First Aid for the Pediatrics Clerkship, 3 Ed.

Dermatologic Disease

 

CLASSIFICATION OF SKIN LESIONS

Primary Skin Lesions

Image Macule: Flat, nonpalpable, skin discoloration.

Image Plaque: Elevated, > 2 cm diameter.

Image Wheal: Elevated, round or flat-topped area of dermal edema, disappears within hours.

Image Vesicle: Circumscribed, elevated, fluid-filled, < 0.5 cm diameter.

Image Bullae: Circumscribed, elevated, fluid-filled, > 0.5 cm diameter.

Image Pustule: Circumscribed, elevated, pus-filled.

Image Papule: Elevated, palpable, solid, < 0.5 cm diameter.

Image Nodule: Elevated, palpable, solid, > 0.5 cm.

Image Petechiae: Red-purple, nonblanching macule, < 0.5 cm diameter, usually pinpoint.

Image Purpura: Red-purple, nonblanching macule, > 0.5 cm diameter.

Image Telangiectasia: Blanchable, dilated blood vessels.

Secondary Skin Lesions

Image Scale: Accumulation of dead, exfoliating epidermal cells.

Image Crust (scab): Dried serum, blood, or purulent exudate on skin surface.

Image Erosion: Superficial loss of epidermis, leaving a denuded, moist surface; heals without scar.

Image Ulcer: Loss of epidermis extending into dermis; heals with scar.

Image Scar: Replacement of normal skin with fibrous tissue as a result of healing.

Image Excoriation: Linear erosion produced by scratching.

Image Atrophy: Thinning of skin.

Image Lichenification: Thickening of epidermis with accentuation of normal skin markings.

DIAGNOSTIC PROCEDURES USED IN DERMATOLOGY

Image Diascopy: Glass slide pressed firmly against red lesion—blanchable (capillary dilatation) or nonblanchable (extravasation of blood).

Image Gram stain: Identifies some bacterial infections. Identifies infectious agent and finds antimicrobial susceptibilities.

Image KOH prep: Identifies fungi and yeast under microscope.

Image Tzanck prep: Identifies vesicular viral eruptions under microscope.

Image Scabies prep: Skin scraping to identify mites, eggs, or feces under microscope.

Image Wood’s lamp: Tinea capitis will fluoresce green/yellow on hair shaft.

Image Patch testing: Detects type IV hypersensitivity reactions (allergic contact dermatitis).

PAPULOSQUAMOUS REACTIONS

Psoriasis (Figure 20-1)

DEFINITION

Image Chronic, noninfectious, hyperproliferative inflammatory disorder.

Image Polygenic, chronic, relapsing, T cell–mediated inflammatory skin disease.

ETIOLOGY

Image Unknown, but with genetic predisposition.

Image Triggering factors: Trauma, infection, and medications.

PATHOPHYSIOLOGY

Image epidermal cell proliferation due to a shortened epithelial cell cycle.

EPIDEMIOLOGY

Image Rare under 10 years of age.

Image Worse in winter.

SIGNS AND SYMPTOMS

Image Classic: Thick, silvery-scaled, sharply defined, pink plaques occurring on the scalp, elbows, and knee.

Image Thick, adherent, well-demarcated, salmon-pink plaques with adherent silver-white scale.

Image On extensor surfaces of extremities, trunk, and scalp.

Image Nails commonly involved—pitting, “oil spots,” onycholysis, subungual hyperkeratosis.

Image May be associated with arthritis (psoriatic arthritis).

Image Higher streptococcal and staphylococcal skin carriage rates.


Image

Salmon-pink plaques with silvery scale. Think: Psoriasis.


DIAGNOSIS

Image Clinical diagnosis.

Image Potassium hydroxide (KOH) test to differentiate from fungal infection.

TREATMENT

Image Topical coal tar, anthralin, corticosteroids, synthetic vitamin D analogue.

