Dermatitis Eksematosa_dr. Kristo a. Nababan, Sp. KK

7/28/2019 Dermatitis Eksematosa_dr. Kristo a. Nababan, Sp. KK

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DERMATITIS EKSEMATOSA

Dr. Kristo A. Nababan, SpKK


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Nummular eczema

Characteristic: Oval patches with

crusted papulovesicles

Localisation: Trunk

Extremities


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Dermatitis Numularis


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Differential Diagnosis

Acute vesico papular dermatitis:

Contact dermatitis

Infections: Dermatophyte, HS virus,

Varicella Zoster, Bacteria

Chronic vesico papular dermatitis:

Chronic CD, psoriasis, drug eruption,

fungal infect


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Biopsy

- Intercellular edema widening

intercellular spaces sponge like

appearance epidermal (spongiosis) - Acute & severe : intra epidermal

vesicular

- Chronis: Epidermal hyperkeratoticThickened (acanthotic)

Dermis: lymphocyte infiltration


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Therapy

1. Corticosteroid:

- topically

- injectable intralesional

- sistemic2. Wide spread acute/ subacute eczematous:

prednisone/ triamcinolone 40 mg/i. m

wet dressing/bath: acute dermatitis3. Chronic: baths containing oil moisturizers

4. Itching: hydroxyzine/ diphenhydramine


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ATOPIC DERMATITIS

Chronic relapsing inflammatory skin

disease.

It is frequently associated with asthma,

allergic rhinitis.


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Debate

AD is primarily an allergen induced disease

or

Simply an inflammatory skin disorder foundin association with respiratory allergy


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Atopy

Familial hypersensitivity of skin and m.

membrane against environmental substances


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Atopy / Atopic Syndrome

Sindrome consist of :

Bronchial asthma

Allergic rhinitis

Atopic Dermatitis


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Epidemiology

Prevalence: AD Common health

problem

10%> in children


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Natural history

AD start early in life ( 60% of the patients

develop the disease in infancy

Majority improve < 5 years

>> pats: resp. allergic disease: asthma &allergic rhinitis


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Prognosis

- Depend of the severity

- Start early in life

more severe

persist

- recurrent of AD adolescent


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Ethiology

Texture o/ t skin is abnormal with defective

lipid barrier---> TEWL increase

( Transepidermal Water Loss)

This is due to abnormal metabolism of

fatty acid is not clear


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Factors Contribute to the Development

of A. D.

Genetics

Environmental

Immunological

Pharmacologic

A. D.


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Genetics Factors

- Immunological abnormalities/ atopy

- Hypersensitivity o/ t skin

important development AD

-genetic influence elevated Ig E productT cell disregulation


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Role of Allergen

Food: Milk, Egg infancy

Aeroallergen

late childhood(house dust mite) 80% (+) skin prick test


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Food

-50% children AD clinical reactivity tofood protein

-Young children allergic to food: Milk

Peanut

soy

wheat

75% (+) to food

-Fooddirect contact provoke AD


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Aero allergen

Older children, adultaero allergen

(house dust mite, mould)

Food allergy less important

- Prick test and patch tes20-60% (+) tomite


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Role of Infection

Pat AD develop viral, bacterial, fungal

Skin infection

- Staphylococcus Aureus, Beta haemolytic

strept common cutaneous pathogens

- Staphy Aureus exotoxn, exoenzymeinflammatory skin lesion


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Atopic Dermatitis

AD can be divided into three stages:

1. Infantile atopic dermatitis:

2 months-2 years of age2.Childhood atopic dermatitis:

2 years-10 years

3. Adolescent and adult atopic dermatitis


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Infantile Atopic Dermatitis

60 % In the first year of life

Usually . 2 month of age

Clinic: Itchy erythema of the cheeks

Intraepidermal vesiclesrupture

moist, crusted areas extend to

other part of the body (scalp, neck,

forehead, wrist, extensor extremities

buttocks and diaper area spared


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Chidhood Atopic Dermatitis

Childhood

Clinic: less acute lesions

Lesions less exudative, drier,

>papularLocations: antecubital, popliteal

fossae, flexor wrist, eyelids, face,

around the neck

lichenified, slightly scaly/ infiltrated

plaques


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Adolescents and adult AD

Older patients

Clinic: Localized erythematous, scaly, papular/vesicular plaques

Pruritic, lichenified plaquesLocation: antecubital and popliteal fossae, frontand sides of neck, forehead, area about theeyes

Eruptions generalized more severe inflexures lichenified

Plaques often erythematous/ hyperpigmented


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Major Clinical features of AD (base on

Hanifin and Rajka)

