Dermatology

I. Evaluation and Clinical Descriptions of Skin Findings

A. Primary Skin Lesions

  1. 1. Macule: Small, flat, well-circumscribed discolored lesion (<1 cm)
  2. 2. Patch: Large macule (>1 cm)
  3. 3. Papule: Small, elevated, firm, well-circumscribed superficial lesion (<1 cm)
  4. 4. Plaque: Large papule (>1 cm)
  5. 5. Pustule: Small, well-circumscribed elevation of skin containing purulent material (<1 cm)
  6. 6. Vesicle: Small, well-circumscribed elevation of skin containing serous fluid (<0.5 cm)
  7. 7. Bulla: Large vesicle (>0.5 cm)
  8. 8. Wheal: Transient, raised, well-circumscribed lesion with erythematous periphery and central pallor
  9. 9. Nodule: Soft or firm lesion in dermis or subcutaneous fat (>1 cm)
  10. 10. Tumor/mass: Solid, firm lesion (typically >2 cm)
B. Secondary Skin Lesions
  1. 1. Scale: Small, thin plates shedding from the surface of the skin
  2. 2. Crust: Solidified exudative material from erosions or ruptured vesicles/pustules
  3. 3. Erosion: Loss of the most superficial layers of the epidermis from friction, pressure, or inflammation
  4. 4. Ulcer: Full thickness loss of the epidermis and dermis, with clearly defined edges
  5. 5. Fissure: Linear or wedge-shaped epidermal tear associated with inflammation and pain
  6. 6. Excoriation: Superficial linear abrasions secondary to scratching
  7. 7. Lichenification: Thickening of the epidermis with accentuated skin lines, secondary to chronic inflammation and/or scratching
  8. 8. Scar: Formation of new connective tissue after full thickness injury to skin, leaving permanent change in skin
C. Shapes and Arrangements
  1. 1. Linear: Distributed along a line
  2. 2. Dermatomal: Following a dermatome
  3. 3. Filiform: Thread-like
  4. 4. Serpiginous: Wavy, coiled, serpentine pattern
  5. 5. Annular: Ring-like configuration
  6. 6. Nummular/discoid: Disk-like lesion
  7. 7. Targetoid: Resembling a bull’s eye target with central erythema surrounded by pale edema with a peripheral border of erythema
  8. 8. Clustered: Lesions in a group
  9. 9. Herpetiform: Clustered vesicular lesions on erythematous bases
  10. 10. Reticulated: Net or lacey distribution
  11. 11. Geographic: Resembling outlines on a map such as a continent
  12. 12. Morbilliform: Eruption of erythematous to dusky coalescing macules with interspersed healthy skin