Image If extensive or resistant—ultraviolet B (UVB) phototherapy, PUVA (psoralen and ultraviolet A [UVA]), retinoids, methotrexate, cyclosporine.

Image

FIGURE 20-1. Silvery scale plaque of psoriasis.

Image

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.


Image

Herald patch followed by a rash in a Christmas tree distribution (oriented parallel to the ribs). Think: Pityriasis rosea.


ETIOLOGY

Suspected infectious agent.


Image

Absence of herald patch does not exclude the diagnosis of pityriasis rosea.


EPIDEMIOLOGY

Affects children and young adults.

SIGNS AND SYMPTOMS

Image Herald plaque—2- to 10-cm solitary, oval, erythematous, with collarette of scale.

Image 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.

Image Can occur in an inverse form (extremities affected and trunk spared).

Image Pruritus.


Image

Must consider secondary syphilis in a sexually active adolescent if the rash involves palms and soles.


DIAGNOSIS

Image Clinical.

Image Rapid plasma reagin (RPR) to differentiate from syphilis if suspected, KOH to differentiate from fungal infection.

TREATMENT

Image Self-limited, resolves in 6–12 weeks.

Image Symptomatic: The goal is to control pruritus (baths, calamine, topical corticosteroids, oral antihistamines).


Image

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

Image Up to 17% of all children in the United States.

Image Affects all ages, but onset usually in first 6 months of life.

Image Two-thirds outgrow by age 10.

Image Familial tendency and Image risk for other atopic disorders (allergic rhinoconjunctivitis, asthma, and food allergy).

Image AD may be the initial manifestation of the “atopic march.”


Image

Atopic dermatitis is part of the atopic triad: allergic rhinitis, asthma, and eczema.


SIGNS AND SYMPTOMS

Image Pruritic.

Image Lesions vary with patient’s age.

Image Infantile—red, exudative, crusty, and oozing lesions primarily affecting face (especially cheeks) and extensor surfaces.

Image Nose and paranasal areas often spared.

Image Diaper area is also spared.

Image Juvenile/adult: Dry, lichenified, pruritic plaques distributed over flexural areas (antecubital, popliteal, neck).

Image Susceptible to secondary bacterial (S aureus) and viral (herpes simplex virus) infections.


Image

You can think of atopic dermatitis as “the itch that rashes.”


DIAGNOSIS

Clinical; supported by personal or family history of atopy.

TREATMENT

Image Sensitive skin cares (nonperfumed lotions, soaps detergents).

Image Avoid scratching.

Image Lubricate dry skin.

Image Avoid wool, fragrances, and harsh cleansers.

Image Oral antihistamines.

Image Oral antibiotics only if clinical signs of secondary infection.

Image Topical corticosteroids are the mainstay of therapy.

Image Avoid oral corticosteroids: Patients become steroid dependent or rebound when discontinued.


Image

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.


Image

Rhus dermatitis is an allergic dermatitis caused by contact with poison ivy or oak.


ETIOLOGY

Irritant or allergic types.

SIGNS AND SYMPTOMS

Image Sharply demarcated, erythematous vesicles and plaques at site of contact with agent.

Image Chronic lesions may be lichenified.

DIAGNOSIS

Image Clinical: Consider location, relationship to external factors, particular configurations.

Image History alone can identify the sensitizing agent in only 10–20%.

Image Nickel.

Image Plant associated (poison ivy).

Image KOH to differentiate from fungal infection.

TREATMENT

Image Remove offending agent.

Image Topical lubrication.

Image Wet dressings soaked in Burow’s solution (aluminum acetate).

Image 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

Image Affects children and adults.

Image Occurs more often in winter months.

SIGNS AND SYMPTOMS

Image Children age 0–3 months: “Cradle cap”—greasy scales covering scalp, forehead, cheeks, neck, chin, shoulders (“shawl distribution”).

Image Adults: Flaking, greasy scales on erythematous background over scalp (dandruff), ears, eyelids (blepharitis), nasolabial fold, and central chest.

