Dermatitis/eczema DR SK MIREMBE - PowerPoint Presentation

Slide1

Dermatitis/eczema

DR SK MIREMBE

Slide2

Seborrheic eczema

Seborrheic dermatitis is a common mild chronic eczema typically confined to skin regions with high sebum production and the large body folds.

Although

its pathogenesis is not fully elucidated, there is a link to sebum overproduction and the commensal yeast

Malassezia

.

Slide3

epidemiology

An infantile and an adult form of seborrheic dermatitis are distinguished, the former being self-limited and confined to the first 3 months of life, while the latter is chronic with a peak in the fourth to sixth

decades.

Its prevalence is estimated at 5%, but its lifetime incidence is

much higher.

Men

are afflicted more often than women. There is

a suggested

indication of a genetic predisposition

but no

horizontal

transmission of seborrheic dermatitis.

Extensive

and therapy-resistant seborrheic dermatitis is an important cutaneous sign of underlying HIV

infection,

Parkinson's disease, and mood

disorders.

Slide4

Risk factors

Hereditary diathesis (seborrheic state)

Psoriasis

Parkinson’s disease

Facial paralysis

Neuroleptic drugs

Emotional stress

HIV

Slide5

Clinical forms

Infantile seborrheic eczema

Adult seborrheic eczema

Slide6

CLINICAL FEATURES- Infantile seborrheic eczema

B

egins

about 1 week after birth and may persist for several months.

Initially

, mild greasy scales adherent to the vertex and anterior fontanelle regions are

seen(‘

cradle cap

’).

Disseminated lesions, usually of lesser intensity, may arise on the face,

retroauricular

folds, neck, trunk and proximal

extremities.

Lesions

of the axillae and inguinal folds are acutely inflamed, oozing, sharply demarcated and surrounded by satellite

lesions.

Superimposed

infection with

Candida

species may occur.

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Infantile seborrheic dermatitis. Glistening red plaques of the neck, axillary and inguinal folds as well as the penis and umbilicus. Note disseminated lesions on the trunk and extremities

Slide8

ADULT SEBORRHEIC ECZEMA

In adults, seborrheic dermatitis is generally found on the scalp and, usually in a milder form, on the

face.

Less

often, lesions occur on the central upper chest and the intertriginous areas.

Erythrodermic

seborrheic dermatitis has been described but it is extremely rare.

Slide9

Adult seborrheic dermatitis of the face and scalp. A Note the diffuse scaling of the scalp in addition to erythema of the forehead. B Sharply demarcated erythema with yellow, greasy scale, especially in the

melolabial

fold. When this degree of severity is seen, the possibility of underlying HIV infection needs to be considered.

Slide10

Pityriasis

simplex

capillitii

(dandruff)

is

defined as a diffuse, slight to moderate fine white or greasy scaling of the scalp and terminal hair-bearing areas of the face, but without significant erythema or irritation.

Scales

fall from the scalp and beard area and accumulate visibly on the collars of dark clothing.

Slide11

seborrheic dermatitis of the scalp

In seborrheic dermatitis of the scalp, there is inflammation and pruritus in addition to dandruff. The vertex and parietal regions are predominantly affected, but in a more diffuse pattern than the discrete plaques of psoriasis

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Facial seb

eczema

Seborrheic dermatitis of the facial skin is often strikingly symmetric, affecting the following areas: forehead, medial portions of the eyebrows, upper eyelids, nasolabial folds and lateral aspects of the nose,

retroauricular

areas, and occasionally the occiput and neck

Slide13

Truncal seb

eczema

If present, lesions of the trunk are preferentially found in the

presternal

and intertriginous areas

Slide14

Note

In patients with seborrheic dermatitis, the skin is sensitive to irritation, and exposure to sun or heat, febrile illnesses and overly aggressive topical therapy may precipitate flares and dissemination

.

Irritated seborrheic dermatitis lesions can become bright red and erosive

Slide15

Note

Adult seborrheic dermatitis has a chronic relapsing course.

Patients

feel well and systemic signs are absent.

Extensive

and severe seborrheic dermatitis, however, should raise the suspicion of underlying HIV infection.

Slide16

Diagnosis

Dermatopathology

; Focal parakeratosis,

pyknotic

neutrophils, moderate acanthosis,

spongiosis

.

