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Emergency and Acute Medicine – Contact Dermatitis
Overview and Basic Description
Contact dermatitis is an inflammatory skin condition caused by direct exposure to external substances and is broadly classified into irritant, allergic, and photocontact forms. Irritant contact dermatitis is the most common type and presents as an immediate eczematous eruption resulting from a superficial inflammatory process that primarily involves the epidermis. In this condition, the triggering substance directly damages the skin, producing a non-immunologic inflammatory reaction manifested by erythema, dryness, cracking, or fissuring. It typically occurs due to repeated exposure to mild irritants such as water, soaps, heat, or friction. Symptoms often develop gradually and include itching or burning sensations, with lesions that have indistinct borders. The hands are most commonly affected, and the skin may appear dry, red, rough, and occasionally vesiculated or fissured. Frequent irritants include cement, hair dyes, wet diapers, rubber gloves, shampoos, and repeated handwashing.
Allergic contact dermatitis is a delayed type IV hypersensitivity reaction that requires prior sensitization. In this form, exposure to an allergen triggers an immune-mediated response, leading to localized edema, erythema, vesicles, pruritus, or burning. Lesions usually correspond exactly to the area of contact, such as beneath a watchband. In previously sensitized individuals, symptoms typically appear within 12–48 hours, whereas primary exposure may require 14–21 days before clinical manifestations develop. Common allergens include nickel, gold, neomycin, bacitracin, preservatives, fragrances, dyes, and poison ivy.
Photocontact dermatitis occurs when an otherwise harmless substance on the skin interacts with ultraviolet light, producing an inflammatory reaction. This type of dermatitis does not occur without sunlight exposure and is commonly associated with shaving lotions, sunscreens, sulfa-containing ointments, and perfumes.
Pediatric Considerations
Allergic contact dermatitis is less common in children, particularly infants, compared with adults. In pediatric patients, the major sources of contact allergy include metals, shoes, preservatives, and fragrances found in cosmetics, topical medications, and plants. Diaper dermatitis represents the prototype of irritant contact dermatitis in children and results from prolonged exposure to urine and feces. Circumoral dermatitis is seen in infants and young children and may be triggered by certain foods through either irritant or allergic mechanisms.
Etiology and Risk Factors
Irritant contact dermatitis accounts for approximately 80% of all cases and may be caused by soaps, solvents, chemicals, certain foods, urine, feces, diapers, and continuous or repeated exposure to moisture such as frequent handwashing. Physical irritants including coarse paper, glass fibers, and wool may also provoke dermatitis. Shoe dermatitis is a common presentation and is typically identified by lesions limited to the distal dorsal surface of the foot while sparing the interdigital spaces.
Allergic contact dermatitis may result from exposure to plants such as poison ivy, poison oak, and poison sumac, collectively referred to as rhus dermatitis, which is the most common form of allergic contact dermatitis in North America. The reaction is caused by oleoresin urushiol and may occur through direct contact with the plant or indirectly via contaminated pets, clothing, or smoke from burning leaves. Lesions may appear up to three days after exposure in sensitized individuals and may persist for as long as three weeks. The fluid contained within vesicles is not contagious and does not produce new lesions; however, urushiol oil on clothing or animal fur remains contagious until removed. Other allergic causes include cement, which may result in severe alkali burns with prolonged exposure, metals—especially nickel—solvents, epoxy, chemicals in rubber or leather, lotions, cosmetics, topical medications such as neomycin, hydrocortisone, benzocaine, and parabens, and certain foods. The ability to respond to specific antigens is likely influenced by genetic factors.
Photodermatitis represents an inflammatory reaction caused by exposure to an irritant, often plant sap, in combination with sunlight and typically does not occur in the absence of ultraviolet exposure.
Clinical Features and Diagnostic Evaluation
Assessment begins with a detailed history focusing on the date of onset, time course, pattern and distribution of lesions, relationship to occupational or work exposures, presence or absence of pruritus, mucosal involvement, and recent exposure to new products such as soaps, lotions, cosmetics, foods, medications, or jewelry. Physical examination should emphasize the morphology and distribution of the rash. Acute lesions are characterized by erythema and pruritus and may be accompanied by edema, papules, vesicles, bullae, serous discharge, or crusting. Subacute lesions demonstrate less prominent vesiculation, while chronic lesions may present with scaling, lichenification, pigmentation changes, or fissuring, often with little or no vesiculation and a characteristic distribution pattern.
