Many skin findings in childhood are benign and self-limited conditions. Other dermatologic complaints may be the 1st manifestation of a systemic disease or associated condition, recognition of which facilitates appropriate evaluation and treatment.
History, Physical Examination, and Diagnostic Procedures
History
Obtaining a careful and focused history is necessary to establish diagnoses of pediatric skin disorders. It may be helpful to examine the patient first and then proceed with a relevant line of questioning. Important questions to ask include the following:
- 1.
When did the eruption begin?
- 2.
How did the eruption evolve (distribution, spread, change in the structure of individual lesions)?
- 3.
Are the lesions pruritic or painful?
- 4.
Have there been previous similar episodes?
- 5.
Are there associated systemic symptoms?
- 6.
Are there exacerbating or alleviating factors?
- 7.
Has treatment been rendered? If so, what effect has it had?
- 8.
Are there affected family members or close contacts?
- 9.
Is there a family history of skin disease?
Physical Examination
It is necessary to identify the primary skin lesions, secondary skin lesions, or changes, size, color, distribution, and configuration of the lesions. Several specific signs are pathognomonic for certain diseases. Examination of the hair, nails, and mucosal surfaces should be included. Palpation of cutaneous lesions provides additional information, such as firmness, tenderness, mobility, temperature, and ability to blanch with pressure. Precise morphologic descriptions are critical for establishing a differential diagnosis ( Figs. 48.1 and 48.2 ).
Primary Lesions
Macules and Patches. Macules are flat, circumscribed lesions that are detected because of a change in color. Pink or red macules may be caused by inflammation or vasodilatation. Brown, black, or white lesions may be caused by alterations in melanin synthesis. Purple hues may represent extravasation of blood into the skin. Macules greater than 1 cm in diameter are usually described as patches.
Papules, Nodules, Plaques, and Tumors. Papules are circumscribed, palpable, elevated solid lesions. Typically less than 0.5-1 cm in diameter, these lesions may be epidermal or dermal in origin and may be flat-topped or dome-shaped. Papules that are 0.5-2 cm in diameter are described as nodules. Nodules are epidermal, dermal, or subcutaneous lesions that may, in some cases, evolve from preexisting papules. Plaques are elevated flat-topped lesions, larger than 1 cm in diameter, and often formed by the coalescence of papules. Tumors are larger nodules greater than 2 cm in diameter that are usually solid and well circumscribed.
Vesicles and Bullae. Vesicles are elevated fluid-filled lesions. Bullae are large vesicles, usually greater than 1 cm in diameter. The tenseness or flaccidity of the blister indicates whether the level of separation is intraepidermal or subepidermal ( Fig. 48.3 and Table 48.1 ).
| Site of Cleavage | Clinical Example |
|---|---|
| Intracorneal | Miliaria crystallina |
| Granular layer | Bullous impetigo |
| Staphylococcal scalded skin syndrome | |
| Pemphigus foliaceus | |
| Intraepidermal | Dermatophytosis Insect bites Incontinentia pigmenti Scabies Viral blisters |
| Suprabasal | Pemphigus vulgaris |
| Basal cell layer | Epidermolysis simplex |
| Junctional | Junctional epidermolysis bullosa |
| Subepidermal | Toxic epidermal necrolysis |
| Dermatitis herpetiformis | |
| Recessive dystrophic epidermolysis bullosa | |
| Dominant dystrophic epidermolysis bullosa | |
| Linear IgA disease of childhood |
Pustules. Pustules are white or yellow well-circumscribed lesions that contain purulent material. Pustules do not always signify an infectious cause.
Wheals. Wheals are edematous, elevated lesions that are transient in nature and variable in shape and size. They may be white or erythematous and often have central pallor.
Telangiectases. These are ectatic, dilated superficial blood vessels of the skin that typically blanch when pressure is applied.
Secondary Lesions
Secondary lesions may represent the natural evolution of primary lesions or changes that result from external manipulation, such as scratching.
Crusts. Crusts represent serum, pus, blood, or exudate that has dried on the skin surface.
Scales. Scales appear as yellow, white, or brownish flakes on the skin surface that represent desquamation of stratum corneum.
Erosions. Erosions are moist, erythematous, circumscribed lesions that result from partial or complete loss of the epidermis. They often result from rupture of a blister. Erosions do not involve the dermis or subcutaneous tissue; therefore, they heal without scarring.
Ulcers. Ulcers are deeper than erosions and penetrate the dermis or fat and usually heal with scarring.
