Venous Ulcers
- Where is the most common location for venous stasis ulcers?
- What are the distinguishing characteristics of venous stasis ulcers?
- What is the mechanism of venous stasis ulcer formation?
- What is the accepted method of treatment of venous stasis ulcers?
1. Where is the most common location for venous stasis ulcers?
The origin or center of venous stasis ulcers occurs in the anatomical location denoted as the "gaitor area". This is the area from the bulge of the gastrocnemius to the distal border of the malleolus, corresponding to the course taken by the distal saphenous vein in the medial lower leg.
Valencia IC, Falabella A, Kirsner RS, Eaglstein WH.
Chronic venous insufficiency and venous leg ulceration.
J Am Acad Dermatol. 2001 Mar;44(3):401-21; quiz 422-4. Review.
PMID: 11209109 [PubMed - indexed for MEDLINE]
Kirsner, R. et al. The Clinical Spectrum of Lipodermatosclerosis. Journal of the American
Academy of Dermatology, vol 28: no 4, 1993. 623-627.
Holloway G, Ooi S, Weingarten M. Management of venous insufficiency and ulceration. Treatment of Chronic Wounds. Number 3 in a series Curative Health Services, 1996.
Hurley JP. Chronic venous insufficiency: venous ulcers and other consequences. In: Krasner D ed. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. King of Prussia, PA: Health Management Publications lnc.;1990:213-222.
2. What are the distinguishing characteristics of venous stasis ulcers?
Venous stasis ulcers present with well defined borders, in an irregular shape (scalloped), with a ruddy color base, and often a shallow depth. The ulcer may have moderate to heavy exudates. They appear in the Gator area of the lower extremity and are often surrounded by fibrosed, indurated skin (lipodermatoslerosis). Surrounding tissue often appears hyperpigmented (reddened or brown), may have noticeable varicose veins and telengectasias, and have pitting or n0n-pitting edema. The skin should be warm to the touch, peripheral pulses should be palpable, and normal capillary refill is present. The ulcers may be partial thickness or full thickness and their base may range from red granular, white fibrolytic, to black and necrotic.
Valencia IC, Falabella A, Kirsner RS, Eaglstein WH.
Chronic venous insufficiency and venous leg ulceration.
J Am Acad Dermatol. 2001 Mar;44(3):401-21; quiz 422-4. Review.
PMID: 11209109 [PubMed - indexed for MEDLINE]
Kirsner, R. et al. The Clinical Spectrum ofLipodermatosclerosis. Journal of the American
Academy of Dermatology, vol 28: no 4, 1993. 623-627.
Melanin, K., Haapanen, A. and Havu, V. Lowered Peripheral Resistance in Arteries of
Legs With Venous Ulceration. Acta Derm Venereol, 74:1994. 110-112.
Holloway G, Ooi S, Weingarten M. Management of venous insufficiency and ulceration. Treatment of Chronic Wounds. Number 3 in a series Curative Health Services, 1996.
Hurley JP. Chronic venous insufficiency: venous ulcers and other consequences. In: Krasner D ed. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. King of Prussia, PA: Health Management Publications lnc.;1990:213-222.
To top3. What is the mechanism of venous stasis ulcer formation?
There are several theories that explain the pathological mechanism of venous ulcer formation. Two well accepted theories of venous hypertension (insufficiency) explains the formation of edema caused by incompetent venous valves, most notably in the deep venous system allowing blood to leak backward, and the increased ambulatory pressure due to a failing calf muscle pump which normally returns fluid to central circulation. The insufficiency may lie in the superficial, perforators, deep or a combination of venous systems. The fibrin cuff theorizes that there is an inhibition on oxygen transport, the trap theory states that macromolecules such as fibrinogen, alpha sub 2- macroglobin leak in to the dermis due to venous hypertension and act as a trap to inhibit endogenous growth factor from maintaining tissue integrity. The white cell trapping theory proposed that tissue hypoxia is due to an occlusion caused trapped leukocytes in the lower extremity capillaries. Tissue hypoxia may be secondary to A-V shunting as well. With any of these, the blood can pool and stasis ensues in the veins.
Valencia IC, Falabella A, Kirsner RS, Eaglstein WH.
Chronic venous insufficiency and venous leg ulceration.
J Am Acad Dermatol. 2001 Mar;44(3):401-21; quiz 422-4. Review.
PMID: 11209109 [PubMed - indexed for MEDLINE]
Labropoulos, N. et al. Venous Hemodynamic Abnormalities in Patients With Leg Ulceration. American Journal of Surgery, vol 169: no 6, 1995. 572-574.
The microcirculation in venous disease.
Angiology. 1994 Jun;45(6 Pt 2):537-41.
PMID: 8203784 [PubMed - indexed for MEDLINE]
Pericapillary fibrin cuffs in venous disease. A reappraisal.
Dermatol Surg. 1997 Oct;23(10):955-9. Review.
