Acne affects 85% of adolescents. The onset of adolescent acne is between ages 7 and 10 years in 40% of children. The early lesions are usually limited to the face and are primarily closed comedones.
The primary event in acne formation is obstruction of the sebaceous follicle and subsequent formation of the microcomedo (not evident clinically). This is the precursor to all future acne lesions. This phenomenon is androgen-dependent in adolescent acne. The four primary factors in the pathogenesis of acne are (1) plugging of the sebaceus follicle, (2) increased sebum production, (3) proliferation of Propionibacterium acnes in the obstructed follicle, and (4) inflammation. Many of these factors are influenced by androgens.
Drug-induced acne should be suspected in teenagers if all lesions are in the same stage at the same time and if involvement extends to the lower abdomen, lower back, arms, and legs. Drugs responsible for acne include corticotropin (ACTH), glucocorticoids, androgens, hydantoins, and isoniazid, each of which increases plasma testosterone.
Open comedones are the predominant clinical lesion in early adolescent acne. The black color is caused by oxidized melanin within the stratum corneum cellular plug. Open comedones do not progress to inflammatory lesions. Closed comedones, or whiteheads, are caused by obstruction just beneath the follicular opening in the neck of the sebaceous follicle, which produces a cystic swelling of the follicular duct directly beneath the epidermis. Most authorities believe that closed comedones are precursors of inflammatory acne lesions (red papules, pustules, nodules, and cysts). In typical adolescent acne, several different types of lesions are present simultaneously. Severe, chronic, inflammatory lesions may rarely occur as interconnecting, draining sinus tracts. Adolescents with cystic acne require prompt medical attention, because ruptured cysts and sinus tracts result in severe scar formation.
Consider rosacea, nevus comedonicus, flat warts, miliaria, molluscum contagiosum, and the angiofibromas of tuberous sclerosis.
Different treatment options are listed in Table 15–4. Recent data have indicated that combination therapy that targets multiple pathogenic factors increases the efficacy of treatment and rate of improvement.
Table 15–4.Acne treatment. ||Download (.pdf) Table 15–4.Acne treatment.
|Type of Lesion ||Treatment |
|Comedonal acne || |
One of the following:
Tretinoin, 0.025%, 0.05%, or 0.1% cream; 0.01% or 0.025% gel; 0.4% or 0.1% microgel
Adapalene, 0.3% gel, 0.1% gel or solution; 0.05% cream
|Papular inflammatory acne || |
One from first grouping, plus one of the following:
Benzoyl peroxide, 2.5%, 4%, 5%, 8%, or 10% gel or lotion; 4% or 8% wash
Azelaic acid, 15% or 20% cream
Clindamycin, 1% lotion, solution, or gel
Combination products include benzoyl peroxide-erythromycin (Benzamycin); benzoyl peroxide-clindamycin (Duac, BenzaClin, Acanya); tretinoin-clindamycin (Ziana, Veltin)
|Pustular inflammatory acne || |
One from first grouping, plus one of the following oral antibiotics:
Minocycline or doxycycline, 50–100 mg, bid
|Nodulocystic acne ||Isotretinoin, 1 mg/kg/day, goal dose 120–150 mg/kg total |
A. Topical Keratolytic Agents
Topical keratolytic agents address the plugging of the follicular opening with keratinocytes and include retinoids, benzoyl peroxide, and azelaic acid. The first-line treatment for both comedonal and inflammatory acne is a topical retinoid (tretinoin [retinoic acid], adapalene, and tazarotene). These are the most effective keratolytic agents and have been shown to prevent the microcomedone. These topical agents may be used once daily, or the combination of a retinoid applied to acne-bearing areas of the skin in the evening and a benzoyl peroxide gel or azelaic acid applied in the morning may be used. This regimen will control 80%–85% of cases of adolescent acne.
Topical antibiotics are less effective than systemic antibiotics and at best are equivalent in potency to 250 mg of tetracycline orally once a day. One percent clindamycin phosphate solution is the most efficacious topical antibiotic. Most P acnes strains are now resistant to topical erythromycin solutions. Topical antibiotic therapy alone should never be used. Multiple studies have shown a combination of benzoyl peroxide or a retinoid and a topical antibiotic are more effective than the antibiotic alone. Benzoyl peroxide has been shown to help minimize the development of bacterial resistance at sites of application. The duration of application of topical antimicrobials should be limited unless benzoyl peroxide is used. Several combination products (benzoyl peroxide and clindamycin, tretinoin and clindamycin, adapalene and benzoyl peroxide) are available which may simplify the treatment regimen and increase patient compliance.
Antibiotics that are concentrated in sebum, such as tetracycline, minocycline, and doxycycline, should be reserved for moderate to severe inflammatory acne. The usual dose of tetracycline is 0.5–1.0 g divided twice a day on an empty stomach; minocycline and doxycycline 50–100 mg taken once or twice daily can be taken with food. Monotherapy with oral antibiotics should never be used. Recent recommendations are that oral antibiotics should be used for a finite time period, and then discontinued as soon as there is improvement in the inflammatory lesions. The tetracycline antibiotics should not be given to children younger than 8 years of age due to the effect on dentition (staining of teeth). Doxycycline may induce significant photosensitivity, and minocycline can cause bluish-gray dyspigmentation of the skin, vertigo, headaches, and drug-induced lupus. These antibiotics have anti-inflammatory effects in addition to decreasing P acnes in the follicle.
An oral retinoid, 13-cis-retinoic acid (isotretinoin), is the most effective treatment for severe cystic acne. The precise mechanism of its action is unknown, but apoptosis of sebocytes, decreased sebaceous gland size, decreased sebum production, decreased follicular obstruction, decreased skin bacteria, and general anti-inflammatory activities have been described. The initial dosage is 0.5–1 mg/kg/day. This therapy is reserved for severe nodulocystic acne, or acne recalcitrant to aggressive standard therapy. Side effects include dryness and scaling of the skin, dry lips, and, occasionally, dry eyes and dry nose. Fifteen percent of patients may experience some mild achiness with athletic activities. Up to 10% of patients experience mild, reversible hair loss. Elevated liver enzymes and blood lipids have rarely been described. Acute depression and mood changes have been reported, but no definitive relationship to the drug has been proven. Most importantly, isotretinoin is teratogenic. Because of this and other potential side effects, it is not recommended unless strict adherence to the Food and Drug Administration (FDA) guidelines is ensured. The FDA has implemented a strict registration program (iPLEDGE) that must be used to obtain and/or prescribe isotretinoin.
