Acute palmoplantar eczema (dyshidrotic eczema)

INTRODUCTION — Acute palmoplantar eczema (more popularly known as dyshidrotic eczema or pompholyx) is an intensely pruritic, vesicular eruption affecting the palms, soles, or both [1,2]. It is characterized by deep-seated lesions ranging from small vesicles to large, tense bullae clinically and by spongiotic vesicles histologically. Recurrence is common, and patients typically experience frequent episodes for months or years.

This topic will discuss the pathogenesis, clinical presentation, diagnosis, and management of dyshidrotic eczema. Other forms of eczema involving the hands, including irritant and allergic contact dermatitis and atopic dermatitis, are discussed separately.

●(See "Irritant contact dermatitis in adults".)

●(See "Clinical features and diagnosis of allergic contact dermatitis".)

●(See "Management of allergic contact dermatitis in adults".)

●(See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)

●(See "Treatment of atopic dermatitis (eczema)".)

TERMINOLOGY — The terminology for acute palmoplantar eczema is confusing. The term "dyshidrosis" was coined in 1873 to describe a blistering disease of the palms and soles that was believed to be a disorder of the sweat glands [3]. It is now accepted that the sweat glands are not involved in the pathogenesis [4,5]. However, the term "dyshidrotic eczema" continues to be used.

Other terms for acute palmoplantar eczema include "pompholyx," "dyshidrosis," "vesicular palmoplantar eczema," "acute and recurrent vesicular hand dermatitis," "cheiropompholyx" (affecting the hands), or "podopompholyx" (affecting the feet). These terms do not represent a specific diagnosis but, rather, indicate a morphologic pattern of hand/foot eczema that can occur with irritant contact, allergic contact, or endogenous eczema.

EPIDEMIOLOGY — Dyshidrotic eczema occurs most commonly in young adults and in females [6].

The prevalence of either mild or severe dyshidrotic eczema in the general population is unknown. A survey and examination of over 107,000 people in Sweden found a prevalence of 0.05 percent [7]. Among patients with hand dermatitis, dyshidrotic eczema accounts for 5 to 20 percent of cases [3,8-10].

RISK FACTORS — The cause of dyshidrotic eczema is unknown, but it is probably multifactorial. Although, in most cases, a causative or predisposing factor cannot be identified, factors that have been associated with the development of dyshidrotic eczema include:

●History of atopic dermatitis [11,12]

●Exposure to contact allergens, particularly metals [11,13,14]

●Exposure to contact irritants (eg, metalworking fluids) [15]

●Systemic exposure to contact allergens (eg, ingestion of nickel or cobalt) [16]

●Dermatophyte infection at a distant site (id reaction) [12]

●Treatment with intravenous or subcutaneous immune globulin [13,17-22]

●Treatment with secukinumab, an interleukin (IL) 17 inhibitor approved for the treatment of psoriasis and psoriatic arthritis [23]

●Hyperhidrosis [11]

●Smoking [24]

●Exposure to ultraviolet (UV) radiation [25]

PATHOGENESIS — The mechanisms underlying the development of dyshidrotic eczema are largely unknown. One hypothesis is that the overexpression of two water/glycerol channel proteins, aquaporin-3 and aquaporin-10, across all layers of the epidermis may alter the function of the epidermal water permeability barrier, with transepidermal water loss exacerbated by exposure to water and alkaline skin pH [26,27].

CLINICAL PRESENTATION — Episodes of dyshidrotic eczema often start with pruritus followed by a sudden, symmetric eruption of intensely pruritic vesicles on the palms, lateral and dorsal aspects of the fingers (picture 1A-D), or on the soles. In 70 to 80 percent of patients, only the hands are involved [13]. In mild cases, vesicles develop only on the lateral aspect of fingers (picture 1A, 1D). New episodes or worsening tend to be more common during the warmest months of the year.

The vesicles are typically deep seated and multilocular ("tapioca or sago pudding" lesions); they may coalesce into large bullae (picture 2A). In some patients, symptoms may be severe enough to interfere with occupational duties and daily activities (picture 2B).

