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irritant contact dermatitis
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Irritant contact dermatitis
- Ipshita johri.
Definition
• ICD is a cutaneous inflammatory disorder resulting from activation of innate immune system by direct cytotoxic effect of a physical or chemical agent.
• Acute- erythema, edema, vesiculation and erosion.
• Chronic- lichenification, hyperkeratosis and fissures.
Epidemiology
• Most common occupational skin disease ( 70-80%)
• Rubber, soaps, cleansers, wet work, resins, acrylics, nickel
• 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 , with consequent cracking of the stratum corneum
– Occlusion, excessive humidity, and maceration increase percutaneous absorption of water-soluble substances
• 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%
Exogenous causes of ICD in Occupational Dermatology Clinic, Skin and Cancer Foundation, Australia
(total 621 patients over the period 1993–2002)
Australasian Journal of Dermatology (2008) 49, 1–11
Acids
Inorganic and organic acids can be corrosive to the skin
Cause epidermal damage via protein denaturation and cytotoxicity
Symptoms include erythema, vesication, and necrosis
Hydrofluoric and sulfuric acid can cause the most severe burns
Hydrofluoric acid, used in the semiconductor industry, is able to penetrate intact skin with subsequent dissociation in deeper tissues and resultant liquefactive necrosis
Acids
Chromic acid causes ulcerations known as ‘chrome holes’ and often perforates the nasal septum
Chemical burns and irritant dermatitis from nitric acid can cause a distinctive yellow discoloration
In general, organic acids are less irritating than inorganic acids
Formic acid has the greatest corrosive potential of the organic acids
Examples of chrome holes www.cdc.gov/niosh/ocderm
Alkalis Strong Alkalis include sodium,
ammonium, potassium hydroxide, sodium and potassium carbonate, and calcium oxide
Found in soaps, detergents, bleaches, ammonia preparations, drain pipe cleaner, toilet bowl cleansers, and oven cleaner
Often more painful and damaging than acids
No vesicles, necrotic skin that appears dark brown then black, ultimately becomes hard, dry, and cracked
Alkalis disrupt barrier and denature proteins with subsequent fatty acid saponification
Alkalis
Cement mixed with water can cause ulcerative damage due to alkalinity
Changes appear 8 to 12 hours after exposure
Chronic irritant cement dermatitis may also develop over months to years
Can accompany allergic contact dermatitis
Hand dermatitis due to contact with cement dermnetnz.org/dermatitis/chrome
Metal Salts Include:• arsenic trioxide- folliculitis• beryllium compounds, calcium oxide - ulceration• copper salts- greenish black color of skin, hair , “metal
fume” fever.• inorganic mercury- bluish linear pigmentation of tongue and
gums.• thimerosal, and selenium
SolventsAct mainly by dissolving the intercellular lipid barrier of
the epidermis
Prolonged skin contact can result in severe burns and well as systemic toxicity
Examples include: chlorinated hydrocarbons, petrochemicals.
benzene- petechial eruptionTrichloroethylene- Degreaser’s flush
Professional paint and crayon illustrator with bilateral palmar dermatitis secondary to repeated contact with paint solvents. Extensive patch testing excluded allergic contact dermatitis
Detergents and Cleansers
Include any surface active agent (surfactant) that concentrates at the oil-water interfaces and has both emulsifying and cleansing properties
Found in skin cleansers, cosmetics, and household cleaning products
Surfactants cause protein denaturation of the stratum corneum, impairing barrier function
Anionic detergents such as alkyl sulfates and alkyl carboxylate salts are the most irritating
Disinfectants
• Include, alcohols, aldehydes, phenolic compounds, halogenated compounds, surfactants, dyes, oxidizing agents, and mercury compounds
• Weak toxic agents that can cause chronic ICD
Practicing dentist with moderately severe irritant hand dermatitis from chronic exposure to disinfecting solutions and antiseptics. The results of patch testing, latex challenge testing, and RAST testing were negative.
Food Agriculture, fishing, catering, and
food processing
Often work without gloves, in damp working conditions with frequent hand washing
Mechanical, thermal, and climatic factors
Nearly 100% of exposed persons in food handling and fishing professions may be affected by chronic irritant hand dermatitis
Water
Ubiquitous skin irritant
Tropical immersion foot, seen during Vietnam War
Hairdressers, hospital cleaners, cannery workers, bartenders
Irritancy of water is exacerbated by occlusion
9 year old is an habitual hand washer who develops a contact irritant dermatitis every winter. At times she washes over 10 times a day.
Pathogenesis of ICD
• Denaturation of epidermal keratins
• Disruption of the permeability barrier
• Damage to cell membranes
• Direct cytotoxic effects
Acute phase
Chronic phase
•Stratum corneum is disrupted•Loss of cohesion bw corneocytes, desquamation,increased transepidermal water loss.
triggers •Lipid synthesis, keratinocyte proliferation•hyperkeratosis
result •Increased epidermal turnover•Chronic eczematoid irritant reaction.
