eMedicine Specialties > Ophthalmology > Dermatologic Disorders

Dermatitis, Atopic

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: Apr 10, 2009

Introduction

Background

Atopy is the hereditary predisposition to allergy or hypersensitivity. Symptoms may present as a dermatitis, hay fever, or asthma. According to Rapoza, Besnier first characterized atopic dermatitis, and many Europeans still use his name to describe the disease (prurigo Besnier).¹ This disease was labeled eczema for many years in the United States until Coca and Cooke coined the term atopy as a skin hypersensitivity seen in patients with hereditary allergies. Wise and Sulzberger have been credited with the term atopic dermatitis to describe a group of diseases associated with atopic conditions that may be seen in all age groups.²

Pathophysiology

Atopic dermatitis is primarily caused by cellular immune deficiency and elevated immunoglobulin E (IgE). The pathogenesis can be traced to a genetically inherited, bone marrow–derived cell associated with chromosome 11q. Abnormal skin reactivity also plays a major role in the development of the disease. Irritants to the skin are believed to predispose an individual to develop dermatitis more often than simply exposure to an allergenic trigger. Nonetheless, patients frequently have a history of food or inhalant allergies or eventually develop them.³

Frequency

United States

An estimated 3-12% of the population will be affected at some time.

Race

The highest incidence is in urban areas and in cooler temperature zones, although no clear racial predisposition appears to exist.

Sex

According to Bezan, males appear to be affected more frequently by vernal and atopic conjunctivitis than females.⁴

Age

Children most commonly are affected, with 80% developing the disease before age 7 years. Less than 2% will have an onset after age 20 years. Most sources agree that persistence after age 20 years is uncommon. Only an estimated 10% of patients older than 20 years continue to be symptomatic.⁵

Clinical

History

• The most common symptoms include pruritus, erythema, and skin lesions of the antecubital and/or popliteal skin, eyelids, corners of the mouth, neck, outer canthi, or behind the ears.
• In infants, the eruption particularly involves the face, scalp, and extensor surfaces.
• In older children and adults, the neck and antecubital or popliteal areas more commonly are involved.
• Adult patients usually have a history of infantile disease that may require anecdotal history or contacting their caregivers from infancy.
• Most patients have a familial occurrence of symptoms of atopy.

Physical

• The most common physical findings are erythematous, exudative skin lesions of the antecubital and/or popliteal skin, eyelids, corners of the mouth, neck, outer canthi, or behind the ears.
  • Scaling, lichenification (thickening of the skin due to scratching and irritation), and pigmentary changes (eg, vitiligo, hyperpigmentation [often seen in patients with darker skin types]) are common in adolescents and adults.
  • In severe cases, generalized eruptions over the entire body may occur.
• Possible physical findings on slit lamp examination include blepharitis, atopic keratoconjunctivitis (AKC), scarring of the palpebral conjunctiva, papillary conjunctival reaction, Trantas dots (limbal deposits of eosinophils), atopic cataracts, and keratoconus.
  • Unlike vernal conjunctivitis, the lower tarsus is involved more frequently.
  • Hyperemia, chemosis, and discharge are more common than papillary or cobblestone reaction.
• Atopic cataracts develop in patients with long-standing atopic disease (10 or more years).
  • These patients usually are older children or young adults.
  • The incidence of atopic cataracts is estimated to be 10%, and they are most frequently bilateral.
  • These cataracts tend to evolve rapidly and may opacify within 6 months.
  • The cataracts often begin as a posterior subcapsular opacity and develop into an anterior cortex opacity that frequently resembles the shape of a shield or a bearskin rug.
• Spontaneous retinal detachment is more common in patients with atopic disease than the general population.
• In a few rare, advanced cases, symblepharon, entropion, and trichiasis may be seen.

Causes

• Abnormal skin reactivity is a feature of the disease, and exposure to skin irritants, most frequently water and chemicals, may predispose patients to the development of atopic dermatitis.
• Additionally, since many of these patients have allergic sensitivities to food or inhaled allergens, exposure to these may increase the chances of development of the dermatitis.
• Skin irritants, thought to trigger this more frequently than other allergens, also may be more readily avoidable.
• Psychological stress has been implicated as a possible contributor to disease development.
• Recent studies have implicated loss-of-function mutations in the barrier protein filaggrin and diminished expression of certain antimicrobial peptides in atopic dermatitis skin, which may lead to further treatment research.

