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Skin Lesions and Rashes

This chapter focuses on many skin lesionsand rashes seen in pediatric practice. Note that some lesions andrashes fall into more than 1 category in the classification.

Principal Causes of Skin Lesions and Rashes

1. Blistering(vesiculobullous) lesions
   1. Miliaria
   2. Allergic contact dermatitis
   3. Chemical and thermal burns
   4. Friction blisters
   5. Frostbite
   6. Bullous impetigo
   7. Papular urticaria (insect bites)
   8. Hand-foot-mouth disease
   9. Varicella-zoster virus infections
   10. Herpes simplex virus infections
   11. Erythema multiforme
   12. Staphylococcal scalded skin syndrome
   13. Epidermolysis bullosa
   14. Chronic bullous dermatitis of childhood(linear immunoglobulin A dermatosis)
   15. Dermatitis herpetiformis
   16. Bullous pemphigoid
   17. Incontinentia pigmenti
2. Pustular lesions
   1. Erythematoxicum
   2. Transient neonatal pustular melanosis
   3. Acne
   4. Folliculitis
   5. Eosinophilic pustular folliculitis
   6. Infantile acropustulosis
   7. Miliaria
   8. Candidiasis
   9. Herpes simplex virus infections
   10. Local bacterial infections (Staphylococcusaureus)
   11. Scabies
3. Skin-colored papules and nodules
   1. Smoothsurface
      1. Milia
      2. Molluscum contagiosum
      3. Acne
      4. Epidermal cyst
      5. Granuloma annulare
      6. Lipoma
      7. Juvenile xanthogranuloma
      8. Xanthoma
      9. Neurofibroma
   2. Rough surface
      1. Epidermal nevi
      2. Warts
      3. Corns and calluses
      4. Keratosis pilaris
4. White lesions
   1. Flat lesions
      1. Postinflammatory hypopigmentation
      2. Pityriasis alba
      3. Tinea versicolor
      4. Vitiligo
      5. Piebaldism
      6. Ash-leaf macules
      7. Hypomelanosis of Ito
      8. Chediak-Higashi syndrome
      9. Waardenburg syndrome
   2. Raised lesions
      1. Milia
      2. Acne
      3. Keratosis pilaris
      4. Molluscum contagiosum
5. Brown, blue-black, or black lesions
   1. Flat lesions
      1. Freckles(ephelides)
      2. Mongolian spots (dermal melanosis)
      3. Café au lait spots
      4. Lentigines
      5. Nevi of Ota and of Ito
      6. Congenital nevocellular nevi
      7. Acquired nevocellular nevi
      8. Nevus spilus (speckled lentiginousnevus)
      9. Spitz nevi (spindle epithelioid nevi)
      10. Epidermal nevi
   2. Raised lesions
      1. Postinflammatoryhyperpigmentation
      2. Mastocytoma and urticaria pigmentosa
      3. Pyogenic granuloma
      4. Dysplastic melanocytic nevi
      5. Melanoma
6. Yellow lesions
   1. Jaundice
   2. Carotenemia
   3. Sebaceous gland hyperplasia
   4. Nevus sebaceous of Jadassohn
7. Inflammatory papules and nodules
   1. Insectbites
   2. Acne
   3. Roseola (exanthem subitum)
   4. Enteroviruses (coxsackie A and B viruses,echoviruses)
   5. Epstein-Barr virus
   6. Parvovirus B19 (fifth disease)
   7. Postnatal rubella
   8. Measles (rubeola)
   9. Scarlet fever
   10. Cellulitis
   11. Furuncle
   12. Candidiasis
   13. Kawasaki disease
   14. Mycoplasma infections
   15. Erythema marginatum
   16. Panniculitis
   17. Erythema chronicum migrans
   18. Cutaneous larva migrans
   19. Urticaria (hives)
8. Vascular reactions
   1. Blanching
      1. Mottling(cutis marmorata)
      2. Salmon patch
      3. Spider angioma
      4. Port-wine stains
      5. Hemangiomas
      6. Drug hypersensitivity reactions
      7. Erythema toxicum
      8. Urticaria
      9. Viral infections (exanthems)
      10. Scarlet fever
      11. Erythema multiforme
      12. Kawasaki disease
      13. Toxic shock syndrome
      14. Erythema chronicum migrans
      15. Syphilis
      16. Pyogenic granuloma
      17. Pityriasis rosea (early lesions)
      18. Guttate psoriasis (early lesions)
   2. Nonblanching (purpuric rashes)
      1. Meningococcemia
      2. Toxic shock syndrome
      3. Rocky Mountain spotted fever
      4. Other
9. Papulosquamous disorders
   1. Diaperdermatitis (irritant dermatitis)
   2. Atopic dermatitis
   3. Nummular eczematous dermatitis
   4. Juvenile plantar dermatosis (foot eczema)
   5. Seborrheic dermatitis (infantile)
   6. Contact dermatitis
   7. Tinea corporis
   8. Tinea pedis
   9. Candidiasis
   10. Sunburn
   11. Pityriasis rosea
   12. Drug eruptions
   13. Scabies
   14. Polymorphous light eruption
   15. Psoriasis
   16. Parapsoriasis
   17. Lichen nitidis
   18. Lichen striatus
   19. Lichen planus
   20. Lupus erythematosus
   21. Dermatomyositis
   22. Langerhans cell histiocytosis
   23. Acrodermatitis enteropathica
   24. Human immunodeficiency virus infection
   25. Secondary syphilis
   26. Ichthyoses
       1. Ichthyosis vulgaris
       2. X-linked ichthyosis
       3. Classic lamellar ichthyosis and congenitalnonbullous ichthyosiform erythroderma
       4. Congenital bullous ichthyosiform erythroderma(epidermolytic hyperkeratosis)

Clinical Features and Diagnosis

Blistering (Vesiculobullous) Lesions

Miliaria

Miliariacrystallina is produced by obstruction of sweat ducts in stratumcorneum. Clear, thin-walled, 1- to 2-mm vesicles usually occur onface, neck, and upper trunk in neonates or in areas of sunburn inolder children.

Characteristic lesions of miliariarubra (heat rash) are 2- to 4-mm papules or vesicles surroundedby erythema, which are commonly seen in neck, axilla, and groinareas.

Allergic Contact Dermatitis

Delayedhypersensitivity reaction to contact allergens, which include poisonivy, oak, and sumac; nickel-containing earrings or belt buckles;nail polishes; hair dyes; perfumes; cosmetics; and deodorants.

Presence of linear or geometric areasof vesiculation usually indicates allergic contact dermatitis.

Patch testing for contact allergenscan be useful in diagnosis.

Chemical and Thermal Burns

Both chemical and thermal burns produce blisteringof skin with vesicle and bulla formation. Exposed areas are commonlyinvolved where rubbing against hot object has occurred. Cigaretteburns on skin or scald burns of feet suggest child abuse.

