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The treatments to prevent the formation of blood clots is balanced against the risk of bleeding. [5] One of the goals of blood clot prevention is to limit venous stasis as this is a significant risk factor for forming blood clots in the deep veins of the legs. [6] Venous stasis can occur during the long periods of not moving.
This valvular incompetence combined with persistent venous obstruction from thrombus increases the pressure in veins and capillaries. Venous hypertension induces a rupture of small superficial veins, subcutaneous hemorrhage [7] and an increase of tissue permeability. That is manifested by pain, swelling, discoloration, and even ulceration.
A venous ulcer tends to occur on the medial side of the leg, typically around the medial malleolus in the 'gaiter area' whereas arterial ulcer tends to occur on lateral side of the leg and over bony prominences. A venous ulcer is typically shallow with irregular sloping edges whereas an arterial ulcer can be deep and has a 'punched out' appearance.
Venous ulcers are common and very difficult to treat. Chronic venous ulcers are painful and debilitating. Even with treatment, recurrences are common if venous hypertension persists. Nearly 60% develop phlebitis which often progresses to deep vein thrombosis in more than 50% of patients. The venous insufficiency can also lead to severe hemorrhage.
Potential complications of venous stasis are: Venous ulcers; Blood clot formation in veins (venous thrombosis), that can occur in the deep veins of the legs (deep vein thrombosis, DVT) or in the superficial veins; Id reactions [1]
Oral ulcers, genital ulcers, papulopustular lesions, uveitis, superficial venous thrombosis and deep vein thrombosis. [23] Cogan’s syndrome: Interstitial keratitis, ocular redness, vertigo, and tinnitus. [24] Single-organ vasculitis [25] [8] Cutaneous small-vessel vasculitis: Palpable purpura, necrosis, ulceration, bullae, and nodules. [26]
Venous thrombi are caused mainly by a combination of venous stasis and hypercoagulability—but to a lesser extent endothelial damage and activation. [7] The three factors of stasis, hypercoagulability, and alterations in the blood vessel wall represent Virchow's triad, and changes to the vessel wall are the least understood. [8]
Aching, heavy legs [10] [11] Appearance of spider veins (telangiectasia) in the affected leg; Ankle swelling [10] [11] A brownish-yellow shiny skin discoloration near the affected veins; Redness, dryness, and itchiness of areas of skin, termed stasis dermatitis or venous eczema [11] Muscle cramps when making sudden movements, such as standing ...