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Dermatitis

Dermatitis
Derives from Greek
Derma = skin, +it is =
inflammation

Inflammation of the skin


Dermatitis

Contact
Eczema
Dermatitis

Atopic
Non Allergic
Dermatitis Non Atopic Allergic Contact
Contact
(Eczema / Dermatitis Dermatitis
Dermatitis
Atopic Eczema)
Contact
Dermatitis
Prof. Dr. dr. Irma D. Roesyanto-Mahadi, Sp.KK(K)

Dermatovenereolgy Department
Medical Faculty University of Sumatera Utara
RSUP H.Adam Malik
Medan
CONTACT DERMATITIS

An inflammatory reaction of the


skin precipitated by an exogenous
chemical
CONTACT DERMATITIS

skin reaction (dermatitis) resulting from


exposure to:
Allergic contact Irritant contact
dermatitis
Allergens Irritans dermatitis
IRRITANT CONTACT DERMATITIS
(ICD)
Non-immunologic inflammation of the skin
caused by contact with chemical, physical
or biologic agents

Allergic contact dermatitis (ACD)


An acquired delayed sensitivity to various
substances that produce inflammatory
reactions in only those who have been
previously sensitized to the allergen
ETI
OLO
GY
ICD

Multifactorial disease;
ETIOL
OGY
ACD

Low molecular
weight
electrophilic or
hydrophilic
hapten chemicals
(<50-1000d)
The most common
Sensitizers : ACD
Pentadecylcatechol

• Poison Ivy
• Paraphenylene diamine : hair dye
• Nickel : ear piercing
• Rubber compounds : mercapthobenzothiazole,
thiuram
• Ethylenediamine : preservative in mycology cream,
dyes, rubber accelerators
PATHOGENESIS
ICD ACD
Removal of surface Characterized by 3
lipid & water phases:
holding substance  1. Sensitization
damage to cell
2. Elicitation
membrane 
epidermal keratin 3. Resolution
denaturation 
direct cytotoxic
effects
journal of Investigative Dermatology (2010) 130, 641–643.
type IV
antigens

inflammatory
mediators
lymphokines

activated macrophage
CLINICAL
PRESENTATIONS

IC
a.
D Mild irritants require
prolonged or repeated
exposure before
inflammation is noted. AC D
b. Strong irritants  a. Lesion appear w/I 24
immediate reactions. -96 hrs of exposure
b. Main symptom : pruritus
c. Pain, burning,
stinging. c. Localization of the
dermatitis is helpful
d. ICD will only erupt in
in identifying the
areas of the skin that
cause
have direct contact
with the irritant
Clinical
presentation
Most cases of contact dermatitis have similar

s
appearance regardless of the mechanism or cause
of inflammation

Inflammatory response :
Acute, sub acute & chronic phase

KEY FEATURE: LOCALIZATION TO THE AREA OF


CONTACT
Tattoo’s ACD

Upper left arm

Lower left arm

Courtesy of Prof. Dr. dr. Irma D. Roesyanto-Mahadi Sp.KK (K).


DIAGNOSIS

H
I
S
T
O
R • Onset, location, temporal associations,
treatments.

y
PATCH TEST
Often essential to help distinguish ACD from ICD or to
diagnose concomitant ICD & ACD
Results
• - Negative reaction
• ? Doubtful reaction
• + Weak reaction
• ++ Positive reaction

• +++ Extreme reaction

• IR Irritant reaction
• NT Not tested
TREATMENT
•Avoidance of allergic or irritant
contactants

•Pharmacologic interventions :
Topical corticosteroid, calcineurin
inhibitors (pimecrolimus & tacrolimus),
oral antihistamines

•Phototherapy
Shortwave UVB
DD
• Other eczematous eruptions
• Atopic dermatitis
• Seborrhoic dermatitis
• Stasis eczema
• Superficial fungus infections
• Bacterial cellulitis
Dermatitis Kontak Iritan

