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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTA4NDgxMy10cmVhdG1lbnQ=\nDrugs & Diseases > Dermatology\nStasis Dermatitis Treatment & Management\nAuthor: Scott L Flugman, MD; Chief Editor: Dirk M Elston, MD more...\nSections Stasis Dermatitis\nTopical Therapy\nSystemic Therapy\nPrevention and Management of Infection\nTreatment-Related Allergic Contact Dermatitis\nAntibiotics, Other\nTopical Immunomodulators\nAlthough extensive work has been completed in the study of venous ulcer treatment, no large, well-controlled trials have examined the treatment of stasis dermatitis. The overall mainstay of treatment has always been aimed at lessening the clinical impact of the underlying venous insufficiency and edema, a goal that is typically accomplished with high-level compression therapy. [29, 30]\nStasis dermatitis related to an arteriovenous fistula or incompetent perforators may respond to ligation of the vessels.\nCombination therapy with autologous platelet-rich plasma and light-emitting diodes shows some promise in the treatment of refractory stasis ulcers. [31]\nStasis pigmentation, resulting from hemosiderin deposition, is notoriously difficult to treat and typically does not resolve even when the underlying stasis dermatitis is well controlled with topical therapy. However, some authors have reported improvement of stasis pigmentation after treatment with a noncoherent intense pulsed light (IPL) source. [32]\nAssessing the patient's peripheral arterial circulation (clinically or with a Doppler study) before recommending compression therapy is important. Adding compression to a leg with compromised arterial circulation could increase claudication and put the patient at risk for ischemic damage. [33]\nCompression accomplished by means of specialized stockings that deliver a controlled pressure gradient (measured in mm Hg) to the affected leg are suitable for long-term management of edema, but not for healing of stasis ulcers. Compression stockings should be applied early in the morning, before the patient rises from bed, in order to facilitate application when leg edema is at its lowest point.\nHigh-level compression can be performed by using elastic wraps, compression (Unna) boots, and more sophisticated devices, such as end-diastolic compression boots. Most of these modalities require administration in a physician's office or wound care center. Frequent leg elevation is a necessary adjunct to leg compression.\nAllogeneic cultured dermal substitutes have been used, but are expensive. Most patients respond to high-level compression alone. [34]\nCounseling patients regarding the use of compression therapy is vital to the successful management of stasis dermatitis. Although the benefits of compression therapy are widely recognized, patient noncompliance with regard to compression stockings remains a major barrier to treatment. Difficulty in stocking application and patient concerns about appearance are among the reasons why patients may fail to comply with this therapy. [35]\nIn addition, patients frequently resist the idea of using compression dressings and/or stockings because these modalities may cause considerable discomfort when first applied to edematous, inflamed lower extremities. However, it is important to reassure patients that the discomfort lessens considerably as leg edema is reduced and to inform them that this therapy must be maintained permanently in order to prevent a recurrence of dermatitis and leg ulcers.\nTopical treatment of stasis dermatitis has much in common with the treatment of other forms of acute eczematous dermatitis. Weeping lesions can be treated with wet to damp gauze dressings soaked with water or with a drying agent, such as aluminum acetate. Topical corticosteroids are frequently used to reduce inflammation and itching in acute flares; midpotency corticosteroids, such as triamcinolone 0.1% ointment, are generally effective. [36, 37]\nBe wary of the use of high-potency topical corticosteroids in stasis dermatitis, because the chronically inflamed skin can increase the risk of systemic absorption and because steroid-induced cutaneous atrophy can predispose the patient to ulceration. [38, 39] Furthermore, prolonged use of topical steroids can cause their efficacy to decrease, a phenomenon known as tachyphylaxis. (Systemic corticosteroids are not part of stasis dermatitis treatment, although they may be required in very severe cases of widespread autoeczematization.)