II. Vascular Anomalies

Section references: [1]
A. Vascular Tumors

  1. 1. Infantile hemangiomas (Fig. 8.1, Color Plates).2,3
    1. a. Pathogenesis: Benign vascular tumor with rapid proliferation followed by spontaneous involution. Most present before 4 weeks of age. Undergo rapid growth between 1 and 2 months of age, with 80% of size reached by 3 months. Most begin to regress between 6 and 12 months of age, with the majority of tumor regression occurring by 4 years of age. 50% to 70% resolve completely.
    2. b. Clinical presentation: Newborns may demonstrate pale macules with threadlike telangiectasias that later develop into hemangiomas. May be superficial, deep, or mixed. After involution, can have residual skin changes including scarring and atrophy.
    3. c. Indicators that should prompt consideration for early treatment:
      1. (1) Potential for life-threatening complications: Airway hemangiomas, liver hemangiomas (associated with high-output heart failure and severe hypothyroidism), and profuse bleeding from an ulcerated hemangioma.
      2. (2) Risk of functional impairment: Interference with the development of vision (if near eye) and interference with feeding (if near mouth).
      3. (3) Ulceration: Most common complication (5% to 21%). Can be extremely painful and usually scars; risk greatest in large hemangiomas and those located in skin creases, particularly the diaper area.
      4. (4) Associated structural anomalies: PHACES syndrome ( Posterior cranial fossa malformations, large segmental facial Hemangiomas, Arterial lesions, Cardiovascular anomalies (aortic anomalies), Eye anomalies, Sternal cleft anomalies/supraumbilical raphes4) and LUMBAR syndrome ( Lower body hemangioma, Urogenital anomalies, Ulceration, Myelopathy, Bony deformities, Anorectal malformations, Arterial anomalies, Renal anomalies).
      5. (5) Potential for disfigurement: Risk of permanent scarring or distortion of anatomic landmarks.
    4. d. Diagnosis: Usually diagnosed clinically. Atypical clinical findings, growth pattern, and equivocal imaging should prompt tissue biopsy to exclude other neoplasms or unusual vascular malformations. See Table 8.1 for indications to order imaging.
    5. e. Treatment:
      1. (1) Most are uncomplicated and can be observed with watchful waiting. Photo documentation is used to follow the growth and regression process.
      2. (2) If an infantile hemangioma is identified as high risk, the child should be evaluated by a hemangioma specialist promptly, as there is a narrow window of opportunity in which to intervene and prevent poor outcomes.
      3. (3) β-adrenergic blockers such as propranolol are considered first-line therapy for complicated infantile hemangiomas and should be initiated under supervision of a pediatric dermatologist or experienced practitioner.5 While patients should be clinically screened for cardiac disease, EKG and/or echocardiogram are not required unless there is clinical concern. Contraindications include: Reactive airways, sinus bradycardia, decompensated heart failure, greater than 1st degree heart block, hypotension, hypoglycemia, hypersensitivity to propranolol. Off label use of selective beta-blockers may be considered in certain patients. Duration should be at least 6 months and up to 12 months of age.6
      4. (4) Corticosteroids are considered second line. Similar efficacy to propranolol in a prospective, randomized, investigator-blinded trial, but propranolol is better tolerated and with fewer severe side effects.7
      5. (5) Topical timolol is effective in superficial, uncomplicated hemangiomas (recommend 0.5% gel forming solution).
  2. 2. Pyogenic granuloma (Lobular Capillary Hemangioma) (Fig. 8.2, Color Plates)
    1. a. Clinical presentation: Benign vascular tumor, appears as small (usually 3 to 10 mm but occasionally much larger) bright red papule that grows over several weeks to months into sessile or pedunculated papule with a “collarette,” scale, or crust. Can bleed profusely with minor trauma and can ulcerate. Rarely spontaneously regresses. Seen in all ages; average age of diagnosis 6 months to 10 years. Located on head and neck, sometimes in oral mucosa but can be at any skin site and often misdiagnosed as hemangiomas.
    2. b. Treatment: Usually required, given frequent bleeding and ulceration. Options include shave excision or curettage with cautery of base, surgical excision, carbon dioxide laser excision, or pulsed dye laser therapy. For most cases, shave and cautery are quick, safe, low risk, and can be performed quickly with local anesthesia.
B. Vascular Malformations
Include capillary (port-wine stains and salmon patch/stork bite/angel kiss), lymphatic, venous, and arteriovenous malformations.
Note: For a comparison of vascular malformations to vascular tumors, please see Table EC 8.A .8