PMID: 9357508 [PubMed - indexed for MEDLINE]
Yang D, Vandongen YK, Stacey MC.
Changes in calf muscle function in chronic venous disease.
Cardiovasc Surg. 1999 Jun;7(4):451-6.
PMID: 10430530 [PubMed - indexed for MEDLINE]
Stacey MC, Burnand KG, Bhogal BS, Black MM.
Pericapillary fibrin deposits and skin hypoxia precede the changes of lipodermatosclerosis in limbs at increased risk of developing a venous ulcer.
Cardiovasc Surg. 2000 Aug;8(5):372-80.
PMID: 10959062 [PubMed - indexed for MEDLINE]
Current concepts in chronic venous ulceration.
Eur J Vasc Endovasc Surg. 2000 Sep;20(3):227-32. Review.
PMID: 10986019 [PubMed - indexed for MEDLINE]
Kirsner, R. et al. The Clinical Spectrum ofLipodermatosclerosis. Journal of the American Academy of Dermatology, vol 28: no 4, 1993. 623-627.
Labropoulous: Am J Surg. Volume 169 (6). June 1995.
Browse, N.L. and Burnand, K.G.: The Cause of Venous Ulceration: Lancet, 2:1982. 243-245.
Scurr, J. and Coleridge-Smith, F.R., The Microcirculation in Venous Disease. Angiology: vol 45: no 6, 1994. 537-541.
Falanga, V. and Eaglestein, W., The "Trap" Hypothesis of Venous Ulceration. The Lancet: vol 34: April 17, 1993. 1006-1008
Melanin, K., Haapanen, A. and Havu, V. Lowered Peripheral Resistance in Arteries of Legs With Venous Ulceration. Acta Derm Venereol, 74:1994. 110-112.
To top4. What is the accepted method of treatment of venous stasis ulcers?
The mainstay of therapy for venous insufficiency and venous leg ulceration is COMPRESSION, COMPRESSION, COMPRESSION. To treat edema with no ulceration, specially measured compressive stockings are your starting point. Anti -puritic creams (hydrocortisone), zinc oxide (to prevent possible infection or cracking), and possibly an antifungal (for CVI patients prone to fungal infections) are helpful prophylactants in skin that is still completely intact. Ulcerated tissue requires compression by means of an UNNA’s boot or a multi layer compression dressing. Note: patients with combined arterial and venous insufficiency (ABI 0.5-0.8) should receive less compressive pressure. This may be done by omitting one of the compressive layer wraps, which diminishes the pressure to 25-30 mm Hg rather than 40 mm Hg. Non-adherent gauze should be placed directly over the wound and use of products such as Allevyn (Smith & Nephew) or Cutinova-Foam (Biersdorf-Jobst) may be used to absorb excessive exudate.
Venous ulcers should be treated with moist wound-healing methods. Dressing changes should occur at one week or less. Patients with excessive drainage will require more frequent dressing changes. Patients should elevate their lower extremities when possible and sleep with their feet elevated about 6 inches by propping them on pillows at night. Newer modalities, such as growth factors, matrix materials, and biologically engineered tissue may be added under the compression dressing to speed the healing process in more recalcitrant ulcerations.
Margolis DJ. Management of venous ulcerations.Hosp Pract (Off Ed). 1992 May 15;27(5):32-4, 37, 41-4. Review. No abstract available.
PMID: 1577889 [PubMed - indexed for MEDLINE]
Marston WA, Carlin RE, Passman MA, Farber MA, Keagy BA.
Healing rates and cost efficacy of outpatient compression treatment for leg ulcers associated with venous insufficiency.
J Vasc Surg. 1999 Sep;30(3):491-8.
PMID: 10477642 [PubMed - indexed for MEDLINE]
Valencia IC, Falabella A, Kirsner RS, Eaglstein WH.
Chronic venous insufficiency and venous leg ulceration.
J Am Acad Dermatol. 2001 Mar;44(3):401-21; quiz 422-4. Review.
PMID: 11209109 [PubMed - indexed for MEDLINE]
Kirsner, R. et al. The Clinical Spectrum ofLipodermatosclerosis. Journal of the American
Academy of Dermatology, vol 28: no 4, 1993. 623-627.
Partsch H, Menzinger G, Mostbeck A.
Inelastic leg compression is more effective to reduce deep venous refluxes than elastic bandages.
Dermatol Surg. 1999 Sep;25(9):695-700.
PMID: 10491059 [PubMed - indexed for MEDLINE]
Lyon RT, Veith FJ, Bolton L, Machado F.
Clinical benchmark for healing of chronic venous ulcers. Venous Ulcer Study Collaborators.
Am J Surg. 1998 Aug;176(2):172-5.
PMID: 9737626 [PubMed - indexed for MEDLINE]
Douglas, W.S. and Simpson, N.B. Guidelines For The Management of Chronic Venous Ulceration, Report of a Multidisciplinary Workshop. : B.J. Dermatology. 132: 1995. 446-452.
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