Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Pediatric Contact Dermatitis Treatment & Management

  • Author: Nanette B Silverberg, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: May 13, 2014
 

Approach Considerations

Once the correct diagnosis has been established, many patients improve with adequate hygiene and avoidance of the contactant. Further therapy depends on the degree of involvement, duration, and presence or absence of secondary infection.

In acute contact dermatitis, contaminated clothing must be removed and the contactant rinsed from the skin with large quantities of water. 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.[15]

Acute irritant contact dermatitis from acids or alkalis should be treated with vigorous irrigation with water to remove the irritant and then should be treated as a thermal burn. Treatment of chronic contact dermatitis requires identification and removal of the contactant.

Chronic allergic contact dermatitis should be treated with midpotency topical corticosteroids and general skin care with emollients. Chronic irritant dermatitis is extremely common. Irritant dermatitis of the hands secondary to soaps or volatile solutions is exceedingly common in adolescents and adults.

Patients should be educated about the cause of the dermatitis and instructed in methods of skin protection and care with emollients.

Investigators have found that most people could be immunized against poison ivy through prescription pills; however, this procedure can take months to achieve a reasonable degree of hyposensitization and must be continued over a long period. Immunization can cause uncomfortable side effects and should only be considered for individuals, such as firefighters, who must live or work in areas where they come into constant contact with poison ivy.

The American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology have established a practice parameter for the management of contact dermatitis.[16]

Go to Irritant Contact Dermatitis, Allergic Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.

Next

Emergency Department Care

The definitive treatment of both irritant contact dermatitis and allergic contact dermatitis is the identification and removal of any potential causal agents. Emergency department treatment may include the following:

  • Topical soaks with cool tap water, Burow solution (1:40 dilution), or saline (1 tsp/pint)
  • Lukewarm water baths (antipruritic)
  • Oatmeal baths

Emollients (eg, white petrolatum, Eucerin) may be beneficial chronic cases.

Large vesicles may benefit from therapeutic drainage (but not removing the vesicle tops).[1] These lesions should then be covered with dressing soaked in Burow solution.

Previous
Next

Contactant Removal

In acute irritant dermatitis, the first goal must be to prevent further damage by removal of the irritant. Remove clothing and accessories that the contactant touched. Immediately rinse the site of both acid and alkali burns with large quantities of water. Acid burns can be treated with weak alkali solutions, such as sodium bicarbonate or soap solutions. If believed to be a poison, poison control can be consulted in the United States through the website http://poisonhelp.hrsa.gov/what-can-you-do/ or by calling 800-222-1222.

Following irrigation, alkalis (eg, soaps, detergents, bleaches, ammonia preparations, lye, drain pipe cleaners, toilet bowl and oven cleansers) may be buffered by rinsing the skin with a weak acid solution, such as vinegar or lemon juice. Alkalis cause tissue destruction by dissolving keratin. Oral and topical steroid therapies are of no benefit in irritant contact dermatitis.

Thoroughly wash skin exposed to significant allergens, such as poison ivy, and remove and wash contaminated clothing. Patients may be able to minimize or eliminate allergic contact dermatitis if the skin is adequately washed as soon as possible following exposure.

Previous
Next

Topical Nonsteroidal Therapy

Many cases of localized mild contact dermatitis respond well to cool compresses and adequate wound care. Cool wet soaks applied for 5-10 minutes followed by air-drying may significantly reduce serous drainage from the site. Clean water, isotonic sodium chloride solution, and Burow solution can all be used with good success. Application of topical calamine is usually of minimal benefit.

Gently clear the loose crusts from the affected sites and apply a thin coat of petroleum jelly (Vaseline) or antibacterial ointment. Most episodes of contact dermatitis do not require antibiotic therapy if treated promptly and if adequate wound care can be provided.

Secondary infection usually takes at least 2-3 days to develop. Initial yellow crusts are simply dried serum from ruptured bullous lesions. If a significant degree of purulent material is present, a wound culture may be performed and oral antibiotics may be of benefit. Adequate coverage for staphylococci and streptococci can usually be achieved with a 5- to 10-day course of erythromycin, dicloxacillin, or a cephalosporin.

Previous
Next

Topical Steroids

Low-strength topical steroids, such as hydrocortisone, may be effective in decreasing inflammation and symptoms associated with very mild contact dermatitis in infants. However, they are useless as therapy for significant areas of allergic contact dermatitis.

Potent topical steroids, such as clobetasol propionate (Temovate) or betamethasone dipropionate (Diprolene) applied twice daily for 1-2 weeks, are effective for treating small areas of moderate allergic contact dermatitis. Usage of a midpotency agent is often more appropriate in children for milder disease. In the setting of proven allergic contact dermatitis due to topical corticosteroids, the choice of product must be modified to avoid the allergen and known cross-reactive agents.

Topical steroid therapy is of no benefit in irritant contact dermatitis.

Previous
Next

Systemic Steroids

Systemic steroids are the mainstay of therapy in acute episodes of severe extensive allergic contact dermatitis. Without therapy, an episode of rhus dermatitis may be expected to persist as long as 3-4 weeks. Early adequate use of prednisone can significantly shorten this course.

The duration of prednisone therapy is generally 7-10 days, but severe episodes of allergic contact dermatitis may recur when therapy is stopped; thus, an additional few days of systemic therapy may be required. In otherwise healthy individuals, a tapering dose of prednisone is not required for short courses of systemic therapy (7-10 d). In the setting of proven allergic contact dermatitis due to topical corticosteroids, the choice of product must be modified to avoid the allergen and known cross-reactive agents.

In adolescents and adults, an alternative to oral therapy is a single intramuscular (IM) dose of 4 mg (1 mL) of betamethasone sodium phosphate (Celestone) mixed with 40-60 mg of triamcinolone (Kenalog). This provides rapid onset and prolonged action over 2-4 weeks.