Lichenification. Lichenification, or thickening of the skin, usually results from chronic scratching or rubbing. Accentuation of skin markings or hyperpigmentation is observed.
Fissures. A fissure is a linear crack in the epidermis extending to the dermis.
Atrophy. Atrophy represents loss of substance of the skin. Epidermal atrophy is characterized by loss of skin markings, increased wrinkling, and transparency with visibility of underlying vasculature. Dermal or subcutaneous atrophy results in depression of the skin with minimal, if any, epidermal changes.
Excoriations. Excoriations are linear erosions on the skin caused by scratching.
Diagnostic Techniques
Potassium Hydroxide Test
This simple and rapid test can confirm the diagnosis of dermatophyte or candidal infections. Scale is scraped with a curved blade onto a microscope slide. Hair or nail fragments can also be examined. A glass coverslip is then placed on the slide after 1-2 drops of 10-20% KOH are added. The slide is heated gently but not boiled, which can result in KOH crystallization and subsequent difficulty in interpretation. Dermatophyte infections are confirmed by identifying fungal hyphae , which appear as long, branching septate filaments. Pseudohyphae or budding spores are characteristic of candidiasis. Short, broad hyphae and clusters of budding cells resembling “spaghetti and meatballs” are diagnostic of tinea versicolor.
Tzanck Smear
A Tzanck smear is useful for the diagnosis of varicella-zoster virus and herpes simplex virus (HSV) infections. The smear is prepared by unroofing a blister with a curved blade and gently scraping the blister base and underside of the roof. The material is spread in a thin layer onto a glass slide. The slide is air-dried and stained with Giemsa or Wright stain. Identification of multinucleated giant cells , a syncytium of epidermal cells with multiple overlapping nuclei, establishes the diagnosis. These cells may have 2-15 nuclei and are much larger than other inflammatory cells. Although a positive result of Tzanck preparation is confirmatory, a negative test result does not rule out herpes viral infection. Viral specimens should be obtained for culture or polymerase chain reaction (PCR) to differentiate HSV from varicella-zoster virus infections.
Scabies Test
A scabies preparation exhibiting the mite, egg, or feces (scybala) confirms the diagnosis of scabies infestation with Sarcoptes scabiei . The mite is most often found within burrows (serpiginous or elongated papules), which may have a vesicle or pustule at one end. A drop of mineral oil should be applied to the lesion so that the scraped material adheres to the blade. The site is then scraped firmly with a curved blade, which occasionally induces minimal bleeding. The material is applied to a microscope slide, another drop of mineral oil is added, and a glass coverslip is placed. Mites are 8-legged arachnids that are easily identified under low magnification. Eggs are frequently observed as smooth ovals approximately half the size of the mite. Feces are smaller than ova and appear as red-brown pellets, often in clusters.
Gram Stain
A Gram stain can be useful in the diagnosis and treatment of suspected bacterial infections. After the site is disinfected, the pustule or blister roof is carefully removed with a needle or straight blade. The contents of the pustule are removed in a sterile manner and spread thinly onto a glass slide. The specimen is air-dried or heat-fixed, stained, and examined microscopically. Results help determine which antibiotic, if any, is indicated. Bacterial cultures are typically obtained simultaneously.
Wood Lamp Examination
A Wood lamp emits low-intensity ultraviolet light at 365 nm and is useful for accentuating pigmentary alterations such as those of piebaldism or ash leaf macules in the newborn and detecting several fungal or bacterial infections. The examination is performed in a darkened room, and the lamp is held 4-6 inches from the patient’s skin. Characteristic color changes of infectious etiologies are outlined in Table 48.2 .
| Fluorescence | Clinical Appearance | Organisms/Disease |
|---|---|---|
| Coral, red, pink | Brown or red thin plaques on the groin, axillae, or toe webs | Erythrasma ( Corynebacterium minutissimum ) |
| Pale green or yellow | Hypopigmented or hyperpigmented macules and plaques on the trunk | Tinea versicolor ( Pityrosporum orbiculare, P. ovale, Malassezia furfur ) |
| Bright yellow-green | Infection of the toe web space; often in burn patients | Pseudomonas aeruginosa |
| Yellow-green | Scaling of the scalp with patchy hair loss | Tinea capitis ( Microsporum canis, M. audouinii ) Not Trichophyton tonsurans |
Skin Biopsy
A skin biopsy can be performed when a clinical diagnosis is unclear. Histologic evaluation of a small skin specimen may reveal changes in the epidermis, dermis, or subcutaneous tissue that confirm or rule out specific disorders. Direct immunofluorescence testing can be extremely helpful in the diagnosis of collagen vascular and autoimmune bullous diseases ( Table 48.3 ).
