eMedicine Specialties > Emergency Medicine > Dermatology

Dermatitis, Atopic

Author: Jamie Alison Edelstein, MD, Staff Physician, Department of Emergency Medicine, State University of New York, Kings County Hospital Center
Coauthor(s): Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Contributor Information and Disclosures

Updated: Jun 30, 2009

Introduction

Background

Eczema, or atopic dermatitis, is a common inflammatory disease of the skin. The condition often has its start in childhood and follows a variable and sometimes unremitting course. Historically, this disease has been considered a part of a triad of "atopy" that included asthma and allergic rhinitis, though this association has recently come into question. Although not a cause of significant mortality, the visible and chronic nature of eczema can be a source of emotional stress.

Pathophysiology

The precise mechanism for the development of eczema is unknown. Whether the clinical manifestations of atopic dermatitis (AD) are the result of violation of the epidermis and the subsequent contact between environmental irritants and immune cells, or the reverse sequence, is debatable. Nonetheless, the epidermis is the first line of defense between the body and the environment and, when intact, shields the body from a variety of irritants, allergens, and microbes. This barrier, which is maintained by differentiated keratinocytes and structural proteins, can be compromised by inheritance, trauma, decreased humidity, change in pH, and infection.
 
Atopic skin additionally has diminished ability to maintain water; this dry skin leads to scratching, which further contributes to the release of proinflammatory mediators. Eczema is a biphasic T-cell – mediated disease: TH2 is more prevalent in the acute phase, and TH1 predominates in the chronically affected skin.¹ Patients with atopic dermatitis have elevated serum IgE levels, peripheral eosinophilia, and overall greater numbers of immune mediators and cytokines.

Frequency

Atopic dermatitis is the most common inflammatory skin disease in children, affecting up to 17% of the pediatric population in the United States, with increasing prevalence over the past several decades.

United States

Prevalence of atopic dermatitis ranges from approximately 7-17% in children.² 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 atopic dermatitis.

Mortality/Morbidity

Mortality is not associated with atopic dermatitis. The impact of eczema is hard to measure but has real personal, social, and financial consequences. The burden includes but is not limited to professional fees, hospitalization, pain/suffering, social isolation, poor self-esteem, and work and/or school performance or absence. Additionally, patients suffering from atopic dermatitis are prone to bacterial superinfection.

Sex

Data shows a slightly increased prevalence of atopic dermatitis in female children.

Age

Atopic dermatitis predominantly affects infants and young children. Eczema is apparent in the first year of life in 60% of cases, and its onset is before 5 years in 75% of cases.³ Onset of eczematous appearing disease in adulthood should lead the physician to consider another diagnosis.

A triphasic course of atopic dermatitis across the lifespan has been proposed. Phase I develops before IgE sensitization has taken place and occurs mostly in infants who are likely genetically predisposed to the disease. Phase II involves IgE sensitization to food, environmental antigens, or both. Phase III is the product of chronic scratching and is characterized by the formation of IgE autoantibodies against proteins of keratinocytes and endothelial cells.

Clinical

History

The hallmarks of atopic dermatitis are intense pruritus, chronic eczematous skin lesions, and epidermal thickening and hypertrophy.

• The emergency physician often is the first to diagnose atopic dermatitis. 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. Atopic dermatitis 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.

Physical

Atopic dermatitis is a spectrum of disease that varies in presentation, severity, and distribution. Eczema defies a simple definition as the disease has differing characteristics depending on the age of the patient and the stage of the disease course.

• Lesions may be acute, subacute, or chronic, each with a characteristic appearance. Lesions from one stage can convert into another stage at any time due to processes such as manipulation, irritation, allergy, or infection.
  • Acute lesions are intensely itchy and present as vesicles and blisters with intense redness.
  • Subacute disease is characterized by slight-to-moderate itching, pain, stinging, burning and redness, scaling, and fissuring of the skin with a parched and scalded appearance.
  • Chronic eczematous inflammation demonstrates thickened skin, accentuated skin lines, excoriations, and fissuring accompanying a moderate-to-intense itch.
• The pattern of skin manifestations also differs across the lifespan.
  • In infantile atopic dermatitis, pruritic, red, scaly, and crusted lesions are typically found on the extensor surfaces and cheeks or scalp, with severe cases possibly presenting with vesicles, serous exudates, or crusting. The diaper area is protected and usually spared.
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    Irritation around mouth of an infant with atopic dermatitis.

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    Irritation around mouth of an infant with atopic dermatitis.

  • The lesions in the childhood stage have less exudation; the skin often demonstrates lichenified plaques in a flexural distribution, commonly antecubital and popliteal fossae, volar aspect of the wrists, ankles, and neck.
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    Flexural involvement in childhood atopic dermatitis.

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    Flexural involvement in childhood atopic dermatitis.

  • Adult eczema has a similar distribution to that in childhood atopic dermatitis but is increasingly localized and lichenified with thickened skin, increased skin markings, and excoriated and fibrotic papules.
• Certain characteristic patterns are worth mentioning.
  • Eczema that appears as one or several coin-shaped plaques is called nummular eczema.
  • Plaques with prominent skin lines are referred to as lichen simplex chronicus. These lesions are characterized by intense pruritus that ceases when pain replaces itch.

Diagnosis of atopic dermatitis is made by observing representative clinical features of the disease. The Hanifin and Rajka diagnostic criteria, which consist of 4 major and 23 minor criteria has traditionally been used, but it is time consuming and not manageable. The UK working group on atopic dermatitis has the following criteria for diagnosis, which has been most extensively validated in clinical trials.⁴ Evidence of itchy skin with 3 more of the following:

• History of skin crease involvement
• Presence of generally dry skin within in the past year
• Symptoms in a child beginning before the age of 2 years
• Visible involvement of dermatitis involving flexural surfaces

The complete Hanifin and Rajka criteria are included below:

• 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

Causes

Atopic dermatitis is a complex genetic disease that results from an array of gene-gene and gene-environment interactions. Most experts believe that atopic dermatitis has a genetic basis. This is supported by twin studies and chromosome studies that suggest the trait might be inherited via a maternal gene located on chromosome 11. Clinical studies have also shown a higher risk of atopy in children with maternal atopy than in children with paternal atopy.⁵

Two theories have been proposed to explain the manifestations of atopic dermatitis. Atopic dermatitis was traditionally thought to be caused by an innate immunologic disturbance leading to IgE sensitization, which later results in disruption of the epithelial barrier, though this supposed mechanism is falling out of favor. Alternatively, it is thought that skin breakdown precedes the inflammatory process and an intrinsic epithelial cell defect leads to barrier disruption of the skin and that immunologic imbalance is an "epiphenomenon".¹ Genetic defects in filaggrin, a group of structural proteins, have been cited as a major cause of atopic dermatitis.^6,7 The upregulation of a protease stratum corneum chymotryptic enzyme is also being investigated in the cause of atopic dermatitis.

Chronic eczema is a disease that is somewhat behaviorally mediated. Skin thickening and plaque formation is dependent on habitual scratching.

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