Description

Atopic dermatitis (AD) is a chronic inflammatory state of the skin characterized by pruritus, erythema, induration, and scale of the skin. It is the result of chronic inflammation resulting from abnormalities of skin barrier structures, an immunologic response to environmental allergens, defects in innate immunity, and an altered microbiome.

Epidemiology

• 45% of those with AD have symptoms in the first 6 months of life; 60% during the 1st year and 85% before the age of 5 years old
• There is higher prevalence in urban versus rural populations.
• Prevalence of AD is 20% in the United States. Internationally, estimates range widely between 0.3% and 20.5%.
• 13.4% have AD by the age of 1 year and 21.5% have AD by 2 years of age.

Risk Factors

General Prevention

• One key factor in preventing AD flares is through using emollients to retain moisture of the skin.
• Another useful tactic is the avoidance of exacerbating factors. These include heat, low humidity, sweat, excess saliva, nonbreathable clothing fabrics, infections, bathing without moisturizing immediately afterwards, harsh solvents, and detergents.

Pathophysiology

• AD is due to a combination of impairment of skin barrier and an abnormal immune response.
• Defects in skin barrier integrity result in increased water loss in both skin marked with lesions as well as unaffected skin. Irritants and allergens impair the skin’s barrier functions leading to cytokine production, inflammation, and development of eczematous lesions. Defects in the skin barrier lead to allergen penetration leading to sensitization.
• Abnormalities of the immunologic reaction such as a strong type 2 T-helper cell (TH2) response to environmental allergens and defects in innate immunity lead to an increased inflammatory state.
• On histology typical findings of AD include spongiosis (edema of the epidermis), acanthosis, hyperkeratosis, and lymphohistiocytic infiltrate of the dermis. Spongiosis leads to stretching and rupture of intercellular attachments with vesicle formation.
• AD is a disorder of immune dysregulation with increased T-cell activation and increased cytokine production of interleukin (IL)-4, IL-5, and IL-13, which lead to increased IgE production.

Etiology

• The exact cause of AD is still under debate but it is the result of dysfunction of the innate skin barrier, genetic predisposition, environmental exposures, and immune dysregulation. Increased viral (warts and molluscum) and dermatophyte infections seen in atopic patients appear to be related to cytokine-induced suppression of endogenous antimicrobial peptides.
• Patients often have elevated IgE levels and decreased chemotaxis of neutrophils.

History

• Diagnosis is based on history of symptoms, family history, and physical exam.
• Important elements of the history include sleep impairment, age of onset, pruritus, soap and detergent use, family history of atopy, asthma, or allergic rhinitis.
• Assessment of sleep disturbance, itching, impact on daily activities, area of body covered by lesions, skin thickening, bleeding, alteration of pigmentation, oozing or cracking of skin

Physical Exam

• Skin findings include erythema, xerosis, diaper area spared, lichenification, dyspigmentation.
• Infants have red, scaly pruritic, crusted lesions on extensor surfaces, trunk, extensor surfaces, cheeks, or scalp with sparing of diaper area.
• Children: flexor surfaces (wrists, ankles, antecubital, or popliteal fossae)
• Older children and adolescents often have lichenified plaques with distribution in flexural surfaces especially antecubital and popliteal fossae, volar aspect of wrists, ankles, and neck; also may have reticulate pigmentation of the neck
• Adults have more localized and lichenified lesions in skin flexures also involving the face, neck, or hands.
• Acute flares reveal erythematous and scaly maculopapular exudative patches.
• Chronic disease is characterized by hyperpigmentation or hypopigmentation, lichenification, and scaling.
• Severe AD can present as exfoliative erythroderma with diffuse scaling and erythema.
• Other associated findings include Dennie-Morgan folds (infraorbital folds), pityriasis alba (dry white patches), hyperlinear palms, facial pallor, infraorbital darkening, follicular accentuation, keratosis pilaris (dry, rough hair follicles on extensor surfaces of upper arms and thighs), and ichthyosis.

