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How to Differentiate Hemosiderin Staining

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How to Differentiate Hemosiderin Staining What’s causing your patient’s lower-extremity redness? How to differentiate hemosiderin staining, lipodermatosclerosis, In left image, note pronounced varicose veins and hemosiderin staining in gaiter area (ankle to venous dermatitis, and knee) of light-skinned patient. In right image, note similar conditions hemosiderin staining in dark-skinned patient and medial ankle flare of dilated small veins By Robyn Bjork, MPT, CWS, WCC, CLT-LANA associated with chronic venous hypertension. he ability to understand or “read” lower-extremity redness in your pa - Ttient is essential to determining its cause and providing effective treatment. Redness can occur in multiple condi - tions—hemosiderin staining, lipoder - matosclerosis, venous dermatitis, chronic inflammation, cellulitis, and dependent ru - Note inverted champagne-bottle appearance of bor. This article provides clues to help you leg and ankle, indicating chronic lipodermato - sclerosis. Also note lumpy, bumpy skin (papillo - differentiate these conditions and identify matosis) and thickened, fibrotic skin with positive the specific cause of your patient’s lower- Stemmer’s sign, which indicate secondary phle - extremity redness. bolymphedema. Redness results from chronic in - flammation and resolves with compression ther - Hemosiderin staining and apy and manual lymphatic drainage. lipodermatosclerosis Hemosiderin staining is dark purple or dermatosclerosis may be misdiagnosed as rusty discoloration of the lower legs cellulitis. Active lipodermatosclerosis caus - caused by chronic venous disease. A 2010 es painful, sharply demarcated red patch - study found hemosiderin staining in all es on medial aspects of the lower leg. subjects with lipodermatosclerosis and ve - Unlike in cellulitis, redness in lipoder - nous ulcers. When vein valves fail, regurgi - matosclerosis is localized to areas of he - tated blood forces red blood cells (RBCs) mosiderin staining and induration. Also, out of capillaries. Dead RBCs release iron, the skin isn’t hot and the patient is which is stored in tissues as hemosiderin, afebrile and unresponsive to antibiotics. staining the skin. Lipodermatosclerosis progresses to fibro - Hemosiderin staining and active lipo - sis and constriction, causing an inverted 16 www.WoundCareAdvisor.com Wound Care Advisor July/August 2013 • Volume 2, Number 4 • champagne-bottle appearance of the legs. common in patients with lower-extremity Treat active lipodermatosclerosis with venous disease. Signs and symptoms in - compression therapy and topical corticos - clude scaling, crusting, weeping, erythema, teroids, if needed. Control chronic venous erosions, and intense itching. This disorder hypertension with compression, and he - increases the risk of contact sensitivity. Ad - mosiderin staining will fade. Refer the pa - vise the patient to avoid such products as tient for potential corrective venous surgi - lanolin, balsam of Peru, rubber, adhesives, cal procedures. fragrances, dyes, preservatives, skin sealants, silver sulfadiazine, neomycin, and Venous dermatitis bacitracin—all known to exacerbate ve - Defined as inflammation of the epidermis nous dermatitis. and dermis, venous (stasis) dermatitis is Venous dermatitis commonly is con - fused with cellulitis. A 2011 study found that 28% of 145 patients hospitalized for cellulitis had been misdiagnosed. The most common mistaken diagnosis was venous dermatitis. Unlike cellulitis, venous der - matitis causes itching and crusting; also, the skin isn’t acutely painful or hot and the patient is afebrile. Treat acute venous dermatitis with com - pression therapy and mild-potency topical corticosteroids. Apply corticosteroids spar - ingly to affected areas once or twice daily for 2 weeks; be aware that premature dis - continuation can lead to recurrence, while prolonged use can cause skin thinning and reduced efficacy. Domeboro soaks also de - crease weeping, irritation, and itching. Paste bandages impregnated with calamine or zinc oxide are soothing and drying. However, some patients may react to the preservatives in paste bandages, so a patch test is prudent. Top image shows redness, weeping, and crust - ing from acute venous dermatitis, coupled with secondary phlebolymphedema. Bottom image Chronic inflammation shows scaling from venous dermatitis on right leg Lymphedema causes chronic inflammation. and hemosiderin staining on left leg. Notice skin About 50% of plasma proteins leak into pallor on left leg (top of image), which becomes the interstitial space daily and are recycled more prominent with leg elevation, indicating through the lymphatics. Lymphatic failure concurrent peripheral arterial disease. Redness traps proteins in the tissues; the