Contact dermatitis is an acute or chronic skin inflammation caused by cutaneous interaction with a chemical, biologic, or physical agent. Contact dermatitis after a single exposure or multiple exposures may be irritant or allergenic—clinically it may be difficult to differentiate between these processes. Irritant contact dermatitis (ICD) is caused by direct tissue damage following a single exposure or multiple exposures to a known irritant. By contrast, in allergic contact dermatitis, tissue damage by allergic substances is mediated through immunologic mechanisms. A complete history related to exposures at home, the workplace, and in recreational activities is essential to making the diagnosis and identifying the causative agent. Acutely, eczematous or nonspecific dermatitis is the most common clinical expression of this induced inflammation. The severity of the dermatitis ranges from a mild, short-lived condition to a severe, persistent, job-threatening, and possibly life-threatening disease. Treatment of both irritant contact dermatitis and allergic contact dermatitis begins with removal of the offending substance(s).
The American Academy of Allergy, Asthma & Immunology and the American College of Allergy, Asthma & Immunology published updated clinical practice guidelines on contact dermatitis in 2015.[1] Recommendations pertaining specifically to irritant contact dermatitis are briefly summarized in the Guidelines section.
Irritant contact dermatitis (ICD) is a nonspecific, nonallergic response of the skin to direct chemical damage from a corrosive agent that releases mediators of inflammation predominantly from epidermal cells. Irritant contact dermatitis can be acute or chronic. Irritants can be classified as cumulatively toxic (eg, hand soap causing irritant dermatitis in a hospital employee), subtoxic, degenerative, or toxic (eg, hydrofluoric acid exposure at a chemical plant).[2] Acutely, this inflammation is manifested by redness, erythema, mild edema, and scaling. Chronic irritant contact dermatitis presents with lichenification, hyperkeratotic scale, fissures, or ulcerations. Note the image below.
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Chronic irritant contact dermatitis of the hands in an older worker; the condition resulted in early retirement.
The hands are the most important sites of irritant contact dermatitis. Irritant contact dermatitis from repeated workplace exposure of the hands to soaps, cleansers, and solvents is the source of most occupational skin disorders.
Although it is much more common, irritant contact dermatitis remains understudied compared with allergic contact dermatitis. Most articles on contact dermatitis concern allergic contact dermatitis. This largely reflects the fact that with history and patch testing, a specific hypersensitivity and a probable cause of dermatitis can be identified in most cases of allergic contact dermatitis.
No reliable diagnostic test exists for irritant contact dermatitis. The diagnosis rests on the exclusion of other cutaneous diseases (especially allergic contact dermatitis) and on the clinical appearance of dermatitis at a site sufficiently exposed to a known cutaneous irritant. Laboratory studies may be of value in eliminating some disorders from the differential diagnosis. (See Workup).
The definitive treatment of irritant contact dermatitis is the identification and removal of any potential causal agents. For hand irritant contact dermatitis, advise individuals to use ceramide-containing creams or bland emollients after washing hands with soap and before sleep. (See Treatment.)
Although the term hypoallergenic is used widely in the marketing of consumer products, no Food and Drug Administration (FDA)–approved definition of "hypoallergenic" exists. Individuals with susceptible skin (eg, atopic dermatitis, facial skin of individuals with rosacea) would benefit greatly from hypoirritating cleansers, cosmetics, moisturizers, and protectants, but there is no standard method for identifying such products.
Go to Allergic Contact Dermatitis, Pediatric Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.
Irritant contact dermatitis (ICD) is the clinical result of sufficient inflammation arising from the release of proinflammatory cytokines from skin cells (principally keratinocytes), usually in response to chemical stimuli. Irritant contact dermatitis arises as a result of activated innate immunity without prior sensitization, which differentiates it from allergic contact dermatitis. Different clinical forms may arise. The three main pathophysiological changes are skin barrier disruption, epidermal cellular changes, and cytokine release.[3]
With sufficient concentration or duration of exposures, a wide range of chemicals can act as cutaneous irritants. Common cutaneous irritants include solvents, microtrauma, and mechanical irritants.
Cumulative irritant contact dermatitis from repeated mild skin irritation from soap and water is common. For example, hand-washing frequency of more than 35 times per shift was associated strongly with occupational hand dermatitis in intensive care unit workers (odds ratio = 4.13). Similarly, most cases of "homemaker's" eczema are irritant contact dermatitis resulting from repeated skin exposure to low-grade cutaneous irritants, particularly soaps, water, and detergents.
