Are You Confident of the Diagnosis?

Irritant contact dermatitis is a cutaneous inflammation caused by exposure of an exogenous agent. Endogenous and exogenous factors play a role in the skin barrier disruption and damage to keratinocytes and pro-inflammatory mediator release resulting in a clinical presentation of contact dermatitis. Irritant dermatitis can be further divided into 10 phenotypes, which vary in morphology, onset and prognosis. The 10 phenotypes are listed below in Table I.

Table I.
Phenotype Description
Acute irritant dermatitis Acute onset often after single exposure
Signs of acute skin irritation – erythema, edema, inflammation, vesiculation
Heals quickly after exposure
Delayed acute irritant dermatitis Delayed onset, 12-24 hours or more
Similar clinical appearance as acute irritant dermatitis
May be confused with allergic contact dermatitis due to delayed onset
Irritation reaction Acute, often multiple exposures required
Monomorphic presentation with only one of the following parameters present: scaling, erythema, vesiculation, pustules or erosions
Frequently heals spontaneously with hardening of the skin
Chronic irritant dermatitis (cumulative irritant dermatitis, wear and tear dermatitis) Slowly developing (weeks to years)
Erythema, xerosis, hyperkeratosis, erythema, pruritus, pain
Traumatic irritant dermatitis Slowly developing after preceding trauma (i.e. burn, lacerations, acute irritant dermatitis)
Presents with unhealed skin, erythema, vesicles, papules, scaling at site of injury
Prolonged healing period
Chronic and resistant to therapy
Acneiform irritant dermatitis (pustular irritant dermatitis, follicular irritant dermatitis) Moderately slow-developing (weeks to months)
Acneiform lesions, sterile and transient pustules
Nonerythematous (suberythematous) irritation Slowly developing
Subtle skin damage with no visible inflammation
Subjective (sensory) irritation Acute
No visible signs of irritation but experiences itching, stinging, burning or tingling with chemical contact
Friction dermatitis Slowly developing
Repetitive, low-intensity friction leading to hyperkeratosis and acanthosis, hardening of skin, hyperpigmentation, friction blisters, erythema, scaling, fissuring, itching around affected area often associated with paper work
Asteotic irritant eczema (asteotic dermatitis, exsiccation eczematid, eczema cracquele) Slowly developing
Partially due to low humidity
Primarily seen in elderly patients during dry, winter months
Xerosis, loss of smoothness, icthysoiform scale, cracking of superficial epidermal layers
What you should be alert for in the history

Due to the fact that irritant dermatitis is most often the result of occupational exposures to irritants, the diagnosis of acute irritant dermatitis is usually evident with rapid onset of changes to the skin after initial exposure to the irritating agent. Chronic irritant dermatitis and allergic contact dermatitis are often indistinguishable, and a thorough history of the patient’s chemical environment is crucial to proper diagnosis. Patch testing may be needed to rule out allergic contact dermatitis.

The diagnosis of irritant dermatitis depends on careful clinical examination, patient history and assessment of exposure to irritants including occupational and nonoccupational exposures as listed in Table II. The mode of irritant exposure and history of other skin diseases should be considered. Patients who are receiving workers’ compensation due to their irritant dermatitis may continue to work second jobs that expose them to other irritants and may cause ersistent irritant dermatitis.

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Table II.

Clinical characteristics of dermatitis

Characteristics of initial lesions and clinical evolution

Time of onset and possible relationship with exposure to allergens or irritants

Dermatitis area corresponding to exposure site

Dermatitis morphology suggesting specific contacts

History of occupational exposure

Job description; occupational gestures and characteristics of the working mileu

Potential allergens and irritants in the working environment

Characteristics of the exposure: dose, frequency and site

Concomitant exposure factors: temperature, humidity, or occlusion

Time relationship to occupation; effect of holidays and time off work

Personal protective measures at work (gloves, masks and barrier creams)

Other workers similarly affected?

