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ECZEMA
1. INTRODUCTION
1.1 Terminology
ECZEMA : Use as a clinical descriptive term, it describe a process that is clearly superficial in form and that, early, is erythematous, papulo-vesicular, oozing and crusting and, later, red-purple, scaly, lichenified and possibly pigmented. Epithelial disruption and non-sharp margination are its characteristics.
ECZEMA can be defined histologically by the presence of a predominantly lymphohistiocytic infiltrate around the upper dermal blood vessels, associated with varying degrees of spongiosis and acanthosis.
The terms 'ECZEMA' and 'DERMATITIS' are regarded as synonymous.
1.2 Table 1 : Stages of Eczematous Inflammation
STAGE MORPHOLOGY OF SYMPTOMS EXAMPLES TREATMENT
LESIONS
Acute vesicles, blisters, intense acute contact cold wet
intense red itch, dermatitis, acute compresses,
stinging, nummular eczema, steroid,
burning stasis dermatitis, antihistamine,
pompholyx antibiotics
Subacute red, scale, slight contact allergy, topical
fissuring, parched to irritation, atopic steroid,
appearance, scalded moderate dermatitis, stasis emollients,
appearance itch, dermatitis, nummular antihistamine,
stinging, eczema, asteatotic antibiotics
Chronic thickened skin, moderate atopic dermatitis, topical
lichenified to lichen simplex steroid
excoriation, intense chronicus, fingertip antihistamine
fissuring itch eczema, antibiotics,
hyperkeratotic emollients
eczema 1.3 Table 2 : Common Types of Eczema
EXOGENOUS ENDOGENOUS
IRRITANT DERMATITIS ATOPIC
ALLERGIC CONTACT DERMATITIS SEBORRHOEIC DERMATITIS
PHOTOALLERGIC CONTACT ASTEATOTIC DERMATITIS
DERMATITIS
ECZEMATOUS POLYMORPHOUS LIGHT DISCOID ECZEMA
ERUPTION
INFECTIVE DERMATITIS PITYRIASIS ALBA
DERMATOPHYTIDE HYPERKERATOTIC ECZEMA
GRAVITATIONAL ECZEMA
JUVENILE PLANTAR DERMATOSIS
ECZEMA ASSOCIATED WITH SYSTEMIC
DISEASE
ECZEMATOUS DRUG ERUPTION
2. ATOPIC ECZEMA
Atopic eczema (AD) is a characteristic type of chronic dermatitis frequently associated with atopy and an elevated IgE level. There are no single distinguishing features of AD; however, the diagnosis can be made on a combination of history, and morphological findings.
2.1 Epidemiology
AD has a world-wide distribution and affects all races. About 3% of children under age 5 years had AD with a male to female ratio of 1.2 : 1. Majority of patients presents within the first 5 years.
AD runs in family. About 75% of patients have a personal or family history of other atopic diseases, e.g., allergic rhinitis, asthma, hay fever.
2.2 Aetiology and Pathogenesis
The aetiology is unknown and the pathogenetic mechanisms are speculative. However, a number of clinical, pathological and immunological abnormalities are frequently observed in these patients and are briefly discussed below :
(i) Elevated IgE
Occur in about 80 percent of AD patients and are directed against a wide variety of antigen like pollens, molds, foods, house dust mites (HDM) and bacterial antigens etc. A high IgE level is not a unique feature of AD but appears to correlate with the clinical severity and falls with remission.
(ii) Skin Prick Test and RAST
Patients with AD often show positive Prick test and RAST to common household allergens like egg, milk, wheat, fish, soy, peanut, pollens, HDM and animal danders etc. However, avoidance of such allergens does not necessarily bring about a clinical response.
(iii) Bacterial Antigens
Staph. aureus colonization occurs in over 50% of AD patients and compared to less than 5% in normal individuals, and is frequently isolated (> 90%) from acute exudative lesions and lichenified plaques. The density of the organism correlates with the severity of eczema and antibiotics that clear Staph. aureus improve eczema.
(iv) Impaired Cellular Immunity
This includes a reduced CD8+ suppressor T cells, a reduced natural killer cell function, a reduced IFN- production, a reduced response to mitogens; peripheral eosinophilia in some and abnormal neutrophil chemotaxis.
