Are You Confident of the Diagnosis?

What you should be alert for in the history

A careful history should be taken in all patients presenting with hand eczema. Past medical history, including information about a history of atopic dermatitis and previous episodes of hand eczema, should be identified. Hand eczema is usually remitting and relapsing, so the time course of flares and remissions should be noted and can sometimes aid in diagnosis. Flares can correspond with seasons, workdays, weekends, or holidays.

Exposures should be assessed, including possible irritants or allergens in the home, at work, or those associated with hobbies and leisure activities. Patients with hand eczema have often been treated extensively and exposed to numerous topical agents, which can sometimes themselves cause allergic reactions and worsen hand eczema, so all previous treatment regimens should be explored.

Characteristic findings on physical examination

Hand eczema can vary in location and extent of involvement, morphology, and severity. On physical examination, the localization of the lesions should be noted, which can include palmar, dorsal, interdigital, and involvement of other areas of the body, particularly the wrists and feet. In cases of allergic contact dermatitis, the location and shape of the lesions may point to a cause, as the affected areas may correspond directly to contact with an allergen. For example, eczema on the thumb and index finger of a florist is characteristic of allergic contact dermatitis to alstroemeria. The characterization of the lesions is also important–vesicular, scaling, hyperkeratotic, with or without fissuring, nummular, etc.

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Depending on the acuity of the eczema, the morphology will vary from vesicles and bullae, to scaling, lichenified plaques. The skin may become dry and chapped, indicating a breakdown in the barrier of the skin that has promoted water loss typical of mild irritant contact dermatitis from hand washing. This may progress to fissuring and become red and tender. The inflammation can become more acute, with vesicles and bullae, and weeping and crusting can develop, as is found in dyshidrotic eczema.

As the lesions become increasingly pruritic, excoriations can be seen. Sometimes secondary infections occur, manifested by pustules and purulent drainage. However, this also could be sterile pustules of pustular psoriasis. As the patient continues to scratch, scaling and lichenification can become more prominent as the inflammation becomes chronic, typical of atopic dermatitis.

Expected results of diagnostic studies

Work-up for hand eczema is summarized in Table I. Patch testing, in combination with the patient’s history, can be helpful in identifying the cause of hand eczema (Figure 1). Patients who have not responded to standard therapies with topical steroids and a good skin care regimen should be considered for patch testing. Patch testing employs a series of standard allergens to assess for Type IV, delayed type allergic reactions. In addition to commercially available materials in screening patch test series, materials that the patient commonly uses can also be patch tested as long as they are not irritants. The exposure time should be 2 days, and evaluation for reactions should take place on day 2, as well as day 3 or 4.

Table I.
History Patch Test
Physical RAST (occasionally)
KOH prep Rarely biopsy

Though patch testing is often a fundamental component in diagnosing hand eczema, results of the test are not always clinically relevant. Therefore, the patient’s medical and exposure history, as well as the physical examination, should be taken into consideration in conjunction with the results of the patch test to make a diagnosis of allergic contact dermatitis of the hands.

Secondary testing includes skin prick testing and radioallergosorbent testing (RAST). Both tests assess for Type-I, IgE-mediated immediate hypersensitivity reactions. Skin prick testing consists of pricking the skin with a small needle to introduce a small amount of purified allergen into the skin to assess for a response. Immunologic response can manifest as a rash, urticaria, or, if severe, anaphylaxis.

If an individual’s risk of anaphylaxis is sufficient, skin prick testing should be avoided, and RAST testing can be used instead. This test is a blood test that assesses levels of specific IgE antibodies to suspected allergens and has no risk of anaphylaxis since no allergen is being introduced into the body. RAST testing also avoids unnecessary sensitization to allergens. Allergists normally perform skin prick testing because of the concern of anaphylaxis. Testing for Type I allergy is now only occasionally done for hand dermatitis since the improved manufacture of surgical and exam gloves that have no or very low levels of natural rubber latex protein.

Eczema is largely a clinical diagnosis, but histologic examination can be useful in excluding other possible causes. On histopathology, acute eczema is characterized by spongiosis, or intercellular edema leading to intraepidermal vesicles, and an inflammatory lymphocytic infiltrate is present in the epidermis and dermis. As the eczema becomes more chronic, spongiosis and inflammation is reduced, and acanthosis and parakaratosis develop. However, a skin biopsy is not commonly accomplished unless to rule uncommon causes of eczematous appearing eruptions, such as mycosis fungoides or dyshidrosifom bullous pemphigoid.