Solvents cause cutaneous irritation because they remove essential fats and oils from the skin, which increases transepidermal water loss and renders the skin susceptible to the increased direct toxic effects of other previously well-tolerated cutaneous exposures. The alcohol propanol is less irritating to the skin than the detergent sodium lauryl sulfate.
p Ka, an acid dissociation constant, is a quantitative measure of the strength of an acid in solution. p Ka has been shown to be highly predictive of acute skin irritation for acids and bases: acids with a p Ka of less than 4 and bases with a p Ka of greater than 8 are highly irritative.[4]
Microtrauma may produce skin irritation. A common example is fiberglass, which may produce pruritus with minimal visible inflammation in susceptible individuals. Many plant leaves and stems bear small spicules and barbs that produce direct skin trauma.
Physical irritants (eg, friction, abrasive grains, occlusion) and detergents such as sodium lauryl sulfate produce more irritant contact dermatitis in combination than singly.[5] Propanol and sodium lauryl sulfate are not additive irritants, however.
Skin irritation predisposes the skin to develop sensitization to topical agents. Skin irritation by both nonallergenic and allergenic compounds induces Langerhans cell migration and maturation.[6] An exacerbation of irritant contact dermatitis may reflect development of allergic contact dermatitis to topical creams, medications, or rubber gloves.
The pathogenesis of irritant contact dermatitis involves resident epidermal cells, dermal fibroblasts, endothelial cells, and various leukocytes interacting with each other under the control of a network of cytokines and lipid mediators. Keratinocytes play an important role in the initiation and perpetuation of skin inflammatory reactions through the release of and responses to cytokines. Resting keratinocytes produce some cytokines constitutively.
A variety of environmental stimuli (eg, ultraviolet light, chemical agents) can induce epidermal keratinocytes to release the following cytokines[3] :
Intercellular adhesion molecule 1 promotes the infiltration of leukocytes into the epidermis in cutaneous inflammatory reactions, including irritant contact dermatitis.
Significantly increased numbers of dividing keratinocytes are present 48 and 96 hours after exposure to the anionic emulsifying agent sodium lauryl sulfate (used in shampoos, skin cleansers, acne treatments, and toothpastes and in laboratories as an experimental irritant). However, Heinemann et al found that repeated occlusive application of 0.5% sodium lauryl sulfate over 3 weeks often resulted in adaptation (the so-called hardening phenomenon), with an increase in ceramide 1 in the lipid composition of the stratum corneum.[7]
All irritants provoke a similar pattern of cellular infiltration in the dermis; the densities of most of the cell types rise in proportion to the intensity of inflammation. Within the epidermis, marked differences exist in the patterns of cellular infiltration among different irritants.
Individuals with a history of atopic dermatitis are prone to develop irritant contact dermatitis of the hands. Polymorphisms in the filaggrin (FLG) gene, which result in loss of filaggrin production, may alter the skin barrier and are a predisposing factor for atopic dermatitis. FLG null alleles are associated with increased susceptibility to chronic irritant contact dermatitis.[8, 9]
Almost any material may be a cutaneous irritant, if the exposure is sufficiently prolonged and/or the concentration of the substance sufficiently high. The likelihood of developing irritant contact dermatitis (ICD) increases with the duration and intensity of exposure to the irritant.[2] Environmental factors may enhance the effect of other irritants.[10, 11, 12]
Dry air and temperature variation
Dry air renders the skin more susceptible to cutaneous irritants. Sufficiently dry air alone may provoke irritant contact dermatitis. Most cases of winter itch are a result of dry skin from the drier air found during sustained periods of cold weather.
An increase in temperature (up to 43°C from 20°C) increases the cutaneous effect of an irritant.[13]
Water
Continual exposure to water may produce maceration or repeated evaporation of water from the skin may produce cutaneous irritation by desiccation of the skin. Even distilled water experimentally provokes increased CD11c+ cells and neutrophils in the epidermis.
Solvents
Many individuals are exposed to solvents, particularly at work. Solvents such as alcohol or xylene remove lipids from the skin, producing direct irritant contact dermatitis and rendering the skin more susceptible to other cutaneous irritants, such as soap and water.
Irritant contact dermatitis from alcohol most often is cumulative. Manual workers may wash their hands inappropriately with solvents to remove oil, grease, paints, or other materials; thus, they develop irritant contact dermatitis.
