Any condition that obstructs normal venous drainage will lead to a backlog of blood which will increase the pressure within the veins. This increased pressure damages venous valves which have a poor ability to recovery. As a result an episode of acute venous hypertension may result in a permanent reduction in the efficiency of the venous return mechanisms. Reduced efficiency of the venous return will lead to a chronic increase in the pressure within the effected peripheral veins. These factors explain why DVT is the most important pathogenic mechanism in the causation of chronic venous insufficiency. This insufficiency can contribute to the development of varicose veins and venous leg ulcers.
As a result of the venous insufficiency there is a chronic backlog of blood in the peripheral veins. As the volume of blood in the veins increases so does the pressure. Increased hydrostatic pressure in the veins also increases hydrostatic pressure in the capillaries. A backlog of blood in the capillaries reduces the rate of circulation, as arterial blood is not able to enter efficiently. This results in a reduction in the delivery of oxygen and nutrients to the tissue as well as inhibiting the removal of waste products such as carbon dioxide and nitrates.
Increased pressure in the venous ends of the capillaries also reduce the rate of reabsorption of tissue fluid; this increases the volume of tissue fluid, resulting in edema. Edema in tissue increases the volume of fluid through which nutrients must diffuse in order to pass from the capillaries into the cells. Also edematous swelling increases the diffusional distance from blood to tissue cells. This reduces the efficiency of transporting oxygen and nutrients to cells and removing carbon dioxide and other metabolic waste products. Both of these effects reduce the viability of tissue cells in the presence of edema.
Increased pressure in a capillary will also lead to dilation of the vessel. This will stretch the capillary walls and widen the gaps between individual endothelial cells. Increased capillary pore size allows larger molecules such as proteins to migrate from blood into the tissue spaces. One of these plasma proteins is fibrinogen which can easily pass through these enlarged pores. Once in the tissue fibrinogen is converted into the clotting protein fibrin. Fibrin is composed of long sticky strands which form a cuff around a dilated capillary. My researchers believe that the presence of such a “fibrin cuff” further reduces the interchange of oxygen, nutrients and waste products between capillary blood and tissue fluids which furthers reduces tissue viability and often result in leg ulcers.
Leg ulcers are classified according to their causes. Chronic venous hypertension caused by venous insufficiency is the most common cause and are called venous ulcers. Ulcers may also be caused by chronic ischemia as seen in peripheral vascular disease; these are termed as arterial ulcers. Leg ulcers are also seen as a long-term complication of diabetes mellitus; such lesions are therefore classified as diabetic ulcers. Diabetic ulcers may be primarily ischemic or neuropathic. Rheumatic ulcers may occur as a complication of rheumatoid vasculitis.
Venous hypertension causes dilation of capillaries which allows red blood cells to escape into the tissue through dilated capillary walls. Over time this leads to a characteristic brown staining caused by the presence of hemosiderin, a breakdown product of hemoglobin. Venous ulcers are typically described as wet as tissue fluid oozes onto the wound bed. The ulcers are usually shallow with diffuse edges and edema is often present in the whole limb. Venous ulcers are usually painful. It is important to decide if a given ulcer is venous or arterial. If an ulcer is purely venous then the arterial blood supply will be normal. Quality of the arterial supply should be assessed by determination an ankle brachial index (ABI). This assessment is vital as arterial ulcers must not receive compression therapy. In a purely venous ulcer, the ABI will be greater than 0.9. In practice some patients have both venous and arterial insufficiency in the same leg; this can give rise to a mixture of venous and arterial features. Such ulcers are described as having a mixed or arterial etiology.
The treatment of venous ulcers requires compression therapy. Leg compression progressively compresses leg veins and also improves venous return by supporting the calf pump. If the venous return is improved the adverse effects of chronic venous hypertension are relieved. In addition to aiding healing, compression also significantly reduces the risk of recurrence of venous ulcers. Compression therapy can be broken down into two types; elastic and inelastic. It is important to understand that inelastic (or nonelastic) compression therapy (Unna Boot) is only effective for actively ambulating patients, as it only supports the calf pump. These patients must also have 45O of ankle movement in order for the calf pump to be fully engaged. Non-ambulating or patients with less than 45O of ankle movement should be treated with elastic compression therapy that is appropriate for their corresponding ABI. Tubular sleeves should never be used as compression therapy, as these products reverse the pressure gradient, by providing more pressure at the knee than at the ankle.
References
1. Bryant, R. A., & Nix, D. P., (Eds.). (2012). Acute & chronic wounds: current management concepts. (4th Ed.). St. Louis: Mosby.
2. Campbell J. (2006) Campbell’s pathophysiology notes. Carlisle: Lorimer, UK.
3. Krasner, D.L. (Ed). (2014). Chronic wound care: the essentials. A clinical source book for healthcare professional. Wayne: HMP.
4. Gloviczki P., (Ed). (2009). Hand book of venous disorders; Guidelines of the American venous forum. Hodder: Hachette UK.
5. Partsch H., Rabe E., & Stemmer R. (Eds). (2000). Compression therapy of the extremities. phlébologiques françaises: Paris, FR.