Friction Blisters

Mild trauma may produce friction with blisteringand vesicle formation of skin. Common cause is wearing of new shoesor skates.

Frostbite

Affects fingers, toes, nose, and ears mostcommonly. Rewarming produces erythema, swelling, and burning painfollowed by vesicles and bullae.

Bullous Impetigo

Skin infectioncaused most commonly by S. aureus. Group A Streptococcus is commoncopathogen but does not form bullae alone.

Bullae containing clear fluid on erythematousbase may become pustular, with subsequent oozing and crusting.

Diagnosis is usually clinical. Positivebacterial culture of lesion is definitive.

Papular Urticaria (Insect Bites)

Insect bitesby fleas (most common), mosquitoes, bedbugs, fire ants, spiders,and chigger mites often produce urticarial papules, which may befollowed by vesicle formation.

Observing particular insect causingbite is diagnostic. Otherwise, inquiry into which insects may havebeen seen in house or immediate surroundings helps narrow possibilities.

Hand-Foot-Mouth Disease

Infectionusually associated with coxsackievirus A16.

Characteristic findings are fever andvesicles on erythematous base located on hands, feet, and in themouth.

Usually a clinical diagnosis, whichmay be confirmed by culture of skin vesicle.

Varicella-Zoster Virus Infections

Primaryinfection causes varicella (chickenpox). Incubation period is 10–21 days.

Illness begins with fever and macularrash; subsequently, lesions become papular, vesicular, and crusted.

When all stages of skin lesions occurat once, diagnosis is easily made clinically. Positive viral cultureis confirmatory.

Small number of children who receivevaricella vaccine may develop mild rash consisting of macules, papules,and vesicles within 1 mo of vaccination.

Reactivation of varicella-zoster viruscauses herpes zoster (shingles). Groups of painful vesicles on erythematousbase follow ≥1 of skin dermatomes. Diagnosis is usually clinical.Polymerase chain reaction (PCR) or positive viral culture confirmsdiagnosis.

Herpes Simplex Virus Infections

Infectionusually produces painful vesicles on erythematous base.

In neonates, herpes simplex virus (HSV)may be transmitted by mothers who have active infection of cervix,vulva, or perineum; however, positive history of maternal herpesinfection is often lacking. Neonates may develop localized lesionsinvolving skin, eye, or pharynx; encephalitis; or disseminated infectionwith hepatitis, pneumonia, and encephalitis.

In infancy and childhood, lesions alsomay occur on the lips and mouth (gingivostomatitis), fingers, andgenitalia.

Herpes genital infection is transmittedalmost exclusively by sexual contact and occurs in sexually activeindividuals or in younger children who have been sexually abused.

Diagnosis may be made by culture ofskin vesicles, nasopharynx, eyes, urine, blood, rectum, or CSF.Direct fluorescent antibody staining of vesicle scrapings or enzymeimmunoassay detection of HSV antigen are other diagnostic techniques.PCR is sensitive method to detect HSV DNA, especially in evaluationof spinal fluid for suspected herpes encephalitis.

Erythema Multiforme

Most commoncauses are infection, especially with HSV, and drugs (e.g., penicillins, sulfonamides,and barbiturates).

Oval or round, fixed, symmetric, violaceousmacules and papules 1–2 cm in diameter may occur anywhereon body, but their occurrence on palms and soles is characteristic.Lesions progress over a few days to develop concentric zones ofcolor with dusky center that can develop blisters. These are calledtarget or iris lesions.

When there is extensive skin and mucousmembrane involvement along with systemic symptoms (e.g., fever),this is known as Stevens-Johnson syndrome. Severe exfoliative variantof Stevens-Johnson syndrome is called toxic epidermal necrolysis.

Staphylococcal Scalded Skin Syndrome

S. aureusphage group II produces exfoliative toxins A and B, which causescalded skin syndrome.

Most common in children <5yrs of age.

Usual source of this pathogen is conjunctivitisor nasopharyngitis.

Clinical spectrum varies from mildillness with erythema, skin tenderness, and mild desquamation totoxic illness with high fever and widespread skin exfoliation. Skincan often be peeled off just by rubbing it (Nikolsky'ssign). Vesicles, bullae, and pustules may occur during exfoliativephase. Mucous membranes are generally spared, although crustingmay occur around eyes and mouth.

S. aureus may be cultured from skin,pharynx, eyes, ears, nose, and rectum. Cultures of blood and bullaeare usually negative.

Skin biopsy shows absence of epidermalnecrosis and inflammatory cells in contrast to toxic epidermal necrolysis,which shows epidermal necrosis and perivascular dermal inflammatory cells.

Epidermolysis Bullosa

Group ofgenetic disorders characterized by noninflammatory blisters. 3 majortypes are epidermolysis bullosa simplex, junctional epidermolysisbullosa, and dystrophic epidermolysis bullosa.

All types may appear similarly in neonateswith blisters, erosions, and mucous membrane involvement.

Diagnosis is based on clinical findings,routine histopathology, electron microscopy, and immunofluorescentantibody mapping of basement membrane.

Chronic Bullous Dermatitis of Childhood (Linear ImmunoglobulinA Dermatosis)

This raredisorder usually occurs in first decade of life.

Polycyclic lesions with blisters atedges can appear on trunk, perineum, legs, hands, and feet. Mucousmembranes are uninvolved.

Skin biopsy with immunofluorescentstaining shows linear immunoglobulin A (IgA) deposits within basementmembrane adjacent to blister.

Dermatitis Herpetiformis

Characteristiclesions of this rare disorder occur in school-aged children andconsist of pruritic groups of vesicles and blisters that appearin symmetric distribution over elbows, knees, back, and buttocks.Mucous membranes are uninvolved.

Diagnostic skin biopsy adjacent tovesicles shows granular IgA deposits at tips of dermal papillae.These individuals also may be gluten sensitive.

Bullous Pemphigoid

Large tensebullae on trunk and flexural areas of extremities characterize thisdisorder, which may last months to years. Mucous membrane involvementoccurs in some cases.

Skin biopsy with immunofluorescencereveals linear IgG and C3 deposits in basement membrane. CirculatingIgG against basement membrane also may be found in serum.

Incontinentia Pigmenti

Transmittedas X-linked dominant trait and only occurs in girls because it islethal in boys. In early infancy, vesicles and pustules appear.

Second stage occurs 2–6 wkslater and consists of papules and verrucous lesions.

Third stage usually occurs at 3–6mos of age with whorls of skin hyperpigmentation appearing in thelines of Blaschko.

Fourth stage consists of skin atrophyand hypopigmentation. In some cases, microcephaly, seizures, andmental retardation may occur.

Pustular Lesions

Pustularlesions commonly seen in neonates include erythema toxicum, transientneonatal pustular melanosis, miliaria, acne neonatorum, folliculitis,candidiasis, herpes simplex, and local bacterial infections usuallycaused by S. aureus.