CLINICAL COURSE AND COMPLICATIONS — Vesicles and bullae persist for several weeks, desiccate, and resolve with desquamation (picture 3) [1,3]. Frequent relapses may result in chronic hand dermatitis, characterized by red, lichenified, and scaling patches or plaques with fissures (picture 1E).

Episodes may recur at intervals of three to four weeks for months or years. In some patients, flares may be associated with emotional or physical stress, but most often, they occur in the absence of an identifiable trigger. Between episodes, the skin returns to a normal appearance, in contrast to the persistent signs and symptoms of chronic vesicular hand dermatitis secondary to irritant or allergic contact dermatitis or atopic dermatitis.

Severe episodes can affect the nail matrix and produce dystrophic nail changes such as horizontal ridging and color changes (picture 1E). Secondary infection, usually with Staphylococcus aureus, may occur.

DIAGNOSIS

Clinical diagnosis — The diagnosis of dyshidrotic dermatitis is usually made based upon clinical findings, symptoms, and history:

●Tense, deep-seated vesicles or bullae localized on the palms and soles and often on the lateral aspect of the fingers (picture 1B, 1D)

●Tiny vesicles limited to the lateral aspect of fingers (picture 1A)

●Intense pruritus

●Acute onset

●History of recurrence

Assessment of severity — The severity of dyshidrotic eczema is generally assessed subjectively. A scoring tool called the Dyshidrotic Eczema Area and Severity Index (DASI), based upon the number of vesicles, intensity of erythema, desquamation, and itch, was designed for use in clinical trials but is not routinely used in clinical practice [28]:

●Mild to moderate − We consider dyshidrotic eczema to be mild to moderate if it does not involve the entire palmar or plantar surface; presents as a few crops of vesicles or scattered, small vesicles with absent or modest erythema (picture 1B, 1E-G); and the patient does not complain of intolerable pruritus, burning, or pain.

●Severe − We consider dyshidrotic eczema to be severe if it involves the entire palmar or plantar surface and presents with large vesicles or bullae that are disabling (picture 2A-C) (ie, prevent walking or use of the hands) or if it is intensely painful or pruritic (regardless of the size of the lesions).

Indications for biopsy — A skin biopsy for histopathologic examination is rarely needed. Potential indications for skin biopsy include lack of response to treatment and exclusion of other conditions in the differential diagnosis (eg, psoriasis or palmoplantar pustulosis).

If a skin biopsy is performed, periodic acid-Schiff (PAS) staining for fungal elements may be useful in excluding a fungal infection. (See 'Differential diagnosis' below.)

Histopathology — The histologic features of dyshidrotic eczema depend upon the stage (acute or chronic) of the disease:

●Acute stage − The acute form is characterized by intraepidermal spongiotic vesicles or bullae that do not involve the intraepidermal portion of the eccrine sweat duct (acrosyringium). A sparse, superficial, perivascular infiltrate of lymphocytes is usually present. The epidermal thickness is normal, and the thick stratum corneum of acral skin is intact.

●Chronic stage − In chronic cases, there is a predominance of parakeratosis and acanthosis with minimal or no spongiosis and a dermal, lymphocytic infiltrate.

Patch testing — Patch testing is generally not helpful in making the diagnosis of dyshidrotic eczema. However, it is often performed by dermatologists to determine whether there is a component of allergic contact dermatitis. Patch testing may also be warranted in patients who do not respond to initial therapy [1,3]. (See "Patch testing" and "Management of allergic contact dermatitis in adults", section on 'Allergen avoidance'.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of dyshidrotic eczema includes inflammatory and infectious vesicobullous skin diseases [1,3]:

●Allergic contact dermatitis – Allergic contact dermatitis may be clinically indistinguishable from dyshidrotic eczema (picture 4A-B). The correct diagnosis is based upon the assessment of allergen exposure and results of patch testing. (See "Clinical features and diagnosis of allergic contact dermatitis", section on 'Diagnosis'.)

