Section 2. Eczematous 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.

Epidemiology

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.

Pathophysiology

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.

History

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.

Physical Examination

Skin Findings

Type Patches and plaques with scale, crust, and lichenification. Lesions usually confluent and ill defined.

Color Erythematous.

Special Clinical Features

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.

Differential Diagnosis

Atopic dermatitis can be confused with seborrheic dermatitis, contact dermatitis, psoriasis, or scabies. Some 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).

Dermatopathology

Acute lesions show intraepidermal intercellular edema (spongiosis) with occasional vesicle formation and a dermal infiltrate is comprised largely of lymphocytes with few eosinophils. Chronic lesions show acanthosis, hyperkeratosis, and spongiosis.

Laboratory Examination

May have an increased IgE and/or eosinophilia. Radioallergosorbent testing is frequently positive for multiple antigens but direct applicability to the dermatitis is exceedingly rare.

Course and Prognosis

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.

Management

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.

Moisturization

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 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:

1. 1. Bathing in lukewarm water for approximately 15 minutes daily.

   2. Using a mild nonsoap cleanser such as Dove, Aveeno, or Cetaphil.

   3. Patting the skin dry lightly with a towel to remove most of the water.

   4. While still moist, applying the moisturizer liberally.

Anti-Inflammatory Agents

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.

1. a. Low-potency steroids (e.g., hydrocortisone 2.5%) 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.

   b. Mid-potency steroids (e.g., triamcinolone 0.1% and fluticasone 0.005%) may be used on the body or extremities twice daily, no more than 2 weeks per month.

   c. High-potency steroids (e.g., fluocinonide and clobetasol) 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 was approved in 2000 as a 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 much 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 many clinicians and patients to avoid their use. 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.

Antibiotics

Topical or oral antibiotics may be needed if the skin becomes secondarily infected, a very common scenario in atopic dermatitis. 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 sensitizers and should be avoided. 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. The most commonly prescribed antibiotics include 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.

Antipruritics

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.

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.

Infantile Atopic Dermatitis

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.

Epidemiology

Age Symptoms appear between age 2 and 6 months and the majority clear by age 2 to 3 years.

Physical Examination

Skin Lesions

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).

Childhood-Type Atopic Dermatitis

Epidemiology

Age Typically follows infantile atopic dermatitis and is seen from age 4 to 10 years.

Physical Examination

Skin Lesions

Type Papules coalescing into lichenified plaques with erosions and crusts (Figs. 2-3 and 2-4).

Distribution Wrists, ankles, antecubital, and popliteal fossae.

Adolescent-Type Atopic Dermatitis

Epidemiology

Age Begins at age 12 years and continues into adulthood.

Physical Examination

Skin Lesions

Type Papules coalescing into lichenified plaques.

Distribution Flexor folds, face, neck, upper back, hands, and feet (Fig. 2-5).

Atrophic, scarlike lesions that may be seen from topical or systemic corticosteroid use. While they do not cause significant morbidity, numerous striae can be disfiguring.

Epidemiology

Age Persons of all ages may be affected, but seen more commonly in adolescents and adults.

Gender F > M.

Incidence Common.

Pathophysiology

Damage to the connective tissue (collagen and elastin) due to mechanical stretching, particularly in genetically susceptible individuals causes permanent breakage and alteration of elastic fibers. During the adolescent growth spurt striae frequently develop on the back and arms; during pregnancy they are frequently found on the abdomen. Topical or systemic corticosteroids (endogenous or exogenous) facilitate striae while topical retinoids mitigate against their formation.

History

Duration of Lesion(s) Years. The lesions often start as deep red–blue plaques and over time become more white in color and thinner.

Physical Examination

Skin Lesions

Type Atrophic linear plaques with fine wrinkling of the epidermis.

Size 1 to 10 cm.

Color Erythematous in younger lesions to hypopigmented in older lesions.

Shape Linear.

Distribution Frequently on the lower back, upper arms, and abdomen, but may occur anywhere topical steroids are applied (Fig. 2-6).

Differential Diagnosis

Striae secondary to rapid growth or weight gain must be distinguished from endogenous or exogenous Cushing syndrome.

Management

Cautious use of topical and corticosteroids with frequent breaks from the medication can minimize the risk of striae. Avoiding high-potency steroids to more delicate skin such as that of the face or groin is also helpful. Concurrent use of tretinoin cream or gel has been shown to prevent the formation of striae and improve the appearance even after their development. Pulsed dye laser is helpful for decreasing the erythema and may increase the collagen in the lesions.

Lichen simplex chronicus (LSC) is a localized, well-circumscribed area of lichenification (thickened skin with enhanced skin markings) resulting from repeated rubbing, itching, and scratching of the skin. It is frequently seen in individuals with atopic, seborrheic, contact dermatitis, and psoriasis.