DKI pd tangan & ujung-ujung jari akibat asam


Dermatitis Kontak Alergi

DKA akibat kalung nikel DKA akibat semen


Fotoalergi
(Dermatitis Berloque)
DKA semen
DKA plester
Nummular eczema
• Characteristic: Oval patches with crusted
papulovesicles

• Localisation: Trunk
Extremities
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
Therapy
• 1. Corticosteroid:
- topically
- injectable intralesional
- sistemic
2. Wide spread acute/ subacute eczematous:
prednisone/ triamcinolone 40 mg/i. m
wet dressing/bath: acute dermatitis
3. Chronic: baths containing oil moisturizers
4. Itching: hydroxyzine/ diphenhydramine
Dermatitis Numularis
Dermatitis numularis
LICHEN SIMPLEX
CHRONICUS/neurodermatitis

-Definition:

A chronic eczematous eruption o/ t skin, that is


result of scratching
LSC

Pruritus  scratching and precipitated by frustration,


depression and stress lichenification further itching,
resulting “itch-scratch-itch”cycle
LSC pada daerah pubis dan skrotum
Dermatitis atopik pada orang dewasa
ATOPIC
DERMATITIS

Irma D.Roesyanto
Departement of Dermato-Venerology
Medical Faculty, North Sumatera
University
occurs most commonly during early
infancy and childhood.

• Prevalence peak of 15–20% in early


childhood in industrialized countries

• Frequently associated with


abnormalities in skin barrier function,
allergen sensitization, and recurrent
skin infections.

• No single distinguishing feature of AD or


a diagnostic laboratory test.

• The diagnosis is based on the


constellation of clinical findings listed in
EPIDEMIOLOGY

Etiology and Pathogenesis
complex interactions between genetic
susceptibility genes


immunologic
defects in the
defective skin responses to
innate immune
barrier allergens and
system
microbial
antigens

highly pruritic inflammatory skin


disease →Atopic Dermatitis
↓regulation of
cornified
↑ endogenous ↑
envelope ↓ ceramide
proteolytic transepidermal
genes levels
enzymes water loss
(filaggrin and
loricrin)

↑ allergen
exposure to
absorption into
↓ Skin exogenous
(-) certain
the skin and Barrier endogenous
proteases
microbial from house
colonization Function protease
dust mites
inhibitors
and S.
aureus

breakdown
↑activity of of epidermal
Soap & pH skin ↑ endogenous barrier
Detergent proteases function
BASIC OF PRURITUS IN
AD
Allergen ,Humidity, Sweating, Low concetration of
irritant

T-cell-derived cytokines, e.g: IL-31, stress-induced


neuropeptides, and proteases

cutaneous hyperreactivity and scratching

• Topical
corticosteroids
PRURIT • Calcineurin
US inhibitors
• Anti histamine→ not
effective
CLINICAL PRESENTATION
• Intense pruritus and cutaneous reactivity are
cardinal features of AD
• 3 stages of skin reaction : acute, subacute and
chronic
• Acute : Intense pruritus and cutaneous reactivity
are cardinal features of AD
• Subacute : erythematous, excoriated, scaling
papules
• Chronic : (1) thickened plaques of skin, (2)
accentuated skin markings (lichenification), and
(3) fibrotic papules
Major Features Other common findings
• Pruritus • Dryness
• Rash on face and/or extensors in • Dennie–Morgan folds (accentuated lines
infants and youngchildren or grooves belowthe margin of the
• Lichenification in flexural areas in lower eyelid)
older children • Allergic shiners (darkening beneath the
• Tendency toward chronic or eyes)
chronically relapsing dermatitis • Facial pallor
• Personal or family history of atopic • Pityriasis alba
disease: asthma, allergic rhinitis, • Keratosis pilaris
atopic dermatitis • Ichthyosis vulgaris
• Hyperlinearity of palms and soles
• White dermatographism (white line
appears on skin within1 minute of being
stroked with blunt instrument)
• Conjunctivitis
• Keratoconus
• Anterior subcapsular cataracts
• Elevated serum immunoglobulin
EImmediate skin test reactivity

