AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Atopic dermatitis (AD) is a chronic, highly pruritic, eczematous skin disease that follows patients from early childhood into puberty and sometimes adulthood. Also referred to as eczematous dermatitis, the disease often has a remitting/flaring course, which may be exacerbated by social, environmental, and biological triggers.

Atopic dermatitis is characterized as an immediate (type I) hypersensitivity reaction similar to that of allergic rhinitis, bronchial asthma, atopic dermatitis, and food allergy. Although not all patients who have atopic dermatitis are atopic (a misnomer of the disease), the correlation is high, around 80%, and patients with AD often manifest other atopic diseases.

Pathophysiology

The exact etiology of AD is unknown. It is immunologically mediated, with a large majority of affected patients having elevated serum immunoglobulin E (IgE) concentrations, although no relationship exists between IgE levels and severity of disease. A strong familial inheritance pattern seems to exist for both AD and other atopic diseases, with more than half of patients with AD reporting a family history of respiratory atopy.

Researchers are continuing to examine the role that chromosomal markers (chromosomal 11), eosinophilia, cell-mediated immunity, interleukins, and other inflammatory mediators play in the pathophysiology of AD.

Frequency

United States

Prevalence of AD ranges from approximately 7-17% in children. A small percentage of affected children will have the disease into adulthood.

International

Studies in Japan and Northern Europe have found similar prevalence, with industrialized and westernized nations noting increasing trends of patients with AD.

Mortality/Morbidity

This disease itself is not life threatening.

Sex

Some studies have found a higher incidence, although not statistically significant, in females, although females do seem to have a worse prognosis.

Age

AD typically manifests in infants aged 1-6 months. Approximately 60% of patients experience their first outbreak by age 1 year and 90% by age 5 years. Disease manifestations can be divided into 3 stages: acute, subacute, and chronic. Onset of AD in adolescence or later is uncommon and should prompt consideration of another diagnosis.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• The emergency physician often is the first to diagnose AD. The most common presentation is that of infants, usually younger than 6 months, brought in by their parents for a persistent rash. Before coming to the ED, the parents may have tried a number of over-the-counter and home remedies. Parents usually report that the rash has waxed and waned for months with a history of dry skin since birth.
• Clinicians should inquire about a family history of asthma, hay fever, allergy, and other atopic diseases. Patients with pertinent medical or family history of such disease tend to have a worse prognosis.
• Parents may also give a history of poor sleep or increased irritability in the patients, which is due to the desire to scratch the skin during sleep. AD begins with intense pruritus, leading the patient to scratch, which results in the characteristic rash.
• Atopic dermatitis typically is not associated with fever or other constitutional symptoms, and the presence of these should prompt the clinician to look for bacterial superinfection.
• First published in 1977 by Hanifin et al, the diagnosis of AD can be made by fulfilling major and minor criteria:
• • Major criteria (need 3 or more)
    • Pruritus
    • Typical morphology and distribution
    • Flexural lichenification in adults
    • Facial and extensor involvement in infants and children
    • Dermatitis - Chronically or chronically relapsing
    • Personal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis)
  • Minor criteria (need 3 or more)
    • Cataracts
    • Cheilitis
    • Conjunctivitis - Recurrent
    • Eczema - Perifollicular accentuation
    • Facial pallor or erythema
    • Food intolerance
    • Hand dermatitis - Nonallergic
    • Ichthyosis
    • IgE- Elevated
    • Immediate (type I) skin test reactivity
    • Infections (cutaneous)
    • Dennie-Morgan infraorbital fold
    • Itching when sweating
    • Keratoconus
    • Keratosis pilaris
    • Nipple dermatitis
    • Orbital darkening
    • Palmar hyperlinearity
    • Pityriasis Alba
    • White dermographism
    • Wool intolerance
    • Xerosis

