eczema

Eczema

‘to boil’,

is a clinical and histological pattern of inflammation of the skin seen in a variety of

dermatoses with widely diverse aetiologies

‘dermatitis’ and ‘eczema’ are generally regarded as synonymous, although some authors still use the term ‘dermatitis’

to include all types of cutaneous inflammation, so that all eczema is dermatitis, but not all dermatitis is eczema

Exogenous eczemas Irritant eczema Allergic contact eczema Photoallergic contact eczema Infective eczema* Dermatophytide* Post-traumatic eczema*

Classifi cation of the principal forms of eczema.

Endogenous eczemas Atopic eczema Seborrhoeic eczema* Asteatotic eczema* Discoid eczema* Eyelid eczema* Exudative discoid and lichenoid chronic dermatosis* Chronic superfi cial scaly dermatitis* Pityriasis alba* Hand eczema* Venous eczema* Juvenile plantar dermatosis* Metabolic eczema or eczema associated with systemic disease* Eczematous drug eruptions*

acute papular, oedematous, exudative (Fig. 23.1a) and, , vesicobullous. More longstanding or ‘chronic’ Predominant features are dryness,

hyperkeratosis and ‘lichenifi cation

Acute versus chronic eczema.

In the acute phase , the histological picture is dominated by spongiosis, an intercellular epidermal oedema

In chronic eczema , hyperkeratosis gradually replaces parakeratosis. Acanthosis is more prominent than spongiosis.

Infl ammatory cells are less evident in the epidermis, but dermal changes become more prominent.

DEFINITION Atopic Dermatitis – is an itchy, chronic or

chronically relapsing inflammatory skin disease that occurs most commonly during early infancy & childhood which frequently associated with:

» Abnormalities in Skin Barrier Function & » Allergen sensitization » With no single distinguishing feature or a

diagnostic laboratory test- Dx is based on d/t criteria.

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GENETIC FACTORS

SKIN BARRIER DEFECT

ENVIRONMENTAL FACTORS

IMMUNOLOGIC RESPONSE

ETIOPATHOGENESIS - MULTI FACTORIAL

CLINICAL FINDINGS Intense Pruritus and Cutaneous Reactivity are cardinal features

of AD. Pruritus may be intermittent throughout the day but is usually

worse in the early evening and night. Its consequences are Scratching, Prurigo Papules, lichenification

and eczematous skin lesions

FIGURE 14-1 Prurigo papules in a patient with Atopic Dermatitis.FIGURE 14-2 Lichenification of the neck and shoulders in an adult with Atopic Dermatitis.

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Intensely Pruritic, Erythematous Edematous Papules & Plaques

Oozing, Serous Exudate

Often with 2ndry Excoriations.

Erythematous Papules & Plaques

With Scaling, Excoriation mark as 2ndry Change

Thickened, Hyperkeratotic Plaque

Lichenification &

Fibrotic Papules (Prurigo Nodularis)

Postinflamatory Hyper/ Hypo/ De-Pigmentation.

ALL 3 PHASES OF SKIN REACTION CAN COEXIST.

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CLINICAL STAGES OF ATOPIC DERMATITIS

PHASE DISTRIBUTION MORPHOLOGY CLEARINGINFANTILE

(2 months to 2 years)

Cheeks, face and scalp, extensor surfaces of extremities & trunk (due to friction from crawling)

Erythema, papules, vesicles, oozing, and crusting

Dermatitis clears in half of the patients by 3 years of age

CHILDHOOD(3 to 11 years)

Wrists, ankles, backs of the thighs, buttocks, and antecubital and popliteal fossae

Chronic, lichenified scaly patches and plaques that may have crusting and oozing

Two thirds of patients clear by age 6

ADOLESCENT/YOUNG ADULT

(12 to 20 years)

Face, neck, arms, back, and flexures

Thick, dry, lichenified plaques without weeping, crusting, or oozing

90% or patients clear by age 18

ADULT(>20 years)

Most commonly involves the hands, sometimes the face and neck, and rarely diffuse areas

Lichenified plaques, fissures on the hands, occasional vesicular outbreaks, one subset of “sensitive skin” patients

50% of all patients will have recurrences as adults 

STAGES OF ATOPIC DERMATITIS

INFANTILE PHASE(2 months_2 years) DISTRIBUTION

Cheeks, Face and Scalp, Extensor Surfaces of Extremities & Trunk (due to friction from crawling)

Anywhere on the skin surface Often, Napkin area is spared

MORPHOLOGY - Mainly Acute Lesions lesions consist of Erythema Papules (Discrete or Confluent) The papules are intensely itchy &

may become exudative oozing, & crusting

2ndry infection & LAP are common

CLEARING / COURSE Has chronic, fluctuating course,

varying ê factors: teething, RIs, emotional upsets & climatic changes

Dermatitis clears in 1/2 of the patients by 3 years of age

AD IN INFANT

AD IN INFANTS

CHILD HOODsometimes nail change.

Involvement of the hands, often with exudativelesions, and sometimes with nail changes, is common

ADULT PHASE

DISTRIBUTION Most commonly the Flexures &

Hands, Sometimes predominant head and

neck with eye lid dermatitis rarely diffuse areas some -chronic hand dermatitis localized patches of AD on nipple

(adolecent and young women) involvement of vermilion of lip

MORPHOLOGY – Prominent chronic lesions

Lichenified plaques, & prurigo nodularies

Fissures on the hands, Follicular lichenified papules are a

frequent feature in black people & the Japanese

occasional vesicular outbreaks, one subset of “sensitiveskin” patients photosensitivity

CLEARING / COURSE Subsides as the pt grows older,

leaving an adult with skin that is prone to itching & inflammation w/n exposed to exogenous irritants

Pityriasis alba

MAJOR FEATURES PRURITIS TYPICAL MORPHOLOGY AND DIST. CHORONIC OR CHRONICALY RELAPSI-NG

DERMATITIS. PERSONAL OR FAMILY HX OF ATOPY.