Slide17

Differential diagnoses

Atopic dermatitis (infantile)

Psoriasis (infantile)

Langerhans cell

histiocytosis

(infantile)

Wiskott

–Aldrich syndrome

(infantile)

Tinea

capitis

(scalp)

Dermatomyositis

(scalp)

Rosacea (face)

SLE (face)

Pityriasis

rosea

(

trunk

)

intertriginous areas must be distinguished from

erythrasma

, inverse psoriasis, intertriginous dermatitis, candidiasis and, rarely, Langerhans cell

histiocytosis

Slide18

Seborrheic-like dermatitis due to

dermatomyositis

Slide19

Treatment for Infantile seb

eczema

skin

care measures such as bathing and the application of emollients.

Ketoconazole

cream (2%) is indicated in more extensive or persistent cases.

Short

courses of low-potency topical corticosteroids may be used initially to suppress inflammation.

Mild

shampoos are recommended for the removal of scalp scales and crusts.

Avoidance

of irritation (e.g. the use of strong

keratolytic

shampoos, or mechanical measures to remove the scales from the scalp) is important.

Slide20

Treatment for adult seb

eczema

Topical

azoles (e.g. ketoconazole), either as shampoos (scalp) or as creams (body

).

Additional

measures, particularly in the initial stages of treatment, include low-potency topical corticosteroids and emollients.

Second-line

treatment options are zinc

pyrithione

and tar shampoos.

Hydroxypyridone

ciclopirox

Topical

calcineurin

inhibitors (e.g.

pimecrolimus

and tacrolimus)

Slide21

Contact eczema

Acute or chronic inflammatory reaction to substances that come in contact with the skin.

Irritant (non immunologic) contact dermatitis is caused by a chemical irritant

Allergic (immunologic) contact eczema is caused

by an

antigen allergen that elicits a type IV hypersensitivity reaction.

Slide22

Epidemiology

Irritant (80%) more common than allergic contact eczema (20%)

Gender differences may be attributed to social and environmental factors

Slide23

Pathogenesis of irritant contact eczema

Any substance can be irritant

Irritants produce direct toxic injury to the skin

An irritant substance is one that causes an inflammatory reaction in most individuals when applied in sufficient concentrations for an adequate length of time.

Potential for an individual compound to cause dermatitis include; substances' chemical and physical properties, concentration, vehicle, duration of exposure, patient age, area of exposure, underlying dermatitis, genetic make up, humidity, temperature

Slide24

Subtypes of irritant contact eczema

Acute toxic

Cumulative insult

Slide25

Pathogenesis of allergic contact eczema

Type IV hypersensitivity reaction

Low molecular

hapten

contacts the skin. Forms

hapten

-carrier protein complex.

Complex associates with epidermal Langerhans cells, that presents the complete antigen to T-helper cell causing the release of various mediators.

T -cell expansion occurs in regional lymph nodes producing specific memory and T-effector lymphocytes which circulate in general blood stream. This is called sensitization and takes 5-21 days

Slide26

Pathogenesis of ACD

Re- exposure to specific antigen

Proliferation of activated T-cells, mediator release and migration of cytotoxic T cells resulting in cutaneous eczematous inflammation at the site of contact. This is also called elicitation and takes 48-72 hours

Small concentration of allergens may be required as compared to ICD

Slide27

CLINICAL FEATURES OF ACUTE ICD

Erythema

Vesicles

Bullae

Skin sloughing

Reactions occur within minutes to hours of contact

Localize to area of contact

Sharp borders

Healing soon after exposure

Slide28

Clinical features of chronic ICD

Multiple exposures to low level irritants over time

Eg

soaps, shampoos

May take weeks, months, years to appear.

