Allergic and irritant contact dermatitis

2. INTRODUCTION
• CD defined as an inflammatory process affecting skin
• Induced by contact with chemical, physical and/or
biotic agents in environment,
• Causes lesions of skin, mucosa and semi-mucosa by
means of allergic and irritant pathogenic mechanisms .
• Allergic form generally starts at age of 2-3 years
(sometimes as early as six months) because of
progressive exposure to sensitizing agents and
immaturity of CMI,
• Irritant contact dermatitis may develop from birth.
• CD grows in frequency with age.

3. Epidemiology of ICD
• Clinical manifestations of ICD are determined by:
– Properties of the irritating substance
– Host factors
– Environmental factors including concentration, mechanical
pressure, temperature, humidity, pH, and duration of contact
– Cold alone may also reduce the plasticity of the horny layer, with
consequent cracking of the stratum corneum
– Occlusion, excessive humidity, and maceration increase
percutaneous absorption of water-soluble substances

4. Epidemiology of ICD
• Important predisposing characteristics of the individual
include:
– Age, race, sex, pre-existing skin disease, anatomic region
exposed, and sebaceous activity
– Both infants and elderly are affected more by ICD because
of their less robust epidermal layer
– Patients with darkly pigmented skin seem to be more
resistant to irritant reactions
– Other skin disease such as active atopic dermatitis may
predispose an individual to develop ICD
– The most commonly affected sites are exposed areas such
as the hands and the face, with hand involvement in
approximately 80% of patients and face involvement in
10%

5. Pathogenesis of ICD
• Denaturation of epidermal keratins
• Disruption of the permeability barrier
• Damage to cell membranes
• Direct cytotoxic effects

7. Pathology of ICD
• Variable mix of inflammation, necrosis of epidermal
keratinocytes, and mild spongiosis
• Combination of an upper dermal perivascular infiltrate of
lymphocytes with minimal extension of inflammatory cells into
the overlying epidermis, and widely scattered necrotic
keratinocytes is most typical picture
• True features of interface dermatitis are absent, and spongiosis
should be focal or absent
• Over time additional histologic findings include acanthosis with
mild hypergranulosis and hyperkeratosis

8. Epidemiology of ACD
• Affects the old and young, individuals of all races, and both
sexes
• Differences in genders usually based on exposure patterns,
such as nickel allergy being seen more frequently in women,
presumably due to greater exposure to jewelry
• Occupations and avocations play an important role
• Allergens differ from region to region, e.g. preservatives used
in personal care products can vary based on government
legislation

9. ACD: Causes:
• M/C agents are plants of Toxicodendron genus
– eg : poison ivy, poison oak, poison sumac
• Other common agents
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Nickel sulfate (various metal alloys)
Sunscreens
Potassium dichromate (cements, household cleaners),
Chromate (leather products)
Lanolin (emollients)
Formaldehyde
Ethylenediamine (dyes, medications)
Mercaptobenzothiazole (rubbers)
Thiram (fungicides)
Paraphenylenediamine (Hair dyes, Henna, photographic chemicals)
Balsam of peru (fragrnce)
CAPB (COCOAMIDOPROPYL BETAINE) (shampoos, bath products,
and eye and facial cleaners)

10. PATHOGENESIS
TWO PHASES
• Sensitization phase
– Hapten penetrates skin ->
– Biochemically transformed by epidermal enzymatic processes ->
– Conjugated with a carrier protein to become immunogenic ->
– Captured by antigen presenting cells (APCs), particularly
Langherans cells ->
– Processed, bound to class II MHC molecules, and exposed on cell
surface ->
– Cytokines produced by keratinocytes and APCs ->
– Langherans cells migrate towards locoregional lymph nodes ->
– Specific effector and memory T lymphocytes selected and clonally
proliferated ->
– Enter bloodstream and reaches to skin and subject is sensitized to
hapten.

