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

During and following significant surgical intervention, deep venous thrombosis prophylaxis by application of anticoagulants is routinely used. However, patients with malignant disorders are subject to an especially high risk of deep venous thrombosis progressing in severe cases to subsequent pulmonary embolism. The present study focuses on appraising modern markers of deep vein thrombosis in 34 patients undergoing major maxillofacial surgery, with some malignant disorders. No significant differences between the two patient groups were noted using the markers of the kallikrein-kinin-system. From the first postoperative day plasma levels of the coagulation indicator thrombin-antithrombin-III complexes were significantly higher in the group of tumour patients. Markers of fibrinolysis indicated corresponding results: on the first postoperative day tissue-plasminogen activator values rose to 18.9 +/- 3.2 micrograms/l in the group of malignant patients, but only to 7.4 +/- 1.1 micrograms/l (P < 0.05) in the control group. Also postoperative D-dimer concentrations in the malignancy group were significantly above those of the control group. In the present study it could be demonstrated that patients with malignant neoplasia undergoing major maxillofacial surgery are exposed postoperatively to a particularly high risk of developing thromboembolic complications. All in all, the status of anti-thrombotic therapy requires reappraisal with respect to the current treatment approach adopted in tumour patients.
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PMID:Evaluation of markers of deep vein thrombosis in patients undergoing surgery for maxillofacial malignancies. 1062 61

To increase thrombolytic specificity of urokinase (uPA), we engineered a recombinant chimeric plasminogen activator SZ51Hu-scuPA, which consists of a humanized monoclonal antibody (SZ-51Hu) specifically against P-selectin on activated human platelet and a single-chain urokinase (scuPA). The cDNA, encoding scuPA amino acids 1-411, was inserted in 5' end to 3' end orientation immediately after the CH3 of SZ-51Hu heavy-chain sequence in the expression vector alphaLys30. The resulting construct alphaLys30-SZ51VH/Hu-scuPA was used to transfect into SP2/0 murine myeloma cell line, which was pretransfected with SZ51Hu light chain. The fusion protein SZ51Hu-scuPA was expressed at 5 mg/L in the supernatant of cell culture. The fusion protein purified by affinity chromatography had a molecular weight of 160 kDa with fibrinolytic activity of 39,000 IU/mg and its affinity to activated human platelet was 67% of the parent murine mAb SZ-51. The thrombolytic property of the fusion protein was first characterized in an in vitro system, which consists of a 125I-fibrin-labeled human plasma clot containing different concentrations of human platelets suspended in citrated human plasma. Fifty percent lysis was reached with SZ51Hu-scuPA in 1 hour at a concentration of 20 IU/mL or in 2 hours at a concentration of 10 IU/ mL, which was much faster than uPA at the same concentration. The maximal lysis of the clots by SZ51Hu-scuPA was 4.1 to 8.4 times more potent than that by uPA. The fusion protein was further characterized in the hamster pulmonary embolism model with clots prepared from fresh platelet-rich human plasma containing 125I-labeled fibrinogen. The thrombolytic activity of SZ51-scuPA was 3.9 times more potent than that of uPA at 2,000 IU/kg in this model. Almost no significant fibrinogen breakdown was observed either in vitro and in vivo.
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PMID:A recombinant antibody-targeted plasminogen activator with high affinity for activated platelets increases thrombolytic potency in vitro and in vivo. 1068 Jun 44

