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

Acute massive pulmonary embolism (AMPE) is an event that places the recipient at an unusually high risk of sudden death. Among 183 patients with thromboembolic disease, AMPE has been diagnosed clinically in 58 cases (32%). Diagnostic criteria: cardiac arrest (24 cases--41%), shock (12--21%) acute cor pulmonale (ACP 15--26%) and ACP with shock (7 cases--12%). There were 33 women and 25 men aged 22-88 years in this group. In 25 patients heparin (H), in 7 streptokinase (S), in 1 tPA, in 7 S after H have been used, 26 patients (45%) survived, 32 (55%) died: there were 20 sudden deaths. Advanced underlying cardiopulmonary diseases or/and recurrent pulmonary embolism seem to be the most important predictors of fatal outcome of AMPE.
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PMID:[Outcome of patients with clinically acute massive pulmonary embolism]. 806 37

Pulmonary embolism after lung resection (PEALR) has a high mortality rate, and it is one of the most severe complications after lung resection. Early diagnosis and treatment are essential for PEALR. Here we present 3 cases of severe PEALR. In these cases, transthoracic Doppler echocardiography was useful for confirming the diagnosis of PEALR. Thrombolysis with recombinant tissue plasminogen activator (r-tPA) was used to treat the embolism, and these patients were subsequently discharged. Thus echocardiography may become a primary procedure to confirm the diagnosis of severe PEALR, and thrombolysis with second-generation r-tPA may be the preferred choice for treatment.
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PMID:Pulmonary embolism after lung resection: diagnosis and treatment. 1290 12

A 24-year-old man known to have a double outlet right ventricle, status post-modified Fontan procedure at age 10, taking coumadin after having a stroke one year prior, presented with a massive pulmonary embolism and hemodynamic instability. Locally delivered tPA was unsuccessful, and the pulmonary artery thrombus was finally removed with a thrombectomy catheter (Angiojet thrombectomy); the patient recovered soon thereafter. This is the first report of the successful use of a thrombectomy catheter in a patient with pulmonary emboli and an occluded Fontan conduit.
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PMID:A pulmonary embolism treated with the Angiojet technique in a patient with double outlet right ventricle. 1469 24

We studied changes in platelet aggregation and fibrinogen levels during thrombolysis with massive or submassive pulmonary embolism. Fifteen patients were randomized into ultrahigh-dose streptokinase (UH-SK n = 8) or alteplase (tPA n = 7) groups. Arterial blood samples were taken before and after thrombolysis every 4 h between 4 and 36 h, and once daily between 2 and 30 days. In-vitro platelet aggregation was examined as spontaneous (0.9% NaCl) and induced aggregation with adrenaline 10 micromol/l, collagen 2 microg/ml and ADP 10 micromol/l. D-dimer and fibrinogen were measured every 8 h on first day, and later as above. In the UH-SK group, adrenaline-induced platelet aggregation decreased at 4 and 8 h compared with baseline (P < 0.03). Adrenaline-induced platelet aggregation was significantly lower in the UH-SK group than in the tPA group at 36 h and on day 3 (P < 0.03). Platelet aggregation induced by ADP was lower at 4 h than at baseline in the UH-SK group (P < 0.05). Collagen-induced platelet aggregation was lower at 4 and 8 h than at baseline (P < 0.05) in the UH-SK group. Compared with baseline, fibrinogen levels decreased in both groups after thrombolysis. D-dimer levels were elevated in both groups at 8 h (tPA group, P < 0.0004; UH-SK group, P < 0.05). Spontaneous platelet aggregation, major bleeding or re-embolism was not documented. Platelet aggregation decreased after thrombolysis with UH-SK for 12 h, in comparison tPA caused an insignificant decrease. Fibrinogen level decreased with UH-SK treatment for 5 days but in case of tPA we could not measure significant changes. According to our findings, tPA is a more suitable drug but streptokinase is also effective because of its cost-benefit ratio.
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PMID:Time course of platelet aggregation during thrombolytic treatment of massive pulmonary embolism. 1789 Sep 54

