CLASSIFICATION OF SKIN LESIONS
Primary Skin Lesions
Macule: Flat, nonpalpable, skin discoloration.
Plaque: Elevated, > 2 cm diameter.
Wheal: Elevated, round or flat-topped area of dermal edema, disappears within hours.
Vesicle: Circumscribed, elevated, fluid-filled, < 0.5 cm diameter.
Bullae: Circumscribed, elevated, fluid-filled, > 0.5 cm diameter.
Pustule: Circumscribed, elevated, pus-filled.
Papule: Elevated, palpable, solid, < 0.5 cm diameter.
Nodule: Elevated, palpable, solid, > 0.5 cm.
Petechiae: Red-purple, nonblanching macule, < 0.5 cm diameter, usually pinpoint.
Purpura: Red-purple, nonblanching macule, > 0.5 cm diameter.
Telangiectasia: Blanchable, dilated blood vessels.
Secondary Skin Lesions
Scale: Accumulation of dead, exfoliating epidermal cells.
Crust (scab): Dried serum, blood, or purulent exudate on skin surface.
Erosion: Superficial loss of epidermis, leaving a denuded, moist surface; heals without scar.
Ulcer: Loss of epidermis extending into dermis; heals with scar.
Scar: Replacement of normal skin with fibrous tissue as a result of healing.
Excoriation: Linear erosion produced by scratching.
Atrophy: Thinning of skin.
Lichenification: Thickening of epidermis with accentuation of normal skin markings.
DIAGNOSTIC PROCEDURES USED IN DERMATOLOGY
Diascopy: Glass slide pressed firmly against red lesion—blanchable (capillary dilatation) or nonblanchable (extravasation of blood).
Gram stain: Identifies some bacterial infections. Identifies infectious agent and finds antimicrobial susceptibilities.
KOH prep: Identifies fungi and yeast under microscope.
Tzanck prep: Identifies vesicular viral eruptions under microscope.
Scabies prep: Skin scraping to identify mites, eggs, or feces under microscope.
Wood’s lamp: Tinea capitis will fluoresce green/yellow on hair shaft.
Patch testing: Detects type IV hypersensitivity reactions (allergic contact dermatitis).
PAPULOSQUAMOUS REACTIONS
Psoriasis (Figure 20-1)
DEFINITION
Chronic, noninfectious, hyperproliferative inflammatory disorder.
Polygenic, chronic, relapsing, T cell–mediated inflammatory skin disease.
ETIOLOGY
Unknown, but with genetic predisposition.
Triggering factors: Trauma, infection, and medications.
PATHOPHYSIOLOGY
epidermal cell proliferation due to a shortened epithelial cell cycle.
EPIDEMIOLOGY
Rare under 10 years of age.
Worse in winter.
SIGNS AND SYMPTOMS
Classic: Thick, silvery-scaled, sharply defined, pink plaques occurring on the scalp, elbows, and knee.
Thick, adherent, well-demarcated, salmon-pink plaques with adherent silver-white scale.
On extensor surfaces of extremities, trunk, and scalp.
Nails commonly involved—pitting, “oil spots,” onycholysis, subungual hyperkeratosis.
May be associated with arthritis (psoriatic arthritis).
Higher streptococcal and staphylococcal skin carriage rates.
Salmon-pink plaques with silvery scale. Think: Psoriasis.
DIAGNOSIS
Clinical diagnosis.
Potassium hydroxide (KOH) test to differentiate from fungal infection.
TREATMENT
Topical coal tar, anthralin, corticosteroids, synthetic vitamin D analogue.
If extensive or resistant—ultraviolet B (UVB) phototherapy, PUVA (psoralen and ultraviolet A [UVA]), retinoids, methotrexate, cyclosporine.
FIGURE 20-1. Silvery scale plaque of psoriasis.
FIGURE 20-2. Pityriasis rosea.
Note “Christmas tree” distribution of macules. Note “herald patch” that precedes other lesions.
Pityriasis Rosea (Figure 20-2)
DEFINITION
Common, self-limited eruption of single herald patch followed by a generalized secondary eruption.
Herald patch followed by a rash in a Christmas tree distribution (oriented parallel to the ribs). Think: Pityriasis rosea.
ETIOLOGY
Suspected infectious agent.
Absence of herald patch does not exclude the diagnosis of pityriasis rosea.
EPIDEMIOLOGY
Affects children and young adults.
SIGNS AND SYMPTOMS
Herald plaque—2- to 10-cm solitary, oval, erythematous, with collarette of scale.
After few days to a few weeks, followed in 80% by generalized eruption of multiple smaller, pink, oval, scaly patches over trunk and upper extremities in “Christmas tree” distribution.
Can occur in an inverse form (extremities affected and trunk spared).
Pruritus.
Must consider secondary syphilis in a sexually active adolescent if the rash involves palms and soles.
DIAGNOSIS
Clinical.
Rapid plasma reagin (RPR) to differentiate from syphilis if suspected, KOH to differentiate from fungal infection.
TREATMENT
Self-limited, resolves in 6–12 weeks.
Symptomatic: The goal is to control pruritus (baths, calamine, topical corticosteroids, oral antihistamines).
The herald patch may be mistaken for tinea corporis.
ECZEMATOUS REACTIONS
Eczema: Broad term used to describe several inflammatory skin reactions; used synonymously with dermatitis.
Atopic Dermatitis (AD)
DEFINITION
Hypersensitivity inflammatory reaction.
ETIOLOGY
Type 1 (IgE) immediate hypersensitivity response.
PATHOPHYSIOLOGY
Sensitized mast cells release vasoactive mediators.