(v) Inflammatory Cells and Mediators
A very characteristic feature of AD is intense pruritus. It has been shown that an increased population of mast cells occurs in the skin of AD patients which releases histamine, leukotrienes and cytokines much more readily compared with normal subjects.
(vi) Abnormal Vascular Responses
Disturbed vascular reactivity like white dermographism, nicotine blanching, and delayed blanch with methacholine are well documented.
(vii) Sweat and Sebum Production
AD patients tend to produce more sweating than nonatopic controls. It has been suggested that an increase in transepidermal water loss, and a possible deficiency of lipids in the epidermis account for the skin dryness.
2.3 Clinical Features
(i) Pruritus
Is the hallmark of AD. It is more severe at night and is attributed to the absence of distraction, capillary dilatation, and increased skin temperature. A natural response to itch would be scratching, and scratching results in erosions, weeping, crusts, secondary infections, prurigo papules and lichenification.
(ii) Dry Skin (Xerosis)
Manifests as scaling, chapping and a feeling of skin roughness. It is worse in winter times due to reduced ambient humidity and coldness. Dry skin is enhanced by frequent use of detergents or defatting substances.
(iii) Eczematous Lesions
The most typical skin sign of infantile AD. They are polymorphic, with an erythematous, papulovesicular, erosive and crusted appearance.
(iv) Prurigo
Is a dome-shaped papule, sometimes with a tiny vesicle on top. Excoriation is frequent. Prurigo papules vary in number and distribution.
(v) Lichenification
A lichenified plaque is a poorly demarcated, slightly tan to red plaque with grossly accentuated skin markings. Lichenified plaques take long time to resolve. The antecubital and popliteal fossae and the neck are predilected sites.
(vi) Dennie Morgan Fold
Is an extra infraorbital eyelid fold. About 80% is bilateral. Some consider this is a consequence of scratching of the eyelids.
(vii) Hand and Feet Ivolvement
Dry, nonpruritic plaques and recurrent hyperkeratosis and fissuring of the finger pulps (and soles) are common. Linear furrows running across thenar and/or hypothenar eminences referred to as hyperlinearity of palms occurs in about 1/3 to 1/2 of AD patients. Coarse pitting and ridging of nails may occur.
2.4 Four Phases of AD
(i) Infantile Phase
Lesions first appear on the cheeks, forehead, and scalp, but may occur on the trunk, neck, hands and feet. Eczema with oozing and crusts are more typical. Nocturnal restless, irritability and crying are prominent. When the child begins to crawl, the exposed areas especially the extensor aspects of knees are affected.
(ii) Childhood Phase
At about 18 months, the eczematous lesions tend to be replaced by lichenification. Prurigo papules occur and are very itchy. Elbow and knee flexures, wrists and ankles and neck are commonly involved. The neck may show striking reticulate repigmentation (dirty neck). Hands may be dry and lichenified; sole involvement may mimic juvenile plantar dermatosis. The face is less frequently affected. Problems with schooling may occur.
(iii) Adolescent/Young Adult Phase
Predominant features are pruritus, lichenification, prurigo papules, scratch marks, and crusting. Lesions occur mostly on the face, neck, flexures, and upper trunk. Localized patches of eczema around the nipple or vermillion of the lips can occur. Psychological difficulties occur in some.
(iv) Adult Phase
AD resolves spontaneously in most patients after age of 20. Majorities of the patients, however, still have sensitive, unstable skin and a higher tendency to develop dermatitis. Full blown AD occurs in only a small percentage of patients throughout adulthood.
2.5 Associations
The association of AD with allergic rhinitis, asthma and conjunctivitis is well documented. Eczematous conditions like contact dermatitis, discoid eczema, pityriasis alba, lip-stick eczema and follicular eczema are more frequently seen in atopic subjects. Others like ichthyosis vulgaris, keratosis pilaris, Netherton's syndrome, alopecia areata and vitiligo etc. also have linkage.
2.6 Complications
(i) Infection
Bacterial especially Staph. aureus, viral, and fungal infections are common, and so as scabies. Eczema herpeticum, which is herpes simplex infection in eczematous skin is characterized by multiple, painful, vesiculopustular lesions; and often become haemorrhagic, eroded and crusted. Affected areas may be very edematous; regional lymphadenopathy occurs and secondary bacterial infection is common. Diagnosis can be established by Tzanck smears or electronmicroscopy from scarping of the skin lesions.