There are no specific laboratory studies or imaging modalities that are routinely helpful in the emergency department for diagnosing contact dermatitis. Patch testing is generally not performed acutely and should be arranged through referral to an allergist or immunologist. When a fungal infection is suspected, a Wood lamp examination may be used to assess for fluorescence suggestive of tinea.
Differential Diagnosis
Conditions that may mimic contact dermatitis include atopic dermatitis, often associated with a family history of atopy; seborrheic dermatitis with greasy, scaly lesions; nummular dermatitis characterized by coin-shaped plaques; and intertrigo involving areas where skin surfaces are in apposition such as the axillae and groin. Other considerations include infectious eczematous dermatitis with secondary bacterial infection, usually due to Staphylococcus aureus; cellulitis presenting as a warm, painful, blanching lesion; impetigo with yellow crusting; scabies with intensely pruritic interdigital tracks; psoriasis with well-demarcated silvery plaques affecting extensor surfaces, scalp, or genital region; herpes simplex infection with painful grouped vesicles; herpes zoster following a dermatomal distribution; bullous pemphigoid with diffuse bullae; tinea with maximal involvement at the margins and Wood lamp fluorescence; pityriasis alba with asymptomatic hypopigmented lesions; urticaria with pruritic wheals and surrounding erythema; acrodermatitis enteropathica due to zinc deficiency, associated with failure to thrive, diarrhea, and alopecia; dyshidrotic eczema; drug-induced rashes; Stevens–Johnson syndrome; toxic epidermal necrolysis; and erythema nodosum.
Management in the Emergency Department
Initial stabilization is rarely required unless there is significant concomitant pathology. Treatment is primarily symptomatic and includes gentle cleansing of the affected area with mild soap and water, removal and avoidance of the offending agent, and washing of contaminated clothing. Cool, wet compresses are particularly effective during the acute blistering phase. Antipruritic therapy may include topical agents such as calamine lotion and topical corticosteroids, although corticosteroids do not penetrate intact blisters and benzocaine- or hydrocortisone-containing products should be avoided due to the risk of further sensitization. Systemic therapy may include antihistamines and corticosteroids when indicated. Aluminum acetate (Burrow solution) may be applied to weeping surfaces.
For irritant contact dermatitis, management focuses on removal of the offending agent, thorough washing with soap and warm water, reduction of wet–dry cycles such as frequent handwashing, and use of alcohol-based cleansers to decrease repetitive trauma. Bland emollients are recommended, and topical corticosteroids of medium to high potency, preferably in ointment form, may be used for severe cases on the hands twice daily for several weeks.
Allergic contact dermatitis is treated with topical corticosteroids applied twice daily for two to three weeks, with potency adjusted by location: low potency for the face, medium potency for the arms, legs, and trunk, and high potency for the hands and feet. Oral corticosteroids may be required for severe reactions. In rhus dermatitis, additional measures include washing all clothing and pets that may have come into contact with the plant, as the oil remains contagious. Oatmeal baths may provide symptomatic relief, and aseptic aspiration of tense bullae can reduce discomfort. Severe reactions involving more than 10% of total body surface area require systemic corticosteroids for two to three weeks with a gradual taper, as premature discontinuation may result in rapid rebound of symptoms. Shoe dermatitis management includes wearing open-toe, canvas, or vinyl shoes, controlling perspiration through frequent sock changes, and using absorbent powders. Diaper dermatitis management includes topical zinc oxide, petrolatum, or aquaphor and frequent diaper changes after each soiling.