| Disease | Involved Skin | Uninvolved Skin | Direct IF Findings | Indirect IF Findings | Circulating Antibodies |
|---|---|---|---|---|---|
| Dermatitis herpetiformis | Negative | Positive | Granular IgA ± C in papillary dermis | None | IgA antiendomysial and transglutaminase antibodies |
| Bullous pemphigoid | Positive | Positive | Linear IgG and C band in BMZ, occasionally IgM, IgA, IgE | IgG to BMZ | IgG anti-BP180 and anti-BP230 |
| Pemphigus (all variants) | Positive | Positive | IgG in intercellular spaces of the epidermis between keratinocytes | IgG in intercellular spaces of the epidermis between keratinocytes | IgG antidesmoglein 1 and 3 (pemphigus vulgaris and foliaceus). IgA antidesmocollin 1 (IgA pemphigus) |
| Linear IgA bullous dermatosis (chronic bullous dermatosis of childhood) | Positive | Positive | Linear IgA at BMZ, occasionally C | Low titer, rare IgA, anti-BP180 | None |
| Discoid lupus erythematosus | Positive | Negative | Linear IgG, IgM, IgA, and C3 at BMZ (lupus band) | None | Usually ANA-negative |
| Systemic lupus erythematosus | Positive | Variable; exposed to sun, 30–50%; nonexposed, 10–30% | Linear IgG, IgM, IgA, and C3 at BMZ (lupus band) | None | ANA Anti-Ro (SSA), anti-La (SSB) Anti-RNP Anti-dsDNA Anti-Sm |
| Henoch–Schönlein purpura | Positive | Positive | IgA around vessel walls | None | None |
Dermatologic Disorders in Older Infants and Children
Many forms of skin lesions are acquired during childhood and adolescence with a range from benign asymptomatic dermatoses to infectious or chronic skin disorders. A thorough history to understand the symptomatology and time course, as well as a detailed skin examination to evaluate the morphology of the lesions, can help distinguish between childhood dermatoses.
Scaling Disorders
The term papulosquamous refers to conditions in which the primary lesions are papules or plaques associated with scale. These disorders are typically benign but can be chronic and therapeutically challenging.
Pityriasis Rosea
Pityriasis rosea is an acute, common, self-limited eruption that has no gender predilection. Although the precise cause is unknown, a viral origin is suspected because there have been reports of epidemics, clusters of cases among closely related individuals, and low recurrence rates. Pityriasis rosea has been associated with systemic reactivation of human herpesvirus 6 (HHV-6) and HHV-7. Furthermore, a prodrome of malaise, headache, and respiratory symptoms is occasionally observed.
The eruption usually begins with a solitary oval, pink scaly plaque approximately 3-5 cm in diameter, typically located on the trunk or proximal extremities ( Fig. 48.4 ). Referred to as the herald patch , this finding is observed in 50-70% of cases. When the herald patch has an elevated red border and central clearing, it resembles tinea corporis. Performing a KOH preparation can differentiate these two conditions. Within 1-2 weeks after appearance of the herald patch, numerous small, pink scaly papules or plaques arise over the trunk and proximal extremities, sparing the face and distal extremities. The lesions classically have a fine cigarette paper–like peripheral collarette of scale. These oval 0.5- to 2-cm lesions have their long axis oriented along skin lines, and when present on the trunk, result in a “Christmas tree” pattern on the back ( Fig. 48.4 ). Young children, particularly African-Americans, may have an “inverse” type of pityriasis rosea, with most lesions distributed on the distal extremities, face, neck, and intertriginous regions. Other variants seen in children demonstrate lesions that are papular, vesicular, pustular, purpuric, or lichenoid.
