ATOPIC DERMATITIS
Atopic dermatitis is a chronic disorder characterized by xerosis, pruritus, scaly erythematous patches, and thickening of the skin with enhancement of normal skin markings (lichenification). It is frequently associated with a personal or family history of hay fever, asthma, or allergic rhinitis. It can be divided into three phases based on the age of the individual: infantile, childhood, and adolescent.
INSIGHT 
Although many patients and families will insist on “finding the cause,” experience and studies confirm that specific allergen identification and avoidance or dietary modification is less helpful than focusing on skin treatment and maintaining healthy skin barrier function.
AGE Onset usually from age 2 to 12 months, and almost all cases by age 5 years. Nearly 80% of cases will resolve by adulthood.
GENDER M = F.
INCIDENCE Common and thought to be increasing.
HEREDITARY PREDISPOSITION More than two-thirds have personal or family history of allergic rhinitis, hay fever, or asthma. Many children with atopic dermatitis develop asthma and/or hay fever later in life.
PREVALENCE 10% to 15% of the childhood population with significant regional variability. Up to 11% of the US pediatric population affected.
The cause of atopic dermatitis is unknown; however, multiple factors are known to play a role in the development of atopic dermatitis. Certain genetic factors (such as filaggrin gene abnormalities) may lead to xerosis while others may result in immune dysregulation. Factors such as stress, climate, infections, irritants, and allergens seem to play a role in many patients as well. For the vast majority of patients, there is no one “trigger” or “cause,” but rather an unfortunate collection of constituents that all can worsen the disease. A central tenet in the pathophysiology of atopic dermatitis is believed to be the interplay between epidermal disruption and inflammation mediated by T-cells and Langerhans cells.
Atopic dermatitis is sometimes called “the itch that rashes.” Dry skin and pruritus are found in essentially all patients. Scratching the skin leads to the characteristic eczematous changes and a vicious itch-scratch cycle. Itching may be aggravated by cold weather, frequent bathing (particularly with hot water), wool, detergent, soap, and stress. The disease can wax and wane unpredictably, however, which probably contributes to the numerous misattributions of causes and remedies.
TYPE Patches and plaques with scale, crust, and lichenification. Lesions usually confluent and ill defined.
COLOR Erythematous.
Atopic children may demonstrate increased palmar markings, periorbital atopic pleats (Dennie–Morgan lines), keratosis pilaris, or white dermatographism. They also can develop widespread herpetic, wart, molluscum, or tinea infections because of their impaired skin barrier function.
Atopic dermatitis can be confused with seborrheic dermatitis, contact dermatitis, psoriasis, or scabies. Several metabolic disorders may manifest eczematous dermatitis and should be considered, including acrodermatitis enteropathica and phenylketonuria. Some disorders of immunity may also include atopic dermatitis, such as Wiskott–Aldrich syndrome, X-linked agammaglobulinemia, and hyper-IgE syndrome (Job syndrome).
Acute lesions show intraepidermal intercellular edema (spongiosis) with occasional vesicle formation and a dermal infiltrate comprised largely of lymphocytes with few eosinophils. Chronic lesions show acanthosis, hyperkeratosis, and spongiosis.
Laboratory studies are not needed to make the diagnosis of atopic dermatitis. Patients may have an increased IgE and/or eosinophilia. Radioallergosorbent testing (RAST) is frequently positive for multiple antigens but direct applicability to the dermatitis is exceedingly rare.
Conflicting data and great individual variability preclude definitive prognostication. However, the majority of patients significantly improve by school age with a minority requiring life-long management. A significant portion of affected children will develop asthma or hay fever later in life.
Because atopic dermatitis cannot be cured, the goal is to keep the condition under control and maintain the quality of life for the patient and the family. A four-pronged approach can be helpful in maximizing treatment, addressing each major aspect of atopic dermatitis, summarized in Figure 2-1: the treatment tetrahedron.
Improving moisturization is universally helpful and is the foundation of treatment for atopic dermatitis. The best moisturizer is the one that the patient will use. While greasier ointment preparations are better, such as hydrated petrolatum, Aquaphor, or Eucerin, low compliance limits the use in some patients. Less greasy creams such as CeraVe, Cetaphil, and Aveeno can still be highly effective and used more frequently throughout the day.
The “soak and seal” technique is highly effective in locking in moisture and consists of the following:
-
Bathing in lukewarm water for approximately 15 minutes daily.
-
Using a mild nonsoap cleanser such as Dove, Aveeno, or Cetaphil.
-
Patting the skin dry lightly with a towel to remove most of the water.
-
While still moist, applying the moisturizer liberally.
For the mildest cases, improved moisturization can often suffice. However, for more significant disease, anti-inflammatory agents are necessary. Systemic corticosteroids are generally best avoided; while incredibly effective in the short term, the rebound effect can be devastating and can create systemic corticosteroid dependence that is extremely difficult to manage.
While topical corticosteroids are the traditional cornerstone of treatment for atopic dermatitis, the topical calcineurin inhibitors tacrolimus and pimecrolimus have an important defined role in the management of this disease.
TOPICAL CORTICOSTEROIDS The most frequent reason for treatment failure is using a potency that is too low for the body site and severity. Fear of side effects from corticosteroids is very common and not necessarily without good reason, but must be tempered by the knowledge that proper use minimizes such adverse effects while providing true relief from the disease. In general, ointments are preferred but as with moisturizers, compliance may dictate use of a cream despite the fact that these can be more drying and even irritating in some cases.
-
Low-potency steroids (e.g., hydrocortisone 2.5% or desonide 0.05%) may be used for mild disease or on sensitive skin areas such as the face, axillae, or groin twice daily, no more than 2 weeks per month.