DIAGNOSIS

Image Clinical.

Image KOH to differentiate from fungal infection.

TREATMENT

Image Symptomatic: Antiseborrheic shampoo (selenium sulfide), topical corticosteroids (brief course) in the presence of inflamed lesions.

Image Topical immunomodulatory agents (tacrolimus, pimecrolimus) > 2 yr.

Image 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.


Image

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

Image Initial development of oral blisters that rupture easily (see Figure 20-3).

Image Months later, flaccid bullae emerge and rupture, leaving eroded, denuded, and crusted surfaces.

Image Localizes to mouth, or generalized on scalp, face, axillae, chest, and groin, sparing palms and soles.


Image

Painful oral ulcers may be the only presentation of pemphigus for the first few weeks.


DIFFERENTIAL DIAGNOSIS

Bullous pemphigoid:

Image Rare in children.

Image Blisters in crops (flexural aspects of the extremities, in the axillae, and on the groin).

Image Large, tense bullae (smaller, flaccid bullae in pemphigus vulgaris).

Image Oral lesions less frequent.

Image Biopsy: Subepidermal bulla and a dermal inflammatory infiltrate, predominantly of eosinophil.

DIAGNOSIS

Image Clinical.

Image Confirm by biopsy showing acantholysis (separation of keratinocytes).

Image

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.)

Image Intercellular immunoglobulin G (IgG) deposits on direct immunofluorescence.

Image Circulating antibodies levels that correlate with disease activity.


Image

Best site for biopsy: Fresh small blisters show acantholytic epidermal cells (cell-cell dyshesion).


TREATMENT

Image Often fatal if not treated.

Image 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.


Image

Herpes simplex viruses account for most cases of recurrent erythema multiforme that are not idiopathic.


ETIOLOGY

Image Drugs (eg, penicillin, sulfonamides, barbiturates, nonsteroidal anti-inflammatory drugs [NSAIDs], thiazides, phenytoin, vaccinations).

Image Viruses (herpes simplex, hepatitis A and B).

Image Bacteria (Streptococcus).

Image Fungi, mycoplasma, malignancy, radiotherapy, pregnancy.

Image Idiopathic in 20–50%.

Image Morphologically, two types: Iris type (target lesions) and vesiculo-bullous type.

Image Clinically, three groups:

Image Erythema multiforme “minor”: “Target lesions.”

Image Erythema multiforme “major”: Rash + mucosal involvement + constitutional symptoms.

Image Maximal variant erythema multiforme (Stevens-Johnson syndrome): Erythema major + systemic complications.


Image

Mycoplasma pneumoniae can cause a similar presentation.


Image

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

Image Systemic illness (fever, malaise).

Image Severe mucous membrane involvement (oral, vaginal, conjunctival).

Image Extensive target-like lesions and mucosal erosions covering < 10% of body surface area.

Image Ocular involvement (purulent uveitis/conjunctivitis) may result in scarring or corneal ulcers.

Image May evolve to toxic epidermal necrolysis.

TREATMENT

Image Discontinue offending agent (if identified).

Image Symptomatic and supportive.

Image Observe closely for strictures developing upon mucous membrane healing.

Image Mouthwashes, topical anesthetics, pain control.

Toxic Epidermal Necrolysis (TEN)

DEFINITION

Image severe variant/progression of erythema multiforme with widespread involvement:

Image Widespread blister formation and morbilliform or confluent erythema with skin tenderness.

Image Absence of target lesions.

Image Sudden onset and generalization within 24–48 hr.

Image 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

Image Widespread, full-thickness necrosis of skin, covering > 30% body surface area.

Image Abrupt onset of fever and influenza-like symptoms.

Image Pruritus, pain, tenderness, and burning.

Image Complications: Secondary skin infections, fluid and electrolyte abnormalities, prerenal azotemia.

Image Thirty percent mortality rate.

