Many diseases of the skin have different clinical presentations and outcomes in the pediatric age group.

This lecture will focus on the more common clinical entities encountered in clinical practice. Diseases will be subdivided into those commonly seen in the following age divisions: neonates and infants, childhood, and adolescence.

Transient Dermatoses of the Newborn: Caput succedaneum - subcutaneous edema over the presenting part of the head and is a common occurrence in newborns

Cephalohematoma - subperiosteal collection of blood and is less common Both lesions are due to shearing forces on the scalp skin and skull during labor.

Milia
multiple pinpoint- to 1-mm papules benign, superficial keratin cysts seen most commonly on the nose of infants may be present in the oral cavity as well, where they are called Epstein's pearls expected findings in the newborn resolve spontaneously within a few weeks of life

Transient mottling of the skin in the newborn period Normal physiologic response to ambient temperature changes; accentuates with decreased temperatures and improves with rewarming Symmetrical, blanchable, redblue reticulated mottling of trunk and extremities More common in premature infants, but also affects full-term newborns

Prominent sebaceous glands present in the newborn period Affects up to 50% of term infants Characteristic pinpoint yellow papules with no surrounding erythema Location: nose, cheeks, upper lip and forehead Due to maternal androgen stimulation of sebaceous glands

4070% of full-term infants Characteristic eruption with macular erythema and discrete, scattered yellow papules and pustules with surrounding erythematous wheals primarily face, trunk and extremities with sparing of the palms and soles occurs on day 12 of life

Acne neonatorum is a benign, self-limited, acneiform eruption that develops within the first 30 days of life. Benign eruption appears to be hormonally mediated Multiple discrete papules develop between the age 2 and 4 weeks of life, evolve into pustules, and spontaneously resolve

Self-limited, benign dermatosis of the newborn Occurs in 0.24% of all term infants; 4.4% ofvBlack infants affected, 0.6% of White infants affected Lesions may be present in utero and are almost always present at birth Location: distributed diffusely on trunk, face, extremities and palms and soles

Three stages: 1. 15 mm, fragile pustules present at birth; may not be evident at birth due to rupture with birth trauma or initial cleaning Resolution of pustules with surrounding fine white collarettes of scale Hyperpigmented macules represent postinflammatory hyperpigmentation. this stage may not be present in lightskinned infants

Cutaneous findings seen in 50% with two variants:

Location most common on the face and scalp with characteristic patterns: 1. Raccoon eyes or owl-like periocular involvement 2. Headband distribution with lesions on the forehead and bilateral temporal areas Skin lesions rarely present at birth and usually develop in the first few weeks of life after light exposure

Clinical findings confirmed by blood tests Serologic studies: anti-Ro (SS-A), anti-La (SS-B), anti-RNP, anti-DNA, anticardiolipin antibodies, antinuclear antibodies and rheumatoid factor may be positive Treatment - Broad-spectrum sunblock daily - Topical steroids: low- or high-potency depending on severity - Oral corticosteroids (rarely needed)

asymptomatic subcutaneous nodules or erythematous plaques in otherwise healthy full-term and post-term infants at 1 6 weeks of life Often follows a difficult delivery with perinatal complications such as hypothermia and asphyxia cheeks, shoulders, buttocks, thighs and legs

Approximately 1 : 5000 births Characterized by the absence of skin (i.e. epidermis, dermis and/or subcutaneous tissues) in localized or widespread areas at birth Most common on the scalp May be isolated finding, associated with underlying defects or seen with other isolated anomalies, syndromes and chromosomal disorders

Characteristic yellowish hairless plaque on the scalp More prominent in the newborn period because of maternal hormone influence Location: head and neck Localized developmental anomaly of appendageal structures

Postnatal colonization of Candida albicans More common in low-birthweight infants (<1500 g) Develop classic mucocutaneous eruption with satellite lesions and diaper area involvement Dissemination to the lungs, meninges and urinary tract with sepsis more common in low-birth-weight infants

Herpes neonatorum Congenital varicella Infantile herpes zoster Congenital syphilis toxoplasmosis, cytomegalovirus (CMV), human immunodeficiency virus (HIV), and rubella (TORCH)

