eMedicine Specialties > Ophthalmology > Dermatologic Disorders
Dermatitis, Contact
Updated: Nov 21, 2006
Introduction
Background
Contact dermatitis is probably the most commonly encountered immunologic disease by dermatologists. In 1895, Jadassohn described contact allergy to mercury and is regarded as the father of contact dermatitis. Prior to this described observation, few physicians recognized the concept of contact hypersensitivity.
The field began to grow in the 1920s with further studies describing the phenomenon and has culminated in the modern era, present day, when volumes of information on the topic are available. Entire books are available listing compounds that have been noted to cause the disease process. An example is Fisher's Contact Dermatitis, a 1,117 page text that breaks down the subject by occupation, plants, and every other conceivable classification.
Pathophysiology
Contact dermatitis is due to either allergic reaction or, more commonly, irritant exposure. Irritants usually are acids, alkalis, resins, or other chemicals and frequently are found in drugs, dyes, plants, preservatives, cosmetics, and metals. Excessive moisture also may act as an irritant.
Irritants (as small molecular weight haptens) form a complete antigen by binding to dermal proteins and causing a sensitization (of T lymphocytes) on first contact and an inflammatory response on subsequent exposure. Allergic contact dermatitis occurs in sensitized individuals through the mechanism of type IV, cell-mediated immunity. Reexposure to sensitized antigens causes delayed hypersensitivity.
Frequency
United States
Incidence is extremely common; estimates vary.
Race
No racial predisposition seems to exist.
Sex
Men and women appear to be affected equally.
Age
With regard to irritant contact dermatitis, all age groups appear to be affected in similar proportions. Allergic contact dermatitis generally does not occur in children younger than 5 years or in elderly individuals because their immune systems do not respond to antigens in this manner.
Clinical
History
Patients will have a history of exposure to an offending substance; in ophthalmology, it is most commonly topical ocular medications, such as neomycin, atropine, and preservatives (frequently benzalkonium chloride), and glaucoma medications. Of course, many common household items can be the culprit. In general, patients often have a history of exposure, through work or recreation, to a different environment than usual.
Physical
- Early contact dermatitis is characterized by erythema, edema, chemosis, eyelid induration, and exudative vesicular lesions. Chronic scaling, crusting, eczema, and lichenification occur.
- Areas of exposure to the offending substance are frequently the hands, face, arms, legs, and neck, and may give clues to the origin of the irritant or allergen.
- Irritant lesions usually occur 1-2 hours after exposure. Allergic lesions do not usually appear until 48 hours after exposure.
- In the eye, conjunctivitis with a papillary or cobblestone appearance, chemosis, injection, and tearing frequently occur.
- Blepharitis also may occur and may be accompanied by a keratitis. This keratitis frequently is appreciated as small yellow opacities near the limbus, often described as a fine punctate keratitis.
- Patients whose rash occurs in an elongated or linear pattern often will have had exposure to a plant, such as poison ivy or oak.
Causes
Irritant and/or allergen exposure causes contact dermatitis. Frequently encountered agents that may be responsible include drugs, soaps, lotions, cosmetics, metals, foods, dyes, preservatives, and plants. The list is almost endless, but the offending agent will have been encountered within 72 hours (if an allergic reaction) and within a few hours (if an irritant).
More on Dermatitis, Contact |
 Overview: Dermatitis, Contact |
| Differential Diagnoses & Workup: Dermatitis, Contact |
| Treatment & Medication: Dermatitis, Contact |
| Follow-up: Dermatitis, Contact |
| References |
| Next Page » |
References
Ayala F, Fabbrocini G, Bacchilega R. Eyelid dermatitis: an evaluation of 447 patients. Am J Contact Dermat. Jun 2003;14(2):69-74. [Medline].
Cohen DE. Contact dermatitis: a quarter century perspective. J Am Acad Dermatol. Jul 2004;51(1 Suppl):S60-3. [Medline].
Friedlander MH. Contact dermatitis. In: Current Ocular Therapy. 5th ed. Elsevier Science; 2000:143-146.
Garrott HM, Walland MJ. Glaucoma from topical corticosteroids to the eyelids. Clin Experiment Ophthalmol. Apr 2004;32(2):224-6. [Medline].
Guin JD. Eyelid dermatitis: experience in 203 cases. J Am Acad Dermatol. Nov 2002;47(5):755-65. [Medline].
Kanski JJ. Disorders of the conjunctiva. In: Clinical Ophthalmology: A Systematic Approach. 4th ed. Elsevier Science; 1999:69-75.
Kulkarni PS, Meredith TA. Steroids in ocular therapy, antiallergic therapies. In: Zimmerman TJ, ed. Textbook of Ocular Pharmacology. Lippincott Williams & Wilkins; 1997:61-74, 363-85, 609-33, 683-701, 801-4.
Kutting B, Brehler R, Traupe H. Allergic contact dermatitis in children: strategies of prevention and risk management. Eur J Dermatol. Mar-Apr 2004;14(2):80-5. [Medline].
Kwan TH. Spongiotic dermatitis. In: Textbook of Dermatopathology. McGraw-Hill Co; 1998:17-32.
Manni G, Centofanti M, Sacchetti M. Demographic and clinical factors associated with development of brimonidine tartrate 0.2%-induced ocular allergy. J Glaucoma. Apr 2004;13(2):163-7. [Medline].
Marks JG, Martini MC. Contact dermatitis and contact urticaria. In: Principle and Practice of Dermatology. 2nd ed. Churchill Livingstone; 1996:419-427.
Rietschel RL, Fowler JF. Fisher's Contact Dermatitis. 4th ed. Lippincott Williams & Wilkins; 1995.
Roy FH. Ocular Differential Diagnosis. 6th ed. Lippincott Williams & Wilkins; 2000.
Weisbecker CA, Fraunfelder FT, Rhee D. Physicians' Desk Reference for Ophthalmology. 28th ed. Medical Economics Co; 2000.
Further Reading
Keywords
contact allergy, contact sensitivity, dermatitis venenata
