Table Of Contents
Overview
Atopic dermatitis AKA eczema is a chronically relapsing, pruritic, inflammatory skin condition characterized by papules and vesicles on an erythematous base, eczematous lesions, xerosis (dry skin) and lichenification (thickening of skin and accentuated skin markings). It is caused by a breakdown/reduced effectiveness of the epidermal barrier which leads to an IgE-mediated, T-cell auto-immune response causing inflammation. Diagnosis is clinical.
There is a genetic predisposition, and often a family history of atopy (70%). Atopic dermatitis patients have a predilection for other atopic diseases (atopic March) such as allergic rhinitis, asthma, and food allergies. There is a genetic predisposition, and often a family history of atopic dermatitis. Most cases present before 5 years of age. It affects 30% of children and about 10% of adults. Breastfeeding as the sole nutrition in the first 3 months of life decreases the risk in children with a family history of atopy.
- Causes of atopic dermatitis
- Genetics: A family history of atopy is the strongest risk factor. Loss of function mutation in the gene coding for Filaggrin causes reduced production of proteins important for maintaining the integrity of the epidermal barrier.
- Hygiene: increased childhood exposure to antigens protects against allergic diseases by strengthening the immune system. Children not exposed to allergens and pathogens are at risk of developing atopic dermatitis.
- Infections: colonization of skin by Staphylococcus aureus increases inflammation and worsens atopic dermatitis.
- Allergens: pet fur, dust, pollen, and food may elicit atopic dermatitis.
- Environmental factors: sweating due to warm climate and hard water increases the risk of developing atopic dermatitis.
- Pollution: exposure to pollutants early in life predisposes to developing atopic dermatitis
- Exacerbating factors (Triggers)
- Emotional stress can worsen the condition
- Clothing – itchiness flares up when taking off clothes.
- Infection – Staphylococcus aureus
- Extreme heat or cold weather – sweating can worsen AD
- Soaps, detergents, shower gels, bubble baths, washing-up liquids
- Protective factors
- Early day care
- Exposure to pets and farm animals
- Multiple siblings
There are two main factors at play in the development of AD: barrier and immune response. Thinking this way helps to understand the treatment: Emollients help to improve the barrier, Steroids help to reduce the inflammation.
- Defective epidermal barrier The barrier function of the skin is primarily carried out by the stratum corneum. When the stratum corneum is damaged this leads to increased transepidermal water loss and resultant drying of the skin as well as allows allergens into the skin. Various factors that cause damage to the skin barrier include:
- Loss of function mutation in the filaggrin gene – filaggrin protein stimulates epidermal cells to release moisturizing factors and lipid material that contributes to the integrity of the epidermal barrier. Its loss leads to a weakened barrier.
- Tight junction abnormalities
- Imbalance between protease and antiprotease activity
- Microbial colonization by the overgrowth of Staphylococcus aureus.
- Itch-scratch cycle whereby scratching a lesion makes it itchier hence the more scratching the more mechanical damage to the skin.
- Immune dysregulation Due to the disrupted skin barrier, allergens enter freely into the skin eliciting an inflammatory reaction with:
- Increased expression of the Th2, Th17 and Th22 cells
- Release of pro-inflammatory cytokines IL-4, IL-13, IL-31 (which also act as pruritogens)
- Activation of B lymphocytes and the release of specific IgE
- Histopathology
- Spongiotic tissue reaction pattern (epidermal edema)
- Acanthosis (Thickening of the stratum spinosum of the epidermis)
- Hyperkeratosis (Thickening of the stratum corneum)
- Lymphohistiocytic infiltrate in the dermis
- Signs and symptoms
- Rash on the flexor surfaces, eyes, and neck. Erythematous papules and vesicles with serous exudation
- Adults: chest, neck and flexural
- Infants: scalp, face and flexural
- Pruritus (this is the main feature – Incessant pruritus)
- Dry skin (Xerosis)
- Thickened skin (Xerosis)
- Rash on the flexor surfaces, eyes, and neck. Erythematous papules and vesicles with serous exudation
- Associated findings that are non-specific but suggest the diagnosis of atopic dermatitis include:
- Keratosis pilaris – rough patches of bumps
- Hertoghe’s sign – thinning or loss of the outer third of the eyebrows due to incessant itching.
- Pityriasis alba – round/oval hypopigmented lesions with fine scales
- Retroauricular fissuring
- Dennie-Morgan fold – folds or crease of skin under the lower eyelid
- Palmar hyperlinearity – thickening of the skin on palms and soles as well as increase in the number of lines
- Periorbital darkening
- White dermatographism – Applying pressure on involved skin leads to blanching
- Centrofacial pallor
- Nipple eczema
Clinical variants
| Variant | Description |
|---|---|
| Hand dermatitis | Worsened by using harsh products such as detergents |
| Exfoliative dermatitis | Extensive skin involvement with generalized redness, scaling, weeping, lymphadenopathy, and fever |
| Eczema herpeticum | Eczema that co-exists with herpes simplex infection. Rapid onset with large patches of eczema with concurrent herpetic-type blisters. |
- NICE (UK) clinical diagnostic criteria of eczema
- Itchy skin folds PLUS 3 of
- History of asthma or hay fever
- Generally dry skin
- Visible patches of eczema in the skin fold
- Onset in the first 2 years of life
- Differentials
- Psoriasis: usually on the extensor surfaces. Has a more shiny appearance and there may be fingernail signs. Umbilical involvement in children is more likely to be psoriasis. Chronic psoriasis is easy to differentiate due to plaque formation.