History of nonoccupational exposure

Domestic products: cleaners and detergents, hand washing frequency

Skin care products, fragrances, nail and hair products, soaps

Pharmaceutical products (prescription and over the counter)

Personal protective measures at home (gloves)

Jewelry and clothing

Homework and hobbies

Variants on exposure

Direct contact with the agent

Contact through fomites or contaminated surfaces

Combination of contact with the causative agent and sun exposure resulting in a photocontact or photoaggravated dermatitis

Contact with spouses or partners, relatives, or friends who convey the agent, which results in connubial or consort dermatitis

Transfer from other body sites, generally by hands, to more sensitive areas, such as eyelids or neck, resulting in ectopic dermatitis

History of previous dermatitis, atopy, or other skin/general diseases

Past contact dermatitis (occupational or not)

Previous patch testing

Other exogenous or endogenous dermatitis: atopic dermatitis, stasis dermatitis, psoriasis, and sensitive skin

Mucosal atopy (asthma and rhinoconjunctivitis)

Family history of atopy and other skin diseases

Characteristic findings on physical examination

Early on in the course of the disease, patients with irritant dermatitis and acute irritant dermatitis may complain of burning, stinging, soreness of skin and pain. Generally, irritant dermatitis is characterized by eczematous inflammation and presents with erythema, edema, vesicles that may coalesce, bullae, and oozing. Acute irritant dermatitis presents with the cardinal signs of erythema, edema, vesiculation, and pruritus.

Acute irritant dermatitis also manifests with inflammation, pustules, oozing, possibly exudative cutaneous inflammation, ulcerative lesions, epidermal necrosis, asymmetrical distribution, and sharply demarcated borders. Subacute or chronic irritant dermatitis morphologically presents with erythema, lichenification, excoriation, scaling, and hyperkeratosis (Figure 1).

Figure 1.

Chronic irritant contact dermatitis of the hand secondary to extensive water exposure. (Courtesy of Howard I. Maibach, MD.)

The shape, pattern and distribution of the eczematous lesions are primarily confined to the areas of irritant contact. This is suggestive of a diagnosis of irritant dermatitis. However, there are cases where the location of lesions presents atypically and irritant dermatitis should still be considered in the differential diagnosis.

Expected results of diagnostic studies

Diagnosis of irritant dermatitis relies primarily on clinical recognition. Histopathologically irritant dermatitis shows pleomorphism. The epidermis shows moderate spongiosis, intracellular edema, exocytosis with diffuse distribution of the inflammatory infiltrate in the epidermis. Occasionally neutrophil rich infiltrates are present and pustulation and necrosis may develop along with decreased CD1+ Langerhans cells. CD4+ T cells predominate with some CD8+ T cells present. There is increased expression of ICAM-1 by keratinocytes and increased expression of HLA-DR by keratinocytes. Irritant dermatitis presents with an increase in epidermal volume at 24 hour after challenge. Proliferating epidermal cells reach a peak 4 days after challenge. Keratin 16 and involucrin expression in the epidermis increased rapidly after challenge reaching a peak after 3 days and fading thereafter.

Diagnosis confirmation

Irritant dermatitis and ACD may both be clinically and histologically difficult to differentiate. However, there are some histological and histochemical differences. ACD presents with spongiosis with microvesicles predominating, but pustulation is rare in ACD. ACD also presents with focal distribution of the inflammatory infiltrate in the epdiermis. There is an initial decrease in number, then an increase in CD+1 Langherhans cells.

IL-2 is expressed, as is increased expression of ICAM-1 and HLA-DR by keratinocytes. The epidermal volume increases 72 hours after the challenge. Keratin 16 and involucrin expression in the epidermis increases more slowly and reaches a peak 4 days after initial exposure. If the correct diagnosis is established removal of the irritant will lead to recovery.

Patch testing is currently used in clinical practice as a diagnostic tool for ACD along with a thorough clinical history and physical exam. A negative patch test can indicate an irritation or endogenous disease, however, is insufficient to diagnose irritant dermatitis. A negative patch test cannot conclusively exclude ACD either due to the possibility that the causal agent was not represented during the test or the possibility of a false negative. A positive or negative patch test cannot eliminate the possibility of concomitant disease of both irritant dermatitis and ACD. There are no direct clinical tests for ICD at this time.

Who is at Risk for Developing this Disease?

