Irritant Contact Dermatitis

Practice Essentials

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 and coexisting irritant and allergic contact dermatitis is possible.^[1]

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. ICD is classified as follows^[2] :

• Acute irritant contact dermatitis 
• Acute toxic contact dermatitis
• Chronic irritant contact dermatitis
• Cumulative-(sub)toxic contact dermatitis (eg, hand soap causing irritant dermatitis in a hospital employee)
• Degenerative contact dermatitis
• Phototoxic contact dermatitis (eg, triggered by the combined exposure to a phototoxic substance and UV light)

Acutely, this inflammation is manifested by redness, erythema, mild edema, and scaling. Chronic irritant contact dermatitis presents with lichenification, hyperkeratotic scale, fissures, or ulcerations. (See the image below.)

View Image

Chronic irritant contact dermatitis of the hands in an older worker; the condition resulted in early retirement.

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.

The hands are the most important sites of ICD. ICD 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, ICD remains understudied in comparison 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 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 known cutaneous irritant. In ICD, it is rare for lesions to spread to unexposed skin areas.^[1] Laboratory studies may be of value in eliminating some disorders from the differential diagnosis. (See Workup).

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. 

Protein contact dermatitis (PCD) is a rare, distinct form of allergic or irritant contact dermatitis induced by proteins of either animal or plant origin. Four groups of proteins can cause protein contact dermatitis: plant, animal, flour, and proteolytic enzymes.  Individuals with chronic irritant or allergic contact dermatitis are at increased risk for PCD.^[1]

The definitive treatment of ICD is the identification and removal of any potential causal agents. For hand ICD, advise individuals to use ceramide-containing creams or bland emollients after washing hands with soap and before sleep. (See Treatment.)

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.^[3]  Recommendations pertaining specifically to irritant contact dermatitis are briefly summarized in the Guidelines section.

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.

• References

Pathophysiology

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. ICD 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 pathophysiologic changes are skin barrier disruption, epidermal cellular changes, and cytokine release.^[4]

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 ICD from repeated mild skin irritation from soap and water is common. For example, a hand-washing frequency that exceeds 35 times per shift has been associated strongly with occupational hand dermatitis in intensive care unit (ICU) workers (odds ratio, 4.13).^[5] Similarly, most cases of "homemaker's" eczema are ICD 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.

pK_a, an acid dissociation constant, is a quantitative measure of the strength of an acid in solution. pK_a has been shown to be highly predictive of acute skin irritation for acids and bases: acids with a pK_a lower than 4 and bases with a pK_a higher than 8 are highly irritative.^[6]

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, or occlusion) and detergents such as sodium lauryl sulfate produce more ICD in combination than singly.^[7] 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.^[8] An exacerbation of ICD may reflect development of allergic contact dermatitis to topical creams, medications, or rubber gloves.

The pathogenesis of ICD 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^[4] :

• Inflammatory cytokines (interleukin [IL]-1, tumor necrosis factor [TBF]-α)
• Chemotactic cytokines (IL-8, IL-10)
• Growth-promoting cytokines (IL-6, IL-7, IL-15, granulocyte-macrophage colony-stimulating factor [GM-CSF], transforming growth factor [TGF]-α)
• Cytokines regulating humoral versus cellular immunity (IL-10, IL-12, IL-18)

Intercellular adhesion molecule 1 promotes the infiltration of leukocytes into the epidermis in cutaneous inflammatory reactions, including ICD.

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.^[9]

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 ICD 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 ICD.^{[10, 11]}

• References

Etiology

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 ICD increases with the duration and intensity of exposure to the irritant.^[2] Environmental factors may enhance the effect of other irritants.^{[12, 13, 14]}

Dry air and temperature variation

Dry air renders the skin more susceptible to cutaneous irritants. Sufficiently dry air alone may provoke ICD. 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.^[15]

Water

Continual exposure to water may produce maceration, or repeated evaporation of water from the skin may produce cutaneous irritation through 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 ICD and rendering the skin more susceptible to other cutaneous irritants, such as soap and water.

ICD from alcohol most often is cumulative. Manual workers may wash their hands inappropriately with solvents to remove oil, grease, paints, or other materials and develop ICD as a consequence.

Inappropriate skin cleansing is a primary cause of ICD in the workplace. Washing facilities and methods must be inspected when investigating the workplace for one or more cases of occupational ICD. 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 ICD (as well as allergic dermatitis). Water-based metalworking fluids often cause ICD in exposed workers; surfactants in these fluids are the main culprit.

Cumulative irritant contact dermatitis

This is common in many "wet work" occupations. Healthcare workers wash their hands 20-40 times a day, producing cumulative ICD. 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 dermatologic 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.^[16]

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 ICD 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.^[17]

Rubber gloves

Some rubber gloves may provoke direct cutaneous irritation. Many workers complain of irritation from the powder in rubber gloves.