Pulmonary embolism is a common and sometimes devastating disease caused by many factors, most commonly deep venous thrombosis. Treatment is typically systemic anticoagulation depending on patient clinical presentation. For patients with life threatening pulmonary embolism, IV tPA (Activase, Genentech, South San Francisco, CA) is the most common medication given emergently at the time of presentation. Computed tomography angiography (CTA) of the chest has advanced the diagnosis and potential treatment options for patients with life threatening pulmonary embolism. Combination percutaneous transcatheter directed pharmacological and mechanical thrombolysis has become extremely useful in these difficult cases.
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PMID:Bilateral EKOS EndoWave catheter thrombolysis of acute bilateral pulmonary embolism in a hemodynamically unstable patient. 2037 46

A 53-year-old man developed a deep venous thrombus (DVT) and pulmonary embolism (PE) shortly after an open Roux-en-Y gastric bypass was performed. He later suffered a life-threatening gastrointestinal bleed while on anticoagulation for the DVT. Thus, anticoagulation was held and an inferior vena cava (IVC) filter (G2, Bard Inc., Tempe, AZ, USA) was placed for PE prophylaxis. About 10 days after filter placement, he presented with severe low back pain and syncope. He also presented with hypotension and anuria unresponsive to intravenous fluids. A STAT non-contrast CT scan of the abdomen revealed that his IVC filter had migrated from an infrarenal to a suprarenal position. Given the high clinical suspicion for renal vein thrombosis, an attempt at IVC filter retrieval was made. The filter could not be retrieved because it was embedded in a large IVC thrombus that extended from the hepatic veins down to the common iliac veins. The patient received nearly 4 days of tPA that was administered at the site of the thrombus with a long thrombolytic catheter (UNIFUSE, Angiodynamics, Queensbury, NY, USA). While his creatinine peaked at 7.6 on hospital Day 4, he eventually began to produce urine and his creatinine had declined to his baseline of 1.0 on follow-up 1 month later. About 18 months after admission, his creatinine had further declined to 0.8. We report the first published case of acute renal failure due to bilateral renal vein thrombosis in the setting of IVC filter migration and thrombosis. This report highlights an important, but rare complication of IVC filter placement as well as the non-operative management of acute bilateral renal vein thrombosis.
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PMID:Bilateral renal vein thrombosis and subsequent acute renal failure due to IVC filter migration and thrombosis. 2042 Aug 4

Extract: When we are wounded, either externally (for instance, when we cut ourselves) or internally (for instance, due to gastric ulcer or brain hemorrhage), blood clots -- sponge-like plugs that are rapidly formed in response to the injury by activated blood platelets and fibrin in a process called coagulation -- prevent profound bleeding. Thus, good or hemostatic clots save our lives. However, under pathological conditions blood clots can also form inside vessels. Such bad or thrombotic clots occlude blood vessels and cause oxygen starvation of vital organs including the brain (stroke), heart (acute myocardial infarction) or lungs (pulmonary embolism). Thrombosis is one of the leading causes of morbidity and mortality from cardiovascular and other disease conditions. Diverse anti-thrombotic means are being developed. For instance, anticoagulants (such as heparin) and platelet inhibitors (such as aspirin) help to prevent formation of clots (blood thinners). Fibrinolytics, known as plasminogen activators (such as tissue-type plasminogen activator, or tPA) dissolve formed clots by degrading the fibrin meshwork. Both types of therapeutics are widely used in medical practice, e.g., for treatment of two forms of ischemic heart disease caused by thrombi in coronary vessels -- acute myocardial infarction and unstable angina.
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PMID:Coupling of anti-thrombotic agents to red blood cells offers safer and more effective management of thrombosis. 2070 55

