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Dermatitis

Authors: Dr Ian Coulson, Consultant Dermatologist, Burnley, Lancashire, UK. April 2022. Previous author: Dr Amanda Oakley, Dermatologist, New Zealand, 1997. Copy edited by Gus Mitchell.


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What is dermatitis?

Dermatitis refers to a group of itchy inflammatory conditions characterised by epidermal changes.

Dermatitis can be classified in a variety of ways. It may be classified by:

In many cases, various factors may all act as underlying triggers together (allergic, irritant, and endogenous factors, especially in hand dermatitis). 

The terms dermatitis and eczema are often used interchangeably. All eczema is a dermatitis, but not all dermatitis is eczema.

  • Dermatitis, strictly speaking, includes any cause of skin inflammation affecting the epidermis.
  • Eczema is derived from the Greek word for “to boil or bubble over”, which pathologically manifests as oedema within the epidermis (called spongiosis).

The term dermatitis is sometimes mistakenly attributed to mean an eczema induced by an occupational factor; this is erroneous.

Dermatitis

Who gets dermatitis?

Dermatitis is common, affecting about one in every five persons at some stage in their life. 

Different types of dermatitis are more frequent at different stages of life, for example:

There are no consistent racial factors influencing disease frequency.

What are the clinical features of dermatitis? 

Dermatitis may be either acute or chronic, and although the mechanism by which the dermatitis develops may be the same, the appearances may be starkly different.

  • Acute dermatitis will show redness or swelling, papulation, vesiculation, oozing and weeping, and even blistering.
  • Chronic eczema will show skin thickening with accentuation of the skin creases, hyperkeratosis, scaling, fissuring, excoriation, and hyperpigmentation.
  • Subacute dermatitis will show features of both.

How do the clinical features vary in different racial groups?

Redness may be more difficult to appreciate in darker skin types. 

Post-inflammatory hypo- and hyperpigmentation are more frequent in darker skin types.

What are the types of dermatitis?

Exogenous dermatitis is the result of an external factor or insult that induces skin inflammation. Common causes include:

  • Allergic contact dermatitis — due to immune sensitisation of an individual to an allergen, often at even low concentration, such as nickel, hair dye, rubber, or perfumes; identified by patch testing.
  • Irritant contact dermatitis — will occur in anyone exposed to an irritant at sufficient concentration for long enough; irritants include soaps, detergents, organic solvents, degreasing agents, abrasives, desiccants, dust, urine, and even water
  • Photosensitive dermatitis — triggered by light or UV radiation
  • Post-traumatic dermatitis — due to physical injuries such as abrasions, burns, or surgery
  • Dermatitis induced by local skin infections such as bacterial, fungal, and viral e.g. molluscum contagiosum and HTLV-1 disease
  • Drug-induced dermatitis.

Endogenous dermatitis occurs because of often ill-understood internal factors. Common types include:

What is the differential diagnosis of dermatitis?

How is dermatitis investigated?

A detailed history and examination may be all that is required to make an accurate diagnosis. 

The following investigations may sometimes be needed:

  • Skin scraping to exclude a fungal infection mimicking a dermatitis
  • Skin swab looking for bacterial or viral superadded infection
  • Patch testing to identify contact allergens
  • Light testing if a photosensitive dermatitis is considered
  • Skin biopsy to exclude mimics of dermatitis
  • Blood tests — IgE (usually elevated in atopic dermatitis), thyroid function (in some hand dermatitis and asteatotic dermatitis).

How is dermatitis treated?

General principles are covered here. Specific management of specific types of dermatitis are detailed on the relevant pages. 

  • Potential allergen identification and avoidance — made on the basis of history e.g. hobbies, products used, and occupation. A patch test will confirm.
  • Potential irritant identification and avoidance — avoid soaps, shower gels, dust, organic solvents, and drying/desiccating agents.
  • Protect the skin with personal protective equipment — especially hand dermatitis, by the use of cotton gloves for dry work, and cotton with an occlusive glove appropriate to the suspected allergen or irritant.

Topical therapies

  • Emollients — both in place of soap, after bathing or washing, and at any time if the skin feels dry.
  • Potassium permanganate soaks — useful for drying up weepy exudative or blistering acute eczema.
  • Paste bandages — useful to help topical steroids penetrate the skin, soothe, and reduce skin trauma from scratching.
  • Topical steroids — generally use an ointment if the skin is dry, and a cream if it is wet and weepy.
    • Most work just as well if applied only once daily. 
    • Help reduce skin inflammation that causes the eczema, and should be applied where the skin is inflamed (red and itchy). 
    • Potent products are often used for 7–14 days, then the frequency of application is reduced to alternate days, then twice weekly, and the potency of the steroid reduced. 
    • Twice weekly steroid treatment is often recommended to prevent disease relapse, and prevent flare-ups for extended periods.
  • Topical anti-inflammatory agents
    • Calcineurin inhibitors such as pimecrolimus and tacrolimus suppress eczema and do not have the long-term side effects of potent steroids, particularly for the face. 
    • Newer small molecules such as JAK inhibitors (ruxolitinib) are being developed for the treatment of dermatitis.

Physical therapies

Systemic agents

  • Antihistamines — to suppress the itch of eczema, a sedating antihistamine, rather than a non-sedating agent is generally needed. 
  • Antibiotics and antivirals — should be considered if the eczema is super-infected with bacteria (Staphylococcus) and herpes simplex
  • Immunosuppressive therapies — less than 2% of chronic eczema sufferers will fail to be adequately controlled with the above therapies. Agents that reduce the overactive immune response seen in dermatitis may help. Methotrexate, azathioprine, and ciclosporin are the agents usually considered. 
  • Biological therapies — antibody treatments that specifically block the key mediators of inflammation in dermatitis (cytokines) are in use and in active development for severe dermatitis. These injection treatments include dupilumab, tralokinumab, labrkizumab, and nemolizumab. 
  • Oral small molecules — baricitinib, upadacitinib, and abrocitanib are currently being considered for licence and use in severe resistant atopic dermatitis in many countries. These agents block the JAK/STAT pathways that in turn regulate cytokine production. 

 

 

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