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

Retrospective study about the frequency of hemorrhagic complications (258 patients) in the treatment of venous thrombosis and/o pulmonary embolism, with heparin. Heparin was intermittently administered by endovenous way and controlled during the ten first days. Mostly of the big hemorrhages happened between the seventh and the tenth day, in digestive and urinary system mainly.
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PMID:[Heparin-induced hemorrhage in the treatment of venous thromboembolism]. 232

The therapeutic regimen in acute pulmonary embolism of different severity is discussed. Heparin is indicated in patients with only small and submassive embolism without impairment of the circulation. Fibrinolysis is the therapy of choice in submassive pulmonary embolism with circulatory insufficiency and massive embolism. In fulminant embolism with circulatory shock or cardiac arrest embolectomy should be performed. If the course of lung embolism is subacute, fibrinolysis may improve the late prognosis in respect to chronic pulmonary hypertension.
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PMID:[Therapy of pulmonary embolism]. 242 13

Heparin has been used in clinical practice since 1936 as anticoagulant for: the treatment of thromboembolic disorders, the prevention of deep vein thrombosis and pulmonary embolism and the maintenance of blood fluidity in extracorporal circuits. Its use in these indications has been complicated by an increased risk of hemorrhage such as major bleeding during the treatment of pulmonary embolism and wound hematoma after surgery. Bleeding problems associated with the use of heparin in extracorporal circuits are the following: hemorrhages after cardiopulmonary bypass, serious hemorrhagic complications in patients treated with hemodialysis during acute renal failure and in patients on chronic intermittent hemodialysis and increased occult blood loss from the gastrointestinal tract and from other sites. The precise contribution of the use of heparin to the enhanced bleeding in these conditions has not yet been established. The effects on platelets, coagulation factors and/or fibrinolytic activity by the exposure of blood to foreign surfaces together with uremia present in hemodialysis patients may also contribute to abnormalities in clinical hemostasis. Recently heparin fractions and a heparinoid of low molecular weight (LMW) have been developed because of their potential to diminish the hazard of hemorrhage while retaining their antithrombotic properties. Preliminary reports from pilot studies have confirmed the increased efficacy in preventing deep vein thrombosis (DVT) of some of the new LMW heparin(oid)s; however, improved safety with regard to bleeding still needs to be shown. The use of LMW heparins and of a new LMW heparinoid in acute and chronic hemodialysis has also been shown to be effective.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin and its biocompatibility. 243 41

Twenty six patients with acute (less than 5 days) pulmonary embolism (PE) confirmed by bilateral pulmonary angiography with a Miller index greater than 15 were given tissue plasminogen activator (Alteplase) (rt-PA) intravenously (n = 20) or directly into the pulmonary artery (n = 6). The dosage was 100 mg/7 hours (bolus 10 mg + 40 mg/2 hours + 50 mg/5 hours). Heparin (5000 IV as a bolus and 1000 IV/hour) was associated in all cases. The Miller index decreased from 24 +/- 1 (n = 26) before treatment to 12 +/- 1 (n = 25) (p less than 0.001) after 100 mg of Alteplase, and from 25 +/- 0.4 (n = 14) to 22 +/- 0.5 (n = 14) (p less than 0.001) after 50 mg. The mean pulmonary arterial pressures fell from 30 +/- 2 mmHg to 21 +/- 2 mmHg after 50 mg (n = 26) (p less than 0.001) and to 14 +/- 1 (n = 25) (p less than 0.001) after 100 mg of Alteplase. A decrease in mean pulmonary artery pressures (-22%, p less than 0.001) and total pulmonary resistances (-29%, p less than 0.001) was obtained after one hour of thrombolysis in 12 monitored patients. There were no fatalities. Severe haemorrhage occurred in 6 cases. Therefore, Alteplase induced a rapid dissolution of recent intrapulmonary thrombi without inacceptable haemorrhagic complications. Its action could be particularly beneficial in patients with right ventricular failure due to life threatening pulmonary embolism.
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PMID:[Tissue plasminogen activator (alteplase) in acute massive pulmonary embolism. A pilot study]. 251 32

