Medical School · Year 3 · Pediatrics · includes a quiz and discussion video

Seminar 13: Pediatric Dermatology

Unit 3: Pediatrics Clerkship

Learning Objectives

1. Recognize and differentiate benign transient neonatal skin findings from conditions requiring evaluation or treatment
2. Diagnose atopic dermatitis using clinical criteria and develop age-appropriate treatment plans emphasizing skin barrier restoration
3. Identify common viral, bacterial, and fungal skin infections in children and select appropriate antimicrobial therapy
4. Recognize parasitic infestations including scabies and pediculosis and apply treatment to patients and close contacts
5. Evaluate urticaria and drug reactions including recognition of life-threatening Stevens-Johnson syndrome and toxic epidermal necrolysis
6. Identify cutaneous manifestations of systemic diseases including Henoch-Schonlein purpura, Kawasaki disease, and dermatomyositis

Lecture Outline

Section 1: Neonatal Skin Findings

The newborn skin examination reveals a variety of findings that may concern parents but represent normal transient phenomena requiring only reassurance. Understanding the appearance, natural history, and distinguishing features of these benign conditions allows clinicians to provide confident counseling while maintaining vigilance for conditions requiring evaluation. The neonatal skin differs from older children in several important ways including increased permeability, immature thermoregulation, and susceptibility to specific conditions that resolve spontaneously within the first weeks to months of life.

Benign transient neonatal skin eruptions occur commonly and resolve without intervention. Erythema toxicum neonatorum affects approximately half of term newborns, presenting between twenty-four and seventy-two hours of life with erythematous macules and papules that may have central pustules, distributed over the trunk and proximal extremities while sparing the palms and soles. The pustules contain eosinophils on Wright stain, distinguishing this condition from infectious causes containing neutrophils and bacteria. Milia appear as small white or yellow papules on the face, particularly the nose and cheeks, representing keratin-filled epidermal cysts that resolve spontaneously within weeks. Miliaria results from eccrine sweat duct obstruction and presents in several forms depending on the level of obstruction, with miliaria crystallina showing superficial clear vesicles and miliaria rubra presenting as erythematous papules in areas of occlusion or heat exposure. Sebaceous hyperplasia manifests as tiny yellow papules over the nose resulting from maternal androgen stimulation and resolves within the first few weeks. Neonatal acne develops at two to four weeks of age with inflammatory papules and pustules on the face, attributed to maternal androgen stimulation, and resolves spontaneously by three to four months without treatment.

Birthmarks constitute another category of neonatal skin findings with varying natural histories and significance. Mongolian spots appear as blue-gray patches most commonly over the lumbosacral area in infants with darker skin pigmentation, representing dermal melanocytosis that typically fades by early childhood and requires no treatment though documentation prevents misinterpretation as bruising. Salmon patches, also called nevus simplex, present as pink patches on the nape of the neck, forehead, glabella, or eyelids, representing dilated capillaries that fade over the first one to two years on the face but may persist on the nape. Infantile hemangiomas are not present at birth but appear within the first two to four weeks of life as proliferating vascular tumors that grow during the first several months before gradually involuting over years. Port-wine stains are present at birth as flat pink to red patches that do not fade and may darken over time, representing malformed capillaries rather than tumors. Cafe-au-lait macules appear as uniformly tan patches that persist throughout life, with clinical significance when multiple lesions are present suggesting neurofibromatosis or other syndromes.

Certain neonatal skin findings require prompt evaluation to exclude serious underlying conditions. Pustules and vesicles in neonates should raise concern for herpes simplex virus infection or bacterial sepsis until proven otherwise, particularly when accompanied by systemic symptoms. Grouped vesicles or erosions suggest herpes and require immediate viral testing and empiric acyclovir therapy pending results. Petechiae and purpura may indicate sepsis, coagulopathy, or congenital infection and warrant urgent evaluation. Collodion membrane, a tight shiny covering encasing the newborn, indicates ichthyosis and requires specialized skin care and monitoring for complications. Midline lesions over the spine including dimples, tufts of hair, or skin tags may indicate underlying spinal dysraphism and warrant imaging evaluation. Large segmental hemangiomas, particularly on the face, raise concern for PHACE syndrome with associated structural abnormalities requiring comprehensive evaluation. Multiple cafe-au-lait spots exceeding five in number warrant evaluation for neurofibromatosis type 1. Port-wine stains in the V1 distribution should prompt evaluation for Sturge-Weber syndrome with associated brain and eye involvement.

<image>Panel A: Clinical photograph comparing erythema toxicum neonatorum with scattered erythematous macules and central pustules to the vesicles of neonatal herpes simplex requiring emergent evaluation. Panel B: Series of images showing natural history of infantile hemangioma from early proliferative phase through complete involution at school age. Panel C: Comparison of benign Mongolian spot over sacrum versus concerning petechial rash requiring sepsis evaluation. Panel D: Infant with midline lumbosacral dimple and hair tuft requiring spine imaging to evaluate for occult spinal dysraphism.</image>

Section 2: Atopic Dermatitis

Atopic dermatitis represents the most common chronic inflammatory skin condition in children, affecting approximately fifteen to twenty percent of children in developed countries with onset typically in the first year of life. This condition profoundly impacts quality of life for affected children and families through intense pruritus that disrupts sleep, activity limitations, and the psychological burden of visible skin disease. Understanding the pathophysiology, diagnostic criteria, and stepwise management approach allows clinicians to effectively control symptoms, reduce flares, and minimize complications.