Pustular lesions seen in infants, children,and adolescents include acne, folliculitis, candidiasis, scabies,infantile acropustulosis, and local bacterial infections.

Some of these disorders are discussedin other sections of this chapter.

Erythema Toxicum

Rash of erythema toxicum consists of blotchy,erythematous macules 2–3 mm in diameter with tiny centralpustule or vesicle. May appear anywhere from 1–2 days ofage up to 10 days of age on the face, trunk, and extremities. Resolutionusually occurs in 4–5 days.

Transient Neonatal Pustular Melanosis

Characterized by 2- to 3-mm pustular lesionsdistributed over face, neck and upper chest, and less often on extremities.When lesions rupture, they leave hyperpigmented macules surroundedby collarette of fine white scale. Fade in a few weeks or months.

Acne

Accumulationof sebum and keratin produce basic lesion of acne, which is calledmicrocomedo.

These firm papules, which are <1mm in diameter, usually appear at 2–8 wks of age on face, chest,and back.

When they become red and inflamed,they may evolve into pustules.

During puberty, acne lesions commonlyappear on face, chest, and back (see discussion of skin-coloredpapules and nodules below).

Folliculitis

Manifestationsof folliculitis, an infection of hair follicles, depend on depthof bacterial invasion. Superficial folliculitis appears as tinypustules 1–2 mm in diameter, whereas deep folliculitis orfurunculosis appears as tender, erythematous nodules. Confluenceof lesions may produce an abscess.

Usual pathogen is S. aureus. P. aeruginosafolliculitis may be associated with use of hot tubs.

Eosinophilic Pustular Folliculitis

Uncommon disorder characterized by recurrentcrops of pruritic papules and pustules that occur on scalp, trunk,and extremities in infants. In some cases, peripheral eosinophiliamay be found at the time of outbreak of pustules.

Infantile Acropustulosis

Benign, self-limited disorder of unknowncause that usually occurs at 2–10 mos of age. Crops of pruriticpapules, pustules, and vesicles occur on fingers, palms, and soles,and occasionally on scalp, face, trunk, and extremities. Lesionslast for 7–10 days, but new crops can occur every 2–3wks, usually disappearing by 2–3 yrs of age.

Skin-Colored Papules and Nodules

Smooth Surface

Milia

Firm, white or yellow, 1- to 2-mm papules,usually appearing on cheeks, forehead, and nose. May also may beseen on palate (Epstein pearls) and gingiva (Bohn nodules). Theyrepresent keratin-filled epidermal inclusion cysts and usually disappeara few weeks after birth.

Molluscum Contagiosum

DNA poxviruscauses this viral disease involving the skin. Transmission occursby person-to-person contact or fomites.

Lesions are discrete, flesh-colored,dome-shaped papules, 1–5 mm in diameter, with umbilicatedcenter.

Diagnosis is usually clinical; however,Wright stain of papule contents can demonstrate characteristic intracytoplasmicinclusion bodies, known as molluscum bodies.

Acne

Closed comedones (whiteheads) and open comedones(blackheads) are noninflammatory lesions that do not scar. Withrupture of walls of hair follicles. inflammatory papules and pustulesappear. Involvement of many follicles may produce cysts and noduleswith more pronounced scarring. See the section Pustular Lesions: Acne.

Epidermal Cyst

This firm, round nodule may be 1–15cm in diameter. In neonates, may be seen on lateral border of eyebrowor in scalp.

Granuloma Annulare

This annular lesion consists of firm papulesand nodules, which form semicircle or circle with uninvolved orslightly discolored central area. Lesions are 1–15 cm indiameter and may be multiple. Often involve fingers, wrists, ankles,and dorsa of hands and feet. Lack of scaling and deep palpable portionhelp distinguish this lesion from tinea corporis.

Lipoma

Soft, mobile, nontender nodule composed offat and commonly found on arms, chest, and neck.

Juvenile Xanthogranuloma

Characterized by skin-colored or orange-brownpapules or nodules, which can appear anywhere on the skin. Whenblanched, underlying color is usually yellow. Spontaneous involutionmay occur over several years.

Xanthoma

Papule, plaque, nodule, or tumor that containslipid. Usually associated with increased serum lipids but is unusualin childhood.

Neurofibroma

Skin-coloredlesion that can occur anywhere on skin and at any age.

May be solitary or associated withneurofibromatosis.

Biopsy is confirmatory.

Rough Surface

Epidermal Nevi

Raised, linear or oval, hairless, flesh-coloredor brown lesions, often present at birth, and their long axis parallelslong axis of dermatome. May become scaly, verrucous-like, inflamed,and pruritic.

Warts

Caused byvarious types of human papilloma virus.

Common warts (verruca vulgaris) aresingle, flesh-colored papules with roughened, irregular, scaly surface.Commonly occur on hands and periungual areas but may occur anywhereon skin.

Plantar warts are common warts thatoccur on soles of feet.

Filiform warts appear as projectionsfrom stalk and usually are seen on nose, eyelids, or lips.

Flat warts (verruca plana) are flat,broad, multiple, flesh-colored or tan papules, 2–5 mm in diameter,that usually appear in groups on face and extremities.

Venereal warts (condyloma acuminata)are flesh-colored papules with irregular surface that are usuallyconfluent. Appear on genital mucosa, adjacent skin, or in both areas.

In most circumstances, diagnosis isclinical.

Corns and Calluses

Corns areareas of thickened skin, usually appearing because of prolongedfriction or pressure. Occur primarily on feet and have central core,when surface is pared off lesion.

Calluses are diffuse areas of thickenedskin, not as circumscribed as corns, which occur on palmar surfacesof hands or fingers and on weight-bearing areas of feet. Paringsurface of calluses reveals normal skin grooves.

Keratosis Pilaris

Stratum corneum follicular plugs, 1–2mm in diameter, usually occur on exterior aspects of arms and legs,buttocks, and lateral aspects of facial cheeks.

White Lesions

Flat Lesions

Postinflammatory Hypopigmentation

Irregular hypopigmentation may occur followingany inflammation of skin. Particularly noticeable in African-Americanchildren and usually resolves in a few months.

Pityriasis Alba

Oval, flat, scaly, poorly demarcated, hypopigmentedmacules 0.5–2 cm in diameter may occur on face, upper trunk,thighs, or arms. Sometimes lesions are associated with atopic dermatitis.

Tinea Versicolor

Yeastlikeorganism M. furfur produces lesions of tinea versicolor.

Oval macules with fine scale occuron neck, upper back, shoulders, and upper arms.

Although they appear as hypopigmentedmacules in tanned or dark-skinned individuals, with fading of skinpigmentation in winter, they appear as tan-brown macules.

Wood light exam reveals orange fluorescence.Diagnostic KOH preparation using skin scrapings reveals short curvedhyphae and circular spores.

