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Dermatitis

Dermatitis

Dermatitis is a nonspecific inflammatory response of the skin to a combination of exogenous and endogenous factors. It is manifest as an itchy, erythematous, and sometimes scaly rash. In the acute stage, there may be weeping, crusting and blisters. Histologically there is spongiosis (intercellular oedema) and superficial inflammation. There is not a clear distinction between dermatitis and eczema, and the two terms are interchangeable.

A classification of the types of dermatitis is shown in Table 1, below.

Endogenous dermatitis

When exogenous factors can be excluded as a major cause then the dermatitis is termed constitutional or endogenous dermatitis. The different types of endogenous dermatitis represent a pattern of disease rather than a definitive aetiology.

Atopic dermatitis is a multifaceted disease the cause of which is still unknown. Patients with atopic dermatitis frequently have elevated IgE levels and a personal or family history of asthma or hayfever. Other associations include dry skin, facial pallor, low finger temperature, pronounced vasoconstriction on exposure to cold, white dermographism, and a susceptibility to cutaneous viral and bacterial infections. Ophthalmological manifestations of atopy include the Dennie-Morgan infraorbital fold, infraorbital darkening of the skin, conjunctivitis, keratoconus and cataract formation.

Patients have an inherently dry and irritable skin. Itching and scratching are responsible for most of the skin changes. The clinical features include erythema, scaling and weeping, along with lichenification and prurigo papules. These changes are most common in the cubital and popliteal fossae, wrists, ankles and face, but may be generalised. Sixty % of patients present in the first year of life, with 30% presenting between the ages of 1 and 5 years. However, it may present for the first time during adult life. Further details are given in the chapter on Paediatric atopic dermatitis.

Discoid dermatitis presents as round or oval plaques of dermatitis with a clearly demarcated edge. The plaques are prone to secondary bacterial infection and need to be distinguished from tinea corporis (ringworm). The condition is not uncommon and usually presents in middle to late adult life but may occur in children. The cause is unknown, but dry skin and overheating are important aggravating factors.

Asteatotic dermatitis is caused by drying of the skin and is most often seen in the elderly where it is relatively common. It may be a presenting sign of hypothyroidism and can be seen with drugs such as diuretics or the lipid-lowering agents. It presents as a dry cracked dermatitis with a ‘crazy-paving’ appearance.

Gravitational or varicose dermatitis is secondary to incompetent valves leading to venous hypertension. There are other changes of varicose disease, including varicosities, oedema, purpura, haemosiderosis, diffuse brown pigmentation due to haemosiderosis, and ulceration, see Venous ulcers.

Hand and/or foot dermatitis presents in two main ways – a vesicular dermatitis (pompholyx) or a scaly or hyperkeratotic dermatitis.

The cause of pompholyx is unclear but there is an association with atopic dermatitis. It presents as small vesicles and if severe, bullae. These occur on the palms and extend along the fingers, particularly the lateral sides, and on the soles. Pompholyx of the hand can be precipitated by an acute inflammatory tinea of the feet and this should be looked for and treated, see Tinea. Other aggravating factors include overheating, irritants and stress.

A scaly or hyperkeratotic dermatitis can affect the palms and extend to involve the volar aspect of the fingers. It usually develops later in life (40 to 60 years of age) and is a chronic disorder. Irritants may play a significant role in some patients.

A dermatitis occurring on the dorsum of the hands or fingers without palmar changes is usually an exogenous dermatitis and external causes should be sought.

Seborrhoeic dermatitis is discussed elsewhere.

Lichen simplex is thickening of the skin caused by repeated rubbing or scratching. It usually occurs on the extensor forearms, neck, arms, groin or ankles. The early changes are erythema and swelling with exaggeration of the normal skin creases. Thickening, hyperkeratosis and pigmentation follow, leading to thick plaques.

Treatment needs to break the itch-scratch cycle, and potent topical corticosteroids with occlusion, see Points on use of modified dressings, or intralesional corticosteroids are needed, see Topical treatment - General treatment of dermatitis.

