Pediatric Contact Dermatitis Medication

  • Chief Editor: Dirk M Elston, MD   more...
 
Updated: May 2, 2011
 

Medication Summary

Therapy depends on the etiology and severity of contact dermatitis. Mild-to-moderate acute allergic contact dermatitis responds to topical care with astringents in a wet compress, topical corticosteroids, and systemic antipruritics. Acute severe allergic contact dermatitis with marked edema and bullae should receive the same treatment but may also require the addition of systemic corticosteroids.

Chronic allergic contact dermatitis should be treated with midpotency topical corticosteroids and general skin care with emollients.

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Wet compresses with an astringent

Class Summary

These agents are used to reduce pain, pruritus, and serous drainage in acute weeping contact dermatitis.

Aluminum acetate solution (Burow solution, Domeboro)

 

Moist compresses are soothing, have a mild antipruritic effect, reduce serous drainage, and gently débride the wound. They are effective in the early stages of acute contact dermatitis when serous drainage is most severe.

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Emollients

Class Summary

These agents may be used as adjunctive treatment to moisturize dry skin in subacute and chronic contact dermatitis.

Eucerin, Lubriderm, Moisturel, Vaseline Intensive Care

 

Numerous emollients are available as creams, ointments, or lotions. Use ointments on dry or cracked skin and creams on inflamed or weeping lesions. Most patients prefer creams. These may be helpful in subacute and chronic contact dermatitis because they help add moisture to skin, minimize moisture loss, or both.

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Antihistamines

Class Summary

These agents may be used as adjunctive therapy to relieve pruritus. They are used to treat minor allergic reactions and anaphylaxis and may be used to pretreat patients with prior documentation of minor allergic reactions. These agents may control itching by blocking effects of endogenously released histamine.

Hydroxyzine HCl (Vistaril)

 

Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in subcortical region of the central nervous system. This agent is available in 10 mg/5 mL syrup and as 10- and 25-mg tablets.

Diphenhydramine (Benadryl, Allerdryl)

 

Diphenhydramine is used for symptomatic relief of allergic symptoms caused by released histamine.

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Topical corticosteroids

Class Summary

These agents decrease the inflammatory reaction associated with allergic contact dermatitis.

Triamcinolone topical (Triderm, Kenalog)

 

Use ointments on dry or cracked skin and creams on inflamed or weeping lesions. Most patients prefer creams. A moderate-potency topical corticosteroid, triamcinolone is available in both ointment (0.1%) and cream (0.1% or 0.5%). This agent decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.

Hydrocortisone topical (Cortaid, Dermarest, Westcort)

 

Lower-potency topical steroids such as hydrocortisone are useful on the face and intertriginous areas.

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Superpotent topical corticosteroids

Class Summary

Low- or moderate-strength topical corticosteroids are useless as therapy for moderate-to-severe allergic contact dermatitis. Superpotent topical corticosteroids, such as clobetasol propionate (Temovate) or betamethasone dipropionate (Diprolene), applied 2-3 times daily for 1-2 weeks may be effective in small areas of acute allergic contact dermatitis or in lichenified areas of chronic contact dermatitis.

Clobetasol propionate (Temovate)

 

Clobetasol decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Betamethasone dipropionate (Diprolene, Celestone, Luxiq)

 

Betamethasone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

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Systemic corticosteroids

Class Summary

These agents are reserved for severe cases of allergic contact dermatitis with involvement of more than 20% of the total body surface area (TBSA), significant bullae, or significant facial involvement. They have anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. Glucocorticoids cause profound and varied metabolic effects and modify the body's immune response.

Prednisone (Deltasone)

 

Approximately 7-10 d of therapy is usually adequate and does not require a tapering dosage schedule. Lesions occasionally recur following a course of therapy, and an additional few days of therapy may be required.

Prednisone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Prednisolone (Pedia-Pred, Delta-Cortef)

 

Prednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Betamethasone sodium phosphate (Celestone) mixed with triamcinolone (Kenalog)

 

In adolescents and adults, an alternative to oral therapy is an IM dose of betamethasone sodium phosphate (Celestone) mixed with triamcinolone (Kenalog). This provides rapid onset and prolonged action over 2-4 weeks.

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Barrier products

Class Summary

Barrier creams, such as zinc oxide or Desenex, are common effective agents to treat or prevent irritant diaper dermatitis. In the past, barrier creams or preexposure treatments offered little hope for protection from poison oak and ivy. However, new over-the-counter products, such as a lotion containing bentoquatam (IvyBlock), may offer some protection. Bentoquatam creates a clay-like barrier on the skin that protects against urushiol, the oily resin in poison ivy, oak, and sumac.

Bentoquatam is not a replacement for accepted protective devices, such as gloves, boots, and clothing. When exposure cannot be avoided completely, barrier products may protect areas of exposed skin, such as the neck and face.

Bentoquatam (Ivy block)

 

Zinc oxide provides relief of minor skin irritations and may provide a barrier against future exposures to irritants and allergens.

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Contributor Information and Disclosures
Coauthor(s)

Mark A Crowe, MD  Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine

Mark A Crowe, MD is a member of the following medical societies: American Academy of Dermatology and North American Clinical Dermatologic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Kevin P Connelly, DO  Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University School of Medicine; Medical Director, Paws for Health Pet Visitation Program of the Richmond SPCA; Pediatric Emergency Physician, Emergency Consultants Inc, Chippenham Medical Center

Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Department of Dermatology, Geisinger Medical Center

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

References
  1. Lee PW, Elsaie ML, Jacob SE. Allergic contact dermatitis in children: common allergens and treatment: a review. Curr Opin Pediatr. Aug 2009;21(4):491-8. [Medline].

