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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombolytic therapy has been used fairly extensively in the management of acute proximal deep-vein thrombophlebitis of the extremities, acute pulmonary embolism, and acute peripheral arterial thrombosis and embolism in addition to acute thrombotic coronary events. In the presence of acceptable indications and a favorable benefit to risk ratio, this form of therapy, when successful, has served as a useful adjunct in the management of these disorders. In deep-vein thrombophlebitis, lysis of the thrombus before permanent pathological changes (eg, organization, scarring) have occurred can prevent venous valvular dysfunction and postural venous hypertension and its complications, especially the postphlebitic syndrome. In the more severe forms of acute pulmonary embolism, thrombolytic therapy, when applied early after symptom onset, decreases morbidity and is likely to prevent a chronic increase in pulmonary vascular resistance and persistent pulmonary hypertension. In peripheral arterial thrombo-occlusive events, early restoration of flow through thrombolysis has been shown to limit ischemic damage and serve as a useful supplement to angioplasty or surgery. Thrombolytic therapy has been used less extensively in acute strokes. Here the danger of reperfusion causing bleeding into a softened area of brain undergoing infarction has slowed its evaluation for this disorder; its application to stroke remains experimental.
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PMID:Thrombolytic therapy for noncoronary diseases. 200 69

The results of a retrospective study comparing two equally large groups of patients treated either surgically for restoration of venous patency and valvular function (24 patients) or medically with heparine, oral anticoagulants and compression stockings (25 patients) are presented. Follow-up time was 7.6 and 7.9 years respectively, operative mortality nil. Assessment of venous function was based on clinical observations as well as on measurements of haemodynamic parameters. Non-fatal pulmonary embolism after onset of treatment occurred in both cohorts with an equal frequency of 13%. Patients operated on for ilio-femoral deep venous thrombosis (DVT) were with few exceptions totally independent of any form of adjunctive hosiery which was in sharp contrast to the conservatively managed group. If onset of DVT had occurred more than three days earlier and extended from the ilio-femoral axis to the popliteo-crural level, surgery usually failed and patients were no better off than in the comparable medical subgroup. The same pattern of late outcome was found for all other clinical and haemodynamic parameters; i.e. clinical signs of venous hypertension, valvular competence as judged by sonography, patient's self-assessment and the expelled volume and refilling time measured by dynamic plethysmography after standardized leg-work. The mean expelled volume was 1.1 +/- 0.5 ml/100 g/min for the surgical subgroup treated early for ilio-femoral DVT and 0.7 +/- 0.5/100 g/min for the corresponding medical group (p = 0.05). Recovery or refilling time was 50 +/- 21 sec for the surgical group and 28 +/- 26 sec for the medical group (p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Surgical thrombectomy versus conservative treatment of ileo-femoral phlebothrombosis. Functional comparison of long-term results]. 207 75

In contrast to pulmonary parenchyma metastases or lymphangitic carcinomatosis, neoplastic emboli of small pulmonary arteries and capillaries frequently go unrecognized and are only discovered at autopsy. Five patients (48 +/- 12 years old) were admitted to 3 intensive care units for severe acute respiratory failure and died between the first and the tenth day following hospitalization. Each patient had a history of rapidly progressive dyspnea, and physical examination showed clinical evidence of right ventricular failure. The lungs were clear on chest X-rays and the ECG revealed sinus tachycardia with a right QRS axis. The mean partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) were, respectively, 50.8 +/- 9.1 mm Hg and 22.2 +/- 2.4 mm Hg. A swan-Ganz catheter, inserted into 4 patients, revealed pulmonary arterial hypertension (55, 43, 37, 28) with capillary wedge pressure within the normal limits and cardiac output normal or low (3.0, 3.8, 4.4, 5.0 l/min). Pulmonary angiograms from each patient showed decreased distal lung perfusion without any proximal defects suggestive of pulmonary embolism. The inferior vena cava always appeared clear. Malignant cells were found upon autopsy (4 cases) in the lumina of the pulmonary arterioles and the primary site of the cancer was determined in 3 patients (2 hepatomas and 1 pancreatic carcinoma). The last patient had a known breast cancer with bone marrow metastases and clinical, hemodynamic and angiographic evidence of neoplastic emboli. The clinical course of neoplastic emboli can suggest acute pulmonary embolism, but the diagnosis can only be advanced after pulmonary angiography, especially if the patient is to have a cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute respiratory distress caused by distal neoplastic pulmonary emboli]. 209 8