Hormonal therapy (oral contraceptives) is often an effective option for girls who have perimenstrual flares of acne or have not responded adequately to conventional therapy. Adolescents with endocrine disorders such as polycystic ovary syndrome also see improvement of their acne with hormonal therapy. Oral contraceptives can be added to a conventional therapeutic regimen and should always be used in female patients who are prescribed oral isotretinoin unless absolute contraindications exist. There is growing data regarding the use of light, laser, and photodynamic therapy in acne. However, existing studies are of variable quality, and although there is evidence to suggest that these therapies offer benefit in acne, the evidence is not sufficient to recommend any device as monotherapy in acne.
F. Patient Education and Follow-up Visits
The multifactorial pathogenesis of acne and its role in the treatment plan must be explained to adolescent patients. Good general skin care includes washing the face consistently and using only oil-free, noncomedogenic cosmetics, face creams, and hair sprays. Acne therapy takes 8–12 weeks to produce improvement, and this delay must be stressed to the patient. Realistic expectations should be encouraged in the adolescent patient because no therapy will eradicate all future acne lesions. A written education sheet is useful. Follow-up visits should be made every 12–16 weeks. An objective method to chart improvement should be documented by the provider, because patients’ assessment of improvement tends to be inaccurate.
HC: Epidemiology of acne vulgaris. Br J Dermatol 2013 Mar;168(3):474–485
A: Oral antibiotic therapy for acne vulgaris: an evidence-based review. Am J Clin Dermatol Mar 2, 2017; Epub ahead of print.
et al: New insights into the management of acne: an update from the Global Alliance to Improve Outcomes in Acne Group. J Am Acad Dermatol 2009;60:S1–S50
BACTERIAL INFECTIONS OF THE SKIN
Erosions covered by honey-colored crusts are diagnostic of impetigo. Staphylococci and group A streptococci are important pathogens in this disease, which histologically consists of superficial invasion of bacteria into the upper epidermis, forming a subcorneal pustule.
Impetigo should be treated with an antimicrobial agent effective against Staphylococcus aureus (β-lactamase–resistant penicillins or cephalosporins, clindamycin, amoxicillin–clavulanate) for 7–10 days. Topical mupirocin, polymyxin, gentamycin, and erythromycin are also effective. In severe and recalcitrant cases, skin swab for bacterial culture should be performed prior to initiation of empiric antibiotic therapy.
In bullous impetigo there is, in addition to the usual erosion covered by a honey-colored crust, a border filled with clear fluid. Staphylococci may be isolated from these lesions, and systemic signs of circulating exfoliatin are absent. Bullous impetigo lesions can be found anywhere on the skin, but a common location is the diaper area.
Treatment with oral antistaphylococcal drugs for 7–10 days is effective. Application of cool compresses to debride crusts is a helpful symptomatic measure.
Ecthyma is a firm, dry crust, surrounded by erythema that exudes purulent material. It represents invasion by group A β-hemolytic streptococci through the epidermis to the superficial dermis, therefore it is often referred as a deeper form of impetigo. This should not be confused with ecthyma gangrenosum. Lesions of ecthyma gangrenosum may be similar in appearance, but they are seen in a severely ill or immunocompromised patient and are due to systemic dissemination of bacteria, usually Pseudomonas aeruginosa, through the bloodstream.
Treatment is with systemic penicillin.
Cellulitis is characterized by erythematous, hot, tender, ill-defined, edematous plaques accompanied by regional lymphadenopathy. Histologically, this disorder represents invasion of microorganisms into the lower dermis and sometimes beyond, with obstruction of local lymphatics. Group A β-hemolytic streptococci and coagulase-positive staphylococci are the most common causes; pneumococci and Haemophilus influenzae (in younger unvaccinated children) are rare causes. Staphylococcal infections are usually more localized and more likely to have a purulent center; streptococcal infections spread more rapidly, but these characteristics cannot be used to specify the infecting agent. An entry site of prior trauma or infection (eg, varicella, dermatophyte) is often present. Septicemia is a potential complication.
Treatment is with an appropriate systemic antibiotic.
A pustule at a follicular opening represents folliculitis. Deeper follicular infections are called furuncles (single follicle) and carbuncles (multiple follicles). Staphylococci and streptococci are the most frequent pathogens. Lesions are painless and tend to occur in crops, usually on the buttocks and extremities in children. Methicillin-resistant Staphylococcus aureus (MRSA) is now an increasing cause of folliculitis and skin abscesses. Cultures of persistent or recurrent folliculitis for MRSA are advisable.
Treatment consists of measures to remove follicular obstruction—either warm, wet compresses for 24 hours or keratolytics such as those used for acne. Topical or oral anti-staphylococcal antibiotics may be required.
An abscess occurs deep in the skin, at the bottom of a follicle or an apocrine gland, and is diagnosed as an erythematous, firm, acutely tender nodule with ill-defined borders. Staphylococci are the most common organisms.
Recent studies have suggested that incision and drainage alone may be adequate for uncomplicated MRSA skin abscesses in otherwise healthy patients. In more extensive cases adjuvant systemic antibiotics may be required.
This entity consists of the sudden onset of bright red, acutely painful skin, most obvious periorally, periorbitally, and in the flexural areas of the neck, the axillae, the popliteal and antecubital areas, and the groin. The slightest pressure on the skin results in severe pain and separation of the epidermis (positive Nikolsky sign). The disease is caused by a circulating toxin (exfoliatin) elaborated by phage group II staphylococci. Exfoliatin binds to desmoglein-1 resulting in a separation of cells in the granular layer. The causative staphylococci may be isolated from the nasopharynx, an abscess, sinus, blood culture, joint fluid, or other focus of infection, but not from the skin.
Treatment is with systemic antistaphylococcal drugs.
et al: Trends and antibiotic susceptibility patterns of methicillin-resistant and methicillin-sensitive Staphylococcus aureus
in an outpatient dermatology facility. JAMA Dermatol 2013Apr;4(149):427–432
FUNGAL INFECTIONS OF THE SKIN
1. Dermatophyte Infections
Dermatophytes become attached to the superficial layer of the epidermis, nails, and hair, where they proliferate. Fungal infection should be suspected with any red and scaly lesion.
