Hand Dermatitis: A Review of Clinical Features, Prevention and Treatment

Dimitar Antonov; Sibylle Schliemann; Peter Elsner

Disclosures

Am J Clin Dermatol. 2015;16(4):257-270. 

In This Article

Clinical Features

Hand dermatitis is a heterogeneous entity and this review focuses on the clinical features of its various types. Hand dermatitis is considered chronic if it lasts more than 3 months or relapses two or more times per year.[2,4] The longer the hand eczema persists, the stronger its tendency to become chronic, even after the causative agents have been withdrawn.[3] Other definitions suggest a duration longer than 6 months for chronic eczema.[5]

The identifiable etiologic factors are given in Table 1 , but in real life these factors are often concomitantly present and in approximately 20 % of cases no etiologic factors can be found.[6]

There are no reliable morphologic features that would allow distinction between irritant and allergic chronic eczema. In all cases of chronic hand dermatitis and not just in cases with suspected contact sensitization, a patch testing should be performed with the relevant standard series or patient substances.[2,7]

In acute irritant contact dermatitis, lesions vary according to the intensity of the provoking agent from mild irritation to deep chemical burns, graded similarly to thermal burns. There is usually a single or a limited number of short contacts with caustic or physical irritants and the lesions are limited to the contact area and accompanied by a burning or stinging sensation rather than itching, with a variable degree of redness, exudation or oozing, formation of vesicles or bullae and swelling.

Acute allergic contact dermatitis is caused by one or more type IV sensitizations. It spreads beyond the contact area, with more swelling, more infiltration, and more itching than acute irritant contact dermatitis.

Most patients searching for dermatological help for hand dermatitis have a chronic condition.[8]

For the irritant type of chronic eczema, the most common mechanism is the cumulative irritant one, where subclinical insults to the skin barrier are not strong enough to induce an acute reaction, but lead to cumulative damage over a longer period of time. The development of clinically apparent lesions is only the tip of the iceberg of the functional derangement of the skin barrier.[9,10] Typical risk factors are exposures to wet work, detergents, wearing occlusive glove material, and frequent hand washings per day (up to 20–30 times daily). After prolonged contact with mild irritants and/or prolonged wet work, redness, dryness and some desquamation of the affected skin develop, starting in the finger webs or on the back of the hand. These lesions progress to form fissured, infiltrated and desquamative and not very sharply demarcated plaques (Fig. 1). The eczematous changes are initially limited to the exposed areas, with the palms usually becoming involved later in the process.

Figure 1.

Cumulative irritant (chronic) contact dermatitis of the hand. Indistinctly demarcated erythematous plaques with desquamation and fissures on the back of the hands and on the fingers

In patients with chronic hand dermatitis, there is often a mixture of constitutional atopy and irritant factors, sometimes with an additional contact sensitization, and a sharp distinction between an allergic or irritant pathogenesis is not always possible. Itching as a symptom is unreliable in distinguishing between allergic and irritant causation in the chronic phase. A recent study of itching in chronic hand dermatitis unresponsive to topical therapy found an association of itching with atopy and disease severity among other factors.[11]

A very rare variant of hand dermatitis, protein contact dermatitis, develops morphologically as an initial contact urticaria, followed by eczema. It is usually caused by a type I IgE-mediated sensitization against proteins, but non-immunological forms of contact urticaria leading to eczema exist as well.[2] The urticarial stage is, however, only rarely recognized clinically.

Endogenous hand eczema is a manifestation of atopic skin diathesis. Skin barrier dysfunction, such as the one caused by filaggrin mutations, plays a role. The diagnosis might be difficult if hand dermatitis remains the only manifestation, and exogenous causes have to be ruled out to confirm the diagnosis. Finding atopic stigmata or typical lesions of atopic dermatitis elsewhere on the body, e.g. flexural areas, helps establish the diagnosis. Personal and family history of, for example, flexural eczema in childhood, asthma or pollinosis might be helpful; the atopy score is a useful instrument as well.[2] Involvement of the ventral wrists with lichenification is very typical. The hands and feet might be simultaneously involved. Other common signs are the involvement of the tips of the fingers (pulpitis sicca) or of the anatomic 'snuff box'.[2] The morphology is diverse and a recent study found no statistically significant association between atopy and a defined morphological pattern of hand dermatitis.[12]

There is no internationally accepted classification of hand dermatitis,[4] because different etiologies usually act concurrently or sequentially, and a combination of clinical patterns may be seen. An international classification based on the etiology has been proposed in order to provide uniformity in clinical studies and clinical work.[13] The cases without identifiable etiology in this study were classified morphologically into vesicular or hyperkeratotic.[13] Further elaborating on this classification, a newer diagnostic algorithm and classification has been developed.[14]

It is advisable to use an etiologic diagnosis in clinical practice and in clinical studies,[12,13] rather than just describing the morphological pattern. For example, atopic hand dermatitis may present any of the discussed morphological patterns, but defining it as atopic hand dermatitis has implications for treatment and prevention and is therefore preferable as a diagnosis to, for example, vesicular hand dermatitis. Practically, this means that a full diagnostic examination should be undertaken and the etiology should be clarified and addressed in the treatment concept, instead of just moving directly from a morphological diagnosis to therapy.

