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

The division of the venous circulation in to two sectors, one constituted by the superficial and deep venous trunks (macrocirculation) and the other by the capillaries and precapillary venules (microcirculation), is surely schematical but aids the comprehension of many hemodynamic effects connected to hampered venous return and to the incompetence of the valvular devices. In fact many of the effects of stasis and venous hypertension (oedema, red cell diapedesis, skin dystrophies) cannot be explained merely by hydraulic mechanisms but require a primary alteration of the microvascular wall associated with structural changes of the perivascular connective tissue. The alterations that occur in microcirculation are of the utmost importance in the formation of the venules ulcerations. The passage of fibrinogen through large pores in the venules of the patients affected by venous hypertension derived from venous insufficiency creates a pericapillary fibrin deposition that cannot be removed because of inadequate blood and tissue fibrinolysis. This accumulation acts as a barrier to the diffusion of oxygen and other nutrients, determining a stasis dermatitis that may lead to tissue necrosis and ulceration. The more precise knowledge of the phenomena connected with the venous stasis at the level of microcirculation (pericapillary fibrin deposition, endothelial ischemia, blocked lymphatic drainage) will not only allow a deeper comprehension of the clinical signs but hopefully will lead to a more effective treatment of the postphlebitic syndrome.
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PMID:[Physiopathology of venous stasis at the microcirculation level]. 129 20

The postphlebitic syndrome is a significant management problem that affects a large number of patients. Primary prophylaxis of deep-vein thrombophlebitis would reduce the risk of developing the postphlebitic syndrome and should be considered in high-risk patients. Patients who have had a phlebitis should be monitored with noninvasive tests of the deep venous circulation for the development of venous valve incompetence. Patients with venous hypertension should be placed in compression stockings to prevent the postphlebitic syndrome. In patients who progress to venous ulceration, several aggressive measures must be undertaken. Systemic treatment includes management of obesity, edema, immobility, poor nutrition, and comorbid illnesses. Some patients may require a short hospitalization of bed rest, lower limb elevation, and daily dressings and wound care. Outpatient therapy requires sustained compression of 35 to 40 mmHg at the ankle for many months to allow the ulcer to heal. The standard bandage material is Unna's boots, which is applied every one to two weeks by a trained nurse. Cadexomer iodide is an effective local treatment that helps debride the ulcer and accelerate healing. Finally, pentoxifylline therapy has also been shown to significantly improve the healing of venous ulcers.
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PMID:Contemporary treatment of venous lower limb ulcers. 147 73

In patients with venous hypertension due to postphlebitic syndrome or varicose veins skin changes, liposclerosis and ulcerations are associated with increased skin blood flux at rest, a decreased venoarteriolar response and increased capillary filtration. Using laser-Doppler flowmetry we studied skin flux and the venoarteriolar response in the perimalleolar region in 100 normal limbs, 100 limb with varicose veins and 100 postphlebitic limbs with edema, skin changes and liposclerosis. The venoarteriolar response was studied with the leg on dependency, the foot being 50 cm below heart level. Flux at rest and on dependency were increased and the venoarteriolar response decreased in both groups of patients at a significantly greater extent in postphlebitic limbs. In conclusion laser-Doppler flowmetry measurements differentiate between normal limbs and those with venous hypertension and between postphlebitic limbs and limbs with venous hypertension due to varicose veins. The increase in skin flux and decrease in venoarteriolar response may be useful to define and quantify the degree of microangiopathy and the effects of treatments in venous hypertension.
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PMID:Skin blood flux and the venoarteriolar response in the perimalleolar area in patients with venous hypertension. 149 69

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

It is known that deep venous thrombosis (DVT) of the ilio-femoro-popliteal axis is frequently associated with irreversible damage to valvular competence of the veins and consequently with varying degrees of chronic venous insufficiency. Because preservation of the valvular function of deep veins can play an important role in preventing the postphlebitic syndrome we analysed and compared the long-term functional outcome of two equally large cohorts of patients treated either surgically for restoration of venous patency and valvular function (24 patients) or medically with heparin, oral anticoagulants and compression stockings (25 patients). The study was also intended to examine the impact of duration and extent of DVT as predictive factors of late outcome. 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 measurement 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 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 3 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 group. 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 standardised leg work. The mean expelled volume was 1.1 +/- 0.5 ml/100 g/min. for the surgical group treated early for ilio-femoral DVT and 0.7 +/- 0.5 ml/100 g/min for the corresponding medical group (P = 0.05). Recovery or refilling time was 50 +/- 21 s for the surgical group and 28 +/- 26 s for the medical group (P = 0.03). Thus, the clinical and haemodynamic effect of surgical thrombectomy was significantly superior to conservative management in ilio-femoral thrombosis treated within 3 days. For extensive thrombosis treated early the advantage of surgical thrombectomy was also evident, but the difference between the two treatment groups was not significant. The advantage of surgery was however totally lost in patients operated on for extensive DVT of long duration (i.e. greater than 3 days).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Surgical thrombectomy versus conservative treatment for deep venous thrombosis; functional comparison of long-term results. 239 84

