Venous ulcer

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Venous ulcer
Classification and external resources
Venous ulcer dorsal leg.jpg
Venous ulcer on the back of the right leg.
ICD-10 I83.0, I83.2, L97
ICD-9 454.0
DiseasesDB 29114
MedlinePlus 000834
MeSH D014647

Venous ulcers (stasis ulcers, varicose ulcers, or ulcus cruris) are wounds that are thought to occur due to improper functioning of venous valves, usually of the legs (hence leg ulcers). They are the major occurrence of chronic wounds, occurring in 70% to 90% of leg ulcer cases.[1] Venous ulcers develop mostly along the medial distal leg, and can be very painful.

Pathophysiology[edit]

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, and blood is not pumped as effectively into or out of the area.[2][3][4][5]

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]

It is in the crus that the classic venous stasis ulcer occurs. Venous stasis results from damage to the vein valvular system in the lower extremity and in extreme cases allows the pressure in the veins to be higher than the pressure in the arteries. This pressure results in transudation of inflammatory mediators into the subcutaneous tissues of the lower extremity and subsequent breakdown of the tissue including the skin.

Wounds of the distal lower extremities arising from causes not directly related to venous insufficiency (e.g., scratch, bite, burn, or surgical incision) may ultimately fail to heal if underlying (often undiagnosed) venous disease is not properly addressed.

Characteristics[edit]

Edema and fibrinous exudate leads to fibrosis of subcutaneous tissues with localized pigment loss and dilation of capillary loops. This is called atrophic blanche. This can occur around ankles and gives an appearance of inverted champagne bottle to legs. Large ulcers may encircle the leg. Lymphoedema results from obliteration of superficial lymphatics. There is hypertrophy of overlying epidermis giving polypoid appearance, known as lipodermatosclerosis.

Diagnosis[edit]

Classification[edit]

A clinical severity score has been developed to assess chronic venous ulcers. It is based on the CEAP (clinical, etiology, anatomy, and pathophysiology) classification system developed by an expert panel. A high score gives a poor prognosis.[7]

Distinction from arterial ulcer[edit]

An arterial ulcer tends to occur on lateral side of distal leg and leg is pulseless and cool. Venous ulceration is typically seen just above the medial malleolus. Arterial ulcers are seen distally and over bony prominences.

Treatment[edit]

The main aim of the treatment is to create such an environment that allows skin to grow across an ulcer.

Bisgaard regimen[edit]

Most venous ulcers respond to a regimen called Bisgaard regimen for treating ulcers.[8] It has four components: Patient education, elevation of foot, elastic compression and evaluation.

Compression therapy[edit]

Non-elastic, ambulatory, below knee (BK) compression aggressively counters the impact of reflux on venous pump failure. 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 decrease 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.[2]

Regarding effectiveness, compression dressings improve healing.[10] It is not clear whether non-elastic systems are better than a multilayer elastic system.[10] Patients should wear as much compression as is comfortable.[11] The type of dressing applied beneath the compression does not seem to matter, and hydrocolloid is not better than simple low adherent dressings.[12][13]

Intermittent pneumatic compression devices may be used, but it is not clear that they are superior to simple compression dressings.[14]

Pentoxifylline[edit]

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".[15] It works by reducing platelet aggregation and thrombus formation.

Artificial skin[edit]

Artificial skin, made of collagen and cultured skin cells, is also used to cover venous ulcers and excrete growth factors to help them heal.[16] 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".[17]

Surgical correction of superficial venous reflux[edit]

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".[18]

TIRS Technique[edit]

Terminal Interruption of Reflux Source Technique entails blocking off the veins that drain the ulcer bed using Sotradecol or Polidocanol foam, administered by ultrasound guidance.[19]

Prognosis[edit]

Venous ulcers are costly to treat, and there is a significant chance that they will recur after healing;[1][2] one study found that up to 48% of venous ulcers had recurred by the fifth year after healing.[2]

Without proper care, the ulcer may get infected leading to cellulitis or gangrene and eventually may need amputation of the part of limb in future.

Some topical drugs used to treat venous ulcer may cause venous eczema. [20]

Current Research[edit]

The current ‘best’ practice in the UK is to treat the underlying venous reflux once an ulcer has healed. It is questionable as to whether endovenous treatment should be being offered before ulcer healing as current evidence would not support this approach as standard care. EVRA (Early Venous Reflux Ablation) ulcer trial - A UK NIHR HTA funded randomised clinical trial to compare early versus delayed endovenous treatment of superficial venous reflux in patients with chronic venous ulceration opened for recruitment in October 2013. The study hopes to show an increase in healing rates from 60% to 75% at 24 weeks. For more information please see: http://www1.imperial.ac.uk/biosurgerysurgicaltechnology/clinical_trials_outcomes/vasculardisease/clinicaltrials/evra/ or www.evrastudy.org

Additional images[edit]

References[edit]

  1. ^ a b c 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. ^ a b c d e f g h i j 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. ^ a b c 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. ^ a b c 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. ^ a b c d 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. ^ a b "eMedicine - Reperfusion Injury in Stroke : Article by Wayne M Clark, MD". Retrieved 2007-08-05. 
  7. ^ Eklöf B, Rutherford RB, Bergan JJ, et al (2004). "Revision of the CEAP classification for chronic venous disorders: consensus statement". J. Vasc. Surg. 40 (6): 1248–52. doi:10.1016/j.jvs.2004.09.027. PMID 15622385. 
  8. ^ "BMJ responses". Retrieved 3 May 2013. 
  9. ^ 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. 
  10. ^ a b Nelson EA, Cullum N, Jones J (2006). "Venous leg ulcers.". Clin Evid (15): 2607–26. PMID 16973096. 
  11. ^ 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. 
  12. ^ Palfreyman SJ, Nelson EA, Lochiel R, Michaels JA (2006). "Dressings for healing venous leg ulcers". In Palfreyman, Simon SJ. Cochrane database of systematic reviews (Online) 3: CD001103. doi:10.1002/14651858.CD001103.pub2. PMID 16855958. 
  13. ^ 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. PMC 1939774. PMID 17631512. 
  14. ^ Nelson EA, Hillman A, Thomas K (2014). "Intermittent pneumatic compression for treating venous leg ulcers.". Cochrane Database Syst Rev 5: CD001899. doi:10.1002/14651858.CD001899.pub4. PMID 24820100. 
  15. ^ Jull A, Arroll B, Parag V, Waters J (2007). "Pentoxifylline for treating venous leg ulcers". In Jull, Andrew B. Cochrane database of systematic reviews (Online) (3): CD001733. doi:10.1002/14651858.CD001733.pub2. PMID 17636683. 
  16. ^ 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.
  17. ^ Jones JE, Nelson EA (2007). "Skin grafting for venous leg ulcers". In Jones, June E. Cochrane database of systematic reviews (Online) (2): CD001737. doi:10.1002/14651858.CD001737.pub3. PMID 17443510. 
  18. ^ 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. PMC 1914523. PMID 17545185. 
  19. ^ Bush, R. New technique to heal venous ulcers: Terminal interruption of the reflux source (TIRS). Perspectives in Vascular Surgery and Endovascular Therapy. 2010;22(3). http://pvs.sagepub.com/content/22/3/194.abstract
  20. ^ Roxburgh's Common Skin Diseases, 17ed. p. 127. ISBN 9780340762325.