An Elderly Man with Leg Pain and Chronic Rash
An 82-year-old white man with a medical history significant for hypertension, type 2 diabetes mellitus, hyperlipidemia, coronary artery disease, and noncompliance with medications and office visits presents to an outpatient clinic with a several-year history of intermittent bilateral leg pain, edema, pruritus, and bilateral lower extremity color changes. The patient works as a cashier and stands for much of the day. He reports worsening symptoms for the last 6 months, but denies any exertional pain, fever, chills, numbness, or tingling. On examination, he does not have any skin breakdown and he is found to have 2/4 pedal pulses.
Based on the case description and the photograph above, what is your diagnosis?
A. Stasis dermatitis
B. Cellulitis
C. Dermatitis from arterial insufficiency
D. Neuropathic dermatitis
Answer and discussion on next page
Diagnosis: Stasis Dermatitis (A)
Discussion
Stasis dermatitis is an inflammatory skin disease of the lower extremities resulting from chronic venous insufficiency due to underlying venous hypertension. The condition is most commonly caused by valvular incompetence in the low-pressure superficial venous system, the high-pressure deep venous system, or, rarely, both. The resultant pooling and backflow of fluid leads to high pressure buildup in the superficial vessels of the skin, which subsequently causes soft-tissue damage and inflammation.1,2
Skin of the medial ankle (a watershed area with relatively poor blood flow) is often the first to show eczematous changes with erythema, scaling, and pruritis, and therefore is the most frequently affected area.1-3 The rash may progress to involve a small patch on one leg or may gradually involve the entire skin on both legs. In severe cases, the skin breaks down with oozing, crusting, and ulceration. Often, after healing, the ulceration may leave white, shiny scars called atrophie blanche.1,4-6 Chronically, the area may have post-inflammatory hyperpigmentation, excoriations and lichenification due to scratching, or petechiae due to chronic erythrocyte extravasation and hemosiderin deposition.1,6 Often, venous stasis presents with a vague, dull ache or pain in the legs along with some dependent edema that improves with leg elevation.6,7 The risk factors for developing stasis dermatitis include advancing age, female sex, the presence of varicose veins and/or phlebitis, surgery, trauma, prolonged standing, genetics, hypertension, obesity, congestive heart failure, and renal failure.1,2,5,6 In the United States, the prevalence of venous stasis dermatitis is approximately 6% to 7% in persons over age 50 years.2
The classic presentation of arterial insufficiency is claudication pain (pain and/or cramping with exertion that is relieved with rest) with slow, progressive skin changes over time. Arterial disease typically leads to well-demarcated painful ulcers, with evidence of relative ischemia (hair loss, shiny skin, decreased pulses, and/or an abnormal ankle-brachial index [ABI; normal, 0.9-1.2]).8 Dermatitis due to arterial insufficiency may have a similar appearance to venous stasis dermatitis, and, at times, venous and arterial insufficiency may coexist. Neuropathic dermatitis presents with numbness, paresthesia, burning, and/or tingling and is usually found on the pressure point areas of the body. Cellulitis usually appears as a warm, tender area of erythema and induration and is accompanied by fever and leukocytosis with left shift (predominance of immature leukocytes in peripheral blood)4,9 (Table).
Our patient was diagnosed with stasis dermatitis because of his older age; history of hypertension and prolonged standing; and his chronic, painful, pruritic rash. He had no symptoms of infection, such as fever, warmth, induration, or leukocytosis with left shift, to suggest cellulitis. As the patient had normal pulses, denied exertional pain, was found during our workup to have an ABI of 0.9, and had no well-demarcated painful ulcers, arterial insufficiency was less likely. Although he had diabetes, he denied any paresthesia, and thus neuropathic dermatitis was lower on the differential. Our workup of this patient included a complete history, physical examination (with a focus on pulse and ABI measurements and monofilament testing), and skin examination. Duplex ultrasound scanning of the lower extremity revealed great saphenous vein and small saphenous vein incompetence, but no deep vein thrombosis. After a discussion with the patient, a conservative management plan that included control of his chronic medical conditions, compression therapy, and leg elevation was agreed upon.
The evaluation of a patient presenting with lower extremity venous stasis dermatitis should include a complete history and physical examination, as well as duplex ultrasound mapping of the saphenous system and deep veins.1,8 Allergy patch testing or a skin biopsy may be helpful in making the diagnosis for atypical presentations.
Usually, venous stasis dermatitis can be managed with compression hoses that are above the knee and leg elevation.10 Treatment should always include management of the underlying chronic medical condition(s) including hypertension, congestive heart failure, renal failure, obesity, varicose veins, and phlebitis. Compression therapy has been shown to reduce edema and pain, improve venous reflux, and enhance ulcer healing,6,7,11 with success rates ranging from 30% to 60% at 24 weeks and from 70% to 85% after 1 year.7,12 Arterial insufficiency, however, would preclude the use of compression therapy,6 as it may lead to ischemia. This is an important point because, as stated previously, dermatitis due to arterial insufficiency may have a similar appearance to venous stasis dermatitis, and venous and arterial insufficiency may coexist at times. Topical or intralesional steroids have been used for pain and dermatitis, although caution is advised to avoid further skin breakdown and risk for infection.1,3 Although results vary, advanced treatment options include vein stripping, sclerotherapy, laser or intense pulsed light treatment, and endovascular techniques (eg, radiofrequency ablation, transilluminated power phlebectomy). These treatments are usually reserved for situations where conservative approaches such as compression therapy, leg elevation, or topical/intralesional treatments are ineffective.
Dr. Pillai is an Attending Physician and Vice Chair, The Methodist (Houston) Hospital Family Medicine Residency Program, TX, Clinical Assistant Professor, Cornell University, New York, NY, and Clinical Assistant Professor, University of Houston, TX; and Dr. Kabir is a Resident Physician, The Methodist (Houston) Hospital Family Medicine Residency Program.
The authors report no relevant financial relationships.
References
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