Basics

Description

• Chronic, eczematous, erythremic, scaling, and noninflammatory edema of the lower extremities accompanied by cycle of scratching, excoriations, weeping, crusting, and inflammation in patients with chronic venous insufficiency, due to impaired circulation and other factors (nutritional edema)
• Clinical skin manifestation of chronic venous insufficiency usually appears late in the disease
• May present as a solitary lesion
• System(s) affected: Skin/Exocrine
• Synonym(s): Gravitational eczema; Varicose eczema; Venous dermatitis

Epidemiology

Incidence

• In the US: Common in patients >50 (6–7%)
• Predominant age: Adult, geriatric
• Predominant sex: Female > Male

Geriatric Considerations

• Common in this age group
• Estimated to affect 15–20 million patients >50 years in the US

Risk Factors

• Atopy
• Superimposition of itch–scratch cycle
• Trauma
• Previous deep vein thrombosis (DVT)
• Previous pregnancy
• Prolonged medical illness
• Obesity
• Secondary infection
• Low-protein diet
• Old age
• Deposition of fibrin around capillaries
• Microvascular abnormalities
• Ischemia
• Genetic propensity
• Edema
• Tight garments that constrict the thigh
• Vein stripping
• Vein harvesting for coronary artery bypass graft surgery
• Previous cellulitis

Genetics

Familial link probable

General Prevention

• Use compression stockings to avoid recurrence of edema and to mobilize the interstitial lymphatic fluid from the region of stasis dermatitis.
• Topical lubricants twice a day to prevent fissuring and itching

Etiology

• Incompetence of perforating veins causing blood to backflow to the superficial venous system leading to venous hypertension (HTN) and cutaneous inflammation
• Continuous presence of edema in ankles, usually present because of venous valve incompetency (varicose veins)
• Weakness of venous walls in lower extremities
• Trauma to edematous, eczematized skin
• Itch may be caused by inflammatory mediators (from mast cells, monocytes, macrophages, or neutrophils) liberated in the microcirculation and endothelium
• Abnormal leukocyte-endothelium interaction is proposed to be a major factor.
• A cascade of biochemical events leads to ulceration.
• Is associated with amlodipine therapy
• Elevated homocysteine has been noted in patients with stasis dermatitis.

Commonly Associated Conditions

• Varicose veins
• Venous insufficiency
• Other eczematous disease

Diagnosis

History

• Erythema, scaling, edema of lower extremities
• Pruritus
• Excoriations
• Weeping, crusting, inflammation of the skin
• Noninflammatory edema precedes the skin eruption and ulceration.
• Edema initially develops around the ankle.
• Itching, pain, and burning may precede skin signs, which are aggravated during evening hours (1)[B].
• Insidious onset
• Usually bilateral
• Description may include aching/heavy legs

Physical Exam

• Evaluation of the lower extremities characteristically reveals:
  • Bilateral scaly, eczematous patches, papules, and/or plaques
  • Violaceous (sometimes brown), erythematous-colored lesions due to deoxygenation of venous blood (postinflammatory hyperpigmentation and hemosiderin deposition within the cutaneous tissue)
• Distribution: Medial aspect of ankle with frequent extension onto the foot and lower leg
• Brawny induration
• Stasis ulcers (frequently accompany stasis dermatitis) secondary to cuts, bruises, and excoriations to the weakened skin around the ankle
• Mild pruritus, pain (if ulcer present)
• Varicosities are often associated with ulcers.
• Clinical inspection reveals erythematous color with increased pigmentation, swelling, and warmth.
• Skin changes are more common in the lower 3rd of the extremity and medially.
• Early signs include prominent superficial veins and pitting ankle edema.
• May present as a solitary lesion (2)[C]

Diagnostic Tests & Interpretation

Lab

Initial lab tests

Culture stasis ulcers if bacterial infection is suspected.

Imaging

Initial approach

Duplex ultrasound imaging is helpful in diagnosis (3)[C].

Diagnostic Procedures/Surgery

Rule out arterial insufficiency (check peripheral pulses, leg blood pressures).