III. Infections

A. Viral

  1. 1. Warts
    1. a. Pathogenesis: Human papillomaviruses (HPVs) of the epithelium or mucus membrane.
    2. b. Clinical presentation:
      1. (1) Common warts: Skin-colored, rough, minimally scaly papules and nodules found most commonly on the hands, although can occur anywhere. Can be solitary or multiple, range from a few millimeters to several centimeters, may form large plaques or a confluent linear pattern secondary to autoinoculation. Sometimes persistent in immunocompromised patients.
      2. (2) Flat warts: Flesh to brown/yellow-colored, smooth, flat-topped papules commonly found over the hands, arms, and face. Usually <2 mm in diameter and often present in clusters.
      3. (3) Plantar warts: Occur on soles of feet as inward growing, hyperkeratotic plaques and papules. Trauma on weight-bearing surfaces results in small black dots (petechiae from thrombosed vessels on the surface of the wart). Can be painful.
    3. c. Diagnosis: Clinical diagnosis.
    4. d. Treatment9:
      1. (1) Spontaneous resolution occurs in greater than 75% of warts in otherwise healthy individuals within 3 years. No specific treatment clearly better than placebo, except possibly topical salicylic acid.
      2. (2) Keratolytics (topical salicylates): Particularly effective in combination with adhesive tape occlusion. Response may take 4 to 6 months.
      3. (3) Destructive techniques, candida antigen, cantharidin, or “beetle juice” are not clearly more effective than placebo. Additionally, destructive techniques can be painful and cause scarring. These options are not recommended in children.
  2. 2. Molluscum contagiosum (Fig. 8.3, Color Plates)
    1. a. Pathogenesis: Large DNA poxvirus. Spread by skin-to-skin contact.
    2. b. Clinical presentation: Dome-shaped, often umbilicated, translucent to white papules that range from 1 mm to 1 cm. Occur anywhere except palms and soles, most commonly on the trunk and intertriginous areas. Can occur in the genital area and lower abdomen when obtained as a sexually transmitted infection. May be pruritic and can be surrounded by erythema, resembling eczema.
    3. c. Diagnosis: Clinical diagnosis.
    4. d. Treatment: Most spontaneously resolve within 6 to 18 months and do not require intervention other than monitoring for secondary bacterial infection. Surrounding eczematous changes may indicate an immunologic reaction and serve as a harbinger of regression. Treatment may cause scarring and may not be more effective than placebo. Recurrences are common.
  3. 3. Herpes simplex virus
    1. a. Pathogenesis: Either HSV-1 or HSV-2 may be implicated, regardless of lesion location. During the initial outbreak, oral lesions last 2 to 3 weeks whereas genital lesions may last 2 to 6 weeks. Recurrent episodes are usually much shorter.
    2. b. Clinical presentation ( Fig. 8.6 , Color Plate): Symptoms include prodrome of tingling, itching, or burning followed by painful vesicles on erythematous base that may last 7 to 10 days, break open, and crust prior to healing, flu-like symptoms, dehydration (gingivostomatitis), dysuria (genital), ophthalmologic symptoms (keratitis). May be triggered by stress, illness, sun exposure, and menstruation. The first outbreak is typically the worst.
    3. c. Diagnosis: Diagnosed clinically and, in many centers, with viral DNA PCR (more sensitive than culture). To culture a lesion, clean with alcohol, un-roof lesion with sterile needle or wooden side of cotton swab, collect vesicular fluid on sterile swab, and send in viral transport medium.
    4. d. Treatment: Acyclovir or valacyclovir for 7 to 14 days (see Formulary for dosing). For children with herpetic gingivostomatitis, antiviral therapy should be initiated within 72 to 96 hours of onset if they are unable to drink or have significant pain. Valacyclovir is generally preferred as it is more bioavailable than acyclovir and, as a result, is dosed less frequently.
  4. 4. Erythema infectiosum (“fifth disease”)
    1. a. Pathogenesis: Parvovirus B19.
    2. b. Clinical presentation: Pediatric presentation of nonspecific febrile illness with headache, coryza, and gastrointestinal complaints. Two to five days after onset of symptoms, the classic malar rash with “slapped cheek” appearance erupts, followed by a reticular rash to the trunk several days later. Associated signs and symptoms include arthralgias (more common in adults) and a transient aplastic crisis, which may be more of a problem in patients with hemoglobinopathies and pregnant women.
    3. c. Diagnosis: Clinical diagnosis, serum IgM, or serum DNA PCR.
    4. d. Treatment: Supportive care and avoiding contact with pregnant women.
  5. 5. Pityriasis rosea
    1. a. Pathogenesis: Viral etiology (possibly HHV-6, HHV-7) has been hypothesized but no definitive cause has been described.
    2. b. Clinical presentation: Typically asymptomatic or may have mild pruritus. Classic presentation with a round to oval, sharply demarcated, scaly, salmon-colored herald patch with central clearing on trunk followed by a “Christmas tree” distribution of oval crops of lesions similar to herald patch. Pediatric patients may have an atypical distribution involving the scalp, face, distal extremities, and sparing of the trunk. Lesions typically resolve in 4 to 6 weeks.
    3. c. Diagnosis: Clinical diagnosis.
    4. d. Treatment: Typically self-resolving.
  6. 6. Roseola infantum (Fig. 8.5, Color Plates)
    1. a. Pathogenesis: Human Herpesvirus 6 (HHV-6).
    2. b. Clinical presentation: Typically diagnosed in children <2 years old with peak 7 to 13 months. Febrile phase of 3 to 5 days of high fever (often >40°C), viremia, and irritability. As febrile phase resolves, patients develop a morbilliform rash on neck and trunk that spreads centripetally to face and extremities for 1 to 2 days.
    3. c. Diagnosis: Clinical diagnosis.
    4. d. Treatment: Self-resolving.
  7. 7. Hand, foot, and mouth disease
    1. a. Pathogenesis: Most commonly Coxsackievirus A serotypes.
    2. b. Clinical presentation: Oral lesions on the tongue, buccal mucosa, and palate that initially are 1 to 5 mm erythematous macules and evolve to vesicles and ulcers with a thin erythematous halo. Erythematous, non-pruritic 1 to 10 mm macules, papules, and/or vesicles on the palms and soles. Typically resolve in 3 to 4 days. Usually nontender, unless caused by Coxsackie A6 (associated with high fevers, widespread lesions, longer duration [12 days], palmar and plantar desquamation, and nail dystrophy).
    3. c. Diagnosis: Clinical diagnosis.
    4. d. Treatment: Supportive care.
  8. 8. Reactive erythema (Fig. 8.4; Figs. 8.5–8.10, Color Plates)
    1. a. Pathogenesis: Represent cutaneous reaction patterns triggered by endogenous and environmental factors (e.g., viral infections, drug reactions).
    2. b. Clinical presentation: Group of disorders characterized by erythematous patches, plaques, and nodules that vary in size, shape, and distribution.

