Pulmonary embolism clinical

Table 3 Frequency of clinical pulmonary embolism in the absence of prophylaxis...

Thrombolytic Enzymes. Although atherosclerosis and the accompanying vascular wall defects are ultimately responsible for such diseases as acute pulmonary embolism, arterial occlusion, and myocardial infarction, the lack of blood flow caused by a fibrin clot directly results in tissue injury and in the clinical symptoms of these devastating diseases (54). Thrombolytic enzyme therapy removes the fibrin clot by dissolution, and has shown promise in the treatment of a number of thrombo-occlusive diseases (60). 

Outcome parameters for VAP, HAP, and HCAP are similar to those with CAP. Clinical improvement should occur within 48 to 72 hours of the start of therapy. If a patient is not responding to therapy, then, again, consider infectious and noninfectious reasons. Infectious explanations are the same as for CAP, but noninfectious reasons are not. They include atelectasis, acute respiratory distress syndrome (ARDS), pulmonary embolism or hemorrhage, cancer, empyema, or lung abscess. 

Urokinase is used clinically under the same circumstances as streptokinase because of its human origin, adverse immunological responses are less likely. Following acute medical events such as pulmonary embolism, the product is normally administered to the patient at initial high doses (by infusion) for several minutes. This is followed by hourly i.v. injections for up to 12 h. 

It is remarkable that most of the data collected from the available SERMs are unanimous in reproducing an estrogen agonistic profile in venous thrombogenesis. The vast clinical experience acquired with tamoxifen confirms an augmented risk for both deep venous thrombosis and pulmonary embolism. This increase, however, did not presuppose increased mortality in the overview of randomized trials of adjuvant tamoxifen for early breast cancer, where the one extra death per 5000 woman-years of tamoxifen attributed to pulmonary embolus was not statistically significant (Early Breast Cancer Trialists Collaborative Group 1998). 

Clinical phase I and II data reveal arzoxifene to be safe, well tolerated, and efficacious. Two multi-institutional phase II trials including 100 women with metastatic or recurrent endometrial cancer have demonstrated significant activity of arzoxifene at 20 mg/d in patients with metastatic or recurrent endometrial cancer. The observed clinical response rates were 25 and 31%, with a mean response duration of 19.3 and 13.9 months, respectively. Progression of the disease was stabilised in a substantial number of women. Toxicity was mild, except for two cases of pulmonary embolism that might have been drug related (Burke et al. 2003). 

In CEA, the total cost and the total benefits, measured in terms of an efficacy parameter, associated with two or more treatment pathways are added, and the increment is calculated. The incremental costs are then compared (in a ratio) with incremental outcomes (as measured in physical or natural emits). Physical and natural units can include both intermediate (surrogate) clinical endpoints (e.g. millimetres of mercury blood pressure reduction, changes in FEVi) or final endpoints (e.g. deaths averted or life-years gained). In a study that assessed the cost per deaths due to pulmonary embolism averted, Hull and associates reported that subcutaneous administration of... 

Heparin is usually administered for a period ranging from 7 to 10 days. Frequently, during file last half of litis period of heparin liierapy, oral anticoagulation will be commenced with warfann. The time during which oral anticoagulation administration should be continued may be three months or longer after clinical evidence that file venous thrombosis has subsided and for one year after pulmonary embolism. 

Recombinant human erythropoietin (rHuEpo) may increase the risk of thrombosis (201). It has been reported that patients with carcinoma of the cervix who received chemotherapy and rHuEpo have an increased risk of symptomatic venous thrombosis (201). In clinical trials where the maintenance hematocrit was 3% on PROCRIT clotting of the arteriovenous shunts occurred at an annual rate of about 0.25 events per patient per year. However, other thrombotic conditions such as cerebrovascular events, transient ischemic attacks, myocardial infarction, or pulmonary embolism occurred at a rate of 0,04 events per patient per year (202). In a separate study of I, I I I untreated patients on hemodialysis, clotting of arteriovenous shunts occurred at a rate of 0.5 events per patient per year. In patients with chronic renal failure on hemodialysis who also had congestive heart failure, ischemic heart disease and venous thrombosis were increased in patients who were treated with PROCRIT targeted to a hematocrit level of 42 3% compared to those targeted to 30 3% (202). It has also been reported... 