- Intense pruritus & excoriation

- Typical morphology and distribution of skin

lesions:-facial and extensor involvement in

infant and early childhood

-flexural lichenification in adult

- Chronic or chronically relapsing dermatitis

(>6 weeks)- Personal and family history of atopic disease


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Minor features -Dryness of the skin (xerosis)

-Ichthyosis, keratosis pilaris, hyperlinear

palms

-Non specific hand/foot dermatitis

-Scalp dermatitis e.g. cradle cap

-Allergic shiners -Recurrent conjunctivitis and keratoconus

- IgE reactivity

-Dennie-Morgan infraorbital fold

-Orbital darkening -Pityriasis alba

-Food hypersensitivity


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Intense pruritus

Itching, Scratching the day worse atnight sleep disruption

Pat AD threshold of itching decreased

Humidity

Excessive sweating

Exposure to allergens, irritants (soap,

detergent acrylic, wool) itch


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Whats the etiology of pruritus in

AD ?

- Not well understood

- Local release of proinflammatory mediators &

cytokines


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Rukwied and Heyer (1999)

Pruritus:

- Histamine

- Cytokines

- leukotrienes

- neuropeptide

- proteases


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Morphological characteristic of AD

-Acute lesions are papules, vesicles on

erythematous background with sign of erosion,

bleeding and serous exudate

-Sub acute lesions are erythematous and scaly

papules on dry background

-Chronic lesions are fibrotic papules on lichenified

(thickened) back ground

-Excoriation due to scratching in a all stage

-Infection may alter the appearance with the presence of

oozing or local abscess

-Even uninvolved skin is often dry and scaly


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Investigation

Total Ig E > not helpful diagnosis

Skin prick test (SPT) Specific Ig E (RAST) more helpful


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Diagnosis

3 or more major criteria

3 or more minor criteria


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Atopic Dermatitis in Child


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Basic Treatment

Skin care Emollients

Avoidance of irritants, sudden

changes of temperature, humidity

Identification of

specific

Exacerbating factors

Anti inflammatory

Treatment

TREATMENT OF ATOPIC DERMATITIS

Allergens

Microbes

Emotional factors


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Avoidance of trigger factors

1. Irritants detergents

soap

2. Allergens: Food allergen

Airborne allergensChild < 5 years : Usually allergy to 1 or > foodcows milk, egg, wheat, bean

3. House dust mite: older children

young adult

4. Emotional stress


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TOPICAL EMOLLIENT

BASIS TOPICAL TREATMENT :

2 3 X / DAY

WATER LOSS

ITCHING


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Topical treatment

CREAM / LOTION : EARLY PHASE

OINTMENT : LICHENI FIED SKIN

SEVERE CASE :

AFTER OINTMENTWETWRAP DRESSING

EPIDERMAL WATER LOSS

TOPICAL CROMOLYN IN WATER SOLUBLEEMOLLIENT VEHICLE ANTI INFLAMATORYEFFECT


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ANTIBIOTIC FUSIDIC ACID

GRAM (+)

TETRA CYCLINE

SKIN CLEANSER 10% POVIDONE

IODINE

GENERALIZED INFECTION :ANTIMICROBIAL BATH (CHLORHEXIDIN 0,005%)

SISTEMIC ANTIBIOTIC : FLUCLOCXACILLIN :

MUPIROCIN


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OTHER TREATMENT

STRATEGIES

UVA PHOTOTERAPY

CICLOSPORIN

IF


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Atopic Dermatitis in Infant and Child


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CONTACT DERMATITIS

An inflammatory reaction of

the skin precipitated by an

exogenous chemical


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Contact Dermatitis

1. Irritant CD: produced by

substance that has direct toxiceffect on the skin

2. Allergic: trigger an

immunologic reaction

tissueinflammation


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Pathogenesis

Irritant CD: nonspecific inflammatory

reactions due toxic injury of the skin

Allergic CD: Cell mediated immunity/

type IV

A. Sensitization phase

B. Elicitation PhaseSensitization: hapten + protein LCs Th1

t IV


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type IV

antigens

T

inflammatory

mediatorslymphokines

activated macrophage


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Irritants

Subtances direct toxic effect of the skin

Acids

Alkalis Solvents

Detergents


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Allergens

Triggers immunologic reactiontissue

inflammation

Metals

Plants

Rubber chemicals Medicines


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Clinical appearance

Acute (vesicles) Chronic (lichenification)


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Incidence:

- Frequent problem

- 50% occupational illness


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History

First determine: ACD/ICD

Strong irritant several hours skin damage

Weaker irritants multiple application & days

dermatitis Allergic Contact Dermatitis:

