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Irritant contact dermatitis in adults

Irritant contact dermatitis in adults
Anthony F Fransway, MD
Margo J Reeder, MD
Section Editor:
Joseph Fowler, MD
Deputy Editor:
Rosamaria Corona, MD, DSc
Literature review current through: Feb 2023. | This topic last updated: Jul 26, 2021.

INTRODUCTION — Irritant contact dermatitis (ICD) is a localized, inflammatory skin response to a wide range of chemical or physical agents [1]. ICD results from direct cytotoxic effect of irritants and, unlike allergic contact dermatitis, is not immune mediated. ICD is a multifactorial disorder influenced by the physical and chemical properties of the irritating substance, host-related susceptibility factors, and environmental factors.

The clinical manifestations of ICD are similar to those of other acute or chronic eczematous dermatitides, including atopic dermatitis and allergic contact dermatitis. ICD, allergic contact dermatitis, and atopic dermatitis may coexist in the same patient.

This topic will discuss the pathogenesis, clinical manifestations, diagnosis, and management of ICD in adults. Atopic dermatitis and allergic contact dermatitis are discussed separately. Diaper dermatitis, the prototype of ICD in infants and young children, is also discussed separately [2].

(See "Treatment of atopic dermatitis (eczema)".)

(See "Basic mechanisms and pathophysiology of allergic contact dermatitis".)

(See "Clinical features and diagnosis of allergic contact dermatitis".)

(See "Management of allergic contact dermatitis".)

(See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)

(See "Diaper dermatitis".)

EPIDEMIOLOGY — Irritant contact dermatitis (ICD) is the most common type of contact dermatitis. ICD represents approximately 80 percent of occupational contact dermatitis and is considered the most frequent cause of hand eczema [2,3]. In the general population, the estimated prevalence of hand eczema ranges from 0.4 to 4 percent [3,4]. Females are more frequently affected than males, particularly between the ages of 20 to 59 [3,4]. Because many patients with hand eczema do not seek medical care, the true prevalence of hand eczema may be higher [4]. In a study of over 68,000 patients referred for patch testing, approximately 13 percent were diagnosed with ICD, with nearly one-half of the cases related to occupation [5]. The risk of occupational ICD is highest among those with "wet work" exposures, such as food handlers, hairdressers, health care workers, mechanical industry workers, cleaners, and housekeepers (table 1) [6].

PATHOGENESIS — Multiple mechanisms, some of which are not completely understood, are involved in the development of irritant contact dermatitis (ICD), including [7,8]:

Disruption of the epidermal barrier and loss of lipids

Damage of keratinocyte cell membranes

Cytotoxic effect on keratinocytes

Inflammatory cytokine release from keratinocytes

Activation of innate immunity

Most experimental studies of ICD have been performed with provocative testing using sodium lauryl sulfate [9]. The disruption of the epidermal barrier (stratum corneum) by occlusion or chemical or physical irritants, resulting in increased skin permeability and transepidermal water loss (TEWL) and reduction of the natural moisturizing factor, is considered the initiating event of ICD [10].

In experimental animal and human models, the acute disruption of the epidermal barrier from exposure to surfactants (eg, sodium lauryl sulfate) induces the release of preformed cytokines, such as interleukin (IL) 1-alpha, IL-1-beta, IL-6, and tumor necrosis factor (TNF)-alpha, from keratinocytes [11-14]. IL-1-alpha and TNF-alpha act as primary signals for the release of proinflammatory chemokines (eg, CCL20, CCL21, and CXCL8), which attract mononuclear and polymorphonuclear cells at the site of injury [14,15]. In addition, TNF-alpha induces the expression of intercellular adhesion molecule 1 (ICAM-1) on keratinocytes, which promote the infiltration of leukocytes into the epidermis.

Anti-inflammatory cytokines, such as IL-10 and the IL-1 receptor antagonist (IL-1RA), are also released in response to irritant exposure and may be involved in the resolution of the inflammatory process [16].

The pathogenesis of chronic ICD is not completely understood. One hypothesis is that chronic exposure to mild irritants or wet work downregulates the inflammatory response and stimulates cell proliferation and differentiation. A few studies have compared the cytokine levels in normal skin and in skin areas repeatedly exposed to sodium lauryl sulfate. In chronically irritated skin, the levels of IL-1-alpha and TNF-alpha were lower and the levels of IL-1RA were higher than those measured in nonirritated skin [16,17].

Moreover, ICD is associated with specific gene expression changes in affected skin, which distinguishes it from allergic contact dermatitis [18].