Vitiligo

Cause isunknown but is thought to involve autoimmune destruction of melanocytes.

Characterized by appearance of well-demarcated,depigmented macules and patches. Distribution of lesions on face,neck, and extensor surfaces of extremities is often symmetric.

May be associated with alopecia areata,Addison disease, hypoparathyroidism, Hashimoto thyroiditis, myastheniagravis, and pernicious anemia.

Piebaldism

In this autosomal-dominant disorder, circumscribedareas of skin with absence of pigment may be noted in neonates.These white patches may occur on face, chest, abdomen, and extremities.

Ash-Leaf Macules

These hypopigmented macules, which may beleaf shaped, may be only sign of tuberous sclerosis in newborns.Usually occur on trunk or extremities. Other cutaneous manifestationsof tuberous sclerosis are angiofibromas of nose and face (adenomasebaceum), which usually appear at 5–10 yrs of age. See furtherdiscussion of tuberous sclerosis in Chap.13, Developmental Delay.

Hypomelanosis of Ito

Bizarre hypopigmented swirls in lines ofBlaschko characterize hypomelanosis of Ito. Mental retardation maybe associated finding.

Chediak-Higashi Syndrome

Individuals with Chediak-Higashi syndromemay have patches of hypopigmented skin. Have recurrent infectionsbecause of inability to kill bacteria (see Chap. 53, Recurrent Infection).

Waardenburg Syndrome

Characteristic features of this autosomal-dominantdisorder include white forelock and eyelashes, white patches ofskin, heterochromia of irides, and sensorineural deafness. Genelocus has been mapped to chromosome 2q35.

Raised Lesions

Milia, microcomedones of acne, keratosispilaris, and molluscum contagiosum are discussed in previous sections.

Brown, Blue-Black, or Black Lesions

Flat Lesions

Freckles (Ephelides)

1- to 4-mm brown macules that occur on sun-exposedskin. More common in light-haired children, they become darker duringsummer and lighter and smaller during winter.

Mongolian Spots (Dermal Melanosis)

Melanocytesdeep in dermis produce blue-black areas of discoloration calledMongolian spots.

Occur most commonly on buttocks, sacrum,and back.

Can be single or multiple and rangein size up to 20 cm in diameter. Lesions usually disappear overseveral years, although some may persist to adulthood.

Café au Lait Spots

These flat,oval or round, tan macules of varying size and shape with usuallyregular margins are present at birth or appear during first yearof life. May occur anywhere on body but usually are found on trunkand extremities.

Presence of ≥6 lesions >5mm in diameter in prepubertal children or >15 mm in diameterin postpubertal children is presumptive evidence of neurofibromatosis.

McCune-Albright syndrome, which usuallyoccurs in females, is characterized by café au lait spotswith irregular margins, polyostotic fibrous dysplasia, and sexualprecocity.

Lentigines

Tan, darkbrown, or black macules 1–5 mm in diameter, which are scatteredover body. Darker than freckles and do not change with sun exposure.

May be seen in normal individuals,in Peutz-Jeghers syndrome (pigmented mucocutaneous lesions and generalizedintestinal polyposis), and in Leopard syndrome (LEOPARD is acronymfor lentigines, electrocardiographic conduction defects, ocularhypertelorism, pulmonic stenosis, abnormal genitalia, retardationof growth, and deafness).

Nevi of Ota and of Ito

Blue-gray patches of dermal melanosis whoseborders may be distinct or indistinct, regular or irregular. Nevusof Ota typically involves sclera and area of 1 side of face innervatedby first 2 branches of trigeminal nerve. Nevus of Ito occurs inacromioclavicular area.

Congenital Nevocellular Nevi

Round oroval, brown or brown-black macules with well-demarcated border seenat birth.

Vary in size from 1–2 mm toseveral cm in diameter and can appear anywhere on skin.

Giant nevocellular nevi (>10–20cm in diameter) have small risk of evolving into cutaneous melanoma.Infants with smaller congenital nevi also probably have above-normalrisk of melanoma in adult life.

Small lesions are followed until about10 yrs of age and then excised. If excision is possible withoutsevere mutilation, giant nevi should probably be excised in infancy.

Acquired Nevocellular Nevi

May be junctional,intradermal, or compound. Junctional nevi arise from junction betweenepidermis and dermis, intradermal nevi arise from dermis, and compoundnevi arise from both epidermis and dermis.

Junctional nevocellular nevi are usuallyflat, round or oval, brown or brown-black macules with well-demarcatedborder. Vary in size from 1–2 mm to several cm in diameterand can appear anywhere on skin, usually after 6 mos of age. Raisedpapular intradermal or compound nevi usually occur in older children.

Diagnosis is usually clinical; however,skin biopsy can distinguish them.

Nevus Spilus (Speckled Lentiginous Nevus)

Consists of light brown or tan macule thatis sometimes dotted with smaller, darker macules. They are 1–12cm in diameter.

Spitz Nevi (Spindle Epithelioid Nevi)

Pink, brown,black, or blue-black, round or oval papules, up to 1.5 cm in diameter, withdistinct regular border.

Usually appear on face, shoulders,or extremities in school-aged children.

Excisional biopsy is diagnostic.

Epidermal Nevi

See section on Skin-Colored Papules and Nodules.

Raised Lesions

Postinflammatory Hyperpigmentation

In children with dark skin, healing inflammatorylesions may be hyperpigmented.

Mastocytoma and Urticaria Pigmentosa

Mastocytomais single red or red-brown lesion appearing in first months of life.

Multiple red-brown papules 1–3cm in diameter are characteristic of urticaria pigmentosa. Usuallyappear on trunk, extremities, or face before 2 yrs of age.

Rubbing these lesions releases histaminefrom mast cells with production of wheal and flare (Darier sign).

Pyogenic Granuloma

Single, reddish-brown, firm nodule 1–10mm in diameter, which may be smooth but also may ulcerate and crust.Usually occurs on hands, fingers, or trunk in children <5yrs of age but can occur at any age.

Dysplastic Melanocytic Nevi

Usuallyappear around puberty and may be precursors of melanoma.

Individual lesions can be various colors(e.g., brown, pink, or fleshtone). Usually ≥5 mm in diameter.Skin surface is raised, and borders tend to be irregular and poorlydemarcated.

Risk of melanoma is high when thereis family history of dysplastic melanocytic nevi and melanoma.

Excisional biopsy is diagnostic.

Melanoma

This raremalignant lesion appears as pigmented nodule that may have variouscolors, including tan, brown, blue, red, and white.

Nonuniform irregular surfaces withnotched borders and rapid growth should raise suspicion of thislesion, which may arise in preexisting nevi, especially congenitalor atypical ones.

Biopsy is diagnostic.

Yellow Lesions

Jaundice

Jaundice is yellow color of skin due to bilirubindeposition and is discussed in Chap.36, Jaundice.