(ii) Exfoliative Dermatitis
This is severe and requires hospitalization.
(iii) Eye
An increased incidence of anterior subcapsular cataract may be due to extensive use of systemic steroid, and to topical steroid applying around the eyes. Keratoconus is corneal degeneration characterized by increasing conicity of the cornea resulting from a raised intraocular pressure. Visual disturbance occurs.
(iv) Retarded Growth
May be attributed to a combination of reduced exercises, infections, and malnutrition secondary to inappropriate dietary restriction; however, frequent use of systemic/topical steroid is perhaps a more important contributing factor.
2.7 Criteria for Diagnosis of Atopic Eczema
Major criteria Minor criteria
Pruritus Dryness
Typical morphology and distribution Hyperlinearity of palms/Keratosis pilaris
of skin lesions. Increased IgE
Chronic and relapsing course Early age of onset
Personal or family history of atopy Tendency to cutaneous infection
Cheilitis
Dennie-Morgan infraorbital folds
Pityriasis alba
Keratoconus/anterior subcapsular cataracts
White dermographism etc.
There is no single diagnostic feature for AD. However, it has been suggested that a diagnosis of AD can be established with 3 or more major criteria plus 3 or more minor criteria.
2.8 Differential Diagnosis
Infantile seborrhoeic dermatitis has an earlier onset than AD. The presence of family history, scratching, possible food intolerance, and high IgE level in AD is absent in seborrhoeic eczema. Allergic contact dermatitis with autosensitisation, psoriasis, candidiasis, dermatophytosis, pityriasis rosea, scabies, nutritional deficiency may at times cause confusion.
2.9 Treatment
(i) General Measures
(a) Explanation
Explanation on the nature and management of AD improves compliance and efficacy of treatment. AD runs a long course that can be controlled but not cured. AD improves with increasing age, but patients often have a dry, sensitive skin and avoidance of irritants and trigger factors is always necessary.
Good medical compliance is important. Scratching of skin should be discouraged in order to disrupt the itch-scratch cycle; keep nails short.
Immunization is given as non-atopic subjects but should be cautious for vaccines derived from eggs if patient is egg-sensitive. Defer vaccination if the child has an acute flare of eczema.
Career advice emphasizes the selection of a 'clean' job. Occupations like barber, chef, laboratory technician, car mechanic, nurse and jobs that require contact with chemicals are not suitable.
(b) Environmental Modification and Avoidance of Trigger Factors
Woolly underclothes irritate skin and should be avoided Woolly toys tend to house allergens so as carpets. Pets have the similar problem; their hair and excreta can be allergenic and pets are a source of infestation. Avoid excessive heating in the bedroom as this increases dryness and itchiness.
Regular once daily bathing is not strictly required. Over-bathing or over-use of soaps is detrimental to the sensitive skin. Avoid bathe with hot water, use soap substitutes, avoid vigorous rubbing at the skin and keep the bathing time short. The skin should be mopped dry immediately after bathing and emollients applied. Swimming is permitted but chlorinated water irritates skin and hence immediate showering is required afterwards. Many cosmetic products have the potential to trigger a flare.
Foods implicated as allergenic include eggs, milk, wheat, legumes, seafood and peanuts. Few young patients do have a clear relationship between food and eczema flares. In such case, they can try a 3-4 week's period of suspected food elimination. One should aware that unsupervised food restriction in the young may lead to malnutrition.
Avoid unnecessary physical and emotional stress.
(ii) Management of Dry Skin - Emollients and Soap Substitutes
Dry skin is more prone to itch and chapping and hence risk of infection and subsequent perpetuation of eczema. A good dry skin care can be achieved by :
(a) Keep bathing time short and to a minimum necessary
(b) Use lukewarm water not too hot
(c) Use soap substitute e.g. emulsifying ointment
(d) Avoid vigorous rubbing and cleaning at the skin
(e) Pat dry, and
(f) Apply emollients e.g., aqueous cream, as soon as after getting out of the bath.
