Venous ulcer

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Venous ulcer
Classifications and external resources
DiseasesDB 29114
MedlinePlus 000834

Venous ulcers are wounds that are thought to occur due to improper functioning of valves in the veins usually of the legs. They are the major cause of chronic wounds, occurring in 70% to 90% of chronic wound cases (Snyder, 2005).

[edit] Pathophysiology

The exact etiology of venous ulcers is not certain, but they are thought to arise when venous valves that exist to prevent backflow of blood do not function properly, causing the pressure in veins to increase (Brem et al., 2004; Mustoe, 2004; Moreo, 2005; Stanley et al., 2005). The body needs the pressure gradient between arteries and veins in order for the heart to pump blood forward through arteries and into veins. When venous hypertension exists, arteries no longer have significantly higher pressure than veins, blood is not pumped as effectively into or out of the area (Brem et al., 2004; Mustoe, 2004; Moreo, 2005; Stanley et al., 2005) and it pools.

Venous hypertension may also stretch veins and allow blood proteins to leak into the extravascular space, isolating extracellular matrix (ECM) molecules and growth factors, preventing them from helping to heal the wound (Brem et al., 2004; Stanley et al., 2005). Leakage of fibrinogen from veins as well as deficiencies in fibrinolysis may also cause fibrin to build up around the vessels, preventing oxygen and nutrients from reaching cells (Brem et al., 2004). Venous insufficiency may also cause white blood cells (leukocytes) to accumulate in small blood vessels, releasing inflammatory factors and reactive oxygen species (ROS, free radicals) and further contributing to chronic wound formation (Brem et al., 2004; Stanley et al., 2005). Buildup of white blood cells in small blood vessels may also plug the vessels, further contributing to ischemia (Clark, 2005). This blockage of blood vessels by leukocytes may be responsible for the "no reflow phenomenon," in which ischemic tissue is never fully reperfused (Clark, 2005). Allowing blood to flow back into the limb, for example by elevating it, is necessary but also contributes to reperfusion injury (Mustoe, 2004). Other comorbidities may also be the root cause of venous ulcers (Moreo, 2005).

[edit] Treatment

Venous ulcers are costly to treat, and there is a significant chance that they will reoccur after healing (Brem et al., 2004; Snyder, 2005); one study found that up to 48% of venous ulcers had recurred by the fifth year after healing (Brem et al., 2004).

Non-elastic, ambulatory, below knee (BK) compression aggressively counters the impact of reflux on venous pump failure (McDonagh, 2005). Compression therapy is used for venous leg ulcers and can decrease blood vessel diameter and pressure, which increases their effectiveness, preventing blood from flowing backwards (Brem et al., 2004). Compression is also used (Brem et al., 2004; Taylor et al., 2005) to increase release of inflammatory cytokines, lower the amount of fluid leaking from capillaries and therefore prevent swelling, and prevent clotting by decreasing activation of thrombin and increasing that of plasmin (Snyder, 2005). Compression is applied using elastic bandages or boots specificially designed for the purpose (Brem et al., 2004).

Artificial skin, made of collagen and cultured skin cells, is also used to cover venous ulcers and excrete growth factors to help them heal (Mustoe, 2005).

[edit] References

  1. Brem H, Kirsner RS, and Falanga V. 2004. Protocol for the successful treatment of venous ulcers. The American Journal of Surgery, Volume 188, Issue 1, Supplement 1, Pages 1-8.
  2. Clark WM. 2005. Reperfusion Injury in Stroke. Emedicine.com. Available.
  3. Moreo K. 2005. Understanding and overcoming the challenges of effective case management for patients with chronic wounds. The Case Manager, Volume 16, Issue 2, Pages 62-67.
  4. Mustoe T. 2004. Understanding chronic wounds: a unifying hypothesis on their pathogenesis and implications for therapy. The American Journal of Surgery, Volume 187, Issue 5, Supplement 1, Pages S65-S70.
  5. Mustoe T. 2005. Dermal ulcer healing: Advances in understanding. Presented at meeting: Tissue repair and ulcer/wound healing: molecular mechanisms,therapeutic targets and future directions. Paris, France, March 17-18, 2005. Available.
  6. Snyder RJ. 2005. Treatment of nonhealing ulcers with allografts. Clinics in Dermatology, Volume 23, Issue 4, Pages 388-395.
  7. Stanley AC, Lounsbury KM, Corrow K, Callas PW, Zhar R, Howe AK, and Ricci MA. 2005. Pressure elevation slows the fibroblast response to wound healing. Journal of Vascular Surgery, Volume 42, Issue 3, Pages 546-551.
  8. B. McDonagh, S. Sorenson, A. Cohen, T. Eaton, D.E. Huntley, M. Schul, C. Martin, C. Gray, P. Putterman, T. King, J.L. Harry, R.C. Guptan. 2005. Non-elastic, BK, ambulatory compression with sequential duplex ultrasound-guided sclerotherapy appears to be highly efficacious in venous stasis ulcer management. Venous Leg Ulcers
  9. Taylor JE, Laity PR, Hicks J, Wong SS, Norris K, Khunkamchoo P, Johnson AF, and Cameron RE. 2005. Extent of iron pick-up in deforoxamine-coupled polyurethane materials for therapy of chronic wounds. Biomaterials, Volume 26, Issue 30, Pages 6024-6033.
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