Inappropriate skin cleansing is a primary cause of irritant contact dermatitis in the workplace. Washing facilities and methods must be inspected when investigating the workplace for 1 or more cases of occupational irritant contact dermatitis. The irritating agents include aromatic, aliphatic, and chlorinated solvents, as well as solvents such as turpentine, alcohol, esters, and ketones. Some organic solvents produce an immediate erythematous reaction on the skin and remove lipids from the stratum corneum.
Metalworking fluids
Neat oils most commonly produce folliculitis and acne. They may cause irritant contact dermatitis (as well as allergic dermatitis). Water-based metalworking fluids often cause irritant contact dermatitis in exposed workers; surfactants in these fluids are the main culprit.
Cumulative irritant contact dermatitis
This is common in many occupations that often are termed "wet work." Healthcare workers wash their hands 20-40 times a day, producing cumulative irritant contact dermatitis. Similar exposures occur among individuals who wash hair repeatedly or in cleaners or kitchen workers.
Multiple skin irritants may be additive or synergistic in their effects. Alcohol-based hand-cleansing gels cause less skin irritation than hand washing and therefore are preferred for hand hygiene from the dermatological point of view. An alcohol-based hand-cleansing gel may even decrease, rather than increase, skin irritation after a hand wash, owing to a mechanical partial elimination of the detergent.[14]
Microtrauma
Fiberglass produces direct damage to the skin, usually manifested by pruritus that may result in excoriation and secondary skin damage. Cutaneous irritation primarily is caused by fiberglass with diameters exceeding 4.5 µm. Most workers with irritant contact dermatitis resulting from fiberglass develop hardening, in which they tolerate further cutaneous exposure to fiberglass.
Many plant leaves and stems bear small spicules and barbs that produce direct skin trauma.
Mechanical trauma
Pressure produces callus formation. Pounding produces petechia or ecchymosis. Sudden trauma or friction produces blistering in the epidermis. Repeated rubbing or scratching produces lichenification. Sweating and friction appear to be the main cause of dermatitis that appears under soccer shin guards in children.[15]
Rubber gloves
Some rubber gloves may provoke direct cutaneous irritation. Many workers complain of irritation from the powder in rubber gloves.
Remember that gloves compromised by a hole may allow an irritant to enter; occlusion dramatically increases skin damage from the irritant. Occlusion accentuates the effects, good or bad, of topical agents. Kerosene may produce skin changes similar to that of toxic epidermal necrolysis following occluded cutaneous exposure. Excessive amounts of ethylene oxide in surgical sheets also may produce similar changes.
Sodium lauryl sulfate
This chemical is found in some topical medications, particularly acne medications, as well as a range of soaps and shampoos. It is also a classic experimental cutaneous irritant.
Hydrofluoric acid
A hydrofluoric acid burn is a medical emergency. Remember that onset of clinical manifestations may be delayed after the acute exposure (this is crucial to diagnosis). Unfortunately, hydrofluoric acid burns are most frequent on the digits, where the pain is most severe and management is most difficult (see Hydrofluoric Acid Burns).
Alkalies
Skin surfaces normally have an acidic pH, and alkalies (eg, many soaps) produce more irritation than many acids. The "acid mantle" of the stratum corneum seems to be important for both permeability barrier formation and cutaneous antimicrobial defense. Use of skin cleansing agents, especially synthetic detergents with a pH of approximately 5.5 rather than alkaline pH, may help prevent skin disease.[16]
Irritant contact dermatitis (ICD) is common in occupations that involve repeated hand washing or repeated exposure of the skin to water, food materials, and other irritants. High-risk occupations include cleaning, hospital care, food preparation, and hairdressing.[17, 18]
The prevalence of occupational hand dermatitis was found to be 55.6% in two intensive care units and was 69.7% in the most highly exposed workers. Hand-washing frequency of more than 35 times per shift was associated strongly with occupational hand dermatitis.[19]
International statistics
In some European studies among employees in high-risk occupations, such as hairdressing, healthcare, and metal working, the 1-year prevalence was between 20% and 30%.[9] Specifically, in Denmark, cleaners comprise the greatest number of affected workers, but culinary workers have the highest incidence. A higher proportion of prolonged sick leave is seen among those in food-related occupations compared with those in wet occupations.[20] The incidence rates of contact dermatitis in Germany were 4.5 cases per 10,000 workers for irritant contact dermatitis, compared with 4.1 cases per 10,000 workers for allergic contact dermatitis. The highest irritant contact dermatitis annual incidence rates were found in hairdressers (46.9 cases per 10,000 workers per year), bakers (23.5 cases per 10,000 workers per year), and pastry cooks (16.9 cases per 10,000 workers per year.[21]
Sexual differences in incidence
Irritant contact dermatitis is significantly more common in women than in men. The high frequency of hand eczema in women in comparison with men is caused by environmental factors, not genetic factors.