A potassium hydroxide (KOH) preparation can be used in to rule out fungal infection if it is in the differential diagnosis. For example, a KOH prep should be considered when the eruption affects one hand and both feet.

Diagnosis confirmation

When treatment for hand eczema is unsuccessful, other causes for the dermatitis should be considered. Commonly, hand eczema is a hybrid of several types of eczema, and treating one cause can result in an apparent partial response or failure of treatment. Long standing atopic hand dermatitis in a hairdresser can be complicated by irritant or allergic contact dermatitis to salon products, eg, shampoos, permanent hair colors, and permanent-wave solutions. In addition, preexisting hand eczema may become secondarily infected, which will change its presentation and response to treatment.

Patients with psoriasis may be misdiagnosed with hand eczema, as palmoplantar psoriasis and eczematous dermatitis of the hands share similar clinical and histologic features. Usually, psoriasis is redder in color with a thicker, silvery scale and well demarcated borders. In addition to the morphology, the distribution of accompanying lesions on the rest of the body can be helpful, as psoriasis tends to involve extensor surfaces, while eczema favors flexor surfaces. Further, nail changes can occur in eczema and other conditions, but nail pitting is more specific to psoriasis and helps to confirm the diagnosis.

Fungal infections of the hands, or tinea manuum, can also resemble hand eczema. It can be ruled out by a KOH preparation or fungal culture. Also, in many cases, tinea manuum is unilateral, and the fungal infection may also involve both feet (“one hand, two feet syndrome”), whereas hand eczema is frequently bilateral.

Infestations, such as scabies, should also be in the differential. Scabies can be ruled out with a microscopic examination (oil or KOH) of a scraping of a burrow. Typically scabies is widespread, but it can be initially localized to the hands. Other infections should be considered when clinically indicated and can be tested for with cultures or microscopic examination.

Who is at Risk for Developing this Disease?

Hand eczema is one of the most frequently encountered dermatologic disorders. It is estimated that the point prevalence of hand eczema is around 4% and the lifetime prevalence around 15%. Women are more commonly affected than men, mainly due to domestic and occupational environmental exposures, and hand eczema generally peaks in young women in the 20s and 30s and decreases with age.

A history of childhood atopic dermatitis is the most important risk factor for both the development and persistence of hand eczema, and even more so if the atopic dermatitis was severe. Hand dermatitis can be the only manifestation of atopic dermatitis in adults. Further, atopic individuals may be particularly susceptible to contact dermatitis due to their impaired epidermis at baseline and chronic use of topicals. Certain occupational groups are also of increased risk, particularly those involving wet work or exposures to chemical irritants and allergens, including hairdressers, health care workers, food service workers, florists, and cleaners.

What is the Cause of the Disease?

The major physical barrier of the skin is the stratum corneum of the epidermis. This layer is composed of corneocytes and lipids, which prevent water from leaving the body and keep materials from crossing through the skin. The stratum corneum of the palms is thicker than that of most other areas of the body, so it is less susceptible to exogenous irritants. However, the barrier of the skin is dynamic, and it can become compromised by chemicals, irritants, allergens, immunologic factors, and low humidity, which can result in dermatitis of the hands.

The most common types of hand eczema are irritant contact dermatitis, allergic contact dermatitis, essential (no-specific), and atopic hand eczema. Other variants include nummular, psoriasiform, dyshidrotic, and fingertip dermatitis (Table II). Hand eczema is often a hybrid of several types of eczema, and treating one of the causes may cause some, but not total, relief. It is important to identify all causes and target treatment individually, and failure to do so may contribute to its chronic course and apparent poor response to treatment.

Table II.
Essential (non-specific) Atopic
Irritant Allergic
Dyshidrotic (pomphylox) Psoriasiform
Nummular Lichen simplex chronicus
Fingertip  

Irritant contact dermatitis is one of the most common causes of hand inflammation. It is a nonimmunologic toxic reaction to a physical or chemical change to the barrier function of the epidermis, and all people are susceptible. Chemicals, such as alkaline soaps, organic solvents, or acids extract lipids and water from the skin to cause dehydration and eventual compromise to its protective function.