Physical

• Acute lesions are erosions with serous exudate or intensely itchy papules and vesicles on an erythematous base.
• Subacute lesions are characterized by scaling, excoriated papules, or plaques over erythematous skin.
• In its chronic phase, skin shows lichenification and pigmentary changes (increased or decreased) with excoriated papules and nodules.
• The pattern of disease varies based on the age of the patient.
• • Infants: Lesions typically develop during the third month of life. Dry, red, scaly areas appear on the cheeks but spare the perioral and perinasal areas.
    • The lips may become affected as the child smacks and licks the lips during winter months.
    • Usually, the diaper area is spared, although infants may develop lesions and lichenification at easy to reach crevices: directly below the diaper, extensor surface of the forearm, or back of the hand.
    • If the scalp is involved, it may be very difficult to distinguish AD from seborrheic dermatitis.
  • Children: Atopic dermatitis appears in areas of repeated flexion and extension (antecubital fossae, neck wrists, and ankles). Areas of high perspiration are most often affected, especially when combined with form-fitting clothing. Lesions are red, scaly, have sharply demarcated borders, and develop lichenification over time.
    • These patients develop generalized eruptions. These are the patients whose mood and behavior are most affected by AD, especially as the disease causes social embarrassment and sleep disruption.
    • The disease may actually remit in many of the pubescent patients.
  • Adults
    • Atopic dermatitis during adulthood most commonly manifests as hand dermatitis, because adults are exposed to irritating chemicals and they wash their hands more frequently than children.
    • Eyelid inflammation is common in adults with AD and causes patients to rub excessively at their eyes. This may cause atopic pleats (Dennie-Morgan infraorbital fold), an extra line on the lower eyelid that, although common in patients with AD, is also seen in patients without the disease.
• Other associations
• • Dry skin and xerosis: A hallmark of AD, patients have rashes and severely dry skin that itches. Even infants with AD have excessively dry skin, especially in the winter months. Continued moisturized and mild soaps help with this.
  • Ichthyosis vulgaris can be observed in patients with atopic dermatitis. Characterizing features are dry, rectangular scales on the extensor surfaces of the arms and legs. This condition is treated with 1% ammonium lactate lotion and often improves with age.
  • Hand and foot dermatitis may be the only manifestation in adults and adolescents. Fissuring of the palms, soles, and fingers often occurs.
  • Keratosis pilaris is an asymptomatic condition where horny follicular papules on the extensor surfaces of the upper arms, buttocks, and anterior thighs (sparing the palms and soles). Lesions may also appear on the face and may be confused with acne, especially in the adolescent patient. Treatment may be with topical steroids or ammonium lactate cream.
  • Hyperlinear palmar creases may be seen in patients with AD often associated with continued itching and scratching.
  • Keratoconus is an elongation and protrusion of the corneal surface, which is seen in a few patients with AD. Its appearance is not associated with cataracts.
  • Patients with AD do have a higher likelihood of cataracts; however, most of these are asymptomatic. The appearance of cataracts may be related to the use of systemic steroids throughout the lifetime of the patient with AD.
  • Pityriasis alba (asymptomatic, hypopigmented scaling plaques on the face and arms) may also be seen in patients with AD. No acute treatment is indicated.

Causes

• Exact etiology is unknown, but several triggers have been identified. Anything that could dry the skin may exacerbate atopic dermatitis. Potential triggers include excessive bathing, swimming, hand washing, and lip licking.
• Contact with solvents, detergents, deodorants, cosmetics, and soaps can exacerbate the disease. Cigarette smoke has also provoked inflammation.
• Patients are extremely sensitive to temperature changes. They should avoid clothing that traps heat or causes sweating. They will also see increased flare-ups during times of low humidity, as dry air exacerbates the disease. Commercial humidifiers may help with the symptoms.
• Although no direct correlation has ever been documented, most AD show increased sensitivity to aeroallergens like dust mites. Some researchers believe these allergens can trigger exacerbations of AD, but this has not been proven.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Lichen simplex chronicus
Seborrheic dermatitis
Nummular eczema
Xerotic eczema
Dyshidrotic eczema
Prelymphomatous
Drug reactions
Hyperimmunoglobulin E syndrome
Photosensitivity rashes
Wiskott-Aldrich syndrome

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• The diagnosis of AD is based on history and physical examination. Laboratory tests are not helpful for diagnosing atopic dermatitis; however, they may be used to exclude other disorders.
• Serum immunoglobulin E (IgE) levels usually are elevated. This may be useful for treating refractory AD with anti-IgE antibodies (omalizumab). This medication is not currently approved for AD treatment.

Procedures

• Biopsy: Pathologic findings include spongiosis with a severely damaged stratum corneum, with hyperproliferation in advanced cases.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Emergency Department Care

