Venous ulcer
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Template:WikiDoc Cardiology News Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Chronic venous ulcers are formed due to the deformed venous valves causing back flow of the blood and stasis of the venous blood. Management of venous ulcers include education, elevation, elastic compression and evaluation. Antibiotic therapy are reserved for the ulcers with secondary infection.
Venous Ulcers
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.[1]
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.[2][3][4][5] 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,[2][3][4][5] 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.[2][5] 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.[2] 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.[2][5] Buildup of white blood cells in small blood vessels may also plug the vessels, further contributing to ischemia.[6] This blockage of blood vessels by leukocytes may be responsible for the "no reflow phenomenon," in which ischemic tissue is never fully reperfused.[6] Allowing blood to flow back into the limb, for example by elevating it, is necessary but also contributes to reperfusion injury.[3] Other comorbidities may also be the root cause of venous ulcers.[4]
Treatment
Venous ulcers are costly to treat, and there is a significant chance that they will reoccur after healing;[1][2] one study found that up to 48% of venous ulcers had recurred by the fifth year after healing.
Ulcerated Skin: Venous/Arterial Insufficiency; Pressure With Secondary Infection (Infected Decubiti) Treatment
- Ulcerated skin: venous/arterial insufficiency; pressure with secondary infection (infected decubiti) treatment[7]
- Preferred regimen (1): Imipenem 0.5 g IV q6h (OR Meropenem 1 g IV q24h OR Doripenem 500 mg IV q8h)
- Preferred regimen (2): Ticarcillin-Clavulanate 3.1 g IV q8h
- Preferred regimen (3): Piperacillin-Tazobactam 3.375 g IV q6h
- Preferred regimen (4): Ertapenem 1 g IV q24h
- Alternative regimen (1): Ciprofloxacin 500 mg PO bid OR Levofloxacin PO 500 mg qd AND Metronidazole 500 mg PO qid
- Alternative regimen (2): Cefepime 2 g IV q12h OR Ceftazidime 2 g IV q8h AND Metronidazole 500 mg PO qid
- Note (1): If gram positive cocci on gram stain add Vancomycin.
- Note (2): If the ulcer is inflamed, treat with parenteral antibiotics with no topical treatment.
- Note (3): If the ulcer is not clinically inflamed, consider debridement, removal of foreign body, reduce the pressure for weight bearing limbs and leg elevation.
- Note (4): If not inflamed, healing improved on air bed, protein supplement, radiant heat and electric stimulation.
- Note (5): Avoid chlorhexidine and povidone iodine as it may harm the granulation tissue.
Bisgaard regimen
Most venous ulcers respond to a regimen called Bisgaard regimen for treating ulcers.[citation needed] Best remembered as a mnemonic 4E's - education, elevation, elastic compression and evaluation.
Compression therapy
Non-elastic, ambulatory, below knee (BK) compression aggressively counters the impact of reflux on venous pump failure.[8] 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.[2] Compression is also used [2][9] 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.[1]
Compression is applied using elastic bandages or boots specifically designed for the purpose. It is not clear whether non-elastic systems are better than a multilayer elastic system. Patients should wear as much compression as is comfortable. [10] The type of dressing applied beneath the compression does not seem to matter, and hydrocolloid is not better than simple low adherent dressings.[11][12]
Pentoxifylline
A meta-analysis of randomized controlled trials by the Cochrane Collaboration found that "Pentoxifylline is an effective adjunct to compression bandaging for treating venous ulcers and may be effective in the absence of compression".[13]
Artificial skin
Artificial skin, made of collagen and cultured skin cells, is also used to cover venous ulcers and excrete growth factors to help them heal.[14] A meta-analysis of randomized controlled trials by the Cochrane Collaboration concluded "Bilayer artificial skin, used in conjunction with compression bandaging, increases the chance of healing a venous ulcer compared with compression and a simple dressing".[15]
Surgical correction of superficial venous reflux
A randomized controlled trial found that surgery "reduces the recurrence of ulcers at four years and results in a greater proportion of ulcer free time".[16]
See Also
References
- ↑ 1.0 1.1 1.2 Snyder RJ (2005). "Treatment of nonhealing ulcers with allografts". Clin. Dermatol. 23 (4): 388–95. doi:10.1016/j.clindermatol.2004.07.020. PMID 16023934.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Brem H, Kirsner RS, Falanga V (2004). "Protocol for the successful treatment of venous ulcers". Am. J. Surg. 188 (1A Suppl): 1–8. doi:10.1016/S0002-9610(03)00284-8. PMID 15223495.