proteins from stasis dermatitis obscures arterial disease on right leg. Skin tears on right ankle result from pa - act like sponges, attracting and binding tient tearing off itchy, flaky scales. fluid. The proteins then denature, trigger - Wound Care Advisor www.WoundCareAdvisor.com 17 • July/August 2013 • Volume 2, Number 4 Stemmer’s sign confirms lymphedema. Complete decongestive physiotherapy pro - motes protein reabsorption and resolves chronic inflammation. Cellulitis Cellulitis is a rapidly spreading infection of the dermis and subcutaneous tissue. In adults, it most commonly stems from Staphylococcus aureus infection of the legs. Erysipelas, a superficial form of cel - lulitis, involves the lymphatic system and is differentiated by “streaking” toward a re - gional lymph node. Cellulitic skin is hot, acutely painful, edematous, and indurated. Redness spreads and the borders usually are irreg - ular, sharply defined, and slightly elevat - ed. Blisters, hemorrhagic bullae, abscesses, erosions, and necrosis may develop. About 30% to 80% of patients with lower limb cellulitis are afebrile. The white Top image demonstrates phlebolipolym - blood cell count, erythrocyte sedimenta - phedema, a combination of venous disease (phlebo), lipedema (lipo), and early secondary tion rate, and C-reactive protein levels lymphedema. Note the chronic inflammation just commonly are elevated, but normal values above the ankle, where there is significant lym - don’t rule out cellulitis. phatic congestion. Also note the dilated veins Treat cellulitis with oral antibiotics effec - near the medial heel, which indicate venous hy - tive against staphylococcus and streptococ - pertension. The foot appears spared of swelling cus. Adding a brief course of oral corticos - compared to the rest of the leg, indicating li - pedema. The redness resolves with compression teroids significantly shortens cellulitis therapy. In the bottom image, note the scale and duration. Severe cases may necessitate crust of chronic venous dermatitis on the lateral hospitalization and I.V. antibiotics, plus ab - aspect of the left ankle. scess incision and drainage. Control edema with bed rest and leg elevation. ing a chronic inflammatory response. This Recurrent cellulitis is common in patients response sometimes is misdiagnosed and with lymphedema. With compromised skin treated as chronic cellulitis. immunity, bacteria invade and spread with Compared to cellulitis, high-protein little resistance. If lymphedema is present, chronic inflammation is diffuse and non - refer the patient for treatment after acute tender, with light redness and mildly in - cellulitis resolves. If the patient already is creased warmth. Local skin changes may being treated for lymphedema, suspend include thickening or papillomatosis (a manual lymphatic drainage and compres - lumpy, bumpy appearance). A positive sion until acute cellulitis resolves. 18 www.WoundCareAdvisor.com Wound Care Advisor July/August 2013 • Volume 2, Number 4 • The most common disorders mistaken veins when the leg is elevated and regurgi - for lower-limb cellulitis are venous der - tates back into the tissues when the leg is matitis, lipodermatosclerosis, irritant der - dependent. matitis, and lymphedema. It also may be If you detect dependent rubor, obtain mistaken for deep vein thrombosis (DVT) the ankle-brachial index (ABI) to confirm or dependent rubor. Rule out DVT using PAD. For moderate PAD (ABI of 0.5 to venous duplex ultrasound. Dependent ru - 0.79), refer the patient for a routine vascu - bor disappears with leg elevation, whereas lar specialist consultation. For severe PAD cellulitic redness doesn’t. (ABI below 0.5), maintain dry, stable Click here to view image of cellulitis. wound eschar and urgently refer the pa - tient to a vascular specialist for potential Dependent rubor revascularization. Dependent rubor is a fiery to dusky-red Click here to view images and read a case coloration visible when the leg is in a de - study on dependent rubor. pendent position but not when it’s elevat - ed above the heart. The underlying cause Knowledge summary is peripheral arterial disease (PAD), so the “Reading” the common causes of leg red - extremity is cool to the touch. To test for ness helps you determine what’s causing dependent rubor, position the patient your patient’s redness so you can provide supine and elevate the legs 60 degrees for effective treatment. Remember—chronic 1 minute; then examine sole color. PAD venous disease causes hemosiderin stain - causes the soles to change from pink to ing, lipodermatosclerosis, and venous der - pale in fair-skinned people and to gray or matitis. Dermatitis is itchy and crusty; lipo - ashen in dark-skinned people. The faster dermatosclerosis causes sclerosis and an the pallor appears, the worse the PAD. Pal - inverted champagne-bottle
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