Carotenemia

Yellow-orange hue of skin due to ingestionof carotene, which is found in carrots and squash. Commonly occursbefore 2 yrs of age.

Sebaceous Gland Hyperplasia

Yellow macules and papules, 1–2mm in diameter, occur on nose and cheeks of infants and usually recedeby 4–6 mos of age.

Nevus Sebaceous of Jadassohn

Nevus sebaceous appears on scalp as slightlyraised, smooth or pebbly, linear or oval, yellow or orange, waxyplaque. These lesions do not contain any hair. Adnexal tumors canappear within lesions after puberty.

Inflammatory Papules and Nodules

Insect Bites

Common feature of insect bites is erythematouspapule with central punctum. Wheals and even bullae may occur.

Acne

Mild acne consists of inflammatory papulesand pustules. Nodules are seen with moderate involvement. In severeacne, extensive number of inflamed papules, pustules, and nodulesoccur.

Roseola (Exanthem Subitum)

Human herpesvirus6 infection.

Usually presents with fever for severaldays in children 6 mos–3 yrs of age.

Within 24 hrs after fever subsides,macular or papular rose-colored rash appears on trunk and spreadsto face and extremities with gradual fading over next 2–3days.

Diagnosis is usually clinical.

Enteroviruses (Coxsackie A and B Viruses, Echoviruses)

Coxsackieand echoviruses may cause various rashes, which can be macular orpapular. Rash usually appears 1–2 days after onset of fever.Headache, malaise, and vomiting also may occur.

These self-limited illnesses usuallylast for a few days.

Positive viral culture or PCR of respiratorytract secretions is diagnostic.

Epstein-Barr Virus

This virusis responsible for infectious mononucleosis.

Characteristic features include fever,malaise, sore throat, lymphadenopathy, and splenomegaly. Liver alsomay be enlarged. Macular, papular, or morbilliform rash may occuron trunk and proximal extremities. There is usually lymphocytosiswith ≥10–20% atypical lymphocytes.

Slide test for heterophil antibodyis generally positive in older children, but it is often negativein children <4 yrs of age.

Elevated antibody titer against viralcapsid antigen (IgM anti-VCA) confirms diagnosis.

Fever may last several weeks, whereasfatigue and lassitude may last ≥3 mos in severe cases.

Parvovirus B19 (Fifth Disease)

Viral infectionalso called erythema infectiosum. Usually affects children ≥3yrs of age.

Erythematous rash is most prominenton cheeks and gives "slapped cheek" appearance. Lacelike,macular or papular rash also may occur on arms, trunk, and thighsfor up to 3 wks. Fever may or may not occur.

This is usually clinical diagnosis,which can be confirmed by presence of IgM antibodies to parvovirus-specificantigens.

Postnatal Rubella

Since rubellavaccine licensure in U.S. in 1969, this infection has become muchless common.

Initial sign of illness may be malaise,which lasts 1–2 days. Macular or papular rash appears onface and spreads to trunk and extremities. Postauricular, posteriorcervical, and occipital adenopathy is also common. Rash usuallyresolves by fourth day and does not become confluent. Fever mayor may not occur.

Positive rubella virus culture fromnasal secretions, 4-fold increase in antibody titer, or seroconversionconfirms diagnosis.

Measles (Rubeola)

Althoughincidence of measles (rubeola) has decreased since immunizationbegan in 1963, outbreaks continue to occur.

Initial findings are fever, coryza,hacking cough, and nonpurulent conjunctivitis. In 2–3 days,white macular 1-mm lesions called Koplik spots appear on buccalmucosa, especially opposite the lower premolars. Their appearanceis pathognomonic for measles. Within 12–24 hrs after thesespots become visible, macular or papular rash that often becomesconfluent appears on forehead and behind ears and spreads downwardto involve trunk and extremities, only to fade in the same orderin which it began.

Although diagnosis of measles usuallycan be made clinically, single elevated IgM level, 4-fold increasein antibody titer with paired sera, or positive nasopharyngeal cultureconfirms diagnosis.

Scarlet Fever

Toxin releasedfrom group A streptococci produces scarlet fever, which usuallyoccurs in children 2–10 yrs of age.

Usual presenting findings are feverand sore throat. In 1–2 days a diffuse, papular, erythematousrash appears around neck and spreads over trunk and extremities.Rash has sandpaper-like feel and is more prominent in elbow creasesand inguinal areas. Perioral pallor, flushed cheeks, strawberrytongue, and generalized adenopathy also may occur. Rash usuallyfades in 3–4 days, with desquamation beginning around fingertipsin 10–20 days.

Positive pharyngeal group A streptococcalantigen test or culture confirms diagnosis.

Scarlet fever also can occur followingpyoderma or infection of a wound.

Cellulitis

Inflammation of soft tissues that may beassociated with fever and localized adenopathy. Skin abrasion orpenetrating wound may have preceded infection. Most common pathogensare S. aureus and group A Streptococcus.

Furuncle

Is a deep folliculitis that appears as tender,erythematous nodule. Confluence and abscess formation can occur.S. aureus is usual pathogen.

Candidiasis

Candidallesions commonly involve diaper area in infants. Satellite lesions(scaly papules, pustules, vesicles) and inflammatory involvementof creases are common features.

Diagnosis is usually clinical but maybe confirmed by positive KOH preparation (budding yeasts) or bypositive culture.

Inflammation around base of nail alsomay be caused by Candida infection.

Kawasaki Disease

Vasculitiswhose cause is unknown. Usually occurs in children <5 yrsof age.

Diagnostic criteria are presence offever for ≥5 days associated with at least 4 of the following5 signs in absence of any other disease process:

Bilateralconjunctival injection

Cervical lymphadenopathy

Erythematous macular, papular, or scarlatiniformrash primarily on trunk

Mucous membrane involvement, includingdry fissured lips, strawberry tongue, pharyngeal injection, anderythema of lips

1 or more changes in extremities (e.g.,palmar erythema and peripheral edema)

Desquamation around nails and involvingpalms, soles, or perineal area may develop 1–2 wks followingonset of illness (see Chap. 21,Fever).

Mycoplasma Infections

Macularor papular rashes may occur in some children with M. pneumoniaeinfection. Usual clinical presentation consists of low-grade fever,malaise, and persistent cough.

Typically, chest radiograph shows patchy,unilateral or bilateral, segmental or subsegmental involvement.

Serologic tests are diagnostic.

Erythema Marginatum

Transient eruption consisting of curvilinearmigrating areas of erythema that form incomplete circles and moveover the skin within a few hours. It is 1 of the major Jones criteriafor rheumatic fever but also can be seen with streptococcal infectionswithout evidence of rheumatic fever.

Panniculitis

Inflammationof subcutaneous fat tissue may produce painful, erythematous nodules.

Cold panniculitis can be caused bypopsicles held too long in a child's mouth.