\nNonsteroidal treatment\nThe nonsteroidal calcineurin inhibitors tacrolimus and pimecrolimus may prove to be useful tools in the management of stasis dermatitis. Although these topical medications are approved only for atopic dermatitis, they have been shown to be effective in many steroid-responsive dermatoses. Because the calcineurin inhibitors do not carry the risks of skin atrophy or tachyphylaxis, they have the potential to become valuable agents in the treatment of chronic dermatoses such as stasis dermatitis.\nA single-arm, interventional pilot study by Maroo et all indicated that combination therapy with topical tacrolimus and oral doxycycline may be effective against stasis dermatitis. The study evaluated treatment results in 15 patients with stasis dermatitis resulting from chronic venous insufficiency in the lower limbs. The patients were treated for 4 weeks with topical tacrolimus 0.1% and oral doxycycline 100 mg. [40]\nThe investigators found that 86.6% of the patients demonstrated improvement of the dermatitis area, while 6.7% showed no improvement, and another 6.7% experienced worsened dermatitis. Two patients showed adverse effects.\nThe researchers also found that patients had significant improvement in pain, edema, erythema, pigmentation, and exudation, as well as a statistically significant reduction in ulcer size.\nLong-term management\nPatients with chronic, quiescent stasis dermatitis can be treated with bland topical emollients to maximize epidermal moisture. Plain white petrolatum is an inexpensive occlusive moisturizer that is very effective and, importantly, does not contain any contact sensitizers.\nAlso see the guideline for venous ulcer care from the Association for the Advancement of Wound Care.\nBased on theories regarding the pathogenesis of cutaneous inflammation in venous insufficiency, systemic therapies that have been hypothesized to have beneficial modulating effects on neutrophil function have been investigated.\nTreatments that have been studied for venous ulcers, such as prostaglandin-E1 (PGE1) and pentoxifylline therapies, have been hypothesized to decrease cytokine-mediated neutrophil activation, leading to reduced inflammation. [41] However, even if these systemic therapies are proven to be unequivocally effective, it is unlikely that their use will extend beyond the scope of treatment of recalcitrant venous ulcers.\nBe wary of infection in stasis dermatitis. This becomes more problematic when using topical corticosteroids, which make the patient more susceptible to infection. Open excoriations and erosions should be treated with a topical antibiotic, such as bacitracin or Polysporin. Obvious superficial impetiginization should be treated with topical mupirocin or a systemic antibiotic with activity against Staphylococcus and Streptococcus species (eg, dicloxacillin, cephalexin, cefadroxil, levofloxacin).\nCulture with sensitivity testing is important when managing suspected superinfection, because community-acquired methicillin resistance is becoming increasingly prevalent. Expanded coverage may be necessary in patients who are immunocompromised.\nSuspected deep cellulitis should always be treated with oral or intravenous antibiotics. Necrotizing fasciitis would be a rare complication but is a surgical emergency.\nThe development of contact dermatitis is especially problematic in the treatment of patients with stasis dermatitis. Chronic inflammation of the skin, coupled with the use of multiple topical medications (prescription and over-the-counter), frequently results in contact sensitization as a complication of stasis dermatitis. In addition, patients may become sensitized to rubber products found in some wraps and stockings.\nSome of the most frequent contact allergens complicating stasis dermatitis include the topical antibiotics neomycin and bacitracin. Patients should be instructed against applying over-the-counter antibiotics or other topical agents without the direction of a physician.