What’s Causing This Woman’s Painful, Itchy, Fissured Fingers and Palms?

AUTHORS:
Alexander K. C. Leung, MD, and Benjamin Barankin, MD

CITATION:
Leung AKC, Barankin B. What’s causing this woman’s painful, itchy, fissured fingers and palms? Consultant. 2016;56(10):915-917.

A 34-year-old woman presented with mildly pruritic and somewhat painful hands of approximately 6 months’ duration. She had been seen by a physician, who had prescribed her a midpotency topical corticosteroid and a moisturizer, which provided modest relief.

She had 3 young children and was preoccupied with housework, including cooking and laundry. She had a history of childhood atopic dermatitis.

Physical examination revealed xerosis, scaling, and fissuring of the digits and palms. There were no skin lesions in other lcations. The rest of the physical examination findings, particularly in the nails and joints, were normal.

What’s Your Diagnosis?

1. Tinea manuum
2. Hand eczema
3. Palmar psoriasis
4. Palmoplantar pustulosis

Answer and discussion on next page.

Answer: Hand Eczema

Hand eczema, also known as hand dermatitis, is a common inflammatory disorder involving the skin of the hands. The condition is characterized by pruritus, soreness, erythema, edema, weeping, and vesiculation in the acute stage, and pruritus, scaling, hyperkeratosis, and fissuring of the skin in the chronic stage.¹ Hand eczema is regarded as chronic if the eczematous process lasts for more than 3 months or relapses twice or more per year.^1,2 The disorder can be aggravated by occupational or routine household activities.³

EPIDEMIOLOGY

The estimated point prevalence of hand dermatitis among adults in the general population is approximately 4%, the 1-year prevalence is approximately 10%, and the lifetime prevalence is approximately 15%.⁴ The peak age of onset is between 20 and 30 years of age.⁵ The condition is more common in females than in males.^2,5,6 Other predisposing factors include wet work, contact allergy, past or present history of atopic dermatitis, friction, and emotional stress.^2,7,8 Construction workers, food industry workers, hairdressers, barbers, homemakers, and hospital personnel engaged in wet work are at risk for hand eczema.⁹

ETIOPATHOGENESIS

Hand eczema is a heterogeneous disorder, the pathogenesis of which is multifactorial and involves both genetic and environmental factors.¹ These factors are not mutually exclusive.

Irritant contact dermatitis is the most common cause of hand eczema and accounts for up to 80% of cases.^5,10,11 Immunologic reactions are not involved, and the dermatitis can occur without prior sensitization.^3,6 Rather, it is a nonspecific response of the skin to direct chemical damage resulting in the release of inflammatory mediators and cytokines (tumor necrosis factor-α, interleukin 1, interleukin 2, interleukin 6, interleukin 8, interferon-γ, and granulocyte monocyte-colony stimulatory factor), predominately from epidermal cells.^9,10

 The condition occurs as a result of exposure of the skin to irritant agents such as water, soaps, detergents, alcohols, disinfectants, fruits such as oranges and lemons, and chemicals found in common cleansers such as ammonia and organic solvents.^6,11,12 In general, the intensity of reaction to irritants is directly proportional to the concentration of the irritant and exposure time.⁹ Frequent and prolonged water exposure in combination with various chemicals is an important cause of irritant contact dermatitis, as is illustrated in the case presented here.

Allergic contact dermatitis is a type IV delayed-hypersensitivity reaction caused by T-cell-mediated immune response to skin sensitizers. Contact allergens require prior exposure for sensitization. Common allergens include nickel, chromium, cobalt, acrylics, topical neomycin, fragrances, rubber, and latex.^1,11

Atopic dermatitis is an endogenous cause of hand eczema.¹² A strong association between atopic dermatitis during childhood and hand eczema in adolescence and adulthood has been documented.⁷ Endogenous hand eczema results from an exaggerated response to external stimuli as a result of a defective epidermal barrier secondary to loss-of-function mutations in the filaggrin gene.^1,2

Dyshidrotic eczema (dyshidrotic dermatitis, pompholyx) may also result in hand eczema.¹³

HISTOPATHOLOGY

In the acute phase, histologic features include spongiosis and a superficial dermal inflammatory infiltrate composed mainly of lymphocytes.¹ In the more chronic phase, the degree of spongiosis is often mild, and epidermal parakeratosis, acanthosis, and hyperkeratosis predominate, with a superficial perivascular inflammatory infiltrate composed mainly of lymphocytes and histiocytes.¹

CLINICAL MANIFESTATIONS

Pruritus is a prominent symptom, especially with allergic contact dermatitis.³ Lesions are usually bilateral involving the palmar or dorsal surfaces or both.¹ In the acute stage, typical findings include erythema, edema, soreness, weeping, and vesiculation. In the chronic stage, typical findings include scaling, hyperkeratosis, desquamation, fissuring, and, sometimes, lichenification.^1,3 Nail changes such as loss of the cuticle, thickening of the nail folds, and thickening of the nail plate may be seen.¹ The condition is typically recurrent and both the acute and chronic phases can coexist.