Previous
Next

Antihistamines

Severe pruritus may respond to antihistamines. Popular choices include hydroxyzine (Atarax) or diphenhydramine (Benadryl).

Previous
Next

Deterrence/Prevention

Prevention of contact dermatitis is better than cure. The most important part of the treatment is to identify and eliminate further exposure to the causative agent.

Urushiol is the oily resin in poison ivy, poison sumac, and poison oak, which causes an allergic reaction. Keep in mind this resin can remain active for years on virtually any surface. Thoroughly wash everything that might have brushed against the plants, including clothing, shoes, tools, camping equipment, and pets.

Wearing a long-sleeved shirt, pants, gloves, and boots when in an infested area and bathing as soon as possible after exposure are effective methods to limit rhus dermatitis.

The only places in the United States where poison ivy is not found are areas above 4000 ft elevation, Alaska, Hawaii, and some desert areas of California and Nevada. Poison ivy usually grows east of the Rocky Mountains and in Canada. Poison oak grows in the western United States, Canada, and Mexico (western poison oak), and in the southeastern states (eastern poison oaks). Poison sumac grows in the eastern states and southern Canada.

Patients should learn to recognize poison ivy, poison sumac, and poison oak and have them removed from areas where children are likely to play. Several features of poison ivy, oak, and sumac are useful in identification.

Poison ivy and oak may be shrubs or climbing vines. All species of poison ivy and oak have 3 leaflets per leaf, hence the reminder, "Leaves of 3, let them be." The leaf stalk has a groove where it attaches to the branch. Blooms and fruits arise in the angle between the leaf and the branch. Young leaves frequently are reddish in color, and the mature fruit is tan or cream colored.

Poison sumac is a shrub or small tree usually 5-10 feet tall and grows in swampy areas or peat bogs. Poison sumac contains 7-13 paired leaflets in a row. The American Academy of Dermatology has handouts with color photographs available for purchase or viewing on their web site.

Poison ivy, poison sumac, and poison oak are most dangerous in the spring and summer when sap is plentiful. The leaves, branches, and trunk may show black marks where they have been injured, as the sap turns black after exposure to air.

Do not let pets run through wooded areas where poison ivy, poison sumac, and poison oak grow. After contacting these plants, pets may carry urushiol on their fur, causing contact dermatitis in family members who come in contact with the animal. Urushiol can travel in smoke if it burns in a fire; do not burn plants that look like poison ivy, poison sumac, or poison oak.

Previous
Next

Activity

Warm weather, hot showers, and activities vigorous enough to cause perspiration increase pruritus. Individuals with severe acute allergic contact dermatitis may be incapacitated temporarily

Previous
Next

Consultations

The following consultations may be indicated:

  • A primary care provider can treat most cases of contact dermatitis on an outpatient basis.
  • Deep chemical burns, extensive bullous reactions, or pulmonary symptoms related to inhaled agents may require admission and consultation as appropriate.
  • Refer patients who have recurrent episodes of dermatitis with unclear etiology to a dermatologist.
Previous
 
 
Contributor Information and Disclosures
Author

Nanette B Silverberg, MD Clinical Professor of Dermatology, Icahn School of Medicine at Mount Sinai; Chief, Pediatric Dermatology, Mt Sinai Health Systems, Mount Sinai St Luke's-Roosevelt Hospital and Mt Sinai Beth Israel Medical Centers

Nanette B Silverberg, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Society for Pediatric Dermatology, Women's Dermatologic Society, European Society for Pediatric Dermatology, Dermatology Foundation, American Association of University Women, Pediatric Dermatology Research Alliance, Vitiligo Support International, American Academy of Pediatrics, American Medical Association, American Medical Womens Association, Phi Beta Kappa, Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

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

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

Additional Contributors

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, American Osteopathic Association

Disclosure: Nothing to disclose.

Acknowledgements

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.

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

  2. Militello G, Jacob SE, Crawford GH. Allergic contact dermatitis in children. Curr Opin Pediatr. 2006 Aug. 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. Silny W, Bartoszak L, Jenerowicz D, Zukiewicz-Sobczak W, Gozdziewska M. Prevalence of contact allergy in children suffering from atopic dermatitis, seborrhoeic dermatitis and in healthy controls. Ann Agric Environ Med. 2013 Mar 25. 20(1):55-60. [Medline].

  5. Munivrana Skvorc H, Plavec D, Munivrana S, Skvorc M, Nogalo B, Turkalj M. Prevalence of and risk factors for the development of atopic dermatitis in schoolchildren aged 12-14 in northwest Croatia. Allergol Immunopathol (Madr). 2012 Dec 17. [Medline].

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

  7. Kennedy JL, Stallings AP, Platts-Mills TA, Oliveira WM, Workman L, James HR, et al. Galactose-a-1,3-galactose and Delayed Anaphylaxis, Angioedema, and Urticaria in Children. Pediatrics. 2013 Apr 8. [Medline].

  8. Salvaggio HL, Scheman AJ, Chamlin SL. Shock Treatment: Swimming Pool Contact Dermatitis. Pediatr Dermatol. 2012 Nov 7. [Medline].

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

  10. 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. 1997 Dec. 37(6):286-93. [Medline].

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

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

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

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

  15. Fonacier LS, Aquino MR, Mucci T. Current strategies in treating severe contact dermatitis in pediatric patients. Curr Allergy Asthma Rep. 2012 Dec. 12(6):599-606. [Medline].

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

 
Previous
Next
 
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. Many other foods can cause similar reactions, i.e. the phytophotodermatitis. 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 dilute concentrations of 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.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.