●Bullous tinea – Bullous tinea occurs more often on the feet than on the hands and is usually unilateral (picture 5A-B). Potassium hydroxide (KOH) microscopic examination of scrapings from the lesions reveals fungal elements. (See "Dermatophyte (tinea) infections", section on 'Tinea pedis'.)

●Irritant contact dermatitis – Irritant contact dermatitis usually involves the dorsal aspect of the hands and web spaces (picture 6A-B). Patients often report a history of irritant exposure. Vesicles and bullae are rarely present, unless there was exposure to a strong irritant with a resultant chemical burn. (See "Irritant contact dermatitis in adults".)

●Atopic hand dermatitis – Atopic hand dermatitis commonly involves the dorsum of the hands (picture 7). Patients report a history of atopic dermatitis, seasonal allergies, or asthma and may present with eczema lesions or lichenification involving flexural areas (ie, antecubital and popliteal fossae) (picture 7). (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis", section on 'Diagnosis'.)

●Dermatophytid (id) reaction – A dermatophytid reaction, also called "autoeczematization," is a secondary, pruritic, papulovesicular eruption that may occur on the palms in association with a dermatophyte infection at a distant site, more often on the foot but also on the scalp or other body area (picture 8). A complete skin examination and a KOH preparation of scrapings from suspicious lesions at a distant site are necessary to confirm the diagnosis. (See "Dermatophyte (tinea) infections", section on 'Id reactions' and "Dermatophyte (tinea) infections", section on 'Diagnosis'.)

●Herpetic whitlow – Herpetic whitlow may mimic dyshidrotic eczema [29]. Typically, it presents as grouped vesicles on a red base, is more often painful than pruritic, and is usually unilateral (picture 9). The diagnosis can be made by viral culture, immunofluorescence staining, polymerase chain reaction, or Tzanck smear. (See "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection", section on 'Diagnosis'.)

●Palmoplantar pustulosis – Palmoplantar pustulosis may have an early, vesicular stage, but pustules usually develop in a few days (picture 10A-B). In 8 to 10 days, the pustules change their color to dark brown, become dry, and desquamate (picture 11). (See "Palmoplantar pustulosis: Epidemiology, clinical features, and diagnosis".)

●Autoimmune bullous diseases – Bullous pemphigoid and pemphigus vulgaris may rarely present as localized disease involving the hands or feet (picture 12). The history reflects a longer and unremitting course. Biopsy for routine histology, direct immunofluorescence, and serologic testing for specific autoantibodies provide the correct diagnosis. (See "Clinical features and diagnosis of bullous pemphigoid and mucous membrane pemphigoid", section on 'Diagnosis' and "Pathogenesis, clinical manifestations, and diagnosis of pemphigus", section on 'Diagnosis'.)

CLINICAL COURSE — Episodes of dyshidrotic eczema tend to spontaneously resolve over several weeks. However, dyshidrotic eczema is a recurrent disease, and patients typically experience frequent attacks of vesicular dermatitis for many years. Episodes tend to occur less frequently with age, and most patients eventually experience a complete remission [30].

MANAGEMENT — Treatment is required for most patients who present with complaints of pruritus or other symptoms. The approach to management is guided by the severity of the disease (see 'Assessment of severity' above) and involves the following:

●Identification and avoidance of causative or exacerbating factors

●Treatment of skin inflammation

●Adoption of skin care measures to reduce skin irritation

General measures — In clinical experience, the avoidance of irritants or exacerbating factors is beneficial for most patients with dyshidrotic eczema. General skin care measures aimed at reducing skin irritation and restoring the skin barrier include [31]:

●Using lukewarm water and mild, synthetic detergent (nonsoap) cleansers to wash hands. Most liquid body cleansers are actually synthetic detergent products with a neutral pH. In contrast, "natural" soaps (eg, Castile soap) have an alkaline pH and tend to be more aggressive detergents.

●Drying hands thoroughly after washing.

●Applying emollients (eg, petroleum jelly) immediately after hand drying and as often as possible.

●Wearing cotton gloves under vinyl or other nonlatex gloves when performing wet work.