Erythema

Scaling

Fissuring

Pruritus

Lichenification

Poor demarcation from surrounding skin

Slide29

Clinical features of ACD

Acute ACD

; Erythema, edema, vesicles, pruritus, frequently spreads beyond the areas of contact and becomes generalized

CHRONIC ACD;

Pruritus, erythema, scaly,

lichenified

, excoriation. These may mimic chronic ICD

Slide30

Allergy to chromate in cement

Slide31

Comparison between ACD and ICD

ICD

ACD

EXAMPLES

Soap, water

Nickel, fragrance, hair dye

Number of compounds

Many

fewer

Distribution of reaction

localized

May spread beyond

area of maximal contact. May be generalized

Concentration

of agent

high

minute

Time course

Immediate to late

delayed

immunology

nonspecific

Type IV

Diagnostic

test

none

patch

Slide32

ACD VS ICD

ICD

ACD

MARGINATION

sharp

Sharp, spreading to periphery

incidence

everyone

Only in sensitized

Slide33

Diagnosis

Dermatopathology

Patch test

RAST

ROAT (Repeated open application test)

KOH examination

Slide34

Differential diagnoses of contact eczema

Atopic dermatitis

Nummular eczema

Neurodermatitis

Stasis dermatitis

Seborrheic dermatitis

Photo dermatitis

Dermatophyte infection

Drug eruptions

Dyshydrotic

eczema

Slide35

Treatment of contact eczema

Avoid allergen

Drain large vesicles

Wet dressings with gauze soaked in burrows solution

Topical steroids

Systemic steroids in severe cases

Other immune modulators

Immune suppressive agents

Slide36

Prevention

Avoid irritant/allergen

If contact occurs wash with water or weak neutralizing agent

Barrier creams

Occupational change

Protective gloves

Slide37

Prognosis of ICD

Healing usually occurs within 2 weeks of removal of noxious stimuli; in more chronic cases, 6 weeks or longer may be required

In the setting of occupational ICD, ONLY 1/3 of individuals have complete remission

Atopic individuals have a worse prognosis

In cases of chronic subcritical levels or irritant, some workers develop tolerance or hardening.

Slide38

Atopic dermatitis

Is an inflammatory, chronically relapsing, non contagious and extremely pruritic skin disease.

Atopy refers to the predisposition to develop asthma, allergic rhinitis, and atopic dermatitis.

While allergic rhinitis and asthma are associated with histamine release, atopic dermatitis presents with scaly plaques reminiscent of Type IV hypersensitivity reaction.

Slide39

Epidemiology

Prevalence of 20% in children

3

% in young adults

Concordance in monozygotic twins 75-85%

Concordance in dizygotic twins 30%

Onset occurs mostly between 3 and 6 months with about 60% developing the condition before 1 year and 90% by 5 years of age

Most patients have elevated serum

IgE

levels and a personal or immediate family history of atopy (allergic rhinitis, asthma, atopic eczema)

Slide40

pathogenesis

Complex interaction of genetic predispositions, environmental triggers, and immune dysregulation.

Inherited in a polygenic fashion with many genes involved

Loss of function mutations within the Epidermal Differentiation complex gene

fillagrin

Fillagrin

is an

i

mportant protein in the formation of the epidermal barrier through binding to and aggregation of the keratin

c

ytoskeleton.

Slide41

pathogenesis

Disturbed epidermal barrier; leads to dry skin due to high trans epidermal water loss and enhanced penetration of

irritative

substances and allergens into the skin

Slide42

Pathogenesis continued

Epidermal barrier function also depends on the immune system. Th2 cytokines inhibit the expression of

filaggrin

a

nd S100protein and therefore impair the epidermal barrier.

AE is characterized by Th2 dominated immune response both in skin and in circulation in the acute phase

Th2 cytokines include;IL-4, IL-5, IL-13

In the chronic phase is mediated mostly by Th1 immune response

Slide43

Triggers

Excessive washing without appropriate skin lubrication

Wool

Synthetic fabrics

Poorly fitting clothes

Mineral oils

Solvents

Sand

Excessive perspiration

Tobacco smoke

Animal dander

Molds

House dust mites

Infections (staph aureus,

pityrosporum

orbiculare

)

Slide44

Triggers of itch

Heat and perspiration

Wool

Emotional stress

Certain foods

Alcohol

Common cold

Dust mites

Slide45

Clinical forms

Infantile phase (2months-2 years)

Childhood phase (3-11 years)

Adolescent/ young adult (12-20 years)

Adult phase (>20 years)

Slide46

Clinical features of infantile phase

Intense itching

Erythema

Papules

Vesicles

Oozing

Crusting

Typical eruptions on the cheeks, forehead and scalp. Diaper area is usually spared