Some individuals develop a tolerance to chronic exposure to irritants. The adaptation of the skin to repeated irritant exposures is called the "hardening phenomenon." The mechanisms underlying the hardening phenomenon are unknown. Irritant-induced changes in skin morphology (eg, acanthosis and hyperkeratosis), lipid composition of the stratum corneum, barrier permeability, and expression of inflammatory mediators may contribute [19,20].

PREDISPOSING FACTORS — The development of irritant contact dermatitis (ICD) is influenced by host-related and environmental factors.

Host-related factors

Age – The skin reactivity to irritants is highest in infants and tends to decrease with age. The reactivity to irritants is lower among individuals >65 years than in those <30 years [21].

Sex – The prevalence of ICD in general, and of hand dermatitis in particular, is greater in females than in males. However, the higher risk in females is probably due to increased domestic and occupational exposure to detergents and "wet work" rather than to genuine sex differences in susceptibility [3]. The clearance rate and prognosis are similar in males and females [22].

Body site – The response to irritants varies from site to site on the body, reflecting differences in the thickness of the stratum corneum and barrier function. The face, dorsum of the hands, and finger webs are more prone to irritation from chemical substances than the palms, soles, or back [2,23].

Atopy – Individuals with atopic dermatitis have a chronically impaired barrier function that increases their susceptibility to irritants [24,25]. In a population-based study of patients with occupational skin disease, 64 percent of the subjects with ICD reported a personal or family history of atopic dermatitis or had typical and/or minor signs of atopic dermatitis [26].

Genetic factors – Twin studies indicate that genetic factors other than atopy (eg, cytokine gene polymorphisms) may influence the susceptibility to ICD [27]. Individuals with a low threshold for the irritant effect of sodium lauryl sulfate and benzalkonium chloride have a high prevalence of a tumor necrosis factor alpha (TNFA) gene polymorphism that is correlated with increased tumor necrosis factor (TNF)-alpha production [28,29]. Another study examining the genetic basis of irritant susceptibility in a larger population of health care workers identified nine significant single nucleotide polymorphisms in seven candidate genes involved in inflammation and skin homeostasis [30].

Environmental factors — Environmental factors, such as temperature, air flow, humidity, and occlusion, affect the skin response to irritants [31].

High temperatures and air flow appear to decrease the skin barrier function and increase the penetration of irritants, such as sodium lauryl sulfate (a surfactant contained in many detergents) [32-34]. Cold temperatures and low ambient humidity increase the transepidermal water loss (TEWL) and the skin susceptibility to irritants [35,36].

Increased humidity (eg, sweating from prolonged wearing of occlusive gloves) can disrupt the skin barrier and enhance the inflammatory response to chemical or mechanical irritants [37].

HISTOPATHOLOGY — The histologic features of irritant contact dermatitis (ICD) vary according to the stage and severity of skin lesions:

Acute ICD is characterized by mild spongiosis, intraepidermal vesicles or bullae, and necrosis of keratinocytes. A perivascular mononuclear cell infiltrate may be seen. Electron microscopy shows a condensed cytoplasm containing aggregated keratin filaments, lipid vacuoles, and membrane-bound vesicles; disrupted cell membranes; and pyknotic nuclei with condensed chromatin [38].

Chronic ICD is characterized by hyperkeratosis, parakeratosis, hypergranulosis, and acanthosis.

None of the histopathologic features of ICD can differentiate it from allergic contact dermatitis or eczema [39]. (See "Clinical features and diagnosis of allergic contact dermatitis", section on 'Histopathology'.)

COMMON IRRITANTS — Irritants are physical or chemical agents that can produce cellular perturbation if applied to the skin for sufficient time and in sufficient concentration. Unlike allergens, prior sensitization is not needed. Common chemical irritants include water and wet work, detergents and surfactants, solvents, oxidizing agents, acids, and alkalis. Physical irritants include metal tools, wood, fiberglass, plant parts, paper, and dust or soil. Occupations at high risk for irritant contact dermatitis (ICD) and common irritants encountered are listed in the table (table 1) [6].

MECHANISM OF ACTION OF IRRITANTS — The level of irritancy for an individual substance depends upon its chemical properties (eg, acid dissociation constant, ionization status, molecular size, or liposolubility) and the duration of the contact [2]. High concentrations of most chemicals are sufficient to induce an irritant reaction in almost all individuals, whereas mild irritants may induce an inflammatory response only in susceptible individuals or after repeated or prolonged contact [40].

Different chemicals may act synergistically in inducing dermatitis. Solvents remove the lipids from the stratum corneum whereas detergents remove both lipids and hygroscopic (water-holding) substances (eg, filaggrin breakdown products). The combined exposure to solvents and detergents produces an additive effect [41].