Differential Diagnoses

Workup

Laboratory Studies

• Diagnosis of atopic dermatitis is usually a clinical one based on history and physical findings.
• Laboratory tests that may be of use early in the diagnostic process include various types of skin testing and serum testing for elevated immunoglobulin E (IgE).
• Patients with atopic dermatitis display immediate skin test reactivity and may display skin blanching to cholinergic agents.
• Culture of eyes with conjunctivitis associated with atopic dermatitis usually grows Staphylococcus aureus.
• Once a clinical diagnosis of atopic dermatitis has been established, lab testing is generally unnecessary.

Histologic Findings

Examination of histopathologic sections early in the disease process shows parakeratosis, hyperkeratosis, acanthosis, intercellular and intracellular fluid accumulation, and perivascular infiltration of the dermis and epidermis by lymphocytes, monocytes, and macrophages. Later in the disease, observation reveals hyperkeratosis, dyskeratosis, acanthosis, and a thickened epidermis. Lysosomes have been demonstrated by electron microscopy.

Treatment

Medical Care

• No cure exists, and treatment is aimed at the multifactorial nature of the disease.⁶
• The most commonly used treatments include stress control, avoidance of allergens (most commonly dust mites, peanuts, egg, milk, fish, rice, soy, and wheat), and irritants (particularly chemicals, soaps, heat, humidity, wool, and acrylic).
• Atopic dermatitis frequently can be controlled with topical steroids.
• Management of atopic dermatitis and AKC is similar to management of vernal keratoconjunctivitis (VKC), but the chronic nature of AKC requires more prolonged treatment.
• The treatment regimen for AKC typically consists of topical steroids, mast cell stabilizers, systemic antihistamines, and systemic and topical antibiotics.⁷
• Recent studies have shown that patients with eye involvement may have an increased likelihood of food sensitivity.

Consultations

Ophthalmic consultation is recommended if eye involvement is noted. Dermatology consultation may be necessary to confirm a diagnosis of atopic dermatitis.⁸

Diet

Patients with known atopic disease may have various food allergies that trigger or exacerbate their disease. Avoidance of these foods is essential.

Medication

The most commonly used treatment strategies include antibiotics, corticosteroids, antihistamines, and, less commonly, immunosuppressives (other than steroids), UV light, and hospitalization (rare). For most cases of atopic dermatitis (without AKC), application of topical steroids to the affected area is usually sufficient. Eye involvement may be treated with topical steroids alone, or if symptoms persist, additional mast cell stabilizers (topical), and oral antihistamines (eg, over-the-counter diphenhydramine). AKC may require all of these, and some ophthalmologists recommend that an oral antibiotic be given in addition to a topical antibiotic for the affected eye(s). Antibiotic treatment should target S aureus, the most likely pathogen, and should be chosen based on the patient's allergies and compliance. Immunosuppressives, other than steroids, will only very rarely be required, and these likely will not be prescribed by the ophthalmologist.

Corticosteroids

As anti-inflammatory and immunosuppressive agents, corticosteroids are beneficial in treating atopic dermatitis. Dexamethasone, fluorometholone, hydrocortisone, and prednisolone are the most commonly available preparations of ophthalmic steroids in the United States. Preparations range from 0.05-2.5%. For most topical purposes, a 0.5% preparation of prednisolone, cortisone, or hydrocortisone is adequate.