Occupational irritant contact dermatitis affects women almost twice as often as men, in contrast to other occupational diseases that predominantly affect men. Women are exposed more highly to cutaneous irritants from their traditionally disproportionately greater role in housecleaning and the care of small children at home. In addition, women predominantly perform many occupations at high risk for irritant contact dermatitis (eg, hairdressing, nursing).
Age-related differences in incidence
Irritant contact dermatitis may occur at any age. Many cases of diaper dermatitis are irritant contact dermatitis resulting from direct skin irritants present in urine and, especially, feces. Older persons have drier and thinner skin that does not tolerate soaps and solvents as well as younger individuals. Occupational hand eczema often is associated with persistent dermatitis and prolonged sick leave, with substantially greater severity among those with occupational irritant contact dermatitis and atopic dermatitis and age older than 50 years.
Prognosis is good for nonatopic individuals in whom irritant contact dermatitis (ICD) is diagnosed and managed promptly. Individuals with atopic dermatitis remain highly susceptible to irritant contact dermatitis and may find that the tasks of many common occupations (eg, nursing, hairdressing) produce too much direct skin inflammation to continue with these careers.
Hardening may be specific to the irritant inducing the hardening phenomenon and does not occur in all persons exposed long term to an irritant.[4] Hardened skin may also have a thickened stratum granulosum, with changes in the expression of various inflammatory mediators and markers.[4] An induction of an increase in the stratum corneum lipid ceramide 1 may play a key role as a protection mechanism against irritation by repeated application of sodium lauryl sulfate.[5, 7]
Activities of daily living and work may be reduced by severe irritant contact dermatitis.
Acute irritant contact dermatitis reactions to potent irritants (eg, acids, alkaline solutions) are comparable to a chemical burn and can be graded like thermal burns (ie, first-, second-, or third-degree burns). With appropriate symptomatic management, the prognosis for this type of irritant contact dermatitis is usually good, and, unless the dermis is damaged, no permanent scarring should occur. See Chemical Burns for more information.
Mortality
Hydrofluoric acid is a potent cutaneous irritant used in low-technology and high-technology industries and at home in rust removal.[22] Death from hypocalcemia may ensue if as little as 1% of the skin's surface area is exposed sufficiently to this strong inorganic acid and if complications are not managed optimally (see Hydrofluoric Acid Burns).
Remind individuals that they must continue to avoid cutaneous irritants; they will redevelop or aggravate dermatitis if they continue to have the same skin care exposures that resulted in irritant contact dermatitis (ICD). The possibility of secondary or complicating allergic contact dermatitis or impetigo always must be considered as well.
For patient education information, see the Skin Conditions & Beauty Center, as well as Contact Dermatitis.
A detailed history is required because the diagnosis of irritant contact dermatitis (ICD) rests on the history of exposure of the affected body site to the cutaneous irritant. Patch testing also is used in severe or persistent cases to exclude allergic contact dermatitis as a component of the individual's cutaneous manifestations.
Onset of symptoms occurs within minutes to hours of exposure in simple acute irritant contact dermatitis. Acute delayed irritant contact dermatitis is characteristic of certain irritants, such as benzalkonium chloride (eg, zephiran, a preservative and disinfectant), which elicits a deferred (8-24 h after exposure) inflammatory reaction.[23]
The onset of signs and symptoms may be delayed by weeks in cumulative chronic irritant contact dermatitis. Cumulative irritant contact dermatitis is a consequence of multiple incidents of subthreshold damage to the skin, with the time between exposures being too short for a full resolution of skin barrier function. Patients with sensitive skin (ie, atopic individuals) have a decreased irritant threshold or a prolonged restoration time, making them more vulnerable to clinical irritant contact dermatitis.
Cumulative irritant contact dermatitis typically occurs with exposure to weak irritants rather than strong ones. Often, the exposure (eg, water) is not only at work but also at home.