Clinical features
Acute Irritant Contact Dermatitis • Burning, stinging, painful sensations can occur
immediately within seconds after exposure or may be delayed up to 24 hour
LESIONErythema with a dull, nonglistening surface
vesiculation (blister formation) erosion crusting shedding of crusts and scaling or erythema necrosis shedding of necrotic tissue ulceration healing
21
Chemical irritant dermatitis occurs after doing mehendi
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 developLESIONDryness chapping erythema hyperkeratosis
and scaling fissures and crusting• Lichenification, vesicles, pustules, and erosions
27
Different types of irritant contact dermatitis:
1. Acute delayed irritant contact dermatitis2. Irritant reaction ICD3. Cumulative contact dermatitis4. Asteatotic Dermatitis5. Traumatic Irritant Contact Dermatitis6. Subjective or sensory ICD7. Pustular and Acneiform Irritant Contact
Dermatitis8. Airborne Irritant Contact Dermatitis9. Frictional Irritant Contact Dermatitis10. Contact urticaria
Acute delayed ICD
• Retarded inflammatory response characterstic of certain irritants such as anthralin , benzalkonium chloride ( preservative/ disinfectant) and ethylene oxide.
• Seen 8-24 hours exposure.• This form of ICD is commonly seen during
patch testing.
Cumulative Irritant Contact Dermatitis
• Consequence of multiple sub-threshold skin insults, without sufficient time between them for complete barrier function repair
• lesions are less sharply demarcated
• Itching and pain due to fissures of hyperkeratotic skin.
• Skin findings include lichenification, hyperkeratosis, xerosis, erythema, and vesicles
Asteatotic Dermatitis
• Exsiccation eczematid ICD• Seen mainly during the
winter months in elderly individuals who frequently bath without remoisturizing
• Skin appears dry with ichthyosiform scale and patches of eczema craquele
Traumatic Irritant Contact Dermatitis
• May develop after acute skin trauma, such as burns, lacerations, or acute ICD
• Patients should be asked if they have cleansed with strong soaps or detergents
• Characterized by eczematous lesions most commonly on the hands, that persist
• Healing is delayed with redness, infiltration, scale, and fissuring in the affected areas
Subjective or sensory Irritant Contact Dermatitis
• Reports of stinging or burning in the absence of visible cutaneous signs of irritation
• Response to irritants such as lactic or sorbic acid,hydroxy acids, azelaic acid, benzoyl peroxide, mequinol, tretinoin.
Pustular and Acneiform Irritant Contact Dermatitis
Result to certain irritants such as metals, croton oil, mineral oils, tars, greases, cutting and metal working fluids, and naphthalenes
Should be considered in conditions in which folliculitis or acneiform lesions develop in setting outside of typical acne
Pustules are sterile and transient
Milia may develop in response to occlusive clothing, adhesive tape, ultraviolet and infrared radiation Chloracne. Note heavy involvement
of retroauricular skin with comedones and cysts
Airborne Irritant Contact Dermatitis
Develops on irritant-exposed skin of the face and periorbital regions
Often simulates photoallergic reactions
Involvement of the upper eyelids, philtrum, submental regions and wilkinson’s triangle help to differentiate from photoallergic reaction
Frictional Irritant Contact Dermatitis
Results from repeated low-grade frictional trauma
Plays adjuvant role in ACD and ICD
Characterized by hyperkeratosis, acanthosis, and lichenification, often progressing to hardening, thickening, and increased toughness
9 year old girl demonstrates a lichenified hyperpigmented round plaque on the top of her thumb produced by chronic thumbsucking. www.dermatlas.org
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
Differential diagnosis
Differentiation between ICD and ACD
J Allergy Clin Immunol 2010;125:S138-49.
Management Avoidance of causative irritants at home or in the workplace is the
primary TX
Engineering controls to reduce exposure in the workplace
Shielding and personal protection such as gloves and special clothing
Pre-exposure protection by protective creams, removal of irritants by mild cleaning agents, and enhancement of barrier function generation by emollients and moisturizers
Emphasizing personal and occupational hygiene
Establishing educational programs to increase awareness in the workplace
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.• 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?
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
Treatment
• Restoration of barrier function by use of Emolients- lipid rich.
• Moisturizers containing ceramide.• Systemic corticosteroids- acute inflammation• Severe cases- PUVA, NB-UVB, azathioprine,
cyclosporin, methotrexate, systemic retinoids.
Prognosis
• In many individuals, ICD resolves spontaneously even with continuous exposure – “ accomodation” or “hardening”.
Mechanism-• Improvement of physical barrier via formation of a
thicker stratum corneum and granulosum and increased formation of ceramide 1.
• Increased skin permeability to irritants and changes in vascular reactivity that allow faster removal of irritants.
• Immunologic alterations that favour an anti-inflammatory response to irritants, eg. Increased ratio of IL-1RA (anti-inflammatory cytokine) to IL-1α ( proinflammatory cytokine)
• A systemic hyporeactive state following repetetive exposure to low- dose irritants.