Another type of panniculitis is subcutaneousfat necrosis of newborns.

Erythema Chronicum Migrans

Earliestfeature of Lyme disease is erythema chronicum migrans that begins4–20 days after tick bite.

Red papule occurs at site of bite andenlarges over several weeks to form ring with flat red border andclearing of its center. Multiple secondary rings may develop 1–6days after primary lesion appears. Skin lesion is associated withheadache, fatigue, myalgia, and low-grade fever.

About 1 mo after tick bite, other complicationsmay occur, including arthritis, meningitis, myocarditis, peripheralneuropathy, and facial nerve palsy (see Chap. 37, Limp).

Cutaneous Larva Migrans

Infectivelarvae of dog and cat hookworms are usual causes of cutaneous larvamigrans, which is most common in southeastern U.S.

Pruritic red papules occur at siteof entry, usually on feet or hands, and intensely pruritic serpiginoustracks are formed in the skin.

Diagnosis is usually clinical.

Urticaria (Hives)

Characterizedby oval or round, flat or papular wheals and flares that are pruritic. Usuallytransient phenomenon lasting few hours or a few days. Clinical characteristicis their disappearance and reappearance within hours. Angioedemaof eyelids, lips, face, scrotum, and larynx also may occur.

Some known causes are

Drugs (penicillins,sulfonamides, opiates, radiocontrast media)

Foods (milk, shellfish, nuts, eggs,chocolate)

Inhalants (pollens, molds)

Infectious agents (enteroviruses, adenoviruses,group A Streptococcus)

Insect and arthropod bites and stings(bees, wasps, fleas, mites, bedbugs, mosquitoes, scorpions, spiders,jellyfish)

Skin contactants (cosmetics, animaldanders, chemicals)

Physical factors (heat, cold, stress,exercise, prolonged local pressure, sunlight)

Diagnosis is usually clinical. Evenafter exhaustive history, specific cause may remain unknown.

Vascular Reactions

Blanching

Erythema toxicum, urticaria, viral exanthems,scarlet fever, erythema multiforme, Kawasaki disease, toxic shocksyndrome, erythema chronicum migrans, syphilis, pyogenic granuloma,and early lesions of pityriasis rosea and guttate psoriasis arediscussed in other sections of this chapter.

Mottling (Cutis Marmorata)

When exposed to decrease in temperature,lacelike pattern of erythema called mottling appears on extremities,only to disappear with rewarming.

Salmon Patch

Formed byectatic dermal capillaries. Most common of vascular nevi.

Pink macules and patches 1–3cm in size and appear most commonly on nape of neck, glabella, andupper eyelids. They blanch with pressure and become more intensewith crying. Most of them fade or regress with age.

Spider Angioma

Telangiectaticlesions that have legs radiating from central punctum (arteriole). Rangein size from a few mm to 2 cm in diameter and may occur anywhereon body, usually on face and hands.

They are found in normal children,in individuals with chronic liver disease, and during pregnancy.Most involute at puberty.

Port-Wine Stains

Is a typeof capillary malformation which is a purple-red, macular lesionthat may present on face or extremity at birth.

Port-wine stain that involves distributionof ophthalmic branch of trigeminal nerve is known as Sturge-Webersyndrome. Clinical manifestations include seizures, ipsilateralglaucoma, contralateral hemiparesis, and mental retardation. Angiomasof cerebral cortex are likely with involvement of upper eyelid.CT is diagnostic.

Port-wine stain of an extremity associatedwith overgrowth of subcutaneous tissue and bone is known as Klippel-Trenaunay-Webersyndrome. Parkes-Weber syndrome is similar but includes arteriovenousmalformations rather than venous malformations.

Hemangiomas

May be superficial,deep, or mixed (possessing both superficial and deep components).

At birth, only blanched macule withfine telangiectasias may occur, but after a few weeks of age, brightred, raised capillary hemangioma develops. They are usually 1–3cm in diameter, although they can be larger. During the first 6–12mos of life, they often increase in size. Involution begins at about 1yr of age and slowly progresses during next 5–10 yrs.

Deep capillary hemangiomas often havebluish hue and indistinct borders. They regress but not to sameextent as capillary hemangiomas.

Drug Hypersensitivity Reactions

Can be associatedwith almost any type of rash, although macular and papular rashes, urticaria,and erythema multiforme are most common.

Most common drugs implicated in causinghypersensitivity reactions are penicillins, sulfonamides, barbiturates,and phenytoin.

Drug-related macular or papular rashesusually begin a few days after initiation of drug therapy and seldomoccur >1 wk later. Eruption may be diffuse, generalized,and confluent, with resolution usually 1–2 wks after drughas been discontinued.

Presence of fever, lymphadenopathy,and eosinophilia, and increase in serum aminotransferases supportdiagnosis. Clinical diagnosis depends on likelihood that a givendrug can cause particular rash, temporal relationship between administrationof drug and onset of rash, and associated findings.

Nonblanching (Purpuric Rashes)

Purpuraare macular discolorations that do not blanch or disappear withpressure.

Types of purpura include petechiae(<3 mm in diameter) and ecchymoses (larger lesions).

Purpuric rashes are discussed in Chap. 52, Purpura and Bleeding,but 3 life-threatening causes are discussed here.

Meningococcemia

Petechialor purpuric rash occurs in about 50% of cases of meningococcemia.In severe cases, purpura fulminans may be seen.

Acute onset of fever and spreadingpetechial or purpuric rash in ill child is meningococcemia untilproven otherwise.

Gram-stained smear of petechial lesionmay show gram-negative intracellular diplococci. Confirmatory testsinclude positive blood or spinal fluid culture.

Toxic Shock Syndrome

Usuallycaused by toxin produced by certain strains of S. aureus. May alsobe caused by group A Streptococcus. Some cases occur in adolescentfemales following menstrual period in which tampons were used.

Clinical features include fever, vomiting,diarrhea, headache, myalgia, diffuse macular or papular rash, hypotension,and alteration in consciousness. Desquamation of extremities, palms,and soles occurs 1–2 wks after onset of the illness.

Lab tests may reveal leukocytosis,pyuria, azotemia, thrombocytopenia, elevated serum aminotransferasesand bilirubin, and abnormal coagulation studies.

Initially, diagnosis is clinical, andtreatment must begin without delay. Isolation of toxin-producingstrains of S. aureus or group A Streptococcus from nose, pharynx,vagina, cervix, or blood in this clinical setting is diagnostic.

Rocky Mountain Spotted Fever

Tick bitetransmits R. rickettsii, which causes Rocky Mountain spotted fever.History of recent exposure to ticks usually exists, but negativehistory is not uncommon.

Prodrome consists of fever, headache,vomiting, and myalgia. Rash, which initially consists of red macules,appears in 2–4 days on wrists, ankles, and lower legs,and may involve palms and soles. Rash usually becomes petechialand is more intense on extremities than on face and trunk.