It is important to remember that gloves compromised by a hole may allow an irritant to enter and that 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 those 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. It must be kept in mind that the 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.^[18]

• References

Epidemiology

United States statistics

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.^{[19, 20]}

The prevalence of occupational hand dermatitis was found to be 55.6% in two ICUs and was 69.7% in the most highly exposed workers.^[5] A hand-washing frequency greater than 35 times per shift was associated strongly with occupational hand dermatitis.

International statistics

In some European studies among employees in high-risk occupations (eg, hairdressing, healthcare, and metalworking) the 1-year prevalence was between 20% and 30%.^[11] 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 than among those in "wet work" occupations.^[21]

The incidence figures reported for contact dermatitis in Germany were 4.5 cases per 10,000 workers for ICD, compared with 4.1 cases per 10,000 for allergic contact dermatitis. The annual incidence of ICD was found to be highest 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).^[22]

Age-related demographics

ICD may occur at any age. Many cases of diaper dermatitis are ICD 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 ICD and atopic dermatitis and those older than 50 years.

Sex-related demographics

ICD is significantly more common in women than in men. The higher frequency of hand eczema in women as compared with men is caused by environmental factors, not genetic factors. Occupational ICD affects women almost twice as often as men, in contrast to other occupational diseases that predominantly affect men. Women experience greater exposure 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 ICD (eg, hairdressing and nursing).

• References

Prognosis

For nonatopic individuals in whom ICD is diagnosed and managed promptly, the prognosis is good. Individuals with atopic dermatitis remain highly susceptible to ICD and may find that the tasks of many common occupations (eg, nursing and hairdressing) produce too much direct skin inflammation to allow them to continue with these careers.

Hardening may be specific to the irritant inducing the hardening phenomenon and does not occur in all persons with long-term exposure to an irritant.^[6] Hardened skin may also have a thickened stratum granulosum, with changes in the expression of various inflammatory mediators and markers.^[6] 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.^{[7, 9]}

Activities of daily living (ADLs) and work may be reduced by severe ICD.

Acute ICD reactions to potent irritants (eg, acids and alkaline solutions) are comparable to a chemical burn and can be graded similarly to a thermal burn (ie, as first-, second-, or third-degree). With appropriate symptomatic management, the prognosis for this type of ICD 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.^[23] 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).

• References

Patient Education

Individuals must be reminded to continue to avoid cutaneous irritants; they will redevelop or aggravate dermatitis if they continue to have the same skin care exposures that resulted in ICD. The possibility of secondary or complicating allergic contact dermatitis or impetigo must always be considered as well.

For patient education information, see the Skin Conditions & Beauty Center, as well as Contact Dermatitis.

• References

History

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 ICD. Acute delayed ICD 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.^[24]

The onset of signs and symptoms may be delayed by weeks in cumulative chronic ICD. Cumulative ICD 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 ICD.

Cumulative ICD typically occurs with exposure to weak irritants rather than strong ones. Often, the exposure (eg, water) occurs 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 ICD include the onset of dermatitis within 2 weeks of exposure, as well as reports of many other coworkers or family members affected.

Occupational history

ICD 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 suspected ICD.

Occupational ICD typically affects workers who are new to a job, who are constitutionally more susceptible to ICD, 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 ICD, particularly of the hands.

• References

Physical Examination

Rietschel and Fowler proposed the following as primary diagnostic criteria for ICD^[25] :

• 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 ICD 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 ICD and may develop secondary neurodermatitis or lichen simplex chronicus (lichenification). This may be accepted as a sequela of an occupational injury.

• References

Complications

Skin lesions may become colonized secondarily or infected, particularly by Staphylococcus aureus. Secondary neurodermatitis (lichen simplex chronicus) may develop in individuals with ICD, particularly in those with workplace exposures or under psychological stress.

Postinflammatory hyperpigmentation or hypopigmentation may occur in areas affected by ICD or persist after resolution of ICD in individuals with more pigmented skin.

Scarring may occur after corrosive agent exposure, excoriation, or artifact, causing ulceration.

ICD increases the risk of sensitization to topical medications.

• References

Approach Considerations

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.

See Allergic Contact Dermatitis, Pediatric Contact Dermatitis, and Protein Contact Dermatitis for further information on these topics.

• References

Laboratory Studies

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 the sites and morphology of lesions.

• References

Other Tests

Patch testing

Patch testing can be performed to diagnose contact allergies, but there is no patch test capable of proving that a cutaneous irritant is responsible for a particular case of ICD. Diagnosis rests on exclusion of allergic contact dermatitis and a history of sufficient exposure to a cutaneous irritant.