DIAGNOSIS

Clinical; confirm by biopsy.

TREATMENT

Image Removal and/or treatment of causative agent.

Image Hospitalization for severe disease.

Image Fluid and electrolyte replacement.

Image Systemic corticosteroids.

Image Antibiotics (for secondary bacterial infection).

CUTANEOUS BACTERIAL INFECTIONS

Impetigo (Figure 20-5)

Image

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

Image Contagious, superficial, bacterial infection transmitted by direct contact.

Image Nonbullous impetigo (70%).

Image Bullous impetigo (most commonly affects neonates).

Image

FIGURE 20-5. Impetigo.

Note characteristic honey-colored crusted lesion, typically seen at corners of mouth and over face.

ETIOLOGY

Image Staphylococcus aureus (bullous lesions).

Image Group A β-hemolytic Streptococcus pyogenes (GAS) (nonbullous lesions).

PATHOPHYSIOLOGY

Only epidermis is affected.

EPIDEMIOLOGY

Image Common in children.

Image Warm and humid climates.

Image Crowded conditions.

SIGNS AND SYMPTOMS

Image Mild burning or pruritus.

Image Initial lesion is a transient erythematous papule or thin-roofed vesicle that ruptures easily and forms a honey-colored crust.

Image Lesions can progress for weeks if untreated.


Image

“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

Image Remove crusts by soaking in warm water.

Image Antibacterial washes (benzoyl peroxide).

Image Topical antibiotic if disease is limited (Bactroban).

Image Oral antibiotics (cephalexin or macrolide) if more severe.

Cellulitis

DEFINITION

Acute, deep infection of dermis and subcutaneous tissue.

ETIOLOGY

Image S aureus (rapidly changing epidemiology now places community-acquired methicillin-resistant S aureus [CA-MRSA] as one of the common organisms).

Image Group A β-hemolytic S pyogenes.

Image Haemophilus influenzae (children).

PATHOPHYSIOLOGY

Image Precipitating factors include injury, abrasions, burns, surgical wounds, mucosal infections, bites, underlying dermatosis, and preexisting lymphatic stress.

Image Risk factors include cancer, chemotherapy, immunodeficiency, diabetes, cirrhosis, neutropenia, and malnutrition.

EPIDEMIOLOGY

Any age.

SIGNS AND SYMPTOMS

Image Erythematous, edematous, shiny area of warm and tender skin with poorly demarcated, nonelevated borders.

Image Fever, chills, and malaise can develop rapidly.

DIAGNOSIS

Image Clinical; confirmed by Gram stain demonstrating gram-positive cocci in clusters or chains.

Image Culture of lesion or blood will be positive only 25% of the time.

TREATMENT

Image First-generation cephalosporin or oxacillin.

Image Vancomycin if allergic or if MRSA is involved.

Image Cefotaxime or ceftriaxone for H influenzae.

Erysipelas

DEFINITION

Image Variant of cellulitis.

Image Others include erysipeloid (hands from handling infected food) and necrotizing fasciitis (medical emergency).

Image Clear line of demarcation between involved and uninvolved tissue.

Image Raised lesions above the surrounding normal skin.

ETIOLOGY

GAS.

EPIDEMIOLOGY

Image incidence in young children and adults.

SIGNS AND SYMPTOMS

Image Local pain and tenderness.

Image Acute onset of fever, malaise, and shivering may precede lesion.

Image Well-demarcated, indurated, and elevated advancing border; less edematous (versus cellulitis).

Image 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

Image S aureus.

Image Epidermolytic toxins that separate the epidermal cells Image blisters.

PATHOPHYSIOLOGY

Image 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.

Image Begins with localized infection, usually around the umbilicus, perioral region conjunctivae, or perineum.

Image 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

Image Skin is initially red and tender with flaccid bullae.

Image Epidermis sloughs off and appears wrinkled, usually beginning in the face, neck, axillae, and groin.

Image Becomes widespread within 24–48 hours, resembling scalding.