The extent and severity of the eczema that results is dependent upon the length of exposure, concentration and strength of the irritant, and the susceptibility of the individual person. Patients are highly variable in their sensitivity to irritants, but with sufficient exposure, everyone is reactive to irritating agents.

Allergic contact dermatitis is a Type-IV, delayed-type hypersensitivity reaction caused by antigen-specific T cells that react to specific antigens that cross the epidermal barrier. Langerhans cells, or antigen presenting cells of the epidermis, mediate the interaction between antigens and T cells, and this interaction results in the activation and proliferation of T cells by cytokines and other inflammatory mediators.

Only certain individuals are susceptible to reacting to particular antigens. Contact allergens require prior exposure for sensitization. Once sensitization has occurred, subsequent exposures cause allergic contact dermatitis to develop within 12 to 48 hours and can persist for several weeks. Often, the shape and location of the dermatitis can be indicative of the causative agent, but this is not always the case.

Systemic Implications and Complications

Hand eczema is generally not associated with systemic disorders. The main concerns with hand eczema and systemic effects stem from the immunomodulating treatments that are sometimes employed. Systemic corticosteroids, in particular, can cause many adverse effects if used long-term, including adrenal suppression, immunosuppression, cataracts, glaucoma, hypertension, osteoporosis, skin atrophy, weight gain, and an increase in blood sugar levels.

Treatment Options

Treatment options are summarized in Table III.

Table III.
Lifestyle Changes Topical Treatments Systemic Treatments Physical Treatments
·        Avoidance of possible irritants/ allergens·        Decrease exposure to wet work and frequency ofhand washing·        Liberal use of moisturizers, emollients·        Use of mild, hypoallergenic soaps·        Protective measures (gloves, barrier creams) ·        Potent topical steroids·        Calcineurin inhibitors·        Coal tar and derivatives·        Tazarotene ·        Short course of systemic steroids·        Azathioprine·        Methotrexate·     Cyclosporine·        Mycophenolate mofetil·        Alitretinoin·        Acitretin ·        Phototherapy (UVA1,UVB, narrow-band UVB, PUVA)

Optimal Therapeutic Approach for this Disease

Most patients with hand eczema can be managed with a combination of skin protective measures and topical treatments. When these options are insufficient, systemic therapies can be utilized.

Before beginning pharmacologic interventions, lifestyle changes should first be recommended. These changes include avoidance of possible irritants and allergens, using protective measures when in contact with potential irritants and allergens, such as gloves and barrier creams, and decreasing the amount of wet work and mechanical irritation of the hands. When using gloves, white cotton gloves should be worn underneath vinyl gloves to prevent maceration from sweating. Manual dexterity and safety depending on the occupation must be considered when recommending gloves.

Skin care is a critical part of treating hand eczema, which focuses on moisturizers, emollients, and the use of mild, hypoallergenic soaps. Patients should apply a protective moisturizing cream or ointment after each hand washing or exposure to water. Ointments are generally preferred because preservatives in creams pose a risk of contact sensitivity. White petroleum jelly is highly recommended, as it is nonsensitizing, cheap, and it remains in the stratum corneum to help restore barrier function. However, the greasy texture may diminish compliance.

Potent topical steroids are the initial pharmacologic treatment of choice. The thick stratum corneum of the hands and particularly of the palms requires the use of more potent preparations of topical steroids. In general, ointments are more effective and have fewer preservatives than creams. A treatment trial of emollients and potent topical steroids should last a few weeks.

In general, subacute inflammation should be treated with group III to IV topical steroids. Chronic inflammation should be treated with group I topical steroids without occlusion or group II to V topical steroids with occlusion until the inflammation subsides. The exact length of time is dependent on the clinical presentation, but assessment for improvement is reasonable approximately 4 weeks into treatment. If improvement is noted, treatment should be continued for several more weeks before re-assessment. If response is poor, adherence to the treatment regimen should be investigated, and alternative options should be considered.

Long-term use of topical steroids can result in several adverse effects, including skin thinning or atrophy and allergic contact dermatitis to the steroid itself or its excipient. Tachyphylaxis can also occur. Intermittent dosing or alternating the use of a topical steroid with a topical calcineurin inhibitor may reduce the risk of these adverse effects. The topical calcineurin inhibitors tacrolimus and pimecrolimus can be used to reduce the use of topical steroids. Adverse effects of topical calcineurin inhibitors include marked stinging upon application. Other topical agents include coal tar and its derivatives, and retinoids.