EPIDEMIOLOGY
Up to 17% of all children in the United States.
Affects all ages, but onset usually in first 6 months of life.
Two-thirds outgrow by age 10.
Familial tendency and risk for other atopic disorders (allergic rhinoconjunctivitis, asthma, and food allergy).
AD may be the initial manifestation of the “atopic march.”
Atopic dermatitis is part of the atopic triad: allergic rhinitis, asthma, and eczema.
SIGNS AND SYMPTOMS
Pruritic.
Lesions vary with patient’s age.
Infantile—red, exudative, crusty, and oozing lesions primarily affecting face (especially cheeks) and extensor surfaces.
Nose and paranasal areas often spared.
Diaper area is also spared.
Juvenile/adult: Dry, lichenified, pruritic plaques distributed over flexural areas (antecubital, popliteal, neck).
Susceptible to secondary bacterial (S aureus) and viral (herpes simplex virus) infections.
You can think of atopic dermatitis as “the itch that rashes.”
DIAGNOSIS
Clinical; supported by personal or family history of atopy.
TREATMENT
Sensitive skin cares (nonperfumed lotions, soaps detergents).
Avoid scratching.
Lubricate dry skin.
Avoid wool, fragrances, and harsh cleansers.
Oral antihistamines.
Oral antibiotics only if clinical signs of secondary infection.
Topical corticosteroids are the mainstay of therapy.
Avoid oral corticosteroids: Patients become steroid dependent or rebound when discontinued.
Don’t culture skin in atopic dermatitis—90% of atopic patients are carriers of Staphylococcus aureus.
Contact Dermatitis
DEFINITION
Inflammatory skin reaction resulting from contact with an external agent.
Rhus dermatitis is an allergic dermatitis caused by contact with poison ivy or oak.
ETIOLOGY
Irritant or allergic types.
SIGNS AND SYMPTOMS
Sharply demarcated, erythematous vesicles and plaques at site of contact with agent.
Chronic lesions may be lichenified.
DIAGNOSIS
Clinical: Consider location, relationship to external factors, particular configurations.
History alone can identify the sensitizing agent in only 10–20%.
Nickel.
Plant associated (poison ivy).
KOH to differentiate from fungal infection.
TREATMENT
Remove offending agent.
Topical lubrication.
Wet dressings soaked in Burow’s solution (aluminum acetate).
Topical corticosteroids.
Seborrheic Dermatitis
DEFINITION
Chronic and recurrent skin disease occurring at sites with sebaceous gland activity, characterized by erythema and scaling.
ETIOLOGY
Unknown; however, Malassezia furfur has been implicated.
PATHOPHYSIOLOGY
Unknown.
EPIDEMIOLOGY
Affects children and adults.
Occurs more often in winter months.
SIGNS AND SYMPTOMS
Children age 0–3 months: “Cradle cap”—greasy scales covering scalp, forehead, cheeks, neck, chin, shoulders (“shawl distribution”).
Adults: Flaking, greasy scales on erythematous background over scalp (dandruff), ears, eyelids (blepharitis), nasolabial fold, and central chest.
DIAGNOSIS
Clinical.
KOH to differentiate from fungal infection.
TREATMENT
Symptomatic: Antiseborrheic shampoo (selenium sulfide), topical corticosteroids (brief course) in the presence of inflamed lesions.
Topical immunomodulatory agents (tacrolimus, pimecrolimus) > 2 yr.
Consider Langerhans cell histiocytosis X and HIV in the presence of chronic seborrhea.
BULLOUS DISEASES
Pemphigus Vulgaris
DEFINITION
Potentially fatal, chronic, autoimmune, blistering disease of the skin and mucous membranes.
Nikolsky’s sign: Direct pressure applied to surface of bulla causes it to extend laterally.
ETIOLOGY
Autoimmune.
PATHOPHYSIOLOGY
Circulating antibodies adhere to cell surface glycoproteins that hold epidermal cells together, causing intraepidermal blisters.
EPIDEMIOLOGY
Very rare in children, but may occur. Often follows a viral infection.
SIGNS AND SYMPTOMS
Initial development of oral blisters that rupture easily (see Figure 20-3).
Months later, flaccid bullae emerge and rupture, leaving eroded, denuded, and crusted surfaces.
Localizes to mouth, or generalized on scalp, face, axillae, chest, and groin, sparing palms and soles.
Painful oral ulcers may be the only presentation of pemphigus for the first few weeks.
DIFFERENTIAL DIAGNOSIS
Bullous pemphigoid:
Rare in children.
Blisters in crops (flexural aspects of the extremities, in the axillae, and on the groin).
Large, tense bullae (smaller, flaccid bullae in pemphigus vulgaris).
Oral lesions less frequent.
Biopsy: Subepidermal bulla and a dermal inflammatory infiltrate, predominantly of eosinophil.
DIAGNOSIS
Clinical.
Confirm by biopsy showing acantholysis (separation of keratinocytes).
FIGURE 20-3. Pemphigus.
(Reproduced, with permission, from Weinberg S, Prose NS, and Kristal L. Color Atlas of Pediatric Dermatology. New York: McGraw-Hill, 2008: 180.)
Intercellular immunoglobulin G (IgG) deposits on direct immunofluorescence.
Circulating antibodies levels that correlate with disease activity.
Best site for biopsy: Fresh small blisters show acantholytic epidermal cells (cell-cell dyshesion).
TREATMENT
Often fatal if not treated.
Systemic corticosteroids, immunosuppressive agents.
