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by Dr N Raboobee MBChB (Natal), FFDerm (SA)

Eczema

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Eczema

A pattern of inflammatory response defined histologically by:

1. Spongiosis

2. Acanthosis

3. Lymphocytic infiltrate around upper dermal vessels

Cardinal symptom

itch

Cardinal signs:

redness

papules

vesicles

scaling

exudation

crusting

Pathology

1.     Acute

2.     Subacute

3.     Chronic

Acute eczema

spongiosis

fluid around prickle cells

coalescence -> vesicles -> bullae

leakage of fluid -> serous exudation -> coagulation crusts

Subacute

acanthosis (thickening - prickle layer)

parakeratosis - (retention of nuclei in horny layer)

 

Chronic

acanthosis

parakeratosis

hyperkeratosis (thickening of horny layer)

lichenification (tree bark appearance)

 

Classification of eczema

According to aetiology and clinical features

Endogenous

Atopic

Seborrhoeic

Discoid

Pompholyx (Palms & Soles)

Hand Dermatitis

Pityriasis Alba

Gravitational Eczema

Asteatotic

Juvenile Plantar Dermatosis

Eczematous Drug Eruptions

Exogenous

Contact Dermatitis

    i)     Primary Irritant Contact Dermatitis

    ii)     Allergic Contact Dermatitis

Infective

Photosensitive

Dermatophytide

 

 

 

Endogenous eczema

 

Atopic eczema

Clinical type of dermatitis associated with asthma, hay fever & eczema.

Aetiology unknown

70% f/h

itchy skin

Trigger factors

food

clothing

preservatives

chemicals

climate & temperature

psychological/ emotional

Immunological

increased IgE

decreased IgA

decreased suppressor t cells

increased colonisation with staph

Clinical features

age of onset: 2 - 6/12 in 75 %

sites:

infantile: face

knees

childhood: elbow and knee flexures

eyelids - dennie morgan fold

lichenification

adult: flexures and hands

(lichenification)

Associations:

Asthma/ Hay Fever

Urticaria

Food/ Drugs

 

Complications:

Impetigo

Kaposiís Varicelliform Eruption

Conjunctivitis

Cataract

Prognosis

50% clear by age 13

30% develop asthma and hay fever.

Investigations not helpful

ige, rast, prick and patch testing

Management

general:

avoid soap, wool, preservatives, chemicals, extreme climate, small pox vaccine, herpes

cows milk < 6/12 (controversial)

elimination diet

drug treatment

topical steroids

emollients

soap substitutes, eg. Ung emulsificans

antihistamines (orally)

antibiotics (oral or topical)

evening primrose oil

For Resistant Patients (Dermatologist Only)

oral steroids (only for the most severe cases) no place in routine management.

cyclosporin (for extremely severe cases)

azathioprine

methotrexate

puva therapy

narrow band uvb (tlo1)

 

Seborrhoeic dermatitis

Characteristic distribution: (childhood and adult varieties)

scalp, eyebrows, nasolabial folds

trunk

major flexures (neck, axillae, groins, submammary)

Pathology: ?pityrosporon yeasts

Exclude underlying immunosuppression (hiv)

Treatment:

shampoo (ketoconazole shampoo/selsun

scalp: sal acid/sulphur mixture

face: 1% hydrocortisone

body: topical steroid/ sulphur/ ichthammol

systemic ketoconazole

 

Atopic

Seborrhoeic

Age of onset

2-6 months

2-6 weeks

Atopic history

70%

Absent

Sites

Face,

Elbow and knee flexures

Scalp, neck, axillae, groins and ears

Pruritus

++

-

General condition

Miserable

Well

Course

Chronic

Self limiting approx 6 weeks.

Prognosis

Good

Treatment

Topical steroids

Emollients

(reduction of irritants and allergens

Topical steroids

Anti fungals

Aetiology

?

