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Dermatitis ANTHONY PAULO SUNJAYA 406162114 Pembimbing: dr. Euis Nana Resna, Sp.KK SMF ILMU KULIT DAN KELAMIN, RSUD CIBINONG JULI 2017 1

ANTHONY SUNJAYA 406162114

INTRODUCTION The word ‘eczema’ comes from the Greek for ‘boiling’ – a reference to the tiny vesicles (bubbles) that are often seen in the early acute stages of the disorder, but less often in its later chronic stages.

‘Dermatitis’ means inflammation of the skin and is therefore, strictly speaking, a broader term than eczema

The terms eczema and dermatitis are used interchangeably, denoting a polymorphic inflammatory reaction involving the epidermis and dermis

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Epidemiology • One of the most common dermatologic disorders

• Associated with Occupations • 10% prevalence worldwide, increasing year by year • 15-25% of all dermatologic patients

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Classification • No clear classification system • Difficult to classify as not all eczemas have known etiologies • Current Classification based on ◦ Morphology ◦ Location ◦ Known Etiology

• Alternatively classified according to ◦ Endogenous and Exogenous cause ◦ Acute and Chronic 4

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Classification

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Etiology •

Exogenous (contact) factors ◦ Irritant ◦ Allergic ◦ Photodermatitis

•

Other types of eczema (endogenous) ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦

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Atopic Seborrhoeic Discoid (nummular) Pompholyx Gravitational (venous, stasis) Asteatotic Neurodermatitis Ptyriasis alba ANTHONY SUNJAYA 406162114

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Pathogenesis Acute vs Chronic Dermatitis

In acute eczema, epidermal oedema (spongiosis), with separation of keratinocytes, leads to the formation of epidermal vesicles ( Fig. 17.3a ). Dermal vessels are dilated, and inflammatory cells invade the dermis and epidermis. In chronic eczema, there is thickening of the prickle cell layer (acanthosis) and stratum corneum (hyperkeratosis) with retention of nuclei by some corneocytes (parakeratosis) ( Fig. 17.3b ). The rete ridges are lengthened, dermal vessels dilated and inflammatory mononuclear cells infiltrate the skin.

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Acute Dermatitis

• • • •

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Erythema and oedema are seen with papules, vesicles and sometimes large blisters. Exudation and crust formation follow. The eruption is painful and pruritic. This case resulted from a contact allergy to a locally applied cream. ANTHONY SUNJAYA 406162114

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Chronic Dermatitis

• Lichenification, scaling and fissuring of the hands due to repeated exposure to irritants. • Allergic contact dermatitis cannot be excluded on the appearance alone. 9

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Laboratory and Skin Tests • IgE, specific IgE • Prick testing

• Patch testing • Atopy patch test • Exposition tests • Mycology, bacteriology • Histopathology

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ATOPIC DERMATITIS The word ‘atopy’ comes from the Greek (a-topos meaning ‘without a place’) It was introduced by Coca and Cooke in 1923 and refers to the lack of a niche in the medical classifications

then in use for the grouping of asthma, hay fever and eczema.

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Definition Atopic dermatitis is a difficult condition to define because it lacks a diagnostic test and shows variable clinical features. Atopic dermatitis is an (( itchy, chronic, or chronically relapsing, inflammatory skin condition)). The rash is characterized by itchy papules (occasionally vesicles in infants) which become excoriated and lichenified, and typically have a flexural distribution.

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Epidemiology Age of Onset First 2 months of life and by the first years in 60% of patients. 30% are seen for the first time by age 5, and only 10% develop AD between 6 and 20 years of age. Rarely AD has an adult onset.

Gender Slightly more common in males than females. Prevalence Between 7 and 15% reported in population studies in Scandinavia and Germany, Prevalence of AD has been increasing since World War II. 13

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Epidemiology

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Etiopathogenesis • Large genetic contribution, with dominant role of mutations in gene encoding filaggrin. • Allergic responses play a role in disease flares. • 60% of adults with AD had children with AD. • The prevalence in children was higher (81%)when both parents had AD 15

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Eliciting Factors • Inhalants Specific aeroallergens, especially dust mites and pollens, have been shown to cause exacerbations of AD. • Microbial Agents Exotoxins of Staphylococcus aureus may act as superantigens and stimulate activation of T cells and macrophages. • Autoallergens IgE antibodies directed at human proteins, release of autoallergens from damaged tissue trigger IgE or T cell responses, suggesting maintenance of allergic inflammation by endogenous antigens. • Foods Subset of infants and children have flares of AD with eggs, milk, soybeans, fish, and wheat. 16