These patients report both itching and pain caused by fissuring of the hyperkeratotic skin (chapping). Pain, burning, stinging, or discomfort exceeding pruritus occur early in the clinical course.
Less important subjective criteria for irritant contact dermatitis include the onset of dermatitis within 2 weeks of exposure, and reports of many other coworkers or family members affected.
Occupational history
Irritant contact dermatitis is a major occupational disease; skin disorders comprise up to 40% of occupational illnesses. The physician needs to take an occupational history from adults with suspect irritant contact dermatitis.
Occupational irritant contact dermatitis typically affects workers who are new to a job, who are constitutionally more susceptible to irritant contact dermatitis, or who have not learned to protect their skin from cutaneous irritants. Individuals with history of atopic dermatitis (especially of the hands) are more susceptible to irritant contact dermatitis, particularly of the hands.
Most affected workers have a degree of permanent injury that is lower than that of other occupational diseases; however, the compensation pay was higher for skin diseases than for diseases of the respiratory system or musculoskeletal disorders, according to a study in Denmark.
Rietschel and Fowler proposed the following as primary diagnostic criteria for irritant contact dermatitis (ICD)[24] :
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 the offending agent
Negative results on patch testing that includes all possible allergens
Minor objective criteria for irritant contact dermatitis include the following:
Sharp circumscription of the 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
Individuals may develop a habit of continuing to rub a site initially affected by irritant contact dermatitis and may develop secondary neurodermatitis or lichen simplex chronicus (lichenification). This may be accepted as a sequela of an occupational injury.
Skin lesions may become colonized secondarily and/or infected, particularly by Staphylococcus aureus. Secondary neurodermatitis (lichen simplex chronicus) may develop in individuals with irritant contact dermatitis (ICD), particularly in those with workplace exposures or under psychological stress.
Postinflammatory hyperpigmentation or hypopigmentation may occur in areas affected by irritant contact dermatitis or persist after resolution of irritant contact dermatitis in individuals with more pigmented skin.
Scarring may occur after corrosive agent exposure, excoriation, or artifact, causing ulceration.
Irritant contact dermatitis increases the risk of sensitization to topical medications.
No single diagnostic test exists for irritant contact dermatitis (ICD). The diagnosis rests on the exclusion of other cutaneous diseases (especially allergic contact dermatitis) and on the clinical appearance of dermatitis at a site sufficiently exposed to a suspected or known cutaneous irritant. Laboratory studies are generally of little value in proving a diagnosis of contact dermatitis. However, they may be of value in eliminating some disorders from the differential diagnosis.
Findings of significantly elevated serum immunoglobulin E occasionally are useful to substantiate an atopic diathesis in the absence of a personal or family history of atopy.
Go to Allergic Contact Dermatitis, Pediatric Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.
A bacterial culture can be obtained and is especially useful in cases complicated by secondary bacterial infection. A potassium hydroxide (KOH) examination of scrapings may be performed and samples for mycology may be obtained to exclude superficial tinea infections or candidal infections, depending on site and morphology of lesions.
Patch testing can be performed to diagnose contact allergies, but no patch test exists that proves that a cutaneous irritant is responsible for a particular case of irritant contact dermatitis. Diagnosis rests on exclusion of allergic contact dermatitis and history of sufficient exposure to a cutaneous irritant.
Skin biopsy can help exclude other disorders, such as tinea, psoriasis, or cutaneous T-cell lymphoma.
Skin biopsy of skin lesions of the palms and soles has several potential pitfalls. The stratum corneum and epidermis are particularly thick there, which makes the histologic diagnosis of psoriasis more difficult and increases the possibility that the specimen lacks sufficient dermis for optimal diagnosis. In the thenar area, an overly deep biopsy can cut the recurrent branch of the median nerve. A biopsy from the sole may leave a chronic painful scar on which the patient must walk.
Skin scrapings of cutaneous lesions may help exclude scabies or may reveal fiberglass fibers as a cause of a patient's pruritus. To asses for scabies, superficial epidermal cells can be scraped lightly from the skin surface with a No. 15 blade. Skin scrapings can be evaluated with light microscopy on a glass slide containing mineral oil.
The histopathology of acute experimental irritant contact dermatitis (ICD) has been studied to a greater extent than chronic irritant contact dermatitis, which is the primary clinical complaint. Cellular changes seen in the skin vary according to the chemical nature and concentration of the irritant applied, duration of exposure, severity of ensuing response, and time of sampling for acute irritant contact dermatitis. Many primary irritants cause overt necrosis if applied in a sufficiently high concentration for sufficient time.