Erythema Multiforme (Figure 20-4)
DEFINITION
General name used to describe an immune complex–mediated hypersensitivity reaction to different causative agents.
Herpes simplex viruses account for most cases of recurrent erythema multiforme that are not idiopathic.
ETIOLOGY
Drugs (eg, penicillin, sulfonamides, barbiturates, nonsteroidal anti-inflammatory drugs [NSAIDs], thiazides, phenytoin, vaccinations).
Viruses (herpes simplex, hepatitis A and B).
Bacteria (Streptococcus).
Fungi, mycoplasma, malignancy, radiotherapy, pregnancy.
Idiopathic in 20–50%.
Morphologically, two types: Iris type (target lesions) and vesiculo-bullous type.
Clinically, three groups:
Erythema multiforme “minor”: “Target lesions.”
Erythema multiforme “major”: Rash + mucosal involvement + constitutional symptoms.
Maximal variant erythema multiforme (Stevens-Johnson syndrome): Erythema major + systemic complications.
Mycoplasma pneumoniae can cause a similar presentation.
FIGURE 20-4. Erythema multiforme.
Note the many different-sized lesions. (Reproduced, with permission, from Stead LG, Stead SM, Kaufman MS. First Aid for the Emergency Medicine Clerkship, 2nd ed. New York: McGraw-Hill, 2006: 356.)
PATHOPHYSIOLOGY
Unknown, likely hypersensitivity reaction.
EPIDEMIOLOGY
Older children and adults.
SIGNS AND SYMPTOMS
Pruritus or pain.
Stevens-Johnson Syndrome (Erythema Multiforme Major)
DEFINITION
Severe variant of erythema multiforme with systemic illness.
ETIOLOGY
Often viruses (herpes) or drugs (see above).
SIGNS AND SYMPTOMS
Systemic illness (fever, malaise).
Severe mucous membrane involvement (oral, vaginal, conjunctival).
Extensive target-like lesions and mucosal erosions covering < 10% of body surface area.
Ocular involvement (purulent uveitis/conjunctivitis) may result in scarring or corneal ulcers.
May evolve to toxic epidermal necrolysis.
TREATMENT
Discontinue offending agent (if identified).
Symptomatic and supportive.
Observe closely for strictures developing upon mucous membrane healing.
Mouthwashes, topical anesthetics, pain control.
Toxic Epidermal Necrolysis (TEN)
DEFINITION
severe variant/progression of erythema multiforme with widespread involvement:
Widespread blister formation and morbilliform or confluent erythema with skin tenderness.
Absence of target lesions.
Sudden onset and generalization within 24–48 hr.
Full-thickness epidermal necrosis and a minimal to absent dermal infiltrate.
ETIOLOGY
Hypersensitivity, triggered by many of above list.
PATHOPHYSIOLOGY
Damage to basal cell layer of epidermis.
SIGNS AND SYMPTOMS
Widespread, full-thickness necrosis of skin, covering > 30% body surface area.
Abrupt onset of fever and influenza-like symptoms.
Pruritus, pain, tenderness, and burning.
Complications: Secondary skin infections, fluid and electrolyte abnormalities, prerenal azotemia.
Thirty percent mortality rate.
DIAGNOSIS
Clinical; confirm by biopsy.
TREATMENT
Removal and/or treatment of causative agent.
Hospitalization for severe disease.
Fluid and electrolyte replacement.
Systemic corticosteroids.
Antibiotics (for secondary bacterial infection).
CUTANEOUS BACTERIAL INFECTIONS
Impetigo (Figure 20-5)
A 3-year-old girl had an upper respiratory infection for the past week. Two days ago, her parents noted a rash immediately under her nose. On examination, she is afebrile with multiple round and oval areas of erythema with golden-colored crusts. Think: Impetigo.
Impetigo is a highly contagious superficial skin infection that is limited to the epidermis. It is transmitted by direct contact. The nonbullous form is more common, which begins as a single papule that quickly becomes a vesicle. When this vesicle ruptures and the contents dry, characteristic honey or golden-colored crusts develops.
DEFINITION
Contagious, superficial, bacterial infection transmitted by direct contact.
Nonbullous impetigo (70%).
Bullous impetigo (most commonly affects neonates).
FIGURE 20-5. Impetigo.
Note characteristic honey-colored crusted lesion, typically seen at corners of mouth and over face.
ETIOLOGY
Staphylococcus aureus (bullous lesions).
Group A β-hemolytic Streptococcus pyogenes (GAS) (nonbullous lesions).
PATHOPHYSIOLOGY
Only epidermis is affected.
EPIDEMIOLOGY
Common in children.
Warm and humid climates.
Crowded conditions.
SIGNS AND SYMPTOMS
Mild burning or pruritus.
Initial lesion is a transient erythematous papule or thin-roofed vesicle that ruptures easily and forms a honey-colored crust.
Lesions can progress for weeks if untreated.
“Honey-colored crust” is classic for impetigo.
DIAGNOSIS
Clinical; can confirm with Gram stain and culture showing gram-positive cocci in clusters (S aureus) or chains (GAS).
TREATMENT
Remove crusts by soaking in warm water.
Antibacterial washes (benzoyl peroxide).
Topical antibiotic if disease is limited (Bactroban).
Oral antibiotics (cephalexin or macrolide) if more severe.
Cellulitis
DEFINITION
Acute, deep infection of dermis and subcutaneous tissue.
ETIOLOGY
S aureus (rapidly changing epidemiology now places community-acquired methicillin-resistant S aureus [CA-MRSA] as one of the common organisms).
Group A β-hemolytic S pyogenes.
Haemophilus influenzae (children).