Image Direct pressure applied to surface of bulla causes it to extend laterally (Nikolsky’s sign).

Image Self-limited in 5–7 days, though death can occur in neonates with extensive disease.


Image

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

Image Hospitalize newborns with extensive skin sloughing.

Image Warm baths for debridement of necrotic epidermis.

Image Systemic antibiotics (oxacillin, dicloxacillin).

Image Pain control.

Image 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

Image Children.

Image Untreated streptococcal infection of pharynx, tonsils, or wound.

SIGNS AND SYMPTOMS

Image Finely punctate pink-scarlet exanthem first appears on upper trunk 12–48 hr after onset of fever.

Image As exanthem spreads to extremities, it becomes confluent and feels like rough sandpaper-like texture.

Image Fades in 4–5 days, followed by desquamation.

Image Circumoral pallor.

Image Linear petechiae evident in body folds (Pastia’s sign).

Image Pharynx is beefy red and tongue is initially white, but within 4–5 days the white coating sloughs off and tongue becomes bright red.


Image

“Strawberry tongue” or “sandpaper rash.” Think: Scarlet fever.


DIAGNOSIS

Image Clinical; confirmed by culture from throat or wound.

Image Rapid direct antigen tests detect GAS antigens.

Image Gram stain reveals gram-positive cocci in chains.

TREATMENT

Image Acetaminophen for fever and pain.

Image Antibiotics (penicillin, macrolide, or cephalosporin).

Image 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

Image incidence in atopic and immunocompromised patients.

SIGNS AND SYMPTOMS

Image Tender if irritated.

Image Types:

Image Verrucae vulgaris: Hands, fingers, knees; skin-colored papule.

Image Verrucae plantaris: Rough; over pressure points on plantar aspect of foot.

Image Verrucae planar: Flat; on face and dorsum of hands and fingers.

Image Condyloma acuminata: Anogenital warts.


Image

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

Image Transmitted by direct contact with skin and mucous membranes.

Image After primary infection, virus remains latent in a neural ganglion.

Image Reactivation of latent virus results in recurrent disease commonly occurring in the same area.

Image Recurrences become less frequent over time.

EPIDEMIOLOGY

Image Primary infection affects children and young adults.

Image Image incidence of infection in immunocompromised patients.

SIGNS AND SYMPTOMS

Image Grouped vesicles on an erythematous base, occurring primarily on lips, mouths, genitals, and eyes, but can occur at any site.

Image Erosions and crusted lesions form after a couple of days.

Image Fever, malaise, headache, and adenopathy may occur with primary infection.

Image Prodrome of burning, tingling, or itching occurs with recurrent infection.

Image Complications include ocular disease, secondary infection, and dissemination (especially in immunocompromised patients).


Image

Herpetic whitlow (herpes-infected finger)—can occur in children with herpes gingivostomatitis secondary to sucking of fingers.


DIAGNOSIS

Image Clinical.

Image Confirmed by Tzanck preparation, revealing multinucleated giant cells.

Image Viral culture of vesicle fluid.


Image

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

Image Oral acyclovir, valacyclovir, or famciclovir ↓ viral shedding time and accelerate healing time. Consider if herpetic whitlow or at risk for severe disease.

Image 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.

Image

FIGURE 20-6. Molluscum contagiosum.

(Photo courtesy of Danial Stuhlberg, MD, Utah Family Practice Residency, Provo, UT.)

ETIOLOGY

Molluscum contagiosum virus (poxvirus).


Image

Umbilicated, pearly papules. Think: Molluscum contagiosum.


EPIDEMIOLOGY

Image Affects children and sexually active adults.

Image Image incidence in atopic and immunocompromised patients.

SIGNS AND SYMPTOMS

Image Single or multiple, 2- to 5-mm, firm, umbilicated, skin-colored or pearly-white papules.

Image Commonly found on face, eyelids, axillae, and anogenital region.