Pityrosporon yeasts

Gravitational eczema

Inner lower legs

Secondary to venous hypertension

Pathogenesis

Increased venous pressure -> fibrinogen -> deceased nutrition

Treatment

avoid sensitisers

topical steroids

supportive bandages

treat underlying varicosities

 

Asteatotic eczema

Elderly

Lipid retention

Reticulate cracks

 

Discoid eczema

Coin shaped

Scaling and crusting

Treatment: mild topical steroid

emollient

retinoids (resistant cases)

 

Pompholyx

Palms - cheiropompholyx

Soles - podopompholyx

Cf: deep seated vesicles

Sago like grains

Treatment:

Rest

Kmno4 soaks

Open bullae

Topical steroids

Topical / oral antibiotics

Oral steroids (severe cases)

Pityriasis alba

Oval patches

Initial erythema

Hypopigmented with branny scales

Majority 3 - 16 years

Hypopigmentation may persist for 6 months

Diff diag. Vitiligo

pityriasis versicolor

Rx: bland emollient

mild topical steroid for two weeks in acute phase

sunscreen

 

 

 

 

 

 

Principles of management of eczema

Patient education

explanation, reassurance, sympathy

support, reduction of stress

Avoidance of irritants and allergens

imitation jewellery, hand cleaner, medicaments

Wet dressings (acute stage)

kmno4 soaks 1:8000 - light pink solution

aluminium acetate lotion 5% in sterile water

Soap substitutes

ung emulsificans

Bath oils

Emollients

mainstay of treatment

aqueous cream

urea based compounds

Topical steroids

creams - acute

ointments - subacute and chronic

fatty ointments - chronic

combinations

antibiotics - secondary infection

keratolytics - scaling

(antifungal)

varying strengths (teach patient)

weak - face eg. 1% hydrocortisone

moderate

potent

very potent (palms and soles, short duration)

Non steroidal topical agents (new)

Tacrolimus (Protopic)

Pimecrolimus (Elidel)

Tar

Ichthamol

Zinc

Antihistamines

These are given orally as topical antihistamines are associated with sensitisation ie development of an eczema/ contact dermatitis.

Antimicrobials

Topical Antiseptic - Savlon

Topical Antibiotic

Systemic Antibiotic

Systemic therapy (dermatologist only)

Oral Steroids (Very Severe Cases Only)

IV Steroids

Cyclosporin

Azathioprine

Methotrexate

Puva

Narrow Band Uvb (Tlo1)

 

 

 

Eczema

 

 

Exogenous eczema

1. Contact dermatitis

i) primary irritant

ii) allergic

2. Infective

3. Photosensitivity dermatitis

4. Dermatophytide

 

 

Primary irritant contact dermatitis

Primary irritant: a substance which will produce an eczematous reaction if applied in high enough concentration on any individual. Single or cumulative exposure.

Allergic contact dermatitis

Only in individuals previously sentitised by an allergen.

 

Differences

Primary irritant

Allergic

Prior exposure

Not required

Essential

Sites

Only sites of contact

Sites of contact and distant sites

Susceptibility

Everyone

Only some patients

Association

Atopy

Prolongued use of topical medication

Timing

Rapid

4 - 12 hours following first exposure

> 24 hours

No lesions on first exposure

Examples of irritants

Caustic liquids

acids }-

alkalis }- strong irritants

Soaps ]

Detergents ] mild irritants

Mineral oils ] - cumulative damage

Cleaning agents ]

 

Acute irritant contact dermatitis

Clinical features

I) immedate burning / stinging

Ii) limited to site of application

Iii)spectrum:

transient erythema/ chapping

- florid eczema with oedema, inflammation, pain, vesiculation,

- severe exudation - bullae, tissue necrosis

Treatment

1. Prevention - protective clothing

gloves, goggles, shields

2. Wash immediately with cold water or nutralising solution

3. Wet compresses: soaks/ lotions

4. Bland creams/ antibacterial creams

5. Topical steroids

Diagnosis

History - not patch test

Chronic (cumulative) contact dermatitis

Repeated insusts with chemical and physical factors

Occupations at risk

Housewives/ domestic servants

Nursing

Hair dressing

Building

Motor mechanics

Gardeners

Clinical features

Dryness, redness, fissuring

Eczema (whole spectrum)

Thin exposed skin

Finger webs

Face & eyelids

Treatment

Remove all adverse factors

Barrier creams to clean

Emollient to prevent dryness

Cotton lined gloves

Topical steroid only if severe

Emulsifying oint

Oral antibiotics

Oral antihistamines

Eg chronic hand dermatitis

 

Allergic contact dermatitis

I) dermatitis caused by prior exposure to allergen

delayed hepersensitivity - type 4 allergy

Ii) high concentration will not cause eczema in normal individual

Iii) in sensitised individual, even low conc may cause eczema

Iv) may develop after many years of handling the substance.