Classification & Clinical Findings
Thickened, broken-off hairs with erythema and scaling of underlying scalp are the distinguishing features (Table 15–5). Hairs are broken off at the surface of the scalp, leaving a “black dot” appearance. Diffuse scaling of the scalp and pustules are also seen. A boggy, fluctuant mass on the scalp called a kerion, represents an exaggerated host response to the organism. Microsporum canis and Trichophyton tonsurans are the cause. Fungal culture should be performed in all cases of suspected tinea capitis.
Table 15–5.Clinical features of tinea capitis. ||Download (.pdf) Table 15–5.Clinical features of tinea capitis.
|Most Common Organisms ||Clinical Appearance ||Microscopic Appearance in KOH |
|Trichophyton tonsurans (90%) ||Hairs broken off 2–3 mm from follicle; “black dot”; diffuse pustule; seborrheic dermatitis-like; no fluorescence ||Hyphae and spores within hair |
|Microsporum canis (10%) ||Thickened broken-off hairs that fluoresce yellow-green with Wood lamp ||Small spores outside of hair; hyphae within hair |
Tinea corporis presents either as annular marginated plaques with a thin scale at the periphery and clear center or as an annular confluent dermatitis. The most common organisms are Trichophyton mentagrophytes, Trichophyton rubrum, and M canis. The diagnosis is made by scraping thin scales from the border of the lesion, dissolving them in 20% potassium hydroxide (KOH), and examining for hyphae.
Symmetrical, sharply marginated lesions in inguinal areas occur with tinea cruris. The most common organisms are T rubrum, T mentagrophytes, and Epidermophyton floccosum.
Tinea pedis presents with red scaly soles, blisters on the instep of the foot, or fissuring between the toes. T rubrum and T mentagrophytes are the cause.
E. Tinea Unguium (Onychomycosis)
Loosening of the nail plate from the nail bed (onycholysis), giving a yellow discoloration, is the first sign of fungal invasion of the nails. Thickening of the distal nail plate then occurs, followed by scaling and a crumbly appearance of the entire nail plate surface. T rubrum is the most common cause. The diagnosis is confirmed by KOH examination and fungal culture. Usually only one or two nails are involved. If every nail is involved, psoriasis, lichen planus, or idiopathic trachyonychia is a more likely diagnosis than fungal infection.
The treatment of dermatophytosis is quite simple: If hair is involved (ie, scalp infections), systemic therapy is necessary. Griseofulvin and terbinafine are both effective. Terbinafine does not work for Microsporum canis. Topical antifungal agents do not enter hair or nails in sufficient concentration to clear the infection. The absorption of griseofulvin from the gastrointestinal tract is enhanced by a fatty meal; thus, whole milk or ice cream taken with the medication increases absorption. The dosage of griseofulvin is 20 mg/kg/day divided BID (maximum 500 mg/dose). With hair infections, cultures should be done every 4 weeks, and treatment should be continued for 4 weeks following a negative culture result. The side effects are few, and the drug has been used successfully in the newborn period. Terbinafine dosing is (62.5 mg/day, < 20 kg–125 mg/day, 20–40 kg–250 mg/day, > 40 kg). For nails, daily administration of topical ciclopirox 8% (Penlac nail lacquer) can be considered, as can terbinafine for 6–12 weeks or pulsed-dose itraconazole (50 mg/twice a day < 20 kg–100 mg/twice a day, 20–40 kg–200 mg/twice a day, > 40 kg) given in three 1-week pulses separated by 3 weeks.
Tinea corporis, tinea pedis, and tinea cruris can be treated effectively with topical medication after careful inspection to make certain that the hair and nails are not involved. Treatment with any of the imidazoles, allylamines, benzylamines, or ciclopirox applied twice daily for 3–4 weeks is recommended.
Tinea versicolor is a superficial infection caused by Malassezia globosa, a yeast-like fungus. It characteristically causes polycyclic connected hypopigmented macules and very fine scales in areas of sun-induced pigmentation. In winter, the polycyclic macules appear reddish brown. Recurrent infection is common.
Treatment consists of application of selenium sulfide (Selsun), 2.5% suspension, zinc pyrithione shampoo, or topical antifungals. Selenium sulfide and zinc pyrithione shampoo should be applied to the whole body and left on overnight. Treatment can be repeated again in 1 week and then monthly thereafter. It tends to be somewhat irritating, and the patient should be warned about this difficulty. Topical antifungals are applied twice a day for 1–2 weeks. Fluconazole 400 mg single dose may also be used.
3. Candida albicans Infections
Candida albicans causes diaper dermatitis; thick, white patches on the oral mucosa (thrush); fissures at the angles of the mouth (perleche); and periungual erythema and nail plate abnormalities (chronic paronychia) (See also Chapter 43). Candida dermatitis is characterized by sharply defined erythematous patches, sometimes with eroded areas. Pustules, vesicles, or papules may be present as satellite lesions. Similar infections may be found in other moist areas, such as the axillae and neck folds. This infection is more common in children who have recently received antibiotics.
A topical imidazole cream is the drug of first choice for C albicans infections. In diaper dermatitis, the cream form can be applied twice a day. In oral thrush, nystatin suspension should be applied directly to the mucosa with the parent’s finger or a cotton-tipped applicator. In candidal paronychia, the antifungal agent is applied over the area, covered with occlusive plastic wrapping, and left on overnight after the application is made airtight. Refractory candidiasis will respond to a brief course of oral fluconazole.
VIRAL INFECTIONS OF THE SKIN
1. Herpes Simplex Infection
Painful, grouped vesicles or erosions on a red base suggest herpes simplex (See also Chapter 40). Rapid immunofluorescent tests for herpes simplex virus (HSV) and varicella-zoster virus (VZV) are available. A Tzanck smear is done by scraping a vesicle base with a No. 15 blade, smearing on a glass slide, and staining the epithelial cells with Wright stain. The smear is positive if epidermal multinucleated giant cells are visualized. A positive Tzanck smear indicates herpesvirus infection (HSV or VZV). In infants and children, lesions resulting from herpes simplex type 1 are seen most commonly on the gingiva, lips, and face. Involvement of a digit (herpes whitlow) will occur if the child sucks the thumb or fingers. Herpes simplex type 2 lesions are seen on the genitalia and in the mouth in adolescents. Cutaneous dissemination of herpes simplex occurs in patients with atopic dermatitis (eczema herpeticum) and appears clinically as very tender, punched-out erosions among the eczematous skin changes. Herpes gladiatorum occurs on the face, lateral neck, and medial arms and is commonly seen in wrestlers and rugby players.