Chemical irritants

Water and wet work – Water is hypotonic and acts as a cytotoxic agent on eroded skin. On intact skin, prolonged contact with water causes swelling of the stratum corneum, disruption of the intercellular lipids, and enhancement of skin permeability and susceptibility to irritants [42]. Wet work is defined as skin exposure to liquids or wearing occlusive gloves more than two hours daily or hand washing or disinfection more than 20 times daily [43]. Food handling and preparation, health care-related occupations, cleaning, and hairdressing are examples of wet work.

Detergents and surfactants – Detergents used for domestic and industrial cleaning remove lipids and hygroscopic substances in the stratum corneum, denature proteins, and damage the cell membranes.

Solvents – Solvents remove lipids and hygroscopic substances and damage cell membranes. Their irritating capacity depends upon their chemical structure; aromatic solvents (eg, benzene or toluene) are stronger irritants than alcohols or ketones (eg, acetone).

Oxidizing agents – Oxidizing agents, such as sodium hypochlorite (bleach) or benzoyl peroxide, are cytotoxic agents.

Acids – Strong acids (eg, sulfuric acid) cause protein coagulation and cell necrosis.

Alkalis – Alkaline solutions saponify the surface lipids, dissolve water-holding substances, break the cross-linkages of keratin, and cause swelling of cells. Soap, soda, ammonia, potassium and sodium hydroxides, cement, and chalk are examples of alkaline substances.

Physical irritants — Chronic microtrauma or friction damages the stratum corneum, impairs the skin barrier, and induces the release of preformed cytokines from keratinocytes [44]. Physical agents that may cause skin irritation include [45-47]:

Metal tools



Plant parts (eg, thorns, spines, sharp-edged leaves) [45,46]



Physical irritants may act synergistically with chemical irritants, such as detergents or water, in inducing a more severe disruption of the skin barrier [37].

CLINICAL MANIFESTATIONS — The clinical manifestations of irritant contact dermatitis (ICD) range from mild skin dryness and erythema to acute or chronic eczematous dermatitis and even skin necrosis (chemical burn) (picture 1A-D). The type of skin response, nature of the irritant, and exposure pattern define several clinical variants, which are summarized in the table (table 2). However, acute and chronic ICD are the most common forms encountered in clinical practice:

Acute irritant contact dermatitis − Acute ICD often results from a single exposure to an irritant or caustic chemical. Clinical features include erythema, edema, vesicles, bullae, and oozing. The reaction is generally limited to the site of contact and is associated with a sensation of burning, stinging, or pain. Mild cases may present with only transient erythema. An example of acute irritant dermatitis common in Asia and tropical areas is Paederus dermatitis (also called blister beetle dermatitis or dermatitis linearis) (picture 1B) [48,49]. It is caused by the accidental crushing on the skin of an insect of the genus Paederus with release of pederin, a potent vesicant toxin produced by Pseudomonas bacteria in the hemolymph of the female beetle.

Chronic irritant contact dermatitis − Chronic ICD results from repeated exposures to mild irritants or low concentrations of strong irritants. Clinically, chronic ICD is characterized by erythema, scaling, lichenification, hyperkeratosis, and fissuring (picture 1C-D). Itch is often a less prominent symptom than burning and pain.

In a large, patch-tested population in Europe (n = 68,072), the hands (61.9 percent) and the face (10.6 percent) were the most commonly affected sites [5]. Hand ICD tends to involve the dorsum of the hands, fingertips, and finger webs. The face may be involved in individuals exposed to volatile irritants, through direct or airborne contact, or cosmetics.

Chronic ICD is particularly frequent in certain categories of workers (table 1). However, host and environmental factors, such as history of atopic dermatitis and exposure to friction, dust, or temperature extremes, are contributing factors in the persistence of ICD.

DIAGNOSIS — The diagnosis of irritant contact dermatitis (ICD) is based upon the clinical finding of a localized dermatitis in a patient with a history of exposure to chemical or physical irritants (table 3). Complete skin examination and accurate history taking are crucial to making the correct diagnosis.

For chronic ICD, patch testing may be performed to exclude allergic contact dermatitis. In some cases, a skin biopsy for histologic examination is necessary to exclude other skin disorders. (See 'Differential diagnosis' below.)