This review analyses literature reports from 1970 to 1998 assessing the use of streptokinase (SK), urokinase (UK) or recombinant tissue-type plasminogen activator (rt-PA) for thrombolytic therapy in neonates and infants. From 1970 to 1998 182 infants were reported to have received SK (n = 54; 29.5%), UK (n = 41; 22.5%) or rt-PA (n = 87; 48%). During thrombolytic therapy no concomitant heparin administration or low dose heparin therapy (5 U/kg/h) were recorded. To perform reocclusion prophylactics heparin was reinitiated at the end of thrombolytic therapy usually in the recommended dosage of 20 U/ kg/h. The overall thrombolytic patency rate in neonates varied from 39% to 86%. Besides bleeding from local puncture sites or recent catheterisation sites (10.4%), pulmonary embolism was reported in 1.1% of the 182 infants. Major bleeding complications, i.e. pulmonary bleeding (0.6%), gastrointestinal bleeding (0.6%) or intraventricular haemorrhage (IVH 2.7%) are rarely reported side effects and only 2 thrombolysis related deaths due to haemorrhage were mentioned. Bleedings reported in the central nervous system (n = 4) mainly occurred in preterm infants (n = 3). In conclusion, data of this preliminary analysis suggest that there is no big difference (p = 0.09; chi2-test) in the efficacy rate between the 3 thrombolytic agents used in the first year of life. In each case an assessment must be made with respect to the relative benefit conferred by thrombolytic therapy in preventing organ or limb damage versus the potential side effects, costs and inconvenience for the childhood patient. Controlled prospective multicentre studies on thrombolytic therapy in neonates and infants are recommended to evaluate patency rates and adverse effects for the different thrombolytic agents used.
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PMID:Thrombolysis in newborns and infants. 1069 99

The diagnosis of major pulmonary embolism should be considered in case of acute respiratory distress, particularly when there is high thromboembolic risk. Although clinical symptoms are not specific, some are suggestive: syncope or dizziness with cyanosis and polypnoea, and especially arterial hypotension and cardiogenic shock. Diagnostic workup should be rapid and straight forward. Transthoracic echography is particularly useful to detect right heart thrombi and right ventricular overload. More information could be provided by helical computed tomography or perfusion lung scan or less commonly now by pulmonary angiography, depending on the patient's clinical condition and the available equipment. The mortality rate can reach 20 to 30%, and up to 65% after resuscitated cardiac arrest. Rapid desobstruction is justified through surgical embolectomy or intravenous thrombolysis favouring short duration protocols (alteplase over 2 h), in spite of the bleeding risk.
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PMID:[Major pulmonary embolism]. 1073 26

Paradoxical embolism through a patent foramen ovale (PFO) can involve multiple organs simultaneously. The most commonly involved sites are the cerebrum and the extremities. Paradoxical embolism to coronary arteries or upper extremities is relatively uncommon. We report a case of acute pulmonary embolism and paradoxical embolism through a patent foramen ovale involving the left upper extremity, brain, and coronary artery. Early diagnosis in the emergency department was made by a trans-esophageal echocardiogram, and the patient was successfully treated with intravenous t-PA and heparin. Patients with acute pulmonary embolism or deep venous thrombosis who also develop signs of systemic embolism should be evaluated for a patent foramen ovale.
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PMID:Paradoxical embolism-report of a case involving four organ systems. 1180 70

A 33 year old male with no known risk factors for hypercoagulability developed a massive thrombi in the inferior vena cava (IVC). The patient had a history of both pulmonary embolism and embolism related syncope. The thrombus which extended proximally to the level of the renal vein and distally to the left superficial femoral vein did not respond to anticoagulant therapy or thrombolysis. Thirteen days after admission, we decided to use a temporary caval filter to provide protection from migration of the thrombus while attempting invasive thrombolytic therapy, which was performed using a tissue type plasminogen activator through a coaxial catheter of the temporary filter. This resulted in a marked decrease in the size of the thrombus, and multiple thrombi were found to be trapped in the temporary filter. Although the temporary caval filter was effective in capturing emboli, resulting in a decrease in the thrombus size, the thrombus was not completely dissolved within two weeks, which is the maximal implantation time. A permanent filter was eventually used to prevent pulmonary embolism, which could arise from the remaining thrombus. We have found placement of a temporary caval filter to be a safe and effective adjunct, in select cases, when attempting thrombolysis of massive thrombi in the IVC. Since we inserted the temporary filter 13 days after admission, use of a temporary filter during thrombolysis may have been more effective if conducted earlier in our patient's clinical course.
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PMID:Use of a temporary caval filter in a young man with pulmonary embolism to prevent migration of massive caval thrombus during an attempt of caval thrombolysis. 1087 Jun 77

