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DERMATITIS, STASIS

Joseph A. Florence, MD Fereshteh Gerayli, MD, FAAFP

BASICS

DESCRIPTION

Chronic, eczematous, erythema, scaling, and noninflammatory edema of the lower extremities accompanied by cycle of scratching, excoriations, weeping, crusting, and inflammation in patients with chronic venous insufficiency (CVI), due to impaired circulation and other factors (nutritional edema)

Clinical skin manifestation of CVI usually appears late in the disease.

May present as a solitary lesion; can be associated with venous leg ulcer, which is located on the medial or lateral side of the ankle

System(s) affected: skin/exocrine

Synonym(s): gravitational eczema; varicose eczema; venous dermatitis

EPIDEMIOLOGY

Incidence

In the United States: common in patients age >50 years (6–7%)

Predominant age: adult, geriatric

Predominant sex: female > male

Geriatric Considerations

Common in this age group:

Estimated to affect 15 to 20 million patients age >50 years in the United States

ETIOLOGYAND PATHOPHYSIOLOGY

Incompetence of perforating veins, superficial venous thrombosis from varicose veins, and deep vein thrombosis can each contribute to CVI leading to venous hypertension (HTN) and cutaneous inflammation. This can be a pathway to venous leg ulcer.

Deposition of fibrin around capillaries

Microvascular abnormalities Ischemia

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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.

Acascade of biochemical events leads to ulceration.

Genetics

Familial link probable

RISK FACTORS

Atopy

Chronic edema

Old age

Obesity

Previous DVT

Previous pregnancy

Prolonged standing

Secondary infection

Superimposition of itch–scratch cycle

Trauma

Low-protein diet

Genetic propensity

Tight garments that constrict the thigh

Vein stripping

Vein harvesting for coronary artery bypass graft surgery

Previous cellulitis

GENERALPREVENTION

Use compression stockings to avoid recurrence of edema and to mobilize the interstitial lymphatic fluid from the region of stasis dermatitis and also following DVT.

Topical lubricants twice a day to prevent fissuring and itching

COMMONLYASSOCIATED CONDITIONS

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Varicose veins

Venous insufficiency

Other eczematous disease

Hyperhomocysteinemia

Venous HTN

DIAGNOSIS

HISTORY

Itching, pain, and burning may precede skin signs, which are aggravated during evening hours.

Insidious onset

Usually bilateral

Description may include aching/heavy legs.

Erythema, scaling, edema of lower extremities

Noninflammatory edema preceded the skin eruption and ulceration.

Edema initially develops around the ankle.

PHYSICALEXAM

Evaluation of the lower extremities characteristically reveals:

–Bilateral scaly, eczematous patches, papules, and/or plaques

–Violaceous (sometimes brown), erythematous 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, occasionally lateral side of ankle

Brawny induration

Stasis ulcers (frequently accompany stasis dermatitis) secondary to minor trauma

Excoriations

Weeping, crusting, inflammation of the skin

Varicosities are often associated with ulcers.

Clinical inspection reveals swelling and warmth.

Skin changes are more common in the lower 1/3 of the extremity and medially.

Early signs include prominent superficial veins and pitting ankle edema. May present as a solitary lesion mimicking a neoplasm

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DIFFERENTIALDIAGNOSIS

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

DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

Duplex ultrasound imaging is helpful in diagnosis.

Diagnostic Procedures/Other

Rule out arterial insufficiency. Check peripheral pulses; ankle brachial pressure index (ABPI or ABI)

Check for diabetes.

Test Interpretation

ABPI <0.8 is suggestive of arterial insufficiency.

ABPI can be elevated, >1.2 in diabetic patients and others with distal small vessel calcifications.

Arterial duplex ultrasound and angiography are the gold standards.

TREATMENT

GENERALMEASURES

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

Outpatient:

–Reduce edema:

Leg elevation: legs above the level of heart for 30 minutes, 3 to 4 times daily. Avoid prolonged dependent position.

Compression therapy: This is the mainstay of treatment of venous stasis plus/minus ulcers. Compression bandages can be safely applied in patients with ABI of 0.8 to 1.2.