Irritant contact dermatitis most commonly involves the palms and distal aspect of the dorsum of the fingers.^1,6 Allergic contact dermatitis usually involves the dorsum of the hands, fingers, web spaces, and the volar aspects of the wrists, where the skin is thinner and allergens can penetrate more easily.^1,6 Atopic hand dermatitis usually involves the dorsum of the hands and fingers and/or the sides of the fingers.¹ There often is involvement of other body parts. Dyshidrotic eczema is characterized by pruritic, tense, deep-seated vesicles mainly on the palms and lateral surfaces of the fingers.¹³

DIAGNOSIS

The diagnosis is mainly clinical based on a detailed history, physical finding of the characteristic lesions, and patch testing. Referral to a dermatologist should be considered when the diagnosis is in doubt.

Differential Diagnosis

Differential diagnosis includes tinea manuum, palmar psoriasis, nummular eczema, palmoplantar pustulosis, lichen planus, porphyria cutanea tarda, keratosis palmoplantaris, scabies, and fixed drug eruption.³

LABORATORY INVESTIGATIONS

Patch testing is used to assess for type IV delayed-hypersensitivity reaction and should be considered in patients with chronic hand eczema to possibly identify an allergen. It is the gold standard for diagnosis of allergic contact dermatitis.^2,10 Skin prick testing and radioallergosorbent testing (RAST) can be used to assess for type I, immunoglobulin E-mediated, immediate hypersensitivity reactions.⁵ RAST rather than skin prick testing should be performed if the risk of anaphylaxis is considerable.⁵ Skin prick testing and RAST are of limited value except in cases of protein contact dermatitis and contact urticaria caused by latex proteins or fish proteins.¹² If necessary, a potassium hydroxide wet-mount examination of the skin scraping can be used to rule out a dermatophyte infection.⁵ Skin biopsy is seldom necessary.

COMPLICATIONS

Hand eczema has a significant negative impact on health-related quality of life due to pruritus, discomfort, esthetic concerns, social embarrassment, and impairment of professional performance.¹⁴ The negative impact is greater for females than for males.¹⁵ Affected individuals may have lower self-esteem.¹⁴ Secondary bacterial infection, especially with Staphylococcus aureus, may occur. Nail dystrophy may result if the nail matrix is affected. The condition has a significant health economic and sociomedical impact.²

Prognosis and Management

Although hand eczema is benign, it tends to run a chronic and relapsing course.⁵ The average duration of the disease is approximately 12 years.¹ Patients with childhood or current atopic dermatitis, widespread lesions at the time of initial examination, young age of onset, and nickel sensitivity tend to have a poorer prognosis.⁷

Successful treatment requires a multipronged approach that consists of avoidance of triggering factors, optimal skin care, pharmacotherapy during acute exacerbations, and maintenance therapy. Potential irritants and allergens should be avoided in the home and work environments. Protective measures such as heavy-duty vinyl gloves should be used when contact with potential irritants and allergens is inevitable. Exposure to water should be minimized.⁶

Hydration of the skin helps to improve the dryness and pruritus and restore the skin’s barrier function. As such, hydration of the skin is of paramount importance in the prevention and management of hand eczema.¹³ A quality moisturizer, emollient, or barrier cream should be used liberally and regularly to keep the skin soft and well hydrated and to prevent transepidermal water loss. In general, ointments are most effective but messy; creams (preferably nonfragranced) are often better tolerated. The type of moisturizer or emollient should be tailored to the skin conditions and the patient’s needs and preferences.

Ultrapotent topical corticosteroids are the mainstay of therapy for allergic contact dermatitis and dyshidrotic eczema.^2,5 Topical corticosteroids should not be applied more than twice a day; frequent use does not improve efficacy and increases the risk of adverse effects. Topical immunomodulators such as tacrolimus and pimecrolimus are not as fast or effective as ultrapotent topical corticosteroids in the treatment of allergic contact dermatitis or dyshidrotic eczema, although they can be considered in the maintenance phase of treatment.² On the other hand, topical immunomodulators can be used for irritant contact dermatitis.²

Although pruritus in hand eczema does not appear to be mediated by histamine release, oral antihistamines can provide symptomatic relief to some patients because of their sedative properties and may be effective for intense pruritus refractory to moisturizers and conservative measures. Of the H₁ antihistamines, hydroxyzine is more effective than diphenhydramine and cyproheptadine.

Alexander K. C. Leung, MD, is clinical professor of pediatrics at the University of Calgary and a pediatric consultant at the Alberta Children’s Hospital in Calgary, Alberta, Canada.

Benjamin Barankin, MD, is a dermatologist and the medical director and founder of the Toronto Dermatology Centre in Toronto, Ontario, Canada.

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