Prednisolone (AK-Pred, Pred Forte, Inflamase Forte)

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

Dosing

Adult

Dosage depends on severity of disease
For AKC, a higher concentration for a longer period may be required
1-2 gtt bid/qid, not to discontinue prematurely; reevaluate in 2 d if symptoms fail to improve

Pediatric

Not established

Interactions

Decreases effects of salicylates and toxoids (for immunizations); phenytoin, carbamazepine, barbiturates, and rifampin decrease effects of corticosteroids

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin infections; glaucoma; immunosuppression; myopathy

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 hyperthyroidism, osteoporosis, cirrhosis, nonspecific ulcerative colitis, peptic ulcer, diabetes, and myasthenia gravis; long-term treatment with high-dose steroids has been shown to cause posterior subcapsular cataracts; hypokalemic alkalosis has been observed; glaucoma, myopathy, psychosis or mood disorders, corneal and scleral thinning, secondary infection, and retardation of wound healing are possible; with prolonged steroid treatment, pediatric patients may develop growth retardation, Cushing syndrome, striae, osteoporosis, avascular necrosis, myopathy, hypertension, ulcers, acne, fluid and electrolyte imbalance, mood alterations, and diminished immunity; pseudotumor cerebri may result on discontinuation; may increase IOP; prolonged use may result in glaucoma

Mast cell stabilizers

May be useful as prophylaxis against exacerbation of the disease.

Lodoxamide (Alomide)

Inhibits degranulation of mast cells and helps prevent histamine release.

Dosing

Adult

1-2 gtt qid for 10 d to affected eye(s); not to use >3 mo

Pediatric

<2 years: Not established
>2 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Not for injection; often experience transient burning or stinging from instillation; soft contact lens wearers should refrain from using them while under treatment

Cromolyn (Crolom, Opticrom)

Inhibits degranulation of sensitized mast cells following exposure to specific antigens.

Dosing

Adult

Not to exceed 1-2 gtt in each eye 4-6 times/d at regular intervals

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Often experience transient burning or stinging from instillation; soft contact lens wearers should refrain from using them while under treatment

Oral antihistamines

Useful in decreasing itching and scratching associated with atopic dermatitis.

Hydroxyzine (Atarax, Vistaril, Vistazine)

Antagonizes H1 receptors in periphery; may suppress histamine activity in subcortical region of CNS; may assist in sleep.

Dosing

Adult

25 mg PO/IM tid/qid

Pediatric

<6 years: 50 mg/d PO divided into several doses
>6 years: 50-100 mg/d PO divided into several doses

Interactions

May potentiate CNS depressants such as alcohol, narcotics, barbiturates, and other analgesics (reducing dose in combination with these is necessary)

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 requiring avoidance of driving, operating heavy machinery, and alcohol use

Topical antibiotics

Atopic conjunctivitis requires the use of topical antibiotics that particularly target S aureus, the most common pathogen. Since most ophthalmic antibiotics will target this bacterium, physician discretion, reference to package inserts, and the ophthalmic Physicians' Desk Reference are recommended. Patients' allergies and compliance should be considered.

Gatifloxacin ophthalmic (Zymar)

Fluoroquinolone with activity against streptococci, staphylococci, Corynebacterium propinquum, and Haemophilus influenzae; inhibits bacterial DNA synthesis and, consequently, growth.

Dosing

Adult

2 gtt q15min for the first 6 h, then 2 gtt q30min for remainder of first day
Day 2: 2 gtt qh
Days 3-14: 2 gtt q4h

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity

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

Serious anaphylactic reactions have occurred; superinfections and opportunistic infections may occur; contact lenses should be removed before instillation; white crystalline precipitates may occur

Follow-up

Further Outpatient Care

• Prophylaxis against scratching should be taken.
  • Scratching the lesions can worsen them and lead to the lichenification process characteristic of long-standing disease.
  • Corneal abrasions and further eye irritation also may occur. Antihistamines, mast-cell stabilizers, and corticosteroids will aid in reducing the itching but may require some time to take effect.
  • Nails should be kept clean and trimmed.
  • In pediatric patients, mittens may be used at night or even daily, when possible, if itching and scratching are severe.

Deterrence/Prevention

• Stress control, avoidance of allergens (most commonly dust mites, peanuts, egg, milk, fish, rice, soy, and wheat), and irritants (particularly chemicals, soaps, heat, humidity, wool, and acrylic) may help control the disease.

Complications

• The use of corticosteroids is fraught with potential ocular and systemic complications. In particular, cataract formation, glaucoma development, and potential corneal thinning must all be considered when deciding to use steroids for this disease. Long-term use should be avoided if at all possible.