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Exacerbating Factors • Skin Barrier Disruption: increase transepidermal water loss by frequent bathing and hand washing and dehydration • Infections: S. aureus present in severe cases; rarely fungus (dermatophytosis, candidiasis). • Season: AD improves in summer, flares in winter. • Clothing: Wool is an important trigger; wool clothing or blankets (also wool clothing of parents) • Emotional Stress: results from or an exacerbating factor in flares of the disease. 17

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Pathogenesis • Deficient skin barrier protein filaggrin Skin Barrier

Immunologic

Genetic

Environmental

Pharmacologic

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CLINICAL FEATURES Atopic dermatitis is an itchy, chronic, fluctuating disease that is slightly more common in boys than girls, with a range of clinical features. The age of onset is between 2 and 6 months in the majority of cases, but it may start at any age, even before the age of 2 months in some cases. The distribution of the eruption varies with age. 20

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Skin Lesion and Distribution • Prominent involvement of flexures, but can be widespread. • Often also the face and hands. Usually spares nose. • Erythema, papules and scaling. • Secondary excoriations, lichenification, and infection may also be seen. 21

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Associated Features

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Pruritus

Xerosis

(hallmark, plaques, prurigo nodularis)

(80-90% of patients)

Keratosis pilaris

Ichtyosis vulgaris

(lateral upper arms, thighs and cheeks)

(50% of patients, excessive scaling spares flexures)

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Associated Features

Dennie Morgan Lines

Hyperlinea Palmaris

Allergic shiners

Pityriasis alba

Cheilitis Common in infants and children

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Diagnostic Criteria (Hanifin and Rajka)

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American Academy of Dermatology (AAD) Criteria Essential features (must present) Important features (support) Associated features (helpful, less specific) 27

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Essential features (must present) Pruritus Eczematous changes • Typical morphology and age-specific distribution patterns: • Facial, neck and extensor involvement in infants and children • Current or prior flexural lesions in any age group • Sparing of groin and axillary regions

Chronic or relapsing course 28

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Important features (support) Early age of onset Personal and/or family history of atopy (IgE reactivity)

Xerosis 29

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Associated features (helpful, less specific) Keratosis pilaris/ichthyosis vulgaris/palmar hyperlinearity Atypical vascular responses

Perifollicular accentuation/lichenification/prurigo Ocular/periorbital changes Perioral/periauricular lesions 30

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UK Criteria (NICE) An itchy skin condition (or parental report of scratching or rubbing in a child) 31

•

Plus three or more of the following:

1. Onset below age 2 years 2. History of skin crease involvement 3. History of a generally dry skin 4. Personal history of other atopic disease 5. Visible flexural dermatitis (or dermatitis of cheeks/forehead and outer limbs in children under 4 years)

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DIFFERENTIAL DIAGNOSIS

Numular

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Dermatophytosis

ANTHONY SUNJAYA 406162114

Early stages of mycosis fungoides.

DERMATITIS

DIFFERENTIAL DIAGNOSIS DIFFERENTIAL DIAGNOSIS

ICD 33

ACD ANTHONY SUNJAYA 406162114

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DIFFERENTIAL DIAGNOSIS DIFFERENTIAL DIAGNOSIS

PSORIASIS

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Management • Avoidance of triggers (including irritants and allergens),

• reparation of skin barrier (emollients), • anti inflammatories (topical corticosteroids, • topical calcineurin inhibitors) and • anti-infectives (as indicated).

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Prevention

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Hydration a specific Foaming detergents and soaps should be avoided. Oilated baths or baths with oatmeal powder followed by unscented emollient (eg petrolatum), 12% ammonium lactate or 10% α-hydroxy acid lotion is very effective for xerosis.

The regular use of emollients protect against inflammation provoked by irritants such as detergent, and increase the benefit obtained from topical corticosteroid therapy.

Ceramide-rich emollients may lead to improvements in childhood atopic dermatitis through barrier repair mechanism

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Management

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Management of acute AD 1) Wet dressings and topical glucocorticoids; topical antibiotics (mupirocin ointment)

2) Hydroxyzine, 10–100 mg four times daily for pruritus. 3) Oral antibiotics (dicloxacillin, erythromycin) to eliminate S. aureus and treat MRSA according to sensitivity as shown by culture. 41

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Management of chronic AD TOPICAL SYSTEMIC PHOTOTHERAPY ADVANCED TTT

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TOPICAL Emollients

Topical steroids topical calcineurin inhibitors (TCIs) 43

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Topical steroids  Principles of treatment with topical corticosteroids.