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

Slide47

CF OF Childhood phase

More chronic

Lichenified

scaly patches and plaques with crusting and oozing

Predilection areas; wrists, ankles, backs of thighs, buttocks, antecubital and popliteal fossae

2/3 of patients clear by age of 6

Slide48

CF OF Adolescent/ adult phase

Thick, dry,

lichenified

plaques without weeping , crusting or oozing

Sites; face, neck, upper arms, back and flexures

Slide49

CF of adult phase

Mostly involves the hands, face, neck and rarely diffuse areas

Only 10% of infantile or childhood cases persist into adulthood

Slide50

AE on face of an infant

Slide51

Atopic dermatitis on the extensor surface of an infant's arm.

Slide52

Severe chronic hand dermatitis in an adult with atopic dermatitis

Slide53

Adult with severe atopic dermatitis and facial involvement

Slide54

African-American infant with atopic dermatitis of the forehead and cheeks. Note the

Dennie

– Morgan lines, central facial pallor, and central facial sparing.

Slide55

Lichenification

Slide56

Infected hand dermatitis

Slide57

Angular chelitis

Slide58

Pityriasis alba

Slide59

Palmoplantar hyperlinearity

Slide60

Diagnostic criteria

Hanifin

and

Rajka

3 major and 3 minor

Slide61

Major

Pruritus

Distribution; flexural surfaces in adults or face and extensor surfaces in infants

Chronic or relapsing dermatitis

Personal or family history of atopy

Slide62

Minor criteria

Facial features; pallor, erythema,

hypopigmented

patches, infra orbital darkening,

cheilitis

, infra orbital folds, recurrent conjunctivitis, anterior neck folds

Triggers; emotional factors, environmental factors, skin irritants,

Complications; susceptibility to skin infections, impaired cell mediated immunity, predisposition to

keratoconus

and anterior

subcapsular

cataracts, immediate skin reactivity

Other; early age of onset,

xerosis

,

itchthyosis

, keratosis pilaris, hand and foot eczema, white

dermatographism

., perifollicular accentuation

Slide63

Investigations

Serum

IgE

RAST

PRICK TESTS

BACTERIOLOGY AND VIROLOGY SWABS

HISTOPATHOLOGY

Slide64

Differential diagnosis

Seborrheic dermatitis

Contact eczema

Psoriasis

Nummular eczema

Dermatophytosis

Early stages of mycosis

fungoides

Acrodermatitis

enteropathica

Gluten sensitive enteropathy

Wiskott

- Aldrich syndrome

Hyper

IgE

syndrome

Selective Ig A deficiency

X-linked

agammaglobulinemia

Slide65

Treatment

Avoid provoking factors ( scrubbing, too frequent bathing, scented soaps

Reduce dryness and pruritus by using emollients to moisten skin

Apply moisturizer within 3 minutes of exiting shower or bath

Urea and alpha-hydroxyl acid containing products are effective for skin

moisturization

Slide66

Treatment

Wear cotton clothing all the entire, including long sleeved shirts if possible

For acutely inflamed and weeping skin, use open wet to dry compresses for their soothing effect

Topical steroids for acute or chronic lesions is the main stay

For resistant lesions. Topical steroids under occlusion improves penetration

Tar preparations that are

vasoconstrictive

, disinfectant, and anti pruritic

Slide67

Treatment

Oral or topical antipruritic agents. Oral antihistamines for sedation

Antibiotics in case of secondary infection

Immune modulators; cyclosporine, methotrexate

Calcineriun

inhibitors;

pimecrolimus

, tacrolimus

Azathioprine

UVB. PUVA for severe cases

Slide68

complications

Kaposi’s

varicelliform

eruption; appears after exposure to certain infectious agents.

The altered skin barrier allows HSV (eczema

herpaticum

), vaccinia (eczema

vaccinatum

),

coxsackie

A16 (Eczema

coxsackium

) to widely infect the body.

Slide69

Disease course and prognosis

60% first outbreak by age of 1

90% by the fifth year.

Dermatitis clears in about half by age of 3

Two thirds clear by age of 6

10% may persist in adulthood

Adult onset atopic dermatitis often runs a severe course

Staph aureus infections lead to extensive erosions and crusting, HSV to eczema that may be life threatening.