Occupational exposures to exogenous agents are the most common cause of irritant dermatitis. Irritant dermatitis acquired through occupational hazards is referred to as occupational contact dermatitis. Table III lists the high-risk occupations and the exogenous agents commonly associated with those occupations.

Table III.
Occupation Exogenous Agents



Construction workers



Asphalt vapors/ Tar


Technical oils and grease



Acidic and alkaline building chemicals

Solvents (building chemicals)


Phototoxic plants and lichens

Furniture industry workers

Wood dust

Mechanical abrasion


Stains, shellac, lacquer, varnish

Soaps and detergents


Hospital workers, including nurses

Antibacterial soaps with sweating induced occlusion of gloves




Alcohol (ethyl, isopropyl)

Drying agents (aluminum acetate)




Kitchen workers




Hair dressers

Detergents in shampoos

Hydrogen peroxide as oxidizing agent in a permanent

Coloring and blonding products

Thioglycates in permanent wave solutions

Persulphates used in blonding/bleaching products

Chemical industry workers

Extensive list of irritants

Dry cleaners

Dry cleaning chemical agents


Warehouse workers

Handling cardboard

Metal workers




Metal chips and dust



Heat and humidity


Soaps and detergents


Metal-work fluids


Occurrence of irritant dermatitis is affected by numerous factors. An identified factor is variation in individual skin barrier function as well as changes in the stratum corneum over time. Studies observing transepidermal water loss (TEWL) in aging skin have demonstrated decreased TEWL with increasing age and decreased percutaneous penetration of some drugs.

The risk of acquiring irritant dermatitis decreases with age due to reduction in sensitivity to exogenous and exposure to cutaneous irritants. However, discrepancies between visual and microscopic appearance are present. In a group of aged patients there was no visual reaction when exposed to irritants, but significant barrier damage was present microscopically.

Due to cultural, socioeconomic and multiple gender-associated traditions in society, females account for the majority of irritant dermatitis patients. Many of the high-risk occupations listed in Table II, such as hairdressers, cleaners, kitchen workers, and hospital workers, all of which involve daily water exposure, are known to predominantly employ females. Again due to social norms, women are more likely to be exposed to irritants at home, particularly in homes with young children. Atopic dermatitis is a known risk factor for irritant dermatitis. Atopic dermatitis itself is more common in females, further predisposing women to irritant dermatitis.

The environment one lives in plays a factor in irritant dermatitis development as well. Environments that are hot, cold, with low humidity or ultraviolet (UV) irradiation increase one’s susceptibility to irritant dermatitis. The heat leads to sweating and retention of sweat, which is an irritation in itself but also increases the penetration of irritants. Low environmental humidity lowers ceramide levels in the stratum corneum.

What is the Cause of the Disease?

Irritant contact dermatitis is primarily the result of direct stimulation of the cells in the stratum corneum by a harmful agent. Exposure of an external agent is often associated with certain high-risk occupational exposures listed in Table II. The resulting irritation depends greatly on the type of chemical, concentration of the chemical, mode of exposure, concomitant environmental factors and individual responses.

Depending on these factors, symptoms may develop as early as 5 hours or as late as 7 days to years after initial contact. In other situations, irritants may result in an invisible inflammatory response and visible inflammation may not be seen until 8-24 hours or even longer after exposure.


The irritant may cause any of three pathophysiologic changes: skin barrier disruption, cellular epidermal change and mediator release. Irritant dermatitis is the manifestation of an inflammatory response emerging from the disruption of the epidermis and the release of cytokines from damaged keratinocytes. The pro-inflammatory mediators recruit and activate T-lymphocytes. Other cytokines and cell adhesion molecules such as ICAM-1, lymphocyte function-associated antigen (LAF)-1, IL-1 alpha, IL-1ß, TNF-alpha, colony-stimulating factor (GM-CSF) and INF-gamma are present in the dermis and epidermis.

As opposed to allergic contact dermatitis (ACD), irritant dermatitis is not caused by a delayed (type IV) hypersensitivity reaction and thus does not require prior sensitization. Although there is a distinction histologically and morphologically the two may be indistinguishable clinically. It seems that the same inflammatory immunomechanisms are the cause of both allergic and irritant contact dermatitis.