Presumptive diagnosis is based on clinicalfindings alone. Affected children must be treated immediately becausethis can be a fatal disease. Diagnosis can be confirmed by serologic tests.

Papulosquamous Disorders

Diaper Dermatitis (Irritant Dermatitis)

Most commonform of diaper rash is irritant dermatitis, which occurs when skin comesinto direct contact with an irritant.

Erythematous plaques with minimal scaleoccur in diaper area, sparing the creases.

Common causes of irritant dermatitisbesides urine and stool are detergents, perfumed baby lotions andoils, and harsh soaps.

Atopic Dermatitis

Usuallyoccurs at 1–4 mos of age with dry, itchy, scaly rash. Before2 yrs of age, commonly occurs on cheeks, trunk, and extensor surfacesof elbows and knees. Later in childhood, flexural areas, includingantecubital and popliteal fossae, and neck are affected. Diaperarea characteristically is spared. Excoriation with secondary staphylococcalinfection is common. Atopic dermatitis also can produce scalingof scalp.

There is often personal or family historyof allergic rhinitis, hay fever, or asthma.

Nummular Eczematous Dermatitis

Characterized by scaly, symmetric, coin-shapedlesions, which usually occur on extremities and are 1–10cm in diameter.

Juvenile Plantar Dermatosis (Foot Eczema)

Dryness, redness, cracking, and scaling ofweight-bearing surface of foot characterizes juvenile planter dermatosis.Common in childhood and represents a form of atopic dermatitis.

Seborrheic Dermatitis (Infantile)

Rash is erythematous, dry, and scaly andoccurs in diaper area, in flexural areas, and behind ears. Greasy,yellow scales are seen on scalp (cradle cap).

Contact Dermatitis

May be producedby local exposure to irritating substance (irritant contact dermatitis) orby allergic response to sensitizing substance (allergic contactdermatitis).

Rash is erythematous and pruritic andmay consist of macules, papules, and vesicles.

Common causes of irritant dermatitisinclude detergents, harsh soaps, and rough sheets or clothes. Allergicdermatitis is seen with exposure to poison ivy, oak, and sumac aswell as nickel-containing jewelry.

Tinea Corporis

T. mentagrophytesis dermatophyte that most commonly causes tinea corporis, which canoccur anywhere on skin.

Lesions are round and reddish withraised, scaly, papular border and clearer center.

Diagnosis is usually clinical, butpositive KOH preparation or culture is confirmatory.

Tinea Pedis

Tinea pedis(athlete's foot) presents with dryness, redness, and crackingof skin between toes. Erythematous papules or vesicles on solesor scale around borders of foot in "moccasin" distributionalso may occur.

More common in adolescence but canoccur at all ages.

Diagnosis is usually clinical.

Candidiasis

C. albicansproduces intensely red, confluent rash in diaper area that may beaccompanied by scaly, erythematous papules and pustules. May producesimilar lesions in neck, axilla, and gluteal folds.

Diagnosis is usually clinical. PositiveKOH preparation or fungal culture is confirmatory.

Sunburn

Produces painful erythema, which may be followedby blistering and desquamation.

Pityriasis Rosea

Cause isnow thought to be human herpesvirus 7.

Usually presents with annular, scaly,erythematous lesion (herald patch). In 1–2 wks, oval, papular,scaly lesions appear and follow lines of skin cleavage on back,chest, and abdomen. Rash usually resolves within 1–3 mos.Pruritus is variable finding.

Drug Eruptions

Certain drugs (e.g., penicillins, sulfonamides,barbiturates, and phenytoin) may be associated with exfoliativedermatitis. Diffuse erythema is followed by bullae and loss of largesheets of epidermis.

Scabies

Human miteS. scabiei produces papular, pustular, and vesicular pruritic lesionsthat can occur anywhere on body.

Hallmark lesion is linear tract orburrow that is a few millimeters long, with central black dot (themite). However, burrows may not be found because of frequent itchingand scratching. Generalized urticarial or "id" reactionmay develop occasionally.

Microscopic visualization of mites,eggs, or fecal pellets from skin scraping confirms diagnosis.

Polymorphous Light Eruption

Patchy dermatitis that usually occurs onface and extremities on exposure to sun in spring or early summer.Papules and vesicles may occur with crusting.

Psoriasis

Familialdisorder of unknown cause in which red, well-demarcated plaqueswith silvery scales commonly occur on elbows, knees, and scalp;around eyebrows; and in genital region. Nail changes include pitting,thickening, and crumbling.

Streptococcal infection often precedesflare of psoriasis.

Skin biopsy is diagnostic.

Parapsoriasis

This disorderof unknown cause has 2 distinct forms: childhood acute parapsoriasis [pityriasislichenoides et varioliformis acuta (PLEVA)] and guttateparapsoriasis (pityriasis lichenoides chronica).

Onset of both forms is usually 5–15yrs of age. In acute parapsoriasis, erythematous papules with scale,2–4 mm in diameter, occur mainly on trunk. They crust overand heal with scars. Eruption may last for several months with lesionsin different stages. In guttate parapsoriasis, salmon-colored papules withcentral thin scales occur primarily on trunk, thighs, and perinealarea. These lesions may persist for several years. Itching seldomoccurs with either form.

Skin biopsy is diagnostic.

Lichen Nitidus

Groups of pinpoint, shiny, flesh-coloredor hypopigmented papules in linear array are most often seen onabdomen, trunk, or forearm. Köbner's phenomena(rash found in areas of skin trauma) may be seen.

Lichen Striatus

This benign disorder is composed of flat-toppedpapules arranged in linear fashion along lines of Blaschko. Papulesare first red and scaly and become flesh-colored in whites and hypopigmentedin African-Americans.

Lichen Planus

Disorderof unknown cause characterized by flat-topped, shiny, blue-red orpurple, intensely pruritic, polygonal papules, which commonly occuron volar surfaces of wrists and forearms, knees and lower legs,and shaft of the penis. Surface of papules may have white cross-hatchingcalled Wickham striae. Nails are often pitted and dystrophic.

Resolution usually occurs in 9–18mos, leaving areas of hyperpigmentation where lesions had been.

Lupus Erythematosus

More commonin girls than boys and can be systemic or limited to skin.

Most common skin manifestation is erythematousmacular rash over cheeks and nose in butterfly distribution andcovered by fine scale. Next most common lesion consists of discoid,scaly, red macules, which commonly occur on face, hands, and scalp.

Positive antinuclear antibody is screeningtest for this disease. Presence of antibody against double-strandedDNA is diagnostic. In most cases, direct immunofluorescence of skinbiopsy is positive for granular deposits of IgG or C3 at dermal-epidermaljunction.

