 13 of 28 (45%) patients with 12 of 25 lower extremity occlusions and one of three upper extremity occlusions. Successful lysis in the native artery occlusion group fell into three categories: five patients were successfully treated for arterial thrombosis complicating percutaneous transluminal angioplasty (PTA); four patients required PTA after complete lysis revealed an underlying arterial stenosis; and only three required no further therapy after SILDT. SILDT failed in all three patients with the aortoiliac occlusions. Eleven patients with femoral artery occlusions and unsuccessful SILDT required six bypass procedures, three amputations, one embolectomy, and one PTA. In group 2 only 3 of 14 treatments (21%) were successful. Bypass revision was not possible in 11 patients and all required amputation. Systemic fibrinolysis was seen in 20 (59%) of 34 patients with available data. Neither fibrinogen levels nor fibrin degradation products predicted the occurrence of complications. Minor complications occurred in 18 of 43 (43%) treatments; small hematomas at the catheter entry site were most common. Minor complications occurred in 20 of 43 treatments (44%) and included severe local hemorrhage (four), distant bleeding (three), pulmonary embolism (four), myocardial infarction (three), unmasking of an aortoduodenal fistula (one), and clot migration requiring emergency thrombectomy (four). SILDT is most effective in acute arterial thrombosis complicating arteriography or percutaneous angioplasty. It may play a role in the patient in whom thrombolysis can reveal an underlying stenosis amenable to percutaneous angioplasty. This experience shows SILDT to be of limited value in the management of prosthetic autogenous graft occlusions. Finally, thrombolytic therapy is associated with significant morbidity and mortality rates and requires cautious monitoring to detect arterial thrombus migration, worsening tissue ischemia, venous thromboembolism, intracerebral hemorrhage, and local or systemic bleeding.
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PMID:Thrombolytic therapy for acute arterial occlusion. 396 60

Intrapulmonary arterial infusions of urokinase (mean 1724 IU/kg X h) and heparin (mean 17 IU/kg X h) were given to 7 patients with acute massive pulmonary embolism. Pulmonary angiography and pulmonary artery pressure measurements were performed before, during and 15 months after the drug infusion. During the acute phase, pulmonary artery pressures were recorded daily while urokinase and heparin were administered until the pressures had become normal (after a mean of 6 days). 15 months later right heart catheterization was undertaken before and after ergometric exercise as well as bilateral leg venography. Before treatment pulmonary angiography demonstrated massive vascular obstruction which regressed markedly during and after drug infusion. Treatment also led to normalization of previously elevated pulmonary artery pressures. In addition, pulmonary artery mean pressures and total pulmonary vascular resistance became normal both at rest and on exercise in 6 patients. All patients had signs of acute leg vein thrombosis before treatment, but 15 months later phlebography demonstrated normal findings in 4 and residual findings of previous thrombosis in 3. Local thrombolysis of acute massive pulmonary embolism is thus a highly successful form of treatment.
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PMID:[Long-term results after local thrombolysis in acute massive pulmonary embolism]. 397 80

This report concerns 34 cases of heparin-associated thrombocytopenia in which standard heparin has been systematically replaced by LMW heparin CY 216 Choay. There were 21 women and 13 men, mean age, 69 years. Twenty-six of the 34 cases had thrombotic complications. All of the patients were treated by standard heparin of porcine mucosal origin, in most cases for prevention of deep vein thrombosis and pulmonary embolism. Twenty-six cases occurred along with orthopedic and traumatologic surgery (especially for total hip replacement, 15 cases). Four cases involved vascular surgery and three involved medical thrombotic disease. Standard heparin treatment was always replaced by LMW heparin CY 216. Initial doses were 0.30 ml three times daily, later increased to obtain global hypocoagulability. Surgical procedures (embolectomy and vena cava filter) were carried out when necessary. Five patients had thrombolytic treatment (urokinase) in conjunction with LMW heparin. The overall results were 31 recoveries, but with seven severe sequelae (three amputations and four hemiplegias) most often attributable to the first ischemic attack, and three deaths. For the last 16 patients, indirect platelet aggregation tests were performed (control platelet-rich plasma plus patient platelet-poor plasma plus LMW heparin): nine cases had negative tests, with nine recoveries and seven cases had positive tests, with five recoveries and two deaths.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of heparin-associated thrombocytopenia and thrombosis with low molecular weight heparin (CY 216). 404 56

