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Query: UMLS:C0020538 (hypertension)
 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

Recent histological and immunocytochemical analyses of venous leg ulcers suggest that lesions observed in the different stages of chronic venous insufficiency (CVI) may be related to an inflammatory process. This inflammatory process leads to fibrosclerotic remodeling of the skin and then to ulceration. The vascular network of the most superficial layers of the skin appears to be the target of the inflammatory reaction. Hemodynamic forces such as venous hypertension, circulatory stasis, and modified conditions of shear stress appear to play an important role in an inflammatory reaction accompanied by leukocyte activation which clinically leads to CVI: venous dermatitis and venous ulceration. The leukocyte activation is accompanied by the expression of integrins and by synthesis and release of many inflammatory molecules, including proteolytic enzymes, leukotrienes, prostaglandin, bradykinin, free oxygen radicals, cytokines, and possibly other classes of inflammatory mediators. The inflammatory reaction perpetuates itself, leading to liposclerotic skin and subcutaneous tissue remodeling. In light of the mechanisms of venous ulcer formation cited above, therapy in the future might be directed against leukocyte activation in order to diminish the magnitude of the inflammatory response. With this in mind, the attention of many investigators has been drawn to two different drugs with an anti-inflammatory effect: pentoxifylline and flavonoids.
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PMID:Microcirculation and venous ulcers: a review. 1624 8

Cushing's syndrome is a condition caused by high levels of glucocorticoids, or most commonly as a result of prolonged exposure to exogenous steroids. Clinical features include diabetes, hypertension, obesity, skin atrophy, immune suppression and delayed wound healing. We report a patient with iatrogenic Cushing's syndrome, in whom long-term topical steroid therapy was used to treat varicose eczema, which contributed to the development of type 2 diabetes, morbid obesity, sleep apnoea and chronic wound sepsis. In this case, repeated hospital admissions and systemic antibiotics were associated with considerable comorbidity. Aggressive local treatment, consisting of potassium permanganate soaks and irrigating gels, was highly effective in reducing the amount of exudate, pain and preventing from further deterioration of the patient's legs.
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PMID:Cushing's syndrome and chronic venous ulceration--a clinical challenge. 2107 30

Effective management of stasis ulcer, and the frequently coexisting stasis dermatitis, depends on correct diagnosis. Significant morbidity and disability result, often over a long period of time. The usual defect involved is incompetence of the intrinsic valves in either the superficial or deep veins. Treatment is geared towards correction of venous hypertension in the lower leg, clearing of secondary infection and inflammation, protection from further injury, and correction of predisposing factors. Treatment failure is usually due to non-compliance, since many treatment methods are irksome. A simplified method, using the Unna paste boot, partly eliminates dependence on patient compliance.
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PMID:Office management of stasis ulcer and stasis dermatitis. 2128 18

A clinical model to examine the hypothesis that venous hypertension of the lower leg per se can cause lower leg stasis dermatitis is described. To prove this concept, we retrospectively studied a consecutive series of 38 patients with lower leg dermatitis who underwent phlebological examination at our consultation over a period of four years. Among those patients who had an insufficiency of the superficial veins only, without insufficiency of the deep veins, 22 had undergone patch testing to common allergens in phlebology. We found 10 patients with a stasis dermatitis of the lower leg and an incompetent great saphenous vein, six of whom had no detectable contact sensitization at all and another four exclusively to phlebologically irrelevant substances, e.g. nickel, cobalt, chromate or epoxid resin. All these 10 patients showed long saphenous vein incompetence from the groin to the medial aspect of the leg. All were operated by classical flush ligation and saphenectomy. Lower leg dermatitis healed in all 10 patients within 8-12 weeks and no recurrence was observed (1 year follow-up). These results support clinical experience that venous hypertension alone indeed can cause lower leg dermatitis.
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PMID:Evidence that venous hypertension causes stasis dermatitis. 2164 4

Stasis dermatitis commonly occurs in older age. It is caused by venous hypertension resulting from retrograde flow due to incompetent venous valves, valve destruction, or obstruction of the venous system. Further tissue changes arise from an inflammatory process mediated by metalloproteinases, which are up-regulated by ferric ion from extravasated red blood cells. Stasis dermatitis presents initially as poorly demarcated erythematous plaques of the lower legs bilaterally, classically involving the medial malleolus. It is one of the spectrum of cutaneous findings that may result from chronic venous insufficiency. Its mimics include cellulitis, contact dermatitis, and pigmented purpuric dermatoses. Duplex ultrasound is useful in demonstrating venous reflux when the clinical diagnosis of stasis dermatitis is inadequate. Conservative treatment involves the use of compression therapy directed at improving ambulatory venous pressure. Interventional therapy currently includes minimally invasive techniques such as endovenous thermal ablation and ultrasound-guided foam sclerotherapy, which have supplanted the use of open surgical techniques.
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PMID:Stasis Dermatitis: Pathophysiology, Evaluation, and Management. 2806 94

Chronic venous insufficiency (CVI) results from long-term venous hypertension in the legs caused by venous obstruction, venous valve incompetency, muscle pump dysfunction, or a combination of these. CVI occurs in 9.4% of men and 6.6% of women. It takes any of several forms, including leg pain and heaviness, leg edema that is worsened by prolonged standing and relieved by elevation, stasis dermatitis, skin fibrosis, skin ulcers, and varicose veins. If the patient history and/or physical examination results are suggestive of CVI, the diagnosis can be confirmed with duplex ultrasonography. The primary conservative treatment is use of compression stockings. Physical therapy and exercise programs often are recommended but little evidence supports their use. If a skin ulcer is present, appropriate wound care is indicated. Flavonoid drugs have been shown to improve venous function but none are approved for use in the United States. Diosmiplex, a flavonoid medical food product derived from oranges, is approved by the Food and Drug Administration for management of CVI and has shown some benefits. Patients with more severe manifestations of CVI should be referred to a vascular subspecialist for consideration of interventional therapies.
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PMID:Cardiovascular Disease: Chronic Venous Insufficiency and Varicose Veins. 3099