\nProducts based on the antimicrobial agent triclosan have been shown to present a low risk for contact sensitization in patients with stasis dermatitis. These products may be a good alternative to decrease bacterial colonization, especially in patients who have a history of cellulitis or other cutaneous infections. [42]\nTopical corticosteroid allergy, while uncommon, is a condition that can worsen stasis dermatitis despite seemingly appropriate prescription therapy.\nConsider contact dermatitis in any patient with stasis dermatitis who becomes clinically worse despite appropriate topical treatment.\nStasis dermatitis is a chronic condition. Acute exacerbations of this disorder should be closely monitored with weekly office visits, with careful observation for signs of infection. However, patients with long-standing stasis dermatitis may be able to manage the disease on their own with the use of compression stockings, elevation, proper skin care, and short courses of topical steroids for inflammatory exacerbations. The clinician must be vigilant in treating any signs of cutaneous ulceration with close follow-up care to ensure that ulceration does not become a chronic problem.\nUncomplicated stasis dermatitis is usually managed in the dermatologist's office. However, a consultation with a vascular surgeon may be required, especially when an underlying surgically correctable vascular abnormality is suspected.\nA consultation with a hematologist may be needed when treating a patient with stasis dermatitis due to deep venous thrombosis; cases such as these may be secondary to congenital or acquired hypercoagulable states.\nDavid CV, Chira S, Eells SJ, Ladrigan M, Papier A, Miller LG, et al. Diagnostic accuracy in patients admitted to hospitals with cellulitis. Dermatol Online J. 2011 Mar 15. 17(3):1. [Medline].\nSundaresan S, Migden MR, Silapunt S. Stasis Dermatitis: Pathophysiology, Evaluation, and Management. Am J Clin Dermatol. 2017 Jun. 18 (3):383-390. [Medline].\nBryan LJ, Callas PW, Criqui MH, Cushman M. Higher soluble P-selectin is associated with chronic venous insufficiency: The San Diego Population Study. Thromb Res. 2012 Aug 11. [Medline].\nCheatle TR, McMullin GM, Farrah J, Smith PD, Scurr JH. Skin damage in chronic venous insufficiency: does an oxygen diffusion barrier really exist?. J R Soc Med. 1990 Aug. 83(8):493-4. [Medline]. [Full Text].\nDodd HJ, Gaylarde PM, Sarkany I. Skin oxygen tension in venous insufficiency of the lower leg. J R Soc Med. 1985 May. 78(5):373-6. [Medline]. [Full Text].\nFalanga V, Moosa HH, Nemeth AJ, Alstadt SP, Eaglstein WH. Dermal pericapillary fibrin in venous disease and venous ulceration. Arch Dermatol. 1987 May. 123(5):620-3. [Medline].\nPappas PJ, You R, Rameshwar P, et al. Dermal tissue fibrosis in patients with chronic venous insufficiency is associated with increased transforming growth factor-beta1 gene expression and protein production. J Vasc Surg. 1999 Dec. 30(6):1129-45. [Medline].\nPeschen M, Lahaye T, Hennig B, Weyl A, Simon JC, Vanscheidt W. Expression of the adhesion molecules ICAM-1, VCAM-1, LFA-1 and VLA-4 in the skin is modulated in progressing stages of chronic venous insufficiency. Acta Derm Venereol. 1999 Jan. 79(1):27-32. [Medline].\nCheatle TR, Scott HJ, Scurr JH, Coleridge Smith PD. White cells, skin blood flow and venous ulcers. Br J Dermatol. 1991 Sep. 125(3):288-90. [Medline].\nColeridge Smith PD, Thomas P, Scurr JH, Dormandy JA. Causes of venous ulceration: a new hypothesis. Br Med J (Clin Res Ed). 1988 Jun 18. 296(6638):1726-7. [Medline]. [Full Text].\nHerouy Y, Mellios P, Bandemir E, et al. Inflammation in stasis dermatitis upregulates MMP-1, MMP-2 and MMP-13 expression. J Dermatol Sci. 2001 Apr. 25(3):198-205. [Medline].\nBeauregard S, Gilchrest BA. A survey of skin problems and skin care regimens in the elderly. Arch Dermatol. 1987 Dec. 123(12):1638-43. [Medline].\nWeismann K, Krakauer R, Wanscher B. Prevalence of skin diseases in old age. Acta Derm Venereol. 1980. 60(4):352-3. [Medline].\nBeebe-Dimmer JL, Pfeifer JR, Engle JS, Schottenfeld D. The epidemiology of chronic venous insufficiency and varicose veins. Ann Epidemiol. 2005 Mar. 15(3):175-84. [Medline].