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

From 1957 to 1982, 115 patients underwent radical vulvectomy and bilateral inguinal lymphadenectomy for invasive squamous carcinoma of the vulva. From 1957 to 1971, 57 patients received perioperative prophylactic sodium warfarin (Coumadin) as prophylaxis against pulmonary embolism. From 1971 to 1976, 27 consecutive patients received dextran-40 as prophylaxis for pulmonary embolism and to improve the microcirculation to the inguinal skin flaps. Because of the report that dextran-40 is a cause of acute renal failure, this study was terminated and the subsequent 19 patients were treated with mini-dose heparin because of the reported benefit as prophylaxis against thromboembolic disease. During the 25-year period, 12 patients received no prophylactic anticoagulants. Mini-dose heparin resulted in a significant morbidity not previously reported in patients undergoing inguinal lymphadenectomy: 43% (8/19) of the mini-dose heparin patients, 7% (2/27) of the dextran-40 patients, 0% (0/57) of the sodium warfarin patients, and none of the 12 patients not receiving perioperative prophylaxis developed inguinal lymphocysts (P less than .001). There was no significant difference in the prevention of pulmonary embolism between the mini-dose heparin (0/19), dextran-40 (0/27), and no treatment groups (0/12) as compared to the 5% (3/57) incidence in the sodium warfarin patients (.10 less than P less than .50). The significant relationship between prophylactic heparin and the subsequent development of inguinal lymphocysts and the need to reassess its role in prevention of pulmonary embolism in patients undergoing lymphadenectomy is discussed.
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PMID:Prophylactic anticoagulation as a possible cause of inguinal lymphocyst after radical vulvectomy and inguinal lymphadenectomy. 685 17

Anticoagulant therapy has stood the test to time. Full-dose heparin and warfarin prevent recurring pulmonary embolism and deep venous thrombosis. Their use is indicated in patients who have experienced venous thromboembolism unless contraindications are compelling. Low-dose heparin is successful in preventing the initial episode of venous thrombosis in most patients at high risk for the development of thrombophlebitis. Warfarin reduces the incidence of systemic embolization in patients with heart disease and atrial fibrillation and in patients with artificial heart valves. Evidence is accumulating to suggest that warfarin may still retain an important role in the management of patients with myocardial infarction. However, bleeding remains an inevitable risk in patients receiving anticoagulant therapy. The risk, however, can be diminished when both the physician and patient understand the mechanism of action of the drugs and the factors that predispose to bleeding.
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PMID:Current status of anticoagulant therapy. 707 46

A case study report is presented of a 20 year old black woman with a past history of oral contraceptive (OC) use who developed Budd-Chiari syndrome (hepatic vein thrombosis) associated with decreased levels of antithrombin 3. This combination has not been previously reported. The woman presented on December 28, 1979 with midepigastric pain. She had no previous illnesses, but OCs had been used up to 2 years prior to admission. Shortly after admission the patient became hypotensive, developed oliguric renal failure, and began to rapidly accumulate ascites. During this admission, the patient's transaminase levels abruptly declined. A percutaneous liver biopsy obtained on January 9, 1980 showed centrilobular hemorrhagic necrosis of a severe degree. An inferior vena cavagram was repeated on January 14, 1980 demonstrating hepatic vein thrombosis. Streptokinase, followed by heparinization, was given in an effort to lyse the thrombi, but repeat inferior cavagram on January 24th proved this to be unsuccessful. Thrombosis of the left iliac and left femoral vein then appeared. Because of her apparent "hypercoagulable state," the antithrombin 3 level was measured on January 31st and found to be 27%. A simultaneous serum fibrinogen was 255 mg/dl. Family members (father, mother, and 4 children) were studied. All had normal antithrombin 3 levels, thus excluding a familial defect. The patient gradually improved and was discharged on February 25, 1980 on Coumadin, diuretics, and a 3 g sodium diet. Because of ascites and peripheral edema, a LeVeen shunt was placed on March 25, 1980. At surgery, she was noted to have obstruction of the right internal jugular and right cephalic veins. Because of possible thrombosis in the superior inferior vena cava branches, venography was performed on March 31st and demonstrated thrombosis of the right subclavian, inferior vena cava, and internal iliac veins. Despite the therapy, patient again began to reaccumulate ascites and was readmitted on May 17th. The then nonfunctioning shunt was repositioned in the patient's right atrium. Postoperatively, the patient's course was complicated by DIC. Because heparin induced thromboycytopenia was suspected, heparin was discontinued and Coumadin begun. On June 6th the patient became suddenly short of breath. A lung scan was consistent with pulmonary embolism. She could not be adequately ventilated and died on June 8th. Although the patient discontinued OC use 2 years prior to initial presentation of the disease, the morphologic features of the venous thrombosis and hepatic damage were indicative of a chronic, ongoing process of longer than 6 months' duration, thus raising the possibility of a cause-effect relationship between the OC and thrombotic process. Prospective studies are needed to substantiate the view of a relationship between OC use, antithrombin 3 deficiency, and the Budd-Chiari syndrome.
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PMID:Budd-Chiari Syndrome and antithrombin III deficiency. 710 23