PATHOPHYSIOLOGY
Precipitating factors include injury, abrasions, burns, surgical wounds, mucosal infections, bites, underlying dermatosis, and preexisting lymphatic stress.
Risk factors include cancer, chemotherapy, immunodeficiency, diabetes, cirrhosis, neutropenia, and malnutrition.
EPIDEMIOLOGY
Any age.
SIGNS AND SYMPTOMS
Erythematous, edematous, shiny area of warm and tender skin with poorly demarcated, nonelevated borders.
Fever, chills, and malaise can develop rapidly.
DIAGNOSIS
Clinical; confirmed by Gram stain demonstrating gram-positive cocci in clusters or chains.
Culture of lesion or blood will be positive only 25% of the time.
TREATMENT
First-generation cephalosporin or oxacillin.
Vancomycin if allergic or if MRSA is involved.
Cefotaxime or ceftriaxone for H influenzae.
Erysipelas
DEFINITION
Variant of cellulitis.
Others include erysipeloid (hands from handling infected food) and necrotizing fasciitis (medical emergency).
Clear line of demarcation between involved and uninvolved tissue.
Raised lesions above the surrounding normal skin.
ETIOLOGY
GAS.
EPIDEMIOLOGY
incidence in young children and adults.
SIGNS AND SYMPTOMS
Local pain and tenderness.
Acute onset of fever, malaise, and shivering may precede lesion.
Well-demarcated, indurated, and elevated advancing border; less edematous (versus cellulitis).
High morbidity if untreated.
DIAGNOSIS
Clinical; Gram stain reveals gram-positive cocci in chains.
TREATMENT
Oral antibiotics (penicillin, cephalosporin, macrolide, vancomycin).
TOXIN-MEDIATED DISEASES
Staphylococcal Scalded Skin Syndrome
DEFINITION
Toxin-mediated blistering disease.
ETIOLOGY
S aureus.
Epidermolytic toxins that separate the epidermal cells 
blisters.
PATHOPHYSIOLOGY
Pathogen colonizes nose or conjunctivae without causing clinical signs of infection, but produces exfoliatin and epidermolytic toxins that spread hematogenously to skin, resulting in blistering and sloughing of the epidermis.
Begins with localized infection, usually around the umbilicus, perioral region conjunctivae, or perineum.
Toxin is produced at the primary site of infection and then spreads hematogenously to distant sites.
EPIDEMIOLOGY
Newborns and infants (< 2 years old).
SIGNS AND SYMPTOMS
Skin is initially red and tender with flaccid bullae.
Epidermis sloughs off and appears wrinkled, usually beginning in the face, neck, axillae, and groin.
Becomes widespread within 24–48 hours, resembling scalding.
Direct pressure applied to surface of bulla causes it to extend laterally (Nikolsky’s sign).
Self-limited in 5–7 days, though death can occur in neonates with extensive disease.
Culture of epidermolytic skin in staphylococcal scalded skin syndrome will not demonstrate the pathogen.
DIAGNOSIS
Clinical; confirmed by culture of colonized site (nose, eyes, throat) revealing gram-positive cocci.
TREATMENT
Hospitalize newborns with extensive skin sloughing.
Warm baths for debridement of necrotic epidermis.
Systemic antibiotics (oxacillin, dicloxacillin).
Pain control.
Intravenous (IV) fluids in severe cases.
Scarlet Fever
DEFINITION
Toxin-mediated disease characterized by sore throat, high fever, and mucous membrane erythema.
ETIOLOGY
GAS.
PATHOPHYSIOLOGY
Toxin mediated.
EPIDEMIOLOGY
Children.
Untreated streptococcal infection of pharynx, tonsils, or wound.
SIGNS AND SYMPTOMS
Finely punctate pink-scarlet exanthem first appears on upper trunk 12–48 hr after onset of fever.
As exanthem spreads to extremities, it becomes confluent and feels like rough sandpaper-like texture.
Fades in 4–5 days, followed by desquamation.
Circumoral pallor.
Linear petechiae evident in body folds (Pastia’s sign).
Pharynx is beefy red and tongue is initially white, but within 4–5 days the white coating sloughs off and tongue becomes bright red.
“Strawberry tongue” or “sandpaper rash.” Think: Scarlet fever.
DIAGNOSIS
Clinical; confirmed by culture from throat or wound.
Rapid direct antigen tests detect GAS antigens.
Gram stain reveals gram-positive cocci in chains.
TREATMENT
Acetaminophen for fever and pain.
Antibiotics (penicillin, macrolide, or cephalosporin).
Follow-up recommended if history of rheumatic fever present.
CUTANEOUS VIRAL INFECTIONS
Verrucae (Warts)
DEFINITION
Viral infection of skin and mucous membranes spread by direct contact.
ETIOLOGY
Human papillomavirus (HPV).
EPIDEMIOLOGY
incidence in atopic and immunocompromised patients.
SIGNS AND SYMPTOMS
Tender if irritated.
Types:
Verrucae vulgaris: Hands, fingers, knees; skin-colored papule.
Verrucae plantaris: Rough; over pressure points on plantar aspect of foot.
Verrucae planar: Flat; on face and dorsum of hands and fingers.
Condyloma acuminata: Anogenital warts.
HPV subtypes 6, 11, 16, 18, 31, 33, 35, and 44 are associated with cervical dysplasia (precancerous).
DIAGNOSIS
Clinical—absence of normal skin lines and presence of black dots.
TREATMENT
Cryotherapy, topical keratolytic agents (eg, salicylic acid), destructive agents (podophyllin), curettage and desiccation, topical imiquod.