\nChiesa R, Marone EM, Limoni C, Volonté M, Schaefer E, Petrini O. Chronic venous insufficiency in Italy: the 24-cities cohort study. Eur J Vasc Endovasc Surg. 2005 Oct. 30(4):422-9. [Medline].\nDooms-Goossens A, Degreef H, Parijs M, Maertens M. A retrospective study of patch test results from 163 patients with stasis dermatitis or leg ulcers. II. Retesting of 50 patients. Dermatologica. 1979. 159(3):231-8. [Medline].\nGooptu C, Powell SM. The problems of rubber hypersensitivity (Types I and IV) in chronic leg ulcer and stasis eczema patients. Contact Dermatitis. 1999 Aug. 41(2):89-93. [Medline].\nJappe U, Schnuch A, Uter W. Frequency of sensitization to antimicrobials in patients with atopic eczema compared with nonatopic individuals: analysis of multicentre surveillance data, 1995-1999. Br J Dermatol. 2003 Jul. 149(1):87-93. [Medline].\nMorris SD, Rycroft RJ, White IR, Wakelin SH, McFadden JP. Comparative frequency of patch test reactions to topical antibiotics. Br J Dermatol. 2002 Jun. 146(6):1047-51. [Medline].\nErfurt-Berge C, Geier J, Mahler V. The current spectrum of contact sensitization in patients with chronic leg ulcers or stasis dermatitis - new data from the Information Network of Departments of Dermatology (IVDK). Contact Dermatitis. 2017 Feb 14. [Medline].\nErfurt-Berge C, Geier J, Mahler V. The current spectrum of contact sensitization in patients with chronic leg ulcers or stasis dermatitis - new data from the Information Network of Departments of Dermatology (IVDK). Contact Dermatitis. 2017 Sep. 77 (3):151-158. [Medline].\nIsoda H, Shimauchi T, Ogaki T, et al. Stasis ulcer and dermatitis caused by artificial arteriovenous fistula created 33 years previously for the treatment of poliomyelitis. Clin Exp Dermatol. 2006 May. 31(3):470-2. [Medline].\nGosnell AL, Nedorost ST. Stasis dermatitis as a complication of amlodipine therapy. J Drugs Dermatol. 2009 Feb. 8(2):135-7. [Medline].\nWeaver J, Billings SD. Initial presentation of stasis dermatitis mimicking solitary lesions: a previously unrecognized clinical scenario. J Am Acad Dermatol. 2009 Dec. 61(6):1028-32. [Medline].\nHuang TM, Lee JY. Lipodermatosclerosis: a clinicopathologic study of 17 cases and differential diagnosis from erythema nodosum. J Cutan Pathol. 2009 Apr. 36(4):453-60. [Medline].\nDavid CV, Chira S, Eells SJ, Ladrigan M, Papier A, Miller LG. Diagnostic accuracy in patients admitted to hospitals with cellulitis. Dermatol Online J. 2011. 17(3):1. [Medline].\nKeller EC, Tomecki KJ, Chadi Alraies M. Distinguishing cellulitis from its mimics. Cleve Clin J Med. 2012 Aug. 79(8):547-52. [Medline].\nKirsner RS, Pardes JB, Eaglstein WH, Falanga V. The clinical spectrum of lipodermatosclerosis. J Am Acad Dermatol. 1993 Apr. 28(4):623-7. [Medline].\nTrayes KP, Studdiford JS, Pickle S, Tully AS. Edema: diagnosis and management. Am Fam Physician. 2013 Jul 15. 88(2):102-10. [Medline].\nSundaresan S, Migden MR, Silapunt S. Stasis Dermatitis: Pathophysiology, Evaluation, and Management. Am J Clin Dermatol. 2017 Jan 6. [Medline].\nPark KY, Kim IS, Yeo IK, Kim BJ, Kim MN. Treatment of refractory venous stasis ulcers with autologous platelet-rich plasma and light-emitting diodes: a pilot study. J Dermatolog Treat. 2013 Oct. 24(5):332-5. [Medline].\nPimentel CL, Rodriguez-Salido MJ. Pigmentation due to stasis dermatitis treated successfully with a noncoherent intense pulsed light source. Dermatol Surg. 2008 Jul. 34(7):950-1. [Medline].\nDillon RS. Treatment of resistant venous stasis ulcers and dermatitis with the end-diastolic pneumatic compression boot. Angiology. 1986 Jan. 37(1):47-56. [Medline].\nTaniguchi T, Amoh Y, Tanabe K, Katsuoka K, Kuroyanagi Y. Treatment of intractable skin ulcers caused by vascular insufficiency with allogeneic cultured dermal substitute: a report of eight cases. J Artif Organs. 2012 Mar. 15(1):77-82. [Medline].\nRaju S, Hollis K, Neglen P. Use of compression stockings in chronic venous disease: patient compliance and efficacy. Ann Vasc Surg. 2007 Nov. 21(6):790-5. [Medline].\nCheatle TR, Scurr JH, Smith PD. Drug treatment of chronic venous insufficiency and venous ulceration: a review. J R Soc Med. 1991 Jun. 84(6):354-8. [Medline].