Dermatomyositis

Erythematous plaques with fine scale areusually seen over elbows and knees. Flat-topped red papules alsomay be seen over knuckles (Gottron papules). Violaceous hue of eyelids,periorbital edema, and photosensitive facial rash involving malarareas also may occur (see Chap.33, Hypotonia and Weakness).

Langerhans Cell Histiocytosis

Skin findingsconsist of crusting, scaling dermatitis that may involve scalp,perineum, and axillae. Presence of purpuric papules or nodules withinor peripheral to dermatitis is characteristic. In dark-skinned children,papules may be hypopigmented.

Skin biopsy is diagnostic.

See Chap.38, Lymphadenopathy.

Acrodermatitis Enteropathica

This autosomal-recessivedisorder is due to impaired zinc transport in intestine.

Characteristic features include bullousdermatitis with plaquelike scaly lesions, diarrhea, failure to thrive,and alopecia of scalp, eyebrows, and eyelashes.

Diagnosis is confirmed by low plasmazinc level.

HIV Infection

Dermatitis that mimics seborrheic dermatitismay be seen with HIV (see Chap.53, Recurrent Infection).

Secondary Syphilis

Morbilliformrash of secondary syphilis occurs on any skin surface, especiallytrunk, palms, and soles. Pustules, nodules, and papulosquamous lesionsalso may occur. Clues to diagnosis are history of primary chancre,condyloma lata, or white mucous patches on tongue or buccal mucosa.Associated findings include generalized adenopathy, fatigue, headache,and fever.

Positive serologic tests (rapid plasmareagin and fluorescent treponemal antibody absorption tests) confirmdiagnosis.

Ichthyoses

Refers to excessive scaling of the skin ("fishskin"). Major types are

Ichthyosisvulgaris

X-linked ichthyosis

Classic lamellar ichthyosis and congenitalnonbullous ichthyosiform erythroderma

Congenital bullous ichthyosiform erythroderma(epidermolytic hyperkeratosis)

Ichthyosis Vulgaris

This autosomal-dominantdisorder is most common of the ichthyoses.

Onset is usually after 3 mos of agewith fine white scales that are often larger and coarser on lowerextremities. Abdomen, neck, and face are much less involved, andflexural areas and axillae are usually spared.

Skin biopsy shows hyperkeratosis anddecreased or absent granular layer but is usually unnecessary.

X-Linked Ichthyosis

This formof ichthyosis involves deficiency of steroid sulfatase, which hydrolyzes cholesterolsulfate and other sulfated steroids. Gene locus has been mappedto Xp22.3.

Presents in infancy with scales overextensor surfaces of extremities and upper trunk. Palms and solesare usually spared in contrast to other ichthyoses.

Diagnosis can be confirmed by moleculargenetic analysis.

Classic Lamellar Ichthyosis and Congenital Nonbullous IchthyosiformErythroderma

Both ofthese autosomal-recessive disorders usually present as collodionbabies.

Infants with lamellar ichthyosis havelarger platelike scales, whereas those with nonbullous ichthyosiformerythroderma have increased erythroderma with finer whiter scales.

There is evidence that mutations ingene encoding keratinocyte transglutaminase located on chromosome14q11.2 are responsible for these disorders.

Congenital Bullous Ichthyosiform Erythroderma (EpidermolyticHyperkeratosis)

Onset ofthis autosomal-dominant disorder is usually at birth, with generalizederythroderma, scaling, and bulla formation. Hyperkeratosis, especiallyon arms and legs, begins later. Tendency toward blistering tendsto decrease with age.

Histopathologic pattern is diagnostic.

Mutations in keratin genes on chromosomes12q13 and 17q21-22 have been found in this disorder.

Diagnostic Approach

Classificationof skin lesions into 1 of the 9 types described above is helpfulin diagnosis. Knowledge of specific skin lesions, especially theirmorphology and distribution, is necessary for diagnosis. Age ofchild, mode of inheritance, whether child is well or ill, presenceof fever and other systemic symptoms, and nature of primary lesionhelp narrow diagnostic possibilities. In most cases, history andphysical exam are diagnostic.

Most important tests to confirm someof disorders discussed above include the KOH preparation; bacterial,viral, and fungal cultures; PCR; and skin biopsy, including immunepathology and electron microscopy, if necessary.

References

1. Drago F, et al. Human herpesvirus 7 inpityriasis rosea. Lancet 1997;349:1367–1368.
2. Feigin RD, Cherry JD, eds. Textbook of pediatric infectiousdiseases, 4th ed. Philadelphia: WB Saunders, 1998.
3. Fine JD, et al. Revised classification system for inheritedepidermolysis bullosa: Report of the Second International ConsensusMeeting on Diagnosis and Classification of Epidermolysis Bullosa.J Am Acad Dermatol 2000;42:1051–1066.
4. Fleisher GR, Ludwig S, eds. Textbook of pediatric emergencymedicine, 4th ed. Philadelphia: Lippincott Williams & Wilkins,2000.
5. Harper J, et al., eds. Textbook of pediatric dermatology.Oxford: Blackwell Science, 2000.
6. Hurwitz S. Clinical pediatric dermatology, 2nd ed.Philadelphia: WB Saunders, 1993.
7. Long SS, et al., eds. Principles and practice of pediatricinfectious diseases. New York: Churchill Livingstone, 1997.
8. Lynch PJ. Dermatology for the house officer, 3rd ed.Baltimore: Williams & Wilkins, 1994.
9. McGuire J. The biologic basis of the ichthyoses. DermatolClin 1986;4:67–78.
10. Online Mendelian Inheritance in Man (OMIM). McKusick-NathansInstitute for Genetic Medicine, Johns Hopkins University (Baltimore,MD) and National Center for Biotechnology Information, NationalLibrary of Medicine (Bethesda, MD), 2000. World Wide Web URL: http://www.ncbi.nlm.nih.gov/omim.
11. Paller AS. Laboratory tests for ichthyosis. DermatolClin 1994;12:99–107.
12. Pickering LK, ed. 2000 Red book: report of the Committeeon Infectious Diseases, 25th ed. Elk Grove Village, IL: AmericanAcademy of Pediatrics, 2000.
13. Rudolph AM, ed. Rudolph's Pediatrics, 20thed. Stamford, CT: Appleton & Lange, 1996.
14. Schachner LA, Hansen RC, eds. Pediatric dermatology,2nd ed. New York: Churchill Livingstone, 1995.
15. Weston WL, et al. Color textbook of pediatric dermatology,2nd ed. St. Louis: Mosby-Year Book, 1996.
16. Williams ML. The ichthyoses—pathogenesis andprenatal diagnosis: a review of recent advances. Pediatr Dermatol1983;1:1–24.

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Book Source Details

• Book Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
• Author(s): Paul S. Bellet
• Year of Publication: 2006
• Copyright Details: The Diagnostic Approach to Symptoms and Signs in Pediatrics, Copyright © 2006 Lippincott Williams & Wilkins.

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