AD impacts not only the patient with the disease but impacts other family members, particularly parents who may find absences from work in order to stay home to care for their child affecting income and health benefits. Healthy siblings compete for attention and interface with parents, who find themselves consumed with the overwhelming task of caring for the child with AD. Research has suggested that caring for a child with type I diabetes mellitus is comparable to caring for a child with moderate-to-severe AD. Atopic dermatitis has more impact on the quality of life in childhood than any other childhood dermatoses with the exception of scabies. General pain and pruritus in any disease have a negative impact on the quality of life, but in AD when the pruritus is often intense and relentless, the negative burden is even greater, leading to disruptions in sleep, disruptions with play and recreational activities, as well as interference with normal social interactions and development. The economic impact of caring for a family member with AD has been compared to the cost of other chronic diseases such as emphysema or epilepsy. Within the past decade, the cost of care for AD was estimated to be over $ 300 million, with visits to the emergency room for acute extensive flares largely responsible for this cost.

The ability for the skin barrier to absorb and hold water is essential in AD as well as in other xerotic skin diseases such as ichthyosis vulgaris. In the past 8 years, breakthrough research has uncovered filaggrin as a key protein in the normal skin barrier. Mutations of this essential protein for an intact skin barrier were found in the epidermis of patients with ichthyosis vulgaris as well as in patients with AD. These mutations represent a strong genetic predisposition for atopic eczema, asthma, and allergies.

Loss of filaggrin means a poorly formed stratum corneum and xerotic barrier that is prone to water loss and unable to protect the body. Xerosis leads to pruritus, which then promotes scratching and excoriations. As the skin barrier is further disrupted by prolonged itching and scratching, it becomes vulnerable to a host of potential infections and penetration of allergens that trigger IgE production.

The hallmark of AD is pruritus, which is often intense and relentless, disrupting every aspect of the patient’s life. The course of AD tends to be chronic and relapsing. As an inflammatory skin disease, AD will present with varying degrees of erythema, inflammatory papules, which often coalesce to form eczematous plaques, as well as areas of weepy dermatitis. Often areas of involvement will evolve into scaly, xerotic plaques, and as the disease becomes chronic, lichenified changes are evident and indicative of extended periods of itching and scratching. Morphology and distribution vary with age (Figure 3-1). Typically in infants and very young children, AD will affect the face and extensor arms and legs (Figures 3-2 and 3-3A). The diaper region, where moisture tends to be retained, is often spared. In older
children and adults, distribution favors flexural areas, including anterior neck, antecubital fossa, and popliteal space, and can affect the breasts, nipples, and trunk (Figures 3-3B 3-3C, and 3-4). The scalp, face, and eyelids can also be affected, and in general, the axillae and groin folds are spared at any age.

AD is a clinical diagnosis with common cutaneous features used to diagnose AD (Box 3-1). Additionally, the diagnoses can only be made after exclusion of differential diagnoses (above) with similar presentations. A KOH test can differentiate tinea from AD. Punch biopsy will identify psoriasis and other noneczematous dermatoses.

When flares are severe and extensive, oral corticosteroids may be necessary to regain control. Generally, a tapering dose of prednisone over the course of 6 days is adequate with the addition of a TCS at the end of the taper. In patients with recalcitrant disease, a course of cyclosporine (CSA) can be utilized. This is generally prescribed when intense topical therapy and/or courses of prednisone have not halted the AD flare. Baseline labs of chemistry panel, complete blood count, and urinalysis need to be obtained prior to starting this therapy and monitored monthly. Blood pressure is also monitored regularly. Due to the potential for renal toxicity and hypertension, it is not a therapy that can be used indefinitely, and after a 6-month course, transition to another therapy is warranted. Patients with known renal disease or uncontrolled hypertension should not take CSA. The starting dose of CSA when prescribed is usually at 5 mg/kg/day. This dose will quickly reduce both pruritus and inflammation and induce a remission, giving patients worn down by their disease a reprieve. After 6 months of therapy, transition to another therapy is usually indicated. Ultraviolet therapy or other systemic therapies, including methotrexate, azathioprine, mycophenolate mofetil, and interferon-γ, have shown varying levels of efficacy in AD patients.

It is important for AD patients to recognize possible extrinsic factors that may trigger a flare of their skin disease. Common trigger factors for AD flares are any type of infection, including viral, bacterial, fungal, and yeast infections (Figures 3-5A and B). Counseling patients to recognize signs of infection and treating quickly is important. Primary outbreaks of herpes simplex virus (HSV) can result in eczema herpeticum (Figure 3-5C). Treating HSV with acyclovir 400 mg t.i.d. for 1week is adequate; however, treatment for eczema herpeticum should include zoster doses of antivirals. Checking for tinea when AD is flaring should be part of your physical exam. Checking toe web spaces, groin, and other intertriginous areas is important when looking for causes of a continued flare. Widespread fungal infections may need treatment with a systemic antifungal. Stress, dry climate, allergic reactions are also potential triggers. AD can severely impact a patient’s (and their caregivers) quality of life and should be discussed with the patient. Abnormal pigmentation, lichenification, scars, striae, and secondary infections are complications from AD (Figure 3-5D).

Severe AD patients require enormous amounts of clinic time to gain control of their disease. Psychological factors are often addressed, as are sleep, trigger factors, explanation of treatments, side effects, and detailed instructions regarding use of medications. An AD patient who becomes erythrodermic will need inpatient hospitalization. A referral to a dermatologic professional who specializes in atopic disease is appropriate. The National Eczema Association (NEA) is a nonprofit patient-centered organization for patients and their families. They offer a host of valuable educational information and support for families as well as for health care professionals.

AD patients require long periods of time and educational dialogue in order to understand the fundamentals of how to manage flares, then maintain control of the disease, and how to recognize signs of skin infections. Compliance to treatment plans is essential for maintenance once the skin disease is under control. Ideally a dermatology nurse will be involved in the teaching and demonstration of treatments, as this can be a time-consuming process that may not automatically be built into the providers’ schedule. Studies have shown that nurse-led clinics help reduce the severity of AD outcomes in children and compliance increase up to 800%.