The treatment of HSV infections is discussed in Chapter 40.
2. Varicella-Zoster Infection
Grouped vesicles in a dermatome, usually on the trunk or face, suggest varicella-zoster reactivation. Zoster in children may not be painful and usually has a mild course. In patients with compromised host resistance, the appearance of an erythematous border around the vesicles is a good prognostic sign. Conversely, large bullae without a tendency to crusting and systemic illness imply a poor host response to the virus. Varicella-zoster and herpes simplex lesions undergo the same series of changes: papule, vesicle, pustule, crust, slightly depressed scar. Lesions of primary varicella appear in crops, and many different stages of lesions are present at the same time (eg, papules), eccentrically placed vesicles on an erythematous base (“dew drop” on a rose petal), erosions, and crusts.
The treatment of VZV infections is discussed in Chapter 41.
3. Human Immunodeficiency Virus Infection
The average time of onset of skin lesions after perinatally acquired HIV infection is 4 months; after transfusion-acquired infection, it is 11 months (See also Chapter 41). Persistent oral candidiasis and recalcitrant candidal diaper rash are the most frequent cutaneous features of infantile HIV infection. Severe or recurrent herpetic gingivostomatitis, varicella zoster infection, and molluscum contagiosum infection occur. Recurrent staphylococcal pyodermas, tinea of the face, and onychomycosis are also observed. A generalized dermatitis with features of seborrhea (severe cradle cap) is extremely common. In general, persistent, recurrent, or extensive skin infections should make one suspicious of HIV infection.
The treatment of HIV infections is discussed in Chapter 46.
Molluscum contagiosum is a poxvirus that induces the epidermis to proliferate, forming a pale papule. Molluscum contagiosum consists of umbilicated, flesh-colored papules in groups anywhere on the body. They are common in infants and preschool children, as well as sexually active adolescents.
Treatment for molluscum is either immunological (topical imiquimod, oral cimetidine, intralesional candida antigen injection) or cytodestructive (topical cantharidin, cryotherapy with liquid nitrogen, and curettage). Left untreated, the lesions resolve over months to years.
Warts are skin-colored papules with rough (verrucous) surfaces caused by infection with human papillomavirus (HPV). There are over 200 types of this DNA virus, which induces the epidermal cells to proliferate, thus resulting in the warty growth. Flat warts are smoother and smaller than common warts and are often seen on the face and other sun-exposed areas. Certain types of HPV are associated with certain types of warts (eg, flat warts) or location of warts (eg, genital warts).
Thirty percent of warts will clear in 6 months. As with molluscum, the treatment of warts is also immunological (topical imiquimod, oral cimetidine, intralesional candida antigen injection, and squaric acid contact therapy) or cytodestructive. Liquid nitrogen is painful, user dependent, and can lead to blistering and scarring. Topical salicylic acid may also be used. Large mosaic plantar warts are treated most effectively by applying 40% salicylic acid plaster cut with a scissors to fit the lesion. The adhesive side of the plaster is placed against the lesion and taped securely in place with duct or athletic tape. The plaster and tape should be placed on Monday through Friday. Over the weekend, the patient should soak the skin in warm water for 30 minutes to soften it. Then the white, macerated tissue should be pared with a pumice stone, cuticle scissors, or a nail file. This procedure is repeated every week, and the patient is seen every 4 weeks. Most plantar warts resolve in 6–8 weeks when treated in this way. Vascular pulsed dye lasers are a useful adjunct therapy for the treatment of warts.
For flat warts, a good response to 0.025% tretinoin gel or topical imiquimod cream, applied once daily for 3–4 weeks, has been reported.
Surgical excision, electrosurgery, and nonspecific burning laser surgery should be avoided; these modalities do not have higher cure rates and result in scarring. Cantharidin may cause small warts to become larger and should not be used.
Venereal warts (condylomata acuminata) (see Chapter 44) may be treated with imiquimod, 25% podophyllum resin (podophyllin) in alcohol, or podofilox, a lower concentration of purified podophyllin, which is applied at home. Podophyllin should be painted on the lesions in the practitioner’s office and then washed off after 4 hours. Re-treatment in 2–3 weeks may be necessary. Podofilox is applied by the patient once daily, Monday through Thursday, whereas imiquimod is used three times a week on alternating days. Lesions not on the vulvar mucous membrane but on the adjacent skin should be treated as a common wart and frozen.
No wart therapy is immediately and definitively successful. Realistic expectations should be set and appropriate follow-up treatments scheduled.
EF: Human papillomavirus and genital warts: a review of the evidence for the 2015 Centers for Disease Control and Prevention Sexually Transmitted Diseases Treatment Guidelines. Clin Infect Dis 2015 Dec 15;61 Suppl 8:S849–S855
Scabies is suggested by linear burrows about the wrists, ankles, finger webs, areolas, anterior axillary folds, genitalia, or face (in infants). Often there are excoriations, honey-colored crusts, and pustules from secondary infection. Identification of the female mite or her eggs and feces is necessary to confirm the diagnosis. Apply mineral oil to a No. 15 blade and scrape an unscratched papule or burrow and examine microscopically to confirm the diagnosis. In a child who is often scratching, scrape under the fingernails. Examine the parents for unscratched burrows.
Permethrin 5% is the treatment of choice for scabies. It should be applied as a single overnight application and repeated in 7 days to patient and household contacts. Oral ivermectin 200 mcg/dose × 1 and repeated in 7 days may be used in resistant cases.
2. Pediculoses (Louse Infestations)
The presence of excoriated papules and pustules and a history of severe itching at night suggest infestation with the human body louse. This louse may be discovered in the seams of underwear but not on the body. In the scalp hair, the gelatinous nits of the head louse adhere tightly to the hair shaft. The pubic louse may be found crawling among pubic hairs, or blue-black macules may be found dispersed through the pubic region (maculae cerulea). The pubic louse is often seen on the eyelashes of newborns.