Herpes Gingivostomatitis (Fever Blisters, Cold Sores)
DEFINITION
Highly contagious viral eruption characterized by painful vesicles, commonly occurring around the mouth (type 1) and genitals (type 2).
ETIOLOGY
Herpes simplex virus (HSV) types 1 and 2.
PATHOPHYSIOLOGY
Transmitted by direct contact with skin and mucous membranes.
After primary infection, virus remains latent in a neural ganglion.
Reactivation of latent virus results in recurrent disease commonly occurring in the same area.
Recurrences become less frequent over time.
EPIDEMIOLOGY
Primary infection affects children and young adults.
incidence of infection in immunocompromised patients.
SIGNS AND SYMPTOMS
Grouped vesicles on an erythematous base, occurring primarily on lips, mouths, genitals, and eyes, but can occur at any site.
Erosions and crusted lesions form after a couple of days.
Fever, malaise, headache, and adenopathy may occur with primary infection.
Prodrome of burning, tingling, or itching occurs with recurrent infection.
Complications include ocular disease, secondary infection, and dissemination (especially in immunocompromised patients).
Herpetic whitlow (herpes-infected finger)—can occur in children with herpes gingivostomatitis secondary to sucking of fingers.
DIAGNOSIS
Clinical.
Confirmed by Tzanck preparation, revealing multinucleated giant cells.
Viral culture of vesicle fluid.
Do not try to excise herpetic whitlow—opening the lesion will only serve to spill more virus onto surrounding skin and spread the infection.
TREATMENT
Oral acyclovir, valacyclovir, or famciclovir ↓ viral shedding time and accelerate healing time. Consider if herpetic whitlow or at risk for severe disease.
Suppressive therapy with acyclovir for more than six recurrences per year.
Molluscum Contagiosum (Figure 20-6)
DEFINITION
Self-limited, contagious, viral infection transmitted by direct contact.
FIGURE 20-6. Molluscum contagiosum.
(Photo courtesy of Danial Stuhlberg, MD, Utah Family Practice Residency, Provo, UT.)
ETIOLOGY
Molluscum contagiosum virus (poxvirus).
Umbilicated, pearly papules. Think: Molluscum contagiosum.
EPIDEMIOLOGY
Affects children and sexually active adults.
incidence in atopic and immunocompromised patients.
SIGNS AND SYMPTOMS
Single or multiple, 2- to 5-mm, firm, umbilicated, skin-colored or pearly-white papules.
Commonly found on face, eyelids, axillae, and anogenital region.
Multiple lesions on face suggest human immunodeficiency virus (HIV) infection.
DIAGNOSIS
Clinical.
TREATMENT
Curettage, cryosurgery, electrodesiccation, laser surgery, or tincture of time.
CUTANEOUS FUNGAL INFECTIONS
Tinea (Dermatophytoses)
DEFINITION
Group of noninvasive fungi that can infect keratinized tissue of epidermis, nails, and hair.
Clinical presentation depends on anatomic site of infection and is named accordingly.
Tinea corporis lesions are annular with peripheral scale and central clearing.
ETIOLOGY
Trichophyton, Microsporum, Epidermophyton.
EPIDEMIOLOGY
Exacerbated by warm, humid climates.
SIGNS AND SYMPTOMS
Tinea pedis (“athlete’s foot”).
Tinea cruris (“jock itch”): Groin.
Tinea corporis (“ringworm”): Body (see Figure 20-7).
Tinea manuum: Hand.
Tinea facialis: Face.
Tinea capitis: Scalp.
Tinea barbae: Beard/mustache area.
Onychomycosis: Nails.
Tinea versicolor: Superficial, asymptomatic.
Tinea versicolor has hyphae and yeast forms in a “spaghetti-and-meatball” distribution on KOH preparation.
DIAGNOSIS
Clinical presentation and history.
KOH preparation reveals multiple, septated hyphae.
Wood’s lamp reveals bright green fluorescence of hair shaft in tinea capitis.
Fungal culture of affected area may demonstrate dermatophyte.
TREATMENT
Prevention: Wearing well-ventilated shoes and clothing.
Topical antifungal agents (imidazoles and terbinafine).
Systemic antifungal agents if unresponsive to topical or if involvement of nails or hair (griseofulvin, systemic azoles, terbinafine).
Mild-potency topical corticosteroids if inflammation and pruritus are severe.
Griseofulvin can cause elevation of liver enzymes.
Candidal Skin Infections (Candida)
DEFINITION
Superficial infection occurring in moist cutaneous sites.
FIGURE 20-7. Tinea corporis (ringworm).
FIGURE 20-8. Oral candidiasis (thrush).
(Reproduced, with permission, from Yong-Kwang T, Seow C. What syndrome is this? Pediatric Dermatology 2001;18(4): 353.)
ETIOLOGY
Candida albicans.
Thrush is a candidal infection of mucosal surfaces, presenting as creamy white, easily removable papules on an erythematous mucosal surface (see Figure 20-8).
PATHOPHYSIOLOGY
Predisposing factors: Diabetes mellitus, obesity, immunosuppression, chronic debilitation, recent use of antibiotics.
SIGNS AND SYMPTOMS
Pruritus and soreness.
Confluent, bright red papules and pustules forming a sharply demarcated eroded patch with pustular lesions at the periphery (satellite lesions).
Distributed over intertriginous regions, including axillae; groin; web spaces; genital, anal, and inframammary areas.
Oral form is thrush: Thick white plaque on tongue or inside of cheeks that can’t be scraped off (Figure 20-8).