Descriptive text is not available for this image

Figure 8.4
Reactive erythema.
Modified from Cohen BA. Atlas of Pediatric Dermatology. 4th ed. China: Elsevier Limited; 2013:206.


Descriptive text is not available for this image

Figure 8.21
Evaluation of neonatal rashes.
Modified from Cohen BA. Atlas of Pediatric Dermatology. 4th ed. China: Elsevier Limited; 2013:62.

B. Parasitic
  1. 1. Scabies (Fig. 8.11, Color Plates)
    1. a. Pathogenesis: Caused by the mite Sarcoptes scabiei. Spread by skin-to-skin contact and through fomites. Can live for 2 days away from a human host. Female mites burrow and lay eggs under the skin.
    2. b. Clinical presentation: Initial lesion is a small, erythematous papule that is easy to overlook. Can have burrows (elongated, edematous papulovesicles, often with a pustule at the advancing border) which are pathognomonic. Most commonly located in interdigital webs, wrist folds, elbows, axilla, genitals, buttocks, and belt line. In temperate climates, the face and scalp are usually spared. In young infants, the palms and soles are also commonly involved. Burrows are most dramatic in patients who are unable to scratch (e.g., infants). Disseminated eczematous eruption results in generalized severe pruritus, especially at night. Can become nodular, particularly in intertriginous areas, or be susceptible to superinfection due to frequent excoriations. Immunosuppressed patients may develop diffuse scaly crusted eruption and lack pruritus.
    3. c. Treatment10:
      1. (1) Permethrin cream: 5% cream applied to skin from neck down in normal hosts including under fingernails and toenails. Rinse off after 8 to 14 hours. Can repeat in 7 to 10 days.
      2. (2) Ivermectin (off-label use): Single dose; can repeat in 2 weeks. Efficacy comparable to permethrin cream. May be the best choice for immunodeficient patients where total body application may be difficult.
      3. (3) Environment: Mites cannot live away from human skin for more than 2 to 3 days. Launder clothing and sheets. Bag and seal stuffed animals and pillows for 2 to 3 days. Consider treatment of close contacts.
C. Fungal (Figs. 8.12–8.16, Color Plates)
  1. 1. Tinea capitis (see Fig. 8.12, Color Plates)
    1. a. Pathogenesis: Mostly caused by fungi of the genus Trichophyton in North America (95%), less commonly Microsporum (5% or less), and spread through contact and fomites.
    2. b. Epidemiology: Usually occurs in young children, with higher incidence in African American children, but any age and ethnicity can be affected.
    3. c. Clinical presentation:
      1. (1) Black dot: Most common. Slowly growing, erythematous, scaling patches. These areas develop alopecia and black dots are visible on scalp where hair has broken.
      2. (2) Gray patch (“seborrheic dermatitis type”): Erythematous, scaling, well-demarcated patches that grow centrifugally. Hair breaks off a few millimeters above the scalp and takes on a gray/frosted appearance.
      3. (3) Kerion (see Fig. 8.13, Color Plates): Complication of tinea capitis or tinea corporis. Type IV hypersensitivity to fungus. Raised, boggy/spongy lesions, often tender and covered with purulent exudate. Most commonly occurs months after primary infection.
      4. (4) All can be associated with posterior cervical lymphadenopathy.
    4. d. Diagnosis: Can be made clinically, but since oral antifungal therapy is indicated, tinea capitis should be confirmed by direct microscopic exam of a potassium hydroxide (KOH) preparation of the proximal ends of hairs, gently and painlessly scraped from the affected area. Cultures may be obtained by using a sterile toothbrush or cotton swab. The scale can be scraped directly into a sterile plastic cup and/or the cotton swab tips can be broken off and placed into the sterile plastic cups.
    5. e. Treatment11 : Always requires systemic therapy. First-line therapy includes oral griseofulvin for 10 to 12 weeks (which should be taken with fatty foods for improved absorption) and terbinafine for 6 weeks (see Formulary for dosing). Most experts consider terbinafine superior to griseofulvin for T. tonsurans because of its shorter duration of therapy and superior effectiveness. The FDA recommends baseline and follow-up hepatic function testing in children taking terbinafine, though most clinicians forego laboratory testing in healthy children without history of liver disease if treatment is 6 weeks or less. Though not FDA-approved for tinea capitis, fluconazole at 6 mg/kg/day (max 400 mg/day) for 6 weeks is recommended by the AAP Red Book as an alternative treatment of tinea capitis in children younger than 2 years old.12 All family members, particularly other children, should be examined carefully for subtle infection. Selenium sulfide 2.5% shampoo may shorten the period of shedding of fungal organisms and reduce risk of infection of unaffected family members.
  2. 2. Tinea corporis and pedis11 (see Figs. 8.14 and 8.15, Color Plates)
    1. a. Pathogenesis: Spread through direct contact and fomites, especially in sports with close contact.