Initial treatment of head lice is often instituted by parents with an over-the-counter pyrethrin or permethrin product. If head lice are not eradicated after two applications 7 days apart with these products, malathion 0.5% is highly effective but is toxic, if ingested, and flammable. A second application 7–9 days after initial treatment may be necessary. Treatment of pubic lice is similar. Treatment of body lice is clean clothing and washing the infested clothing at high temperature.
Papular urticaria is characterized by grouped erythematous papules surrounded by an urticarial flare and distributed over the shoulders, upper arms, legs, and buttocks in infants. Although not a true infestation, these lesions represent delayed hypersensitivity reactions to stinging or biting insects. Fleas from dogs and cats are the usual offenders. Less commonly, mosquitoes, lice, scabies, and bird and grass mites are involved. The sensitivity is transient, lasting 4–6 months. Usually no other family members are affected. It is often difficult for the parents to understand why no one else is affected.
The logical therapy is to remove the offending insect, although in most cases it is very difficult to identify the exact cause. Topical corticosteroids and oral antihistamines will control symptoms.
The terms dermatitis and eczema are currently used interchangeably in dermatology, although the term eczema truly denotes an acute weeping dermatosis. All forms of dermatitis, regardless of cause, may present with acute edema, erythema, and oozing with crusting, mild erythema alone, or lichenification. Lichenification is diagnosed by thickening of the skin with a shiny surface and exaggerated, deepened skin markings. It is the response of the skin to chronic rubbing or scratching.
Although the lesions of the various dermatoses are histologically indistinguishable, clinicians have nonetheless divided the disease group called dermatitis into several categories based on known causes in some cases and differing natural histories in others.
ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
Clinical features of atopic dermatitis:
Atopic dermatitis is a polygenic disease with positive and negative modifiers. Atopic dermatitis results from an interaction among susceptibility genes, the host environment, skin barrier defects, pharmacologic abnormalities, and immunologic response. The case for food and inhalant allergens as specific causes of atopic dermatitis is not strong. There is significant evidence that a primary defect in atopic dermatitis is an abnormality in the skin barrier formation due to defects in the filaggrin gene. Not all people with filaggrin abnormalities have atopic dermatitis and not all people with atopic dermatitis have filaggrin abnormalities.
Many (not all) patients go through three clinical phases. In the first, infantile eczema, the dermatitis begins on the cheeks and scalp and frequently expresses itself as oval patches on the trunk, later involving the extensor surfaces of the extremities. The usual age at onset is 2–3 months, and this phase ends at age 18 months to 2 years. Only one-third of all infants with infantile eczema progress to phase 2 childhood or flexural eczema in which the predominant involvement is in the antecubital and popliteal fossae, the neck, the wrists, and sometimes the hands or feet. This phase lasts from age 2 years to adolescence. Only one-third of children with typical flexural eczema progress to adolescent eczema, which is usually manifested by the continuation of chronic flexural eczema along with hand and/or foot dermatitis. Atopic dermatitis is quite unusual after age 30 years.
All other types of dermatitis must be considered.
A few patients with atopic dermatitis have immunodeficiency with recurrent pyodermas, unusual susceptibility to HSVs, hyperimmunoglobulinemia E, defective neutrophil and monocyte chemotaxis, and impaired T-lymphocyte function (see Chapter 33).
A faulty epidermal barrier predisposes the patient with atopic dermatitis to dry, itchy skin. Inability to hold water within the stratum corneum results in rapid evaporation of water, shrinking of the stratum corneum, and cracks in the epidermal barrier. Such skin forms an ineffective barrier to the entry of various irritants. Chronic atopic dermatitis is frequently infected secondarily with S aureus or Streptococcus pyogenes. HSV virus may also superinfect atopic dermatitis and severe widespread disease is known as Kaposi’s varicelliform eruption or eczema herpeticum. Patients with atopic dermatitis have a deficiency of antimicrobial peptides in their skin, which may account for the susceptibility to recurrent skin infection.
Application of wet dressings and medium-potency topical corticosteroids is the treatment of choice for acute, weeping atopic eczema. The use of wet dressings is outlined at the beginning of this chapter. Superinfection with S aureus, S pyogenes, and HSV may occur, and appropriate systemic therapy may be necessary. If the expected improvement is not seen, bacterial and HSV cultures should be obtained to identify the possibility of a superinfection.
Treatment is aimed at avoiding irritants and restoring moisture to the skin. No soaps or harsh shampoos should be used, and the patient should avoid woolen or any rough clothing. Bathing is minimized to every second or third day. Twice-daily lubrication of the skin is very important.
Nonperfumed creams or lotions are suitable lubricants. Plain petrolatum is an acceptable lubricant, but some people find it too greasy and during hot weather it may also cause considerable sweat retention. Liberal use of a thick moisturizer four to five times daily as a substitute for soap is also satisfactory as a means of lubrication. A bedroom humidifier is often helpful. Topical corticosteroids should be limited to medium strength (see Table 15–2). There is seldom a reason to use super or high-potency corticosteroids in atopic dermatitis. In superinfected atopic dermatitis, systemic antibiotics for 10–14 days are necessary.
Tacrolimus and pimecrolimus ointments are topical immunosuppressive agents that are effective in atopic dermatitis. Because of concerns about the development of malignancies, tacrolimus and pimecrolimus should be reserved for children older than 2 years with atopic dermatitis unresponsive to medium-potency topical steroids. It has been argued that an increased risk of malignancy has not been seen in immunologically normal individuals using these products. Recommendations for usage likely will change with time. Narrow-band UV-B is recommended for extensive disease, starting with twice-weekly sessions in addition to topical steroids. Treatment failures in chronic atopic dermatitis are most often the result of noncompliance. This is a frustrating disease for parent and child. Return to a normal lifestyle for the parent and child is the ultimate goal of therapy.
M: Differential diagnosis of atopic dermatitis. Immunol Allergy Clin North Am 2017 Feb;37(1):11–34
HC: What’s new in atopic eczema? An analysis of systematic reviews published in 2008 and 2009. Clin Exp Dermatol 2010;35:823
Nummular eczema is characterized by numerous symmetrically distributed coin-shaped patches of dermatitis, principally on the extremities. These may be acute, oozing, and crusted or dry and scaling. The differential diagnosis should include tinea corporis, impetigo, and atopic dermatitis.
