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Atopic dermatitis is a very common skin condition that affects approximately 20% of children in developed countries. Ninety percent of patients have onset of disease before age 5 and 65% will have symptoms by 18 months of age. Rates continue to increase in developing countries, but have stabilized in developed countries. Diagnostic criteria, established by Hanifin and Rajka, and adapted by the UK Working Party in 1994, are based on clinical manifestations (Table 8-5).5,6 More than 75% of patients will report a family history of atopy (allergic rhinitis, asthma, and dermatitis). Asthma and allergic rhinitis are seen in many patients with atopic dermatitis; however, asthma flares do not necessarily occur at the same time as skin flares. The atopic march is commonly referred to as the march from atopic dermatitis to asthma and allergic rhinitis. It is estimated that approximately 33% of all children with atopic dermatitis will go on to develop asthma. However, 50% of children with severe atopic dermatitis will go on to develop asthma and 75% will develop allergic rhinitis.7
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The psychosocial effects of atopic dermatitis have been emphasized in recent years, and were summarized in a recent review by Kelsay et al.8 Chamlin et al identified 4 domains of distress9:
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Physical health (sleep disruption, itching, and related scratching)
Emotional health (fussiness in children, various emotional stresses for parents)
Physical functioning (activity restrictions, missed work)
Social functioning (feelings of isolation, negative reactions from family members)
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The etiology of atopic dermatitis is multifactorial, including a combination of genetic susceptibility and environmental triggers and/or exposures. Many gene loci have been linked to atopic dermatitis, including genes associated with increased immunoglobulin E (IgE) levels, or T lymphocyte activation. Filaggrin, a protein that is important in the barrier function of the epidermis, is also a factor in the pathogenesis of the disease.10
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The association of atopic dermatitis and food allergy is a very controversial topic, as many believe that food allergies are responsible for skin flares. In rare cases, specific foods may cause worsening of atopic dermatitis. Usually elimination diets do not result is significant skin improvement.
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Patients with atopic dermatitis have increased susceptibility to Staphylococcus aureus and other infections such as molluscum, herpes simplex virus (HSV), human papilloma virus (HPV), and Trichophyton rubrum and Malasezzia species. About 90% of atopic dermatitis skin lesions are colonized with microbes, usually S. aureus. This is thought to be related not only to an altered epidermal barrier but also to decreased production of antimicrobial peptides.11 Recurrent infections can be problematic and drive the inflammatory cascade.
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Clinical Presentation
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The parent or patient usually complains of a rash and moderate to severe itching.
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The morphology of the skin lesions in atopic dermatitis is similar in all age groups. Excoriations, erythematous, scaly papules and plaques, vesicles, serous drainage, and crusts are common findings.
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Three classic distributions of atopic dermatitis are recognized: infantile, childhood, and adult variants.
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Infants usually present with dermatitis involving the cheeks, trunk, and extensor extremities (Figure 8-7). The scalp may also be involved, but the diaper area is notably spared.
Young children tend to have involvement of the posterior neck, flexor extremities (antecubital fossae and popliteal fossae), wrists, hands, ankles, and feet (Figure 8-8). Keratosis pilaris may be present on the extensor arms and thighs (Figure 8-9).
Older children and adults have posterior neck, flexor extremities, and hand involvement. Changes of chronic atopic dermatitis, including thickened hyperkeratotic plaques with lichenification and prurigo nodularis, may also be present. Postinflammatory hypopigmentation or hyperpigmentation are common associated findings. Xerosis is a common feature.
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Patients with atopic dermatitis are frequently colonized with S. aureus and they may have plaques with erosions, drainage with yellow crusting, or hemorrhagic crusting. Infections with warts and molluscum contagiosum are also more common in patients with atopic dermatitis. Susceptibility to widespread HSV infection is characteristic of atopic dermatitis. Eczema herpeticum is the result of a severe HSV infection. It presents with multiple widespread monomorphic, "punched-out" discrete erosions with hemorrhagic crusting (Figure 8-10). Usually this can be treated with oral antiviral medications. Concurrent staphylococcal infection is common in patients with eczema herpeticum. Patients may be ill-appearing or have associated fever. Parenteral antiviral medications and hospital admission may be appropriate in these cases. Rapid initiation of antiviral therapy has been shown to improve outcomes.12
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Skin biopsies are usually not required, but they can be helpful to rule out other disorders. Elevated serum IgE levels are common. Radioallergosorbent (RAST) testing has not been shown to be clinically relevant in the treatment of atopic dermatitis.