Two patients with familial antithrombin III deficiency developed deep venous thrombosis of the lower limb. The diagnosis of venous thrombosis was made by the indium labelled platelet technique which also allowed for the daily assessment of thrombus size. Each patient received treatment with Warfarin, subcutaneous heparin, and infusions of antithrombin III concentrates. The authors conclude that infusions of antithrombin III concentrates may be of value in limiting the extent of acute thrombosis in patients with a severe deficiency of this protein and may help prevent pulmonary embolism. The haemorrhagic risk of continuing modest doses of heparin with high dose ATIII therapy appears small. In addition to its value in the diagnosis of venous thrombosis the indium platelet technique may give an early indication of thrombus extension and may thus indicate the effectiveness of treatment.
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PMID:Treatment of venous thrombosis in antithrombin III deficient patients with concentrates of antithrombin III. 711 92

Deep vein thrombosis (DVT) is a common condition. Most cases arise as complications during the perioperative period. This can largely be prevented by adequate prophylaxis, principally using low-dose subcutaneous heparin. Only a minority of DVTs produce serious complications, but it is not currently possible to predict the clinical behaviour of any DVT, once formed. For this reason, any identified DVT should be vigorously treated. The mainstay of treatment remains systemic anticoagulation with heparin and then warfarin. Warfarin should be continued for 1 month in postoperative cases and 3 months in spontaneous cases, provided there is no ongoing predisposing factor. Recurrent spontaneous DVT formation is an indication for lifelong anticoagulation. Recent evidence suggests that the subcutaneous route of administration of heparin has advantage over traditional intravenous infusion. Some large DVTs require thrombolysis, and it is now possible to treat the underlying anatomical defects with angioplasty and endovascular stenting, although the long-term outcome of these procedures has not yet been established. For patients with contraindications to the use of anticoagulants, a variety of (temporary and permanent) percutaneously inserted vena caval filters are now available. The principal complications of DVT are pulmonary embolism, which may be fatal, and the development of a postphlebitic leg. The avoidance of these depends on adequate prophylaxis and vigorous treatment of the primary DVT.
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PMID:Deep vein thrombosis. 749 62

Thromboembolic disease is common in patients with malignant brain tumors and represents a major cause of morbidity and mortality in these patients. The presenting signs and symptoms of deep venous thrombosis and pulmonary emboli can be subtle; thus, a high index of suspicion is required to ensure a timely diagnosis. The accuracy of non-invasive studies of the lower extremities and lungs have significant limitations. Venography and pulmonary angiography remain the best diagnostic techniques when difficult decisions arise regarding the need for anticoagulants in these patients. Patients with malignant brain tumors can be safely anticoagulated with heparin and warfarin, if these agents are monitored carefully. Continuous intravenous infusions of heparin are associated with lower risks of bleeding than intermittent boluses. Clinicians may wish to modify the recommended initial bolus dose of heparin in patients without life-threatening thromboembolic disease. Warfarin reduces the incidence of recurrent thromboembolic events. The incidence of warfarin-related bleeding can be lowered without compromising efficacy by maintaining the PT ratio at 1.3. Potential warfarin drug interactions must be considered, aspirin containing medications and NSAIDS should be avoided, and the platelet count should be kept above 50,000 using transfusions if required to prevent potentially life-threatening bleeding in anticoagulated patients. Thrombolytics are contraindicated in this patient population. Vena caval filters and thrombectomy are rarely required. Additional research is needed to determine the best techniques to prevent deep venous thrombosis and pulmonary embolism in patients with brain tumors.
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PMID:Treatment of thromboembolic complications in patients with brain tumors. 774 65