Elastic bandage wraps: Ace bandages or Unna paste boot (zinc gelatin) or compression stockings (compression stockings)

Graduated elastic compression of 30 to 40 mm Hg at the ankle improves ulcer healing rate and may prevent ulcer recurrence (1)[A].

Compression bandages containing both elastic and inelastic components (mixed component systems) are as effective as four-layer bandages, are easier to apply, and have less slippage and associated with favorable quality of life outcomes.

High compression is contraindicated in arterial insufficiency.

Pneumatic compression devices are beneficial, especially in nonambulatory patients and those with a component of arterial insufficiency (2)[B].

Improvement of lipodermatosclerosis:

–Activity:

Avoid standing still.

Stay active and exercise regularly.

Elevate foot of bed unless contraindicated.

Inpatient, for endovascular radiofrequency ablation, vein stripping, sclerotherapy, or skin grafts:

–Venous ulcer treatment: Treat infection: Débride the ulcer base of necrotic tissue (surgical necrotomy if possible, or enzymatic débridement with collagenase).

Autolytic: Modern wound dressings (hydrogel, hydrocolloids, alginate, foam bandages, plain nonadherent dressing) are better than traditional wet to dry dressing as they maintain moist wound environment, with less tissue damage on removal and less frequent changing requirement (2)[A]. However, there is no difference in healing rate of venous stasis ulcers by use of hydrocolloid dressing versus simple nonadherent dressing when used beneath compression.

Biologic: Topical application of granulocyte-macrophage colony-

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stimulating factor promotes healing of ulcers (insufficient evidence).

Mechanical: wet to dry dressings, hydrotherapy, and irrigation

Surgical: modifying cause of venous HTN (by venous ligation, valvuloplasty, and endoscopic perforator vein surgery); treat ulcer by graft.

MEDICATION

First Line

Pentoxifylline 400 mg TID is effective in treating venous leg ulcer.

Enteric-coated aspirin (at least 300 mg) daily may improve venous ulcer healing.

In light of increasing bacterial resistance to antibiotics, current guidelines recommend the use of antibacterial preparations only for clinical infection (cellulitis, increased pain, warmth, malodorous exudate), not for bacterial colonization (3)[A].

If secondary infection, treat with PO antibiotics for Staphylococcus or Streptococcus organisms (e.g., dicloxacillin 250 mg QID, cephalexin 500 mg BID, or levofloxacin 500 mg daily).

If MRSAsuspected, clindamycin 300 mg QID, doxycycline 100 mg BID, TMP/SMX or IV vancomycin

There is no reliable evidence in the effectiveness of topical antiseptics such as povidone-iodine, peroxide-based preparations, mupirocin, chlorhexidine (3) [A].

Uncomplicated stasis dermatitis can be treated with short courses (about 2 weeks) of topical steroids (2)[B] (topical triamcinolone 0.1% cream/ointment BID).

Topical antipruritic: pramoxine, camphor, menthol, and doxepin

Topical anesthetic (lidocaine/prilocaine) may reduce pain during débridement.

Systemic steroids for severe cases

Silver sulfadiazine (SSD) has a positive effect in wound healing (2)[A].

Second Line

Consider antibiotics on basis of culture results of exudate from infected ulcer craters.

Lubricants when dermatitis is quiescent

Chronic stasis dermatitis can be treated with topical emollients (e.g., white petroleum, lanolin).

Antipruritic medications (e.g., diphenhydramine, cetirizine hydrochloride)

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Hydrocolloid or a foam dressing may reduce ulcer pain; no evidence that ibuprofen dressings offer pain relief

ISSUES FOR REFERRAL

Consider referral for:

Nonhealing ulcer

Arterial insufficiency

Uncertain diagnosis

Rheumatoid arthritis

Patch testing to evaluate for contact dermatitis

Associated disease (e.g., symptomatic varicose veins)

ADDITIONALTHERAPIES

If the patient is on amlodipine, consider discontinuing.

SURGERY/OTHER PROCEDURES

Sclerotherapy and surgery may be required for associated disease.

ONGOING CARE

FOLLOW-UPRECOMMENDATIONS

Patient Monitoring

If Unna boot compression is used: Cut off and reapply boot once a week. Unna boots reduce edema by compression and prevent scratching.