Clinical features

Acute/ subacute lesions

Sites of contact and distant sites

Aetiology suspected according to site of involvement

 

Nickel (jewellery)

Ear lobes, neck, wrist, thighs

Acute: erythema

swelling

papules

vesicles

Subacute/ chronic

dryness

scaling

fissuring

 

Localisation of allergic contact dermatitis

Clue to the allergens

Localisation

Possible causative product

Possible allergens

Head

Hair cosmetics

Paraphenylamine diamine

Periorbital

Cosmetics for eyes, face and hair

Nail varnish

Contact lens fluid

Plants

Fragrance

Colophony

Primula

Lips

Lipstick

Toothpaste

Nail cosmetics

Topical medication

Foods

Lanolin

Flavouring

Formaldehyde

Antioxidants

Ears

Earrings

Ear drops

Nickel

Neomycin

Axillae

Deodorant

Antiperspirant

Clothing

Fragrance

Formaldehyde

Hands

All contactants

Nickel

Potassium dichromate

Trunk

Clothes

Metal objects eg zips buttons

Nickel

Legs

Topical medications for stasis ulcers

Neomycin

Clioquinol

Lanolin

Povidone iodine

Feet

Shoes

 

 

Rubber, chromate

Glue-formaldehyde

Dyes (potassium

Dichromate

Perianal

Topical medication

 

Moist toilet paper

Neomycin

Local anaesthetic

Local antihistamine

Isothiazolinone

Investigations

Careful history

1. Occupational

2. Recreational

3. Medicament

Patch testing

Investigation of choice for allergic contact dermatitis

European standard battery (23 allergens)

Treatment

Avoidance of allergen

Eg imitation jewellery

Acute: wet soaks

Subacute: topical steroids

By no means straightforward

 

Photosensitivity

Phototoxicity

Photoallergy

Non immunologic

Immunologic

Majority of individuals if conc. Of substance andamount of radiation of proper wavelength are sufficient

Only some individuals

Occurs on first exposure

Only in previously sensitised individuals

Appears within hours ffg 1st and subsequent exposure

Takes 1 - 2 weeks to develop

Clinically resembles sunburn

Painful tingling, blistering

Clinical features of acute allergic contact dermatitis

Photopatch tests negative

Photopatch test positive

Common causes:

Coal tar, psoralens, dye, perfumes, cosmetics

Drugs: thiazide, chlrpromazine, tetracycline, amiodorone

Causes:

Fragrance, sunscreens,

Drugs:

Nsaids

Diuretics

Dhlorpropamide

Carbemazepine

Sulphonamides

Phenothiazines (antihistamines)

Management of photosensitivity dermatitis

Reduce sun exposure

Withdraw culprit drugs

Broad spectrum non irritating sunscreens

Topical emollients

Topical steroids

Systemic steroid if severe

Patch/ photopatch testing

 

Dermatophytide

Allergic reaction to inflammatory tinea at distant site

Usually severe inflammatory tinea pedis or kerion

Clinically

1. Eczematous vesicles on hands and feet (pompholyx like) - commonest

2. Pityriasis rosea like

3. Uritcaria

4. Erythema nodosum

5. Annular erythema

Criteria for diagnosis of dermatophytide

1. Proven focus of dermatophyte infection

2. Absence of dermatophytes in dermatophyte lesion

3. Clearing of dermatophytide lesion when fungus eradicated

 

Infective dermatitis

Primary event: bacterial infection, secondary eczema

Controversial

Diff. Diagnosis: infected eczema (infection is secondary to eczema)

 

Dr N Raboobee
Copyright © 2000.   All rights reserved.
Revised:  February 29, 2004
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