| What is dermatitis? | AKA Eczema, cutaneous inflammation that presents w/erythema, vesiculations, pruritis in acute phase.
Chronic phase is characterized by dryness, scaling, lichenification, fissuring, and pruritis.
There are multiple types (atopic, seborrhic, nummular, contact) |
| What is contact dermatitis? | Inflammatory eczematous disease, caused by chemicals or metals exert toxic effects w/out inducing a T cell response (contact irritant) or by small reactive chemicals that modify proteins and induce innate and adaptive immune response. |
| What are types of contact dermatitis? | Irritant contact dermatitis (non-specific response of the skin to a direct chemical damage, usually due to detergent not individual, chemical releases mediators of inflammation from epidermal cells)
Allergic Contact Dermatitis (delayed type IV hypersensetivity rxn due to exogenous contact antigens, affects 20% of children, response due to interaction of cytokines and T cells, some are applied after photo contact (Confined to UV radiation) |
| When does ACD occur? | when contact w/ a particular substance elicits a delayed hypersensitivity reaction, sensitization requires 10-14 days, and when re-exposure occurs dermatitis appear w/in 12-48 hours.
Most common cause is Rhus Dermatitis (poison Ivy/Oak/Sumac)
Other causes topic Abx, benzocaine, Vitamin E, Rubber, Nickel, Formaline, Preservatives (some skin care products), Fragrances. |
| How is epidemiology of contact dermatitis? | Females, infants and elderly and individuals w/atopic tendencies have high risk to get irritant contact dermatitis (80% of occupational dermatitis is ICD)
ACD all individuals are at risk, risk factors include age, occupation, and hx of atopic dermatitis.
Contact dermatitis most common in red hair and fair skin people, women more likely to develop contact due to use of jewelry and fragrances. |
| What are the clinical findings in contact dermatitis? | Main symptom of ACD is pruritis.
Presents as eczematous, scaly edematous plaques w/vesiculations distributed in areas of exposure.
It is bilateral if exposure is bilateral (usually unilateral)
Can't differentiate between ICD and ACD both w/three morphological patterns (acute: erythema, edema, oozing, crusting, tenderness, vesicles, pustules.
Subacute: crusts, scales, hyperpigmentation.
Chronic: Lichenification)
CD is 4-7% of dermato consults, mostly chronic due to nickel and chromate.
Occuptational disease burden (after mental illness and musculoskeletal burndens) |
| What is irritant contact dermatitis? | Likelyhood of getting it depends on duration, intensity, concentration of substance.
Chemical/physical agents and microtrauma could induce it, friction/ abrasions/ occlusions/ detergents produce ICD
Severity depends on quantity and concentration of irritant, duration and frequency of exposure.
All types of skin possible, environmental factors like high or low temperature and humidity determine severity. |
| What are factors causing ICD? | Exogenous (inherent toxicity of chemical for human skin, site differences make face/neck/scrotum/dorsal hands more susceptible)
Atopic dermatitis major risk for ICD of hand due to impaired barrier function and lower threshold for skin irritation |
| What are clinical findings of ICD? | Mild irritants (erythema, chapped skin, dryness, fissuring (repeated exposures over time)
Pruritis from mild to extreme, pain most common symptom when erosions and fissures are present.
Severe cases edema, exudate and tenderness
Potent irritants produce painful blisters w/in hours post-exposure.
It is most common type of CD, affects hands common, for children diaper and dry skin dermatitis most common, due to repititive exposure to water, glazed, parched scalded appearance.
In ICD inflammatory cells play a role, but not lymphocytes so no prior sensitization is needed, affects everyone after sufficient exposure. |
| How is pathogenesis of ICD? | Resident epidermal cells, endothelial cells, leukocytes interact under control of cytokines and lipid mediators.
Keratinocytes initiate skin inflammatory reactions through cytokine release, environmental factor stimulates release of inflammatory cytokines (IL1, TNF-a), chemotactic cytokines (IL8/10), Growth-promoting cytokines (IL6,7,15,TGF-a), humoral vs cellular immunity cytokines (IL10/12/18), ICAM-1 infiltration of leukocytes. |
| What is ACD? | Common etiological allergens are nickel, balsam of Peru, chromium, neomycin, formaldehyde, fragrance, poison Ivy.
Sensitization lasts 10-15 days in man, first step has no clinical consequence but may induce primary ACD (hapten-specific skin inflammation 5-15 days after contact).
It results from inflammation caused by type IV HS cellular immune response.
Acute lesions (papules/vesicles/weeping/crusting/erythema/edema/ pruritis)
Prior sensitization is essential here, and needs re-exposure to occur after 6-12 hours.
Chronic lesions fissuring, skin thickening, lichenification, acneiform eruption, hypo/er pigmentation.
For children occurs by age 6 months |
| How is pathogenesis of ACD? | Two phases, Sensitization phase (Ag-specific T cells induced draining lymph nodes by Ag captured DC from skin)
Elicitation phase (T cells activated after Ag caught by DC produce chemical mediators create inflammation) |
| What is photosensitization? | Photoallergic rxn, sun-exposed areas (face/ V of anterior neck/ dorsal hands/ forearms), spares eyelids/ upper lip.
May develop when UV reacts w/chemical agents inducing photosensitization. |
| What is systemic CD? | Generalized dermatitis/ exanthema in flexural areas (Baboon syndrome)
Can also develop in previous CD/ positive patch test sites w/systemic exposure to allergen (ingestion/infusion..)
Pathophysio similar to ACD, initiated by T cells.
Most common causes are metals (mercury/nickel/gold), medications (Abx, steroids, aminophyllin, estradiol topical), plants and herbal products (Balsam of Peru...) |
| What is subjective irritancy? | W/in minutes of contact on face in absence of visible changes, after applying cosmetics/ sunscreens.
Uncommon for endogenous, irritant and allergic etiologies to co-exist in development of eczemas (hand and foot) |
| How is CD in children? | Reports are increasing (Ni, topical Abx, preservatives, fragrances and rubber are most common)
Eczematous eruption children should be patch tested, particular those w/hand and eyelid eczema. |