\nDissemond J, Knab J, Lehnen M, Franckson T, Goos M. Successful treatment of stasis dermatitis with topical tacrolimus. Vasa. 2004 Nov. 33(4):260-2. [Medline].\nWilkinson SM, English JS. Hydrocortisone sensitivity: clinical features of fifty-nine cases. J Am Acad Dermatol. 1992 Nov. 27(5 Pt 1):683-7. [Medline].\nWilkinson SM. Hypersensitivity to topical corticosteroids. Clin Exp Dermatol. 1994 Jan. 19(1):1-11. [Medline].\nMaroo N, Choudhury S, Sen S, Chatterjee S. Oral doxycycline with topical tacrolimus for treatment of stasis dermatitis due to chronic venous insufficiency: A pilot study. Indian J Pharmacol. 2012 Jan. 44(1):111-3. [Medline]. [Full Text].\nPascarella L, Schonbein GW, Bergan JJ. Microcirculation and venous ulcers: a review. Ann Vasc Surg. 2005 Nov. 19(6):921-7. [Medline].\nSchena D, Papagrigoraki A, Girolomoni G. Sensitizing potential of triclosan and triclosan-based skin care products in patients with chronic eczema. Dermatol Ther. 2008 Oct. 21 Suppl 2:S35-8. [Medline].\nThis patient exhibits the classic hyperpigmentation and varicosities of stasis dermatitis. There is inflammatory eczematous change overlying the medial ankle, with healed scarring from recent ulceration.\nThis patient with chronic stasis dermatitis exhibits classic features, such as erythema, hyperpigmentation, and dilated superficial veins reflecting poor function of the deep venous system. The condition is typically confined to the lower leg, particularly the medial portion of the leg.\nPatient with stasis dermatitis. The large scar on the calf resulted from military shrapnel. Injuries to the venous system due to trauma or surgery are common factors in the development of stasis dermatitis.\nScott L Flugman, MD Consulting Staff, Dermatology Associates of Huntington, PC\nScott L Flugman, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa\nRichard A Clark, MD Professor of Biomedical Engineering, Dermatology and Medicine, Stony Brook University; Director of Burn, Nonscar Healing Program RCCC, Armed Forces Institute of Regenerative Medicine\nRichard A Clark, MD is a member of the following medical societies: American Association for the Advancement of Science, American Society for Clinical Investigation, Alpha Omega Alpha, Wound Healing Society, American Academy of Allergy Asthma and Immunology, American Academy of Dermatology, Association of Clinical Scientists, New York Academy of Medicine, Society for Investigative Dermatology\nDirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine\nDirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology\nJeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio\nJeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society\nJean-Hilaire Saurat, MD Chair, Professor, Department of Dermatology, University of Geneva, Switzerland\nJean-Hilaire Saurat, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, and Society for Investigative Dermatology\nRichard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA\nRichard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association\nencoded search term (Stasis Dermatitis) and Stasis Dermatitis\nDeep Venous Thrombosis (DVT)\nDeep Venous Thrombosis Prophylaxis in Orthopedic Surgery\nAnticoagulation in Deep Venous Thrombosis\nDeep Venous Thrombosis Risk Stratification\nImaging in Deep Venous Thrombosis of the Lower Extremity\nHeparin Use in Deep Venous Thrombosis\nPercutaneous Transcatheter Treatment of Deep Venous Thrombosis\nTreatment of Anemia in Patients With Renal Disease Reviewed\nTailored Doses of Enoxaparin Better Prevent VTE After Cancer Surgery\nDeep Vein Thrombosis Risk Declines After Bariatric Surgery\nRed, Hot, and Swollen Foot in Diabetes: Charcot or No?\nAccording to Dermatologists\nCollagen: 'Fountain of Youth' or Edible Hoax?\nEvidence Growing That Eczema Itch More Than Skin Deep\nShingrix for Herpes Zoster: A Review\nSkin, Hair and Nail Supplements\nSunscreen Photoprotection and Vitamin D Status\n2002 1911303-overview Diseases & Conditions\nDiseases & Conditions Deep Venous Thrombosis (DVT)\nNews Deep Vein Thrombosis Risk Declines After Bariatric Surgery\n2002 1268573-overview Procedures\nProcedures Deep Venous Thrombosis Prophylaxis in Orthopedic Surgery\nDiseases & Conditions Anticoagulation in Deep Venous Thrombosis"