DIAGNOSIS
Clinical; confirmed by KOH preparation revealing pseudohyphae and budding spores and cultures of lesion.
TREATMENT
Keep intertriginous areas dry.
Topical antifungals (azoles).
Topical corticosteroids for symptomatic relief.
Diaper rash is often superinfected with Candida, which manifests as erythematous satellite lesions.
INFESTATIONS
Lice (Pediculosis)
DEFINITION
1. Pediculosis corporis—body.
2. Pediculosis capitis—scalp hair.
3. Pediculosis pubis—pubic hair.
ETIOLOGY
1. Pediculus humanus corporis.
2. Pediculus humanus capitis.
3. Pthirus pubis.
PATHOPHYSIOLOGY
Lice are obligate parasites, feeding on human blood.
EPIDEMIOLOGY
1. Poor hygiene.
2. Head-to-head contact, sharing hair items.
3. Sexual contact.
SIGNS AND SYMPTOMS
Pruritus.
Pyoderma may develop from scratching.
Corporis—primary lesion is an intensely pruritic, small, red macule or papule with central hemorrhagic punctum on shoulders, trunk, or buttocks; secondary lesions include excoriations, wheals, and eczematous, secondarily infected plaques.
DIAGNOSIS
Nits detectable on hair/fibers.
TREATMENT
Hot water laundering.
Boil or dispose of implements.
Comb hair.
Permethrin rinse—once, then again at 1 week (alternatives—pyrethrin, lindane).
Cutaneous Larva Migrans (Figure 20-9)
DEFINITION
Eruption caused by several larval nematodes not usually parasitic to humans.
ETIOLOGY
Most often Ancylostoma braziliense (hookworm of dogs and cats).
FIGURE 20-9. Cutaneous larva migrans.
(Reproduced, with permission, from Berger MS. A serpiginous eruption on the buttocks. American Family Physician 2000;62: 2493.)
PATHOPHYSIOLOGY
Parasite eggs are deposited in feces of animals, then hatch. Larvae penetrate human skin, then migrate along epidermal-dermal junction.
EPIDEMIOLOGY
Warm, moist areas.
SIGNS AND SYMPTOMS
Raised, erythematous, serpiginous tracks, occasionally forming bullae.
Single or multiple.
Usually on an extremity or the buttocks, but can occur anywhere on the body.
DIAGNOSIS
Clinical.
TREATMENT
Self-limited in weeks to months.
Thiabendazole if symptoms warrant treatment.
Scabies
A 4-year-old boy has been treated with hydrocortisone cream for eczema on and off for the last 3 years. Over the past 2 months, parents have noted a pruritic, papular rash that improves when hydrocortisone cream is used but returns when hydrocortisone is discontinued. On examination, he is afebrile with diffusely distributed papules on the trunk and extremities, concentrated in the intertriginous areas. Burrows are noted as well. Think: Scabies.
Scabies. It is a highly contagious disease caused by the mite Sarcoptes scabiei and spreads in households with intimate personal contact or sharing of inanimate object. Schoolchildren are especially at higher risk. Typical presentation is generalized, intense nocturnal itching, and classic sites are hairless areas with a thin stratum corneum (interdigital web spaces of fingers and toes, popliteal fossae, flexor surfaces of the wrists, and gluteal region). Presence of skin burrows is the most supportive finding. Definitive diagnosis is established by finding the scabies mites. The most effective topical treatment is 5% permethrin. One application is usually effective but a second treatment 1 week after the first application may be required.
ETIOLOGY
Female mite Sarcoptes scabiei hominis.
PATHOPHYSIOLOGY
Pregnant female mite exudes keratolytic substance and burrows into the stratum corneum, depositing eggs and feces daily.
Eggs hatch; larvae molt into nymphs, mature in 2–3 weeks, and repeat the cycle.
EPIDEMIOLOGY
Physical contact with infected individual.
Rarely transmitted by fomites, as isolated mites dies within 2–3 days.
SIGNS AND SYMPTOMS
Pruritus at initial infestation.
First sign: 1- to 2-mm red papules, some of which are excoriated, crusted, or scaling.
Threadlike burrows.
Multiple types of lesions.
Threadlike burrows are classic for scabies, but may not be seen in infants.
DIAGNOSIS
Scraping for microscopic identification of mites, ova, and feces.
TREATMENT
Permethrin, neck down, scalp only if involved; leave on 8–12 hr; may be repeated after 1 week.
Infants are particularly susceptible to the neurotoxicity of lindane; therefore avoid.
Alternatives include permethrin or sulfur ointment.
Transmission of scabies mites is unlikely 24 hr after treatment.
GROWTHS
Hemangioma
DEFINITION
Benign vascular proliferation that is usually present at birth or appears soon afterward (eg, capillary hemangioma, port-wine stain, cavernous hemangioma) (Figure 20-10).
ETIOLOGY/PATHOPHYSIOLOGY
Abnormal angiogenesis, perhaps incited by cytokines, such as basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF).
EPIDEMIOLOGY
Approximately 0.5% of infants.
SIGNS AND SYMPTOMS
Capillary (“strawberry”) hemangioma: Red or purple papules or nodules that develop soon after birth and spontaneously involute by fifth year (see Figure 20-11).
If multiple hemangiomas, may also have visceral hemangiomas (hemangomatosis).
TREATMENT
Most resolve without treatment.
Involvement of bone, soft tissue, or organ parenchyma may warrant excision of the hemangioma.
FIGURE 20-10. Port-wine stain seen in Sturge-Weber syndrome.
(Reproduced, with permission, from Wolff K, Johnson RA, Suurmond D. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 5th ed. New York: McGraw-Hill, 2005: 187.)