Skin examination — A complete skin examination should be performed to evaluate the extent of the skin involvement and concomitant skin disorders. The morphology, localization, and temporal course of dermatitis often suggest the diagnosis of ICD. In most cases, the affected sites are exposed areas, such as the dorsum of hands, face, and neck. However, irritants may be transferred to other skin sites by contaminated hands or clothes (eg, genitalia or intertriginous areas). Additional clinical criteria that favor the diagnosis of ICD include [50]:

Onset of symptoms within minutes to hours of exposure

Pain, burning, stinging, or discomfort exceeding itching

Glazed, parched, or scalded appearance of the epidermis

Predominance of scaling, hyperkeratosis, or fissuring over vesicular changes

Improvement of the rash when irritants are removed (decrescendo effect)

History — Important aspects of the history in a patient with suspected ICD include:

Daily activities, including occupation, home exposures, and hobbies

Types of substance or machinery used at the workplace

Workplace environment (temperature, humidity, dusts)

Use of protective gloves or gear

Wet work (including use of occlusive gloves)

Hand washing habits

Use of cleansers and skin protecting creams

Accidental chemical exposure

Previous atopic dermatitis, atopic respiratory disease, or other inflammatory skin disease

For occupational exposures, the material safety data sheets or the list of ingredients may be useful in identifying offending irritants (table 4). In some cases, visiting the work site may be needed. Common irritants encountered in occupational settings are listed in the table (table 1).

Laboratory tests

Patch testing – Patch testing is often necessary to exclude allergic contact dermatitis. A standard series of allergens is usually used for initial screening. Testing for additional series or specific, work-related allergens may be required based upon the patient's exposure history. The techniques and interpretation of patch testing are discussed separately. In cases of ICD, the patch testing is negative. Irritant reactions to certain allergens during patch testing may occur, but they are not indicative of clinical ICD. (See "Patch testing".)

Histologic examination – Skin biopsy is not routinely performed for the diagnosis of ICD. However, in some cases histologic examination is useful to differentiate ICD from psoriasis or other types of inflammatory dermatoses. (See 'Histopathology' above.)

DIFFERENTIAL DIAGNOSIS — The most common disorders that should be differentiated from irritant contact dermatitis (ICD) include:

Allergic contact dermatitis – Differentiating ICD from allergic contact dermatitis may be challenging because they frequently have similar clinical and histopathologic features (table 5 and picture 2A-B). A positive patch test to the relevant exposure is generally diagnostic of allergic contact dermatitis, although a positive patch test to a relevant allergen may not by itself exclude ICD. ICD and allergic contact dermatitis can coexist, especially in individuals exposed to wet work [51]. As an example, allergic contact dermatitis to glove allergens and topical medications used for therapy may complicate irritant hand dermatitis in health care workers. In allergic contact dermatitis, the dermatitis can persist or worsen immediately after the exposure to the chemical is removed, demonstrating a crescendo effect. Conversely in ICD, removal of the irritant begins the healing process (a decrescendo effect). (See "Patch testing", section on 'Patch test interpretation' and "Patch testing", section on 'Determining the clinical relevance' and "Clinical features and diagnosis of allergic contact dermatitis", section on 'Diagnosis'.)

Atopic dermatitis – History of atopic dermatitis and/or involvement of flexural areas suggest the diagnosis of atopic dermatitis. However, individuals with a history of atopic dermatitis are prone to the development of ICD when exposed to irritants (eg, wet work). (See 'Host-related factors' above and "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

Psoriasis – Nonpustular palmoplantar psoriasis may be extremely difficult to differentiate from hyperkeratotic, chronic ICD, and biopsy may not differentiate the two (picture 3A-B) [52]. The presence of psoriatic plaques at distant sites (eg, elbows and knees) and/or nail changes are clues to the correct diagnosis (picture 4). (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

Hand eczema – Acute and chronic (dyshidrosiform or psoriasiform) hand eczema (picture 5) can be difficult to differentiate from ICD. However, acute dyshidrotic eczema is characterized by vesicles and bullae on palms and soles, extending to the interdigital spaces, without involvement of the dorsal aspect of hands or wrists. It occurs more frequently in adolescents and young adults, with exacerbations in the spring and summer months and spontaneous remission in fall and winter. Chronic hand eczema may have an irritant component along with an "endogenous" or idiopathic predisposition. (See "Overview of dermatitis (eczematous dermatoses)", section on 'Dyshidrotic eczema'.)

Fungal infection – Tinea manuum or pedis are typically unilateral or asymmetrical (picture 6). Potassium hydroxide (KOH) examination of scales can clarify the diagnosis. (See "Dermatophyte (tinea) infections", section on 'Tinea pedis'.)