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Infants: The key diagnostic features are red, crusted, scaly, pruritic plaques on cheeks, trunk, and extensor extremities.
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Older children and adults: The key diagnostic features are red, scaly pruritic plaques on the neck, antecubital and popliteal fossae, wrists, ankles, and feet. Lichenification may be present.
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Differential Diagnosis
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✓ Seborrheic dermatitis: Presents with yellow, greasy scale most commonly on head, face, and neck region. Can be widespread in infancy. Not as pruritic as atopic dermatitis.
✓ Psoriasis: Presents with well-demarcated, persistent plaques with overlying scale. The diaper area in infants is commonly affected.
✓ Contact dermatitis (irritant or allergic): Presents with well-demarcated eczematous plaques, usually localized to areas of contact.
✓ Dyshidrotic eczema: Presents with deep-seated noninflammatory 1 to 3 mm vesicles on the palms and soles.
✓ Juvenile palmar–plantar dermatosis: Presents with superficial desquamation of the feet, exacerbated by sweating.
✓ Tinea corporis: Presents with well-demarcated scaly, annular plaques, often with a raised border and central clearing.
✓ Other: Nummular dermatitis, scabies, perioral dermatitis, immune deficiency syndromes, nutritional deficiency syndromes, drug eruption, and graft-versus-host disease.
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Education: Treatment begins with education of the parents, caregivers, and patients on the care of skin in atopic dermatitis.13,14
Hydration and restoration of the skin's barrier function: This plays a vital part in the management of atopic dermatitis. Daily 5-minute baths in lukewarm water are encouraged. Colloidal oatmeal powder (Aveeno) and bath oil (RoBathol) can be added to the tub water. Bubble bath products should be avoided. Low detergent hypoallergenic cleansers are recommended for removal of any surface crusts (Table 8-2). Allowing the water to evaporate off the skin can increase xerosis, but application of a hypoallergenic moisturizing ointment or cream (Table 8-2), within 3 minutes after exiting the tub, increases hydration and improves barrier function. Lotions and products containing alpha or beta hydroxy acids, or urea may improve xerosis, but often sting when applied to inflamed skin. Lotions containing ceramides (eg, CeraVe, Cetaphil Restoraderm) may be better tolerated. Tap water soaks or Burow's wet dressings may be helpful for crusted areas. See Table 6-5 for instructions on wet dressings. Moisturizers or topical steroids can be applied during or after the soaks.
Topical steroids: Mild atopic dermatitis can usually be controlled with cream or ointment-based moisturizers and over-the-counter 1% hydrocortisone ointment. One percent hydrocortisone ointment can be used, once or twice a day, to any area of involvement, including the face and buttocks.
Moderate disease, in children and adults, may require class 4 or class 5 mid-potency steroid ointments or creams (Table 8-3). Good starting regimens for the body and extremities include Derma-Smoothe FS oil twice a day after baths. The oil serves as a moisturizer, so additional moisturizers are not required with this regimen. Additional choices for older children and adults include fluocinolone 0.025% ointment and triamcinolone acetonide 0.025% or 0.1% ointments. For the face and neck, good starting choices include hydrocortisone 2.5% ointment and desonide 0.05% ointment. Creams tend to be preferred by adult patients, and may be more elegant, but also may burn or sting more than ointments when applied, and are considered less potent for a given steroid class. Systemic steroids should be used rarely as discontinuation often leads to more severe flaring.