Branchial cleft cyst/sinus Cysts or sinus tracts on the lateral aspect of the neck which are deep to sternocleidomastoid muscle May be unilateral or bilateral Usually present at birth or become obvious in early childhood Can be apparent on the cutaneous surface or drain into the pharynx

Branchial cleft cyst/sinus Branchial cysts are epithelial cysts arising from incomplete closure of the branchial clefts in embryologic development, most commonly the second or third branchial clefts Branchial sinuses are remnants of branchial clefts with depressions Treatment Preoperative imaging to assess for a fistulous connection to the posterior pharynx Surgical excision

Preauricular cyst/sinus An epithelial cyst, sinus, or swelling in preauricular region Common, occurs in 1% of the population Autosomal dominant or sporadic Bilateral and asymptomatic May become infected and drain purulent material Associated defects include deafness and renal abnormalities Most lesions are asymptomatic and do not require Treatment Secondarily infected cysts can be treated with antibiotics Excision is indicated if there is chronic inflammation, drainage or infection

Accessory tragus Presents with round, pedunculated, skin-colored papule, occurring anywhere along the line from the tragus to the lateral commissure of the mouth Can be unilateral or bilateral; single or multiple Treatment Surgical excision

Tinea capitis Most common in preschool or school-age children (ages 39 years) Incidence is highest in Black children Most common cause is Trichophyton tonsurans in North America (>90%) Clinical presentation is an incomplete alopecia especially prominent on the crown and occipital regions, with scaling

Ectothrix (infection on the outside of the hair shaft). a. Gray patch ringworm. Brittle hair; shafts break off close to scalp surface. Caused by M. audouinii and M. cani

Endothrix (infection on the inside of the hair shaft). a. Black dot ringworm. give appearance of black dots, caused by T. tonsurans and T. violaceum

b. Kerion. Boggy, purulent, inflamed painful nodule drains pus. Hairs do not break but fall out easily. Heals with residual hair loss

c. Favus. Scutula (yellowish crusts) are present on the scalp infected with T. schoenleinii. Favus is endemic in the Middle East and South Africa.

Tinea capitis: Management

Tinea capitis: Management

Selenium sulfide 2.5% shampoo 23 times a week Ketoconazole 12% shampoo 23 times a week Newer oral antifungal therapies shown to be safe and effective: terbinafine, itraconazole, fluconazole Obtain follow-up cultures until negative result is obtained Evaluate household contacts and treat if necessary For severe inflammatory kerion: prednisone 1mg/kg per day in addition to antifungal therapy, can hasten reduction of scaling and pruritus

SCABIES Scabies is an infestation by the mite Sarcoptes scabiei,characterized by severe pruritus and transmitted by close proximity to the infested person Common In children who are younger than 5 years old Equal incidence in Males and Females Incidence: 300 million cases annually worldwide. Seasonal variation: Fall, winter.

Scabies Papules on wrists, fingerwebs, periaxillary skin, genitalia and abdomen In infants, lesions more generalized: feet, scalp and face Multiple excoriations, erythematous papules, crusts, some pustules and secondary impetigo Pruritus, often increased in evening/night Erythematous nodules (nodular scabies) more common on trunk and axillae, particularly in infants

Scabies: Diagnosis Confirmed by scraping an unscratched burrow, demonstrating a mite, egg, feces (scybala) microscopically

Scabies: Treatment Permethrin cream 5% (see Table 10.1) 1. Dispense 60 g per patient; no refills 2. Apply thin layer of cream from neck down to toes 3. Be sure to include finger webs, armpits, groin 4. Leave cream on for 812 hours (overnight) 5. Take a hot shower or bath in the morning 6. Wash clothes used in previous 3 days through the hot cycle of the washer 7. Reapply cream (same technique) 1 week later 8. Do not apply cream more than twice Gamma benzene hexachloride lotion or cream 1% (lindane, Kwell, Gamene) 1. Dispense 60 g per patient; no refills 2. A bath is not recommended before applying the lotion