Image 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

Image Group of noninvasive fungi that can infect keratinized tissue of epidermis, nails, and hair.

Image Clinical presentation depends on anatomic site of infection and is named accordingly.


Image

Tinea corporis lesions are annular with peripheral scale and central clearing.


ETIOLOGY

Trichophyton, Microsporum, Epidermophyton.

EPIDEMIOLOGY

Exacerbated by warm, humid climates.

SIGNS AND SYMPTOMS

Image Tinea pedis (“athlete’s foot”).

Image Tinea cruris (“jock itch”): Groin.

Image Tinea corporis (“ringworm”): Body (see Figure 20-7).

Image Tinea manuum: Hand.

Image Tinea facialis: Face.

Image Tinea capitis: Scalp.

Image Tinea barbae: Beard/mustache area.

Image Onychomycosis: Nails.

Image Tinea versicolor: Superficial, asymptomatic.


Image

Tinea versicolor has hyphae and yeast forms in a “spaghetti-and-meatball” distribution on KOH preparation.


DIAGNOSIS

Image Clinical presentation and history.

Image KOH preparation reveals multiple, septated hyphae.

Image Wood’s lamp reveals bright green fluorescence of hair shaft in tinea capitis.

Image Fungal culture of affected area may demonstrate dermatophyte.

TREATMENT

Image Prevention: Wearing well-ventilated shoes and clothing.

Image Topical antifungal agents (imidazoles and terbinafine).

Image Systemic antifungal agents if unresponsive to topical or if involvement of nails or hair (griseofulvin, systemic azoles, terbinafine).

Image Mild-potency topical corticosteroids if inflammation and pruritus are severe.


Image

Griseofulvin can cause elevation of liver enzymes.


Candidal Skin Infections (Candida)

DEFINITION

Superficial infection occurring in moist cutaneous sites.

Image

FIGURE 20-7. Tinea corporis (ringworm).

Image

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.


Image

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

Image Pruritus and soreness.

Image Confluent, bright red papules and pustules forming a sharply demarcated eroded patch with pustular lesions at the periphery (satellite lesions).

Image Distributed over intertriginous regions, including axillae; groin; web spaces; genital, anal, and inframammary areas.

Image 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

Image Keep intertriginous areas dry.

Image Topical antifungals (azoles).

Image Topical corticosteroids for symptomatic relief.


Image

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

Image Pruritus.

Image Pyoderma may develop from scratching.

Image 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

Image Hot water laundering.

Image Boil or dispose of implements.

Image Comb hair.

Image 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).

Image

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

Image Raised, erythematous, serpiginous tracks, occasionally forming bullae.

Image Single or multiple.

Image Usually on an extremity or the buttocks, but can occur anywhere on the body.

DIAGNOSIS

Clinical.

TREATMENT

Image Self-limited in weeks to months.

Image Thiabendazole if symptoms warrant treatment.

Scabies

Image

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

Image Pregnant female mite exudes keratolytic substance and burrows into the stratum corneum, depositing eggs and feces daily.

Image Eggs hatch; larvae molt into nymphs, mature in 2–3 weeks, and repeat the cycle.

EPIDEMIOLOGY

Image Physical contact with infected individual.

Image Rarely transmitted by fomites, as isolated mites dies within 2–3 days.

SIGNS AND SYMPTOMS

Image Pruritus at initial infestation.

Image First sign: 1- to 2-mm red papules, some of which are excoriated, crusted, or scaling.

Image Threadlike burrows.

Image Multiple types of lesions.


Image

Threadlike burrows are classic for scabies, but may not be seen in infants.


DIAGNOSIS

Scraping for microscopic identification of mites, ova, and feces.

TREATMENT

Image Permethrin, neck down, scalp only if involved; leave on 8–12 hr; may be repeated after 1 week.

Image Infants are particularly susceptible to the neurotoxicity of lindane; therefore avoid.

Image Alternatives include permethrin or sulfur ointment.