The duration of the eruption varies from 2-12 weeks. Therapy is unnecessary; emollients, topical corticosteroids, or oral antihistamines help relieve pruritus. In addition, pityriasis rosea improves significantly with exposure to ultraviolet light. Postinflammatory hypopigmentation or hyperpigmentation may persist for weeks to months, especially in dark-skinned patients. There are many other dermatoses that can resemble pityriasis rosea ( Table 48.4 ). In sexually active adolescents, a rapid plasma reagin (RPR) test should be obtained to rule out the possibility of secondary syphilis, especially if the palms and soles are involved. Persistence of the eruption after 3-4 months necessitates an evaluation for another diagnosis.
|
Psoriasis
Psoriasis is an immune-mediated inflammatory skin condition characterized by well-demarcated, erythematous scaly papules and plaques located most often on the scalp, elbows, knees, genitalia, and lumbosacral regions. The course is more chronic and unpredictable than that of pityriasis rosea. Psoriasis occurs in approximately 1-3% of the population and is estimated to manifest before the age of 20 years in about 30% of patients. It affects both genders equally in adulthood, but childhood psoriasis has a slight female predominance. The cause is multifactorial, but there is a genetic predisposition in many affected individuals and about 50% have a positive family history when onset occurs during childhood. The association between psoriasis, obesity, and metabolic syndrome has been described in both adult and pediatric patients with psoriasis, and screening for individuals with moderate-to-severe involvement should be considered.
Psoriasis encompasses a broad spectrum of clinical manifestations, ranging from mild, asymptomatic, virtually undetectable disease to extensive, chronic, debilitating disease. The course is usually marked by recurrent flares and remissions and is often exacerbated by stress, trauma, infection, climate, hormonal factors, and particular medications.
Although morphologic variations exist, the classic lesions of plaque psoriasis are well-demarcated erythematous papules or plaques with a silvery-white scale ( Fig. 48.5 ). The lesions usually begin as small erythematous papules that gradually enlarge and coalesce to form plaques up to several centimeters in diameter. The micaceous (mica-like) scale of the psoriatic plaque is more adherent centrally than peripherally. Removal of this scale results in multiple small bleeding points. This is referred to as the Auspitz sign and is secondary to disruption of the dilated blood vessels that are located high in the papillary dermis. Although this finding is seen in psoriasis, it is not pathognomonic.
The Koebner phenomenon , another characteristic feature of psoriasis, although observed in a number of dermatologic conditions, is an isomorphic response (development of new or larger lesions) occurring at sites of injury or trauma such as scratching, sunburn, or surgery ( Fig. 48.6 ). Psoriatic lesions tend to be distributed symmetrically. Although extensor surfaces are typically involved, a variant of psoriasis known as inverse psoriasis affects flexural surfaces, such as the axillae and groin.
Scalp lesions are present in most children with psoriasis. Diffuse, thick white scale may be accompanied by erythema. In contrast to seborrhea, psoriasis often extends beyond the hairline, affecting the forehead, ears, and neck. The lesions are variably pruritic and are generally not associated with hair loss. Scalp psoriasis tends to be more resistant to therapy than seborrheic dermatitis.
Nail abnormalities are seen in 25-50% of patients with psoriasis. Nail pits are the most common finding, identified by multiple pinpoint depressions that are irregularly distributed over the nail plate. Although nail pitting is characteristic of psoriasis, it is not a pathognomonic sign; it is also associated with atopic dermatitis, alopecia areata, and trauma. Other nail changes include separation of the nail plate from the nail bed (onycholysis), subungual hyperkeratosis, discoloration, crumbling, and yellowish-brown “oil spots” on the nail plate.
Guttate psoriasis , characterized by numerous droplike lesions, is a variant commonly seen in children and young adults ( Fig. 48.7 ). The round-to-oval, pinkish-red, somewhat scaly papules arise in crops and are widely distributed, particularly on the trunk. Two-thirds of affected patients have a history of an upper respiratory tract infection, usually streptococcal in origin, which was present 1-3 weeks before the onset of lesions. Clinical improvement is often seen after appropriate antibiotic therapy; however, the clinical course may range from spontaneous resolution to chronic disease.
Psoriasis is usually diagnosed from the clinical appearance of skin lesions. However, when the diagnosis is unclear, a skin biopsy may be helpful. Differential diagnosis of psoriasis includes seborrheic dermatitis, dermatophytosis, pityriasis rosea, lichen planus, atopic dermatitis, and subacute cutaneous lupus erythematosus ( Table 48.4 ).
The course of psoriasis is marked by recurrent flares and remissions. Although it is unpredictable, there appears to be a subset of individuals whose disease gradually improves over time. Management of psoriasis varies depending on a number of factors including age of the child, extent of involvement, functional limitations, and psychosocial impact. For limited disease, topical therapy (emollients, corticosteroids, vitamin D derivatives, retinoids, tar, keratolytics) alone may afford control. For more extensive or debilitating disease, the addition of phototherapy or a systemic agent (immunosuppressants, retinoids, “biologic” therapy) may be necessary.