• Many patients with AD present to the ED during acute exacerbation. Therapy is targeted toward alleviation of pruritus and prevention of scratching. ED physicians must also look for signs and symptoms of bacterial superinfection and treat accordingly.
• Skin care
• • In the acute setting patients should be instructed to bathe once-to-twice daily using mild soaps (eg, Dove). There is no preference over showers or baths, whichever makes the patient most comfortable.
  • The patient should dry quickly and immediately (within 3 min) lubricate the skin. Many creams and lotions are available, and the optimal one is the greasiest the patient can tolerate.
  • Creams (eg, Eucerin, Cetaphil) are preferred over lotions, as they have lower or no water content and will not evaporate off of the skin during the day. Parents may use petroleum jelly on infants, but most children and adults will not tolerate the texture.
• Topical steroids
• • Acute attacks should be treated by mid-high strength topical steroids for up to 2 weeks. Medium-to-high potency topical steroids should not be used on the face or neck area because of the potential adverse effects. These are preferred over low-mid strength medications, as they better control exacerbations. Patients should apply the ointment within 5 minutes of twice-daily bathing.
  • Inform the patient about adverse effects of topical steroids (eg, atrophy, hypopigmentation, striae, telangiectasia, thinning of the skin).
• Antihistamines: Physicians have been prescribing antihistamines for years to control the pruritus associated with acute AD. Little evidence exists that antihistamines help with the itching in an awake patient; however, the use of sedating antihistamines is supported to control scratching while the patient is asleep.
• Systemic steroids: The use of systemic steroids in the treatment of acute exacerbation of AD is controversial. Most authors reserve oral prednisone (at least 20 mg/d for 7 d) for the most severe cases, although it seems the disease quickly relapses once the medication is discontinued. Patients also tend to discontinue topical steroid creams and other treatment as they feel better, which contributes to the relapse after oral steroids are done.
• Topical calcineurin inhibitors: Topical calcineurin inhibitors (pimecrolimus 1% and tacrolimus 0.03%, 0.1%) are available for patients older than 2 years. These medications may be used all over skin surfaces (including face, neck, and hairline) because they do not have the side effects seen with topical steroids. Evidence supports the twice-daily use of these creams during acute exacerbation of AD, and some evidence exists to support use up to 4 years. The long-term side effects (including the possibility of increased risk for malignancy) have not fully been elucidated. For these reasons, the Food and Drug Administration (FDA) does not recommend long-term use yet. Side effects of tacrolimus include burning and stinging on broken skin.
• Oral immunosuppressive agents: Patients with refractory AD may benefit from oral immunosuppressive agents, such as cyclosporine A. This medication is effective in treating severe AD in the acute setting. It is not recommended for long-term use.

Consultations

Because AD is likely to be a lifelong disease, refer patients to a dermatologist or their primary care physician for ongoing care.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Drug regimens for eczema should be tailored to the individual patient to reduce the frequency and severity of exacerbations.

Drug Category: Topical steroids

Topical steroids are very effective when used in the induction of remission and in the acute exacerbation of AD.

Low-to-medium potency steroids should be used routinely, with medium-to-high potency steroids for more severe rashes.

Drug Name	Hydrocortisone (CortaGel, Cortaid, Dermacort, Westcort)
Description	An example of a low-potency topical steroid available OTC. An adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. Has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity.
Adult Dose	Apply bid to affected areas
Pediatric Dose	Apply as in adults
Contraindications	Documented hypersensitivity; viral, fungal, and bacterial skin infections
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Prolonged use, applying over large surface areas, application of potent steroids, and occlusive dressings may increase systemic absorption of corticosteroids and may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia, and glycosuria

Drug Category: Topical calcineurin Inhibitors

Topical immune suppressants that block early T-cell activation, degranulation of mast cells, and multiple cytokines.

Drug Name	Tacrolimus (Protopic)
Description	The mechanism of action of tacrolimus in atopic dermatitis is not known. Reduces itching and inflammation by suppressing the release of cytokines from T cells. Also inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha, all of which are involved in the early stages of T-cell activation. Additionally, may inhibit release of preformed mediators from skin mast cells and basophils, and downregulate expression of FCeRI on Langerhans cells. Can be used in patients as young as 2 years. Drugs of this class are more expensive than topical corticosteroids. Available as an ointment in concentrations of 0.03% and 0.1%. Indicated only after other treatment options have failed.
Adult Dose	Apply thin layer to affected skin areas bid and rub in gently and completely; continue treatment for 1 wk after clearing of signs and symptoms; use short-term and intermittent use only
Pediatric Dose	<2 years: Not established 2-15 years: Apply 0.03% ointment bid to affected area(s) >15 years: Administer as adults; use short-term and intermittent use only
Contraindications	Documented hypersensitivity to tacrolimus or components of ointment
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Patients may experience a burning sensation during first few days of application; skin can become photosensitive, and patients should be cautioned about exposure to direct or artificial sunlight and to use sunscreen; safety and efficacy in infected atopic dermatitis is not known; application under occlusion, which may promote systemic exposure, has not been evaluated (do not use tacrolimus ointment with occlusive dressings); absorption of tacrolimus following topical applications of tacrolimus ointment is minimal (relative to systemic administration), but tacrolimus is excreted in human milk and, thus, a decision should be made whether to discontinue breastfeeding or to discontinue drug, taking into account importance of drug to mother (potential for serious adverse reactions in breastfeeding infants from tacrolimus should also be a concern) Caution with conditions that suppress the immune system (eg, AIDS, cancer); possible risk of lymph node or skin cancer based on animal studies and a small number of patients; may increase risk of viral infections; other adverse effects include headache, sore throat, flulike symptoms, fever, and cough

Drug Category: Oral immunosuppressive agents

For use in severe refractory AD.