11. • Elicitation phase
– New contact penetration of skin ->
– Substance undergoes chemical changes ->
– Recognized and processed by Langherans cells ->
– Specific T lymphocytes are recalled at skin level
and, together with keratinocytes, release numerous
cytokines -> Amplify inflammatory response ->
– Give rise to skin damage

12. Pathology of ACD
• ACD is the prototype of spongiotic dermatitis
• Acute stage: variable degree of spongiosis with mixed dermal
inflammatory infiltrate containing lymphocytes, histiocytes, and
variable numbers of eosinophils
• Moderate to severe reactions show intraepidermal vesiculation
• Subacute to chronic stages have epidermal hyperplasia, often
psoriasiform

13. Regional Sites of Predilection
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14. Inflammatory Response in CD:
• Acute
– Bright red edematous skin
– May have clear fluid-filled vesicles or bullae
– As lesions break, skin becomes exudative and weeps clear fluid
• Subacute
– Characterized by the formation of papules instead of vesicles
– Additionally, less edema is seen in subacute phase.
– Dry scales are sometimes seen in subacute contact dermatitis.
• Chronic
– Scaling, skin fissuring, and lichenification but only minimal
edema.
– Excoriations can also be observed in chronic contact dermatitis.

16. ICD
ACD
Morphology
• Acute ICD includes erythema and edema and
sometimes vesicles or bullae, oozing and
pustules
• Pustules, necrosis or ulceration are rarely
seen
• Necrosis and ulceration may also be seen
with corrosive materials
• ACD is mostly characterized by edema,
• ICD is mostly characterized by dryness,
vesicles and oozing, however, these features
roughness, glazed or scalded appearance of the are usually not present in subacute or chronic
skin
ACD
• Chronic ICD may have hyperkeratosis,
desquamation, lichenification and fissuring
• Chronic ACD may display hyperkeratosis,
desquamation, lichenification and fissuring
• Lesions are characteristically sharply
circumscribed to the contact area
• Clinical lesions are more intense in the
contact area, but they usually exceed this area
and their limits are ill defined
• Usually there is absence of distant lesions,
but sometimes dermatitis may be generalized, • Dissemination of the dermatitis with distant
depending on the nature of the exposure
lesions may occur

17. ICD
ACD
Symptoms
• Symptoms of acute ICD are burning,
stinging, prickling, pain and soreness of the
skin (pruritus may be present)
• Pruritus is the main symptom of ACD
Clinical course
• Sensitizing exposure(s) is required
• Acute ICD may appear after first exposure (at
least with strong irritants)
• Clinical lesions appear after subsequent
challenges with re-presentation of the antigen
• In acute ICD, lesions appear rapidly, usually to already primed (memory) T cells
within minutes to a few hours after exposure,
but delayed reactions can be seen
• Lesions usually appear 24–72 h after the last
exposure to the causative agent, but they may
• Irritant reactions are characterized by the
develop as early as 5 h or as late as 7 days after
'decrescendo phenomenon'
exposure
• The reaction reaches its peak quickly, and
then starts to heal
• Allergic reactions are characterized by the
'crescendo phenomenon' and the kinetics of
resolution may be slower

18. Differences between Contact Dermatitis Irritant and Allergic
IRRITANT
ALLERGIC
People at risk:
everyone
Mechanism of response: nonimmunologic
a physical and chemical alteration of epidermis
Number of exposure required: few to many
depends on individual,s ability to maintain
an effective epidermal barrier
Nature of substance: organic solvent, soaps, acids
Concentration of substance required:
usually high
Evolution: rapid (few hours after exposure)
lesions: monomorphical
Margination and site: well-defined to site of
exposure
Investigative procedure: trial of avoidance
Management: protection and reduced incidence
of exposure
Genetically predisposed
Delayed hypersensitivity reaction
One or several to cause
Sensitization
low molecular weight hapten
(metal, formalin, epoxy,...)
May be very low
Not so rapid
Polymorphical
poor-defined, spreading in the
periphery, may become generalized
Trial of avoidance, patch testing
Complete avoidance

19. ACD and ICD
ACD
ICD
Histology
Spongiosis, exocytosis
Epidermal necrosis
Patch tests
Skin
immunology
Blood
immunology
Positive (eczema)
Presence of activated
T cells
Presence of specific T
cells
Negative
No activated T cells
No specific T cells