Successfully utilized contemporary pulmonary embolism thrombolysis reverses right heart failure rapidly and safely. This therapeutic approach may lower mortality from pulmonary embolism and reduce morbidity from chronic pulmonary hypertension. Unlike myocardial infarction thrombolysis, a 2-week 'time window' is available, during which treatment can be initiated. A high concentration of the thrombolytic agent is administered in a brief infusion lasting several hours. No special laboratory testing is needed. Currently, the only contemporary thrombolytic regimen for pulmonary embolism that is approved by the Food and Drug Administration is tissue plasminogen activator, in a dose of 100 mg/2 h. New thrombolytic agents under development for pulmonary embolism include reteplase, saruplase, and recombinant staphylokinase. Future clinical trials will require multicenter collaboration and will focus on relevant endpoints such as the reduction of mortality and recurrent venous thromboembolism.
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PMID:A contemporary approach to thrombolytic therapy for pulmonary embolism. 1094 88

Consensus regarding the use of thrombolysis to treat acute pulmonary embolism has not yet been reached. There is good evidence that thrombolytic agents dissolve clot more rapidly than heparin. However, proving that this benefit reduces the death rate from pulmonary embolism has been difficult. Each of the 3 thrombolytic agents (tissue type-plasminogen activator, streptokinase and urokinase) is equally efficacious at dissolving clot, but all are associated with an increased risk of major hemorrhage when compared with heparin. One evolving position is that, in addition to patients presenting in circulatory collapse, for whom thrombolysis has been demonstrated to be life-saving, a subgroup of patients may be identified by echocardiography, through its ability to assess right ventricular dysfunction, who should also be considered for thrombolytic therapy. It remains to be seen whether this approach can reduce the death rate associated with pulmonary embolism.
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PMID:Thrombolytic therapy for pulmonary embolism. 1112 28

The fibrinolytic system plays an important role in the physiological maintenance of blood flow and the dissolution of thrombi. Administration of fibrinolytic agents in indications such as myocardial infarction, pulmonary embolism, deep vein thrombosis or stroke, therefore, offers a rational means to dissolve pathological thrombi and restore vascular patency. The functional domains of the physiological tissue plasminogen activator (t-PA) provide fibrin specificity and serine protease activity for plasminogen cleavage and binding to liver receptors which gives the molecule a short half-life. In order to combat acute thromboembolic events such as myocardial infarction, the structure of the natural t-PA molecule was genetically modified to prolong its half-life, to increase its fibrin-specificity and to improve its resistance to plasminogen activator inhibitor. These features of TNK-t-PA allow bolus administration in emergency situations, early reperfusion of the blood vessel and a low rate of bleeding complications, thus improving the overall benefit to patients.
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PMID:Improving natural principles with genetic engineering: TNK-tissue plasminogen activator. 1145 85

Successfully utilized contemporary pulmonary embolism thrombolysis reverses right heart failure rapidly and safely. This therapeutic approach may lower mortality from pulmonary embolism and reduce morbidity from chronic pulmonary hypertension. Pulmonary embolism thrombolysis remains a debatable indication because large clinical trials using survival as an endpoint have not been carried out. Instead, thrombolysis trials have been undertaken with surrogate endpoints such as reduction in clot burden, reduction in pulmonary arterial pressure, and improvement in right ventricular function. In an era where hundreds of thousands of myocardial infarction patients have participated in thrombolysis trials that focus on survival as the principal endpoint, the much smaller trials of PE thrombolysis have not been sufficiently definitive to achieve a consensus. Pharmaceutical companies have not considered this area of investigation to be a good return on investment, because PE is a much less common problem than acute coronary syndromes. No government funding agency has targeted PE thrombolysis as a priority for clinical research. Currently, the only contemporary thrombolytic regimen for pulmonary embolism that is approved by the Food and Drug Administration is tissue plasminogen activator, in a dose of 100 mg/2 h. New thrombolytic agents under development for pulmonary embolism include reteplase, saruplase, and recombinant staphylokinase. Future clinical trials will require multicenter collaboration and focus on clinically relevant endpoints such as reduction of mortality and recurrent venous thromboembolism.
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PMID:Thrombolysis in pulmonary embolism: a debatable indication. 1148 35


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