Melanocytic Nevus (Mole) (Figure 20-12)
DEFINITION
Benign proliferation of melanocytes, which are classified according to location of clustering: dermal-epidermal junction (junctional), dermis (dermal), or both (compound).
EPIDEMIOLOGY
Nevi usually arise in childhood, peak during adolescence, and spontaneously regress during adulthood.
TREATMENT
Serial observation for early recognition of premalignancy.
Early excision of suspicious lesions.
FIGURE 20-11. Capillary hemangioma.
FIGURE 20-12. Melanocytic nevus.
(Reproduced, with permission, from Wang SQ, Katz B, Rabinovitz H, Kopf AW, Oliviero M. Lessons on dermoscopy. Dermatologic Surgery 2000;26(4): 397.)
Malignant Melanoma
DEFINITION
Malignant proliferation of melanocytes.
ETIOLOGY
May arise from normal-appearing skin or from preexisting mole or skin lesion.
PATHOPHYSIOLOGY
Horizontal growth phase: Lateral extension within the epidermis and dermis.
Vertical phase: Penetrates into dermis, greatly increasing risk of metastasis.
EPIDEMIOLOGY
incidence in fair-skinned people and with sun exposure.
Adolescents.
Characteristics of mole suspicious for melanoma:
Asymmetric
Borders irregular
Color uneven
Diameter > 0.6 cm
Elevated
Enlarging
SIGNS AND SYMPTOMS
Characteristics of a mole suspicious for melanoma:
Asymmetric.
Border (irregular).
Color (variegated and mottled).
Diameter (> 0.6 cm).
Elevated.
Enlarging.
DIAGNOSIS
Prognosis based on thickness of the primary tumor.
TREATMENT
Surgical excision with margins at least 1 cm beyond borders, depending on depth of lesion.
Close follow-up.
Xeroderma Pigmentosum
DEFINITION
Genetic defect in DNA repair mechanisms, predisposing to certain skin cancers.
ETIOLOGY
Autosomal recessive.
PATHOPHYSIOLOGY
Failure to repair ultraviolet-damaged DNA.
SIGNS AND SYMPTOMS
Predisposes patients to basal and squamous cell skin cancers.
OTHER SKIN CONDITIONS
Henoch-Schönlein Purpura (Figure 20-13)
DEFINITION
Classic example of vasculitis in children.
ETIOLOGY/PATHOPHYSIOLOGY
Immunoglobulin A (IgA) mediated.
Occurs most commonly following streptococcal or viral infection.
Palpable purpura is the classic sign of small-vessel damage.
EPIDEMIOLOGY
Pediatric age group.
SIGNS AND SYMPTOMS
Palpable purpura
Arthritis
Abdominal pain
FIGURE 20-13. Henoch-Schönlein purpura.
DIAGNOSIS
Clinical; may biopsy.
Intestinal wall purpura can serve as a lead point for intussussception.
TREATMENT
Usually benign, self-limited.
If severe, consider systemic steroids.
Monitor for renal dysfunction.
Acne Vulgaris
DEFINITION
Disorder of pilosebaceous glands.
Develops in areas with the greatest concentration of sebaceous glands.
ETIOLOGY/PATHOPHYSIOLOGY
Results from a combination of hormonal (androgens), bacterial (Propionibacterium acnes), and genetic factors.
Initial pathology is microscopic microcomedo.
EPIDEMIOLOGY
Adolescents.
SIGNS AND SYMPTOMS
Comedone: Plug of sebaceous and dead skin material stuck in the opening of a hair follicle; open follicle (blackhead) or almost closed (whitehead).
Pustules, papules.
Painful nodules and cysts if severe.
Seborrhea of face and scalp (greasy skin).
Depressed or hypertrophic scars may develop with healing.
DIAGNOSIS
Clinical; confirmed by presence of comedones.
TREATMENT
Benzoyl peroxide wash.
Topical antibiotics (clindamycin or erythromycin).
Intralesional corticosteroid injections (triamcinolone acetonide).
Topical retinoid: ↑ cell turnover and prevent follicle occlusion.
Oral isotretinoin (Accutane) for severe, recalcitrant, nodular acne.
Dermabrasion for treatment of scars.
Accutane is teratogenic and must be prescribed with oral contraceptives; it also has many side effects.
Diaper Rash
DEFINITION
Rash occurring in the diaper area.
ETIOLOGY
Irritant contact dermatitis: Prolonged dampness, interaction of urine (ammonia) and feces with the skin, reactions to medications/creams, type of diaper.
Candidal or bacterial secondary infection can occur.
Atopic dermatitis.
May be any other dermatologic condition in diaper distribution.
PATHOPHYSIOLOGY
Overhydration, friction, maceration, allergy, etc.
EPIDEMIOLOGY
Most children who wear diapers, to some degree.
SIGNS AND SYMPTOMS
Red, scaly, fissured, eroded skin.
Patchy or confluent.
If secondarily infected: Impetiginous or candidal.
Check for oral candidiasis if present in diaper area.
TREATMENT
Keep infant dry, change diapers often.
Avoid harsh detergents, wipes with alcohol, and plastic pants.
Ointments can reduce friction and protect skin from irritation.
Avoid powders, as they can injure infants’ lungs if inhaled accidentially.
Nystatin or other antifungal cream for yeast infection.
Recurrent Minor Aphthous Ulcers/Stomatitis (Canker Sores)
DEFINITION
Chronic inflammatory disease causing recurrent oral ulcers of varying frequency.