21. Type of irritation
Acute ICD
Onset and type of exposure
Acute; often single exposure to strong irritant
Delayed onset of clinical lesions: 8–24 h or
Acute-delayed ICD longer after exposure; induced by special
irritants
Develops in weeks; often seen in individuals
Irritant reaction
involved in wet work and appears after
multiple exposures
Develops in months to years; multiple
exposures to different agents; often weak
Cumulative ICD
irritants, capable of inducing a reaction only
after repetitive exposure
Develops in months to years; multiple
Traumiterative ICD
exposure to a single agent
Develops in weeks to months after skin
Traumatic ICD
trauma
Develops in weeks to months by repetitive
Friction ICD
microtrauma
Develops in weeks to months; exposure to
Pustular and
special agents (comedogenic-pustulogens),
acneiform CD
frequently occurs with occlusion
Exsiccation
Develops in weeks; multiple exposure
Clinical characteristics
Erythema, edema, weeping, vesicles,
bullae, necrosis, burning, pain
Erythema, papules, vesicles, bullae
Erythema, papules, dryness, scaling; it
may resolve or, with continued exposure,
may progress to a full-blown ICD
Erythema, papules, dryness, scaling,
fissuring, lichenification. Burning, itching,
soreness
Erythema, papules, dryness, scaling,
fissuring, lichenification
Erythema, papules, dryness, scaling,
fissuring, lichenification, callus
Erythema, papules, dryness, scaling,
lichenification
Papules, pustules, comedones
Dryness, scaling, fissuring, itching,

22. Irritant Contact Dermatitis
Acute Irritant Contact Dermatitis
• Burning, stinging, painful sensations can occur
immediately within seconds after exposure or
may be delayed up to 24 hour
LESION
Erythema with a dull, nonglistening surface 
vesiculation (blister formation)  erosion 
crusting  shedding of crusts and scaling or
erythema  necrosis  shedding of necrotic
tissue  ulceration  healing
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23. Irritant Contact Dermatitis
Acute Irritant Contact Dermatitis
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24. Irritant Contact Dermatitis
Acute Irritant Contact Dermatitis
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25. Irritant Contact Dermatitis
Chronic Irritant Contact Dermatitis
• Prolonged and repeated exposures of the skin to
irritants results to a chronic disturbance of the barrier
function, subsequently, elicit a chronic inflammatory
response.
• Stinging and itching, pain as fissures develop
LESION
Dryness  chapping  erythema  hyperkeratosis and
scaling  fissures and crusting
• Lichenification, vesicles, pustules, and erosions
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26. Irritant Contact Dermatitis
Chronic Irritant Contact Dermatitis
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27. Allergic Contact Dermatitis
Acute Allergic Contact Dermatitis
• Well-demarcated erythema and edema on
which are superimposed closely spaced,
nonumbilicated vesicles, and/or papules
LESION:
Erythema Papules vesicles erosions
crusts scaling.
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28. Allergic Contact Dermatitis
Acute Allergic Contact Dermatitis
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29. Allergic Contact Dermatitis
Acute Allergic Contact Dermatitis
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30. Allergic Contact Dermatitis
Chronic Allergic Contact Dermatitis
• Plaques of lichenification (thickening of the
epidermis with deepening of the skin lines in
parallel or rhomboidal pattern), scaling with
satellite, small, firm, rounded or flat-topped
papules, excoriations, erythema, and
pigmentation
LESION
Papules scaling lichenification excoriations
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31. Allergic Contact Dermatitis
Chronic Allergic Contact Dermatitis
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32. Allergic Contact Dermatitis
Chronic Allergic Contact Dermatitis
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33. ICD & ACD
• Differentiation is often difficult in clinical setting,
• Deciding whether dermatitis primarily depends on irritancy
or allergy is not always straightforward.
• No pathognomic clinical signs and symptoms can
unambiguously discriminate between ACD and ICD.
• Diagnosis of CD depends on:
– Patient history,
– Clinical examination,
– Exposure assessment (including hazard identification,
estimation of dermal exposure and risk characterization),
– Analysis of all predisposing and contributory factors,
– Comprehensive diagnostic testing.

35. Clinical characteristics of the dermatitis
• Characteristics of initial lesions and clinical evolution
• Time of onset and possible relationship with
exposure to allergens or irritants
• Dermatitis area corresponding to exposure site
• Dermatitis morphology suggesting specific
contactants

36. History of occupational exposure
• Job description; occupational gestures and characteristics
of working milieu
• Potential allergens and irritants in working environment
• Characteristics of exposure: dose, frequency and site
• Concomitant exposure factors: temperature, humidity,
occlusion, friction, and so on.
• Time relationship to occupation; effect of holidays and
time off work
• Personal protective measures at work (gloves, masks and
barrier creams)
• Other workers similarly affected?