Emollients minimize dryness and is the mainstay in treating mild AD. Some emollients are also humectants, e.g. urea cream. Humectants attract water into the skin, and are useful on unbroken skin but can cause stinging. Emollients should be applied as frequently as possible according to patient's need. It is believed that regular and frequent use of emollients can reduce 10-20% of the amount of topical steroids used in the maintenance treatment of AD. Some emollients contain lanolin that may sensitize skin e.g., Alpha keri, oilatum etc. Chapters 35 and 37 give further description on the property and use of emollients.
(iii) Ichthammol and Tar Preparations (0.5-1%)
Ichthammol impregnated bandages are old remedy but are still used for treating childhood eczema in UK.
Tar can reduce itch. Tar/steroid-impregnated bandages are useful for chronic lichenified eczema. Tar bath is a useful bath additive in reducing itchiness. Tar compounds can induce folliculitis and photosensitisation; and because of its smell and colour, patient compliance is a poor.
(iv) Topical Steroids
Is the mainstay of treatment for inflammatory aspect of atopic eczema. The strength and the base used will depend on the stage and location of the eczema. Acute weeping eczema should first be treated with potassium permanganate (KMnO4) compresses followed by a steroid lotion or cream. In chronic eczema, creams and ointments are both suitable. Twice daily application is usually sufficient. Prolonged use of a potent corticosteroid e.g., clobetasol propionate 0.05% over 50 g per week may result in systemic and local side effects. Fear of side effects, however, should not limit the use to a weaker but ineffective corticosteroid. Potent corticosteroids can be used as a short-term measure aiming to obtain initial control, this is then changed over to a weaker steroid suitable for the situation. Chapter 36 gives an overview on topical corticosteroids.
(v) Control of Infections
Staph. aureus infection is a frequent cause of eczema flare requiring systemic antibiotics, e.g., erythromycin or cloxacillin. Sometimes, a prolonged course of antibiotics may be required. Topical mupirocin twice daily to nasal vestibules and chlorhexidine massaging onto body during bathing can reduce the number of Staph. aureus in a carrier. Systemic antibiotics for treating large area of infected eczema are superior than using large amount of topical antibiotics that carry risk of hypersensitivity and inducing bacterial resistance.
Eczema herpeticum needs systemic acyclovir. Molluscum contagiosum, warts and fungal infections should be treated accordingly.
(vi) Systemic Corticosteroid
It is not a routine management of atopic eczema and it should be avoided at times of puberty. Sometimes, a short course of systemic corticosteroid is effective in gaining control of a severe eczema flare. Whenever systemic steroid is used, any infection must be looked for and treated promptly.
(vii) Systemic Antihistamines
Recommended doses can be given during periods of excessive scratching. Avoid excessive doses as hyperexcitability may be quite marked in young children.
(viii) PUVA
It is useful in chronic lichenified eczema where pruritus is intractable and a useful adjunct to leaving off topical steroids at the time of pubertal growth spurt. Patient selection is important. No PUVA should be given to children under the age of 12 because of risk of cataract in the immature lens and difficulty in co-operation and understanding with the PUVA regime. The same precautions and procedures as PUVA for other conditions should be undertaken. The response of AD to PUVA is not as good as compared with that for treating psoriasis and the total dose required is often larger. The experience in UK showed that approximately one-third showed remission or significant response, one-third remit and relapse, and one-third no response.
(ix) Immunosuppressives
Azathioprine or cyclosporin are helpful in severe cases. Nevertheless, drug toxicity and long-term hazards are a definite risk. They should only be considered for chronic severe AD with poor response to the usual treatment.
(x) Hospitalization
In severe cases, it can be very helpful. Remove the patient from his environment and potential trigger factors, institute regular and intensive treatments can lead to resolution of the eczema.
2.10 Alternative Treatments
(i) Evening primrose oil
Which contains linoleic acid and gamma linolenic acid, was found to be effective in some cases in reducing erythema and pruritus; but it may take 2-3 months to see effect. It is also costly. The precise indications are not clear and it cannot be predicted which patients will respond. It may be tried for patients who failed with conventional therapy.
(ii) Chinese herbs
Recent studies in UK using a certain formulary of Chinese herbs for patients with long-standing, widespread, and non-exudative AD have shown a statistical significant improvement in symptoms and skin signs. At this stage, Chinese herbs do seem to have a therapeutic potential in the treatment of AD but its palatability, efficacy and its safety need further evaluation.