Heparin-associated thrombocytopenia and thrombosis (HATT) syndrome is a severe complication of heparin therapy. Since patients admitted for rehabilitation are at high risk for deep-vein thrombosis and pulmonary embolism, prophylactic doses of subcutaneous heparin are frequently used. We report the case of a 73-year-old woman with a history of heparin exposure, admitted to a comprehensive rehabilitation program for management of severe back pain. The patient was started on subcutaneous heparin. After 18 days of hospitalization, she developed marked thrombocytopenia and a massive venous thrombosis in the right lower extremity. On intravenous heparin therapy, the platelet count continued to decline. The thrombocytopenia resolved with discontinuation of heparin. This case illustrates a devastating complication of heparin therapy and emphasizes that physiatrists should be aware of this acute and preventable drug reaction.
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PMID:Heparin-associated thrombocytopenia and thrombosis syndrome in a rehabilitation patient. 252 17

A 30-year-old woman in the 36th week of her second pregnancy, suddenly developed jaundice with remarkable liver necrosis, accompanied by generalized bleeding due to disseminated intravascular coagulation (DIC). She underwent a caesarean and a dead foetus was extracted from the uterus. Heparin and frozen plasma infusion resulted in a prompt recovery from the haemostatic disorder. The course of the disease involved the successive appearance of haemorrhagic shock, intestinal ileus and pulmonary embolism all of which she recovered from. The liver biopsy showed severe cholestasis without derangement of the lobular structure. Hypotheses of acute veno-occlusive disease caused by the DIC, and acute fatty liver of pregnancy are discussed.
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PMID:[Disseminated intravascular coagulation and acute hepatic necrosis at the end of pregnancy. A case report]. 262 77

The aim of prophylaxis in venous thromboembolism is firstly to prevent fatal pulmonary embolism and secondly to reduce the morbidity associated with deep vein thrombosis and the post-phlebitic limb. Particularly high-risk groups are identifiable and include those over 60 years of age undergoing major surgery, patients with malignancy and those undergoing hip operations. Low-dose subcutaneous heparin (5000 U s.c. commenced two hours preoperatively and continued eight to twelve hourly until the patient is fully mobile) is unequivocally effective in preventing deep vein thrombosis in medical and surgical patients and, most importantly, significantly reduces the incidence of fatal postoperative pulmonary embolism and total mortality. Furthermore, in established deep vein thrombosis, low-dose heparin limits proximal clot propagation, which is the prelude to pulmonary embolism. Despite this, surveys have demonstrated an alarming deficiency amongst clinicians in the application of measures to prevent venous thromboembolism. Heparin prophylaxis carries a small risk of increased bleeding complications, mostly evidenced by the frequency of wound haematoma rather than major haemorrhage. Low molecular heparin fragments (e.g. Fragmin, Choay, Enoxaprin) are now emerging as useful alternative agents, having the advantage of once daily administration and yet providing similar efficacy in the prevention of deep vein thrombosis. However, protection against fatal pulmonary embolism has yet to be demonstrated. Mechanical methods of prophylaxis designed to counteract venous stasis, such as graduated elastic compression stockings, are also beneficial in protection against deep vein thrombosis but by themselves do not achieve such consistently good prophylaxis as low-dose heparin. However, clinical trials with combinations of mechanical methods and low-dose heparin indicate that this may be the optimum approach to very high-risk patients. In the presence of established acute deep vein thrombosis, anticoagulant therapy is the mainstay in preventing pulmonary embolism. Vena caval interruption procedures should be reserved for patients in whom anticoagulation is contraindicated or for those who develop recurrent pulmonary embolism despite adequate anticoagulation.
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PMID:Prevention of venous thromboembolism. 266 85