ETIOLOGY
Local cell-mediated immunity, elevated inflammatory mediators, abnormal cell communication/epithelial integrity.
PATHOPHYSIOLOGY
Triggers may include toothpaste/mouthwash with sodium lauryl sulfate, mechanical trauma, stress, nutritional deficiencies, food sensitivities/allergies, hormones, infection, genetics, medical conditions, and medications.
EPIDEMIOLOGY
Twenty percent of the general population.
SIGNS AND SYMPTOMS
Round/ovoid ulcer with grayish membrane and edges surrounded by reddish halo.
Occur on nonkeratinized skin: Inside of the lips and cheeks, floor of the mouth, under the tongue, soft palate, and tonsillar areas.
High recurrence rate.
Painful.
Usually heal uneventfully in 4–14 days.
DIAGNOSIS
Clinical; rule out herpes stomatitis.
TREATMENT
Avoid individual triggering factors.
Symptomatic: Oral numbing or coating medications.
Antibacterial/cleansing rinses.
Home remedies: Milk of Magnesia, warm salt water, alum rinses.
Prescription anti-inflammatory or antibacterial collagenase inhibitors.
Vitiligo
DEFINITION
Pigmentary defect.
ETIOLOGY/PATHOPHYSIOLOGY
Unknown, possibly autoimmune.
Trauma may be associated with initiation of the lesions.
EPIDEMIOLOGY
Half of cases present before 20 years of age.
SIGNS AND SYMPTOMS
Depigmented macules.
Predilection for hyperpigmented areas.
DIAGNOSIS
Clinical, though melanocyte absence can be confirmed by electron microscopy of biopsy specimen.
TREATMENT
Many months of psoralen and ultraviolet therapy can partially or completely repigment areas.
Potent topical steroids are used on areas such as lips not amenable to phototherapy.
Urticaria-Angioedema
A 12-year-old boy with a history of multiple food allergies ate a candy bar given to him by a friend at school. He complained of throat discomfort and a rash. On examination, he is afebrile. He is wheezing. Multiple discrete erythematous papules are noted on trunk and extremities. Think: Urticaria.
Urticaria with or without angioedema is frequently seen in pediatric practice. Angioedema is due to an urticarial process that involves deeper layers of the skin. Acute urticaria is more common in children. History is often able to identify an inciting factor, especially if the hives occur shortly after ingestion of a food or drug. Common foods that cause urticaria are milk, eggs, peanuts, and shellfish. The mast cell is the mediator in the development of urticaria. These lesions are typically pruritic and erythematous, often showing central clearing. Systemic symptoms develop if it is associated with anaphylaxis.
FIGURE 20-14. Urticaria.
DEFINITION
Allergic response 
edema of the tissues.
ETIOLOGY/PATHOPHYSIOLOGY
Type 1 hypersensitivity reaction of immunoglobulin E (IgE) with mast cells causes the release of histamine, vasodilation, vascular permeability, and axonal response.
EPIDEMIOLOGY
Can occur in response to a large number of entities—ingestion, contact, infectious agents, environmental factors, or genetic conditions.
SIGNS AND SYMPTOMS
Urticaria: Well circumscribed, but can be coalescent, erythematous, raised lesions (wheals or welts) (see Figure 20-14).
Angioedema: Involves the deeper layers of skin, submucosa, and subcutaneous tissues.
TREATMENT
Usually self-limited.
Antihistamines to relieve pruritus.
Watch for signs of airway compromise (especially with angioedema).
Epinephrine for severe cases.
NEONATAL DERMATOLOGIC CONDITIONS
See Table 20-1.
Hair Loss
MOST COMMON ETIOLOGIES
Tinea capitis (see p. 524).
Trichotillomania.
Alopecia areata.
Trichotillomania (Hair Pulling)
DEFINITION
Traumatic hair pulling resulting in breaking of hair shafts at different lengths.
Can also involve eyebrows or eyelashes.
ETIOLOGY
Habitual.
Sign of psychiatric disorder.
Reaction to stress.
SIGNS AND SYMPTOMS
Patchy hair loss of scalp (often on side of dominant hand).
Loss of eyebrows, eyelashes.
Close examination of hair demonstrates hair shafts broken at different lengths.
TABLE 20-1. Neonatal Dermatologic Conditions
TREATMENT
Behavioral modification.
Consider psychiatry/psychology referral.
Alopecia Areata (Figure 20-15)
DEFINITION
Total hair loss in localized area.
ETIOLOGY
Immunologic mediated loss of hair. Infiltration of lymphocytes may be relapsing/remitting in some children.
SIGNS AND SYMPTOMS
Loss of every hair within area.
Exclamation point hairs.
TREATMENT
High rates of spontaneous resolution/regrowth within 12 months.
In some cases, steroids (systemic, topical, or local injection).
Minoxidil or other immune modulation.
Dermatologic Manifestations of Some Infectious Diseases
See Table 20-2.
FIGURE 20-15. Alopecia areata of scalp: solitary lesion.
A sharply outlined portion of the scalp with complete alopecia without scaling, erythema, atrophy, or scarring. Empty follicles can still be seen on the involved scalp. The short, broken-off hair shafts (so-called exclamation point hair) appear as very short stubs emerging from the bald scalp. (Reproduced, with permission, from Wolff K, Johnson RA, Suurmond D. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 5th ed. New York: McGraw-Hill, 2005: 956.)
TABLE 20-2. Dermatologic Manifestations of Some Infectious Diseases
DERMATOLOGIC MANIFESTATIONS OF SYSTEMIC DISEASE
See Table 20-3.
TABLE 20-3. Dermatologic Manifestations of Systemic Disease