Differential Diagnosis

• Tinea corporis
• Severe seborrheic dermatitis
• Contact dermatitis
• Allergic or irritant psoriasis
• Wiskott-Aldrich syndrome
• Langerhans cell histiocytosis
• Acrodermatitis enteropathica
• Secondary syphilis
• HIV/AIDS related skin changes
• Netherton syndrome
• Viral exanthema
• Ichthyosis vulgaris
• Food allergy
• Drug eruptions
• Phenylketonuria
• Nutritional deficiencies
• Scabies
• Xerosis
• Hyper-IgE syndrome
• Metabolic deficiencies (carboxylase or prolidase)

Diagnostic Tests and Interpretation

• AD is a clinical diagnosis without a diagnostic test. Laboratory testing may be used to distinguish from other conditions or to diagnose complications such as infections.
• Biopsy can be helpful to rule out other skin disorders, such as psoriasis.
• IgE levels can be elevated but need not be checked.
• Bacterial cultures of skin can be obtained to rule out superinfections.
• Rapid fluorescent antibody studies, polymerase chain reaction studies, or viral cultures, and Tzanck smear can identify the presence of eczema herpeticum (EH).

General Measures

• Treatment approaches address restoration of skin barrier, removal of allergens, and hydration of the skin.
• Avoid factors such as heat and low humidity.
• Frequent use of emollients to promote moisture retention; creams with low water and high oil content or ointments at least twice a day and immediately after bathing
• Treat skin infections.
• Antihistamines to control itching
• Avoidance of irritants and allergens that could trigger a flare. Common agents are soaps, lotions, and detergents with fragrances.
• Dilute bleach bath: Apply topical steroids to the affected areas and moisturizer to the rest of the skin. Moist gauze or cotton clothing dampened by warm water is then applied with a layer of dry cotton clothing on top. The dressings can be left on for 3 to 8 hours. They can also be used for 24 to 72 hours or overnight for up to 1 week.

Medication (Drugs)

Issue for Referral

Referral should be considered in the following circumstances:

• If the diagnosis of AD is in question
• The patient does not respond to treatment.
• If high potency steroids are being considered for sensitive areas such as face or skin folds
• If the child may need immunosuppressive therapy

Inpatient Consideratons

• Admission for AD alone is uncommon but may be necessary for severe AD flares unresponsive to outpatient therapy.
• Superinfections with bacteria or herpes herpticum requiring IV treatment
• Persistent AD requiring further workup for alternative diagnosis

Follow-Up Recommendations

Prognosis

The majority of children with AD have resolution of symptoms by adulthood. Studies have shown that by 8 years after diagnosis, 80% did not have persistence of symptoms and 20 years after <5% had persistence of symptoms. About 40–70% of children with AD no longer have symptoms by age 6 to 7 years. Children with later onset and severe AD are more likely to have persistent disease into adolescence and adulthood.

Complications

• The major complications are viral and bacterial infections.
• Decreased cell-mediated immunity, decreased chemotaxis, and decreased production of endogenous antimicrobial peptides can result in increased infection. In addition, given the fissures and open excoriations, there is a risk of superinfection. The decreased integrity of the skin can result in widely spread cutaneous infections.
• The most common bacterial infection is with Staphylococcus aureus. AD is a risk factor for MRSA colonization. Colonization rates of MRSA are higher in those with AD (11–34%) than the general population (1–3%). The virulence of this bacteria in patients with AD is partially due to the production of staphylococcal enterotoxins which act as superantigens. MRSA is associated with increased skin infections. Those colonized are less responsive to topical corticosteroids.
• S. aureus infections can be superficial or invasive leading to bacteremia, endocarditis, septic arthritis, or osteomyelitis.
• The most commonly associated fungal infection is Malassezia species and can induce inflammation by cell-mediated immunity and IgE production.
• EH is caused by the herpes simplex virus (HSV). Those with EH usually have more severe or earlier onset of AD as well as increased risk of food allergies and asthma compared to AD patients without EH. EH can cause disseminated vesicles with skin breakdown, viremia, lymphadenopathy, or more severe infections such as meningitis or keratoconjunctivitis. Can be life-threatening. Infections are treated with acyclovir.
• Similar problems can also be seen with coxsackievirus or molluscum contagiosum and used to occur with the smallpox vaccine.
• Early growth delay is not uncommon among children with AD, although later catch-up growth is generally seen. This may be related to impaired growth hormone release. Growth delay can occur independent of topical steroid exposure.
• Increased prevalence of emotional, behavioral, and psychological issues secondary to sleep disturbance

ICD-9

• 691.8 Other atopic dermatitis and related conditions
• 690.12 Seborrheic infantile dermatitis

ICD-10

• L20.9 Atopic dermatitis, unspecified
• L20.83 Infantile (acute) (chronic) eczema
• L20.89 Other atopic dermatitis

SNOMED

• 24079001 Atopic dermatitis (disorder)
• 402195009 Infantile atopic dermatitis
• 402196005 Childhood atopic dermatitis