Deep venous thrombosis (DVT) is often occult and difficult to recognize clinically. The diagnostic approach should begin with color-flow (duplex) ultrasound, noninvasive functional tests such as plethysmography, or both. Because these tests are not 100% sensitive, contrast venography or magnetic resonance imaging may be necessary in a patient with unexplained symptoms. A baseline ventilation-perfusion scan should be considered for any patient with DVT, because there is a high incidence of clinically inapparent pulmonary embolism. In the absence of contraindications, systemic or regional thrombolytic therapy should be considered for every patient with acute DVT. Surgical thrombectomy may be indicated for patients with a large, obstructive proximal thrombus. At a minimum, routine treatment should start with heparin and proceed to oral warfarin (Coumadin, Panwarfin, Sofarin), which should be continued for 3 months. Recurrent DVT after cessation of therapy warrants lifetime use of anticoagulants. A filter should be placed in the inferior vena cava whenever a large, poorly adherent thrombus is identified or when there is progression of thrombosis despite an anticoagulant regimen.
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PMID:Venous thrombosis. Lifting the clouds of misunderstanding. 781 15

Pregnancy is associated with a prethrombotic state. Pulmonary embolism is the major cause of maternal mortality. Anticoagulant prophylaxis and therapy are therefore commonplace in pregnant women. Those with inherited and acquired thrombophilic conditions are at increased risk and special considerations arise in management. Heparin has recently become the favoured anticoagulant drug in pregnancy. Its use carries risks of osteopaenia and thrombocytopaenia, as well as haemorrhage, in the mother. Warfarin is teratogenic and may also cause haemorrhagic complications in mother and fetus. Few clinical trial data exists for guidance on optimal anticoagulant regimes during pregnancy and the puerperium and details of management will depend upon the personal preferences of patient and clinician, after due consideration of the perceived risks and benefits in the individual clinical situation.
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PMID:Anticoagulants in pregnancy. 830 94

The incidence of pulmonary embolism (PE) in osteoarthritic patients prophylaxed with low-dose coumadin after cemented total knee arthroplasty (TKA) was investigated prospectively. Each patient had a preoperative perfusion scan and a ventilation-perfusion scan on the seventh postoperative day. Pulmonary embolism was diagnosed by a high probability ventilation-perfusion scan or positive arteriogram. Patients with a moderate probability scan had an arteriogram to rule out PE. Pulmonary embolus was identified in 48 (5.6%) of 852 TKAs in 755 patients. Of these, six (0.7%) were symptomatic, and no fatal PE was identified. Age, gender, and weight did not show statistical differences comparing the PE and non-PE groups, nor did the incidences of previous PE, contralateral phlebitis, malignancy, and diabetes. A history of ipsilateral phlebitis increased the risk of PE from 5.2% to 13%, and a history of cardiac disease decreased the risk from 7.8% to 4.2%. Type of anesthesia, blood loss, tourniquet time, and prosthesis type were not significant factors. With the exception of previous contralateral phlebitis, traditional risk factors for PE were not found to increase risk of PE with low-dose coumadin prophylaxis. Spinal anesthesia that has been shown to be protective in total hip surgery was not a significant factor in this study.
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PMID:Incidence of pulmonary embolism after total knee arthroplasty with low-dose coumadin prophylaxis. 842 57

With a greater understanding of the prevention of thromboembolic complications, the incidence of fatal pulmonary embolism after total joint arthroplasty has declined. Although much of our knowledge is centered around deep vein thrombosis and its use as a marker for thromboembolic complications, little is known about the natural history of both symptomatic and asymptomatic pulmonary embolism. Although differing methods of prophylaxis have shown some success, the ideal agent has yet to be discovered. The use of serial lung scanning has shown great use in the diagnosis of pulmonary embolism. Additional studies using effective diagnostic tools are needed to evaluate the risk of recurrent embolism. Only then can the duration of treatment and prophylaxis be determined. Despite the many unanswered questions, the following conclusions can be drawn: (1) fatal pulmonary emboli are a preventable complication of total joint arthroplasty; (2) fatal emboli are often preceded by small and frequently asymptomatic emboli; (3) detection and appropriate therapeutic measures for asymptomatic emboli are possible with the use of serial lung scans and judicious use of pulmonary angiography; and (4) low-dose coumadin has proven to be the most effective agent in lowering the risk of asymptomatic, symptomatic, and fatal pulmonary emboli.
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PMID:Pulmonary embolism in total joint arthroplasty. 763 20


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