The diagnosis of atopic dermatitis relies on clinical criteria including the essential features of pruritus and chronic or relapsing eczematous dermatitis with typical morphology and age-specific distribution. Pruritus is the hallmark symptom, often described as the itch that rashes, as scratching exacerbates and perpetuates the dermatitis. The eczematous changes include erythema, papules, vesicles, and weeping in acute phases, progressing to scaling, lichenification, and excoriations in chronic disease. Distribution varies characteristically by age, providing important diagnostic clues. Additional features supporting the diagnosis include early age of onset, personal or family history of atopic conditions including asthma and allergic rhinitis, xerosis, and immunoglobulin E reactivity, though none of these features is required for diagnosis.

The distribution of atopic dermatitis changes characteristically as children age, reflecting differences in skin vulnerability and scratching behavior. In infancy, the face and scalp are prominently involved, with erythematous patches and papules on the cheeks sparing the nasal tip and perioral region, often accompanied by involvement of extensor surfaces of the extremities where crawling infants experience friction. During childhood, the classic flexural distribution emerges with involvement of the antecubital and popliteal fossae, wrists, ankles, and neck representing areas where sweating, friction, and scratching perpetuate disease. Adolescents and adults continue to show flexural predominance with additional involvement of the hands, face, and eyelids. Acute flares manifest with erythema, vesiculation, and weeping, while chronic disease produces thickened, lichenified plaques from persistent scratching. Secondary bacterial infection with Staphylococcus aureus complicates atopic dermatitis frequently, presenting as increased weeping, crusting, or pustules, while herpes simplex virus superinfection produces eczema herpeticum, a dermatologic emergency characterized by monomorphic punched-out erosions requiring systemic antiviral therapy.

Management of atopic dermatitis employs a stepwise approach beginning with foundation therapy applicable to all patients regardless of severity. Skin barrier restoration through liberal and frequent application of thick emollients forms the cornerstone of management, recommended immediately after bathing and multiple times daily. Bathing practices should include lukewarm water, limited soap use, and immediate post-bath moisturizer application to trap water in the stratum corneum. Trigger identification and avoidance address exacerbating factors including irritants such as fragrances and harsh soaps, allergens when identified through history or testing, heat, sweating, and stress. Topical corticosteroids represent first-line anti-inflammatory therapy, with potency selected based on location and severity: low-potency preparations for the face and intertriginous areas, medium-potency for the body, and higher potency reserved for lichenified or refractory areas under supervision. Topical calcineurin inhibitors including tacrolimus and pimecrolimus provide steroid-sparing options particularly useful for sensitive areas. Antihistamines may provide symptomatic relief and sedation to improve sleep but do not reduce inflammation. Wet wrap therapy, applying damp dressings over emollients and topical medications, provides intensive treatment for severe flares. Systemic therapy with immunosuppressants or biologics such as dupilumab is reserved for severe disease refractory to topical management.

<image>Panel A: Series of photographs showing age-specific distribution of atopic dermatitis with infant facial involvement, childhood flexural dermatitis, and adolescent hand eczema. Panel B: Comparison of acute atopic dermatitis with erythema and vesiculation versus chronic lichenified plaques from persistent scratching. Panel C: Clinical photograph of eczema herpeticum showing punched-out erosions requiring emergent antiviral therapy. Panel D: Demonstration of wet wrap therapy application technique with inner damp layer and outer dry layer over topical medications.</image>

Section 3: Other Eczematous Conditions

Several other eczematous conditions affect children and must be distinguished from atopic dermatitis to guide appropriate management. These conditions share features of erythema, scaling, and pruritus but differ in distribution, natural history, and treatment approach. Recognition of the characteristic presentations allows accurate diagnosis and targeted therapy.

Seborrheic dermatitis presents a common eczematous condition with bimodal distribution affecting infants and adolescents through distinct mechanisms. Infantile seborrheic dermatitis, commonly called cradle cap, typically presents in the first few months of life with greasy, yellowish scales on the scalp that may extend to involve the face, retroauricular area, and intertriginous zones including the diaper area. Unlike atopic dermatitis, seborrheic dermatitis is typically non-pruritic and does not disturb the infant. The condition responds well to gentle scale removal with mineral oil and soft brushing, followed by antifungal shampoo or low-potency topical corticosteroids for persistent cases. Infantile seborrheic dermatitis resolves spontaneously by age one in most cases. Adolescent seborrheic dermatitis presents with erythema and greasy scales in seborrheic areas including the scalp, nasolabial folds, and eyebrows, persisting indefinitely with waxing and waning course. Management includes antifungal shampoos containing ketoconazole or selenium sulfide and low-potency topical corticosteroids for facial involvement.