Pityriasis Lichenoides
Pityriasis lichenoides can manifest in two forms: pityriasis lichenoides et varioliformis acuta (PLEVA) or pityriasis lichenoides chronica. These diseases most commonly affect children between ages 5 and 15 years. Both diseases are believed to be part of the same clinical spectrum. PLEVA is characterized by an abrupt eruption of multiple, 2- to 4-mm, nonpruritic, variably scaly erythematous macules and papules that may progress to vesicular, necrotic, or crusted lesions. The lesions often occur in crops, and are thus present in different stages most commonly on the trunk, but may spread to the extremities. The condition may resolve spontaneously within several months, or recurrences and relapses may occur episodically for several years.
Pityriasis lichenoides chronica manifests more gradually and is characterized by pink-to-brown 2- to 5-mm papules with central adherent scale, found primarily on the trunk and proximal extremities. The clinical course is variable, and the lesions may last from months to years. After the papules recede, postinflammatory hypopigmentation or hyperpigmentation commonly occurs. Sequelae are uncommon, and the lesions usually heal without a scar. Pityriasis lichenoides chronica may initially resemble pityriasis rosea and other papulosquamous eruptions ( Table 48.4 ). Reports of cutaneous T-cell lymphoma ( mycosis fungoides ) in the setting of pityriasis lichenoides chronica exist, and the patient with a persistent or atypical eruption should be evaluated with consideration of a skin biopsy ( Fig. 48.8 ).
Treatment may be limited to lubricants in an asymptomatic patient. If treatment is required, first-line agents include oral antibiotics with antiinflammatory properties (erythromycin, doxycycline) for several weeks, which have shown benefit in some children.
Lichen Planus
Lichen planus occurs in patients of all ages but is less commonly seen in children than in adults. It is characterized by the “ 5 Ps ”: purple, polygonal, planar, pruritic papules. The primary lesion is a shiny, violaceous, flat-topped papule, often with angulated borders, measuring from 2 mm to more than 1 cm in diameter. The lesions are very pruritic and demonstrate the Koebner phenomenon, which results in the development of new lesions (often in a linear configuration) at sites of scratching. The distribution may be localized or generalized, and lesions may number from few to numerous. Sites of predilection include the volar wrists, forearms, legs, genitalia, and mucous membranes. A reticulated pattern of delicate white lines or streaks ( Wickham striae ) seen on the buccal mucosa or skin aids in confirming the diagnosis.
Nail changes are seen in approximately 10% of patients. These include longitudinal ridging, generalized nail destruction, red or brown discoloration, subungual hyperkeratosis, and thinning of the nail plate. Pterygium formation results from the overgrowth of fibrous tissue, which extends from the proximal nail fold to the tip of the nail, obliterating the nail plate.
Common medications that can produce a lichenoid eruption that is indistinguishable from lichen planus include antihypertensives (β blockers, angiotensin-converting enzyme inhibitors), diuretics (hydrochlorothiazide), antimalarials, penicillamine, and gold salts. Rarely, tetracycline, griseofulvin, nonsteroidal antiinflammatory medications, phenytoin, and carbamazepine can be causes. Unlike other cutaneous medication reactions, the lichenoid reaction may not occur for months or years after medication initiation.
It is often possible for the experienced clinician to diagnose lichen planus strictly on clinical grounds. If necessary, a skin biopsy specimen can reveal specific findings. The clinical differential diagnosis most often includes psoriasis and drug eruptions ( Table 48.4 ). If oral lesions are present, the clinician must consider the possibility of aphthous stomatitis, erythema multiforme (EM), herpes simplex, or leukoplakia.
Topical corticosteroids are the treatment of choice in most cases. Lichen planus often resolves spontaneously over 1-2 years, but some cases may persist for many years. Generalized eruptions may respond to a short course of systemic corticosteroids. Oral antihistamines provide symptomatic relief.