Table 1. Features of Atopic Dermatitis


Figure 14–1
Ichthyosis vulgaris commonly accompanies atopic dermatitis and is thought to be
responsible for the barrier defect in a subset of patients. Note the larger scales on the
lower extremities.
Figure 14–2
Hyperlinear palms.
F
igure 14–4
Lichenification and excoriations on the dorsal aspect of the hand in a child with atopic
dermatitis.
Figure 14–3
Prurigo papules in a patient with atopic dermatitis.
Figure 14–11
Typical papules, vesicles, and erosions seen in atopic hand dermatitis.
Figure 14–5
A. Pronounced weeping and crusting of eczematous lesions in childhood atopic dermatitis.
B. Excoriated papules and crusting (with secondary infection) in an acute flare of atopic
dermatitis.
Figure 14–6
Confluent erythematous papules on the cheeks of an infant with subacute atopic
dermatitis. Chronic exposure to saliva and moist food at this location has been thought to
contribute to the distribution.
Figure 14–7
Severe lichenification and hyperpigmented prurigo papules seen in a patient with chronic
atopic dermatitis.
Figure 14–7
Severe lichenification and hyperpigmented prurigo papules seen in a patient with chronic
atopic dermatitis.
Figure 14–8
Edematous, erythematous eyelids with lichenification and hyperpigmentation in an
adolescent with atopic dermatitis. Note the infraocular (Dennie–Morgan) folds.
Figure 14–9
Itching infant with atopic dermatitis. (Used with permission from Oholm Larsen, MD.)
Figure 14–10
Childhood atopic dermatitis with lichenification of antecubital fossae and generalized severely
pruritic eczematous plaques.
Differential Diagnosis
1. Seborrhoic dermatitis
2. Contact dermatitis
3. Numular dermatitis
4. Scabies
5. Ichthyosis
6. Psoriasis
7. Dermatitis herpetiformis
8. Sezary syndrome
9. Leterrer-Siwe disease
Figure
Approach to patient with atopic dermatitis (AD). aSee Table . bSecond-line therapy per
black box warning.
TREATMENT
Multipronged approach

• Education about the disease state


• Skin hydration
• Pharmacologic therapy
• Identification and elimination of flare
factors such as irritants, allergens,
infectious agents, and emotional
stressors
TOPICAL THERAPY
SYSTEMIC THERAPY
EDUCATION

• Comprehensive “center-based”
patient/family teaching

• Written “handouts” and care plan


patient/family support groups

• Internet-accessed media
Diaper Dermatitis
Diaper Dermatitis

One of the most common dermatologic


conditions in infants & children
(1 million/ year)

the advent of Irritant and candidal


superabsor bent diaper dermatitis 
disposable diapers >> in diaper-wearing
in the last decade individuals of all ages.
 ↓ incidence
Etiology
Other interrelated etiologic factors…
Irritant Diaper Dermatitis

the most common type


of diaper dermatitis

Appears as
 Erythematous,
 Moist, and
 sometimes scaly occurs in any person
patches who wears diapers,
 Shallow erosions are regardless of age.
sometimes present on
the convex surfaces

It can be asymptomatic or
tender
Candida Diaper Dermatitis

The second most common type of


diaper dermatitis

Candida from intestinal flora frequently


contaminates any type of diaper dermatitis
present for > 3 days, and Candida levels ↑ with
the clinical severity of the dermatitis
Clinical Features
On body
folds as
Oral thrush
well as
can be
convex
associated
convex
surfaces
A = Air.

B = Barrier ointments.

C = Cleansing and anticandidal treatment.

D = Diapers.

E = Education of parents and caregivers


NOTE :

Topical steroid use in


Because of greatly ↑
this anatomic region
percutaneous
should be limited to a
absorption of steroids
short course (3–7 days)
from moisture and
of hydrocortisone (1%
occlusion from diapers,
or 2.5%) ointment
Thank you...

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