Contact dermatitis results from skin reaction to external substances and presents in two distinct forms with different pathophysiology. Irritant contact dermatitis represents direct damage to the skin from chemicals, moisture, or friction without immune mechanism, accounting for the majority of contact dermatitis in children. Diaper dermatitis exemplifies irritant contact dermatitis, with erythema and erosions in convex areas exposed to urine and stool while creases are relatively spared. Drool dermatitis affects the chin and perioral area in teething infants. Management focuses on barrier protection and removal of the irritant. Allergic contact dermatitis involves a delayed-type hypersensitivity reaction to specific allergens and presents with erythema, vesicles, and pruritus distributed in the pattern of exposure. Common allergens in children include nickel from jewelry and belt buckles, poison ivy and related plants containing urushiol, topical antibiotics such as neomycin, and rubber chemicals. Patch testing identifies specific allergens when the clinical history is unclear. Treatment involves allergen avoidance and topical corticosteroids for active dermatitis.

Diaper dermatitis represents one of the most common skin conditions in infancy and requires differentiation of subtypes to guide appropriate management. Irritant diaper dermatitis affects convex surfaces in contact with the diaper while sparing creases, resulting from prolonged exposure to moisture, urine, and fecal enzymes that compromise skin barrier function. Management emphasizes frequent diaper changes, thorough gentle cleansing, and barrier cream application with zinc oxide or petrolatum-based products. Candidal diaper dermatitis involves secondary yeast infection, presenting with bright red erythema extending into skin creases with characteristic satellite papules and pustules beyond the main border. Topical antifungal therapy with nystatin or clotrimazole effectively treats candidal superinfection and should be applied before barrier cream. Seborrheic diaper dermatitis appears as salmon-colored patches with greasy scale in the diaper area, often accompanying scalp involvement. Nummular dermatitis presents as coin-shaped eczematous plaques on the extremities and trunk, typically related to dry skin and irritation, and responds to emollients and topical corticosteroids.

<image>Panel A: Infant with classic cradle cap showing thick yellowish greasy scale on the scalp with mild extension to the forehead and eyebrows. Panel B: Diaper area comparison showing irritant dermatitis with spared creases versus candidal dermatitis with involved creases and satellite lesions. Panel C: Allergic contact dermatitis to nickel showing geometric pattern corresponding to belt buckle exposure with erythema and vesiculation. Panel D: Nummular dermatitis with multiple coin-shaped scaly plaques on the lower extremities in a child with dry skin.</image>

Section 4: Viral Skin Infections

Viral infections produce diverse cutaneous manifestations in children ranging from classic exanthems associated with specific pathogens to more nonspecific morbilliform rashes accompanying systemic illness. Recognition of characteristic patterns allows accurate diagnosis, appropriate management, and counseling regarding contagion and complications.

The classic viral exanthems represent childhood infections producing characteristic skin findings that often allow clinical diagnosis. Measles produces a morbilliform erythematous rash beginning on the face and spreading cephalocaudally over three to four days, accompanied by high fever, cough, coryza, conjunctivitis, and pathognomonic Koplik spots on the buccal mucosa. Rubella presents with pink macular rash spreading similarly from face downward but with milder systemic symptoms and prominent posterior cervical and suboccipital lymphadenopathy. Roseola infantum, caused by human herpesvirus 6, produces a distinctive pattern of high fever for three to four days that resolves abruptly as a pink macular rash appears on the trunk, often providing relief to parents concerned about the prolonged fever. Erythema infectiosum, caused by parvovirus B19, presents with bright red slapped cheek erythema followed by a lacy reticular rash on the trunk and extremities; the rash may wax and wane over weeks with heat or sun exposure. Hand-foot-and-mouth disease, caused by coxsackieviruses, produces painful vesicles on the hands, feet, and oral mucosa, sometimes with more widespread vesicular eruption.

Varicella, caused by varicella-zoster virus, produces one of the most distinctive viral exanthems with important implications for isolation and treatment. The rash progresses through stages from erythematous macules to papules to vesicles described as dew drops on a rose petal to crusted lesions. A hallmark feature is the presence of lesions at all stages simultaneously due to successive crops appearing over several days. Distribution is centripetal, with greater concentration on the trunk than extremities, and involvement of the scalp and mucous membranes commonly occurs. Fever and malaise accompany the eruption. Complications include secondary bacterial skin infection, pneumonia (particularly in adolescents and adults), cerebellar ataxia, and encephalitis. Treatment is supportive for healthy children, with antihistamines and cool baths for pruritus and attention to preventing secondary infection through nail trimming and hygiene. Oral acyclovir is indicated for adolescents, adults, immunocompromised patients, and those with severe disease or complications.