General treatment for dermatitis

The treatment principles are essentially the same for all types of dermatitis. Initial assessment is to determine if there is a treatable cause and which are the important aggravating factors. Treatment is directed at reducing the itch.

There are many irritants to be avoided and these include soaps, bubble baths, shampoos, wool and sheepskins, nylon, carpets, grass and sand.

Dry skin is a major factor and general measures are directed at improving this.

           Reducing the frequency and duration of bathing or showering.

           Adding bath oils to the bath.

           Using emollients regularly after the bath and during the day, see Control of xerosis.

           Taking a cool shower and applying emollients immediately after the use of spas and chlorinated pools.

Scratching should be avoided. Acceptable measures to relieve itching include patting or pressing the skin and cooling the skin with water, followed by soothing emollients.

Overheating should be minimised. In winter, appropriate clothing, avoidance of electric blankets and turning down heaters are worthwhile measures. Central ducted heating also causes drying, which aggravates the dermatitis. In summer, fans and air conditioners are helpful.

In selected cases when patients with severe dermatitis are not responding to treatment, it is worthwhile reducing airborne allergens such as house dust mite. Methods include regular wet dusting and vacuuming, eliminating dust catching objects, frequent washing of bed linen and blankets, the use of plastic pillowcases and mattress protectors and, in severe cases, removal of carpets. Confirmation by prick or RAST tests, see Allergy testing, is worthwhile, especially if extreme or expensive measures are to be undertaken. Similarly, household cats and dogs should be avoided if the dermatitis worsens on contact with them. Allergy to animal dander does not need to be proven, as it can be both irritant and allergic. Patch testing is important in patients with a persistent dermatitis or when there is an unusual distribution, see Allergy testing.

The role of exclusion diets is controversial, and they are rarely needed, particularly in adults where they can be less useful than in children. If the dermatitis is not responding to routine measures then dietary measures can be undertaken. If exclusion diets are to be used then assessment by an allergist and a dietitian is needed.

For topical therapy an appropriate base needs to be chosen, with a cream base for acute weeping dermatitis, an ointment base for dry or lichenified dermatitis, and lotions for hairy areas.

Corticosteroids are the main topical treatment.

For face and flexures, use

a mild topical corticosteroid (the use of topical corticosteroids on the face is discussed further in Points on topical corticosteroid use).

For the initial treatment of dermatitis elsewhere, use

a moderately potent topical corticosteroid.

For lichen simplex and dermatitis involving the thick skin of the palm and sole, use

a potent to very potent topical corticosteroid.

Wet dressings with cool water, see Points on use of modified dressings, used with or without a topical corticosteroid, are useful in moderate to severe dermatitis, especially if the above measures are not working. The use of an antiseptic in the bath water prior to the application of wet dressings can reduce the risk of infection. Use

medicated bath oil OR chlorhexidine 5% solution 5mL in bath water with bath oil.

There should be a good response within a few days. If not, consider using a more potent corticosteroid, more frequent corticosteroids or occlusion, see Points on use of modified dressings.

For lichen simplex or discoid dermatitis, intralesional corticosteroids may be needed. Use

triamcinolone acetonide 10mg/mL OR betamethasone acetate/sodium phosphate 5.7mg/mL intralesionally.

Severe dermatitis not responding to corticosteroids needs a full assessment by a dermatologist.

Tar preparations are useful, especially in a dry or lichenified chronic dermatitis or for an acute dermatitis that has calmed down with initial treatment. Use

liquor picis carbonis (LPC) 2 to 5% and salicylic acid 2 to 5% in aqueous cream or simple ointment, applied to the affected area once daily, most conveniently at night.

Occlusion of tar preparations is not generally advised as it may induce irritation and microbial folliculitis.

In patients with chronic dermatitis, the basis of topical therapy is

Emollients, applied up to 3 times daily, particularly after bathing.

If there is localised infection, use

medicated bath oil OR chlorhexidine 5% solution 5mL in bath water with bath oil, daily.