    2. b. Clinical presentation: Pruritic, erythematous, annular patch or plaque with central clearing and a scaly raised border. Typically affects glabrous skin (smooth and bare).
    3. c. Diagnosis: Usually diagnosed clinically, but a KOH preparation or fungal culture can be used to help guide diagnosis.
    4. d. Treatment: Topical antifungals (terbinafine, azole) through 1 to 2 weeks past lesion resolution. Widespread eruption may require oral antifungals.
  3. 3. Tinea versicolor (see Fig. 8.16, Color Plates)
    1. a. Pathogenesis: Caused by Malassezia. Exacerbated by hot/humid weather, hyperhidrosis, topical skin oil use. Most people are colonized with Malassezia but only a small number are prone to develop clinical lesions. Not associated with poor hygiene. Not contagious.
    2. b. Clinical presentation: Well demarcated, minimally scaly, hypopigmented macules or patches. Hypopigmented areas tend to be more prominent in the summer because affected areas do not tan. Lesions often have a fine scale that may be noted following gentle rubbing and can be mildly pruritic but are usually asymptomatic.
    3. c. Diagnosis: KOH microscopy reveals pseudohyphae and yeast cells that appear like “spaghetti and meatballs.”
    4. d. Treatment: Topical antifungal shampoos and/or creams (miconazole, oxiconazole, ketoconazole) or selenium sulfide are effective. Given the risk of hepatotoxicity, oral azole antifungals are reserved for resistant or widespread disease. Oral terbinafine is not effective. Pigmentation changes may take months to resolve despite successful treatment.
D. Bacterial
  1. 1. Impetigo
    1. a. Pathogenesis: Contagious bacterial infection of the skin, most commonly caused by Staphylococcus aureus (99% MSSA), with a minority of cases caused by Group A Streptococcus.
    2. b. Clinical presentation:
      1. (1) Nonbullous impetigo: Papules that evolve into erythematous pustules or vesicles that break and form thick, honey-colored crusts and plaques. Commonly overlying any break to skin barrier. Primarily face and extremities.
      2. (2) Bullous impetigo: Painless vesicles that evolve into flaccid bullae and crusted patches with undermined border. Seen more in infants and young children. Caused by Staphylococcus aureus exfoliative toxin A.
    3. c. Diagnosis: Clinical diagnosis.
    4. d. Treatment: When impetigo is contained to a small area, topical mupirocin may be used for 5 days. When the infection is widespread, an oral antibiotic such as cephalexin should be used for 7 days. Consider broader coverage if MRSA is suspected, although MSSA accounts for most infections.
  2. 2. Staph scalded skin syndrome
    1. a. Pathogenesis: Staphylococcus aureus infections of the skin with hematogenous dissemination of exfoliative toxin A or B to the epidermis.
    2. b. Clinical presentation: Typical presentation is Ritter disease (generalized exfoliation) in a 3- to 7-day-old infant who initially is febrile and irritable with conjunctivitis and perioral erythema. In addition to newborns, this presentation is seen in young children who do not have antibodies to the toxin and often do not clear the toxin-antibody complex quickly due to decreased renal excretion. One to two days after the prodromal onset, patient develops diffuse erythema, fragile, flaccid bullae and erosions that are Nikolsky positive in areas of mechanical stress such as intertriginous areas. Lesions are not scarring as they are intraepidermal. Older children tend to have a localized bullous impetigo with tender scarlatiniform eruption. Infants and toddlers usually have a combination of the presentations seen in neonates and older children along with white to brown thick flaking desquamation of the entire body, especially the face and neck.
    3. c. Diagnosis: Typically clinically. However, cultures should be obtained from any potential source site of infection or colonization such as the medial canthi or nares.
    4. d. Treatment: Nearly all cases are MSSA, with an increasing number being clindamycin resistant. First-line treatment may include oral penicillinase-resistant beta-lactams such as first or second-generation cephalosporins. Vancomycin should be considered in patients who fail to respond to treatment and/or in areas with a high prevalence of MRSA. Management should also include supportive care with topical emollients and close monitoring of fluid and electrolyte status.
  3. 3. Scarlet fever (Fig. 8.17, Color Plates)
    1. a. Pathogenesis: Exotoxin-mediated response to a Streptococcus pyogenes infection, typically pharyngitis.
    2. b. Clinical presentation: Sandpaper-like, coarse, erythematous, blanching rash that originates in the groin and axilla then spreads to the trunk then extremities but spares the palms and soles. May have Pastia lines. Associated with pharyngitis, circumoral pallor, and a strawberry tongue.
    3. c. Diagnosis: Clinical diagnosis. May benefit from rapid strep test and throat culture.
    4. d. Treatment: No additional treatment aside from treating the patient’s Strep pharyngitis.
  4. 4. Cellulitis: See Chapter 17 .