Eight patients with massive pulmonary thromboembolism documented by angiography were treated with Urokinase (UK) 4.400 IU/Kg/hr for 12 hours. UK i.v. infusion was started immediately after angiographic evaluation (Miller index) and was followed by anticoagulant therapy with heparin and sodium warfarin. All patients survived even though 4 pts. were in shock before treatment. Significant reduction of pulmonary obstruction (reduction of Miller index) was obtained in 7 patients with 48 hours from withdrawal of the drug. Mild superficial bleedings which did not influence the clinical course were the only complication recorded. Neither bleedings nor angiographic improvement showed a correlation with thrombin time prolongation. Indications for thrombolytic therapy of pulmonary embolism and particularly prevention of the major haemorrhagic complications are briefly discussed. It is concluded that the high doses of UK suggested by Food and Drug Administration may be used safely in patients affected by massive pulmonary thromboembolism with or without shock, if patients are adequately selected and prevention of major haemorrhagic complications is continued throughout treatment.
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PMID:[Thrombolytic therapy with urokinase in 8 patients with massive pulmonary thromboembolism]. 409 13

A comparison of the effects of two regimens of urokinase infusion not associated to heparin and of continuous heparin infusion was made assessing the rate of emboli and arterial hypoxemia resolution in patients with acute pulmonary embolism. Twenty-nine patients with acute pulmonary embolism, each one diagnosed by means of perfusion lung scan and selective pulmonary arteriography, were admitted to the study and randomly allocated to three treatment groups: A, 10 patients, urokinase: 800,000 CTA units/day for three days followed by oral anticoagulants; B, 9 patients, heparin: mean daily dose 30,000 units for seven days followed by oral anticoagulants; C, 10 patients, urokinase: 3,300,000 CTA units in 12 hours followed by oral anticoagulants. Pulmonary lung scan and PaO2st (PaO2 standardized to PaCO2 of 40 mmHg) were repeated at 1, 3, 7, and 30 days in all the groups of treatment. The mean daily rate of improvement, assessed from both the perfused lung segments and the PaO2st increment, in group C was highest in the first 24 hours and lowest from the first to the third day of treatment. However, from the third to the seventh day of treatment and onwards the mean daily rate of improvement was roughly the same in all the groups. After one month, lung perfusion and the PaO2st had considerably improved, but had not attained full recovery in any of the treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A controlled clinical trial on the effect of heparin infusion and two regimens of urokinase in acute pulmonary embolism. 639 81

The results of a multicentre trial (10 centres) of urokinase (UK) extracted from human urine in patients with recent massive pulmonary embolism (PE) are reported. The aim of this trial was to compare the efficacy of two protocols of UK therapy: low dose UK: 2 000 IU/kg/hour (UKl) associated with heparin, against high dose UK: 4 400 IU/kg/hour for 12 hours (UKh) followed by heparin. This randomised single blind trial included patients under 80 years of age. The clinical diagnosis of recent PE (less than 5 days) was confirmed by pulmonary angiography showing over 30% vascular obstruction (Miller index greater than 11). The efficacy of treatment was assessed by the degree of early revascularisation on pulmonary angiography 30 to 48 hours after the start of thrombolytic therapy, as analysed by 4 independent vascular radiologists. A total of 133 patients entered the trial between November 1978 and October 1981: 2 died before receiving treatment, 2 were excluded, 129 patients were retained (67 UKl and 62 UKh). The initial clinical, haemodynamic and angiographic parameters were comparable in the two groups: Miller index; 22.6 +/- 3.7 (UKl) and 22.6 +/- 3.4 (UKh), an average vascularisation defect of 66%. The efficacy of treatment was the same: 26% and 20% respectively. The incidence of haemorrhagic complications was the same in both groups: 24% and 29% respectively, but only 2% of patients had spontaneous severe bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Multicenter study of 2 urokinase protocols in severe pulmonary embolism. Research Group on Urokinase and Pulmonary Embolism]. 643 40

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


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