●Removing rings, watches, and bracelets before wet work.

●Wearing protective gloves in cold weather.

●Wearing task-specific gloves for frictional exposures (eg, gardening, carpentry).

●Avoiding cutaneous exposure to irritants (eg, harsh detergents, solvents, hair dyes, acidic foods [eg, citrus fruit]).

In clinical practice, astringent solutions such as aluminum subacetate (Burow's solution) or witch hazel are used for wet, weeping skin. Hands or feet are soaked in the solution for 15 minutes two to four times per day. Alternately, soakings can be replaced by thin, wet dressings through which air will circulate, enhancing the drying effect of astringent solutions. Large bullae may be drained or aspirated using a sterile syringe to reduce pain and prevent spontaneous rupture with risk of local infection.

Mild to moderate disease

●Topical corticosteroids – For patients with mild to moderate dyshidrotic eczema (picture 1B, 1E-G) that has not responded to general measures, we suggest super high-potency or high-potency topical corticosteroids (groups 1 to 3 (table 1)) as first-line therapy. (See 'Assessment of severity' above and 'General measures' above.)

Topical corticosteroids are applied twice daily for two to four weeks. Ointments are generally preferred to other vehicles (creams, solutions, or foams) because they contain fewer potential irritants and allergens, such as additives or preservatives [1,3,31]. However, some patients prefer other vehicles because ointments make their hands too greasy for performing tasks.

The efficacy of topical corticosteroids versus placebo or no treatment for dyshidrotic eczema has not been adequately evaluated in randomized trials. However, they are used in clinical practice because of their anti-inflammatory properties and their efficacy in other forms of hand eczema. (See "Treatment of atopic dermatitis (eczema)", section on 'Topical corticosteroids'.)

The long-term use of topical corticosteroids is limited by their side effects, which include skin atrophy, striae, and telangiectasia. (See "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)

●Topical calcineurin inhibitors – We generally do not suggest a topical calcineurin inhibitor as the first-line anti-inflammatory treatment for dyshidrotic eczema. The anti-inflammatory effect of topical calcineurin inhibitors is approximately equivalent to moderate-potency topical corticosteroids [32]. In addition, topical calcineurin inhibitors are more expensive than many topical corticosteroids.

However, when patients and/or clinicians prefer to avoid long-term use of topical corticosteroids for the treatment of mild to moderate dyshidrotic eczema (picture 1A-B, 1F), the topical calcineurin inhibitor tacrolimus is an alternative [33,34]. Tacrolimus 0.1% ointment is applied twice daily until resolution.

In a randomized trial including 16 patients with moderate to severe dyshidrotic eczema, topical tacrolimus was compared with mometasone furoate, a high-potency topical corticosteroid (group 3) [35]. After four weeks of treatment ointment, both topical tacrolimus 0.1% and mometasone furoate 0.1% reduced the Dyshidrotic Eczema Area and Severity Index (DASI) by more than 50 percent compared with baseline.

Severe disease — In addition to the general measures described above, we suggest a short course of oral corticosteroids for the treatment of severe dyshidrotic eczema (picture 2A-C). (See 'Assessment of severity' above and 'General measures' above.)

We generally start with prednisone 40 to 60 mg once per day in the morning for one week. If there is an adequate response, the dose is then reduced by 50 percent in the next five to seven days and finally tapered and discontinued over the following two weeks.

Oral corticosteroids for dyshidrotic eczema have not been evaluated in clinical trials. However, in clinical experience, they have been beneficial for the short-term treatment of dyshidrotic eczema and other forms of severe, eczematous dermatitis. (See "Management of severe atopic dermatitis (eczema) in children", section on 'Systemic corticosteroids'.)

Superpotent topical corticosteroids applied under occlusive dressings (eg, polyethylene gloves for the hands or plastic wrap for the feet) are a treatment option for severe dyshidrotic eczema in patients for whom systemic glucocorticoids are contraindicated or in patients who prefer to avoid systemic corticosteroids. Occlusive dressings are usually used at nighttime for three to seven days.