Regular use of high-compression stockings reduces chance of recurrent venous ulcer (4)[A].

DIET

Lose weight, if overweight.

PATIENT EDUCATION

Encourage staying active to keep circulation and leg muscles in good condition. Walking is ideal.

Keep legs elevated while sitting or lying.

Do not wear girdles, garters, or pantyhose with tight elastic tops. Do not scratch.

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Avoid leg injury.

Elevate foot of bed with 2- to 4-inch blocks.

Apply compression stockings prior to getting out of bed when less edema is present. Regular use of high-compression stockings may prevent recurrence of venous ulcers.

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.O’Meara S, Cullum N, Nelson EA, et al. Compression for venous leg ulcers.

Cochrane Database Syst Rev. 2012;(11):CD000265.

2.Evidence-based (S3) guidelines for diagnostics and treatment of venous leg ulcers. J Eur Acad Dermatol Venereol. 2016;30(11):1843–1875.

3.O’Meara S, Al-Kurdi D, Ologun Y, et al. Antibiotics and antiseptics for venous leg ulcers. Cochrane Database Syst Rev. 2014;(1):CD003557.

4.Nelson EA, Bell-Syer SE. Compression for preventing recurrence of venous ulcers. Cochrane Database Syst Rev. 2012;(8):CD002303.

ADDITIONALREADING

Coleridge-Smith PD. Leg ulcer treatment. J Vasc Surg. 2009;49:804–808.

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(1):83–92.

Collins L, Seraj S. Diagnosis and treatment of venous ulcers. Am Fam

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Physician. 2010;81:989–996.

Partsch H, Flour M, Smith P; for International Compression Club. 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(3):193–219.

Sippel K, Mayer D, Ballmer B, et al. Evidence that venous hypertension causes stasis dermatitis. Phlebology. 2011;26:361–365.

SEE ALSO

Varicose Veins

Algorithm: Rash

CODES

ICD10

I83.10 Varicose veins of unsp lower extremity with inflammation

I83.11 Varicose veins of right lower extremity with inflammation I83.12 Varicose veins of left lower extremity with inflammation

CLINICALPEARLS

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

Pentoxifylline and aspirin may improve venous ulcer healing.

No difference in healing rate of venous stasis ulcers by use of hydrocolloid dressing versus simple non-adherent dressing when used beneath compression. Decision about the dressing should be based on local cost and patient or physician’s preferences.

Mild topical corticosteroids reduce inflammation and itching; however, these may potentiate infection; high-potency topical corticosteroids should be avoided due to increased risk of atrophy and ulceration.

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DIABETES MELLITUS, TYPE 1

Irfan Siddiqui, MD Armand Krikorian, MD, FACE, FACP

BASICS

DESCRIPTION

Type 1 diabetes mellitus (T1DM) is a chronic disease caused by pancreatic insufficiency (deficiency) of insulin production.

Results in hyperglycemia and end-organ complications (e.g., accelerated atherosclerosis, neuropathy, nephropathy, and retinopathy)

Features include the following:

–Patients are insulinopenic and require insulin.

–Polyphagia, polydipsia, and polyuria

–Ketosis

–Usually rapid onset

–Body habitus: usually normal or thin physique

System(s) affected: endocrine/metabolic

Pregnancy Considerations

Hyperglycemia increases the incidence of congenital malformations. Tight control of blood sugar prior to conception (goal A1C <6.5%) is important (1).

Family planning should be discussed and effective contraception offered until A1C is within goal range to reduce the risk of congenital anomalies.

Women with microalbuminuria during the 1st trimester are at increased risk for preeclampsia and preterm delivery.

Asafe pregnancy is possible with vaginal delivery of a term baby. Close monitoring of blood sugar during labor is important.

Many drugs used to treat diabetic complications are relatively/absolutely contraindicated in pregnancy.

Perinatal and psychological stressors are associated with T1DM in children.

EPIDEMIOLOGY

Age of onset peaks between 5 and 7 years of age and again around puberty; rapid decline in incidence after adolescence

Slightly more common in males than females

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