IV. Hair Loss

A. Telogen Effluvium (see Fig. 8.18, Color Plates)

  1. 1. Pathogenesis: Most common cause of diffuse hair loss. Mature hair follicles switch prematurely to the telogen (resting) state, with shedding within 3 months.
  2. 2. Clinical presentation: Diffuse hair thinning 3 months after a stressful event (major illnesses or surgery, pregnancy, severe weight loss).
  3. 3. Treatment: Self-limited. Regrowth usually occurs over several months.
B. Alopecia Areata (see Fig. 8.19, Color Plates)
  1. 1. Clinical presentation: Chronic inflammatory (probably autoimmune) disease that starts with well-circumscribed small bald patches and normal-appearing underlying skin. New lesions may demonstrate subtle erythema and be pruritic. Bald patches may enlarge to involve large areas of the scalp or other hair-bearing areas. Many experience good hair regrowth within 1 to 2 years, although most will relapse. A minority progress to total loss of all scalp (alopecia totalis) and/or body hair (alopecia universalis).
  2. 2. Diagnosis: Usually clinical diagnosis.
  3. 3. Treatment13: First-line therapy is topical steroids. Referral to dermatology is warranted for consideration of other treatments. No evidence-based data that any therapy is better than placebo. Older children, adolescents, and young adults with longstanding localized areas of hair loss have the best prognosis.
C. Traction Alopecia (see Fig. 8.20, Color Plates)
  1. 1. Pathogenesis: Hairstyles that apply tension for long periods of time.
  2. 2. Clinical presentation: Noninflammatory linear areas of hair loss at margins of hairline, part line, or scattered regions, depending on hairstyling procedures used.
  3. 3. Treatment: Avoidance of styling products or styles that result in traction. If traction remains for long periods, condition may progress to permanent scarring hair loss.
D. Trichotillomania and Hair Pulling
  1. 1. Pathogenesis: Alopecia due to compulsive urge to pull out one’s own hair, resulting in irregular areas of incomplete hair loss. Mainly on the scalp; can involve eyebrows and eyelashes. Onset is usually after age 10 and should be distinguished from hair twirling/pulling in younger children that resolves without treatment in most cases.
  2. 2. Clinical presentation: Characterized by hair of differing lengths; area of hair loss can be unusual in shape.
  3. 3. Treatment: Behavioral modification and consider psychiatric evaluation (can be associated with anxiety, depression, and obsessive-compulsive disorder).