Herpes simplex virus infections present in several distinct clinical patterns depending on the site of infection and the patient's immune status. Primary herpes gingivostomatitis typically affects young children, presenting with high fever, irritability, refusal to eat, and painful vesicles and ulcerations on the gingiva, tongue, and lips accompanied by cervical lymphadenopathy. The illness is self-limited but causes significant morbidity; dehydration may require hospitalization, and oral acyclovir can reduce duration and severity if initiated early. Recurrent herpes labialis presents as clustered vesicles on an erythematous base at the vermilion border, preceded by tingling or burning, and resolves over one to two weeks. Herpetic whitlow involves painful vesicular infection of the finger, often from autoinoculation. Eczema herpeticum represents disseminated herpes simplex infection in patients with atopic dermatitis, presenting with monomorphic punched-out erosions that may become widespread and require intravenous acyclovir. Molluscum contagiosum, caused by a poxvirus, produces characteristic flesh-colored umbilicated papules that spread by autoinoculation and resolve spontaneously over months to years, though treatment with curettage or cryotherapy may be requested for cosmetic reasons or to reduce spread.

<image>Panel A: Clinical photographs comparing classic viral exanthems including measles with morbilliform rash and Koplik spots, slapped cheek appearance of erythema infectiosum, and vesicles on hands in hand-foot-mouth disease. Panel B: Varicella rash demonstrating lesions at multiple stages of development with characteristic dew drops on rose petals vesicles. Panel C: Primary herpes gingivostomatitis showing extensive painful ulcerations on gingiva and lips with associated fever in young child. Panel D: Close-up of molluscum contagiosum showing flesh-colored papules with central umbilication characteristic of poxvirus infection.</image>

Section 5: Bacterial Skin Infections

Bacterial skin infections represent common reasons for pediatric visits and range from superficial localized disease to serious conditions requiring hospitalization. Understanding the clinical presentations, causative organisms, and appropriate antibiotic selection enables effective management while avoiding unnecessary broad-spectrum therapy.

Impetigo represents the most common bacterial skin infection in children and presents in two distinct forms based on the clinical appearance and causative organisms. Non-bullous impetigo begins as small vesicles or pustules that rupture and form characteristic honey-colored crusted lesions, typically on the face around the nose and mouth or at sites of minor skin trauma. Staphylococcus aureus and Streptococcus pyogenes cause non-bullous impetigo either alone or together. Bullous impetigo results from exfoliative toxin production by Staphylococcus aureus, producing flaccid bullae that rupture leaving shallow erosions with collarette scale. The lesions are typically not painful but may be mildly pruritic. Treatment for localized impetigo consists of topical mupirocin applied three times daily for five to seven days after gentle removal of crusts. Extensive impetigo, involvement of multiple sites, or systemic symptoms warrants oral antibiotic therapy with an agent providing staphylococcal and streptococcal coverage such as cephalexin or, in areas with high methicillin-resistant Staphylococcus aureus prevalence, clindamycin or trimethoprim-sulfamethoxazole.

Cellulitis represents bacterial infection of the deep dermis and subcutaneous tissue, presenting with expanding erythema, warmth, swelling, and tenderness without clear borders. Staphylococcus aureus and Streptococcus pyogenes are the most common causative organisms. Periorbital cellulitis, involving the eyelid and periorbital soft tissues anterior to the orbital septum, must be distinguished from orbital cellulitis which extends posterior to the septum. Periorbital cellulitis presents with eyelid swelling and erythema without proptosis, limitation of extraocular movements, or pain with eye movement, and typically responds to oral antibiotics. Orbital cellulitis represents a serious infection with risk of intracranial extension and presents with proptosis, painful or limited extraocular movements, and vision changes, requiring hospitalization, intravenous antibiotics, and often surgical drainage. Facial cellulitis in young children may result from Haemophilus influenzae type b in unimmunized children, presenting with characteristic violaceous discoloration, and has become rare with widespread vaccination.

Staphylococcal scalded skin syndrome represents a toxin-mediated condition distinct from cellulitis, in which staphylococcal exfoliative toxins cause widespread erythroderma and superficial desquamation. The condition primarily affects children younger than five years whose immature kidneys cannot clear the circulating toxin. Clinical presentation begins with fever, irritability, and tender erythema often in a perioral distribution, progressing to widespread erythroderma with subsequent superficial desquamation leaving a glistening denuded surface. The Nikolsky sign, in which lateral pressure causes skin slippage, is positive. Treatment requires hospitalization, intravenous antistaphylococcal antibiotics, fluid and electrolyte management, and skin care similar to burn management. Community-acquired methicillin-resistant Staphylococcus aureus has become increasingly common and often presents as skin abscesses mimicking spider bites in the patient's description. Management of abscesses centers on incision and drainage, which may be curative alone for uncomplicated abscesses. Antibiotics are added for surrounding cellulitis, large abscesses, systemic symptoms, or immunocompromise, with agents such as trimethoprim-sulfamethoxazole or clindamycin providing MRSA coverage. Decolonization with mupirocin to the nares and chlorhexidine washes may reduce recurrence in patients with recurrent MRSA infections.