MINOR Xerosis Ichthyosis(palmar hyper linearity,keratosis

pilaris) Immediate skin type reactivity(type1) Early age of on set Tendency towards cut.inf. Tendency towards non spe.hand,foot

dermatitis.

Contd… Nipple eczema Chelitis Recurrent conjuctivitis Dennie-Morgan infra orbital fold. Keratoconus Anterior subcapsular cataract Orbital darkening Facial pallor/erythema

Contd… Pityriasis alba Anterior neck folds Pruritis when sweating. Intolerance to wool & lipid solvents. Perifollicullar accentuation Food intolerance

Supportive Care a reduction of trigger factors, including

harsh chemicals, alkaline soaps and dust mites, as

well as the avoidance (if possible) of occupational triggers (e.g.

chemicals used in hairdressing or frequent handwashing)

TREATMENT

The frequent use of emollients represents a mainstay of AD treatment.

Topical corticosteroids are frequently the first line of pharmacologic therapy for AD

topical calcineurin inhibitors (TCls)

Topical Pharmacologic Agents

CONTACT DERMATITIS

Definition A dermatitis caused by substances coming

in contact with the skin It has two major categories 1- ICD 2-ACD

Cutaneous inflammatory response resulting from a direct effect of a chemical of physical agent

The most common form of OCD Accounts 70-80% of CD

Etiology and Pathogenesis Immunological memory cells aren’t involved No prior sensitization Many chemicals that penetrate the skin can

alter or damage the cells Occurs when the repair capacity of the skin

is exhausted

Four interrelated mzm have been associated with ICD

Removal of surface lipid and water holding substances

Damage to the cell membrane Epidermal keratin denaturation Direct cytotoxic effect

Characteristic of the exposure Amount Concentration Duration Type of contact Simultaneous exposure with other irritant

Acute ICD Commonly seen in occupational accidents Exposure to single potent irritant Rxn occur within mints to hrs of exposure Burning, stinging and soreness Erythema, edema, bulla and necrosis Lesion is restricted to the area of contact

with sharply demarcated border

Cumulative ICD The most frequent type of ICD A result of multiple sub threshold insult Due to different stimuli or repeated

exposure of one agent No sufficient time for complete restoration

of the skin barrier function Slowly developing over weeks to years

Common marginal irritants include Soap Detergent Organic solvents Oils Cosmetics

Treatment Successful management of ICD requires Identification of susceptible individuals Appropriate career advice Identification of potential irritants and

complicating factors in the working env’t

Advice about irritant management and protection

Advice on use of barrier creams and after work emollients

Treatment of any dermatitis/inflammation Investigation of the cause of persistence

Symptomatic Treatment Topical steroid Calcineurine inhibitor Phototherapy Systemic drugs• Azathioprine, cyclosporine Antibiotics

Allergic Contact Dermatitis One of the more vexing and costly

dermatologic problem First described in 1895 by Jadassohn He developed patch test to identify the

allergen Accounts 20% of contact dermatitis

A delayed type of hypersensitivity response to exogenous agents

Previous exposure is needed The rxn is specific to a specific agent or to a

group of similar chemical All area of skin that are in contact with the

allergen will develop the rash

Eczematous response The dominant symptom is itching The primary signs in the acute cases• Erythema• Swelling • Papules• papulovesicles

Lesions can occur apart from contact site• Inadvertent contact• Autosenstization Palms, soles and scalp are relatively

resistant to ACD

Differential Diagnosis ICD Atopic dermatitis Nummular ezema T cell lymphoma Autosenstization rxn Psoriasis Asteotic eczema

Treatment Symptomatic treatment Drying agents for oozing lesion • Topical aluminum sulfate, calcium acetate Emollients for chronic cases

Topical steroid Short course systemic steroid Topical immunomodulators Immunosupressive drugs PUVA

Prevention Identification of the allergen Advice the pt to avoid the allergen and

cross reacting chemicals

Lichen simplex is a chronic eczematous dermatosis characterized by a small number of heavily lichenified plaques or, very often, a single lesion in which the skin is markedly thickened and skin markings are accentuated.

Thickening of the skin secondary to scratching or rubbing due to felling of pruritus

Lichen simplex ChronicusLSC

During the early stages the skin is reddened and slightly oedematous, and the normal markings are exaggerated.

The redness and oedema subside, and the central area becomes scaly and thickened, and sometimes pigmented.

Surrounding this central plaque is a zone of lichenoid papules, and beyond this an indefinite zone of slight

thickening and pigmentation merges with normal skin.

Lichen simplex is uncommon in childhood. The peak incidence is between 30 and 50 years of age,

but it is seen at any age from adolescence onwards. Women are affected more often than men. Single and multiple sites are involved with about equal

frequency.Almost any area may be affected, but the commonest

sites are those that are conveniently reached. the nape of the neck, the lower legs and ankles, the

sides of the neck, the scalp, the upper thighs, the vulva, pubis or scrotum, and the extensor forearms.

Itching is aggravated by heat, sweating, cloth irritation, psychological stress

GeneralAvoid aggravating factorsEmolients

Treatment

potent topical steroidBethamethasone Clobethasone sedating anti histaminesHydroxizine anti depressants doxepin

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