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

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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.