Systemic Implications and Complications

The only reported incidence of systemic complications associated with irritant dermatitis are due to exposure to hydrofluoric acid (HF). Hydrofluoric acid exposure should be considered if the patient reports a history of occupational exposure, most commonly in the silicon chip industry. Although HF is a comparatively weak acid, penetration of the dermis can lead to serious systemic complications. Systemic complications due to HF are rare but occur due to the chemical’s high permeability coefficient.

Once HF has entered the body, the fluoride ion dissociates from the hydrogen ion and binds to calcium and magnesium, depleting total body stores resulting in hypocalcemia and hypomagnesia. The insoluble ion complexes may causes intense pain, deregulation of Na/K ATPase pump, electrolyte imbalance, enzymatic cellular destruction and cell death. Life-threatening situations may result from cardiac ventricular arrhythmias precipitated by hypocalcemia and hyperkalemia.

Symptoms of HF exposure may be delayed up to 24 hours particularly when involving dilute solutions (5-15%). The presentation is often confusing and leads to errors in triaging. The patient will report agonizing pain, while the appearance of the burn is mild. The treatment protocol for HF burns begins with rinsing the affected area with lukewarm water for 15 minutes followed by measuring serum calcium, magnesium, potassium, and obtaining an ECG. Based on the results serum calcium and/or magnesium should be replaced as necessary. Hyperkalemia and arrhythmias should be treated with standard therapy.

To counteract the painful effects of HF burns, calcium salts are applied to the affected area. Topical application of calcium gel to the dermis is the first line of treatment. The gel can be massaged to the affected area and covered with dressing or with a glove on the hands. If the pain does not diminish within 15 to 30 minutes, parenteral calcium gluconate is indicated and delivered intravenously or intraarteriarly.

Treatment Options

Treatment options are summarized in Table IV.

Table IV.

Moisturizing creams

Barrier creams

Topical creams

Cool compress


Oral antibiotics (when infection is present)

Oral corticosteroids (for severe cases)


Phototherapy (UVB or PUVA) (rarely used)

Grenz-ray therapy

Form of irritation Treatment Efficacy
Acute irritant dermatitis

Cool compress

Topical corticosteroids

Antibiotics (for infection)


Immunosuppressants (infrequently needed)






Chronic (cumulative) irritation





Subacute irritation


Barrier creams





Hydrofluoric acid burns

Calcium gluconate


Sensory irritation

Strontium salts


PUVA, psoralen with ultraviolet B; UVB, ultraviolet B.

Optimal Therapeutic Approach for this Disease

Treatment of irritant dermatitis may vary depending on the stage of dermatitis and type of irritant dermatitis. The treatment protocol may be simplified by categorizing irritant dermatitis as one of three forms: acute irritant dermatitis, chronic (cumulative) irritant dermatitis, or subacute irritant dermatitis.

Acute irritant dermatitis has a rapid onset of symptoms, often after a single exposure to the irritant. The close temporal association of exposure to the irritant and the emergence of symptoms allow for the recognition of the irritant and thus steps can be taken to prevent future dermatitis. Treatment includes removal of the offending substance, cool compresses, potential glucocorticoids ( clobetasol cream or ointment or triamcinalone 0.1% cream or ointment once to twice daily for 1-2 weeks), oral antibiotics, and antihistamines as needed.

Avoiding the irritant

First and foremost, the irritant must be identified and avoided. Prevention is the cornerstone of treatment for irritant dermatitis. Patients thoroughly educated on the sources of the irritant have a better prognosis. Contact with other common household and occupational irritants should also be minimized.

Patients should be vigilant in using protective gear and gloves; however, caution should be used when using gloves. Although gloves prevent contact between the chemical and the skin, the moisture that accumulates within the glove and the occlusive nature of the glove may increase the likelihood or severity of irritant dermatitis. Incidences in which gloves may hinder dexterity of the hands or in occupations with low-grade irritant exposure barrier creams are suggested. Liberal application of moisturizers is advised, as moisturizers may prevent absorption of exogenous substances and accelerate barrier recovery.