(iii) Sodium cromoglycate
It is given as 100-200 mg qid orally. In general, it is not effective.
(iv) Behavioral therapy
May be a useful adjunct for patients who cause excessive self-mutilation in their families.
2.11 Prevention
There is no definite evidence that breast feeding is protective against development of AD. It has been suggested that the early introduction of solid foods (before age 4 months) does have a deleterious effect, and that a greater variety of foods correlated with an increased probability of developing AD.
2.12 Prognosis
Studies investigating the long-term outcome of AD have been unsatisfactory. In general, patients with a family history of AD, associated asthma, hay fever, later-onset disease and the presence of severe dermatitis have higher rates of persistent disease. Many quote 40-50 percent of recovery by age 15 years.
3. OTHER TYPES OF ECZEMA
3.1 Irritant Contact Dermatitis
(i) Diagnostic features :
The affected sites characteristically conform to history of specific contact to a susceptible contactants. Some non-exposed areas are also susceptible to irritant contact dermatitis, e.g., body folds and flexural areas, due to a combination of friction and direct contact with sweat or urine. Once exposure to the irritant ceases, improvement start to occur.
(ii) Clinical presentation :
Strong irritant contact dermatitis can occur after a single brief exposure. the latent period is short. Examples are acid and alkaline burns, thermal burns and frost bites. The offending irritant is usually obvious. Weak irritant contact dermatitis develops after multiple exposures, latent period is long.
(iii) Management :
The offending irritant should be identified and removed. Soap and detergents should appropriately be minimized. Cool water is less detrimental than hot water. Advice on the use of protective barriers whilst at work, e.g., gloves, protective clothes etc. should be strictly followed by the patient. Restoration of the lipid layer can be accomplished by frequent application of emollients. In case of maceration, wet clothing should be changed frequently, non-porous clothing to be avoided. Inflammatiory element can be controlled with topical steroid.
3.2 Allergic Contact Dermatitis ,
(i) Diagnostic features :
The characteristic distribution of the lesions can often gives a clue to a particular allergen (Table 3). Removal of the suspected allergen leads to resolution of the dermatitis. A positive patch test to a suspected offending contactant support the clinical diagnosis.
(ii) Clinical presentation :
(a) Both allergic contact dermatitis and irritant contact dermatitis bear similar clinical signs. In acute cases weeping and crusting will be present, while in chronic cases scaling and fissuring are the dominant findings. Sometimes, allergic contact dermatitis differs from irritant contact dermatitis in that erythema and edema may be more prominent and pruritus more troublesome in the former.
(b) Systemically induced allergic contact dermatitis : Patients who have been sensitized to topical allergens may develop generalized eczematous inflammation if these allergens or chemically related substances are ingested. e.g. Patient with a history of nickel allergy may get a widespread flare when he takes food rich in nickel; patient sensitized to topical ethylenediamine may develop generalized inflammation following treatment with aminophylline.
(c) Airborne allergic contact dermatitis and photodermatitis have a similar distribution. Look for sparing in the upper eyelids, areas below the chin, and the Wilkinson's triangles behind the ear.
Table 3 : Distribution of allergens
Location Material
Scalp and Shampoo, hair dyes, topical medicaments
ears
Eyelid Nail polish, cosmetics, contact lens solution, metal
eyelash curlers, topical medicaments
Face Airborne allergens, cosmetics, sunscreen, acne
medications, aftershave lotion
Neck Necklaces, airborne allergens, perfumes, aftershave
lotion
Trunk Topical medicaments, sunscreens, plants, clothing,
undergarments (e.g., elastic waist band, spandex bra),
metal belt buckles
Axilla Deodorant, clothing
Arms Watch and watchband
Hands Soaps and detergents, foods, poison ivy, industrial
solvents and oils, cements, metal, topical medications
rubber gloves
Genitals Rubber condom, allergens transfers by hands
Anal region Haemorrhoid preparations, antifungal preparations
Lower legs Topical medicaments, dye in socks
Feet Shoes, cements spilling into boots
(iii) Management :
(a) The first step is the identification and removal of the contactant. A detailed history and a careful examination is usually sufficient. Patch testing* is indicated for cases in which inflammation persists despite avoidance and appropriate topical therapy.