AND

mupirocin 2% ointment or cream applied to any crusted areas once or twice daily

AND

mupirocin 2% nasal ointment intranasally, twice daily for 7 days, to reduce confirmed nasal carriage of Staphylococcus aureus.

Antibiotics are needed for widespread secondary bacterial infection. An initial swab is useful to detect the presence and sensitivities of Staphylococcus aureus. Antibiotics are used if the dermatitis has not settled with other measures and there is suspicion that infection is a contributing factor, or if there is obvious secondary infection, particularly if wet dressings are being used or folliculitis is present.

Oral antibiotics aimed at Gram-positive organisms should be used for 7 days. Use

dicloxacillin (child: 25mg/kg up to) 500mg orally, 6-hourly (liquid formulation of flucloxacillin at the same dosage may be used in young children).

For patients hypersensitive to penicillin (excluding immediate hypersensitivity), use

cephalexin (child: 25mg/kg up to) 500mg orally, 6-hourly for 5 to 7 days.

For sensitive strains roxithromycin or erythromycin may be used:

roxithromycin 300mg orally, daily OR erythromycin 500mg orally, 12-hourly.

For sensitive strains, tetracyclines or trimethoprim can also be used.

Antihistamines may be given. Their benefit is mainly due to their sedating effect and therefore the sedating group is recommended. Night-time use is recommended to prevent daytime sedation. They rarely give complete suppression of itch.

Specific treatments for dermatitis

Severe dermatitis needs a full assessment to determine any aggravating factors. Secondary bacterial infection is an important reason for a flare and should be treated in the first instance with an appropriate systemic antistaphylococcal antibiotic, see Antibiotic therapy - General treatment of dermatitis.

Secondary herpes simplex virus infection should always be suspected and swabbed for, although a negative result does not exclude the diagnosis. Refer to Eczema herpeticum for antiviral therapy.

Severe acute dermatitis that is not responding to the above measures may require hospital admission where frequent topical corticosteroids, wet packs and oral corticosteroids are given.

Severe chronic dermatitis may need immunosuppressive drugs such as azathioprine or cyclosporin.

Phototherapy gives variable results either with narrowband ultraviolet B, ultraviolet A (UVA) or psoralen and UVA (PUVA) therapy, see Points on phototherapy. It is usually more effective for control of chronic dermatitis than for treatment of an acute flare. Treatments are given 3 times a week for 2 to 3 months. Once weekly maintenance treatment may be needed for long-term control but may carry the risk of cutaneous malignancy, see Phototherapy - Vitiligo. Treatment times range from 15 seconds to 15 minutes.

Pompholyx, an acute and severe vesicular dermatitis of the hands or feet, often needs systemic corticosteroids. Use

prednisolone 30 to 50mg orally, daily for 3 to 4 days or until a good response is noted then reduce the dose over 2 to 3 weeks.

Antiseptic/astringent soaks are used to help dry up the acute phase. Soak in

sodium chloride, 1 tablespoon in a litre of water, solution OR potassium permanganate (Condy’s crystals) 0.1% solution diluted 1:10 before use OR aluminium acetate 13% (Burow’s) solution diluted 1:20 to 1:40 before use, for 10 to 15 minutes, 2 to 4 times daily.

Moderately potent to potent topical corticosteroids, are started initially or after the soaks have reduced or cleared the weeping. Oral antibiotics are needed when there is secondary bacterial infection, see Antibiotic therapy - General treatment of dermatitis.

Chronic vesicular hand and foot dermatitis needs a potent to very-potent topical corticosteroid initially and a moderately potent corticosteroid for longer-term use, Occlusion (see Points on use of modified dressings) is often needed. Tar preparations (see General treatment of dermatitis) are helpful but may sting when erosions or fissures are present. The use of emollients (see Control of xerosis) is also helpful. Phototherapy (see above) is beneficial in difficult cases.

Hand protection is an important factor, and this is discussed on Contact dermatitis of the hands.

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