Topical and oral corticosteroids

Standard therapy for irritant dermatitis includes topical corticosteroids. Findings on the effectiveness or corticosteroids in treating irritant dermatitis are inconsistent. The usual recommended dosage is two applications of the corticosteroids daily; however, studies comparing single dosing to multiple dosing have failed to demonstrate differences in absorption. Findings suggest that more frequent applications and less frequent applications may be equally effective.

Standard trade concentrations of corticosteroids suffice in treating contact dermatitis; for severe cases, higher concentrations or systemic corticosteroids should be considered. For mild to moderate cases class I and class II corticosteroids, such as clobetasol or fluocinonide. are used. A medium-potency topical steroid such as triamcinalone 0.1% cream or ointment can be used as well. Tapering begins after clinical improvement is seen.

Due to the anatomic variation in percutaneous absorption of compounds, the concentration of corticosteroid prescribed should be adjusted accordingly. Acute cases should respond to a 3-week taper of topical coricosteroids.

More severe and widespread cases may require high-potency topical corticosteroids or a systemic corticosteroid taper. Frequently used drugs include prednisone or prednisolone. Use of oral corticosteroids should be discontinued as early as possible. High potency steroids have been associated with many adverse effects. Most effects are localized; however, systemic effects may be present, the most concerning of which are Cushing’s syndrome, renal failure, hepatitis, lymphoma, among others.

Immunomodulators such as primecrolimus and tacrolimus have been shown to be effective in the treatment of ICD. However, the medications carry a blackbox warning of increased risk of lymphoma and skin cancer.

Cool compress

The application of a cool compress is also recommended. There is only evidence supporting the effectiveness of cool water compresses; however, other solutions may be prescribed, such as cool compress of Burrow’s solution (aluminum acetate in water), which can be found over the counter. A clean cotton cloth or gauze is soaked in the solution and applied to the symptomatic area for 15-30 minutes 2-6 times per day, followed by a moisturizer.

Studies have demonstrated that cool compresses accelerated the healing of the underlying skin, although no signs of the healing process could be observed externally. Cool compress is thought to reduce transepidermal water loss (TEWL) due to the hygroscopic characteristics of the solution, therefore increasing the capacity for intracellular water retention. It also reduces vesiculation and Burow’s solution will help inhibit bacterial growth. A mositurizer should be applied within a few mintues after the compress is removed.

Oral antibiotics and antihistamines

Oral antibiotics have been prescribed to treat secondary bacterial infections. Sedating antihistamines such as dephenhydramine (Benadryl) and hyroxyzine (Vistaril) may be prescribed to reduce pruritus and provide symptomatic relief. Patients should be informed of the sedating effects of the medication.

Phototherapy and radiotherapy

Phototherapy has been an effective treatment for chronic (cumulative) irritant dermatitis. Exposure to narrowband UVB phototherapy or ultraviolet A photchemotherapy (psoralen with UVA: PUVA) is administered two to three times a week concomitantly with a photosensitizer (topical or oral psoralen). Repeated low-level UV therapy may elicity hardening of the skin, suppress cellular proliferation and reduce the number of Langerhans cells, and has immunosuppressive action.

Phototherapy requires frequent visits by the patient for several weeks at a time. This is difficult for patients to comply with and is disruptive to their routine. Long-term therapy, in particular PUVA, increases the risk for skin cancer, which is exacerbated in cases where oral immunosuppressants such as cyclosporin are given.

Another option is Grenz-ray therapy, which has been successful in treating chronic hand eczema. There is a population of patients who respond particularly well to Grenz-ray therapy and is an option for recalcitrant cases. However, Grenz-ray therapy carries the minimal risk of developing nonmelanoma skin malignancies.

Patient Management

If the irritant is properly identified, few follow-up visits are required. Withdrawal of the irritant should lead to recovery. Patient prognosis varies widely, with follow-up periods ranging from a few months to 31 years. Surveys found that only 30.8% of patients treated for irritant dermatitis reported full remission of symptoms. The clinical history of chronic dermatitis is a predictor of future dermatitis. Diagnosis and treatment at late stages of irritant dermatitis have little effect on the course of the irritant dermatitis.

