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Pediatric Contact Dermatitis Workup

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

Approach Considerations

Patch testing may suggest or confirm the etiologic agent in allergic contact dermatitis.[14] Laboratory studies are generally of little value in proving a diagnosis of contact dermatitis. However, they may be of value in eliminating some disorders from the differential diagnosis.

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

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Patch Testing

By placing standard concentrations of common allergens or specific ingredients of an implicated product on the skin and leaving them covered for 2 days, one may identify the allergen. If the patient has been previously sensitized to one of the agents under occlusion, this reexposure produces the elicitation phase of a type IV hypersensitivity reaction resulting in pruritus, erythema, and vesiculation.

Anaphylaxis may occur shortly after application of antigens used in patch testing. This finding is particularly true when testing for latex allergy but may occur with exposure to other antigens.

Monitor patients for anaphylactic reactions to antigens used in patch testing. Appropriate resuscitation must be available should anaphylaxis occur during the early stages of patch testing. Patch testing is contraindicated in the setting of angioedema and/or contact-induced anaphylaxis and should be avoided in patients with contact urticaria.

Atopic patients are more susceptible to irritant patch test reactions, especially when testing with metals. This may lead to false-positive results from routine patch testing. In a study of 101 sets of twins, no correlation was found between positive patch test results and atopy.

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Dimethylgloxime (DMG) Spot Test

For patients with nickel allergy, a simple procedure exists to test jewelry for the presence of nickel. Trace amounts of nickel can be detected using the dimethylgloxime (DMG) spot test.

Two or 3 drops of 1% DMG and 10% hydroxide solution are placed on a white cotton-tipped applicator. The applicator tip is then rubbed against metallic areas of the jewelry. The appearance of a pink color on the applicator tip is a positive result and proof of the presence of nickel. This test is nondestructive. DMG test kits are inexpensive and available from many medical supply stores.

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Biopsy

Biopsies are of little diagnostic help in contact dermatitis. Most types of contact dermatitis show very similar pathologic changes, and allergic and irritant contact dermatitis may not be distinguished with certainty in all cases. However, skin biopsy findings may serve to eliminate some conditions included in the differential diagnosis.

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Histologic Findings

Histologic findings in contact dermatitis are not usually helpful in identifying the specific cause of the contact dermatitis. Findings in acute contact dermatitis include intercellular edema in the epidermis and vesiculation or blister formation.

Mast cells may be increased in urticarial reactions.

Chronic contact dermatitis shows signs of lichenification and varying degrees of nonspecific inflammation.

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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].

 
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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. 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.
 
 
 
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