Prognosis

• The prognosis is good if the inflammation can be kept under control with therapy. Patients need to understand that atopic disease cannot be cured, but rather controlled. However, some patients have such severe disease that treatment will not prevent vision loss and other potential complications.

Patient Education

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

Miscellaneous

Medicolegal Pitfalls

• Steroid use is probably the biggest area of concern in the treatment of ocular atopic dermatitis because of the complications that can result from steroid use. Corneal scarring and long-term vision loss can result, in addition to glaucoma and cataract development. The potential exists for corneal perforation and loss of an eye with, or even without, the use of steroids.

References

1. Rapoza PA, Chandler JW. Atopic dermatitis. In: Weingeist T, Gould D, eds. The Eye in Systemic Disease. Philadelphia: Lippincott; 1990:606-609.

2. Shen CP, Xing H, Ma L. [Research advances in atopic dermatitis]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. Feb 2009;31(1):103-6. [Medline].

3. Jung T, Stingl G. Atopic dermatitis: therapeutic concepts evolving from new pathophysiologic insights. J Allergy Clin Immunol. Dec 2008;122(6):1074-81. [Medline].

4. Bezan DJ. Eye itch. In: Bezan DJ, Larussa FP, Nishimoto JH, et al, eds. Differential Diagnosis in Primary Eye Care. Boston: Butterworth-Heinemann; 1999:67-71.

5. Brenninkmeijer EE, Legierse CM, Sillevis Smitt JH, Last BF, Grootenhuis MA, Bos JD. The course of life of patients with childhood atopic dermatitis. Pediatr Dermatol. Jan-Feb 2009;26(1):14-22. [Medline].

6. Anderson PC, Dinulos JG. Atopic dermatitis and alternative management strategies. Curr Opin Pediatr. Feb 2009;21(1):131-8. [Medline].

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8. Kaujalgi R, Handa S, Jain A, Kanwar AJ. Ocular abnormalities in atopic dermatitis in Indian patients. Indian J Dermatol Venereol Leprol. Mar-Apr 2009;75(2):148-51. [Medline].

9. Clark RAF, Kristal L. Atopic dermatitis. In: Sams J, Lynch PJ, eds. Principles and Practice of Dermatology. 2^nd ed. New York: Churchill Livingstone Inc; 1996:403-418.

10. Friedlander MH. Diseases affecting the eye and the skin. In: Allergy and Immunology of the Eye. 2^nd ed. 1993:75-106.

11. Friedlander MH. Atopic dermatitis. In: Current Ocular Therapy. 5^th ed. Philadelphia: WB Saunders Co; 2000:143-144.

12. Furue M, Terao H, Moroi Y, et al. Dosage and adverse effects of topical tacrolimus and steroids in daily management of atopic dermatitis. J Dermatol. Apr 2004;31(4):277-83. [Medline].

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14. Hanifin JM. Atopic dermatitis: broadening the perspective. J Am Acad Dermatol. Jul 2004;51(1 Suppl):S23-4. [Medline].

15. Kanski JJ. Disorders of the conjunctiva. In: Clinical Ophthalmology. 4^th ed. Boston: Butterworth-Heinemann; 1999:69-71.

16. Liesegang TJ. Atopic keratoconjunctivitis. In: Pepose JS, Holland GN, Wilhelmus KR, eds. Ocular Infection and Immunity. St. Louis: Mosby; 1996:376-390.

17. Roy FH. Ocular Differential Diagnosis. 7^th ed. Philadelphia: Williams & Wilkins; 2002.

18. Shelley WB, Shelley EB. Atopic dermatitis. In: Advanced Dermatologic Diagnosis. Philadelphia: WB Saunders Co; 1992:285-291.

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21. Zimmerman TJ, Kulkarni PS, Meredith TA. Steroids in ocular therapy, antibiotics and antifungals, antiallergic therapies. In: Zimmerman TJ, Kooner KS, Shariv M, Fechtner RD, eds. Textbook of Ocular Pharmacology. Philadelphia: Lippincott-Raven; 1997:61-74, 363-385, 609-633,683-701, 801-804.

Keywords

atopic dermatitis, atopic eczema, Besnier prurigo, prurigo Besnier, Besnier's prurigo, atopy

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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