The same topical measures should be used as for atopic dermatitis, although more potent topical steroids may be necessary.
3. Primary Irritant Contact Dermatitis (Diaper Dermatitis)
Contact dermatitis is of two types: primary irritant and allergic. Primary irritant dermatitis develops within a few hours, reaches peak severity at 24 hours, and then disappears. Allergic contact dermatitis (described in the next section) has a delayed onset of 18 hours, peaks at 48–72 hours, and often lasts as long as 2–3 weeks even if exposure to the offending antigen is discontinued.
Diaper dermatitis, the most common form of primary irritant contact dermatitis seen in pediatric practice, is caused by prolonged contact of the skin with urine and feces, which contain irritating chemicals such as urea and intestinal enzymes.
The diagnosis of diaper dermatitis is based erythema and scaling of the skin in the perineal area and the history of prolonged skin contact with urine or feces, with sparing of inguinal folds. This is frequently seen in the “good baby” who sleeps many hours through the night without waking. In 80% of cases of diaper dermatitis lasting more than 3 days, the affected area is colonized with C albicans even before appearance of the classic signs of a beefy red, sharply marginated dermatitis with satellite lesions. Streptococcal perianal cellulitis and infantile psoriasis should be included in the differential diagnosis.
Treatment consists of changing diapers frequently. The area should only be washed with clean cloth and water following a bowel movement. Because rubber or plastic pants prevent evaporation of the contactant and enhance its penetration into the skin, they should be avoided as much as possible. Air drying is useful. Treatment of long-standing diaper dermatitis should include application of a barrier cream such as zinc oxide with each diaper change and an imidazole cream twice a day.
4. Allergic Contact Dermatitis (Poison Ivy Dermatitis)
Plants such as poison ivy, poison sumac, and poison oak cause most cases of allergic contact dermatitis in children. Allergic contact dermatitis has all the features of delayed type (T-lymphocyte–mediated) hypersensitivity. Many substances may cause such a reaction; other than plants, nickel sulfate, potassium dichromate, and neomycin are the most common causes. Nickel is found to some degree in all metals. Nickel allergy is commonly seen on the ears secondary to the wearing of earrings, and near the umbilicus from pants snaps and belt buckles. The true incidence of allergic contact dermatitis in children is unknown. Children often present with acute dermatitis with blister formation, oozing, and crusting. Blisters are often linear and of acute onset.
Treatment of contact dermatitis in localized areas is with potent topical corticosteroids. In severe generalized involvement, prednisone, 1–2 mg/kg/day orally for 10–14 days, can be used.
et al: Allergens responsible for allergic contact dermatitis among children: a systematic review and meta-analysis. Contact Dermatitis 2011;64:245
Seborrheic dermatitis is an erythematous scaly dermatitis accompanied by overproduction of sebum occurring in areas rich in sebaceous glands (ie, the face, scalp, and perineum). This common condition occurs predominantly in the newborn and at puberty, the ages at which hormonal stimulation of sebum production is maximal. Although it is tempting to speculate that overproduction of sebum causes the dermatitis, the exact relationship is unclear.
Seborrheic dermatitis on the scalp in infancy is clinically similar to atopic dermatitis, and the distinction may become clear only after other areas are involved. Psoriasis also occurs in seborrheic areas in older children and should be considered in the differential diagnosis.
Seborrheic dermatitis responds well to low-potency topical corticosteroids, antifungal shampoos (ketoconazole 1% or 2%) and antidandruff shampoos.
Dandruff is physiologic scaling or mild seborrhea, in the form of greasy scalp scales. The cause is unknown. Treatment is with medicated dandruff shampoos.
7. Dry Skin Dermatitis (Asteatotic Eczema, Xerosis)
Children who live in arid climates are susceptible to dry skin, characterized by large cracked scales with erythematous borders. The stratum corneum is dependent on environmental humidity for its water, and below 30% environmental humidity the stratum corneum loses water, shrinks, and cracks. These cracks in the epidermal barrier allow irritating substances to enter the skin, predisposing the patient to dermatitis.
Treatment consists of increasing the water content of the skin in the immediate external environment. House humidifiers are very useful. Minimize bathing to every second or third day.
Frequent soaping of the skin impairs its water-holding capacity and serves as an irritating alkali, and all soaps should therefore be avoided. Frequent use of emollients (eg, Cetaphil, Eucerin, Vaseline, Vanicream) should be a major part of therapy.
Follicular papules containing a white inspissated scale characterize keratosis pilaris. Individual lesions are discrete and may be red. They are prominent on the extensor surfaces of the upper arms and thighs and on the buttocks and cheeks. In severe cases, the lesions may be generalized.
Treatment is with keratolytics such as urea cream or lactic acid, followed by skin hydration.
White, scaly macular areas with indistinct borders are seen over extensor surfaces of extremities and on the cheeks in children with pityriasis alba. Sun tanning exaggerates these lesions. Histologic examination reveals a mild dermatitis. These lesions may be confused with tinea versicolor.
Low-potency topical corticosteroids may help decrease any inflammatory component and may lead to faster return of normal pigmentation. Strict sun avoidance and sun protection is also recommended.
If the skin moves with the nodule on lateral palpation, the tumor is located within the dermis; if the skin moves over the nodule, it is subcutaneous. Seventy-five percent of lumps in childhood will be either epidermoid cysts (60%) or pilomatricomas (15%).
Epidermoid cysts are the most common type of cutaneous cyst. Other names for epidermoid cysts are epidermal cysts, epidermal inclusion cysts, and “sebaceous” cysts. This last term is a misnomer since they contain neither sebum nor sebaceous glands. Epidermoid cysts can occur anywhere, but are most common on the face and upper trunk. They usually arise from and are lined by the stratified squamous epithelium of the follicular infundibulum. Clinically, epidermoid cysts are dermal nodules with a central punctum, representing the follicle associated with the cyst. They can reach several centimeters in diameter. Dermoid cysts are areas of sequestration of skin along embryonic fusion lines. They are present at birth and occur most commonly on the lateral eyebrow.