A wide variety of systemic therapies have been used in the treatment of hand eczema, though most have not been specifically approved for this purpose. Only alitretinoin, an oral retinoid, has been approved for hand eczema that has refractory to standard topical steroid treatments. It has been tested at 10mg and 30mg daily doses, showing a more significant response with 30mg daily, and typically takes 4 to 6 weeks to become effective. It is rarely prescribed because of cost and side-effects.

Systemic steroids can result in dramatic improvement, but relapse usually occurs soon after, so they are only recommended in the most severe cases or to control acute flares in the short-term. Treatment doses of 0.5-1mg/kg or 40-60mg prednisone tapered over several weeks can be effective. Other systemic therapies that are used are cyclosporine, azathioprine, methotrexate, mycophenolate mofetil, and acitretin. Generally, these systemic treatments are reserved for refractory cases as steroid sparing agents. One may consider starting with cyclosporine 3mg/kg/day.

Phototherapy, such as ultraviolet (UV)A1, BB-UVB, narrow-band UVB, or psoralen plus UVA(PUVA, oral or topical), can be effective in some resistant cases. Ionizing radiation, including X-rays and Grenz rays, have been used and are of mainly historical interest.

Patient Management

Patients should be followed up at regular intervals after the start of treatment, particularly in severe hand eczema. It is appropriate to assess the success of treatment trials every 4-6 weeks, until a good maintenance regimen has been determined. Often, hand eczema is chronic, as in atopic dermatitis and with certain exposures and habits that are difficult to avoid in everyday life, so management is long-term.

Therapy should be altered when treatment trials have failed, or if improvement has only been partially effective. At these junctures, a hybrid cause of hand eczema should be considered to better treat the patient. If initial treatments are unsuccessful, patch testing can be employed. Patients need to remain active in their controlling hand eczema.

Unusual Clinical Scenarios to Consider in Patient Management

The diagnosis of hand eczema is usually straightforward. Rarely, lichen planus, lupus erythematosus, dermatomyositis, pityriasis rubra, pilaris, and cutaneous T cell lymphoma may mimic hand dermatitis. A skin biopsy and typical lesions elsewhere on the body can help make the diagnosis.

What is the Evidence?

Thyssen, JP, Johansen, JD, Linneberg, A, Menné, T. “The epidemiology of hand eczema in the general population–prevalence and main findings”. Contact Dermatitis. vol. 62. 2010. pp. 75-87. (A excellent review of studies published between 1964 and 2007 on the epidemiology, risk factors, and general prognosis of hand eczema.)

English, J, Aldridge, R, Gawkrodger, DJ. “Consensus statement on the management of chronic hand eczema”. Clin Exp Dermatol. vol. 34. 2009. pp. 761-9. (A comprehensive guideline on the management of hand eczema, covering education, lifestyle modifications, topical and systemic therapies, and phototherapies, with a general algorithm on the overall treatment strategy of chronic hand eczema.)

Apfelbacher, CJ, Funke, U, Radulescu, M, Diepgen, TL. “Determinants of current hand eczema: results from case-control studies nested in the PACO follow-up study (PACO II)”. Contact Dermatitis. vol. 62. 2010. pp. 363-70. (Two case-control studies, one with 100 cases of hand eczema and the other with cases of irritant hand eczema, which examined previous occupational and domestic exposures. In the first study, atopic skin diathesis was the only variable that was significantly associated with hand eczema. In the second concerning irritant hand eczema, both wet work of > 2 hours and an atopic skin diathesis were significantly more prevalent in cases when compared to controls.)

Warshaw, EM. “Therapeutic options for chronic hand dermatitis”. Dermatol Ther. vol. 17. 2004. pp. 240-50. (An excellent review on the various types of hand eczema and their current treatment options.)

Veien, NK, Hattel, T, Laurberg, G, Veien, NK, Hattel, T, Laurberg, G. “Hand eczema: causes, course, and prognosis I”. Contact Dermatitis. vol. 58. 2008. pp. 330-34. (Two papers on the results of a cohort study describing the characteristics of 522 consecutive patients at a single dermatology practice. Results characterize the severity of hand eczema, the frequency of the various causes, the nature of the course of the disease, and the overall prognosis hand eczema over 5 years of follow-up.)

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