Unusual Clinical Scenarios to Consider in Patient Management

Dermatitis artefacta or dermatitis factitia is a form of dermatitis, which may present clinically as irritant dermatitis, however the lesions are self-inflicted and intentional and more commonly seen in females. The lesions are often found in areas that are accessible by the patient’s hands. A variety of means may be used to injure the skin, most commonly fingernails. Patients may use tools such as knives or other sharp instruments and common household chemicals such as bleach.

The underlying cause is related to an underlying psychiatric disorder that needs to be addressed directly. Common causes are depressive disorder, general anxiety disorder, obsessive compulsive disorder, and personality disorders. It is also prevalent in patients diagnosed with anorexia nervosa and bulimia nervosa.

What is the Evidence?

Chew, A, Maibach, HI. Irritant dermatitis. 2007. (The most complete and up-to-date source of the clinical and basic science of knowledge of irritant dermatitis.)

Zhai, H, Maibach, HI, Wilhelm, K. Marzulli and Maibach's dermatoxicology. 2007. (The definitive reference for dermatoxicology used by dermatologists and toxocologists for over 30 years.)

Kanerva, L, Elsner, P, Whalbert, JE, Maibach, HI. “Handbook of occupational dermatology”. 2000. (This is the most comprehensive book on occupational dermatology. The book addresses the epidemiology, treatment, prognosis and causes of occupational dermatological disease.)

Gattu, S, Rashid, RM, Khachemoune, A. “Self-induced skin lesions: a review of dermatitis arterfacta”. Cutis. vol. 84. 2009. pp. 247-51. (Addresses the methods patients use to cause the lesions and the difficulties associated with treatment of dermatitis artefacta.)

Carey, JD, Romero, EA. “Dermatitis artefacta [abstract]”. European Society for Dermatology and Psychiatry. 10th International Congress on Dermatology and Psychiatry. 2003. (This abstract argues that the terms dermatitis artefacta and dermatitis factitia are often used interchangeably, but the author argues that dermatitis artefacta is unique because the patients are willing to admit that the lesions are self-inflicted.)

Ale, IS, Maibach, MI. “Diagnostic approach in allergic and irritant contact dermatitis”. Expert Rev Clin Immunol. vol. 6. 2010. pp. 291-310. (Irritant contact dermatitis and allergic contact dermatitis are often difficult to differentiate based on clinical presentation. This paper compares and contrasts the two diseases and important clinical findings to properly diagnose the skin diseases.)

Clark, SC, Zirwas, MJ. “Management of occupational dermatitis”. Dermatol Clin. vol. 27. 2009. pp. 365-83. (Occupational dermatitis is the most common type of irritant contact dermatitis. Clark and Zirwas detail the important points of recognition, treatment, and prevention of occupational contact dermatitis. The risk factors, clinical presentation, pathogenesis, and treatment of both irritant and allergic contact dermatitis (ACD) are outlined.. The diagnosis and physical examination of OCD are further detailed, even addressing worker's compennal aerticle.sation, disability, and filing reports.)

Barlett, D. “Dermal exposure to hydrofluoric acid causing significant systemic toxicity”. J Emerg Nurs. vol. 30. 2004. pp. 317-3. (This article describes the systemic effects of dermal exposure to hydrofluoric acid (HF) and briefly describes the initial treatment protocol. Even minimal dermal exposures to hydrofluoric acid (HF) can have serious systemic implications resulting in morbidity and even death.)

Hogan, DJ, Dannaker, CJ, Maibach, HI. “The prognosis of contact dermatitis”. J Am Acad Dermatol. vol. 23. 1990. pp. 300-7. (There is a similarly poor prognosis for occupational, nonoccupational, irritant, and allergic contact dermatitis. This paper addresses whether various interventions, such as a change in occupation, would benefit the patients.)

Levin, C, Zhai, H, Bashir, S, Chew, A, Anigbogu, A, Stern, R, Maibach, H. “Efficacy of corticosteroids in acute experimental irritant contact dermatitis”. Skin Res and Tech. vol. 7. 2001. pp. 214-8. (This study focused on the efficacy of low- and medium-potency corticosteroids on irritant contact dermatitis. It was concluded that there were no significant benefits to the corticosteroid application subsequent to irritation; however, topical corticosteroids are continually used as a cornerstone of treatment in irritant dermatitis.)