Epidemiology

Age Rarely seen in young children. Occurs in adolescents and adults.

Gender F > M.

Incidence Common.

Pathophysiology

A response to physical trauma by epidermal hyperplasia and acanthosis. The skin becomes highly sensitive to touch, probably related to proliferation of nerves in the epidermis. This leads to an itch-scratch cycle that is difficult to stop.

History

Duration of Lesion(s) Weeks to months or years.

Physical Examination

Skin Lesions

Type Well-defined plaque of lichenification (Figs. 2-7 and 2-8); at times with scale or excoriations.

Size 5 to 15 cm.

Color Usually hyperpigmented but occasionally hypopigmented.

Shape Round, oval, linear (following path of scratching).

Distribution Easily reached areas such as neck, wrists, ankles, pretibial area, thighs, vulva, scrotum, and perianal area.

Differential Diagnosis

LSC can be confused with tinea corporis, psoriasis, contact, or atopic dermatitis.

Laboratory Examinations

Hyperkeratosis, acanthosis, and elongated and broad rete ridges. Spongiosis is infrequent and vesiculation is absent. In the dermis, there is a chronic inflammatory infiltrate with fibrosis.

Management

Topical corticosteriods or calcineurin inhibitors (i.e., tacrolimus or pimecrolimus) will decrease pruritus. Occlusive dressings or wraps such as the Unna boot (gauze impregnated with zinc oxide and calamine) can also prevent scratching. Flurandrenolide, a mid-potency steroid, is available as a tape, which can be very useful for covering an area of LSC. It should be used sparingly as steroids under occlusion are much more potent. The side effects of prolonged or potent topical steroids should be reviewed. Continued use of topical steroids can lead to thinning of the skin, stretch marks, and accentuation of the blood vessels in the skin. For small localized areas of LSC, intralesional corticosteroids are often highly effective.

Prurigo nodularis (PN) is characterized by multiple lichenified intensely pruritic papules on the extremities. It is more frequently seen in individuals with a history of atopic dermatitis or allergies.

Insight

Simply asking the patient to demonstrate how he or she scratches, picks, or rubs will frequently confirm the diagnosis as the patient gladly obliges.

Synonym Nodular prurigo.

Epidemiology

Age Rarely seen in young children. Occurs in adolescents and adults.

Gender M = F.

Incidence Rare.

Pathophysiology

Although the pathophysiology is uncertain, PN may begin as a response to an insect bite or an area of dermatitis that is scratched, picked or rubbed. As with LSC, the trauma results in skin thickening, hyperkeratosis, and increased size of nerve fibers in the skin. Hepatic or renal dysfunction may be an associated factor in some cases, though the relationship may be simply as an underlying cause of pruritus.

History

Duration of Lesion(s) Months to years.

Physical Examination

Skin Lesions

Type Papules and nodules (Fig. 2-9); at times with scale or excoriation.

Size 3 to 20 mm.

Color Usually hyperpigmented but occasionally hypopigmented.

Shape Round, dome-shaped.

Distribution From several lesions in a localized area to hundreds of widespread nodules, frequently on the legs and arms.

Differential Diagnosis

Papular urticaria (insect bites), transepidermal elimination disorders (perforating dermatoses), bacterial or deep fungal infection of the skin including atypical mycobacteria, and some tumors can mimic this condition.

Laboratory Examinations

Skin biopsy can be helpful in confirming the diagnosis and eliminating infectious or neoplastic etiologies. Complete blood count, liver function tests, and chemistries are useful for evaluating the underlying hepatic or renal dysfunction.

Management

Topical corticosteriods or calcineurin inhibitors (i.e., tacrolimus or pimecrolimus) may decrease pruritus but frequently are ineffective. Occlusive dressings or wraps such as the Unna boot (gauze impregnated with zinc oxide and calamine) help prevent picking. Intralesional corticosteroids are often effective but difficult when the lesions are widespread. Phototherapy with ultraviolet B can be effective for some patients. Discussion of avoiding the picking or scratching behavior is important as well.

Dyshidrotic eczema is a special vesicular type of hand and foot eczema. It is an acute, chronic, or recurrent dermatosis of the fingers, palms, and soles characterized by a sudden onset of deep-seated pruritic, clear, “tapioca-like” vesicles; later, scaling, fissures, lichenification, and occasionally, secondary bacterial infection may occur.

Synonym Pompholyx (from the Greek for bubble).

Epidemiology

Age 12 to 40 years old.

Gender M = F.

Pathophysiology

The etiology is unclear and likely multifactorial. Approximately half the patients have an atopic background. Emotional stress is sometimes a precipitating factor. Hyperhidrosis may or may not be present. External contactants may play a role in some cases.