Pathological Findings

Chronic inflammation, characterized histologically by proliferation of small blood vessels in the papillary dermis

Differential Diagnosis

• Other eczematous diseases:
  • Atopic dermatitis
  • Uremic dermatitis
  • Contact dermatitis (due to topical agents used to self-treat)
  • Neurodermatitis
  • Arterial insufficiency
  • Sickle cell disease causing skin ulceration
  • Cellulitis
  • Erysipelas
• Tinea dermatophyte infection
• Pretibial myxedema
• Nummular eczema
• Lichen simplex chronicus
• Xerosis
• Asteatotic eczema
• Amyopathic dermatomyositis

Treatment

Medication

First Line

• Use of antibiotics topically or systemically is controversial, as stasis ulcer may not be infected.
• Antibiotics are indicated if bacterial infection is present, or may be used empirically if bacterial infection is suspected.
• If ulcer is present, local povidone-iodine treatment is as effective as systemic antibiotics (4)[B].
• If secondary infection, treat with oral antibiotics for Staphylococcus orStreptococcus organisms (e.g., dicloxacillin 250 mg q.i.d., cephalexin 250 mg q.i.d. or 500 mg b.i.d., or levofloxacin 250 mg q.i.d.).

• Gram-negative colonization: Treat with topical antimicrobial agents (e.g., benzoyl peroxide, acetic acid, silver nitrate, or Hibiclens) or broad-spectrum topical antibiotics (e.g., neomycin or bacitracin-polymyxin B [Polysporin]).
• 5% Aluminum acetate (Burow solution) wet dressings and cooling pastes
• Topical triamcinolone 0.1% (Kenalog, Aristocort) cream/ointment t.i.d. or topical betamethasone
• Betamethasone valerate (Valisone) 0.1% cream/ointment/solution t.i.d. (5)[A]
• Topical antipruritic: Pramoxine, camphor, menthol, and doxepin
• Systemic steroids for severe cases
• Calcium dobesilate has been shown to be an effective adjuvant therapy (6)[B].
• Vitamin supplementation in patients with hyperhomocysteinemia (7)[C]
• Evidenced-based treatment options for associated venous ulcers include aspirin and pentoxifylline (8)[B].

Second Line

• Consider antibiotics on basis of culture results of exudate from ulcer craters.
• Lubricants when dermatitis is quiescent
• Chronic stasis dermatitis can be treated with topical emollients (e.g., white petroleum, lanolin, Eucerin).
• Antipruritic medications (e.g., diphenhydramine, cetirizine hydrochloride, desloratadine)

Additional Treatment

If the patient is on amlodipine therapy consider discontinuing amlodipine (9)[B].

General Measures

Primary role of treatment is to reverse effects of venous HTN. Appropriate health care:

• Outpatient:
  • Reduce edema (8)[B]:
    • Leg elevation: Heels higher than knees, knees higher than hips
    • Compression therapy: Elastic bandage wraps: Ace bandages or Unna paste boot (zinc gelatin) if lesions are dry or compression stockings (Jobst or nonfitted type) (10,11)[A]
    • Pneumatic compression devices
    • Diuretic therapy
  • Treat infection:
    • Débride the ulcer base of necrotic tissue.
    • Improvement of lipodermatosclerosis
  • Activity:
    • Avoid standing still.
    • Stay active and exercise regularly.
    • Elevate foot of bed unless contraindicated.
• Inpatient for vein stripping, sclerotherapy, or skin grafts:
  • Venous ulcer treatment includes autolytic, biologic, chemical, mechanical, and surgical:
    • Autolytic: Hydrogels, alginates, hydrocolloids, foams, and films
    • Biologic: Topical application of granulocyte macrophage colony-stimulating factor promotes healing of ulcers.
    • Chemical: Enzyme débriding agents
    • Mechanical: Wet to dry dressings, hydrotherapy, and irrigation
    • Surgical modifying cause of venous HTN, treat ulcer by graft

Surgery/Other Procedures

Sclerotherapy and surgery may be required.

