Eczema
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Transcript of 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.
04/08/2023ATOPIC DERMATITIS - Yohannis 9
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.
04/08/2023ATOPIC DERMATITIS - Yohannis 12
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.
AC
UTE
SU
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CU
TE
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RO
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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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