Most histologic examinations of irritant contact dermatitis reveal some degree of intercellular edema or spongiosis in the epidermis. Spongiosis usually is less pronounced than that seen in allergic contact dermatitis reactions.
Parakeratosis also is observed widely in irritant contact dermatitis reactions.
The histology of chronic irritant contact dermatitis is one of hyperkeratosis with areas of parakeratosis, moderate-to-marked epidermal hyperplasia (acanthosis), and elongation of the rete ridges.
The definitive treatment of irritant contact dermatitis (ICD) is the identification and removal of any potential causal agents. An inflammatory reaction from acute delayed irritant contact dermatitis to an agent such as benzalkonium chloride (eg, zephiran) rarely needs treatment and usually resolves with cessation of exposure. Further symptomatic therapy depends on the degree of involvement and the presence or absence of secondary infection.
Advise individuals to use ceramides containing creams or bland emollients after washing hands with soap and before sleep. Cleansers may be ranked by their irritancy.[25] Recommend mild skin cleansers (eg, Aquanil, Cetaphil cleanser, Oilatum AD, Neutrogena cleanser) in place of soap on affected areas. Instruct individuals to refrain from the use of inappropriate solvents (eg, gasoline) or abrasives (eg, pumice stone) to cleanse hands; these directly defat or traumatize the skin.
A summary of the Danish Contact Dermatitis Group guideline for hand eczema includes a diagrammed sequence of general treatment principles and notes that moisturizing cream should be given in combination with all treatments. If hand eczema does not resolve within 1 month, the guideline recommends physicians refer the patient to a dermatologist; longer delays are associated with a poorer prognosis.[26]
Go to Allergic Contact Dermatitis, Pediatric Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.
Emergency department treatment may include the following:
Topical soaks with cool tap water, Burow solution (1:40 dilution), saline (1 tsp/pint)
Lukewarm water baths (antipruritic)
Aveeno (oatmeal) lukewarm baths
Emollients (eg, white petrolatum, Eucerin) may be beneficial chronic cases.
Large vesicles may benefit from therapeutic drainage (but not removing the vesicle tops).[4] These lesions should then be covered with antibiotic dressing or a dressing soaked in Burow solution.
Hospital admission is required only in severe cutaneous irritant contact dermatitis, ie, chemical burns from hydrofluoric acid or, occasionally, from freshly mixed Portland cement.
Creams containing ceramides (eg, Impruv, Cerave, Cetaphil RESTORADERM) may be particularly helpful in restoring the epidermal barrier in persons with irritant contact dermatitis (ICD) and atopic dermatitis. Creams containing dimethicone (eg, Cetaphil cream) can be helpful in restoring the epidermal barrier in persons with wet work–related irritant contact dermatitis.
Most soaps and detergents are alkaline and induce an increase in cutaneous pH, which affects the physiologic protective acid mantle of the skin by decreasing the fat content. Disruption of stratum corneum and changes in pH are key elements in the induction of irritant contact dermatitis (ICD) and pruritus by soaps. These conditions are exacerbated in the winter months in patients with dry, sensitive skin.
Syndets, with a pH approximately 5.5, do not modify skin pH. Most bar soaps and liquid detergents available on the market are a mixture of soap and syndet. A study found that Dove and Cetaphil had a lower irritant effect than the other soaps tested. Interestingly, no significant correlation was made between the price of the products and their irritation potential.
Irritant contact dermatitis is a frequent problem in healthcare workers, owing to frequent hand washing. The best antimicrobial efficacy can be achieved with ethanol (60-85%), isopropanol (60-80%), and N-propanol (60-80%). The antimicrobial efficacy of chlorhexidine (2-4%) and triclosan (1-2%) is both lower and slower and carries a potential risk of bacterial resistance.
The use of alcohol-based hand rubs containing various emollients instead of irritating soaps and detergents is one strategy to reduce skin damage, dryness, and irritation in healthcare workers. Irritant contact dermatitis occurs most frequently with preparations containing 4% chlorhexidine gluconate, less frequently with nonantimicrobial soaps and preparations containing lower concentrations of chlorhexidine gluconate, and least frequently with well-formulated alcohol-based hand rubs containing emollients and other skin conditioners.