-
Mid-potency steroids (e.g., triamcinolone 0.1% and fluticasone propionate 0.005% ointment) may be used on the body or extremities twice daily, no more than 2 weeks per month.
-
High-potency steroids (e.g., fluocinonide 0.05% and clobetasol propionate 0.05% ointment) are reserved for older children on severely affected areas twice daily, no more than 2 weeks per month.
Patients need to be cautioned about steroid side effects. Continuous or overzealous use may cause thinning of the skin, stretch marks (striae), telangiectasia, and significant systemic absorption. Infants are at greater risk for increased absorption because of their increased body surface area-to-weight ratio. Topical steroids applied near the eye area may lead to cataracts and glaucoma.
TOPICAL CALCINEURIN INHIBITORS Tacrolimus has been used as a systemic treatment for transplant rejection and is an approved topical preparation for atopic dermatitis. Tacrolimus and the related chemical pimecrolimus are important additions to the armamentarium as they are not corticosteroids and do not share the same side effects. However, they are very expensive and have a shorter history of safety data than corticosteroids. The FDA has issued a black box warning for these medications highlighting a possible association with skin cancer and lymphoma, prompting concern from clinicians and patients alike. While more than 15 years of clinical practice has yielded minimal data suggesting a significant increase in long-term adverse effects from the use of topical calcineurin inhibitors in the management of atopic dermatitis or other cutaneous conditions, ongoing surveillance is warranted. These medications are probably best used as steroid-sparing agents in patients with moderate-to-severe atopic dermatitis who would be at significant risk from steroid side effects. Side effects reported include burning and itching in some patients, which tend to resolve as the skin improves.
Topical or oral antibiotics may be needed if the skin becomes secondarily infected, a very common scenario in atopic dermatitis. However, systemic antibiotics are not indicated in the absence of infection; use in this context may unnecessarily promote antibiotic resistance.
Open and moist areas, which may weep or become crusted, vesiculation and frank pustules frequently indicate bacterial infection in patients with severe disease. Topical mupirocin is generally the antibiotic of choice because of its efficacy against Staphylococcus and the relatively rare rate of contact allergy. It may be applied thrice daily to such impetiginized areas for 7 to 14 days. Bacitracin and neomycin are frequent contact dermatitis sensitizers and should be avoided. Daily bleach baths—adding a half cup of bleach to a full bathtub, achieving a very dilute bleach solution—can also be helpful for decolonization of skin flora that may contribute to secondary infection.
In more widespread infection, oral antibiotics may be used for 7 to 10 days. In patients with recurrent infections a longer maintenance course of antibiotics may be considered. Commonly prescribed antibiotics include empiric cephalexin (25–50 mg/kg/d divided qid, not to exceed 4 g/d) and dicloxacillin (25–50 mg/kg/d divided qid, not to exceed 2 g/d), though obtaining skin culture with sensitivities can be very helpful in guiding antibiotic therapy, especially in patients with recurrent infections.
This corner of the tetrahedron is least populated with good options and, perhaps as a result of this, most frequently ignored. However, there is still a role for antipruritic treatments.
ANTIHISTAMINES These oral medications are unfortunately not very effective at controlling the itch of atopic dermatitis. They continue to be useful at bedtime as the side effect of drowsiness is often effective at improving sleep. In rare instances, a paradoxical hyperactivity may be seen. The most commonly prescribed antihistamines are hydroxyzine (2 mg/kg/d divided tid or qid) and diphenhydramine (1–2 mg/kg tid, not to exceed 300 mg/d). Topical antihistamines are not recommended because of the relatively high risk of developing allergic contact dermatitis and limited efficacy in controlling atopic dermatitis-associated itch.
ANESTHETICS Topical pramoxine (available as 1% cream and in combination creams) can be helpful at alleviating itch very quickly by literally inhibiting the nerves, which convey the sensation.
COOLING PREPARATIONS Topical preparations of menthol, camphor, and calamine may all be helpful, especially in combination form. Aveeno Anti-Itch cream (regular strength), Sarna Sensitive Skin lotion, and Eucerin Itch-Relief Moisturizing spray all contain combinations of these ingredients and can be helpful for acute pruritus. Encouraging patients to apply the antipruritic preparations instead of scratching can be extremely helpful. In all patients, but especially in children younger than 2 years, camphor use should be carefully limited as camphor toxicity can occur.
Frequently appearing on the face, this common problem is often extremely worrisome to new parents. Many of these patients have atopic diseases in the family. Milk-protein allergy is frequently blamed, but the high rate of improvement with time alone makes this observation very suspect.
AGE Symptoms appear between age 2 and 6 months and the majority clear by age 2 to 3 years.
TYPE Patches and erosions with scaling, exudation with wet crusts, and fissures.
COLOR Erythematous pink to red.
DISTRIBUTION Begins on face (cheeks, forehead, and scalp) and then spreads to body, usually sparing diaper area (Fig. 2-2).
AGE Typically follows infantile atopic dermatitis and is seen from age 4 to 10 years.
DISTRIBUTION Wrists, ankles, antecubital, and popliteal fossae.
AGE Begins at age 12 years and continues into adulthood.
TYPE Papules coalescing into lichenified plaques.
DISTRIBUTION Flexor folds (Fig. 2-5), face, neck, upper back, hands, and feet.
STRIAE DISTENSAE
Atrophic, scar-like lesions that may be seen from topical or systemic corticosteroid use. While they do not cause significant morbidity, numerous striae can be disfiguring and are difficult to reverse.
SYNONYM Stretch marks.
AGE Persons of all ages may be affected; seen more commonly in adolescents and adults.
GENDER F > M.
INCIDENCE Common.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
