eMedicine Specialties > Ophthalmology > Dermatologic Disorders

Dermatitis, Contact

R Scott Lowery, MD, Assistant Professor of Ophthalmology, Department of Pediatric Ophthalmology and Strabismus, University of Arkansas for Medical Center, Arkansas Children's Hospital

Updated: Oct 30, 2009

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.¹

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).^2,3,4,5

Recent studies have shown an increase in positive patch test reactions to carbamates, balsam of Peru, thimerosal, formaldehyde, imidazolidinyl urea, and methyldibromoglutaronitrile.⁶ The rates of positive reactions to Dimethylol dimethyl (DMDM) hydantoin, diazolidinyl urea, and methylchloroisothiazolone/methylisothiazolone remained unchanged. All other antigens were noted to decrease during the studied time period.

Differential Diagnoses

Workup

Other Tests

Patch testing is the criterion standard for diagnosing contact dermatitis. A small portion of the suspected offending agent is placed on the skin and patched for 48 hours. A low dose of the test substance is used to avoid irritation as much as possible. Allergic responses may take longer than 72 hours to become evident. Irritants will show a response in a few hours. If irritation occurs, the substance may be falsely identified, which is the major weakness of this test.

Histologic Findings

Histologically, appearance varies with the clinical spectrum of the disease. With mild contact dermatitis, simple parakeratosis and hyperkeratosis with intracellular edema and small infiltrates are seen. Early in the disease, neutrophils commonly are seen (more often in irritant contact dermatitis than in allergic dermatitis). With chronic disease, ballooning degeneration and frank necrosis may be appreciated. Hyperpigmented lesions show melanin-laden macrophages in the upper dermis with basal pigmentation.

Treatment

Medical Care

The medical care for contact dermatitis simply involves removal of the offending agent from the patient's environment (if it can be identified). This may be impossible because of a patient's work environment or economic situation.⁷

Clothing to limit exposure may be useful. Harsh soaps and detergents should be avoided. Sweating and cold weather may cause exacerbations. Irritating fabrics and scratching also are problematic. Typical treatment involves topical steroids to the affected area and wet saline compresses to exudative skin lesions. Oral antihistamines may be used for control of itching. Oral steroids may be used if control with topical treatment is not sufficient.

Consultations

Dermatologic consultation may be helpful if skin involvement is severe or if patch testing is necessary.

Diet

Food allergens do not commonly cause contact dermatitis, although this may occur. If the offending agent is believed to be in a particular food, atopic dermatitis and urticaria should be considered as possible diagnoses.

Medication

Contact dermatitis is treated by identifying and removing the offending agent (if possible) and treating conservatively based upon the degree of symptoms. Frequently, removing the agent and allowing a short time for the symptoms to resolve will be adequate treatment. Otherwise, symptoms may be too severe and may require one or more of the following: topical corticosteroids, oral antihistamines, and oral corticosteroids.

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli. Various preparations of corticosteroids are available as eye drops that may be used for contact dermatitis affecting the eye.

Triamcinolone (Aristocort, Kenalog, Trilone)

Topical form in a water-soluble base should be sufficient to control most forms of contact dermatitis that occur on skin. Patients must be seen if symptoms do not improve within a few days.

Dosing

Adult

Apply topically tid to affected area of skin

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; fungal, viral, and bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Retardation of wound healing possible with prolonged treatment; may increase IOP; prolonged use may result in glaucoma

Prednisolone (Pred Forte)

Decreases inflammation and corneal neovascularization. Suppresses migration of polymorphonuclear leukocytes and reverses increased capillary permeability.

Dosing

Adult

Solution: 1-2 gtt into conjunctival sac q1h during day and q2h noct; once desired response is obtained, use 1 gtt q4h; may reduce to 1 gtt tid/qid to control symptoms
Suspension: Shake well before using and instill 1-2 gtt into conjunctival sac 2-4 times/d; if necessary, may increase dosing frequency during initial 24-48 h

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; most viral diseases of the cornea and conjunctiva, including epithelial herpes simplex keratitis (dendritic keratitis), vaccinia, and varicella, and also mycobacterial infections of the eye and fungal diseases of ocular structures

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hypertension; known to cause cataract formation with long-term use; may cause secondary glaucoma; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use (obtain fungal cultures when appropriate); may increase IOP; prolonged use may result in glaucoma

Prednisone (Deltasone, Meticorten, Orasone, Sterapred)

Oral form may be necessary if skin lesions are widespread and do not respond initially to topical steroids. A high dose may be given initially with a slow taper for a large affected area. Use should be limited to short periods because of the risks of long-term use, especially in children.

Dosing

Adult

5-10 mg PO qd

Pediatric

Not established

Interactions

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use; may increase IOP; prolonged use may result in glaucoma

Oral antihistamines

Act by competitive inhibition of histamine at the H1 receptor. This mediates the wheal and flare reactions, bronchial constriction, mucous secretion, smooth muscle contraction, edema, hypotension, CNS depression, and cardiac arrhythmias.

Hydroxyzine (Atarax, Vistaril, Vistazine)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS.

Dosing

Adult

5-25 mg PO qd/qid (25 mg tid/qid per PDR)

Pediatric

<6 years: 50 mg PO qd divided into several doses
>6 years: 50-100 mg PO qd divided into several doses (according to PDR)

Interactions

CNS depression may increase with alcohol or other CNS depressants

Contraindications

Documented hypersensitivity; early pregnancy

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Associated with clinical exacerbations of porphyria (may not be safe for porphyric patients); ECG abnormalities (alterations in T-waves) may occur; may cause drowsiness necessitating avoidance of driving, operating heavy machinery, and alcohol use

Follow-up

Further Outpatient Care

• Additional care is needed if the problem continues.