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Use the weakest steroid that controls the eczema effectively

Review their use regularly; check for local and systemic side-effects

In primary care, avoid using potent and very potent steroids for children with atopic eczema

Be wary of repeat prescriptions

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Topical calcineurin inhibitors (TCIs)

Tacrolimus and Pimecrolimus, are gradually replacing glucocorticoids in most patients.

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potently suppress itching and inflammation and do not lead to skin atrophy.

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not effective enough to suppress acute flares but work very well in minor flares and subacute atopic dermatitis.

DERMATITIS

SYSTEMIC ANTI- HISTAMINIC SYSTEMIC GLUCOCORTICOIDS

ANTIMICROBIALS 46

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PHOTOTHERAPY  Improve AD, but some patients cannot tolerate the heat generated by the equipment.

 UVB, UVA, narrowband UVB, combined UVA and UVB, and (PUVA) have all been effective in AD.

 Some patients benefit from natural sunlight.

 Has a favorable side-effect profile compared to systemic immunosuppressive agents, with potential risks of ‘sunburn’ and, with longterm treatment, photoaging and cutaneous malignancies. 47

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Advanced Therapies  For the unusually difficult-to-manage AD patient

CYCLOSPORINE METHOTREXATE AZATHIOPRINE  BIOLOGICS 48

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Complications • Skin infections (bacteria e.g. S. aureus; virus e.g. Herpes simplex; fungus e.g. Malassezzia furfur)

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Prognosis • Generally improves with age • Untreated involved sites persist for months or years. • Spontaneous, more or less complete remission during childhood occurs in >40% with occasional, more severe recurrences during adolescence. • 30-50% of patients develop asthma and/or hay fever • Adult onset AD usually severe • S. aureus infection leads to extensive erosion crusting and HSV infection can lead to eczema herpeticum which may be life threatening 50

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Allergic Contact 51

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Contact Dermatitis • Dermatitis precipitated by an exogenous agent, often a chemical, is known as contact dermatitis. • Skin condition created by a reaction to an externally applied substance (AAD) • particularly common in the home, among women with young children and in industry, where it is a major cause of loss of time from work • Most contact dermatitis (around 80%) is irritant in nature 52

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Definition • ACD occurs when contact with a particular substance elicits a delayed hypersensitivity reaction • Sensitization process requires 10-14 days ◦ Upon re-exposure dermatitis appears within 1248 hours

• Most common cause Rhus dermatitis (from poison ivy, oak, sumac all containing the resin – urushiol)

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Epidemiology • Prevalence 2-9% • Rarely on children • 20% of the adult population are allergic to at least one contact allergen (most common nickel and fragrance, but increasingly methylchloroisothiazolinone) • Females > Male

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Etiology

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Signs and Symptoms • Main symptom is pruritus, occasionally painful during severe reactions

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Skin Lesion and Distribution • Often well demarcated to area of allergen exposure (e.g. unilateral). Can be bilateral if exposure is bilateral • Erythematous, scaly edematous plaques with vesiculation distributed in areas of exposure • Certain sites show increased predisposition (e.g. Face, genitals, hands, chronic wounds) 58

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•

The dermatitis is generally confined to the site of contact with the allergen, although severe cases may extend outside the contact area or it may become generalised.

•

Sometimes the allergen is transmitted from the fingers so unexpected sites can be affected eg the eyelids and genitals. Dermatitis is unlikely to be due to a specific allergen if the area of skin most in contact with that allergen is unaffected. The affected skin may be red, swollen and blistered or dry and bumpy

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Allergen Patch Test 1. Nickel sulfate

2. Wool alcohols 3. Neomycin 4. Potassium dichromate

13. p-tert-butylphenol formaldehyde resin 14. Epoxy resin 15. Carba mix 16. Black rubber mix

6. Fragrance mix

17. Methylchloroisothiazolinone/methylisothiazol inone

7. Colophony

18. Quaternium-15

8. Paraben mix

19. Mercaptobenzothiazole

9. Negative control

20. p-Phenylenediamine

5. Caine mix

10. Balsam of Peru

21. Formaldehyde 11. Ethylenediamine dihydrochloride 22. Mercapto mix 12. Cobalt dichloride

23. Thimerosal

24. Thiuram mix 62

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Allergen Patch Test 25. Diazolidinyl urea 26. Imidazolidinyl urea 27. Budesonide (Rhinocort) 28. Tixocortol-21-pivalate 29. Quinoline mix

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Patch Test Grading

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Irritant vs Allergic Contact

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FEATURE

IRRITANT

ALLERGIC

Location

Usually the hands

Usually exposed areas of skin, often the hands

Symptoms

Burning, pruritus, pain

Pruritus is the dominant symptom

Surface appearance

Dry and fissured skin

Vesicles and bullae

Lesion borders

Less distinct borders

Distinct angles, lines, and borders

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DIFFERENTIAL DIAGNOSIS

Dyshydrotic eczema

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Dermatitis Herpetiformis

ANTHONY SUNJAYA 406162114

Early stages of mycosis fungoides.