(b) For acute inflammation with blisters and intense erythema, cold wet compresses e.g. KMnO4 are highly effective. They should be used for 15 to 30 minutes several times a days until blistering and severe itching is controlled. Prednisolone, in dosage of around 30-40 mg a day in divided doses is used for extensive inflammation. Topical steroids for reduction of local inflammation.
* Patch Testing :
(i) Whether or not the allergy demonstrated by the patch test is relevant to the patient's dermatitis must be determined by the critical judgment of the physician.
(ii) Contraindications to patch testing :
(a) Acute widespread dermatitis.
(b) Ongoing systemic steroid therapy. Defer till at least 1-2 weeks after steroid therapy.
Table 4 : European Standard Screening Series and Examples of common sources
1. Potassium cement
dichromate
2. Neomycin sulphate topical medicaments
3. Thiuram mix rubber products (shoes, balloons),
pesticides
4. Paraphenylenediamin hair dyes, azo dyes, fur dyes, leather
e dihydrochlorate dyes, photodeveloper
5. Cobalt chloride in all almost all trades and industry,
nickel and cobalt often occur together
6. Benzocaine topical anaesthetics
7. Formaldehyde glues, paper, clothing, cosmetic e.g.
shampoo
8. Colophony adhesive plasters, paper, plaster,
polishes and waxes
9. Quinoline mix antiseptics in topical therapeutics
10. Balsam of Peru cosmetics (perfumes, flavours)
11. Black rubber mix rubber products
12. Wool alcohols lanolin, vehicles
13. Mercapto mix shoes, rubber products
14. Epoxy resin glues, pastes, insulator, building
material
15. Paraben mix preservatives and vehicles in medicine and
cosmetics
16. Paratertiary leather, adhesive and rubber systems
Butylphenol
17. Fragrance mix stabilizer in medical products
18. Ethylenediamine medicaments
Dihydrochloride
19. Quaternium 15 cosmetics
20. Nickel sulphate earrings, metal tools, clothing
accessories, cheap ornaments
21. Primin the allergen in P obconica, which mingle
with house dust causing dermatitis.
3.3 Common Patterns of Hand Eczema
3.3.1 Pompholyx
(i) Recurrent eruptions of minute, non-inflammatory, vesicles on fingers, palms and soles is characteristic. Pruritus is common, sometimes lesions can be painful or it may be asymptomatic. Scratching of vesicles leads to weeping and crusting.
(ii) Management :
KMnO4 soaks, oral antihistamines and application of mid to high potency steroids for mild cases. A short course of oral steroid is required for severe cases. Psychological factors are important. Counselling, behavioral modification may be necessary.
3.3.2 Keratolysis Exfoliativa
This is a common chronic asymptomatic non inflammatory bilateral peeling of the palms and soles. Its cause is unknown. The eruption is most common during the summer months and often associated with sweaty palms and soles. Scaling starts simultaneously from several points on the palms or soles with 2 or 3 mm in diameter round scales that appear to have originated from ruptured vesicles; however, such vesicles are never seen. The scales continue to peel and extend peripherally, forming larger roughly circular areas that resemble ringworm, while the central area become slightly red and tender. The condition resolves in 1 to 3 weeks and requires no therapy other than lubrication.
3.3.3 Fingertip Eczema
A very dry chronic form of the palmar surface of finger tip. Usually of unknown cause, but may be the result of an allergic reaction. One or several fingers may be involved. Initially the skin is moist; gradually becomes dry, cracked and scaly. The process usually stops shortly before the distal interphalangeal joint is reached. Fingertip eczema may last for months or years and is resistant to treatment. Treatment is by avoiding irritants and frequent lubrication. Topical steroid with or without occlusion may give temporary relief. Tar is an alternative treatment. Allergy and psoriasis may have to be excluded.
3.3.4 Ring Eczema
An irritable patch of eczema under a ring and tends to spread to adjacent area. This affects mainly young women soon after marriage or childbirth. If the ring is transferred to the other hand, the eczema will appear at the new site. The cause is due to concentrations of detergent beneath the ring and repeated friction. Removal of the ring often brings remission.