Based on a retrospective evaluation of 107 patients with congenital venous angiodysplasia of the Type Klippel-Trenaunay (n = 76) and Type Servelle-Martorell (n = 31) the frequency and pathogenesis of aneurysma formation in the venous system has been analysed. The vascular patterns include both cylindric ectasia and fusiform aneurysms with an incidence of approximately 40%. Preferred locations are subcutaneous drainage veins, the popliteal, external iliac vein and atypic communicating veins between the superficial and the deep venous system. Complications of the aneurysm such as local thrombosis, recurrent pulmonary embolism or bleeding from ruptur were not observed. The aneurysma formation in venous angiodysplasias results probably from the causative factors: congenital weakness of the venous wall and an abnormal hemodynamical stress situation. The latter is caused by concomitant malformations of the deep venous system. The persistent intermittent venous hypertension associated with a more or less pronounced increase of the venous volume in the affected venous system of the limb results in a deep venous insufficiency respectively venous reflux disease. The therapy of choice is predominantly conservative, i.e., external compression bandages or stockings to reduce the deleterious effects of a chronic deep venous insufficiency respectively venous reflux disease. Surgery is indicated under two conditions: a) in the presence of aneurysm complications or b) for the elimination of a pathological short circuit flow in some drainage veins. Antireflux surgery, i.e., venous valve transfer from the brachial vein, is up to recently still in a stage of experimental-clinical investigation.
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PMID:Aneurysma transformation in congenital venous angiodysplasias in lower extremities. 217 53

The authors present the results of their blind prospective comparative study of the postoperative thromboembolic protection of 490 gynecologic patients. Among them 250 (51%) were protected by a low dose heparin (LDH) subcutaneously in 12-hour intervals, 240 (49%) received heparindihydergot (HDHE). Thromboembolisms diagnosed by the 125J fibrinogen uptake test appeared in 26 (10.4%) patients protected by LDH and 23 (9.6%) by HDHE. The most frequent risk factors in patients with thromboembolisms were malignant diseases, obesity, varicose veins, hypertension and a history of deep vein thrombosis or pulmonary embolism. Haemorrhages appeared in 7 (2.8%) patients protected by LDH and 8 (3.3%) by HDHE.
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PMID:[Prevention of thromboembolic disease in gynecologic surgery]. 221 51

Acute fatal pulmonary embolism is one cause of sudden death which should be guarded against. It is the most often missed diagnosis in sudden death cases within the hospital. Clinical pictures of 10 patients with acute fatal pulmonary embolism proved by autopsy were examined to elucidate the problems of diagnosis, and to look for an effective treatment, and a method of prevention. Common risk factors were old age and immobility due to stroke or postoperative state. Common past histories were hypertension, diabetes mellitus, obesity, atrial fibrillation and hyperlipidemia. Electrocardiogram and echocardiogram showed that in these patients there was definite evidence of acute right ventricular overload. High doses of intravenous urokinase should be given whenever acute cardiovascular collapse develops in such high risk patients. Emergent pulmonary angiogram and pulmonary embolectomy could be life-saving in patients with acute massive pulmonary embolism. Prevention is, however, the best treatment. In addition to anticoagulation medication, frequent change of body position and early mobilization are important precautions to prevent fatal pulmonary embolism developing in such patients.
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PMID:[Acute fatal pulmonary embolism: its prevention, diagnosis and treatment]. 236 72

The patient was a 29-year-old woman. She was well until autumn 1983, when she presented with polyarthralgia, fever above 39 degrees C, hepatosplenomegaly, swelling of lymphnode and salmon pink rash. Laboratory tests revealed marked leucocytosis with shift to the left, elevated ESR, strong positivity of CRP and abnormal liver function tests. However, anti-nuclear antibody and RA factor were negative. She was diagnosed as adult onset Still's disease (AOSD) by characteristic clinical course and laboratory data. During her disease course these abnormal findings could be well controlled neither by nonsteroidal anti-inflammatory drugs, immunosuppressive agents nor corticosteroids. Two and half years after the first admission, she began to complain of dry cough, dyspnea on efforts. Auscultation revealed an increased pulmonic sound and systolic murmur of cardiac apex. Chest X-Rays showed enlarged main pulmonary arteries. The lung fields were normal. Pulmonary function tests gave no evidence of a significant obstructive or restrictive defect but showed the low DLco and hypoxemia. Ventilation-perfusion lung scanning failed to reveal pulmonary embolism. Finally, right heart catheterization confirmed the pulmonary precapillary hypertension. Her pulmonary hypertension has progressed rapidly, strongly suggesting poor prognosis. Her pulmonary hypertension associated with no apparent parenchymal involvement was thought to be caused by a pulmonary vascular change probably related to AOSD. This case is a first case of AOSD with pulmonary hypertension.
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PMID:[A case of adult Still's disease with pulmonary hypertension]. 237 40