V. Acne Vulgaris

A. Pathogenetic Factors
Follicular hyperkeratinization, increased sebum production, Cutibacterium acnes (formerly Propionibacterium acnes ) proliferation, and inflammation.
B. Risk Factors
Androgens, family history, and stress. No strong evidence that dietary habits affect acne.
C. Clinical Presentation

  1. 1. Noninflammatory lesions
    1. a. Closed comedone (whitehead): Accumulation of sebum and keratinous material, resulting in white/skin-colored papules without surrounding erythema.
    2. b. Open comedone (blackhead): Dilated follicles filled with keratinocytes, oils, and melanin.
  2. 2. Inflammatory lesions: Papules, pustules, nodules, and cysts with evidence of surrounding inflammation. Typically appear later in the course of acne. Nodulocystic presentations are more likely to lead to hyperpigmentation and/or permanent scarring.
D. Treatment14–16 ( Table 8.2 )
  1. 1. Skin care: Gentle nonabrasive cleaning. Avoid picking or popping lesions. Vigorous scrubbing and abrasive cleaners can worsen acne.
  2. 2. Topical first-line therapies: Recommended for mild to moderate acne.
    1. a. Retinoids ( Table EC 8.B )
      1. (1) Normalize follicular keratinization and decrease inflammation.
      2. (2) A pea-sized amount should be applied to cover the entire face.
      3. (3) Risks: Cause irritation and dryness of skin. Retinoids should be used at night due to inactivation by sunlight. This class should not be used during pregnancy.
      4. (4) Three topical retinoids (tretinoin, adapalene, and tazarotene) are available by prescription in the United States. Adapalene 0.1% gel has been approved for over-the-counter (OTC) use with significant efficacy.17
    2. b. Benzoyl peroxide (BPO)
      1. (1) Oxidizing agent with antibacterial and mild anticomedolytic properties.
      2. (2) Washes may be most convenient formulation, as they can be used in the shower.
      3. (3) Risks: Can bleach hair, clothing, towels, and sheets.
    3. c. Salicylic acid: Topical comedolytic agent that may be found in OTC face washes and serves as an alternative to a topical retinoid.
  3. 3. Topical antimicrobials:
    1. a. Azelaic acid: Antimicrobial, comedolytic, and anti-inflammatory. Recommended by the American Academy of Dermatology (AAD) for the treatment of postinflammatory dyspigmentation (see Figures EC 8.P and EC 8.S). Available in a 15% gel and a 20% cream (more efficacious).18
    2. b. Erythromycin and clindamycin: Avoid topical antibiotics as monotherapy. Topical BPO should be concurrently used to optimize efficacy and avoid bacterial resistance.
  4. 4. Oral antibiotics ( Table EC 8.C ): Recommended for moderate to severe inflammatory acne that is resistant to topical treatment. These medications should be used with BPO or topical retinoid. Do not use as monotherapy. Limit to 3 months to minimize bacterial resistance.
    1. a. ≥8 years old: Doxycycline or minocycline
    2. b. <8 years old, pregnancy, or tetracycline allergy: Azithromycin, erythromycin, or trimethoprim/sulfamethoxazole.
    3. c. Erythromycin should be used with care due to increased risk of resistance. The AAD recommends reserving trimethoprim/sulfamethoxazole for patients who have failed other treatments or are unable to tolerate tetracyclines and macrolides.
  5. 5. Hormonal therapy: Reduces sebum production and androgen levels. Good option for pubertal females who have sudden onset of moderate to severe hormonal acne (often on lower face, jawline) and have not responded to conventional first-line therapies. Should not be used as monotherapy. Combination oral contraceptives (Ortho Tri-Cyclen, Estrostep, and Yaz) or spironolactone (antiandrogen).
  6. 6. Oral isotretinoin: Reserved for patients with severe nodular, cystic, or scarring acne who do not respond to traditional therapy or who cannot be weaned from oral antibiotics. Should be managed by a dermatologist. Most patients have complete resolution of their acne after 16 to 20 weeks of use.
    1. a. Side effects:
      1. (1) Teratogenicity: Patients and physicians are mandated by the FDA to comply with the iPledge program to eliminate fetal exposure to isotretinoin. Female patients with child-bearing potential must use two forms of birth control with routine pregnancy testing.
      2. (2) Hepatotoxicity, hyperlipidemia, and bone marrow suppression, a complete blood cell count, fasting lipid profile, and liver function tests should be obtained before initiation of therapy and repeated at 4 and 8 weeks.