Scabies – Scabies in the interdigital spaces can simulate an irritant dermatitis (picture 7). In scabies, pruritus is the dominant symptom, whereas pruritus is less common and less intense in ICD. Skin scraping, adhesive tape test, or dermoscopy can provide the correct diagnosis. (See "Scabies: Epidemiology, clinical features, and diagnosis", section on 'Clinical manifestations' and "Scabies: Epidemiology, clinical features, and diagnosis", section on 'Diagnosis'.)


Overview — The management of irritant contact dermatitis (ICD) includes:

Identification and avoidance of the offending irritant(s)

Treatment of skin inflammation

Restoration of the epidermal barrier function

Prevention of further exposure

Avoidance — Avoidance of offending irritants and adoption of protective measures are critical in the management of ICD. For hand dermatitis, general measures include:

Minimizing contact with irritants, including detergents or other cleaning agents, fragrances, or solvents

Using vinyl gloves with cotton lining if wet work cannot be avoided (plastic gloves are less likely than rubber gloves to cause allergic contact dermatitis)

Frequently changing gloves when soiled and avoiding prolonged wear

Wearing gloves in cold weather

Using lukewarm water and small amounts of mild, fragrance-free, and soap-free skin cleansers for hand washing

Rinsing and drying hands thoroughly and gently after washing

Using moisturizers multiple times per day

Using barrier creams frequently, particularly with work-associated exposure to irritants and after hand hygiene

In occupational settings, first-line prevention strategies are based on technical and organizational hazard control. Automation of processes to reduce the need of workers to expose their skin to irritants and replacement of dangerous substances by less toxic ones are examples of primary prevention strategies.

Individual avoidance measures may include the use of gloves, sleeves, and/or other personal protective equipment (eg, suits, face masks or shields, and goggles).

The choice of glove material depends upon the type of chemical exposure. As an example, rubber gloves provide protection from hydrosoluble substances but are inappropriate for organic solvents. Information on appropriate gloves is available from glove suppliers and may be found on the material safety data sheet, which provides important safety information about chemical compounds used in the workplace (table 4). (See 'Gloves' below.)

Active treatment — Active treatment of ICD is aimed at reducing the signs and symptoms of inflammation and restoring the epidermal barrier. Emollients and topical corticosteroids are used empirically. Calcineurin inhibitors have not been proven effective in the treatment of ICD and, in some studies, have been found to be irritants [53,54].

Emollients and moisturizers — Emollients and moisturizers are beneficial in all patients with ICD. They soften the stratum corneum, reduce the transepidermal water loss (TEWL), and attract water to the stratum corneum (table 6). Emollients and moisturizers are used to decrease irritation and improve or restore the skin barrier function in ICD. Because they are effective only when present on the skin, emollients and moisturizers should be liberally applied multiple times per day, particularly after hand washing and before bedtime, to support the regenerative capacities of the skin.

Occlusive emollients (eg, petrolatum, lanolin, mineral oil, vegetable oils, beeswax, ceramides, and silicones) retard the TEWL; humectants (eg, glycerin, sorbitol, propylene glycol, or topical urea) are hygroscopic substances with a high capacity to attract water to the stratum corneum from the atmosphere and from the deeper epidermis and dermis. They are combined with occlusive emollients in many commercially available products. Petrolatum-based products are preferred to emollients containing lanolin or fragrances to reduce the risk of contact sensitization. Petrolatum-based products are widely available and inexpensive.

The efficacy of moisturizers has been evaluated in several studies of experimentally induced skin irritation [55]. In one representative study, six different lipid-rich moisturizers were effective in reducing erythema, scaling, and TEWL in skin irritated by sodium lauryl sulfate [56]. This study did not find a difference between moisturizers containing physiologic lipids (eg, cholesterol, ceramide, oleic acid, or palmitic acid) and those containing nonphysiologic lipids, such as petrolatum.

Topical corticosteroids — Topical corticosteroids in combination with emollients are frequently used in clinical practice for the treatment of ICD. Preparations of different potencies are selected based on severity and location of dermatitis, as described below. In general, ointments are preferred to creams:

Severe, nonfacial irritant contact dermatitis − For severe, acute ICD or chronic ICD with conspicuous skin thickening (lichenification) not involving the face or flexural areas, we suggest a super high-potency (group 1 (table 7)) topical corticosteroid (eg, clobetasol propionate). Topical corticosteroids are applied once or twice daily for two to four weeks.

Mild, nonfacial irritant contact dermatitis − For milder forms of ICD not involving the face or flexural areas, we suggest high-potency (groups 2 and 3 (table 7)) corticosteroids (eg, fluocinonide or betamethasone dipropionate). Topical corticosteroids are applied once or twice daily for two to four weeks.