Fondaparinux is a chemically synthesized pentasaccharide that mimics the antithrombin-binding site of heparin and LMWH. Its molecular size (1728Da) is too small to bind to thrombin molecules while it is bound to antithrombin, Therefore, it is a pure anti-Xa inhibitor. It binds very little to platelets, proteins, or endothelium and is excreted in the urine, It does not form a complex with PF4 or other positively charged molecules. It is not neutralizable by protamine sulfate, Recent clinical trials have resulted in FDA approval for prophylaxis of deep vein thrombosis in orthopedic surgery, It has been shown to be effective and safe for the treatment of pulmonary embolism (20,21) and ACS (non-ST-elevation Ml) (OASIS 5—Michelangelo Trial) (17). 

Therapeutic uses Currently alteplase is approved for the treatment of myocardial infarction, massive pulmonary embolism, and acute ischemic stroke. Alteplase seems to be superior to streptokinase and urokinase in dissolving older clots, and may ultimately be approved for other applications. Alteplase administered within 3 hours of the onset of ischemic stroke significantly improves clinical outcome, that is, the patients ability to perform activites of daily living. 

Four major and five minor clinical patterns of acute phencyclidine intoxication have been described in 1000 patients (7). Major patterns were acute brain syndrome (24.8%), toxic psychosis (16.6%), catatonic syndrome (11.7%), and coma (10.6%). Minor patterns included lethargy or stupor (3.8%) and combinations of bizarre behavior, violence, agitation, and euphoria in patients who were alert and oriented (32.5%). Patients with major patterns of toxicity usually required hospitalization and had most of the complications. Patients with minor patterns generally had mild intoxication and did not require hospitalization, except for treatment of injuries or autonomic effects of phencyclidine. There were various types of injuries in 16%, and aspiration pneumonia in 1.0%. There were 22 cases of rhabdomyolysis (2.2%), and three patients required dialysis for renal insufficiency. One patient who had been comatose died suddenly with a pulmonary embolism. 

Approximately 50% of hemiparetic patients in hospital develop a deep vein thrombosis in their paralyzed leg, although this is not usually detectable clinically. However, a swollen and painful leg compromises rehabilitation. A resultant pulmonary embolism causes... 

Pulmonary embolism. Thrombolysis is superior to heparin at relieving obstructed veins demonstrated radiologically. While a reduction in mortality is thus implied, the numbers of cases reported in clinical trials of thrombolytics have been insufficient to... 

A third variety, so-called delayed-onset heparin-induced thrombocytopenia has also been described in several reports. In 12 patients, recruited from secondary and tertiary care hospitals, thrombocytopenia and associated thrombosis occurred at a mean of 9.2 (range 5-19) days after the withdrawal of heparin nine received additional heparin, with further falls in platelet counts (32). In a retrospective case series, 14 patients, seen over a 3-year period, developed thromboembolic complications a median of 14 days after treatment with heparin (33). The emboli were venous (n — 10), or arterial (n — 2), or both (n — 2) of the 12 patients with venous embolism, 7 had pulmonary embolism. Platelet counts were mildly reduced in all but two patients at the time of the second presentation. On readmission, 11 patients received therapeutic heparin, which worsened their clinical condition and further reduced the platelet count. 

Rodvold KA, Erdman SM. Pulmonary embolism. In Carter B, Angaran D, Sisca T, eds. Pharmacotherapy self-assessment program, 1st edition. Kansas City American College of Clinical Pharmacy, 1992 39-53. 

Mini-dose or subcutaneous heparin was reported on briefly in previous reviews.13 14 In 1975-76 more clinical evaluations have been reported.89-71 These smaller doses with lower and more sustained effect are efficacious i n vivo for use before surgery and other thrombotic conditions to prevent venous thrombosis and pulmonary embolism. This new form of dosing was advanced by the development of new understanding of mechanism and development of new methods for measuring activity. Such therapy eliminates the necessity of laboratory monitoring and the danger of bleeding. 

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