Epidermoid cysts can rupture, causing a foreign-body inflammatory reaction, or become infected. Infectious complications should be treated with antibiotics. Definitive treatment of epidermoid and dermoid cysts is surgical excision.
These are benign tumors of the hair matrix. They are most commonly seen on the face and upper trunk. They are firm and may be irregular. Their color varies, flesh colored or blue. The firmness is secondary to calcification of the tumor.
Treatment is by surgical excision.
Violaceous circles or semicircles of nontender intradermal nodules found over the lower legs and ankles, the dorsum of the hands and wrists, and the trunk suggest granuloma annulare. Histologically, the disease appears as a central area of tissue death (necrobiosis) surrounded by macrophages and lymphocytes.
No treatment is necessary. Lesions resolve spontaneously within 1–2 years in most children.
These lesions appear over 1–2 weeks at times following skin trauma as a dark red papule with an ulcerated and crusted surface that may bleed easily with minor trauma. Histologically, this represents excessive new vessel formation with or without inflammation (granulation tissue). It should be regarded as an abnormal healing response.
Pulsed dye laser for very small lesions or curettage followed by electrocautery are the treatments of choice.
Keloids are scars of delayed onset that continue to grow for up to several years and to progress beyond the initial wound margins. The tendency to develop keloids is inherited. They are often found on the face, earlobes, neck, chest, and back.
Treatment includes intralesional injection with triamcinolone acetonide, 20–40 mg/mL, or excision and injection with corticosteroids. For larger keloids, excision followed by postoperative radiotherapy may be indicated.
Papulosquamous eruptions (Table 15–6) comprise papules or plaques with varying degrees of scale.
Table 15–6.Papulosquamous eruptions in children. ||Download (.pdf) Table 15–6.Papulosquamous eruptions in children.
Pityriasis lichenoides (acute or chronic)
Pityriasis rubra pilaris
Pathogenesis & Clinical Findings
Pink to red, oval plaques with fine scales that tend to align with their long axis parallel to skin tension lines (eg, “Christmas tree pattern” on the back) are characteristic lesions of pityriasis rosea. The generalized eruption is usually preceded for up to 30 days by a solitary, larger, scaling plaque with central clearing and a scaly border (the herald patch). The herald patch is clinically similar to ringworm and can be confused. In whites, the lesions are primarily on the trunk; in blacks, lesions are primarily on the extremities and may be accentuated in the axillary and inguinal areas (inverse pityriasis rosea).
This disease is common in school-aged children and adolescents and is presumed to be viral in origin. The role of human herpesvirus 7 in the pathogenesis of pityriasis rosea is debated. The condition lasts 6–12 weeks and may be pruritic.
The major differential diagnosis is secondary syphilis, and a VDRL (Venereal Disease Research Laboratories) test should be done if syphilis is suspected, especially in high-risk patients with palm or sole involvement. Fever and widespread lymphadenopathy is often found in secondary syphilis. “Pityriasis rosea” lasting more than 12 weeks is likely to be pityriasis lichenoides.
Exposure to natural sunlight may help hasten the resolution of lesions. Oral antihistamines and topical steroids can be used for pruritus. Often, no treatment is necessary. Pityriasis rosea that lasts more than 12 weeks should be referred to a dermatologist for evaluation.
ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
Erythematous papules and plaques with thick, white scales.
Elbows, knees, and scalp often affected.
Nail pitting and distal onycholysis.
The pathogenesis of psoriasis is complex and incompletely understood. It has immune-mediated inflammation, is a familial condition, and multiple psoriasis susceptibility genes have been identified. There is increased epidermal turnover; psoriatic epidermis has a turnover time of 3–4 days versus 28 days for normal skin. These rapidly proliferating epidermal cells produce excessive stratum corneum, giving rise to thick, opaque scales.
Psoriasis is characterized by erythematous papules covered by thick white scales. Guttate (droplike) psoriasis is a common form in children that often follows by 2–3 weeks an episode of streptococcal pharyngitis. The sudden onset of small papules (3–8 mm), seen predominantly over the trunk and quickly covered with thick white scales, is characteristic of guttate psoriasis. Chronic psoriasis is marked by thick, large scaly plaques (5–10 cm) over the elbows, knees, scalp, and other sites of trauma. Pinpoint pits in the nail plate are seen, as well as yellow discoloration of the nail plate resulting from onycholysis. Psoriasis occurs frequently on the scalp, elbows, knees, periumbilical area, ears, sacral area, and genitalia.
Papulosquamous eruptions that present problems of differential diagnosis are listed in Table 15–6.
Topical corticosteroids are the initial treatment of choice. Penetration of topical steroids through the enlarged epidermal barrier in psoriasis requires that more potent preparations be used, for example, fluocinonide 0.05% (Lidex) or clobetasol 0.05% (Temovate) ointment twice daily.
The second line of therapy is topical vitamin D3 medications such as calcipotriene (Dovonex) or, calcitriol (Vectical), applied twice daily or the combination of a superpotent topical steroid twice daily on weekends and calcipotriene or calcitriol twice daily on weekdays.
Topical retinoids such as tazarotene (0.1%, 0.5% cream, gel) can be used in combination with topical corticosteroids to help restore normal epidermal differentiation and turnover time.
Anthralin therapy is also useful. Anthralin is applied to the skin for a short contact time (eg, 20 minutes once daily) and then washed off with a neutral soap (eg, Dove). This can be used in combination with topical corticosteroids.
Crude coal tar therapy is messy and stains bedclothes. The newer tar gels (Estar, PsoriGel) and one foam product (Scytera) cause less staining and are most efficacious. They are applied twice daily. These preparations are sold over the counter and are not usually covered by insurance plans.
Scalp care using a tar shampoo requires leaving the shampoo on for 5 minutes, washing it off, and then shampooing with commercial shampoo to remove scales. It may be necessary to shampoo daily until scaling is reduced.