Facial or flexural irritant contact dermatitis − For acute or chronic ICD involving the face or flexural areas, we suggest medium- to low-potency (groups 4 to 6 (table 7)) topical corticosteroids. Topical corticosteroids are applied once or twice daily for one to two weeks.

The use of topical corticosteroids for ICD is controversial. Data evaluating the efficacy of topical corticosteroids in ICD are limited to a few small studies of experimentally induced ICD that did not show a measurable improvement in restoring the epidermal barrier with topical corticosteroids compared with vehicles [57,58]. In one study, 36 healthy volunteers with ICD experimentally induced with sodium lauryl sulfate and nonanoic acid applied triamcinolone acetonide, clobetasol propionate, glycerol, vehicle, or no treatment on separate sites of irritated skin [53]. After 10 days, the treated and untreated sites showed a similar improvement in irritation, evaluated by a visual assessment score and measurement of TEWL and stratum corneum hydration.

Despite the lack of proven benefit in experimentally induced ICD, topical corticosteroids are commonly used as an adjunctive therapy for ICD because of their anti-inflammatory properties and their efficacy in other forms of eczematous dermatitis. These potential benefits must be weighed against the adverse effects of topical corticosteroids. (See "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)

PREVENTION — Gloves and barrier creams combined with adequate skin care are widely recommended as the most important measures of personal protection in occupations at increased risk of irritant contact dermatitis (ICD). Depending on the nature of the irritant exposure, the use of personal protective equipment (eg, suits, face masks, goggles) may be beneficial. Worker education programs are also effective at preventing occupational ICD.

Gloves — Adequate protection from contact with irritants is a key measure to prevent ICD. Since the hands are most frequently exposed to irritants in workplaces and households, the use of appropriate gloves is generally recommended to prevent ICD. The patient should be instructed to use gloves in connection with wet or dirty work at the workplace or at home. Tight-fitting gloves should be used as long as necessary but for the shortest time possible to limit sweating and maceration [59]. Thin cotton gloves should be worn under tight-fitting gloves and changed as soon as they become damp.

The efficacy of gloves in preventing ICD in the workplace has not been evaluated in clinical trials. Guidelines and recommendations on glove use are generally based upon local rules and regulations or clinical experience. It is important to remember that occlusive gloves can be themselves a cause of occupational hand dermatitis if not used properly.

Manufacturers of protective gloves provide lists of applications, hazards, and chemicals for which their gloves have been tested. Additional information can be obtained from the material safety data sheet, which provides important safety information about chemical compounds used in the workplace (table 4).

For optimal protection, the gloves must be used, maintained, and replaced according to the manufacturer's instructions. Failure to provide protection may be due to [60]:

Wrong glove material or thickness

Misuse (eg, contamination of the glove interior from incorrect wearing and/or removal)

Physical damage



Barrier creams — To prevent ICD of the hands, we suggest the use of barrier creams. They are typically applied before work and two to three times during work time, when necessary. They should be applied in adequate amounts and cover all the skin surface exposed to irritants. (See 'Emollients and moisturizers' above.)

Barrier creams include a variety of preparations designed to reduce the penetration of hazardous materials into the skin and help restore a damaged stratum corneum [61]. Some are specifically formulated for individual chemical exposures. In general, barrier creams contain silicones (eg, dimethicone), liquid paraffin, aluminum chlorohydrate, or other water-repellant compounds, such as perfluoropolyethers, that form a thin occlusive layer on the skin surface.

In a 2018 systematic review and meta-analysis of nine randomized trials including nearly 3000 participants in various occupational settings (metalworkers, print and dye industry workers, gut cleaners in swine slaughterhouses, cleaners and kitchen assistants, hospital employees, and apprentice hairdressers), rates of ICD were slightly lower among workers using barrier creams compared with controls, though the difference was not statistically significant (29 versus 33 percent; risk ratio [RR] 0.87, 95% CI 0.72-1.06) [62]. Similar results were noted with the use of moisturizers (RR 0.71, 95% CI 0.46-1.09). However, the individual studies were small and had methodologic limitations.

Barrier creams are generally well tolerated. Side effects are mild and include transient itching, stinging, and dryness [63].

Education — Numerous studies outline the importance of appropriate education on primary prevention of occupational dermatitis, including ICD, for workers involved in health care, hairdressing, wet work, food preparation, cleaning, and manufacturing [64]. Educational training may occur in vocational schools or on-the-job training sessions and includes information on hand hygiene, proper use of personal protective equipment, and application of moisturizers or barrier creams. Simple interventions, such as text messaging programs, have also been shown to increase compliance and regular application of moisturizers in patients with chronic hand eczema [65].