Medications
Systemic therapy may include H1-receptor antagonists from both first- and second-generation antihistamines. Cetirizine may be given at 5–10 mg orally daily in adults and children older than six years, with pediatric dosing of 2.5 mg once or twice daily for ages two to six years. Diphenhydramine may be administered at 25–50 mg intravenously, intramuscularly, or orally every six hours as needed, with pediatric dosing of 5 mg/kg per 24 hours divided every six hours. Fexofenadine may be used at 60 mg orally twice daily or 180 mg once daily in adults, with pediatric dosing of 30 mg twice daily for children aged six to twelve years. Hydroxyzine may be given at 25–50 mg orally or intramuscularly up to four times daily, with weight-based pediatric dosing. Loratadine may be administered at 10 mg orally twice daily. For refractory pruritus, doxepin 75 mg orally daily may be effective.
Systemic corticosteroid therapy includes prednisone at 40–60 mg orally daily in adults, with pediatric dosing of 1–2 mg/kg per day to a maximum of 80 mg, administered once or divided twice daily. Topical therapies include aluminum acetate solution applied for 20 minutes three times daily until the skin is dry, calamine lotion every six hours as needed, and topical corticosteroids such as triamcinolone ointment, cream, or lotion at concentrations of 0.025% or 0.1% applied three to four times daily. Topical corticosteroids should not be applied to the face or eyelids. First-line therapy consists of topical corticosteroids and oral antihistamines, while oral corticosteroids are considered second-line treatment.
Disposition and Follow-Up
Hospital admission is rarely indicated and is generally reserved for patients with severe systemic reactions or significant secondary infections. Patients may be discharged once symptomatic relief is achieved and adequate outpatient follow-up is arranged. Follow-up with a primary care physician is recommended within two to three days for reassessment. Patients should be instructed to return to the emergency department if they develop facial swelling, difficulty breathing, or mucosal involvement that limits oral intake.
Clinical Pearls and Pitfalls
Effective management requires prompt removal of the offending agent. Clinicians should remain vigilant for progression to systemic anaphylaxis, particularly in cases involving latex exposure, and should monitor for concurrent bacterial infections. In rhus dermatitis, lesions are no longer contagious after washing with soap and water; however, all clothing and animals that may have been exposed must be thoroughly cleaned, as the oil remains contagious until removed.
Overview and Basic Description
Contact dermatitis is an inflammatory skin condition caused by direct exposure to external substances and is broadly classified into irritant, allergic, and photocontact forms. Irritant contact dermatitis is the most common type and presents as an immediate eczematous eruption resulting from a superficial inflammatory process that primarily involves the epidermis. In this condition, the triggering substance directly damages the skin, producing a non-immunologic inflammatory reaction manifested by erythema, dryness, cracking, or fissuring. It typically occurs due to repeated exposure to mild irritants such as water, soaps, heat, or friction. Symptoms often develop gradually and include itching or burning sensations, with lesions that have indistinct borders. The hands are most commonly affected, and the skin may appear dry, red, rough, and occasionally vesiculated or fissured. Frequent irritants include cement, hair dyes, wet diapers, rubber gloves, shampoos, and repeated handwashing.
Allergic contact dermatitis is a delayed type IV hypersensitivity reaction that requires prior sensitization. In this form, exposure to an allergen triggers an immune-mediated response, leading to localized edema, erythema, vesicles, pruritus, or burning. Lesions usually correspond exactly to the area of contact, such as beneath a watchband. In previously sensitized individuals, symptoms typically appear within 12–48 hours, whereas primary exposure may require 14–21 days before clinical manifestations develop. Common allergens include nickel, gold, neomycin, bacitracin, preservatives, fragrances, dyes, and poison ivy.
Photocontact dermatitis occurs when an otherwise harmless substance on the skin interacts with ultraviolet light, producing an inflammatory reaction. This type of dermatitis does not occur without sunlight exposure and is commonly associated with shaving lotions, sunscreens, sulfa-containing ointments, and perfumes.
Pediatric Considerations
Allergic contact dermatitis is less common in children, particularly infants, compared with adults. In pediatric patients, the major sources of contact allergy include metals, shoes, preservatives, and fragrances found in cosmetics, topical medications, and plants. Diaper dermatitis represents the prototype of irritant contact dermatitis in children and results from prolonged exposure to urine and feces. Circumoral dermatitis is seen in infants and young children and may be triggered by certain foods through either irritant or allergic mechanisms.