Topical corticosteroids and immunomodulators are of unproven use in treating irritant contact dermatitis (ICD). Corticosteroids were found ineffective in treating the surfactant-induced irritant dermatitis when compared with the vehicle and with the untreated control.[27] However, topical steroids may be helpful for superimposed eczematous features.
Potential complications are associated with the use of steroids, particularly around the eye. The avoidance of long-term steroid use is essential, because such use may cause cataracts, glaucoma, corneal thinning/perforation, and loss of the eye, as well as other problems.
Topical tacrolimus can be used as an alternative to topical corticosteroids, but occasionally is an irritant that may produce further stinging and irritation in persons with irritant contact dermatitis.[28]
Multidisciplinary consultations may be required when many workers become affected with irritant contact dermatitis (ICD) in a workplace. Identifying and remediating the causes of widespread irritant contact dermatitis interfering with workplace productivity and worker quality of life is important.
Any patient with hydrofluoric acid burn should be evaluated as a medical emergency by a physician experienced in the management of hydrofluoric exposures and burns. Consider regional intravenous infusion of calcium gluconate as a therapeutic option in hydrofluoric acid burns to forearm, hand, or digits when topical therapy fails.
Patients with suspected irritant contact dermatitis must first be extensively counseled to avoid further contact with suspected irritants and any potential sensitizers. Topical and oral corticosteroids can be helpful in treatment of symptoms, including mild-to-moderate dermatitis and pruritus. Patch testing can be considered if there is a concern for allergic contact dermatitis and should always be performed by an experienced clinician who understands the nuances of interpreting such tests.[1]
Also see Contact Dermatitis: A Practice Parameter--Update 2015.
After the identification and removal of any potential causal agents, the use of ceramides creams or bland emollients and bland barrier creams such as those containing dimethicone are the mainstays of medical treatment for irritant contact dermatitis (ICD).
A number of agents commonly found in therapeutic products for the skin (eg, propylene glycol, lactic acid, urea, salicylic acid) may produce further skin inflammation and may need to be avoided in these individuals. Topical corticosteroids play a limited role in the treatment of irritant contact dermatitis. They do not address the process directly, but they may be helpful for superimposed eczematous features.
Clinical Context:
Hydrocortisone is an adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. It has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity. Use 0.2% cream or ointment. A thin layer can be applied 1-2 times daily to affected areas on the face, groin, neck, and axilla for 1-2 weeks.
Clinical Context:
Triamcinolone is indicated for inflammatory dermatosis responsive to steroids; it decreases inflammation by suppressing migration of PMNs and reversing capillary permeability. A thin layer can be applied 1-2 times daily to affected areas on the extremities and trunk for 1-2 weeks.
Clinical Context:
A class I superpotent topical steroid, clobetasol suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Use 0.05% cream or ointment. A thin layer can be applied 1-2 times daily to affected areas on the palms and soles for 1-2 weeks.
Corticosteroids are immunosuppressives with anti-inflammatory properties that modify the body's immune response to diverse stimuli. Other actions include vasoconstriction and antiproliferation. These agents have limited use in the treatment of irritant contact dermatitis.
Clinical Context:
Tacrolimus reduces itching and inflammation by suppressing release of cytokines from T cells. It also inhibits transcription for genes that encode interleukin 3 (IL-3), IL-4, IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor–alpha (TNF-alpha), all of which are involved in the early stages of T-cell activation.
Additionally, tacrolimus may inhibit release of preformed mediators from skin mast cells and basophils and may down-regulate expression of high-affinity IgE receptor (FCeRI) on Langerhans cells.
Tacrolimus is approved for moderate-to-severe atopic dermatitis and can be used in patients as young as 2 years. It is more expensive than topical corticosteroids. This agent is available as ointment in concentrations of 0.03 and 0.1%.
Clinical Context:
Pimecrolimus is indicated for eczema and atopic dermatitis. It was the first nonsteroid cream approved in the United States for mild-to-moderate atopic dermatitis. Pimecrolimus is derived from ascomycin, a natural substance produced by fungus Streptomyces hygroscopicus var ascomyceticus.
This agent selectively inhibits production and release of inflammatory cytokines from activated T cells by binding to cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids.