Patients with occupational skin disease who complete a prevention program may fare better. A three-year, follow-up study of 1410 patients with severe occupation skin disease who had completed a tertiary individual prevention program showed decreased disease severity and improved quality of life, with 97 percent of workers returning to work and 75 percent of workers retaining their primary occupation [66].

PROGNOSIS — The prognosis of acute irritant contact dermatitis (ICD) is generally good if the offending irritant is removed and preventive measures are adopted. The recovery of the barrier function after acute ICD is achieved approximately four weeks after irritant exposure, whereas skin hyperreactivity in the affected areas may persist for up to 10 weeks [67,68].

The prognosis of chronic ICD is variable. In a one-year, follow-up study of patients with occupational ICD, 43 percent reported improvement, 26 percent reported persistent dermatitis, and 11 percent reported aggravation [69]. History of atopic dermatitis was the most important determinant of persistence or aggravation.

In a long-term study of occupational hand eczema, healing occurred in 35 percent of patients 7 to 14 years after the initial diagnosis [70]. Negative prognostic factors were history of respiratory or skin atopy, disease duration, food-related occupation, and maintaining the same occupation.

INCONTINENCE-ASSOCIATED DERMATITIS — Incontinence-associated dermatitis (IAD) is a specific type of irritant contact dermatitis (ICD) caused by prolonged contact of the skin with urine or feces and friction [71]. IAD is a subset of moisture-associated skin damage (MASD), where skin breakdown occurs as a result of prolonged exposure to moisture and irritants, including urine, stool, wound drainage, or other bodily fluids [72]. The mechanism of skin injury in IAD involves both chemical and physical irritation, which leads to disruption of the epidermal barrier and increased skin permeability, inflammatory changes, skin breakdown, and increased risk of bacterial colonization and secondary infection [71,73,74]. (See "Female urinary incontinence: Evaluation" and "Urinary incontinence in men".)

The prevalence of IAD varies across different countries, health care settings, and patient populations. A prevalence of approximately 4.3 percent has been estimated among residents of nursing homes and hospitalized patients, but rates as high as 20 to 50 percent have been reported in long-term acute care settings and are highest among persons with limited mobility [75-77]. Independent risk factors for the development of IAD include older age, diabetes, liquid stools, smoking, and not using diapers [78]. IAD is higher in patients with fecal, rather than urinary, incontinence [77].

Clinical presentation — Mild IAD is characterized by persistent erythema and edema of the skin but without skin breakdown; in more severe cases, vesicles, bullae, and erosions may develop [71,73] (figure 1). The sites involved include the perianal skin, buttocks, genitalia, upper thigh, and skin folds between genitalia and thigh [76]. Colonization and secondary infection with bacteria and yeasts can occur in severe IAD.

Diagnosis — The diagnosis of IAD is generally obvious, based upon the clinical presentation (figure 1). However, IAD must be differentiated from stage I and II pressure ulcers, as patients with incontinence are also at higher risk for pressure ulcers (table 8). (See "Clinical staging and general management of pressure-induced skin and soft tissue injury".)

Allergic contact dermatitis should be considered with possible exposures, including topical medicaments, preservatives, and fragrances [79]. Other forms of intertriginous dermatitis that should also be considered in the differential diagnosis of IAD include inverse psoriasis and seborrheic dermatitis. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Inverse (intertriginous) psoriasis' and "Seborrheic dermatitis in adolescents and adults".)

Treatment and prevention — A structured skin care regimen is the mainstay of treatment and prevention of IAD. It should include [71]:

Gentle cleansing of the genital, perianal, and groin area using soap-free cleansers. Regular soaps that have an alkaline pH should be avoided, as they can worsen the irritant effect of urine and stools on the skin. Vigorous washing and rubbing of skin should also be avoided.

Carefully patting the skin dry after washing using a soft cloth without rubbing.

Hydrating the skin by applying moisturizers or barrier creams. Creams are generally preferred to ointments and should be gently applied (without rubbing) on the affected areas in a thin layer. An excess of moisturizers can promote skin maceration. Exuding lesions may benefit from the application of zinc oxide-based barrier creams, films, lotions, or sprays.

These steps can be repeated two to three times per day.