Pediculoses (louse infestations) Body louse infestations present with excoriated papules and pustules on trunk and perineum Pediculosis capitis usually presents with pruritic papules at nape of neck Nits and lice can be detected in scalp or clothing, especially seams of clothing Nits are white ovoid bodies, tightly adherent to hair shafts

Pediculosis Caused by Pediculus humanus (human body louse) with subspecies capitis (head lice) or humanus (body lice) Diagnosis Observation of nits or lice by visual inspection or microscopically

Pediculosis Capitis (Head lice): Management 1. Permethrin 1% (Nix) one application of cream rinse, left on for 10 minutes after shampoo, then rinsed out 2. Pyrethrins with piperonyl butoxide (RID, A-200 Pyrinate Shampoo) two applications (57 days apart) applied undiluted to the scalp, left on 10 minutes, then rinsed out 3. Lindane 1% shampoo (by prescription) 10- minute application then rinsed out; repeat in 1 week 4. Malathion 0.5% (Ovide) excellent ovicidal, but odiferous. Apply to hair, let dry for 812 hours, then shampoo out. Repeat in 1 week. Caution: flammable 5. Ivermectin 200250 g/kg in a single oral dose (off label)

Pediculosis Capitis (Head lice): Other Management a. Apply cream rinse and comb hair to removenits b. Chemicals used to dissolve nits (of questionable value): vinegar, glacial acetic acid, Step 2 (formic acid); use with combing c. Metal nit combs helpful if hair is thick d. Nit picking if hair is thin (may want to cut individual hairs) e. R & C Spray for use on clothing, furniture which cannot be washed or dry cleaned; do not use on people f. Pseudonits flakes of skin on hair shafts which may resemble nits; to differentiate, observe microscopically

Irritant diaper dermatitis (chafing dermatitis) Involves convex surfaces of buttocks, upper thighs, abdomen Spares inguinal folds Common between 7 and 12 months of age Candida albicans dermatitis Beefy-red, confluent erythema (Figure 4.28) Involves inguinal creases Satellite red papules or pustules at the periphery are common Frequently occurs after diaper dermatitis has lasted >72 h KOH: budding yeast and pseudohyphae Commonly seen with thrush (oral candidiasis)

A = Air. The diaper should be left open as much as possible when the infant sleeps to allow drying of the skin. B = Barrier ointments. Zinc oxide pastes, petrolatum, and other bland, unmedicated barrier preparations are mainstays of therapy. A continuous layer of barrier paste or ointment should be maintained, reapplying with every diaper change, if necessary. Baby powder on the diaper area offers no antimicrobial benefit to the infant and adds a risk of aspiration.

C = Cleansing and anti-candidal treatment. Gentle cleansing with plain water, mineral oil, or unscented gentle cleanser is recommended. Avoidance of friction or rubbing is important. A topical anticandidal agent should be added for any signs of candidiasis. Oral nystatin is indicated if oral thrush is present. D = Diapers. Diapers should be changed as frequently and as soon after soiling as possible, especially if cloth diapers are used. E = Education of parents and caregivers.

Candida albicans Topical antifungal therapy (e.g. nystatin, miconazole, ketoconazole, clotrimazole) with every diaper change until clear Erythema Hydrocortisone cream or ointment 1%, 34 times a day until clear (usually <7 days) Avoid steroids stronger than class 7 in diaper area

Appear between age 2 and 6 months and the majority clear by age 2 to 3 years Inherited disorder, presumably autosomal dominant Associated with either a family or a personal history of other allergic conditions (e.g. asthma or allergic rhinitis)

Major features 1. Pruritus 2. Typical morphology and distribution - Facial and extensor involvement during infancy and early childhood - Flexural lichenification in childhood or adolescence 3. Chronic or chronically relapsing dermatitis 4. Personal or family history of atopy

Minor or less specific features 1. Xerosis 2. Periauricular fissures 3. Ichthyosis 4. Hyperlinear palms 5. Keratosis pilaris 6. IgE reactivity (increased serum IgE, RAST, or prick test positivity) 7. Hand or foot dermatitis 8. Cheilitis 9. Scalp dermatitis 10. Susceptibility to cutaneous infections (especially Staphylococcus aureus and herpes simplex) 11. Perifollicular accentuation (especially in darkly pigmented races) 12. Dennies lines 13. Pityriasis alba