Direct microscopy

Skin scrapings of cutaneous lesions may help exclude scabies or may reveal fiberglass fibers as a cause of a patient's pruritus. To assess 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.

• References

Procedures

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.

• References

Histologic Findings

The histopathology of acute experimental ICD has been studied more thoroughly than that of chronic ICD, which is the primary clinical complaint. Cellular changes seen in the skin vary according to the chemical nature and concentration of the irritant applied, the duration of exposure, the severity of the ensuing response, and the time of sampling for acute ICD. Many primary irritants cause overt necrosis if applied in a sufficiently high concentration for a sufficient time.

Most histologic examinations of ICD 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 ICD reactions.

The histology of chronic ICD is one of hyperkeratosis with areas of parakeratosis, moderate-to-marked epidermal hyperplasia (acanthosis), and elongation of the rete ridges.

• References

Approach Considerations

The definitive treatment of irritant contact dermatitis (ICD) is the identification and removal of any potential causal agents. An inflammatory reaction from acute delayed ICD 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.

After the identification and removal of any potential causal agents, the use of ceramide-containing creams or bland emollients and bland barrier creams (eg, those containing dimethicone) are the mainstays of medical treatment for patients with ICD. The ceramide-containing creams or bland emollients should be used after hand washing with soap and before sleep.

Cleansers (eg, soaps and detergents) may be ranked according to their irritancy.^[26] Mild skin cleansers (eg, Aquanil, Cetaphil cleanser, Oilatum AD, Neutrogena cleanser) should be recommended in place of soap on affected areas. Individuals should be instructed to refrain from using inappropriate solvents (eg, gasoline) or abrasives (eg, pumice stone) to cleanse hands; these directly defat or traumatize the skin.

It should be kept in mind that a number of agents commonly found in therapeutic products for the skin (eg, propylene glycol, lactic acid, urea, salicylic acid) may themselves produce further skin inflammation and thus may have to be avoided by individuals with ICD. Topical corticosteroids play a limited role in the treatment of ICD. They do not address the process directly, but they may be helpful for superimposed eczematous features.

See Allergic Contact Dermatitis, Pediatric Contact Dermatitis, and Protein Contact Dermatitis for further information on these topics.

• References

Emergency Department Care

Emergency department (ED) treatment of ICD 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 and Eucerin) may be beneficial in chronic cases.

Large vesicles may benefit from therapeutic drainage (but without removal of the vesicle tops).^[6] These lesions should then be covered with antibiotic dressing or a dressing soaked in Burow solution.

Hospital admission is required only in cases of severe cutaneous ICD (eg, chemical burns from hydrofluoric acid or, occasionally, from freshly mixed Portland cement).

• References

Medical Care

Barrier creams

Creams containing ceramides (eg, Impruv, Cerave, Cetaphil RESTORADERM) may be particularly helpful in restoring the epidermal barrier in persons with ICD and atopic dermatitis. Creams containing dimethicone (eg, Cetaphil cream) can be helpful in restoring the epidermal barrier in persons with wet work–related ICD.

Cleansers

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 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.

ICD 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%), but these quickly produce irritation. 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 for reducing skin damage, dryness, and irritation in healthcare workers. ICD 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 steroids and immodulators

Topical corticosteroids and immunomodulators are of unproven use in treating ICD. In a study by Levin et al, corticosteroids were found ineffective in treating the surfactant-induced ICD when compared with the vehicle and with the untreated control.^[27]

Potential complications are associated with the use of steroids, particularly around the eye. Avoidance of long-term steroid use is essential because such use may cause cataracts, glaucoma, corneal thinning/perforation, and loss of the eye.

Topical tacrolimus can be used as an alternative to topical corticosteroids, but it occasionally is an irritant that may produce further stinging and irritation in persons with ICD.^[28]  European guidelines have recommended tacrolimus ointment for short-term treatment and as second-line treatment for cases unresponsive to corticosteroids. Infection must not be present. Patients should be made aware that this is off-label use.^{[29, 30, 1]}

Systemic therapy

Systemic therapy may be considered if topical therapy is not effective or not feasible. Short-term (≤ 14 d) use of corticosteroids may be considered for severe acute cases and for exacerbations of chronic cases.^[2]

Systemic therapy recommendations for chronic hand eczema (CHE) include the following^{[29, 30, 1]} :

• Alitretinoin as second-line treatment of severe CHE
• Cyclosporine as third-line treatment of severe CHE
• Methotrexate or azathioprine may be considered as third-line treatment of severe CHE; evidence of efficacy is limited, and patients should be made aware that this is off-label treatment

• References

Consultations

Multidisciplinary consultations may be required when many workers become affected with ICD in a workplace. Identifying and remediating the causes of widespread ICD interfering with workplace productivity and worker quality of life is important.