Evaluation of treatment response — Clinical criteria used to evaluate the response to treatment include cessation of vesiculation; clearance of pre-existing vesicles; and reduction of erythema, pruritus, and pain. Resolution is usually associated with increased skin dryness and desquamation.

Refractory disease — Dyshidrotic eczema is considered refractory if there is no improvement/resolution in two to four weeks of adequate treatment. Refractory cases may warrant additional evaluation and reconsideration of the full differential diagnosis.

Additional diagnostic evaluation — Patients with clinical features of dyshidrotic eczema who do not respond or are not adequately controlled after two to four weeks of topical corticosteroids, topical tacrolimus, or systemic corticosteroids may need further evaluation to confirm or rule out the diagnosis.

Additional testing may include (see 'Differential diagnosis' above):

●Potassium hydroxide (KOH) preparation to rule out a fungal infection.

●Bacterial culture to rule out bacterial superinfection. Superinfection with S. aureus is a common cause of inadequate response to treatment in patients with hand eczema, especially with severe disease and wet, weeping lesions. Bacterial superinfection is treated with oral antibiotics. (See "Impetigo", section on 'Systemic antibiotics'.)

●Skin biopsy and histopathologic examination to confirm the diagnosis of dyshidrotic eczema and exclude other conditions. Periodic acid-Schiff (PAS) staining for fungal elements should be included. Direct immunofluorescence may be necessary if bullous pemphigoid or pemphigus are suspected. (See 'Diagnosis' above.)

●Patch testing and detailed history of household- or work-related exposures to exclude an allergic or irritant contact dermatitis. (See "Patch testing" and "Clinical features and diagnosis of allergic contact dermatitis", section on 'History'.)

Treatment

Phototherapy — We suggest oral or topical psoralen plus ultraviolet A (PUVA) therapy or narrowband ultraviolet B (NBUVB) phototherapy for patients with a confirmed diagnosis of dyshidrotic eczema who have frequent or severe episodes that are not adequately controlled with topical or systemic corticosteroids or topical tacrolimus. (See "Psoralen plus ultraviolet A (PUVA) photochemotherapy" and "UVB phototherapy (broadband and narrowband)".)

The use of NBUVB and PUVA for patients with dyshidrotic eczema is largely supported by its use in the treatment of other inflammatory dermatoses, as only a few small clinical trials have demonstrated clinical improvement with PUVA in patients with dyshidrotic eczema [36-42].

Phototherapy may not be available in all communities. Phototherapy treatments are usually delivered two or three times per week. Several weeks of treatment are required to induce clinical improvement, and several months are required for resolution. Thus, the potential benefits of phototherapy should be weighed against the inconvenience of prolonged therapy on a case-by-case basis. Phototherapy that is limited to the palms and soles has few adverse effects. (See "Psoralen plus ultraviolet A (PUVA) photochemotherapy", section on 'Topical PUVA'.)

Systemic therapies

●Systemic immunosuppressive agents – Systemic immunosuppressive agents, such as low-dose methotrexate, mycophenolate mofetil, and cyclosporine, have been occasionally used in the management of patients with severe dyshidrotic eczema [43-45]. However, their use has not been evaluated in high-quality studies, and there is insufficient evidence of benefit to suggest their use in refractory cases.

●Dupilumab – Dupilumab, an interleukin (IL) 4 receptor antagonist approved for the treatment of atopic dermatitis, has been shown to be well tolerated and effective in a small series of patients with dyshidrotic eczema who had previously failed topical corticosteroids [45]. A randomized, placebo-controlled trial evaluating the efficacy of dupilumab for hand eczema uncontrolled by superpotent topical corticosteroids is ongoing (NCT03861455).

●Systemic retinoids – Alitretinoin, not available in the United States, is a systemic retinoid approved for the treatment of chronic, refractory hand eczema in the United Kingdom, Europe, and Canada. This oral retinoid exerts its anti-inflammatory and immunomodulatory effects through both the retinoid X receptor (RXR) and retinoic acid receptor (RAR). Initially expected to work better with hyperkeratotic hand eczema, it was found equally effective in vesicular hand dermatitis [46,47].