<image>Panel A: Non-bullous impetigo on the face showing honey-colored crusted lesions around the nose and mouth typical of streptococcal or staphylococcal infection. Panel B: Bullous impetigo demonstrating flaccid blisters and shallow erosions from staphylococcal exfoliative toxin. Panel C: Child with staphylococcal scalded skin syndrome showing widespread erythema, perioral fissuring, and superficial desquamation with positive Nikolsky sign. Panel D: Comparison of periorbital cellulitis with lid swelling but normal eye versus orbital cellulitis with proptosis and limited extraocular movement requiring emergent intervention.</image>

Section 6: Fungal Infections

Fungal infections commonly affect pediatric skin, hair, and nails, caused primarily by dermatophytes and Candida species. Recognition of clinical patterns and appropriate diagnostic testing guides selection between topical and systemic antifungal therapy.

Dermatophyte infections, commonly called tinea, affect different body sites with characteristic presentations. Tinea corporis presents as annular erythematous plaques with raised scaly borders and central clearing on the trunk and extremities, spreading centrifugally as the fungus advances outward. The advancing border is often more scaly and may contain papules or vesicles. Diagnosis is clinical in typical cases but can be confirmed with potassium hydroxide preparation showing branching hyphae on microscopy. Topical antifungal therapy with terbinafine, clotrimazole, or miconazole applied twice daily for two to four weeks effectively treats limited tinea corporis. Extensive disease, failure of topical therapy, or involvement of hair-bearing areas requires systemic treatment.

Tinea capitis represents dermatophyte infection of the scalp and hair follicles and is the most common fungal infection in children, particularly affecting those with tightly curled hair. Clinical presentation includes scaling patches of alopecia with broken hairs appearing as black dots where hairs have fractured at the follicular opening. Posterior cervical lymphadenopathy commonly accompanies infection. Kerion represents an intense inflammatory response to dermatophyte infection, presenting as a boggy, tender, purulent-appearing nodule that may be mistaken for bacterial abscess; importantly, kerion requires antifungal therapy rather than incision and drainage, and oral corticosteroids may reduce scarring alopecia. Diagnosis of tinea capitis is confirmed by fungal culture, which also identifies the species and guides treatment duration. Topical therapy alone is ineffective for tinea capitis because the fungus resides within the hair follicle beyond topical penetration. Oral griseofulvin has been the traditional treatment, requiring six to eight weeks of therapy with fatty food to enhance absorption. Terbinafine provides shorter treatment duration and is increasingly used. Selenium sulfide or ketoconazole shampoo as adjunctive therapy reduces spore shedding and transmission.

Tinea pedis, or athlete's foot, uncommonly affects prepubertal children but becomes increasingly common in adolescents. The interdigital form presents with maceration, scaling, and fissuring between toes, while the moccasin type produces diffuse plantar scaling. Topical antifungals effectively treat most cases. Candidiasis results from overgrowth of Candida species, normally present on skin and mucous membranes, under conditions of moisture, occlusion, or antibiotic exposure. Oral thrush presents as white plaques on the buccal mucosa and tongue in infants that cannot be wiped away, in contrast to milk residue. Treatment with oral nystatin suspension is typically effective. Candidal diaper dermatitis presents with beefy red erythema involving skin creases with satellite papules and pustules. Intertrigo in other skin folds similarly shows erythema with satellite lesions. Topical nystatin or azole antifungals effectively treat cutaneous candidiasis, applied before barrier cream in the diaper area.

<image>Panel A: Classic tinea corporis demonstrating annular plaque with raised erythematous scaly border and central clearing on the arm. Panel B: Tinea capitis showing patchy alopecia with scale and broken hairs appearing as black dots, with posterior cervical lymphadenopathy visible. Panel C: Potassium hydroxide preparation under microscopy showing branching septate hyphae diagnostic of dermatophyte infection. Panel D: Oral thrush in infant showing white plaques on buccal mucosa and tongue compared with candidal diaper dermatitis with satellite lesions.</image>

Section 7: Parasitic Infestations

Parasitic infestations of the skin cause significant morbidity through intense pruritus and secondary complications while creating social stigma and concern about household hygiene. Understanding the clinical presentations, diagnostic approaches, and treatment protocols for both patients and contacts ensures effective eradication and prevents reinfestation.

Scabies results from infestation with the mite Sarcoptes scabiei, which burrows into the stratum corneum where the female deposits eggs. The clinical presentation results from hypersensitivity reaction to mite proteins, typically developing four to six weeks after initial infestation but occurring within days upon reinfestation. Intense pruritus, characteristically worse at night, represents the hallmark symptom. The distribution differs between infants and older children. In infants and young children, the head, face, palms, and soles may be involved in addition to the interdigital web spaces, wrists, axillae, waistband, and genital areas affected in older children and adults. Primary lesions include burrows appearing as short wavy lines, papules, and vesicles, but the intense scratching usually obscures primary lesions with excoriations, eczematization, and secondary impetiginization. Diagnosis is clinical in typical cases but can be confirmed by skin scraping demonstrating mites, eggs, or fecal pellets under microscopy.