Ongoing Care

Follow-Up Recommendations

Patient Monitoring

If Unna boot compression is used: Cut off and reapply boot once a week (restricts edema and prevents scratching).

Diet

• No special diet
• Lose weight, if overweight

Patient Education

• Stress staying active to keep circulation and leg muscles in good condition. Walking is ideal.
• Keep legs elevated while sitting or lying.
• Don’t wear girdles, garters, or pantyhose with tight elastic tops.
• Don’t scratch.
• Elevate foot of bed with 2–4-inch blocks.

Prognosis

• Chronic course with intermittent exacerbations and remissions
• The healing process for ulceration is often prolonged and may take months.

Complications

• Sensations of itching, pain, and burning have negative impact on the quality of life
• Secondary bacterial infection
• DVT
• Bleeding at dermatitis sites
• Squamous cell carcinoma in edges of long-standing stasis ulcers
• Scarring, which in turn leads to further compromise to blood flow and increased likelihood of minor trauma

References

1. Duque MI, Yosipovitch G, Chan YH, et al. Itch, pain, and burning sensation are common symptoms in mild to moderate chronic venous insufficiency with an impact on quality of life. J Am Acad Dermatol. 2005;53:504–8.

2. Weaver J, Billings SD et al. Initial presentation of stasis dermatitis mimicking solitary lesions: a previously unrecognized clinical scenario. J Am Acad Dermatol. 2009;61:1028–32.

3. Coleridge-Smith P, Labropoulos N, Partsch H, et al. Duplex ultrasound investigation of the veins in chronic venous disease of the lower limbs–UIP consensus document. Part I. Basic principles. Eur J Vasc Endovasc Surg.2006;31:83–92.

4. Daróczy J. Quality control in chronic wound management: the role of local povidone-iodine (Betadine) therapy. Dermatology. 2006;212 (Suppl 1):82–7.

5. Weiss SC, Nguyen J, Chon S, et al. A randomized controlled clinical trial assessing the effect of betamethasone valerate 0.12% foam on the short-term treatment of stasis dermatitis. J Drugs Dermatol. 2005;4:339–45.

6. Kaur C, Sarkar R, Kanwar AJ, et al. An open trial of calcium dobesilate in patients with venous ulcers and stasis dermatitis. Int J Dermatol. 2003;42:147–52.

7. Kartal Durmazlar SP, Akgul A, Eskioglu F et al. Hyperhomocysteinemia in patients with stasis dermatitis and ulcer: A novel finding with important therapeutic implications. J Dermatolog Treat. 2009;1–4.

8. Collins L, Seraj S et al. Diagnosis and treatment of venous ulcers. Am Fam Physician. 2010;81:989–96.

9. Gosnell AL, Nedorost ST et al. Stasis dermatitis as a complication of amlodipine therapy. J Drugs Dermatol. 2009;8:135–7.

10. Partsch H, Flour M, Coleridge Smith P. Indications for compression therapy in venous and lymphatic disease Consensus based on experimental data and scientific evidence. Under the auspices of the IUP. Int Angiol.2008;27:193–219.

11. Coleridge-Smith PD. Leg ulcer treatment. J Vasc Surg. 2009;49:804–8.

Additional Reading

Antignani PL. Classification of chronic venous insufficiency: a review.Angiology. 2001;52 (Suppl 1):S17–26.

13. Durmazlar SPK, Akgul A, Eskioglu F. Hyperhomocysteinemia in patients with stasis dermatitis and ulcer: A novel finding with important therapeutic implications. J Dermatolog Treat. 2009;20:3;1–4.

See Also (Topic, Algorithm, Electronic Media Element)

Varicose Veins

Algorithm: Rash, focal

Codes

ICD9

• 454.1 Varicose veins of lower extremities with inflammation
• 459.81 Venous (peripheral) insufficiency, unspecified

Snomed

• 35498005 Stasis dermatitis (disorder)
• 275700003 Varicose veins of the leg with eczema (disorder)

Clinical Pearls

Treatment of edema associated with stasis dermatitis via elevation and/or compression stockings is essential for optimal results.