What is irritant contact dermatitis (ICD)?How is irritant contact dermatitis (ICD) characterized?What is the most common site of irritant contact dermatitis (ICD)?How is irritant contact dermatitis (ICD) diagnosed?How is irritant contact dermatitis (ICD) treated?Do hypoallergenic products prevent irritant contact dermatitis (ICD)?What is the pathophysiology of irritant contact dermatitis (ICD)?What is the pathophysiology of irritant contact dermatitis (ICD) due to solvents?How is the likelihood of a solution to cause irritant contact dermatitis (ICD) measured?What is the role of microtrauma in the pathophysiology of irritant contact dermatitis (ICD)?What is the role physical irritants in the pathophysiology of irritant contact dermatitis (ICD)?What is the role of skin irritation in the pathophysiology of irritant contact dermatitis (ICD)?What is the pathogenesis of irritant contact dermatitis (ICD)?What is the role of cytokines in the pathogenesis of irritant contact dermatitis (ICD)?How is cellular infiltration characterized in irritant contact dermatitis (ICD)?What is the relationship between atopic dermatitis and irritant contact dermatitis (ICD)?What causes irritant contact dermatitis (ICD)?What is the role of environmental factors in the etiology of irritant contact dermatitis (ICD)?What is the role of exposure to water in the etiology of irritant contact dermatitis (ICD)?What is the role of solvents in the etiology of irritant contact dermatitis (ICD)?What is the role of metalworking fluids in the etiology of irritant contact dermatitis (ICD)?What is the role of frequent handwashing in the etiology of irritant contact dermatitis (ICD)?What is the role of microtrauma in the etiology of irritant contact dermatitis (ICD)?What is the role of mechanical trauma in the etiology of irritant contact dermatitis (ICD)?What is the role of rubber gloves in the etiology of irritant contact dermatitis (ICD)?What is the role of sodium lauryl sulfate in the etiology of irritant contact dermatitis (ICD)?What is the role of hydrofluoric acid in the etiology of irritant contact dermatitis (ICD)?What is the role of alkalies in the etiology of irritant contact dermatitis (ICD)?How common is irritant contact dermatitis (ICD)?What is the international prevalence of irritant contact dermatitis (ICD)?What is the sexual predilection of irritant contact dermatitis (ICD)?What are the age-related differences in the incidence of irritant contact dermatitis (ICD)?What is the prognosis of irritant contact dermatitis (ICD)?What is the mortality associated with hydrofluoric acid burns in irritant contact dermatitis (ICD)?What is involved in patient education for irritant contact dermatitis (ICD)?What is the role of the clinical history in irritant contact dermatitis (ICD)?What is the role of the occupational history in irritant contact dermatitis (ICD)?What are the diagnostic criteria for irritant contact dermatitis (ICD)?What sequela is associated with occupational irritant contact dermatitis (ICD)?What are the potential complications of irritant contact dermatitis (ICD)?What are the diagnostic considerations in irritant contact dermatitis (ICD)?What are the differential diagnoses for Irritant Contact Dermatitis?What are the approach considerations in the workup of irritant contact dermatitis (ICD)?What is the role of bacterial and fungal studies in the workup of irritant contact dermatitis (ICD)?When is patch testing indicated in the workup of irritant contact dermatitis (ICD)?What is the role of skin biopsy in the workup of irritant contact dermatitis (ICD)?What is the role of skin scrapings in the workup of irritant contact dermatitis (ICD)?What are the histologic findings in irritant contact dermatitis (ICD)?What are the approach considerations in the treatment of irritant contact dermatitis (ICD)?What is involved in emergency department care of irritant contact dermatitis (ICD)?How effective are barrier creams in the treatment of irritant contact dermatitis (ICD)?What are the effects of cleansers in the management of irritant contact dermatitis (ICD)?How effective are topical corticosteroids and immunomodulators in the treatment of irritant contact dermatitis (ICD)?Which specialist consultations are indicated in the treatment of irritant contact dermatitis (ICD)?What are the treatment guidelines for irritant contact dermatitis (ICD)?What is the medical therapy for irritant contact dermatitis (ICD)?Which medications in the drug class Emollients are used in the treatment of Irritant Contact Dermatitis?Which medications in the drug class Calcineurin Inhibitors are used in the treatment of Irritant Contact Dermatitis?Which medications in the drug class Corticosteroids, Topical are used in the treatment of Irritant Contact Dermatitis?
Savina Aneja, MD, Dermatologist, Bay Area Dermatology Associates
Disclosure: Nothing to disclose.
Specialty Editors
Michael J Wells, MD, FAAD, Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology
Disclosure: Nothing to disclose.
Paul Krusinski, MD, Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Additional Contributors
Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center
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