Treatment of scabies requires application of a scabicide to all skin from the neck down in older children or including the scalp, face, and behind ears in infants. Permethrin five percent cream represents first-line therapy, applied at bedtime and washed off after eight to fourteen hours, with repeat application one week later to treat newly hatched mites. All household members and close contacts must be treated simultaneously regardless of symptoms, as individuals may harbor mites during the asymptomatic incubation period. Environmental measures include machine washing and drying bedding, clothing, and towels used in the preceding three days on hot cycles, with items that cannot be washed sealed in plastic bags for seventy-two hours. Pruritus often persists for two to four weeks after successful treatment due to continued allergic reaction to mite proteins, and topical corticosteroids may provide relief during this period. Treatment failure or resistance may respond to oral ivermectin.

Pediculosis, or lice infestation, affects the head, body, or pubic area depending on the species involved. Head lice affect primarily school-age children regardless of hygiene or socioeconomic status, transmitted through direct head-to-head contact and less commonly through shared personal items. Clinical presentation includes pruritus of the scalp, particularly the occipital and retroauricular areas, with visible nits cemented to hair shafts near the scalp. Nits within one centimeter of the scalp suggest active infestation. Diagnosis requires identification of live lice or viable nits. Treatment options include permethrin one percent lotion applied for ten minutes then rinsed, with repeat application in seven to ten days. Resistance to permethrin has increased, and malathion, spinosad, or oral ivermectin may be needed for resistant cases. Wet combing to remove nits aids treatment success. Insect bites from fleas, mosquitoes, bedbugs, and other arthropods produce pruritic papules that may become widespread and persistent in sensitized individuals, a condition termed papular urticaria. The distribution provides clues to the source: flea bites predominate on the lower legs, bedbug bites appear in linear groups described as breakfast, lunch, and dinner, and mosquito bites affect exposed areas. Treatment is symptomatic with antihistamines and topical corticosteroids while environmental measures address the source.

<image>Panel A: Distribution diagram showing typical scabies involvement in infants including head and palms versus classic web space and flexural distribution in older children. Panel B: Dermoscopy image showing scabies mite at end of burrow with characteristic triangular head and delta wing sign. Panel C: Hair shaft with attached nit cemented near the scalp demonstrating viable louse egg requiring treatment. Panel D: Linear pattern of bedbug bites in breakfast, lunch, and dinner arrangement on child's arm with urticarial papules.</image>

Section 8: Urticaria and Drug Reactions

Urticaria and adverse drug reactions encompass a spectrum from common self-limited conditions to life-threatening emergencies requiring immediate intervention. Recognition of clinical patterns guides appropriate evaluation, treatment, and counseling regarding future medication use.

Urticaria presents as pruritic erythematous wheals that blanch with pressure and characteristically migrate and resolve within twenty-four hours, distinguishing them from the fixed lesions of vasculitis or other conditions. Classification by duration divides urticaria into acute, lasting less than six weeks, and chronic, persisting longer than six weeks. Acute urticaria in children most commonly results from viral infections or may accompany allergic reactions to foods, medications, or insect stings. Identification of specific triggers proves difficult in many cases, and extensive allergy testing is not routinely indicated for acute urticaria. Chronic urticaria rarely reflects ongoing allergen exposure and more often represents chronic spontaneous urticaria driven by autoimmune mechanisms. Treatment of urticaria centers on second-generation antihistamines such as cetirizine, loratadine, or fexofenadine, which may be uptitrated to two to four times standard dosing for refractory chronic urticaria. First-generation antihistamines such as diphenhydramine provide additional benefit through sedation for nighttime dosing.

Anaphylaxis represents a severe systemic allergic reaction with potential for rapid progression to cardiovascular collapse and death, requiring immediate recognition and treatment. Diagnostic criteria require involvement of two or more organ systems including skin manifestations such as urticaria or angioedema, respiratory symptoms such as dyspnea or wheezing, cardiovascular symptoms such as hypotension or syncope, and gastrointestinal symptoms such as vomiting or abdominal pain. Common triggers in children include foods, particularly peanuts, tree nuts, milk, and eggs, medications, and insect stings. Treatment begins with intramuscular epinephrine at the anterolateral thigh, dosed at 0.01 mg/kg with maximum of 0.5 mg, repeated every five to fifteen minutes as needed. Adjunctive measures include positioning supine with legs elevated unless respiratory distress requires upright positioning, intravenous fluids for hypotension, albuterol for bronchospasm, and antihistamines and corticosteroids though these do not substitute for epinephrine. Discharge planning after anaphylaxis requires prescription of epinephrine auto-injectors with training on use, written action plan, and referral to allergist for evaluation.