History

Duration of Lesions Several days.

Skin Symptoms Pruritus and painful fissures that may be incapacitating. Summer exacerbations are not infrequent.

Physical Examination

Skin Lesions

Type

1. a. Early Vesicles, usually small (1 mm), deep-seated, appear like “tapioca” in clusters (Fig. 2-10), occasionally bullae, especially on the feet.

   b. Late Scaling, lichenification, painful fissures, and erosions (Fig. 2-11).

Arrangement Vesicles grouped in clusters.

Distribution Hands and feet with sites of predilection bilaterally on the sides of fingers, palms, and soles.

Nails Dystrophic changes (transverse ridging, pitting, and thickening) may occur.

Other Hyperhidrosis is present in some patients.

Differential Diagnosis

Pompholyx can mimic a vesicular reaction to active dermatophytosis on the feet, an “id” (autoeczematization) reaction to inflammation or infection elsewhere, or an acute contact dermatitis.

Dermatopathology

Intraepidermal vesicles with balloon cells and sparse inflammation.

Course and Prognosis

Recurrent attacks with intervals of weeks to months with spontaneous remissions in 2 to 3 weeks.

Management

1. 1. Dry skin care with minimization of hand washing and wet-work, mild soap-free cleansers for washing, followed by ointments (e.g., hydrated petrolatum).

   2. For the active vesicular stage (early): Burrow’s wet dressings, commonly available as Domeboro Astringent Solution Powder Packets q6h for 15 minutes; large bullae may be drained but not unroofed.

   3. For the more chronic eczematous stage (late): High-potency topical corticosteroids are successful in some patients; rarely, a short course of systemic corticosteroids may be used, though the disease may rebound severely after cessation.

   4. Bacterial infection may be present and topical (mupirocin ointment tid to open or crusted areas) or oral antibiotics (e.g., cephalexin 25–50 mg/kg/d divided qid, not to exceed 4 g/d (7 days) may be helpful.

   5. PUVA (oral or topical as “soaks” in psoralen with controlled ultraviolet A light treatment) is successful in older patients if given over prolonged periods of time, especially in severe cases.

Nummular eczema is a chronic, pruritic, inflammatory dermatitis occurring in the form of coin-shaped plaques. It is seen in individuals with dry skin and/or atopic dermatitis.

Insight

Nummular eczema may be very refractory to treatment; oftentimes a much more potent corticosteroid must be used to these areas than for routine atopic dermatitis.

Epidemiology

Age Any age. Seen more commonly in older children and adolescents.

Gender M = F.

Incidence Common.

Etiology Unclear. Exacerbated by winter, excessive bathing, irritants.

Pathophysiology

Unclear. A common eczematous reaction pattern, frequently occurring in atopics.

History

Duration of Lesions Weeks, with remissions and recurrences.

Skin Symptoms Pruritus, may be mild or severe.

Physical Examination

Skin Lesions

Type Closely grouped, small vesicles and papules that coalesce into lichenified plaques, often 3 to 5 cm.

Color Deeply erythematous to hyperpigmented.

Shape Round or coin-shaped (Fig. 2-12), hence the adjective nummular (from Latin nummularis, “like a coin”).

Distribution Extensor surfaces of hands, arms, legs.

Differential Diagnosis

Nummular dermatitis must be distinguished from tinea corporis, contact dermatitis, and psoriasis.

Laboratory Examinations

Potassium Hydroxide Examination Scrapings negative for fungal elements excludes tinea corporis.

Dermatopathology Subacute inflammation with acanthosis, intraepidermal vesicles, and spongiosis in the epidermis.

Course and Prognosis

Remissions with treatment but frequent recurrences unless the skin is kept moisturized.

Management

1. 1. Dry skin care consisting of mild soap-free cleansers for washing, followed by frequent moisturization with CeraVe, Aveeno, or hydrated petrolatum.

   2. Topical corticosteroids can be applied for a limited time to the more moderate to severely affected areas. (See Topical Corticosteroids.)

There are two types of contact dermatitis:

1. Allergic contact: caused by sensitization of the skin to a topical allergen with type IV hypersensitivity.

2. Irritant contact: caused by mechanical or chemical injury to the skin without specific immunity.

Both reactions are characterized by pruritus, stinging, or burning of the skin and an eczematous rash.

Epidemiology

Age Irritant dermatitis may occur at any age, whereas allergic contact dermatitis is unusual in <1 year of age given time needed to sensitize/ expose skin to allergen/irritant.

Gender M = F.

Incidence May affect 20% of the pediatric population.

Etiology Exposure to an antigen that has previously caused sensitization in the case of allergic contact. A primary irritant that produces inflammation via injury in the case of irritant contact.