Topical calcineurin inhibitors: These are nonsteroidal anti-inflammatory immunosuppressant agents. They are good choices for the face and intertriginous areas, as secondary cutaneous atrophy is not a risk with their use. Pimecrolimus (Elidel) 1% cream is approved for mild to moderate atopic dermatitis in children older than 2 years, but has been studied in the 3- to 23-month age group with no severe side effects. Tacrolimus (Protopic) 0.03% ointment and 0.1% ointments are approved for moderate to severe atopic dermatitis in children older than 2 years of age. Both medications have US Food and Drug Administration (FDA) black box warnings attached for a theoretical risk of cancer (specifically lymphoma in mice who received 30-50 times higher doses than the maximum recommended human dose). Ongoing safety studies have not revealed any increased systemic immunosuppression or increased malignancy risk.15
Antihistamines: Oral antihistamines can be helpful in breaking the "itch–scratch" cycle, but they are not considered a primary treatment for atopic dermatitis–related pruritus. Sedating agents can be especially helpful in children who have trouble falling asleep due to itching at night. Short courses can be used regularly until pruritus is improved. Diphenhydramine and hydroxyzine may be used. Additionally cetirizine (Zyrtec), loratadine (Claritin), and fexofenadine (Allegra) can be helpful in the morning due to their nonsedating effects.
Management of active infections: Cephalexin (Keflex) is a reasonable antibiotic to start with. Standard dosing for 7 to 10 days is usually appropriate. If there is concern for methicillin-resistant S. aureus (MRSA), a culture should be sent to confirm the susceptibility. Oral trimethoprim–sulfamethoxazole (Bactrim) or clindamycin is usually acceptable in the pediatric age group. Tetracyclines should not be used in children less than 8 years old. Bleach (sodium hypochlorite) baths and mupirocin (Bactroban) ointment can be helpful in reducing bacterial load and staphylococcal carriage.16 Mupirocin ointment should be used twice daily for the first 5 days of each month in the nostrils. Bleach baths with one quarter to one half cup of bleach per full bathtub can be done once or twice a week. Bleach baths do not usually cause burning or stinging, as the chlorine concentration is low. Parents should continue with skin moisturization routine after baths.
Avoidance of triggers: Common triggers include heat and sweat for some individuals and for others, cold, dry air. Other potential triggers include house dust mites, pet fur, wool, synthetic fabrics (eg, nylon), dyed fabrics, tobacco smoke, fragrances (which may be present in shampoos, soaps, lotions, laundry detergents, fabric softeners), saliva, or prolonged exposure to water. Fingernails should be trimmed short.
Food allergy: Allergies to foods such as cow's milk, eggs, fish, peanuts, and wheat are more common in children with atopic dermatitis, but foods are specific triggers for flares in only a small percentage of children. There are blood (RAST) and skin prick tests that can identify specific allergens, but they are often positive in children who are not truly allergic and they are not considered to be helpful before age 2. It is important to determine which foods are relevant and cause clinical symptoms such as urticaria. Extreme food elimination diets, which have become more popular in recent years, are discouraged as they can result in nutrition and lack of essential dietary nutrients.
Ultraviolet light therapy and systemic immunosuppressant agents: Severe widespread disease may require narrow-band ultraviolet light therapy, cyclosporine, methotrexate, azathioprine, or mycophenolate mofetil, but these should be used in consultation with specialists.
Psychological burden of disease and quality of life issues: Controlling pruritus is an important aspect of atopic dermatitis treatment. In a quality of life study, ratings of pruritus intensity, both self-reported and parent reported, were inversely correlated with parents' quality of life (psychosomatic well-being, social life, emotional coping, and acceptance of the disease). Older children's itch has been shown to be negatively correlated with quality of life, and positively with depressed mood and catastrophic thinking.17 Nighttime itching affects both parents and children. Parents try to comfort the children at night and this can result in parental sleep deprivation and daytime exhaustion. Parental depression correlates more strongly with sleep deprivation than with severity of their child's atopic dermatitis. Sleep deprivation also has consequences for school-age children (patients and siblings), affecting cognitive function and behavior.
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Most patients with atopic dermatitis improve with time, but a subset progresses to persistent skin disease and allergic rhinitis and/or asthma.
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Indications for Consultation
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Severe or persistent disease that does not respond to treatment, especially in children, could indicate concurrent serious underlying disease.
Patients with recurrent skin infections requiring oral or topical antibiotics.
Patients with eczema herpeticum should be referred to dermatology and to ophthalmology emergently if there is questionable or confirmed eye involvement.
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