Drug eruptions present with various morphologies, with morbilliform or maculopapular rash being most common. This appears as symmetrically distributed erythematous macules and papules, often beginning on the trunk and spreading to extremities, typically one to two weeks after starting a new medication. Most morbilliform drug eruptions resolve with medication discontinuation and supportive care. Stevens-Johnson syndrome and toxic epidermal necrolysis represent severe cutaneous adverse reactions characterized by mucosal erosions and epidermal necrosis requiring urgent recognition and management. Common culprits include sulfonamide antibiotics, anticonvulsants including phenytoin, carbamazepine, and lamotrigine, and allopurinol. Mycoplasma pneumoniae infection can trigger a similar presentation. Clinical features include prodromal fever and malaise followed by painful mucosal erosions of the mouth, eyes, and genitals, and targetoid or dusky macules that evolve to epidermal necrosis and detachment. Stevens-Johnson syndrome involves less than ten percent body surface area detachment, while toxic epidermal necrolysis exceeds thirty percent. Management requires immediate discontinuation of causative medication, transfer to burn unit or intensive care for supportive care of the denuded skin, and ophthalmology involvement for ocular surface protection.

<image>Panel A: Acute urticaria showing multiple erythematous wheals of varying sizes with characteristic blanching and irregular borders. Panel B: Patient experiencing anaphylaxis with urticaria, angioedema of lips, and respiratory distress requiring immediate epinephrine administration. Panel C: Stevens-Johnson syndrome with hemorrhagic crusting of lips, conjunctival injection, and early cutaneous involvement with targetoid lesions. Panel D: Toxic epidermal necrolysis demonstrating extensive epidermal detachment with positive Nikolsky sign and sheet-like skin sloughing.</image>

Section 9: Pigmentary Disorders

Pigmentary abnormalities in children cause significant cosmetic concern for patients and families and may indicate underlying systemic conditions when certain patterns are recognized. Understanding the common causes of hypo- and hyperpigmentation allows appropriate evaluation, treatment when available, and counseling regarding prognosis.

Vitiligo represents an autoimmune condition causing destruction of melanocytes and resultant depigmentation that affects approximately one percent of the population. The condition presents as sharply demarcated depigmented macules and patches that may occur anywhere but commonly involve the face, particularly perioral and periocular areas, dorsal hands, elbows, knees, and genitalia. Distribution may be generalized, segmental following a dermatomal pattern, or focal. The depigmented areas become particularly apparent with sun exposure as surrounding skin tans while affected areas remain white and may burn easily. Association with other autoimmune conditions, particularly thyroid disease, diabetes, and pernicious anemia, warrants screening with thyroid function tests and awareness of symptoms. Treatment options include topical corticosteroids and calcineurin inhibitors, which may promote repigmentation particularly for facial lesions and recent onset disease. Phototherapy with narrowband ultraviolet B also promotes repigmentation. Cosmetic camouflage provides an important option while awaiting treatment effect or for refractory disease. Sun protection prevents burning of depigmented areas and reduces contrast with surrounding skin.

Post-inflammatory pigmentary changes represent common sequelae of cutaneous inflammation or injury and disproportionately affect individuals with darker skin. Post-inflammatory hyperpigmentation presents as darkened patches at sites of prior inflammation such as acne, eczema, or insect bites, resulting from increased melanin deposition in the epidermis or dermis. The discoloration may persist for months to years but gradually fades without treatment. Post-inflammatory hypopigmentation similarly affects sites of prior inflammation but results in lightened patches from reduced melanin production by damaged melanocytes. Pityriasis alba represents a form of post-inflammatory hypopigmentation commonly seen in children with atopic dermatitis, presenting as ill-defined hypopigmented patches with fine scale, typically on the face. The condition is benign and self-limited, with emollients and mild topical corticosteroids promoting resolution. Albinism encompasses a group of genetic disorders affecting melanin synthesis, presenting with reduced pigmentation of skin, hair, and eyes accompanied by nystagmus, photophobia, and reduced visual acuity. Management focuses on sun protection and ophthalmologic care.

Cafe-au-lait macules deserve specific attention as potential markers of neurofibromatosis and other genetic syndromes. These uniformly tan macules with regular borders, described as coast of California, are present in up to twenty percent of the general population as isolated findings without clinical significance. The presence of six or more cafe-au-lait macules exceeding five millimeters in prepubertal children or exceeding fifteen millimeters in postpubertal individuals meets one of the diagnostic criteria for neurofibromatosis type one. Additional NF1 features to assess include axillary or inguinal freckling, neurofibromas, Lisch nodules of the iris, optic glioma, and family history. Cafe-au-lait macules with irregular borders, described as coast of Maine, suggest McCune-Albright syndrome when accompanied by polyostotic fibrous dysplasia and precocious puberty. Referral to genetics is appropriate when multiple cafe-au-lait macules raise concern for syndromic diagnosis.

<image>Panel A: Vitiligo on the face showing sharply demarcated depigmented patches around the eyes and mouth with contrast to surrounding normally pigmented skin. Panel B: Post-inflammatory hyperpigmentation at sites of healed acne lesions on the cheeks in adolescent with darker skin tone. Panel C: Pityriasis alba showing ill-defined hypopigmented patches with fine scale on the cheeks of a child with atopic dermatitis. Panel D: Multiple cafe-au-lait macules with smooth borders on the trunk warranting evaluation for neurofibromatosis type 1.</image>

Section 10: Skin Manifestations of Systemic Disease

Cutaneous findings may provide the first clue to systemic disease in children, making recognition of characteristic patterns essential for timely diagnosis and appropriate management. Several important pediatric conditions present with distinctive skin manifestations that, combined with other clinical features, enable diagnosis.

