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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
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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, red–blue 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
40–70% 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 1–2 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 0.2–4% 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. 1–5 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: - papulosquamous (most common) - annular
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-birth-weight 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 3–9 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
Topical antifungals not fully effective
Oral griseofulvin:
1. Microsize griseofulvin 20 mg/kg per day
(maximum 1 g/24 hours)
2. Ultramicrosize griseofulvin 10 mg/kg per day
(maximum 750 mg/24 hours)
3. Take BID with fatty foods to increase absorption
4. Minimal duration of treatment is 4–6 weeks;
continue for 2 weeks past clinical resolution
Tinea capitis: Management Selenium sulfide 2.5% shampoo 2–3 times a week
Ketoconazole 1–2% shampoo 2–3 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 8–12 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 (5–7 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 8–12 hours, then shampoo out. Repeat in 1 week. Caution: flammable 5. Ivermectin 200–250 μg/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 anti-candidal 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%, 3–4 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. Dennie’s 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
6–7 steroids) for mild inflammation
2. Mid-strength steroids (class 3–5)
(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-γ, 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, mid-face, 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 5–7) 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 8–10 years
Affects 85% of adolescents aged 15–17 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.
1. 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
2. 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 (20–35 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
5. 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.