3.3.5 Hyperkeratotic Eczema
Plaques of yellow-brown dense scale increase in thickness and form deep interconnecting cracks over the surface, similar to mud drying in a river bed. Occurs on the palms and occasionally soles. Hyperkeratotic eczema may result from allergy or excoriation and irritation, but in most cases the cause is not apparent. Differential diagnoses may be psoriasis and lichen simplex chronicus. They may respond to potent steroid and occlusion, but recurrence are frequent.
3.4 Nummular Eczema
(i) Clinical presentation :
Nummular eczema (discoid eczema) is characterized by circular or oval plaques of eczema with a clearly demarcated margin. The typical lesions are coin-shaped, 1 to 5 cm in diameter itchy plaques. There are commonly distributed on the extremities and can become generalized. Acute lesions may be vesicular; chronic lesions may become scaly, cracked and confluent.
(ii) Differential diagnoses :
Allergic or irritant contact dermatitis have primary lesions conform to area exposing to allergens/irritants, and a contact history is often present. Ringworm infection presents as annular, scaly erythematous patches or plaques with central clearing. Psoriatic plaques are well marginated with prominent scales. Irritation is variable. Lesions of chonic superficial dermatitis are dry, indolent patches.
(iii) Management :
Treatment is similar to other forms of eczema and depends on the stage of activity. A course of mid to potent topical corticosteroid combined with topical or systemic antibiotic is effective since infection is commonly associated; however, relapse is not uncommon.
3.5 Asteatotic Eczema (xerotic eczema, eczéma craquelé)
(i) Diagnostic feature :
Lesions are mainly distributed over the hands and legs; and consist of minute, thin fissures, with minimal inflammation.
(ii) Clinical presentation :
It commonly occurs in the elderly and people with dry skin especially in winter times when the humidity is low. The condition is thought to due to a reduction of in skin surface lipid. Distal parts of the extremities especially the legs are affected. The skin is dry, slightly scaly and criss-crossed on the surface to produce a reticulate pattern. The borders of this reticulation can become erythematous and slightly raised, and finally eczematous. The patient feels itchy, sting and burnt.
(iii) Management :
The mainstay of treatment is to reduce moisture loss and to maintain the surface lipid layer. Reducing the bathing frequency to an acceptable level; avoiding hot bath, restricting soap are good measures. Ordinary soaps should be replaced by soap substitute and emollients should be used as frequently as appropriate. Inflammation can be controlled by application of mid potency topical steroid ointment.
3.6 Stasis Dermatitis (Gravitational eczema, Varicose eczema, Venous eczema)
(i) Diagnostic feature :
A history of preceding non-inflammatory swelling, distributed over the ankles and association with varicose veins.
(ii) Clinical presentation :
Acute inflammation is characterized by a red, superficial, itchy plaque with weeping and crusting on the lower limbs especially the medial side of lower legs, ankles and calves. This is due to a combination of eczematous changes and cellulitis. A vesicular eruption (id reaction) on the palms, trunk, extremities sometimes accompanies this acute inflammation.
In subacute and chronic stages, an increased hydrostatic pressure lead to extravasation of red blood cells from the leg veins. Disintegration of these red blood cells lead to haemosiderin deposition. The skin looks dry, scaly, hyperpigmented and accompanied with white atrophic changes ('atophie blanche'). Ulceration is common in the late stage and is a serious consequence.
(iii) Aetiology :
Venous insufficiency is a major factor but not all patients with venous insufficiency develop stasis eczema. Allergic response to an epidermal protein antigen created through increased venous pressure, susceptibility to minor trauma and irritation are the contributing factors.
Patients with stasis eczema are more prone to develop hypersensitivity reaction to topical medicaments. Topical medicaments that contain potential sensitizers such as lanolin, benzocaine, parabens and neomycin should be avoided by patients with stasis disease.
(iv) Management :
The dry eczematous inflammation can be managed with lubricants and topical corticosteroids. Moist exudative inflammation and moist ulcers respond to tepid wet compress of KMnO4 solution several times a day. Any infection should be identified and treated promptly. Oral antibiotic appropriate to the organism is more preferable than topical antibiotic which should be avoided. Physiotherapy, elevation of legs and compression stocking are helpful. Patients with varicose veins should be referred to the vascular surgeons for early assessment and prompt treatment.