37. History of nonoccupational exposure
• Domestic products: cleansers and detergents
• Skin care products, fragrances, nail and hair products
• Pharmaceutical products (under prescription and
over the counter)
• Personal protective measures at home (gloves)
• Jewellery and clothing
• Homework and hobbies

38. Variants on exposure
• Direct contact with agent
• Contact through fomites or contaminated surfaces
• Combination of contact with causative agent and sun
exposure, resulting in a photocontact or photoaggravated
dermatitis
• Transfer from other body sites, generally by hands, to
more sensitive areas, such as eyelids or neck, resulting in
an ectopic dermatitis
• Exposure to gases, droplets or particles in atmosphere,
which results in airborne dermatitis
• Systemic exposure in previously sensitized patients

39. History of previous dermatitis, atopy and other
skin/general diseases
• Past contact dermatitis (occupational or not)
• Previous patch testing
• Other exogenous or endogenous dermatitis: atopic
dermatitis, stasis dermatitis, psoriasis and sensitive
skin
• Mucosal atopy (asthma and rhinoconjunctivitis)
• Family history of atopy and other skin diseases

40. Physical Examination
• Rietschel and Fowler proposed the following as
primary diagnostic criteria for irritant contact
dermatitis:
• Macular erythema, hyperkeratosis, or fissuring
predominating over vesiculation
• Glazed, parched, or scalded appearance of the
epidermis
• Healing process beginning promptly on
withdrawal of exposure to offending agent
• Negative results on patch testing that includes all
possible allergens

41. • Minor objective criteria for irritant contact
dermatitis include the following:
• Sharp circumscription of dermatitis
• Evidence of gravitational influence such as a
dripping effect
• Lower tendency for the dermatitis to spread than
in cases of allergic contact dermatitis
• Morphologic changes suggesting small
differences in concentration or contact time
producing large differences in skin damage

42. Differential Diagnoses:
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Insects Bites,
Herpes Zoster
Cellulitis
Herpetic Whitlow,
Impetigo ,
Atopic Dermatitis,
Exfoliative Dermatitis
Psoriasis
Erysipelas
Scabies
Erythema Multiforme
Vulvovaginitis
Herpes Simplex

43. Workup Laboratory Studies:
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skin tests,
where a positive result, expressing as a dermatitis at the site of contact with the
chemical, is considered to be synonymous with contact allergy
Patch tests (epicutaneous)
Open-tests or repeated open tests – ROAT
Thin-layer Rapid Use Epicutaneous Test (T.R.U.E. Test)
Photopatch Test
Provocative Use Test
Differentiation between irritation and allergy can therefore be established
clinically by:
– The systematic use of a positive control for irritation during the tests;
– When a reaction is difficult to interpret or there are positive irritation tests:
1) re-test with patch tests for only 24 hours (or 12 hours if the first reaction is
strong);
2) carry out a ROAT test.

44. • immunological tests
• shows the existence of allergen-specific T cells
in the skin or blood of patients;
• Presence of allergen-specific T cells
in the skin found in a punch biopsy of ACD
lesions or in skin tests
• Presence of allergen-specific T cells
in patients’ blood

45. Management for Contact Dermatitis
Prevention
• Avoid exposure to potential allergen
• Avoid repeated and prolonged exposure to
irritants
• Wear protective clothing
• Check skin reactions to cosmetics before
applying
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46. Management for Contact Dermatitis
Treatment for Irritant Contact Dermatitis
• Identify and remove the etiologic agent
• Wet dressings with gauze soaked in Burow's solution,
changed every 2 to 3 hours
• Larger vesicles may be drained, but tops should not
be removed
• Topical class I glucocorticoid preparations
• Severe cases: systemic glucocorticoids
– Prednisone, 2-week course, 60 mg initially, tapering by
steps of 10 mg
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47. Management for Contact Dermatitis
Treatment for Allergic Contact Dermatitis
• Identify and remove the etiologic agent.
• Topical glucocorticoid ointments/gels (classes I to III)
for early nonbullous lesions
• Larger vesicles may be drained, but tops should not
be removed
• Wet dressings with cloths soaked in Burow's solution
changed every 2 to 3 hours
• Systemic glucocorticoids: Severe & Exudative lesions
– Prednisone, initial 70 mg (adults), tapering by 5 to 10
mg/d over a 1- to 2-week period.
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48. • Antihistamines
• Emollients:
• Emollients may be used as adjuncts to moisturize dry skin in
subacute and chronic contact dermatitis.
• Urea Both promote hydration and removal of excess keratin in
conditions of hyperkeratosis
• Barrier creams:
• Primary agents for diaper dermatitis.
• Zinc oxide paste
• Provides relief of minor skin irritations.
• Pediatric: Apply to affected area after gentle cleansing and drying,
between each diaper change
• Camphor and menthol (0.5% each) in emollient base

49. Thank you.
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