Infantile Atopic Dermatitis (AD) (from infants to 2 years) - distribution primarily on cheeks, face extensor surfaces of arms and legs; tends to spare diaper area Childhood AD (from about 2 years to puberty) tends to occur on flexural areas (antecubital fossae, popliteal fossae, hands and feet) Adult/teenage eczema (puberty through adulthood) occurs in flexural areas, hands and face, especially eyelids Face has typical central pallor

Crusty, oozing, eruption with frequent secondary changes from scratching Pruritus is a hallmark and can be severe, often set off by certain environmental or psychological causes

Treatment
Eliminate precipitating factors 1. Bathing can be performed once daily, but excessive bathing causes increased dryness a. Apply ointments immediately after patting skin dry b. Oils in bath are messy, and make children slippery to handle; may be useful for older children c. Tepid temperature is best; avoid very hot water; do not make the water too cool, causing the child to shiver d. Soap cleansers (e.g. Cetaphil Aquanil) are best 2. Excessive sweating, whether heat- or exercise induced, can cause itching 3. Temperature extremes (hot and humid, or cold and dry) can increase itching 4. Avoid coarse or irritating clothing (e.g. wool)

Topical corticosteroids reduce pruritus and inflammation 1. Hydrocortisone 1% or 2.5% ointment (class 67 steroids) for mild inflammation 2. Mid-strength steroids (class 35) (triamcinolone 0.1% ointment) only in isolated areas for young children 3. High-potency steroids may be indicated for hand or foot dermatitis because of the thickness of the stratum corneum. Be careful to avoid dorsa of hands and feet with high-potency steroids

Antihistamines Antibiotics 1. Antistaphylococcal drugs a. Topical agents (e.g. mupirocin) may be helpful for the short term, but some topical antibiotics (e.g. neomycin, bacitracin) can sensitize the skin and cause further allergic contact dermatitis b. Oral antibiotics may be given in short courses to reduce staphylococcal infection of the skin c. Frequent use of antibiotics can lead to resistant bacteria Systemic corticosteroids 1. Short courses for acute, severe exacerbations may be indicated 2. Long-term oral steroids are not recommended For severe, recalcitrant cases consider phototherapy (PUVA, UVB), IFN-, or immunosuppressive drugs (e.g. cyclosporine, methotrexate)

Prognosis Half of the cases of typical atopic dermatitis improve by 2 years of age Most improve by teenage years Patients tend to have dry, sensitive skin throughout life <10% of patients have lifelong problems

Common papular eruption of childhood which tends to continue into adulthood Prominent follicular plugs over extensor surfaces of extremities, especially upper arms, upper legs, buttocks and cheeks Associated with atopic disorders: atopic dermatitis, hay fever, asthma, allergic rhinitis Treatment Lubricants or emollients can improve dry skin Topical keratolytics

SEBORRHEIC DERMATITIS Adolescents: dry, fine, flaky desquamation of scalp, mid-face and eyebrows Common areas: scalp, midface, mid-chest, perineum Less common areas: forehead, anterior chest, axillae, umbilicus, intertriginous areas Facial involvement in adolescents along nasolabial folds

Pathogenesis Mechanism unknown Excess sebu m accumulation Increased quantities of Pityrosporum ovale (Malessezia furfur) are seen in sites of seborrheic dermatitis and may contribute to the disorder Treatment Low-potency topical steroid creams (class 57) twice a day, usually necessary for <7 days Shampoos 1. Keratolytic tar shampoos sulfur or salicylicacid (e.g. T-gel) 2. Zinc pyrithione (e.g. Head & Shoulders) 3. Selenium sulfide 2.5% shampoo (e.g. Selsun) 2% ketoconazole shampoo

Self-limited disorder of the pilosebaceous unit that is seen primarily in adolescents Most cases of acne present with a pleomorphic variety of lesions, consisting of comedones, papules, pustules, and nodule Acne may be self-limiting, the sequelae can be lifelong, with pitted or hypertrophic scar formation Most prevalent skin disorder in pediatrics Affects 40% of children aged 810 years Affects 85% of adolescents aged 1517 years

The pathogenesis of acne is multi-faceted, but four basic steps have been identified. These key elements are: (1) follicular epidermal hyperproliferation (2) excess sebum production (3) Inflammation (4) the presence and activity of Propionibacterium acnes.