There is a paucity of high-quality studies evaluating the efficacy of different skin care measures for the treatment and prevention of IAD. A systematic review of 13 clinical trials, including 1295 patients who were incontinent for urine, stool, or both and were residents in a nursing home or hospitalized, found that structured skin care regimens consisting of gentle skin cleansing and application of moisturizing and protective topicals was more effective for the treatment and prevention of IAD than the use of soap and water [80]. However, the included studies were generally of low quality and showed considerable heterogeneity in the type of skin care products used, skin care procedures, and outcome measurement.  

Patients with IAD should be frequently evaluated for signs of bacterial or fungal secondary infection. Topical antiseptics (eg, povidone iodine) or topical antimycotics can be used for superficial, localized infections. Severe bacterial skin infections require systemic antibiotic therapy. (See "Acute cellulitis and erysipelas in adults: Treatment".)

For patients with chronic incontinence, a urinary or fecal management system may be necessary, though leaking around systems can also be associated with the development of IAD [77]. Caution should be used because of the risk of catheter-associated infection.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Contact dermatitis".)


Epidemiology and risk factors Irritant contact dermatitis (ICD) is a localized, inflammatory skin response to exposure to a wide range of chemical or physical agents. ICD is the most common type of occupational dermatitis, particularly among food handlers, health care workers, mechanical industry workers, cleaners, and housekeepers (table 1). (See 'Epidemiology' above and 'Predisposing factors' above.)

Common irritants – Common chemical irritants include water and wet work, detergents and surfactants, solvents, oxidizing agents, acids, and alkalis. Physical irritants include metal tools, wood, fiberglass, plant parts, paper, and dust or soil (table 1). (See 'Common irritants' above.)

Clinical manifestations – Acute and chronic ICD are the most common variants (table 2). Acute ICD presents with erythema, edema, vesicles and bullae, and oozing (picture 1A-B). In chronic ICD, lichenification, hyperkeratosis, and fissuring are predominant (picture 1C-D). (See 'Clinical manifestations' above.)

Diagnosis – In most cases, the diagnosis of ICD is based upon the clinical finding of a localized dermatitis in a patient with a history of exposure to chemical or physical irritants (table 3 and picture 1A-B). Patch testing may be necessary to exclude allergic contact dermatitis. (See 'Diagnosis' above and 'Differential diagnosis' above.)


Avoidance – Avoidance of offending irritants and adoption of protective measures are the mainstay of ICD management. (See 'Avoidance' above.)

Active treatment – For most patients with ICD, we suggest treatment with emollients and moisturizers plus topical corticosteroids rather than either therapy alone or no treatment (Grade 2C). Emollients and moisturizers are liberally applied multiple times per day. The corticosteroid potency is selected based on severity and location of dermatitis (see 'Active treatment' above):

-Severe, nonfacial, nonflexural irritant contact dermatitis – For severe, acute ICD or chronic ICD with conspicuous skin thickening (lichenification) not involving the face or flexural areas, we generally use super high-potency topical corticosteroids (group 1 (table 7)) once or twice daily for two to four weeks.

-Mild, nonfacial, nonflexural irritant contact dermatitis – For milder forms of ICD not involving the face or flexural areas, we generally use high-potency corticosteroids (groups 2 and 3 (table 7)) once or twice daily for two to four weeks.

-Facial or flexural irritant contact dermatitis – For acute or chronic ICD involving the face or flexural areas, we generally use medium- to low-potency topical corticosteroids (groups 4 to 6 (table 7)) once or twice daily for one to two weeks.

Prevention – Prevention measures for ICD include the use of appropriate protection measures (eg, gloves), barrier creams, and emollients. We suggest using barrier creams and emollients in addition to protection measures for the prevention of ICD in individuals exposed to wet work or other chemical or physical irritants (Grade 2C). Barrier creams and emollients are applied before work and multiple times per day if the exposure continues. (See 'Prevention' above.)

Incontinence-associated dermatitis – Incontinence-associated dermatitis (IAD) is a specific type of moisture-associated skin damage (MASD) caused by prolonged contact of the skin with urine or feces and friction. It presents with persistent erythema, edema, and, in severe cases, bullae or erosions on the perianal skin, buttocks, and genitalia (figure 1). IAD must be differentiated from stage I and II pressure ulcers in patients with incontinence who are also at risk for pressure ulcers (table 8). (See 'Clinical presentation' above and 'Diagnosis' above.)

A careful skin care regimen consisting of gentle skin cleansing with soap-free cleansers followed by the application of moisturizers and barrier creams is the mainstay of treatment and prevention of IAD. (See 'Treatment and prevention' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Papapit Tuchinda, MD, and Ronald Goldner, MD, who contributed to earlier versions of this topic review.

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Topic 13661 Version 23.0


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