Any patient with a hydrofluoric acid burn should be evaluated on an medical emergency basis by a physician experienced in the management of hydrofluoric exposures and burns. Regional intravenous infusion of calcium gluconate should be considered as a therapeutic option for patients with hydrofluoric acid burns to the forearm, hand, or digits when topical therapy fails.

• References

Guidelines Summary

German Association of the Scientific Medical Professional Societies (Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften [AMWF])

In 2022, the German Association of the Scientific Medical Professional Societies (Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften [AMWF]) updated its 2013 guidelines for the diagnosis and management of contact dermatitis.^[2]  Key recommendations include the following2: ​

• The initial diagnostic workup of contact dermatitis is based on medical history, clinical examination, and testing for allergic, photoallergic/phototoxic contact dermatitis, and protein contact dermatitis.
• Correct diagnosis is essential for effective management
• Initial treatment is removal/avoidance of any potential causal agents; Topical corticosteroids are first-line therapy for both irritant and allergic contact dermatitis
• Therapy should be individualized and adjusted to the eczema stage.
• Consider systemic therapy if topical therapy is not effective or not feasible.

American Academy of Allergy, Asthma & Immunology and the American College of Allergy, Asthma & Immunology 

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.^[3]  Recommendations pertaining specifically to irritant contact dermatitis are briefly summarized below.

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.^[3]

For complete guidelines see Contact Dermatitis: A Practice Parameter--Update 2015.

Hand Eczema Guidelines

The following organizations have issued specific guidelines on the diagnosis and management of hand eczema (HE):

• 2021 European Society of Contact Dermatitis (ESCD)^[29]
• 2023 German Association of the Scientific Medical Professional Societies (AMWF)^[31]
• 2020  Spanish Academy of Dermatology and Venereology (AEDV)^[30]

HE is classified into etiologic and clinical subtypes as follows^{[29, 31]} :

• • Irritant contact dermatitis
  • Allergic contact dermatitis
  • Atopic hand eczema
  • Protein contat dermatitis/contact urticaria

   

  

   
• • Hyperkeratotic HE
  • Acute recurrent vesicular HE (previously, dyshidrotic eczema or pompholyx)
  • Nummular HE 
  • Fingertip dermatitis

   

  

   
• Mixed forms:  More than one etiology or clinical subtype is present

All three guidelines generally define acute and subacute HE as localized eczema lasting less than 3 months and not occurring  no more than annually.  Chronic HE (CHE) is symptoms lasting more than 3 months or multiple recurrences within 12 months.^{[31, 29, 30]}

The initial diagnostic workup of HE is based on medical history, clinical examination and patch testing.  Exposure assessment should be conducted prior to patch testing to identify potential allergens for inclusion. Wet work is strongly correlated with irritant contact dermatitis. Skin prick testing should be performed for suspected protein exposure etiology.  Microbiology testing is warranted with clinical signs of infection or in unilateral cases of HE and to exclude scabies.  Skin biopsy may be required to narrow the differential when psoriasis, lichen planus or lymphoma are suspected.^{[29, 30, 1]}   

 In additional to the removal/avoidance of any potential causal agents, the ESCD offers the following guidance for treatment of all HE^{[29, 30, 1]} :

• Frequent use of emollients and moisturizers
• Topical corticosteroids as a short-term initial treatment; long-term intermittent use for maintenance therapy may be considered but evidence of efficacy is weak
• Tacrolimus ointment for short-term treatment, and as second-line treatment for cases unresponsive to corticosteroids.  Patients should be made aware this is off-label treatment except for atopic HE
• Phototherapy for CHE unresponsive to corticosteroids; long-term is not advisable due to an increased risk of skin cancer

Systemic therapy recommendations include the following^{[29, 30, 1]} :

• Alitretinoin as second-line treatment of severe CHE
• Cyclosporine as third-line treatment of severe CHE
• Methotrexate or Azathioprine may be considered as third-line treatment of severe CHE; there is limited evidence of efficacy and patients should be made aware this is off-label treatment

• References

Hydrocortisone topical (AlaCort, AlaScalpt, Aquanil)

• Dosing, Interactions, etc.

Clinical Context: 

• References

Clobetasol (Clobex, Clobex Spray, Cormax)

• Dosing, Interactions, etc.

Clinical Context: 

• References

Triamcinolone topical (Kenalog Orabase, Kenalog topical, Pediaderm TA)

• Dosing, Interactions, etc.

Clinical Context: 

• References

Tacrolimus ointment (Protopic)

• Dosing, Interactions, etc.

Clinical Context: 

• References

Pimecrolimus (Elidel)

• Dosing, Interactions, etc.

Clinical Context: 

• References

Petrolatum & mineral oil topical (Eletone Cream, Tropazone)

• Dosing, Interactions, etc.

Clinical Context: 

• References