Noninflammatory lesions Comedos: Open comedo (blackhead) appears as a flat or slightly raised lesion with a central dark-colored follicular impaction of keratin and lipid Closed comedone (white head) may be difficult to visualize. They appear as pale, slightly elevated, small papules and do not have a clinically visible orifice

Inflammatory acne: Lesions vary from small papules with a red border to pustules to large, tender, fluctuant nodules Some of the large nodules were previously called cysts and the term nodulocystic has been used to describe severe cases of inflammatory acne. True cysts are rarely found in acne, and this term should be abandoned and the term severe nodular acne used Whether the lesion appears as a papule, pustule, or nodule depends on the extent and location of the inflammatory infiltrate in the dermis

Scarring can be a complication of both noninflammatory and inflammatory acne There are four general types of acne scars: ice pick, rolling, boxcar, and hypertrophic Ice pick scars are narrow, deep scars that are widest at the surface of the skin and taper to a point in the dermis. Rolling scars are shallow, wide scars that have an undulating appearance. Boxcar scars are wide, sharply demarcated scars In rare instances, especially on the trunk, the scars may be hypertrophic.

Patients and parents should be educated on factors that may aggravate acne: 1. Repeated pressure, leaning, touching, or scrubbing acne-prone areas. 2. Occlusive garments such as headband, chinstraps, helmets, and hats. 3. Oil and grease in moisturizers, face creams, makeup, or hair products. 4. Greasy-air-filled environments in fast-food kitchens. 5. Squeezing or popping pimples can lead to scarring. 6. Certain medications taken for other problems (e.g., oral contraceptives, lithium, hydantoin, topical, and systemic steroids). 7. Emotional stress. 8. Hormonal changes with menses. 9. Foods typically do not play a major role, but some people find specific foods trigger their acne and are helped by avoiding them.

1. Topical antibiotics such as clindamycin or erythromycin help decrease bacterial load and inflammation. 2. Topical benzoyl peroxide also suppresses P. acnes and microbial resistance has not been reported. 3. Topical salicylic acid or -hydroxy acid preparations can help slough the outer layer of skin preventing follicular blockage. 4. Topical retinoids (tretinoin, adapalene, tazarotene) are effective, but require detailed instructions and gradual increases in concentration. Retinoids help the skin turn over more rapidly to decrease possible follicular blockage and rupture.

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Oral antibiotics such as tetracycline, erythromycin, doxycycline, or minocycline are probably the most effective and can be tapered to lower doses once the acne is under good control In females, acne can be controlled with oral contraceptives. Three OCPs are currently FDA-approved for the treatment of acne: (1) A triphasic OCP with norgestimate (preogestin)ethinyl estradiol 35 g (Estrostep) (2) Graduated ethinyl estradiol (2035 g) with norethindrone acetate (Ortho-tricyclin) (3) 20 g of ethinyl estradiol with 3 mg drospirenone (Yaz or Yasmin)

3. Oral spironolactone blocks androgen receptors and 5-reductase.

- Doses or 50 to100 mg daily can reduce sebum production and improve acne. - Patients taking spironolactone should be cautioned regarding hyperkalemia and hypotension side effects

4. Oral 13-cis-retinoic acid (isotretinoin) is highly effective for cystic acne. - retinoids are teratogenic - female patients must have a pretreatment pregnancy test - must be on two forms of birth control at least 1 month prior to beginning treatment, throughout treatment, and for 1 - month after treatment is discontinued. - a patient must have a negative serum pregnancy test within the 2 weeks prior to beginning treatment

Incising and expressing comedones can improve cosmetic appearance transiently. 6. Intralesional steroids for deep and inflamed lesions can quickly help them resolve. 7. Acne scarring can be treated with dermabrasion, laser resurfacing, chemical peels, filler substances, or punch grafting.
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