3.7 Lichen Simplex (Circumscribed neurodermatitis)
(i) Definition :
Lichenification denotes a cutaneous response to repeated rubbing or scratching. It is characterized clinically by a thickened appearance of the skin, with accentuation of the surface markings so that the affected skin surface resembles tree bark.
Lichen simplex is a circumscribed area of lichenification resulting from repeated rubbing and scratching occurring on some predilected sites. This term is used when there is no known predisposing skin disorder.
(ii) Clinical features:
Women are more common affected than men. Pruritus is the predominant symptom and is often out of proportion to the extent of the objective changes. During the early stages the skin is reddened and slightly oedematous, and the normal markings are exaggerated. The redness and oedema subsided and the central area becomes scaly and thickened and sometimes pigmented.
Almost any sites are affected, but the commonest sites are those that are conveniently reached. The usual sites are the nape of the neck, the lower legs and ankles,. the sides of the necks, the scalp, the upper thighs, the vulva, pubis or scrotum and the extensor forearms.
(iii) Management :
A search for a causation should be made before the lichenification is considered to be primary, then a careful psychological history should be taken and the patient given some assistance in reducing her tensions. Topical steroid is the treatment of choice, sometimes with occlusion to enhance absorption and prevent further scratching. Intralesional triamcinolone is useful for circumscribed chronic lesions. Topical antibiotic may be prescribed if secondary infection is present.
3.8 Seborrhoeic Dermatitis
(i) Diagnostic feature :
Seborrhoeic dermatitis is characterized by a distinctive morphology (red, sharply marginated lesions covered with greasy looking scales) and a distinctive distribution (scalp, face and upper trunk) which are areas rich in sebaceous glands.
(ii) Clinical patterns :
(a) Adult (may be associated with Parkinsonism and HIV infection)
Scalp Dandruff is usually the earliest manifestation. In chronic cases, there may be hair loss which is reversible when the inflammation is controlled. Ears are a common site of involvement.
Face Medial sides of the eyebrows, glabella, nasolabial fold, are predilected sites. Blepharitis is a feature.
Trunk Petaloid form is commoner than the pityriasiform. Follicular papules with greasy scale that may become confluent, and commonly found over the sternum and interscapular region.
(b) Infantile
The eruptions in infants frequently first appear between the third and eighth weeks of life. It may start in the napkin area, the face and scalp, and occasionally on the trunk outside the napkin area. The rash comprises well-defined areas of erythema and scaling with tiny vesicles. Papular and lichenified lesions are not seen. Typically the infant is well and not irritable (c/w atopic dermatitis). The prognosis is usually good. Most uncomplicated cases clear in 3 to 4 weeks.
(iii) Differential diagnoses :
Psoriasis, pityriasis rosea, pityriasis versicolor, drug eruption and lichen simplex in adult. Intertrigo, irritant contact dermatitis, atopic dermatitis, psoriasis and eczematous eruptions in immunodeficiency disorders in infants.
(iv) Management :
(a) Adults
Ketoconazole shampoo is very effective in removing dandruff. Shampoos that contain salicylic acid, selenium sulphide, zinc pyrithione and tar are alternatives. For thick scalp scale and crust, sulphur salicylic emulsion can be applied before bed and shampooed next morning. Steroid lotion applied twice daily provides symptomatic relief but may relapse.
Lesions on face, chest can be treated by weak topical steroid and antiseborrhoeic shampoo. Washing the affected areas with soap can be a useful adjunct. 2% Ketoconazole cream once a day is highly effective in difficult cases.
Scaling of blepharitis may be suppressed by frequent washing with zinc or tar containing antidandruff shampoos. Prolonged use of steroid lotion on the eyelids causes glaucoma and should be avoided. 2% ketoconazole cream once a day should be tried in resistant cases.
(b) Infants
Cradle cap should be oiled regularly with warm olive oil and washed off few hours later with 5% cetrimide shampoo. Erythema and scaling on the body can be treated with weak topical corticosteroid cream topical antibiotic if infection is present. Shampoo that contains salicylic acid or selenium sulphide should be avoided in neonates for the risk of systemic absorption.
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