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

The consequences of chronic deep venous insufficiency are a major medical concern and result in significant loss of human productivity in addition to a significant compromise of lifestyles. The postphlebitic syndrome of chronic venous stasis and ulceration is a result of chronic venous hypertension and reflects a sequela of events occurring secondary to venous valvular insufficiency and reflux. Diagnostic techniques have advanced considerably; however, the prevention and management of this entity continue to be inadequate. Many new areas are being explored, both from a medical and a surgical perspective, and it is hoped that as clinical investigation proceeds, new conceptual approaches and techniques will arise to combat this difficult medical problem. The literature reviewed in this article reflects a spectrum of research attempting to understand the basic underlying hemodynamic as well as cellular and tissue changes that contribute to the development of postphlebitic signs and symptoms. More investigation is needed to enable us to proceed from the descriptive understanding of this entity to the mechanisms that result in this disease state. Preventive and curative management needs to succeed the current palliative approach to therapy.
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PMID:Chronic venous insufficiency. 749 65

The ulcus cruris is an ulcerative lesions caused by chronic venous stasis and chronic venous hypertension. Every pathologic obstacle to venous return can cause ulcus cruris. Ulcus could be brought back to 3 situations: postphlebitic syndrome, chronic venous insufficiency and primitive varicosities. The common denominator is always the increase in venous pressure, the appearance of reflux and venous stasis. Venous ulcers are possibly characterized by tissue degeneration and by bacterial superinfection. A particular bacterial flora is found in these injuries, it is qualitatively different from that of healthy skin. The therapy of ulcus cruris cannot leave out by its etiopathogenesis: the first treatment always consists in the stasis suppression to arrive quickly to a complete cicatricial would repair. In it three moments are recognizable: ulcus abstersion, disinfection and cicatrization. The venous ulcer is not cured when it is closed, but when it has no recurrency: the cicatrization is obtainable treating the principal causes, eliminating the venous stasis and anticipating the relapses.
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PMID:[The trophic venous ulcer. The physiopathological, microbiological and pharmacological aspects]. 802 44

A 65-year-old man was referred to our clinic for the rehabilitation of right hemiparesis caused by ischaemic stroke. Hypertension, postphlebitic syndrome of lower limbs, frequent nose bleeding, and anemia were present in his history; in his adolescence, he was treated for idiopathic hypogonadotropic hypogonadism. Further investigations have revealed also microsomia, suggesting a clinical diagnosis of Kallmann syndrome, that is, an association, possible in males and females, of hypogonadotropic hypogonadism with olfactory deficits. A definite diagnosis of hereditary hemorrhagic telangiectasia was made based on clinical criteria and confirmed by genetic analysis.
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PMID:Hypogonadotropic hypogonadism associated with hereditary hemorrhagic telangiectasia [corrected]. 2395 91

Venous thromboembolism (VTE) is a common condition that can lead to complications such as postphlebitic syndrome, chronic pulmonary artery hypertension, and death. The approach to the diagnosis of has evolved over the years and an algorithm strategy combining pretest probability, D-dimer testing, and diagnostic imaging now allows for safe, convenient, and cost-effective investigation of patients. Patients with low pretest probability and a negative D-dimer can have VTE excluded without the need for imaging. The mainstay of treatment of VTE is anticoagulation, whereas interventions such as thrombolysis and inferior vena cava filters are reserved for special situations. Low-molecular-weight heparin has allowed for outpatient management of most patients with deep vein thrombosis at a considerable cost savings to the health care system. Patients with malignancy-associated VTE benefit from decreased recurrent rates if treated with long-term low-molecular-weight heparin. The development of new oral anticoagulants further simplifies treatment. The duration of anticoagulation is primarily influenced by underlying cause of the VTE (whether provoked or not) and consideration of the risk for major hemorrhage. Testing for genetic and acquired thrombophilia may provide insight as to the cause of a first idiopathic deep vein thrombosis, but the evidence linking most thrombophilias to an increased risk of recurrent thrombosis is limited.
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PMID:The diagnosis and treatment of venous thromboembolism. 2431 19


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