Seborrheic Dermatitis
Seborrheic dermatitis is characterized by an erythematous, scaly, symmetric eruption that occurs most often in hair-bearing and intertriginous regions. Seborrhea of infancy is discussed in Chapter 47 . In adolescents, yellowish, greasy scale of the scalp, eyebrows, nasolabial folds, nasal bridge, posterior auricular regions, and midchest may be accompanied by mild erythema ( Fig. 48.9 ). Immunodeficiency disorders and neurologic dysfunction may be associated with severe, recalcitrant seborrheic dermatitis. Although patients usually respond well to therapy, it is a chronic condition characterized by recurrences. It is often responsive to low-potency topical corticosteroids or topical antifungals (azoles, ciclopirox, selenium sulfide). These preparations may be available in a number of vehicles, including solutions or shampoos for the scalp. Keratolytics may be added when thicker scale is present.
Atopic Dermatitis
Atopic dermatitis ( eczema ) is a chronic condition characterized by pruritus, a personal or family history of atopy, and an age-dependent distribution. It is common during infancy and childhood. Up to 95% of affected individuals have signs before the age of 5 years.
Typical lesions are pink-to-red crusted or scaly plaques or papules. Some individuals have follicular accentuation, particularly on the trunk, manifested by a goosebump-like texture. Lichenification (thickened skin with exaggerated skin markings) is a feature of chronic atopic dermatitis and results from repeated rubbing and scratching. Excoriations are secondary lesions caused by scratching. Postinflammatory pigmentary changes are frequently noted, especially in dark-skinned individuals ( Fig. 48.10 ). Associated findings are noted in Table 48.5 .
| Ichthyosis vulgaris | Affects 20% of patients with atopic dermatitis |
| Primarily involves the legs and trunk | |
| Keratosis pilaris | Asymptomatic hyperkeratotic follicular papules found mainly on the extensor surfaces of the upper arms and anterior thighs, also on the face in children |
| Pityriasis alba | Hypopigmented patches on the cheeks and occasionally upper body |
| Hyperlinear palms/soles | Common physical finding |
| Dennie–Morgan fold | A double line found under the lower eyelids Not pathognomonic |
| Lichen spinulosus | More commonly seen in darker skin |
| Pruritic grouped hyperkeratotic follicular spires | |
| Eye findings | Keratoconjunctivitis, cataracts, keratoconus (abnormally shaped cornea), retinal detachment (rare) |
| Dyshidrotic eczema | Firm vesicles found on the palms and soles and lateral aspects of digits |
| Frequently associated with hyperhidrosis | |
| Nummular eczema | Well-demarcated, scaly, coin-shaped lesions usually on the lower extremities |
| Associated with xerosis | |
| Juvenile plantar dermatosis | Occasionally exudative lesions |
| Painful erythema, scaling, cracking, and fissuring of weight-bearing surfaces of the feet | |
| Often associated with hyperhidrosis | |
| Improvement after puberty |
The distribution of the lesions tends to be age dependent . The cheeks, face, scalp, trunk, and extensor surfaces of the arms and legs are characteristically involved in the infant form. Between the ages of 2 and 10 years (childhood atopic dermatitis), the distribution predominately involves the neck, wrists, ankles, and flexural surfaces of the extremities ( Fig. 48.11 ). After puberty, atopic dermatitis has a predilection for the face, neck, hands, and feet. The clinical features of the skin lesions are not specific to this condition, as other eczematous eruptions (contact dermatitis, seborrheic dermatitis) have a similar appearance. Laboratory tests are of limited value, and histologic findings reveal nonspecific spongiotic dermatitis. The distribution of lesions, age at onset, and history are most important for establishing the diagnosis. Obtaining a complete personal and family history of atopic diatheses is necessary.
Secondary infections are the most common complication. Individuals with atopic dermatitis have increased colonization with Staphylococcus aureus . Most affected children need occasional treatment with antibiotics to eradicate secondary infection, and dilute sodium hypochlorite bleach baths can help reduce infection with S. aureus. The presence of pustules, extensive excoriations, or weeping and crusted lesions suggests the need for antibiotic therapy. Topical therapy with mupirocin may be sufficient for limited areas; however, widespread involvement may necessitate the use of oral antimicrobial agents. The increase in methicillin-resistant S. aureus (MRSA) infections has limited therapeutic options in some patients. Secondary infection with HSV is referred to as eczema herpeticum or Kaposi varicelliform eruption ( Fig. 48.12 ). Transmission may occur during routine child care from a caretaker with a herpetic fever blister, whereby the eczematous skin becomes inoculated with HSV. The hallmark of this condition is the rapid development of numerous umbilicated vesicles and pustules. Later in the course, multiple erosions are seen, and identification of an intact vesicle may be difficult. The infection may be associated with fever and other constitutional symptoms, and expedient treatment with acyclovir is required. Hospitalization may be necessary in young infants or severely affected individuals. Recurrences of eczema herpeticum can be problematic.