Massive pulmonary embolism (MPE) is a life threatening disease, thrombolytic treatment could save lives. The aims of this study are to identify early and late mortality rates in patients with MPE who received thrombolytic treatment, and mortality related risk factors. All the hospital records for the MPE patients who received thrombolytic treatment between 1998 and 2006 were retrospectively investigated. Pulmonary embolism was diagnosed through computed tomografi scan and V/P scintigraphy. Due to MPE, 21 women total 41 patients who undergo tPA or streptokinase were included in the study. Kaplan-Meier for the survival analysis and cox regression analysis for determining the mortality related independent risk factors were used. Dying while staying in hospital was accepted as early or hospital mortality, after discharge from hospital as late mortality. Out of 41 patients, 12 of them died while they are hospitalized (hospital mortality; 29%) 6 of them died after they were discharged (late mortality; 21%). The average survival time among discharged patients was 2304 days (95% confidence interval: 1725-2884). Among those patients who took streptokinase or tPA, late or early mortality rates (p> 0.05) and survival time did not show significant difference (p= 0.8908). The presence of arrhythmia [p= 0.01; odds rate (OR): 6.25] and jugular vein distention (JVD) (p= 0.03; OR: 6.25) for hospital mortality and multiple ongoing health problems for the late mortality were identified as the independent risk factors. For the hospital mortality, the presence of JVD or arrhythmia, for prognostic sensitivity, specificity, positive predictive value and negative predictive value were recorded as 75%, 79%, 60% and 88% respectively. In conclusion, the presence of arrhythmia and/or JVD on a patient with MPE is a negative prognostic factor for hospital mortality. The presence of other ongoing health problems influences the survival time of the discharged patients.
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PMID:[Effecting factors on survival in patients taking thrombolytic treatment due to massive pulmonary embolism]. 2103 37

The incidence of venous thromboembolism (VTE) is increasing in the pediatric population. Individuals with cystic fibrosis (CF) have an increased risk of thrombosis due to central venous catheters (CVCs), as well as acquired thrombophilia secondary to inflammation, or deficiencies of anticoagulant proteins due to vitamin K deficiency and/or liver dysfunction. CVC-associated thrombosis commonly results in line occlusion, but may develop into serious life-threatening conditions such as deep venous thrombosis (DVT), superior vena cava syndrome or pulmonary embolism (PE). Post-thrombotic syndrome (PTS) may be a long complication. Local occlusion of the catheter tip may be managed with instillation of thrombolytics (such as tPA) within the lumen of the catheter; however, CVC-associated thrombosis involving the proximal veins is most often is treated with systemic anticoagulation. Initial treatment with heparin is a standard approach, but thrombolytic therapy, which may carry higher bleeding risks, should be considered for life and limb threatening episodes of VTE. Recommended duration of anticoagulation with low molecular weight heparin (LMWH) or warfarin ranges from 3 to 6 months for major removable thrombotic risks; longer anticoagulation is considered for recurrent thrombosis, major persistent thrombophilia, or the continued presence of a major risk factor such as a CVC. While CVCs are the most common risk for development of VTE in children, studies have not demonstrated a clear benefit with routine use of systemic thromboprophylaxis. The incidence and risk factors of VTE in CF patients will be reviewed and principles of diagnosis and management will be summarized.
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PMID:Venous thromboembolism in cystic fibrosis. 2200 66

Thrombosis, the formation of a clot within a blood vessel, underlies a number of life-threatening cardiovascular disorders such as heart attack, ischemic stroke, pulmonary embolism, and deep vein thrombosis. These conditions affect the lives of millions of people worldwide and result in significant morbidity and mortality. It is thus crucial to develop novel methodologies to enhance the detection and treatment of these disorders. Thrombolysis, or the dissolution of blood clots, relies upon the administration of exogenous plasminogen activators (PAs) that lyse fibrin. Yet, there are several drawbacks to the use of current PAs, including significant risks of uncontrolled bleeding and suboptimal efficacy and pharmacokinetics. Nanomaterials are well positioned to address these priority issues in thrombolysis, via the alteration of PA pharmacokinetics and biodistribution. Additionally, due to the multifunctional nature of nanoparticles, these thrombolytics may be targeted to the site of occlusion, effectively concentrating the drug where it is most needed. Herein, we describe the methodology associated with the synthesis of a novel thrombus-targeted fibrinolytic nanoagent. At each step of the synthesis, we analyze the nanomaterials, including their physical properties and their ability to bind to thrombosis targets of interest. The effect of the conjugation of tPA to the nanoparticle surface on the amidolytic and fibrinolytic activities of nanoagents is also investigated. Lastly, the in vivo binding of the targeted thrombolytic to intravascular thrombi is examined.
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PMID:Detection and treatment of intravascular thrombi with magnetofluorescent nanoparticles. 2244 27


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