Adequate anticoagulation treatment in patients with deep vein thrombosis reduces the risk of thrombus extension or embolization to less than 5%. Thrombolytic treatment may possibly prevent subsequent postthrombotic syndrome. Heparin is the initial treatment of choice for most patients with deep vein thrombosis. The dose is adjusted according to the results of tests such as the whole blood clotting time, thrombin clotting time, activated partial thromboplastin time or plasma heparin concentration. The most commonly used test is the activated partial thromboplastin time which should be maintained at 1 1/2 to two times the control level. Initially the test should be performed two to three times daily and when optimal adjustment has been established, clotting studies are required only at 24-hour intervals. In general, treatment with intravenous heparin should be continued for seven to ten days. Thereafter, for secondary prophylaxis, treatment with oral anticoagulants is carried out for six to eight weeks for symptomatic lower leg thrombosis, for twelve weeks in the case of proximal venous thrombosis and pulmonary embolism. Oral anticoagulant therapy with warfarin should be given overlapping the last few days of heparin with the dose adjusted to prolong the prothrombin time to 1.3 to 1.5 times control. Initially, the prothrombin time should be monitored weekly, thereafter at intervals of two to three weeks. If oral anticoagulant therapy is contraindicated, secondary prophylaxis with subcutaneous heparin given twice daily in doses sufficient to prolong the activated partial thromboplastin time to 1 1/2 times control is an effective and safe alternative. The major side effect of oral anticoagulant therapy, as well as that of heparin, is bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapy of deep vein thrombosis. 269 42

In a prospective study the complications of Heparin-Dihydroergotamine (HDHE) [2,500 units Heparin + 0.5 mg DHE] s c. twice daily as thromboembolic prophylaxis have been studied in patients undergoing a lumbar disc operation. During a two year period 616 patients were operated, 47 patients had to be excluded, 107 patients did not receive HDHE desired by the surgeon; 462 patients received HDHE as described in the protocol. Because the distribution of age, sex, duration of hospitalisation of the 107 patients without HDHE is the same as in the HDHE group, this group can be used as control group. Increased intraoperative bleeding--written down in the operation report--66 patients (14.3%) in HDHE group and 6 patients (5.6%) in the control group. There is no statistic significance between the both groups in superficial and deep wound hematomas, deep vein thromboses or pulmonary embolism. In the HDHE group two death appears. Both patients [a 37 year old, asymptomatic woman and a 65 year old man with mild ischemic symptoms 11 months prior to operation] died because of an acute myocardial infarction. The clinical course and the missing of stenosis or occlusion at autopsy let us think at the possibility of coronary arterial spasm, presumably caused by DHE, as the cause of myocardial infarction. We suggest not to apply HDHE to patients with coronary artery heart disease or with atypical thoracic pain.
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PMID:[Complications of thromboembolic prophylaxis with heparin-dihydroergotamine]. 280 59

728 patients aged 50-75 years who had had Q-wave myocardial infarction 6-18 months previously were enrolled in a randomised, multicentre trial of low-dose heparin in prevention of reinfarction. The control group (365 patients) received their study centres' usual therapy; the heparin group (363 patients) also received subcutaneous calcium heparin (12,500 IU daily). Mean (SD) follow-up was 708 (265) days in the heparin group and 687 (251) in the control group. The reinfarction rate was 63% lower in the heparin than in the control group (4/303, 1.32% v 13/365, 3.56%). The difference in cumulative reinfarction rate between the groups was significant by both drug-efficacy (chi 2 = 3.99, p less than 0.05) and intention-to-treat analysis (chi 2 = 3.84, p = 0.05). Heparin treatment reduced the cumulative general mortality rates by 48% on drug-efficacy analysis (chi 2 = 3.88, p less than 0.05) and by 34% on intention-to-treat analysis (chi 2 = 2.05, not significant). Cardiovascular mortality was also reduced (33%) but not significantly. However, fatal events attributable to thromboembolism (fatal reinfarction, stroke, pulmonary embolism) were significantly less frequent in the heparin than in the control group (1 v 7, p less than 0.05). 60 patients (16.5%) discontinued heparin treatment, but only 23 patients (6.3%) stopped because of side-effects. Low-dose heparin appears to be effective, safe, well tolerated, and free from haemorrhagic risk for the prevention of myocardial reinfarction.
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PMID:Effectiveness of low-dose heparin in prevention of myocardial reinfarction. 288 39


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