Other dermatologic conditions to consider in the differential diagnosis of a rash that looks like atopic dermatitis are presented in Table 48.6 .
| Condition | Similarities | Differences |
|---|---|---|
| Seborrheic dermatitis | Scaly plaques | Earlier onset is typical, can be seen in older children |
| Erythroderma may be seen when severe | Increased severity associated with immunodeficiency disorders and neurologic dysfunction | |
| Pruritus minimal or absent | ||
| Well-demarcated lesions | ||
| Characteristic yellowish-salmon greasy lesions with intertriginous distribution | ||
| Contact dermatitis | ||
| Primary irritant | Common in infants, young children | Usually less pruritic and less eczematoid |
| May have similar distributions depending on the irritant (i.e., cheeks, chin, neck) | Diaper area distribution uncommon in atopic dermatitis | |
| Allergic | Pruritic | Well circumscribed |
| Erythematous, papulovesicular eruption | Uncommon in 1st few months of life | |
| Involutes spontaneously after the removal of the offending agent | ||
| Psoriasis | Scaly, red lesions | Deeper red-violaceous hue Thick micaceous scale Characteristic nail changes Sharply demarcated lesions Distinct distribution Pruritus may be less intense |
| Scabies | Frequent eczematous changes secondary to scratching, rubbing, or irritating therapy Can be very difficult to distinguish in infancy | Presence of hyperpigmented nodules Presence of burrows Isolation of a mite from skin scrapings Acute onset Affected household members |
| Langerhans cell histiocytosis | Scaly, erythematous eruption Usually begins during 1st yr of life | Primarily children <3 yr of age Presence of purpuric papules Associated hematologic abnormalities, hepatosplenomegaly |
| Acrodermatitis enteropathica | Vesiculobullous eczematoid lesions Onset during infancy | Acral, periorificial distribution Associated features: failure to thrive, diarrhea, alopecia, nail dystrophy, low serum zinc levels |
| Wiskott–Aldrich syndrome | Severe eczematous dermatitis | X-linked recessive disorder Associated features of thrombocytopenia, defects in cellular and humoral immunity, bloody diarrhea |
| Phenylketonuria | Eczematous eruption | Hereditary Intellectual disabilty, seizures Diffuse hypopigmentation, blond hair, photosensitivity Elevated blood phenylalanine levels |
| Hyper-IgE syndrome | Symptoms begin in 1st 3 mo of life Eczematous dermatitis involving the face and extensor surfaces Personal or family history of atopy | Coarse facial features, irregularly proportioned jaw and cheeks, broad nasal bridge, prominent nose, severe oral mucositis Lifelong history of severe streptococcal or staphylococcal infections of the skin, limbs, joints Exceptionally high serum IgE levels Diminished neutrophil chemotaxis |
An overview of the management of atopic dermatitis is presented in Table 48.7 .
| Therapeutic Modality | Indications and Recommendations |
|---|---|
| Bathing | Recommended daily for 10–15 min with warm, not hot, water. May use fragrance-free bath oils. Hydrates the skin. |
| Soaps | Mild, fragrance-free cleansers, such as Dove, Basis, Aveenobar, Olay, Cetaphil, or Aquanil, are essential. |
| Emollients | Best applied immediately after bathing/showering. Should be used as often as possible. Petroleum jelly is an ideal emollient: contains no water, additives, or preservatives and prevents evaporative water loss from the skin. Thick creams such as Eucerin, Nivea, Aquaphor, Vanicream, and Cetaphil are some alternatives. |
| Bleach (sodium hypochlorite) | Depending on the size of the bathtub/amount of water used, 0.25–0.5 U.S. cup (60–120 mL) of common bleach solution (6% sodium hypochlorite) is added to a full bath (40 gallon tub). Performed 2–3 times/wk to reduce S. aureus colonization. |
| Compresses | Indicated for acute weeping lesions. Helps cool and dry the skin, reduces inflammation. Use cool tap water or aluminum acetate solutions for 20 min, 2–4 times daily. Follow with topical corticosteroid application. |
| Topical corticosteroids | Indicated to reduce pruritus and inflammation. The potency of the topical corticosteroid is determined by the age of patient, site of involvement, severity of dermatitis, and duration of therapy. Facial and intertriginous skin should be treated with low-potency preparations. Apply before emollient. Use the lowest potency that is effective. Monitor closely for potential side effects, such as striae and cushingoid features. |