Etiology and Risk Factors
Irritant contact dermatitis accounts for approximately 80% of all cases and may be caused by soaps, solvents, chemicals, certain foods, urine, feces, diapers, and continuous or repeated exposure to moisture such as frequent handwashing. Physical irritants including coarse paper, glass fibers, and wool may also provoke dermatitis. Shoe dermatitis is a common presentation and is typically identified by lesions limited to the distal dorsal surface of the foot while sparing the interdigital spaces.
Allergic contact dermatitis may result from exposure to plants such as poison ivy, poison oak, and poison sumac, collectively referred to as rhus dermatitis, which is the most common form of allergic contact dermatitis in North America. The reaction is caused by oleoresin urushiol and may occur through direct contact with the plant or indirectly via contaminated pets, clothing, or smoke from burning leaves. Lesions may appear up to three days after exposure in sensitized individuals and may persist for as long as three weeks. The fluid contained within vesicles is not contagious and does not produce new lesions; however, urushiol oil on clothing or animal fur remains contagious until removed. Other allergic causes include cement, which may result in severe alkali burns with prolonged exposure, metals—especially nickel—solvents, epoxy, chemicals in rubber or leather, lotions, cosmetics, topical medications such as neomycin, hydrocortisone, benzocaine, and parabens, and certain foods. The ability to respond to specific antigens is likely influenced by genetic factors.
Photodermatitis represents an inflammatory reaction caused by exposure to an irritant, often plant sap, in combination with sunlight and typically does not occur in the absence of ultraviolet exposure.
Clinical Features and Diagnostic Evaluation
Assessment begins with a detailed history focusing on the date of onset, time course, pattern and distribution of lesions, relationship to occupational or work exposures, presence or absence of pruritus, mucosal involvement, and recent exposure to new products such as soaps, lotions, cosmetics, foods, medications, or jewelry. Physical examination should emphasize the morphology and distribution of the rash. Acute lesions are characterized by erythema and pruritus and may be accompanied by edema, papules, vesicles, bullae, serous discharge, or crusting. Subacute lesions demonstrate less prominent vesiculation, while chronic lesions may present with scaling, lichenification, pigmentation changes, or fissuring, often with little or no vesiculation and a characteristic distribution pattern.
There are no specific laboratory studies or imaging modalities that are routinely helpful in the emergency department for diagnosing contact dermatitis. Patch testing is generally not performed acutely and should be arranged through referral to an allergist or immunologist. When a fungal infection is suspected, a Wood lamp examination may be used to assess for fluorescence suggestive of tinea.
Differential Diagnosis
Conditions that may mimic contact dermatitis include atopic dermatitis, often associated with a family history of atopy; seborrheic dermatitis with greasy, scaly lesions; nummular dermatitis characterized by coin-shaped plaques; and intertrigo involving areas where skin surfaces are in apposition such as the axillae and groin. Other considerations include infectious eczematous dermatitis with secondary bacterial infection, usually due to Staphylococcus aureus; cellulitis presenting as a warm, painful, blanching lesion; impetigo with yellow crusting; scabies with intensely pruritic interdigital tracks; psoriasis with well-demarcated silvery plaques affecting extensor surfaces, scalp, or genital region; herpes simplex infection with painful grouped vesicles; herpes zoster following a dermatomal distribution; bullous pemphigoid with diffuse bullae; tinea with maximal involvement at the margins and Wood lamp fluorescence; pityriasis alba with asymptomatic hypopigmented lesions; urticaria with pruritic wheals and surrounding erythema; acrodermatitis enteropathica due to zinc deficiency, associated with failure to thrive, diarrhea, and alopecia; dyshidrotic eczema; drug-induced rashes; Stevens–Johnson syndrome; toxic epidermal necrolysis; and erythema nodosum.