Pathophysiology

Allergic contact dermatitis is the classic example of type IV hypersensitivity reaction (delayed type) caused by sensitized lymphocytes (T cells) after contact with antigen. The tissue damage results from cytotoxicity by T cells or from release of lymphokines. Irritant contact dermatitis is caused by immediate physical damage to an area of skin.

History

Duration of Lesion(s) Acute contact: days, weeks; chronic contact: months, years.

Skin Symptoms Pruritus, often severe. Extensive lesions may be painful.

Physical Examination

Skin Findings

Type

1. a. Acute Inflammatory papules and vesicles coalescing into plaques (Fig. 2-13).

   b. Subacute Patches of mild erythema showing small, dry scales or superficial desquamation, sometimes associated with small, red, pointed or rounded, firm papules.

   c. Chronic Patches of lichenified (thickening of the epidermis with enhancment of the skin markings) firm, rounded or flat-topped papules, excoriations, and pigmentation (Fig. 2-14).

Arrangement Well-demarcated patterns suggestive of an external cause or “outside job.” Plant allergic contact dermatitis often results in linear lesions.

Distribution In exposed areas that come into contact with irritant or allergen.

Laboratory Examinations

Dermatopathology Inflammation with intraepidermal intercellular edema (spongiosis) and monocyte and histiocyte infiltration in the dermis suggest allergic contact dermatitis, whereas more superficial vesicles containing polymorphonuclear leukocytes suggest a primary irritant dermatitis. In chronic contact dermatitis, there is lichenification (hyperkeratosis, acanthosis, elongation of rete ridges, and elongation and broadening of papillae).

Patch Testing Numerous allergens may be specifically tested in suspected allergic contact dermatitis. Standardized mixtures of the allergens are placed against the skin for 24 to 48 hours and then removed looking for reactions at each site.

Management

Prompt identification and removal of the offending agent is critical.

Acute Domeboro Astringent Solution soaks 15 minutes 4 times per day may be helpful. High-potency topical corticosteroids can be very helpful for localized reactions. For more widespread reactions and those involving very sensitive skin such as the face or genitals, a short course of systemic corticosteroids may provide relief. It is important to taper systemic steroids slowly (over several weeks) as rebound is common if the taper is performed too quickly.

Subacute and Chronic Short courses of potent topical corticosteroid preparations (such as clobetasol ointment) may be used sparingly bid for up to 2 weeks along with aggressive moisturization and avoidance of scratching and rubbing.

Seborrheic dermatitis is a recurrent, waxing and waning dermatosis, which occurs on the areas of the skin in which the sebaceous glands are most active, such as the face and scalp, and in the diaper area.

Synonym Cradle cap.

Epidemiology

Age Infancy (within the first 10 weeks) and adolescence (puberty).

Gender More common in males.

Incidence 2% to 5% of the population.

Etiology Unknown. Malassezia furfur yeast, a normal skin constituent, is highly associated with seborrheic dermatitis.

Pathophysiology

Malassezia does not appear to be present in higher numbers in these patients, thus an abnormal immune response is postulated.

History

Duration of Lesions Gradual onset, commonly in infancy.

Skin Symptoms Typically asymptomatic or mildly pruritic.

Physical Examination

Skin Lesions

Type Patches with yellowish often greasy scale which can be very thick and adherent.

Color Erythematous.

Arrangement Scattered, discrete patches on the face and chest (Fig. 2-15); diffuse involvement of scalp and diaper area.

Distribution Scalp, face, chest, and diaper area.

Differential Diagnosis

Differential includes dermatophytosis, candidiasis, and atopic dermatitis. There is an overlap seen in some patients with psoriasis, so-called “sebopsoriasis.”

Dermatopathology

Focal parakeratosis, with few pyknotic neutrophils, moderate acanthosis, spongiosis (intercellular edema), nonspecific inflammation of the dermis.

Course and Prognosis

Infantile seborrhea usually is asymptomatic and clears spontaneously within months. Childhood and adolescent seborrheic dermatitis can clear spontaneously but may have a recurrent course.

Treatment

Scalp (Cradle Cap) Removal of the thick scale with mineral oil and fine tooth comb lifting off of scale can provide symptomatic and cosmetic relief. For older children, shampoos containing selenium sulfide, zinc pyrithione, tar, or ketoconazole used intermittently 2 to 3 times a week can control the eruption. It is important to instruct the patient or parent to lather the shampoo and let it sit on the scalp for 5 minutes before rinsing.

Face and Diaper Area Creams containing ketoconazole are helpful and safe; these may be used bid on a regular basis for prevention. Low-potency topical steroid preparations (e.g., 2.5% hydrocortisone cream or fluticasone cream) may be used bid sparingly for 2 to 3 days for acute flares.