Atopic Dermatitis in Emergency Medicine

Updated: Apr 26, 2021
  • Author: Cassandra Bradby, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
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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.



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.


Etiology of Atopic Dermatitis

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. [2]

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. [3, 4, 5] 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.




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. [6] A small percentage of affected children will have the disease into adulthood.


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


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


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. [7] 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.



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.

About 90% of patients with atopic dermatitis have spontaneous resolution by puberty. Adults who continue to have atopic dermatitis usually have localized dermatitis (eg, chronic hand or foot dermatitis, eyelid dermatitis, lichen simplex chronicus). Unfavorable prognostic factors for atopic dermatitis (in order of relative importance) include the following:

  • Persistent dry or itchy skin in adult life

  • Widespread dermatitis in childhood

  • Family history of atopic dermatitis

  • Associated bronchial asthma

  • Early age at onset

  • Female gender

The objective when treating a patient for atopic dermatitis 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

Given the chronic nature of atopic dermatitis 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.