Alitretinoin is usually given at the dose of 30 mg daily for six months. Upon stopping treatment, some patients experience prolonged remissions, while others will relapse more quickly. Treatment can be resumed when relapse occurs. Some patients may require continuous treatment.

The most common adverse effect is headache during the first few weeks of treatment. Pregnancy precautions are similar to isotretinoin. Where available, this medication has found a niche between superpotent topical corticosteroids or phototherapy and systemic immunosuppressive agents.

SUMMARY AND RECOMMENDATIONS

●Epidemiology and risk factors – Acute palmoplantar eczema (also known as "dyshidrotic eczema" or "pompholyx") is a relatively uncommon, recurrent eruption affecting the palms, soles, or both. It occurs most commonly in young adults and more frequently in females. Main risk factors include a history of atopic dermatitis, exposure to contact irritants and allergens, and treatment with intravenous immunoglobulins. (See 'Epidemiology' above and 'Risk factors' above.)

●Clinical features – Dyshidrotic eczema is characterized by the sudden eruption of intensely pruritic vesicles on the palms (picture 1G), soles, or lateral aspects of the fingers (picture 1D). The vesicles persist for several weeks, desiccate, and resolve with desquamation. Episodes may recur at intervals of three to four weeks for months or years. (See 'Clinical presentation' above.)

●Diagnosis – The diagnosis of dyshidrotic eczema is usually based upon the clinical appearance and location of lesions, symptoms, and history. In selective patients with recalcitrant disease, patch testing is useful to determine whether there is a component of allergic contact dermatitis. (See 'Diagnosis' above.)

●Differential diagnosis – The differential diagnosis of dyshidrotic eczema includes bullous tinea (picture 5B), dermatophytid reaction (picture 8), bullous impetigo, herpes simplex infection (picture 9), allergic contact dermatitis (picture 4A), and palmoplantar pustulosis (picture 10A-B). (See 'Differential diagnosis' above.)

●Management:

•General measures – Avoidance of irritants or exacerbating factors is important for most patients with dyshidrotic eczema. (See 'General measures' above.)

•Mild to moderate disease – For patients with mild to moderate dyshidrotic eczema (picture 1B, 1E-G) that has not responded to general measures (see 'General measures' above), we suggest super high-potency or high-potency topical corticosteroids (groups 1 to 3 (table 1)) as first-line therapy (Grade 2C). Topical corticosteroids are applied twice daily for two to four weeks. Ointments are preferred to other vehicles. Topical tacrolimus is an alternative treatment for patients who wish to avoid long-term use of topical corticosteroids. (See 'Mild to moderate disease' above.)

•Severe disease – In addition to the general measures described above, we suggest a short course of oral corticosteroids for the treatment of severe dyshidrotic eczema (Grade 2C). Treatment is started with prednisone 40 to 60 mg per day for one week. The dose may be reduced by 50 percent in the next five to seven days and then tapered and discontinued over the following two weeks. (See 'Severe disease' above.)

•Refractory disease – For patients with clinical features of dyshidrotic eczema whose disease does not respond or is not adequately controlled after two to four weeks of superpotent topical corticosteroids or systemic corticosteroids, further diagnostic evaluation may be needed to confirm or rule out the diagnosis. (See 'Additional diagnostic evaluation' above.)

For patients with confirmed, refractory dyshidrotic eczema, we suggest phototherapy with oral or topical psoralen plus ultraviolet A (PUVA) or narrowband ultraviolet B (NBUVB) therapy rather than systemic immunosuppressants (Grade 2C). (See 'Phototherapy' above.)

Oral alitretinoin, a systemic retinoid approved for the treatment of chronic, refractory hand eczema in the United Kingdom, Europe, and Canada (but not available in the United States), may be an alternative to phototherapy for patients with refractory dyshidrotic eczema. (See 'Systemic therapies' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges David R Adams, MD, PharmD, and James G Marks, Jr, MD, who contributed to earlier versions of this topic review.