| Topical Immunomodulators | Tacrolimus and pimecrolimus may be effective steroid-sparing agents for more severe involvement. |
| Antihistamines | Controversial whether effective in this condition. Topical formulations should be avoided. May help some patients sleep. Hydroxyzine often more effective than diphenhydramine. May induce drowsiness. Nonsedating antihistamines include cetirizine, loratadine and fexofenadine. |
| Antibiotics | Patients have increased colonization with S. aureus . Use if multiple weeping excoriations, crusts, or pustules suggest secondary infection or if severe or resistant eczema is present. Treat with antistaphylococcal antibiotics; specific antibiotic is based on local sensitivities. |
| Ultraviolet light | Useful for severe, uncontrollable atopic dermatitis. May administer narrowband ultraviolet B light (NBUVB). |
| Tars | Useful for chronic, dry, lichenified lesions, not for acute dermatitis. |
| Environmental conditions | Environmental factors may influence the severity of the dermatitis. Some helpful measures:
|
| Systemic immunosuppressants | Oral corticosteroids should be avoided. Cyclosporine, methotrexate, mycophenolate mofetil, and azathioprine have shown some benefit in the management of atopic dermatitis, but given the side effect profile, should be prescribed under the direction of a dermatologist. |
Lumps and Bumps
The presence of cutaneous or subcutaneous nodules and tumors can present a diagnostic challenge. They are also a source of great concern to parents, who fear the possibility of malignancy. Fortunately, most nodules and tumors in children are benign, and cutaneous malignancies are rare ( Table 48.8 ).
| Diagnosed Lesion | Usual Onset | Color | Size | Site | Comments | Therapy |
|---|---|---|---|---|---|---|
| Epidermal cyst | Birth, childhood, adolescence | Skin-colored | 1–3 cm | Face, scalp, neck, trunk | Potential for inflammation and infection | Elective excision vs observation |
| Dermoid cyst | Birth | Skin-colored | 1–4 cm | Face, scalp, lateral eyebrow | When midline, may have sinus tract | Elective excision |
| Pilomatricoma | Any age, 50% before adolescence | Skin-colored, reddish-blue, bluish-gray | 0.5–3 cm | Head, neck | Malignant transformation possible but rare | Elective excision vs observation |
| Dermatofibroma | Adulthood, 20% before age 20 yr | Skin-colored, tan brown, black | 0.3–1 cm | Extremities | May follow trauma | Elective excision vs observation |
| Neurofibroma | Occasionally at birth Usually childhood or adolescence | Usually skin colored Also pink, blue | 2 mm to several centimeters | Any body site | May be associated with neurofibromatosis May see café-au-lait spots | Elective excision vs observation |
| Juvenile xanthogranuloma | Birth Childhood | Yellow to reddish-brown | 0.5–4 cm | Head, neck, trunk, proximal extremities | Extracutaneous lesions involving eye, other organs | Ophthalmology consult; resolves spontaneously |
| Keloids | Peak between puberty and age 30 | Pink to violaceous | Variable | Any site of injury Commonly earlobes after piercing | Often tender or pruritic Familial tendency | Difficult; intralesional steroids, excision |
| Granuloma annulare | Childhood Adolescence | Skin colored to red | 1–4 cm | Distal extremities | May be generalized in approximately 15% of cases | Observe, self-limited Topical steroids if needed |
| Lipoma | Puberty, adulthood | Skin colored | Variable May be >10 cm | Any, but usually neck, shoulders, back; abdomen | Malignant change Very rare | Observe, excision |
| Solitary mastocytoma | Birth Early infancy | Skin colored to light brown or tan Occasionally pink or yellowish hue | 1–5 cm | Any site; but most often on arms, neck, trunk | Positive Darier sign Urticaria with stroking | Usually resolves spontaneously; antihistamines may be helpful |
| Erythema nodosum | Usually >10 yr of age Peak in the 3rd decade | Begins bright to deep red, then develops a brownish-red to violaceous bruiselike appearance | 1–5 cm | Symmetric distribution over pretibial region, legs Occasionally arms | Tender Association with many infectious agents (group A streptococci, tuberculosis, mycoplasma), inflammatory diseases (sarcoidosis, inflammatory bowel disease), medications (birth control pills) | Thorough evaluation and treatment of underlying cause, antiinflammatory agents Bed rest/elevation of legs |
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