DERMATITIS

DIFFERENTIAL DIAGNOSIS DIFFERENTIAL DIAGNOSIS

ICD 68

AD ANTHONY SUNJAYA 406162114

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DIFFERENTIAL DIAGNOSIS DIFFERENTIAL DIAGNOSIS

PSORIASIS

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Management • Avoidance of causative allergen

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Complication • Secondary spread of eczema to nonexposed sites or systemic reactions may arise in severe cases

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Prognosis • Resolves completely with allergen avoidance.

• Occupational allergic contact dermatitis may require career change.

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Irritant Contact

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Definition

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Epidemiology • Estimated 1-2% population • Female > Men • Any age, but infants and elderly more common

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Etiology

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Etiology

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Signs and Symptoms

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Signs and Symptoms • 80% of occupational skin disorders Occupation

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Source

Builders

Cement, friction

Cleaners

Detergents, solvents

Cooks

Meat, vegetables, soaps

Hairdressers

Shampoos, bleach

Healthcare workers

Water, soaps

Metal workers

Cutting oils, water

Office workers

Paper, dry air

Farmers

Animal secretion

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Skin Lesion and Distribution • Restricted to area of irritant exposure.

• Often hard to distinguish from allergic contact dermatitis. • Certain sites show increased predisposition (e.g. hands, finger webs). 81

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DIFFERENTIAL DIAGNOSIS DIFFERENTIAL DIAGNOSIS

ACD 83

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DIFFERENTIAL DIAGNOSIS DIFFERENTIAL DIAGNOSIS

PSORIASIS

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Management

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Prevention

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Prevention

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Prognosis • Often difficult to treat. • Occupational irritant contact dermatitis may require career change.

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Stasis/Venous 89

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Definition • Venous hypertension • Full spectrum of timing • Id reaction common • Complicated by ulceration

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Epidemiology • Common amongst the 15% of adults who suffer venous insufficiency

• Men = Female • Usually in elderly

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Pathogenesis •

•

• •

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Venous hypertension, often due to valvular incompetence, leads to lower leg tissue oedema and extravasation of erythrocytes. incompetence of the deep perforating veins increases hydrostatic pressure in dermal capillaries. Pericapillary fibrin deposition impedes oxygen diffusion and leads to clinical changes This leads to chronic inflammation and itch.

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Signs and Symptoms • Most patients are middleaged or older women. • Leashes of venules and haemosiderin pigmentation around the ankles are early signs • Eczema develops, sometimes with fibrosis of the dermis and subcutaneous tissue (lipodermatosclerosis) and ulceration • Itch 93

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Pseudokaposi’s (acroangiodermatitis) 94

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Lipodermatosclerosis Dispigmentation (chronic) DERMATITIS

Skin Lesion and Distribution • Usually bilateral, confined to the lower legs,

• evident signs of venous hypertension.

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Management • Topical corticosteroids help the acute inflammation, • maintenance treatment requires the venous incompetence to be addressed e.g. compression). • Daily emollients are helpful. • Tar-impregnated bandages applied once or twice a week are useful, especially when ulceration coexists. • Venous disease or ulceration is treated on its own merit 96

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Complication • Venous ulceration is not a direct complication of the venous eczema, but may arise following trauma through scratching in atrophied skin. • Prevalence of allergic contact dermatitis is increased in venous eczema.

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Prognosis • Without correction of the underlying vascular defects, gradual deterioration is seen

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References • • • • • • • • • • • 99

Journal of Clinical Immunology Expert Opinion on Biological Therapy; Nature Reviews Drug Discovery; Immunotherapy Pharmaceutical Journal, Royal Pharmaceutical Society Dermatology Illustrated Colour Text Fitzpatrick Dermatology in General Practice 8th ed Ilmu Kesehatan Kulit dan Kelamin FKUI Derm Net New Zealand Dermis, University of Heidelberg American Osteopathic College of Dermatology (http://www.aocd.org/?page=JuvenilePlantarDerm) American Academy Dermatology ANTHONY SUNJAYA 406162114

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References

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