Requires 24-48 hours

Often exposure Clinical disease

Occasionally dermatitis (8-12 hours) up to 4-7 hours

Detailed history of occupation, hygiene habits, hobbies

Th t S iti


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The most common Sensitizers

Poison Ivy

Para phenylenediamine

Nickel

Rubber compounds Ethylenediamine

Poison ivy: in the summer

Allergen: pentadecylcatechol (oleoresin of the plant)


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PPD

Permanent coloring of hair

Cross reaction : Azo, aniline dye,

Benzocaine, procaine,

Hydrochlorothiazine

Sulfonamides

When completely oxidized (fur coat), PPD not allergenic


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Nickel

Most commonly in woman

Ear piercing

In all metals

Hypoallergenic earring: one cannot be

certain that they are free of nickel

Stainless steel: nickel bound so tightly

ACD (-)


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Rubber compound

Shoes ACD on dorsa of the feet

Allergen: Mercaptobenzothiazole

Thiurams


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Ethylenediamine

Preservative in Mycolog cream, ointment (-)

Dyes, insecticides,

Rubber accelerators,Synthetic waxes,

In aminophyllin

Sensitive individualgeneralizedeczematous dermatitis


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Physical Examination

Acute/chronic

Depend upon the nature of the exposure

patches/plaque, angular corner, geometric on

lines, sharp margin Localization:

Head& neck: cosmetics, hair dyes, permanentwaves, shampoos

Eyelid: eye cosmetic, nail polishPhoto allergic: produce by a photoreactionbetween SUV & allergen, of the neck, arms


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Physical Examination

The dorsum of the hands: industrial

chemicals (irritants): petroleum, solvents

The dorsum of the feet: shoes (rubber,

leather tanning agents)

Groins and buttocks in infants: Diaper

dermatitis: moisture and feces


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DD

Other eczematous eruptions

Atopic dermatitis

Seborrhoic dermatitis

Stasis eczema

Superficial fungus infections

Bacterial cellulitis


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Diagnosis

Patch test: The test material, in different vehicles

(commonly white petrolatum)

Is applied to the skin under a metal disc, called a

Finn chamber A test battery of 20-24 allergens is used as

standard allergens

The sheet is placed on the upper back, scaled

with adhesive tape

The patch is removed after 48 hours read


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Therapy

Prevention

Avoidance of irritant/allergen change in life

style & occupation

Protective clothing Occupational: protective, barrier cream little

benefit

Substituted Topical steroid

Antihistamine


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Dermatitis Kontak Iritan

DKI pd tangan & ujung-ujung jar i akibat asam


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Dermatitis Kontak Alergi

DKA akibat kalung nikel DKA akibat semen

Seborrheic Dermatitis/ Morbus


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Seborrheic Dermatitis/ Morbus

Unna

Definition: a chronic, superficial, inflammatoryprocess affecting the hairy regions of the body

Etiology: unknown/ Pityrosporum ovale

Dandruff is scaling of the scalp withoutinflammation

Incidence: a common problem, 2-5%adult 18-40 years, baby (cradle cap),

children 6-10 years, woman> man

S b h i D i i


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Seborrheic Dermatitis Predilection hairy

region: scalp, eyebrow

eyelid

Nasolabial creases,

ears, chest


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History

The occurrence of Seborrheic

Dermatitis parallels the increased

sebaceous gland activity occurring in

infant, after puberty, pruritus


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Physical examination

Predilection for the hairy regions where thereare numerous sebaceous gland: scalp,eyebrows, eyelids, nasolabial creases, ears,chest, intertriginous area: axilla, groin, buttocks,

infra mammary folds Bilateral and symmetrically

Most mild form, dandruff, fine whittis scalingwithout erythema.

Patch/plaque: indistinct margin, erythema,yellowish, greasy scaling, uncommon hair loss


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Physical examination S.D

Mild form: dandruff fine whitish scaling

without erythema / Pityriasis sica

Mild Moderate: erythema, yellowish

greasy scaling


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DD

1. A.D (infantile eczema)if infant Loc: diaper area & axilla

diagnosis S.D

If lesion: forearms, shins AD

2. Psoriasis: scalp, groin, other area

papilosquamous patches &

plaque

3. T. capitis: hair loss, urban blackBiopsy : non diagnostic


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Therapy S.D

Anti seborrheic shampoos (sulfur, salicylic

acid, selenium sulfide, zinc pyrithione)

Shampoos must be rubbed in to the

scalp 5-10 minutes

Inflam. Seborrrheic:

topical steroid lot/gel in hairy area;

hydrocortisone cream non hairy skin


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Course & Complication

Infancy : to remit after 6-8 months

Adult : chronic, unpredictable


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STASIS DERMATITIS

Defination:

An eczematous eruption of thelower leg secondary to peripheralvenous disease


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STASIS DERMATITIS

Venous incompetence hydrostaticpressure, capillary damage extravasation ofred blood cell & serum inflammatoryeczematous process


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Incidence

Adults (middle age old age)

History: Chronic

pruritic eruption

precede by edema & swelling

Patients with Stasis dermatitis have oftenhad thrombophlebitis



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Varicose vein are prominent1. Edema

2. Brown pigmentation3. Petechiae

4. Sub acute and chronic dermatitis

5. Thickened skin, scaling and /or weeping6. Any portion of the leg prominent site is

above the medial malleolus


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DD

1. Contact Dermatitis

2. Peripheral Arterial Disease

3. Superficial Fungal Infection

4. Bacterial cellulitis

Examination of peripheral pulses, history of

topical agent, KOH, gram steins, bacterialculture should be done


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Biopsy

Sub acute or chronic dermatitis with

hemosiderin, fibrosis, and dilated capillariesin the dermis


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Therapy

- Prevention of venous stasis and edema use of supportive hose

- Standing should be restricted

- Patients who are obese weight reduction- If this fails bed rest with elevation of legs- Topical steroid

- Wet compresses if there is oozing orcrusting


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Course and Complications

Dusky erythema

Ulceration total bed rest with legelevation with antiseptic cleansingSystemic antibiotics not helpfulApplication of skin grafts

Allergy to topical preparation 60% ( topical

antibiotics)

LICHEN SIMPLEX


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CHRONICUS/Neurodermatitis

-Definition:

A chronic eczematous eruption o/ t skin, that isresult of scratching

Pruritus scratching lichenification & itching

LSC


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SC

Pruritus scratching and precipitated byfrustration, depression and stresslichenification further itching, resultingitch-scratch-itch cycle

History


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History

- Patient may have history of emotional or

psychiatric problem

Ph i l E i ti


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Physical Examinations

Patients: anxious

Lichenified plaque, scratching (+)

Liken Simplek Kronikus/


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Liken Simplek Kronikus/

Neurodermatitis


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DD


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DD

1. Chronic dermatitis2. Psychodermatoses (factitious

dermatitis, delusion of parasitosis

Factitious dermatitis: self inflicted injury o/ t

skin

bizarre eruption (often ulcerated), linearand geometric outlines

Delusion of parasitosis: in disturbed/

anxious eccentric individual

Begins intractable pruritus crawling sensation, thatthey are harboring parasites & bring specimens

Active lesions: excoriated, crusted papule secondary to picking

DD


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DD

3. Neurotic excoriations

Linear :dug out lesions:

Upper mid back (Where scratching

fingers cannot reach.

Neurotic woman

Therapy


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Therapy

Difficult

Tranquilizer and anti depressants

Topical steroid and intralesional steroid

Tabel ECZEMATOUS ERUPTIONSIncidence* History Physical Differential

Di i

Lab.


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Diagnosis

Nonspeciffic

eczematous

dermatitis

11.4 Pruritus Acute-vesicles, weeping, crusted

patches

Subacute-juicy papules

Chronic-lichenified, scaling plaques

Contact dermatitis

Atopic dermatitis

Seborrheic dermatitis

Fungal infection

PsoriasisDrug rash

-

Contact

dermatitis

2.8 Irritant-contact

precedes rash by

hours to days

Allergic-contact

precedes rash by 1-4

days

Vesicles, juicy papules, lichenified

plaques

Sharp margins

Geometric or linear configuration

Conforms to area of contact

Eczematous dermatitis

Fungal infection

Cellulites

Patch test

Atopic

dermatitis2.6 Allergic rhinitis

AsthmaVesicles, juicy papules-infants

Lichenified plaques-adults and

older children

Head, neck, antecubital and

popliteal fossa

Contact dermatitis

Scabies

IgE

Seborrheic

dermatitis

3.7 Dandruff Scaling papules and patches

Scalp, eyebrows, nasal, sternum

Atopic dermatitis

Psoriasis

Fungal infection

Histiocytosis XLupus erythematosus

-

Stasis

dermatitis

0.4 Varicose veins

Leg swelling

Thrombophlebitis

Juicy papules

Lichenified plaques

Brown pigmentation

Lower legs

Cellulitis

Contact dermatitis

Arterial disease

Fungal infection

-

Lichen

simplex

chronicus

0.8 Rash subsequent to

pruritus

Lichenified plaque

Within reach of fingers

Psoriasis -


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Dermatitis Eksematosa_dr. Kristo a. Nababan, Sp. KK

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