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Dermatitis — extra information
Synonyms:
Eczema
Categories:
Rashes, Terminology
ICD-10:
L20-L30
ICD-11:
EA8Z
SNOMED CT:
703938007, 26435006, 34936997, 53107009, 414492009
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RashesTerminology

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.

Introduction
Demographics
Clinical features
Variation in skin types
Types
Differential diagnosis
Investigation
Treatment
E-lecture

What is dermatitis?

Dermatitis refers to a group of itchyinflammatory conditions characterised byepidermal 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, andendogenous factors, especially inhand dermatitis).

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

  • Dermatitis, strictly speaking, includes any cause of skininflammation affecting theepidermis.
  • Eczema is derived from the Greek word for “to boil or bubble over”, which pathologically manifests asoedema within the epidermis (calledspongiosis).

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

Acute weepy contact dermatitis due to sticking plaster allergy

Acute weepy contact dermatitis due to sticking plasterallergy 

Allergic contact dermatitis due to nickel in the sides of her spectacle frame

Allergic contact dermatitis due to nickel in the sides of her spectacle frame 

Gravitational eczema compounded by a contact allergy to a bandage constituent

Gravitational eczema compounded by a contact allergy to a bandageconstituent 

Excoriated acute eczema on the extensor aspects of the knees (reverse pattern)

Excoriated acute eczema on theextensor aspects of the knees (reverse pattern) 

Fissuring over the knuckles in atopic dorsal hand eczema

Fissuring over the knuckles inatopicdorsal hand eczema 

Weepy lesions of discoid eczema on the legs

Weepylesions ofdiscoid eczema on the legs 

Weepy and impetigenised discoid eczema on the foot

Weepy and impetigenised discoid eczema on the foot 

Fissuring, hyperkeratosis and vesiculation in chronic fingertip dermatitis

Fissuring,hyperkeratosis andvesiculation inchronic fingertip dermatitis 

Discoid pattern of eczema on the dorsal hands

Discoid pattern of eczema on the dorsal hands 

Hand eczema on the back of the hand - mixture of irritant factors in this atopic person

Hand eczema on the back of the hand - mixture of irritant factors in this atopic person 

Hypopigmentation and fine scale on the cheeks in pityriasis alba

Hypopigmentation and finescale on the cheeks inpityriasis alba 

Cheek and nasolabial fold redness and scaling in seborrhoeic dermatitis

Cheek and nasolabial fold redness andscaling inseborrhoeic 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 withaccentuation of the skin creases, hyperkeratosis, scaling, fissuring,excoriation, andhyperpigmentation.
  • 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 immunesensitisation of an individual to anallergen, often at even low concentration, such as nickel,hair dye, rubber, or perfumes; identified bypatch 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 orUV radiation
  • Post-traumatic dermatitis — due to physical injuries such as abrasions, burns, or surgery(eg,autonomic denervation dermatitis)
  • Dermatitis induced by local skininfections such asbacterial, 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 fungalinfection mimicking a dermatitis
  • Skin swab looking for bacterial or viral superadded infection
  • Patch testing to identify contactallergens
  • Light testing if aphotosensitive dermatitis is considered
  • Skinbiopsy 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 withpersonal protective equipment — especially hand dermatitis, by the use of cotton gloves for dry work, and cotton with anocclusive 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 helptopical steroids penetrate the skin, soothe, and reduce skintrauma from scratching.
  • Topical steroids — generally use anointment if the skin is dry, and acream 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 diseaserelapse, and prevent flare-ups for extended periods.
  • Topicalanti-inflammatory agents
    • Calcineurininhibitors such aspimecrolimus andtacrolimus suppress eczema and do not have the long-term side effects of potent steroids, particularly for the face.
    • Newer smallmolecules such asJAK inhibitors (ruxolitinib) are either approved or 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 withbacteria (Staphylococcus) andherpes 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, andciclosporin are the agents usually considered.
  • Biological therapiesantibody treatments that specifically block the keymediators of inflammation in dermatitis (cytokines) are in use and in activedevelopment for severe dermatitis. These injection treatments includedupilumab,tralokinumab,lebrikizumab, andnemolizumab.
  • Oral small moleculesbaricitinib,upadacitinib, and abrocitanib either are licensed or are being considered for licence and use in moderate/severe atopic dermatitis in many countries. These agents block theJAK/STAT pathways that in turn regulatecytokine production.

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