It is generally considered that clinical morphology is poorly related to etiology.[4,12–14] Molin et al.[14] found that patients with chronic irritant dermatitis more often had a hyperkeratotic rhagadiform and rarely a vesicular morphology; in allergic contact dermatitis, a mixed pattern of vesicular and hyperkeratotic lesions predominated. Similar results were reported from Johansen et al.,[12] who showed that irritant contact dermatitis was the most frequent etiology in the dry fissured variety and allergic contact dermatitis in the vesicular types. In the last study,[12] the most frequent clinical patterns were hyperkeratotic rhagadiform (dry fissured, 36 %), and vesicular (31.8 %). All other types (nummular, pulpitis sicca, hyperkeratotic) were each observed in<10 % of the study population.

  • Dyshidrosiform/vesicular eczema or pompholyx: this type begins with deep-seated vesicles on the palm and/or palmar aspects and the sides of the fingers and is usually very itchy (Figs. 2, 3). The vesicles resolve spontaneously with desquamation, but new attacks of new vesicles usually recur. The term dyshidrotic originates from the belief that the vesicles develop from the sweat glands, because this eczema is usually aggravated by sweating, hot weather and occlusion. It has been shown in histological studies that the dyshidrotic vesicles are the result of progressive spongiosis, just as in other types of eczema.[15,16] The distinct morphology is attributed to the thicker stratum corneum of the volar skin of the hands and feet. Nevertheless, the term dyshidrosiform is still widely used and some therapies against sweating, such as tap water iontophoresis and botulinum toxin, may be effective in some patients. This type is considered generally more difficult to treat than the other types of hand dermatitis. The palmoplantar pustulosis is the most important differential diagnosis. An id reaction on the hands to tinea pedis may have a dyshidrosiform morphology as well.

  • Hyperkeratotic rhagadiform: in this form, the development of erythematous infiltrated plaques with oozing followed by dry hyperkeratosis and cracking is the typical feature. Usually the palms and the volar aspects of the fingers are involved, sometimes the plantar aspects of the feet as well. The loss of skin elasticity and the hyperkeratosis lead to painful fissures in the folds, which is another typical feature. Such eczema is also called tylotic eczema, when a strong dry hyperkeratosis predominates the clinical picture. In some patients, little or no inflammation is evident, just hyperkeratotic thickening of the skin. The differentiation from a variety of disorders, such as hyperkeratotic tinea manus, psoriasis, genetically determined palmoplantar hyperkeratosis, or pityriasis rubra pilaris, may be difficult.

Figure 2.

Vesicular (dyshidrosiform) eczema or Pompholyx

Figure 3.

Vesicular (dyshidrosiform) eczema

The following are other distinct patterns of hand eczema, but these do not exhaust the variety of clinical presentations of hand dermatitis:

  • Nummular eczema: in this pattern of hand dermatitis, discoid or nummular (coin shaped) plaques develop on the back of the hands and possibly on the backs and sides of the fingers or the backs of the feet. These plaques might be scaly or with tiny vesicles on the periphery. The nummular plaques could be limited to the hands but are usually part of a generalized eruption on the body and limbs.

  • Fingertip eczema or pulpitis sicca: in this specific pattern, redness and dryness with desquamation develop on the tips of all or most of the fingers. This leads to little but very painful fissures on the fingertips. Vesicles may also be seen. The condition is usually worse in the winter and is a part of atopic eczema. Allergic or occupational variants are also known; a clue in this direction could be the involvement of just the fingers participating in an occupational activity. One well known example of the latter is allergic contact dermatitis to handling of dental material, such as acrylates, in dental technicians. Spread from the tips to the whole fingers or the palms may occur.

  • Interdigital eczema or finger web eczema develops in the interdigital spaces and on the back of the fingers with redness, chapping and desquamation. Ring eczema is a condition with a similar morphology, starting from the skin under a ring where detergents of allergens are more difficult to rinse off, leading to occlusion. Mechanical rubbing may also play a role.

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