Image

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

Image Capillary (“strawberry”) hemangioma: Red or purple papules or nodules that develop soon after birth and spontaneously involute by fifth year (see Figure 20-11).

Image If multiple hemangiomas, may also have visceral hemangiomas (hemangomatosis).

TREATMENT

Image Most resolve without treatment.

Image Involvement of bone, soft tissue, or organ parenchyma may warrant excision of the hemangioma.

Image

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

Image Serial observation for early recognition of premalignancy.

Image Early excision of suspicious lesions.

Image

FIGURE 20-11. Capillary hemangioma.

Image

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

Image Horizontal growth phase: Lateral extension within the epidermis and dermis.

Image Vertical phase: Penetrates into dermis, greatly increasing risk of metastasis.

EPIDEMIOLOGY

Image Image incidence in fair-skinned people and with sun exposure.

Image Adolescents.


Image

Characteristics of mole suspicious for melanoma:

Image Asymmetric

Image Borders irregular

Image Color uneven

Image Diameter > 0.6 cm

Image Elevated

Image Enlarging


SIGNS AND SYMPTOMS

Characteristics of a mole suspicious for melanoma:

Image Asymmetric.

Image Border (irregular).

Image Color (variegated and mottled).

Image Diameter (> 0.6 cm).

Image Elevated.

Image Enlarging.

DIAGNOSIS

Prognosis based on thickness of the primary tumor.

TREATMENT

Image Surgical excision with margins at least 1 cm beyond borders, depending on depth of lesion.

Image 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

Image Immunoglobulin A (IgA) mediated.

Image Occurs most commonly following streptococcal or viral infection.


Image

Palpable purpura is the classic sign of small-vessel damage.


EPIDEMIOLOGY

Pediatric age group.

SIGNS AND SYMPTOMS

Image Palpable purpura

Image Arthritis

Image Abdominal pain

Image

FIGURE 20-13. Henoch-Schönlein purpura.

DIAGNOSIS

Clinical; may biopsy.


Image

Intestinal wall purpura can serve as a lead point for intussussception.


TREATMENT

Image Usually benign, self-limited.

Image If severe, consider systemic steroids.

Image Monitor for renal dysfunction.

Acne Vulgaris

DEFINITION

Image Disorder of pilosebaceous glands.

Image Develops in areas with the greatest concentration of sebaceous glands.

ETIOLOGY/PATHOPHYSIOLOGY

Image Results from a combination of hormonal (androgens), bacterial (Propionibacterium acnes), and genetic factors.

Image Initial pathology is microscopic microcomedo.

EPIDEMIOLOGY

Adolescents.

SIGNS AND SYMPTOMS

Image Comedone: Plug of sebaceous and dead skin material stuck in the opening of a hair follicle; open follicle (blackhead) or almost closed (whitehead).

Image Pustules, papules.

Image Painful nodules and cysts if severe.

Image Seborrhea of face and scalp (greasy skin).

Image Depressed or hypertrophic scars may develop with healing.

DIAGNOSIS

Clinical; confirmed by presence of comedones.

TREATMENT

Image Benzoyl peroxide wash.

Image Topical antibiotics (clindamycin or erythromycin).

Image Intralesional corticosteroid injections (triamcinolone acetonide).

Image Topical retinoid: ↑ cell turnover and prevent follicle occlusion.

Image Oral isotretinoin (Accutane) for severe, recalcitrant, nodular acne.

Image Dermabrasion for treatment of scars.


Image

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

Image Irritant contact dermatitis: Prolonged dampness, interaction of urine (ammonia) and feces with the skin, reactions to medications/creams, type of diaper.

Image Candidal or bacterial secondary infection can occur.

Image Atopic dermatitis.

Image 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

Image Red, scaly, fissured, eroded skin.

Image Patchy or confluent.

Image If secondarily infected: Impetiginous or candidal.

Image Check for oral candidiasis if present in diaper area.