Drug Category: Antihistamines

Used for the sedating effects. Help to prevent scratching during sleep.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Few patients with AD will require hospitalization. Patients with cellulitis or severe secondary infection may require IV antibiotics and sedation.

Deterrence/Prevention

• The mainstay of treatment for AD is prevention of outbreaks. Patients should continue to take short showers/baths followed by immediate hydration of skin with emollients even during rash-free times.
• They should also continue to avoid any triggers that my exacerbate AD.

Complications

• Because of frequent scratching and fissuring of the skin, secondary infection is not uncommon. Suspect infection in persons with fever, surrounding erythema, or yellow crusting of the lesions. In severe exacerbations, it may be difficult to identify signs of secondary infection; empirical treatment for infection may be warranted.
• Eczema herpeticum (Kaposi varicelliform eruption) can be a life-threatening complication of atopic dermatitis. Most commonly seen during an initial infection with HSV in a child whose AD has recently healed, the vesicular eruption can progress from mild to fatal quickly. This disease should be suspected in any child with a remote history of AD, high fever, lymphadenopathy, and vesicular eruption, especially of the face. Affected patient should be treated with acyclovir (dose appropriate for age) and monitored closely.
• Atrophy or striae occur if fluorinated corticosteroids are used on the face or in skin folds.
• Systemic absorption of steroids may occur if large areas of skin are treated, particularly if high-potency medications and occlusion are combined.

Prognosis

• About 90% of patients with AD have spontaneous resolution by puberty.

  Adults who continue to have the disease usually have localized dermatitis (eg, chronic hand or foot dermatitis, eyelid dermatitis, lichen simplex chronicus).

• Unfavorable prognostic factors for AD (in order of relative importance) include the following:
• • Persistent dry or itchy skin in adult life
  • Widespread dermatitis in childhood
  • Family history of AD
  • Associated bronchial asthma
  • Early age at onset
  • Female gender
• The objective when treating a patient for AD is control of exacerbations, not elimination of the disease. Using the above treatment modalities, patients and their families can hope to minimize the frequency and severity of outbreaks.

Patient Education

• Instruct patients about proper skin care. Patients should bathe appropriately, keep skin well lubricated, use mild soaps, and avoid known triggers.
• The goal is control, not cure.
• For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Eczema.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Special Concerns

• Given the chronic nature of this disease and patients' concerns about appearance, emotional support and psychological counseling may be helpful. Physicians need to be sensitive to the needs of patients and their families.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Ben-Gashir MA, Seed PT, Hay RJ. Predictors of atopic dermatitis severity over time. J Am Acad Dermatol. Mar 2004;50(3):349-56. [Medline].
• Eichenfield LF, Hanifin JM, Luger TA. Consensus conference on pediatric atopic dermatitis. J Am Acad Dermatol. Dec 2003;49(6):1088-95. [Medline].
• Flohr C, Pascoe D, Williams HC. Atopic dermatitis and the 'hygiene hypothesis': too clean to be true?. Br J Dermatol. Feb 2005;152(2):202-16. [Medline].
• Habif TP. Clinical Dermatology: Fourth Edition A Color Guide to Diagnosis and Therapy. 2004;105-128.
• Hanifin JM, Paller AS, Eichenfield L. Efficacy and safety of tacrolimus ointment treatment for up to 4 years in patients with atopic dermatitis. J Am Acad Dermatol. Aug 2005;53(2 Suppl 2):S186-94. [Medline].
• Hoare C, Li Wan Po A, Williams H. Systematic review of treatments for atopic eczema. Health Technol Assess. 2000;4(37):1-191. [Medline].
• Kay J, Gawkrodger DJ, Mortimer MJ. The prevalence of childhood atopic eczema in a general population. J Am Acad Dermatol. Jan 1994;30(1):35-9. [Medline].
• Klein PA, Clark RA. An evidence-based review of the efficacy of antihistamines in relieving pruritusin atopic dermatitis. Arch Dermatol. Dec 1999;135(12):1522-5. [Medline].
• Lane JE, Cheyney JM, Lane TN. Treatment of recalcitrant atopic dermatitis with omalizumab. J Am Acad Dermatol. Jan 2006;54(1):68-72. [Medline].
• Larsen FS, Holm NV, Henningsen K. Atopic dermatitis. A genetic-epidemiologic study in a population-based twin sample. J Am Acad Dermatol. Sep 1986;15(3):487-94. [Medline].
• Laughter D, Istvan J, Tofte RN. The prevalence of atopic dermatitis in Oregon schoolchildren. J Am Acad Dermatol. Oct 2000;43(4):649-55.
• Sauer GC. Manual of Skin Diseases. Lippincott Williams & Wilkins Publishers; 1991:77-84.
• Simpson EL, Hanifin JM. Atopic dermatitis. Med Clin North Am. Jan 2006;90(1):149-67. [Medline].

Article Last Updated: Jun 5, 2006