Henoch-Schonlein purpura represents the most common systemic vasculitis in children, affecting small vessels and typically presenting between ages three and ten years. The hallmark cutaneous finding is palpable purpura, appearing as non-blanching violaceous papules and macules distributed predominantly on the lower extremities and buttocks, the dependent areas subject to hydrostatic pressure. Unlike petechiae from thrombocytopenia, the lesions of HSP are palpable due to the inflammatory component. Associated manifestations include arthralgia or arthritis affecting large joints, particularly knees and ankles; abdominal pain from gastrointestinal involvement with risk of intussusception; and nephritis ranging from microscopic hematuria to nephrotic syndrome. The condition is self-limited in most cases, with supportive care and monitoring for renal involvement. Corticosteroids may be considered for severe abdominal pain or joint symptoms but do not prevent renal disease. Long-term follow-up monitors for nephritis, which may develop weeks after acute presentation.

Kawasaki disease is an acute febrile vasculitis of unknown etiology affecting predominantly children younger than five years, with serious risk of coronary artery aneurysm if untreated. The mucocutaneous manifestations constitute several of the diagnostic criteria and include polymorphous rash of various morphologies distributed on the trunk and extremities, bilateral nonexudative conjunctival injection, changes of the lips and oral mucosa including erythema, cracking, strawberry tongue, and pharyngeal erythema, and changes of the extremities including erythema and edema of the hands and feet acutely with subsequent periungual desquamation in the subacute phase. These findings combined with fever persisting five or more days establish the diagnosis when sufficient criteria are met. Treatment with intravenous immunoglobulin within the first ten days of illness dramatically reduces the risk of coronary artery aneurysm.

Juvenile dermatomyositis represents an inflammatory myopathy with characteristic cutaneous findings that often precede or accompany proximal muscle weakness. The heliotrope rash presents as violaceous discoloration of the upper eyelids, often with edema, resembling the color of the heliotrope flower. Gottron papules are violaceous papules or plaques overlying the metacarpophalangeal and interphalangeal joints, and Gottron sign refers to similar discoloration over the elbows and knees. The V-sign describes erythema in the anterior neck and chest in a V-shaped distribution, while the shawl sign describes erythema over the upper back and shoulders. These cutaneous findings combined with proximal muscle weakness, elevated muscle enzymes, and characteristic findings on MRI or electromyography establish the diagnosis. Treatment involves systemic immunosuppression. Systemic lupus erythematosus may present in childhood with characteristic skin findings including the malar or butterfly rash, an erythematous rash across the cheeks and nasal bridge sparing the nasolabial folds, photosensitivity, discoid lesions, and oral ulcers. Recognition of these findings prompts evaluation for systemic disease.

<image>Panel A: Palpable purpura of Henoch-Schonlein purpura distributed over the lower extremities and buttocks showing non-blanching violaceous papules. Panel B: Kawasaki disease features including bilateral conjunctival injection, cracked erythematous lips, and erythema with edema of the hands. Panel C: Dermatomyositis showing heliotrope rash of the upper eyelids and Gottron papules over the metacarpophalangeal joints. Panel D: Malar rash of systemic lupus erythematosus demonstrating erythema across the cheeks and nasal bridge with characteristic sparing of the nasolabial folds.</image>

Summary

• Erythema toxicum neonatorum is a benign condition with erythematous macules and pustules containing eosinophils that resolves spontaneously, while neonatal vesicles require evaluation for herpes simplex virus

• Infantile hemangiomas appear at 2-4 weeks, proliferate during the first year, then slowly involute, while port-wine stains are present at birth and persist, with facial V1 involvement requiring evaluation for Sturge-Weber syndrome

• Atopic dermatitis is characterized by pruritus and eczematous dermatitis with age-dependent distribution, treated with emollients, topical corticosteroids, and trigger avoidance, with calcineurin inhibitors as steroid-sparing options

• Tinea capitis requires oral antifungal therapy as topical agents cannot penetrate the hair follicle, with griseofulvin or terbinafine as first-line agents

• Scabies presents with intense nocturnal pruritus in characteristic distributions, requiring permethrin treatment of all household members simultaneously and environmental decontamination

• Impetigo presents with honey-crusted lesions treated with topical mupirocin for localized disease or oral antibiotics for extensive involvement

• Staphylococcal scalded skin syndrome is toxin-mediated with widespread erythroderma and superficial desquamation requiring intravenous antibiotics and supportive care

• Stevens-Johnson syndrome and toxic epidermal necrolysis present with mucosal erosions and epidermal necrosis requiring immediate drug discontinuation and burn unit care

• Multiple cafe-au-lait spots exceeding six warrant evaluation for neurofibromatosis type 1

• Henoch-Schonlein purpura presents with palpable purpura on lower extremities, arthritis, abdominal pain, and nephritis requiring monitoring for renal involvement

Key Terms

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