Inpatient & Outpatient Medications

• See Medication.

Deterrence/Prevention

• Take precautions to avoid known irritants and allergens.

Complications

• Potential complications center on the use of steroids, particularly around the eye. The avoidance of long-term steroid use is essential, because its long-term use may cause cataracts, glaucoma, corneal thinning/perforation, and loss of the eye, as well as other problems.

Prognosis

• The prognosis for individuals affected by contact dermatitis is good. Most patients have a mild form that will improve with or without physician intervention.
• Some severe cases with widespread involvement, where the eyes may be swollen shut, typically will respond well to oral corticosteroid therapy and receive much relief from antihistamine treatment.

Patient Education

• For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Contact Dermatitis.

Miscellaneous

Medicolegal Pitfalls

• Attempt to identify and avoid the offending agent.
• Avoid long-term or high-dose steroid use. In addition to the well-documented systemic side effects, the use of steroids around the eye can cause glaucoma, cataracts, corneal thinning, and, ultimately, perforation of the cornea, loss of vision, and/or loss of the eye. 

References

1. Rietschel RL, Fowler JF. Fisher's Contact Dermatitis. 4^th ed. Lippincott Williams & Wilkins; 1995.

2. Geraut C, Tripodi D, Brunet-Courtois B, Leray F, Geraut L. Occupational dermatitis to epoxydic and phenolic resins. Eur J Dermatol. Apr 7 2009;[Medline].

3. Pontén A, Dubnika I. Delayed reactions to reusable protective gloves. Contact Dermatitis. Apr 2009;60(4):227-9. [Medline].

4. Helaskoski E, Kuuliala O, Aalto-Korte K. Occupational contact urticaria caused by cyclic acid anhydrides. Contact Dermatitis. Apr 2009;60(4):214-21. [Medline].

5. Glick ZR, Saedi N, Ehrlich A. Allergic contact dermatitis from cigarettes. Dermatitis. Jan-Feb 2009;20(1):6-13. [Medline].

6. Tudela E, MacPherson C, Maibach HI. Long-term trend in patch test reactions: a 32-year statistical overview (1970-2002), part II. Cutan Ocul Toxicol. 2008;27(3):187-202.

7. Bourke J, Coulson I, English J. Guidelines for the management of contact dermatitis: an update. Br J Dermatol. Mar 19 2009;[Medline].

8. Ayala F, Fabbrocini G, Bacchilega R. Eyelid dermatitis: an evaluation of 447 patients. Am J Contact Dermat. Jun 2003;14(2):69-74. [Medline].

9. Cohen DE. Contact dermatitis: a quarter century perspective. J Am Acad Dermatol. Jul 2004;51(1 Suppl):S60-3. [Medline].

10. Friedlander MH. Contact dermatitis. In: Current Ocular Therapy. 5^th ed. Elsevier Science; 2000:143-146.

11. Garrott HM, Walland MJ. Glaucoma from topical corticosteroids to the eyelids. Clin Experiment Ophthalmol. Apr 2004;32(2):224-6. [Medline].

12. Guin JD. Eyelid dermatitis: experience in 203 cases. J Am Acad Dermatol. Nov 2002;47(5):755-65. [Medline].

13. Kanski JJ. Disorders of the conjunctiva. In: Clinical Ophthalmology: A Systematic Approach. 4^th ed. Elsevier Science; 1999:69-75.

14. 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.

15. 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].

16. Kwan TH. Spongiotic dermatitis. In: Textbook of Dermatopathology. McGraw-Hill Co; 1998:17-32.

17. 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].

18. Marks JG, Martini MC. Contact dermatitis and contact urticaria. In: Principle and Practice of Dermatology. 2^nd ed. Churchill Livingstone; 1996:419-427.

19. Roy FH. Ocular Differential Diagnosis. 6^th ed. Lippincott Williams & Wilkins; 2000.

20. Weisbecker CA, Fraunfelder FT, Rhee D. Physicians' Desk Reference for Ophthalmology. 28^th ed. Medical Economics Co; 2000.

Keywords

contact dermatitis, contact allergy, contact sensitivity, dermatitis venenata

Contributor Information and Disclosures

Author

R Scott Lowery, MD, Assistant Professor of Ophthalmology, Department of Pediatric Ophthalmology and Strabismus, University of Arkansas for Medical Center, Arkansas Children's Hospital
R Scott Lowery, MD is a member of the following medical societies: American Academy of Ophthalmology
Disclosure: Nothing to disclose.

Medical Editor

Jack L Wilson, PhD, Distinguished Professor, Department of Anatomy and Neurobiology, University of Tennessee at Memphis
Jack L Wilson, PhD is a member of the following medical societies: American Association of Anatomists, American Association of Clinical Anatomists, and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

Christopher J Rapuano, MD, Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Co-Chairman of the Cornea Service, Co-Chairman of Refractive Surgery Department, Wills Eye Institute
Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Cornea Society, Eye Bank Association of America, International Society of Refractive Surgery, and Pan-American Association of Ophthalmology
Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; Inspire Honoraria Speaking and teaching; RPS Ownership interest Other; Vistakon Honoraria Speaking and teaching

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

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