TREATMENT

Image Keep infant dry, change diapers often.

Image Avoid harsh detergents, wipes with alcohol, and plastic pants.

Image Ointments can reduce friction and protect skin from irritation.

Image Avoid powders, as they can injure infants’ lungs if inhaled accidentially.

Image 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

Image Round/ovoid ulcer with grayish membrane and edges surrounded by reddish halo.

Image Occur on nonkeratinized skin: Inside of the lips and cheeks, floor of the mouth, under the tongue, soft palate, and tonsillar areas.

Image High recurrence rate.

Image Painful.

Image Usually heal uneventfully in 4–14 days.

DIAGNOSIS

Clinical; rule out herpes stomatitis.

TREATMENT

Image Avoid individual triggering factors.

Image Symptomatic: Oral numbing or coating medications.

Image Antibacterial/cleansing rinses.

Image Home remedies: Milk of Magnesia, warm salt water, alum rinses.

Image Prescription anti-inflammatory or antibacterial collagenase inhibitors.

Vitiligo

DEFINITION

Pigmentary defect.

ETIOLOGY/PATHOPHYSIOLOGY

Image Unknown, possibly autoimmune.

Image Trauma may be associated with initiation of the lesions.

EPIDEMIOLOGY

Half of cases present before 20 years of age.

SIGNS AND SYMPTOMS

Image Depigmented macules.

Image Predilection for hyperpigmented areas.

DIAGNOSIS

Clinical, though melanocyte absence can be confirmed by electron microscopy of biopsy specimen.

TREATMENT

Image Many months of psoralen and ultraviolet therapy can partially or completely repigment areas.

Image Potent topical steroids are used on areas such as lips not amenable to phototherapy.

Urticaria-Angioedema

Image

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.

Image

FIGURE 20-14. Urticaria.

DEFINITION

Allergic response Image edema of the tissues.

ETIOLOGY/PATHOPHYSIOLOGY

Type 1 hypersensitivity reaction of immunoglobulin E (IgE) with mast cells causes the release of histamine, Image vasodilation, Image 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

Image Urticaria: Well circumscribed, but can be coalescent, erythematous, raised lesions (wheals or welts) (see Figure 20-14).

Image Angioedema: Involves the deeper layers of skin, submucosa, and subcutaneous tissues.

TREATMENT

Image Usually self-limited.

Image Antihistamines to relieve pruritus.

Image Watch for signs of airway compromise (especially with angioedema).

Image Epinephrine for severe cases.

NEONATAL DERMATOLOGIC CONDITIONS

See Table 20-1.

Hair Loss

MOST COMMON ETIOLOGIES

Image Tinea capitis (see p. 524).

Image Trichotillomania.

Image Alopecia areata.

Trichotillomania (Hair Pulling)

DEFINITION

Image Traumatic hair pulling resulting in breaking of hair shafts at different lengths.

Image Can also involve eyebrows or eyelashes.

ETIOLOGY

Image Habitual.

Image Sign of psychiatric disorder.

Image Reaction to stress.

SIGNS AND SYMPTOMS

Image Patchy hair loss of scalp (often on side of dominant hand).

Image Loss of eyebrows, eyelashes.

Image Close examination of hair demonstrates hair shafts broken at different lengths.

TABLE 20-1. Neonatal Dermatologic Conditions

Image

TREATMENT

Image Behavioral modification.

Image 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

Image Loss of every hair within area.

Image Exclamation point hairs.

TREATMENT

Image High rates of spontaneous resolution/regrowth within 12 months.

Image In some cases, steroids (systemic, topical, or local injection).

Image Minoxidil or other immune modulation.

Dermatologic Manifestations of Some Infectious Diseases

See Table 20-2.

Image

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

Image

Image

DERMATOLOGIC MANIFESTATIONS OF SYSTEMIC DISEASE

See Table 20-3.

TABLE 20-3. Dermatologic Manifestations of Systemic Disease

Image



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