  2. Militello G, Jacob SE, Crawford GH. Allergic contact dermatitis in children. Curr Opin Pediatr. Aug 2006;18(4):385-90. [Medline].

  3. Fisher AA, Rietschel RL, Fowler JF. Fisher's Contact Dermatitis. 4th ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 1995.

  4. de Lagrán ZM, de Frutos FJ, de Arribas MG, Vanaclocha-Sebastián F. Contact urticaria to raw potato. Dermatol Online J. May 15 2009;15(5):14. [Medline].

  5. Clemmensen O, Hjorth N. Perioral contact urticaria from sorbic acid and benzoic acid in a salad dressing. Contact Dermatitis. Jan 1982;8(1):1-6. [Medline].

  6. Brasch J, Geier J. Patch test results in schoolchildren. Results from the Information Network of Departments of Dermatology (IVDK) and the German Contact Dermatitis Research Group (DKG). Contact Dermatitis. Dec 1997;37(6):286-93. [Medline].

  7. Warshaw E, Lee G, Storrs FJ. Hand dermatitis: a review of clinical features, therapeutic options, and long-term outcomes. Am J Contact Dermat. Sep 2003;14(3):119-37. [Medline].

  8. Raikhlin-Eisenkraft B. Contact dermatitis from occupation-induced injury. Isr Med Assoc J. May 2009;11(5):322. [Medline].

  9. Litvinov IV, Sugathan P, Cohen BA. Recognizing and treating toilet-seat contact dermatitis in children. Pediatrics. Feb 2010;125(2):e419-22. [Medline].

  10. Pigatto P, Martelli A, Marsili C, Fiocchi A. Contact dermatitis in children. Ital J Pediatr. Jan 13 2010;36:2. [Medline]. [Full Text].

  11. American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology. Contact dermatitis: a practice parameter. Ann Allergy Asthma Immunol. Sep 2006;97(3 Suppl 2):S1-38. [Medline].

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Dry, fissured, pruritic eczema is frequently the result of excessive washing and very low humidity in cold climates. Irritant contact dermatitis is due to direct injury of the skin. In this patient, frequent handwashing and use of soap is the cause of damage to the protective layers of the upper epidermis. Patients should be educated about the cause of the dermatitis and instructed in methods of skin protection and care with emollients.
Nickel is the most frequent contact allergen in females older than 8 years, and allergy occurs in as many as 25% of females 14 years or older. Allergens, such as nickel, are impossible to completely avoid. Exposure can be reduced with careful instruction, but occult exposures may produce chronic or recurrent symptoms. Nickel in the watch and watch band produced this episode of allergic contact dermatitis.
Allergic reactions to rubber products are usually caused by antioxidants and accelerators added in the manufacturing process, rather than the rubber itself. Antioxidants help preserve the rubber, and accelerators help in the vulcanization process. Exposure to rubber in gloves, shoes, undergarments, tires, heavy-duty rubber goods, and sport goggles is common.
The typical eruption from poison ivy includes erythema, edema, papules, vesicles, and bullae. Linear streaks as in this patient are characteristic but are not always present. Initial yellow crusts are dried serum from ruptured bullous lesions and not evidence of infection. Oleoresin (urushiol), which exudes from damaged areas of poison ivy, poison oak, and poison sumac, turns black after exposure to air. Fresh oleoresin on the skin dries and may be observed as black smudges or spots.
When limes are squeezed into beverages, excess juice remains on the skin. Sun exposure of this lime juice produces areas of dermatitis or hyperpigmentation. Perfumes are also common sources of photo contact dermatitis.
Most common moisturizers contain various additives and preservatives. The list of ingredients on this bottle is not uncommon, and most of these agents are capable of causing allergic contact dermatitis. Patch testing with the individual ingredients can be used to identify the agent that is a problem for any particular patient.
Areas of acute contact dermatitis respond well to cool compresses and wound care. Moist compresses are soothing, have a mild antipruritic effect, reduce serous drainage, and gently debride the wound. Clean water, isotonic sodium chloride solution, and Burow solution all can be used. Compresses should be kept moist at all times. Wet-to-dry compresses are painful and destroy fragile tissues. Following moist compress applications for 5-10 minutes, affected sites should be gently cleared of loose crusts and a thin coat of Vaseline or antibacterial ointment should be applied.
Urticaria, also known as hives or whelps, involves edematous pale or pink plaques. Agents can produce urticaria by immunologic reactions, by nonimmunologic reactions, or by unknown mechanisms. Nonimmunologic reactions are most common. Other types of environmentally associated urticaria must be excluded. This is an example of cold urticaria produced by application of an ice cube to the dorsum of the arm.
Prolonged use of moderate- to high-potency topical steroids may cause skin atrophy or steroid acne. This patient used a moderate-strength steroid, triamcinolone 0.1%, in this area for several weeks. Steroid acne, also called steroid rosacea, has a classic appearance with monomorphic erythematous papules. If the steroid is discontinued, the condition usually worsens. Patients must understand that symptoms worsen before they improve, and several weeks or months are required to taper off this steroid.
This purpuric reaction was noted after application of eutectic mixture of local anesthetics (EMLA) for 1 hour. EMLA cream is widely used as a local anesthetic for superficial procedures. Blanching and redness are commonly observed side effects. Dramatic purpuric reactions to EMLA, as in this patient, have been reported. Patch test results in these patients with the individual ingredients of EMLA cream, EMLA cream itself, placebo cream, and Tegaderm are negative. Apparently, the purpuric reaction is not of an allergic nature, but the cream may have a toxic effect on the capillary endothelium.
 
 
 
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