Management in the Emergency Department
Initial stabilization is rarely required unless there is significant concomitant pathology. Treatment is primarily symptomatic and includes gentle cleansing of the affected area with mild soap and water, removal and avoidance of the offending agent, and washing of contaminated clothing. Cool, wet compresses are particularly effective during the acute blistering phase. Antipruritic therapy may include topical agents such as calamine lotion and topical corticosteroids, although corticosteroids do not penetrate intact blisters and benzocaine- or hydrocortisone-containing products should be avoided due to the risk of further sensitization. Systemic therapy may include antihistamines and corticosteroids when indicated. Aluminum acetate (Burrow solution) may be applied to weeping surfaces.
For irritant contact dermatitis, management focuses on removal of the offending agent, thorough washing with soap and warm water, reduction of wet–dry cycles such as frequent handwashing, and use of alcohol-based cleansers to decrease repetitive trauma. Bland emollients are recommended, and topical corticosteroids of medium to high potency, preferably in ointment form, may be used for severe cases on the hands twice daily for several weeks.
Allergic contact dermatitis is treated with topical corticosteroids applied twice daily for two to three weeks, with potency adjusted by location: low potency for the face, medium potency for the arms, legs, and trunk, and high potency for the hands and feet. Oral corticosteroids may be required for severe reactions. In rhus dermatitis, additional measures include washing all clothing and pets that may have come into contact with the plant, as the oil remains contagious. Oatmeal baths may provide symptomatic relief, and aseptic aspiration of tense bullae can reduce discomfort. Severe reactions involving more than 10% of total body surface area require systemic corticosteroids for two to three weeks with a gradual taper, as premature discontinuation may result in rapid rebound of symptoms. Shoe dermatitis management includes wearing open-toe, canvas, or vinyl shoes, controlling perspiration through frequent sock changes, and using absorbent powders. Diaper dermatitis management includes topical zinc oxide, petrolatum, or aquaphor and frequent diaper changes after each soiling.
Medications
Systemic therapy may include H1-receptor antagonists from both first- and second-generation antihistamines. Cetirizine may be given at 5–10 mg orally daily in adults and children older than six years, with pediatric dosing of 2.5 mg once or twice daily for ages two to six years. Diphenhydramine may be administered at 25–50 mg intravenously, intramuscularly, or orally every six hours as needed, with pediatric dosing of 5 mg/kg per 24 hours divided every six hours. Fexofenadine may be used at 60 mg orally twice daily or 180 mg once daily in adults, with pediatric dosing of 30 mg twice daily for children aged six to twelve years. Hydroxyzine may be given at 25–50 mg orally or intramuscularly up to four times daily, with weight-based pediatric dosing. Loratadine may be administered at 10 mg orally twice daily. For refractory pruritus, doxepin 75 mg orally daily may be effective.
Systemic corticosteroid therapy includes prednisone at 40–60 mg orally daily in adults, with pediatric dosing of 1–2 mg/kg per day to a maximum of 80 mg, administered once or divided twice daily. Topical therapies include aluminum acetate solution applied for 20 minutes three times daily until the skin is dry, calamine lotion every six hours as needed, and topical corticosteroids such as triamcinolone ointment, cream, or lotion at concentrations of 0.025% or 0.1% applied three to four times daily. Topical corticosteroids should not be applied to the face or eyelids. First-line therapy consists of topical corticosteroids and oral antihistamines, while oral corticosteroids are considered second-line treatment.
Disposition and Follow-Up
Hospital admission is rarely indicated and is generally reserved for patients with severe systemic reactions or significant secondary infections. Patients may be discharged once symptomatic relief is achieved and adequate outpatient follow-up is arranged. Follow-up with a primary care physician is recommended within two to three days for reassessment. Patients should be instructed to return to the emergency department if they develop facial swelling, difficulty breathing, or mucosal involvement that limits oral intake.
Clinical Pearls and Pitfalls
Effective management requires prompt removal of the offending agent. Clinicians should remain vigilant for progression to systemic anaphylaxis, particularly in cases involving latex exposure, and should monitor for concurrent bacterial infections. In rhus dermatitis, lesions are no longer contagious after washing with soap and water; however, all clothing and animals that may have been exposed must be thoroughly cleaned, as the oil remains contagious until removed.
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