- ↑ 3.0 3.1 3.2 Mustoe T (2004). "Understanding chronic wounds: a unifying hypothesis on their pathogenesis and implications for therapy". Am. J. Surg. 187 (5A): 65S–70S. doi:10.1016/S0002-9610(03)00306-4. PMID 15147994.
- ↑ 4.0 4.1 4.2 Moreo K (2005). "Understanding and overcoming the challenges of effective case management for patients with chronic wounds". The Case manager. 16 (2): 62–3, 67. doi:10.1016/j.casemgr.2005.01.014. PMID 15818347.
- ↑ 5.0 5.1 5.2 5.3 Stanley AC, Lounsbury KM, Corrow K; et al. (2005). "Pressure elevation slows the fibroblast response to wound healing". J. Vasc. Surg. 42 (3): 546–51. doi:10.1016/j.jvs.2005.04.047. PMID 16171604.
- ↑ 6.0 6.1 "eMedicine - Reperfusion Injury in Stroke : Article by Wayne M Clark, MD".
- ↑ Greer N, Foman NA, MacDonald R, Dorrian J, Fitzgerald P, Rutks I; et al. (2013). "Advanced wound care therapies for nonhealing diabetic, venous, and arterial ulcers: a systematic review". Ann Intern Med. 159 (8): 532–42. doi:10.7326/0003-4819-159-8-201310150-00006. PMID 24126647. Review in: Evid Based Med. 2014 Jun;19(3):91
- ↑ 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. "Venous Stasis Ulcer".
- ↑ Taylor JE, Laity PR, Hicks J; et al. (2005). "Extent of iron pick-up in deforoxamine-coupled polyurethane materials for therapy of chronic wounds". Biomaterials. 26 (30): 6024–33. doi:10.1016/j.biomaterials.2005.03.015. PMID 15885771.
- ↑ Nelson EA, Harper DR, Prescott RJ, Gibson B, Brown D, Ruckley CV (2006). "Prevention of recurrence of venous ulceration: randomized controlled trial of class 2 and class 3 elastic compression". J. Vasc. Surg. 44 (4): 803–8. doi:10.1016/j.jvs.2006.05.051. PMID 17012004.
- ↑ Palfreyman SJ, Nelson EA, Lochiel R, Michaels JA (2006). "Dressings for healing venous leg ulcers". Cochrane database of systematic reviews (Online). 3: CD001103. doi:10.1002/14651858.CD001103.pub2. PMID 16855958.
- ↑ Palfreyman S, Nelson EA, Michaels JA (2007). "Dressings for venous leg ulcers: systematic review and meta-analysis". BMJ. 335 (7613): 244. doi:10.1136/bmj.39248.634977.AE. PMID 17631512.
- ↑ Jull A, Arroll B, Parag V, Waters J (2007). "Pentoxifylline for treating venous leg ulcers". Cochrane database of systematic reviews (Online) (3): CD001733. doi:10.1002/14651858.CD001733.pub2. PMID 17636683.
- ↑ 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.
- ↑ Jones JE, Nelson EA (2007). "Skin grafting for venous leg ulcers". Cochrane database of systematic reviews (Online) (2): CD001737. doi:10.1002/14651858.CD001737.pub3. PMID 17443510.
- ↑ Gohel MS, Barwell JR, Taylor M; et al. (2007). "Long term results of compression therapy alone versus compression plus surgery in chronic venous ulceration (ESCHAR): randomised controlled trial". BMJ. 335 (7610): 83. doi:10.1136/bmj.39216.542442.BE. PMID 17545185.