Pulmonary embolism can produce severe cardiopulmonary dysfunction characterized by pulmonary artery hypertension, right ventricular failure, and hypoxemia. The search for the source of a pulmonary embolus, by exploration of the veins of the lower limbs and the inferior vena cava should be systematically carried out in all cases of pulmonary embolus which are not immediately life-threatening to the patient. The treatment of deep vein thrombosis associated with pulmonary embolism with thrombolytic agents has been proposed and utilized for approximately 20 years. Although superior results have been claimed with thrombolytic agents, the use of this type of treatment remains limited to massive or sub-massive pulmonary embolism. Fibrinolytic agents with high specificity for fibrin in the thrombi and little systemic activation of the fibrinolytic system have been developed and tested in preliminary clinical trials of patients with acute pulmonary embolism. The largest published experience available has been with recombinant tissue plasminogen activator (rtPA). The acylated streptokinase-plasminogen complex (APSAC) and pro-urokinase also gave promising results. All these agents were accompanied by unexpectedly high incidence of systemic activation of the fibrinolytic system and by hemorrhagic complications with frequencies similar to those that follows the use of first generation products (urokinase and streptokinase). Hence, their superior clinical efficacy must be clearly proven before they are substituted for a more widely available and less expensive drug, such as streptokinase.
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PMID:Pathogenesis and management of acute pulmonary embolism. 251 49

Vascular risk, mainly thromboembolitic risk, attributed to oral contraceptives (OCs) since 1962, has been primarily linked to ethinyl estradiol (EE). OCs which combine estrogen and have been associated with cerebral vascular accidents. A 1977 study showed a 40% increase of mortality due to cardiovascular complications in women taking OCs. There were of both an arterial and a venous character. The risk of myocardial infarction was 3 times more frequent among OC users. Deep venous thrombosis and pulmonary embolism were more numerous. Some other risk factors include smoking, hypertension, diabetes, and age 35. The risk of heart attack vanishes a few years after stopping OC use. The reduction of EE (and similarly progesterone) dosage from 100-50 mcg also lower the risk of hypertension, cerebral vascular accidents, and venous thrombosis. Prolonged use of OCs causes disorders of hemostasis affecting the walls of blood vessels, modifying the viscosity of blood flow (increase of hematocrits, reduction of venous tonus), modifying plasmatic coagulation (increase of platelets, increase of factors VII and X and plasma fibrinogen, and decrease of antithrombin III activity), and increased fibrinolysis. These anomalies are exclusively associated with high doses of estrogens. 5% of women using OCs develop moderate hypertension of 5-10 mm Hg of systolic pressure 5 years later, but after cessation it is reversed. OCs stimulate the renin-angiotensin-aldosterone system causing accelerated production of angiotensin II with the resultant forceful vasotension. 3 months after quitting OC use, high blood pressure returns to normal. EE can provoke diabetes; it increases very low density lipoprotein (VLDL) and high density lipoprotein (HDL) production, but total cholesterol is hardly affected. The androgenic property of progestogens reduces HDL. Combined OCs are contraindicated for women with hypertension, hyperlipidemia, diabetes, and a family history of vascular accidents.
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PMID:[Oral contraception and the vascular risk]. 251 20

Based on a retrospective evaluation of 107 patients with congenital venous angiodysplasia of the Type Klippel-Trenaunay (n = 76) and Type Servelle-Martorell (n = 31) the frequency and pathogenesis of aneurysm formation in the venous system has been analysed. The vascular patterns include both cylindric ectasias and fusiform aneurysms with an incidence of approximately 40%. Preferred locations are subcutaneous drainage veins, the popliteal, external iliac vein and atypic communicating veins between the superficial and the deep venous system. Complications of the aneurysm such as local thrombosis, recurrent pulmonary embolism or bleeding from rupture were not observed. From a pathogenetic point of view the aneurysm formation in venous angiodysplasias results probably from two causative factors, i.e., a congenital weakness of the venous wall (inborn error?) and an abnormal hemodynamical stress situation. The latter is caused by concomitant malformations of the deep venous system (avalvulia, hypo- and/or aplasia). The persistent intermittent venous hypertension associated with a more or less pronounced increase of the venous volume in the affected venous system of the limb results in a deep venous insufficiency respectively venous reflux disease. Surgery is indicated under two conditions: a) in the presence of aneurysm complications or b) for the elimination of a pathological short circuit flow in some drainage veins. Antireflux surgery, e.g., venous valve transfer form the brachial vein, is up to recently still in a stage of experimental-clinical investigation. The therapy of choice is predominantly conservative, i.e., external compression bandages or stockings to reduce the deleterious effects of a chronic deep venous insufficiency respectively venous reflux disease.
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PMID:[Aneurysmic transformation of the venous system in venous angiodysplasias of the limbs]. 254 55


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