More severe cases of psoriasis are best treated by a dermatologist. Narrow band UVB phototherapy and multiple systemic medications and new biologic agents (antibodies, fusion proteins, and recombinant cytokines) are effective in more widespread, severe cases.
et al: Efficacy and safety of treatments for childhood psoriasis: a systematic literature review. J Am Acad Dermatol 2010;62:1013
Hair loss in children (Table 15–7) imposes great emotional stress on the patient and the parent. A 60% hair loss in a single area is necessary before hair loss can be detected clinically. Examination should begin with the scalp to determine whether inflammation, scale, or infiltrative changes are present. The hair should be gently pulled to see if it is easily removable. Hairs should be examined microscopically for breaking and structural defects and to see whether growing or resting hairs are being shed. Placing removed hairs in mounting fluid (Permount) on a glass microscope slide makes them easy to examine.
Table 15–7.Other causes of hair loss in children. ||Download (.pdf) Table 15–7.Other causes of hair loss in children.
Hair loss with scalp changes
Aplasia cutis congenita
Hair loss with hair shaft defects (hair fails to grow out enough to require haircuts)
Monilethrix—alternating bands of thin and thick areas
Pili annulati—alternating bands of light and dark pigmentation
Pili torti—hair twisted 180 degrees, brittle
Trichorrhexis invaginata (bamboo hair)—intussusception of one hair into another
Trichorrhexis nodosa—nodules with fragmented hair
Three diseases account for most cases of hair loss in children: alopecia areata, tinea capitis (described earlier in this chapter), and hair pulling.
Complete hair loss in a localized area is called alopecia areata. This is the most common cause of hair loss in children. An immunologic pathogenic mechanism is suspected because dense infiltration of lymphocytes precedes hair loss. Fifty percent of children with alopecia areata completely regrow their hair within 12 months, although as many may have a relapse in the future.
A rare and unusual form of alopecia areata begins at the occiput and proceeds along the hair margins to the frontal scalp. This variety, called ophiasis, often eventuates in total scalp hair loss (alopecia totalis). The prognosis for regrowth in ophiasis is poor.
Superpotent topical steroids, minoxidil (Rogaine), contact therapy, and anthralin are topical treatment options. Systemic corticosteroids given to suppress the inflammatory response will result in hair growth, but the hair may fall out again when the drug is discontinued. Systemic corticosteroids should never be used for a prolonged time period. In children with alopecia totalis, a wig is most helpful. Treatment induced hair growth does not alter risk of recurrence.
et al: Alopecia areata update: part I. Clinical picture, histopathology and pathogenesis. J Am Acad Dermatol 2010;62:177
et al: Alopecia areata update: part II. Treatment. J Am Acad Dermatol 2010;62:191
Traumatic hair pulling causes the hair shafts to be broken off at different lengths, with an ill-defined area of hair loss, petechiae around follicular openings, and a wrinkled hair shaft on microscopic examination. This behavior may be merely habit, an acute reaction to severe stress, trichotillomania, or a sign of another psychiatric disorder. Eyelashes and eyebrows rather than scalp hair may be pulled out.
If the behavior has a long history, psychiatric evaluation may be helpful. Cutting or oiling the hair to make it slippery is an aid to behavior modification.
Erythema multiforme begins with papules that later develop a dark center and then evolve into lesions with central bluish discoloration or blisters and the characteristic target lesions (iris lesions) that have three concentric circles of color change. Erythema multiforme has sometimes been diagnosed in patients with severe mucous membrane involvement, but Stevens-Johnson syndrome is the diagnosis when severe involvement of conjunctiva, oral cavity, and genital mucosa also occur.
Many causes are suspected, particularly concomitant HSV; drugs, especially sulfonamides; and Mycoplasma infections. Recurrent erythema multiforme is usually associated with reactivation of HSV. In erythema multiforme, spontaneous healing occurs in 10–14 days, but Stevens-Johnson syndrome may last 6–8 weeks.
Treatment is symptomatic in uncomplicated erythema multiforme. Removal of offending drugs is an obvious measure. Oral antihistamines such as cetirizine 5–10 mg every morning and hydroxyzine 1 mg/kg/day at bedtime are useful. Cool compresses and wet dressings will relieve pruritus. Steroids have not been demonstrated to be effective. Chronic acyclovir therapy has been successful in decreasing attacks in patients with herpes-associated recurrent erythema multiforme.
Drugs may produce urticarial, morbilliform, scarlatiniform, pustular, bullous, or fixed skin eruptions. Urticaria may appear within minutes after drug administration, but most reactions begin 7–14 days after the drug is first administered. These eruptions may occur in patients who have received these drugs for long periods, and eruptions continue for days after the drug has been discontinued. Drug eruptions with fever, eosinophilia, and systemic symptoms (DRESS syndrome) is most commonly seen with anticonvulsants, but may be seen with other drugs. Drugs commonly implicated in skin reactions are listed in Table 15–8.
Table 15–8.Common drug reactions. ||Download (.pdf) Table 15–8.Common drug reactions.
Fixed drug eruption, erythema multiforme, toxic epidermal necrolysis, Stevens-Johnson syndrome
Nonsteroidal anti-inflammatory drugs
MISCELLANEOUS SKIN DISORDERS SEEN IN PEDIATRIC PRACTICE
Recurrent erosions on the gums, lips, tongue, palate, and buccal mucosa are often confused with herpes simplex. A smear of the base of such a lesion stained with Wright stain will aid in ruling out herpes simplex by the absence of epithelial multinucleate giant cells. A culture for herpes simplex is also useful in differential diagnostics. The cause remains unknown, but T-cell–mediated cytotoxicity to various viral antigens has been postulated.
There is no specific therapy for this condition. Rinsing the mouth with liquid antacids provides relief in most patients. Topical corticosteroids in a gel base may provide some relief. In severe cases that interfere with eating, prednisone, 1 mg/kg/day orally for 3–5 days, will suffice to abort an episode. Colchicine, 0.2–0.5 mg/day, sometimes reduces the frequency of attacks.
Vitiligo is characterized clinically by the development of areas of depigmentation. These are often symmetrical and occur mainly on extensor surfaces. The depigmentation results from a destruction of melanocytes. The basis for this destruction is unknown, but immunologically mediated damage is likely and vitiligo sometimes occurs in individuals with autoimmune endocrinopathies.
Treatment is with potent topical steroids or tacrolimus. Topical calcipotriene has also been used. Narrow-band ultraviolet B radiation (UVB 311 nm) may be used in severe cases. Response to treatment is slow often requiring many months to years.
JG: Vitiligo in childhood: a state of the art review. Pediatr Dermatol 2010;27:437