- Contact dermatitis
- Seborrhoeic dermatitis
- Fungal skin infection
- Lichen simplex chronicus
- Scabies
- Investigations
- Complete blood count: Eosinophilia
- Swab for MC + S: Bacterial and viral swab tests to check for Staphylococcal and HSV infection
- Serum IgE testing
- Dermatopathology: acanthosis and spongiosis will be present. An infiltrate with lymphocytes, monocytes, mast cells and eosinophils will be present.
- Complications of eczema
- Lichenification: thickened and leathery skin (as a result of epidermal hypertrophy) due to excessive scratching and rubbing
- Staph infection of the lesion
- Eczema herpeticum: Patients become ill with fever and lymphadenopathy, usually about 5 days after vesicles appear. Lesions can also become infected with staphylococci.
- Cataracts: can be a feature of the disease or steroid agents around the eyes. Steroids should not be prescribed for eczema around the eyes
- Erythrodermic eczema: eczema involving >90% of the body.
Differential diagnosis
| Likelihood | Differentials |
|---|---|
| Most likely | Contact dermatitis, Seborrhoeic dermatitis, Scabies, Psoriasis, Keratosis pilaris, Ichthyosis vulgaris, Pityriasis alba, Porphyrias |
| Least likely | Cutaneous T-cell lymphoma (Sezary syndrome), HIV-associated dermatoses, Wiskott-Aldrich syndrome, X-linked agammaglobulinemia, Hyper IgE syndrome, Selective IgA deficiency, Langerhans cell histiocytosis, Lupus erythematosus |
Complications
| Complication | Description |
|---|---|
| Ocular problems | Eyelid dermatitis, chronic blepharitis, Atopic keratoconjunctivitis, Keratoconus, cataracts |
| Infections | Eczema herpeticum, Superficial fungal infections (Tricophyton rubrun), Staphylococcus aureus infection |
| Sleep disturbance | Due to intense pruritus |
| Allergic diseases | Food allergy, urticaria, asthma, allergic rhinitis |
Treatment of Eczema
Its basis is to moisturise the skin, allay pruritus and manage inflammation of eczematous lesions.
- Avoid and remove identified triggers
- Educate to avoid rubbing and scratching
- Change soaps and shower gels to emollients
- Avoid bubble baths
- Avoid woollen clothes, extremes of temperature
- Wear soft clothing
- Wash clothes with mild detergents
- Limit exposure to carpets, vacuuming mattresses, and using mattress protectors (dust mites)
- Avoid dietary factors (not beneficial in adults)
- Definitive treatment
- Emollients: help to improve the skin’s natural barrier by creating and oily, moisturising layer. Used liberally > 500 ml/week. Special shower emollients can also be used. Emollients can also be used as an alternative to soap when washing hands.
- Topical steroids: brings the exacerbation under control. Should be applied before emolients. Mild steroids should be used for < 5 days on the face and < 2 weeks on the rest of the body. Avoid using steroids around the eyes since they cause cataracts. Other side effects are rare (skin thinning, striae formation, telangiectasia, adrenal suppression)
- Systemic glucocorticoids: used only in very severe cases. Prednisone 60-80mg for two days then halving the dose each two days for the next six days.
- Oral antihistamines: to reduce pruritus
- Immune modulating agents (Pimecrolimus and Tacrolimus): used as alternatives or adjuncts to topical steroids. Have topical and oral preparations
- Phototherapy: UVA/UVB is effective in treating disease resistant to topical agents. Avoided in children due to sun damage. At a frequency of 2-3 times a week.
- Treatment of staphylococcal skin infection
- Flucloxacillin 500mg every 6 hours for 1-2 weeks
Types of emollients
| Emollient | Description |
|---|---|
| Creams | Water based and least potent |
| Lotion | Water and oil based and moderately potent |
| Ointment | Oil-based and most potent |
Types of steroids
| Potency | Example | Use |
|---|---|---|
| Mild | 1% hydrocortisone, 0.05% clobetasone | Face and neck, mild flare-ups |
| Moderate | Betamethasone valerate 0.02%, triamcinolone 0.02% | Axilla and groin, severe flare-ups |
| Potent | 0.1% betamethasone valerate, mometasone 1%, methylprednisolone acetylate | Axilla and groin, severe flare-ups |
| Very potent | Clobetasone proprionate 0.05%, betamethasone dipropriate 0.05% | Not for use in children and on the face. Useful for persistent rash with lichenification. |
Treatment of an acute presentation
| Treatment | Description |
|---|---|
| Moisturization/ hydration | Taking lukewarm baths with moisturizing emulsifying oils added in. After showering apply an unscented emollient (such as hydrated petrolatum) to seal in water. |
| Topical corticosteroids | This is the mainstay of treatment. Low-potency steroids such as hydrocortisone applied twice a day can be used as initial therapy. Stronger steroids such as betamethasone can be used for more extensive involvement, applied twice a day. |
| Hydroxyzine | 10-100mg four times daily to alleviate pruritus. |
| Oral/topical antibiotics | Used where indicated in case of superimposed infection |
| Antivirals | In case of secondary herpes infection |