VI. Common Neonatal Dermatologic Conditions

Fig. 8.21
A. Erythema Toxicum Neonatorum (see Fig. 8.22, Color Plates)

  1. 1. Clinical presentation: Most common rash of full-term infants; incidence declines with lower birth weight and prematurity. Appears as small erythematous macules and papules that evolve into pustules on erythematous bases. Rash most often occurs by 24 to 48 hours of life but can be present at birth or emerge as late as 2 to 3 weeks.
  2. 2. Course: Self-limited, resolves within 5 to 7 days; recurrences possible.
B. Transient Neonatal Pustular Melanosis (see Figs. 8.23–8.24, Color Plates)
  1. 1. Clinical presentation: More commonly affects full-term infants with darker pigmentation. At birth, appears as small pustules on non-erythematous bases that rupture and leave erythematous/hyperpigmented macules with a collarette of scale.
  2. 2. Course: Self-limited macules fade over weeks to months.
C. Miliaria (Heat Rash) (see Fig. 8.25, Color Plates)
  1. 1. Clinical presentation: Common newborn rash associated with warmer climates, incubator use, or occlusion with clothes/dressings. Appears as small erythematous papules or pustules usually on face, scalp, or intertriginous areas.
  2. 2. Course: Rash resolves when infant is placed in cooler environment or tight clothing/dressings are removed.
D. Milia (see Fig. 8.26, Color Plates)
  1. 1. Clinical presentation: Common newborn lesions. Appears as 1- to 3-mm white/yellow papules, frequently found on nose and face; due to retention of keratin and sebaceous materials in pilosebaceous follicles.
  2. 2. Course: Self-limited, resolves within first few weeks to few months of life.
E. Neonatal Acne (see Fig. 8.27, Color Plates)
  1. 1. Clinical presentation: Seen in 20% of infants. Appears as inflammatory papules or pustules without comedones, usually on face and scalp. Secondary to effect of maternal and endogenous androgens on infant’s sebaceous glands.
  2. 2. Course: Peaks around 1 month, resolves within a few months, usually without intervention. Does not increase risk of acne as an adolescent.
F. Seborrheic Dermatitis (Cradle Cap) (see Figs. 8.28–8.29, Color Plates)
  1. 1. Clinical presentation: Erythematous plaques with greasy yellow scales. Located in areas rich with sebaceous glands, such as scalp, cheeks, ears, eyebrows, intertriginous areas, diaper area. Unknown etiology. Can be seen in newborns, more commonly in infants aged 1 to 4 months.
  2. 2. Course: Self-limited and resolves within a few weeks to months.
  3. 3. Treatment: Can remove scales on scalp with an emollient (e.g., mineral or olive oil, or petroleum jelly) and a soft brush/fine comb. In more severe cases, antifungal shampoos or low-potency topical steroid can shorten the course, although no shampoos are FDA-approved for children less than 2 years of age.
G. Congenital Dermal Melanocytosis (formerly known as Mongolian Spots)
  1. 1. Clinical presentation: Most common pigmented lesion of newborns, usually seen in babies with darker skin tone. Appear as blue/gray macules without definite disappearance of dermal melanocytes. Can be mistaken for child abuse thus accurate documentation at newborn and well-child visits is important.
  2. 2. Course: Spots typically fade within first few years of life, with majority resolved or much improved by age 10 years.
H. Diaper Dermatitis19 (see Fig. 8.30, Color Plates)
  1. 1. Clinical presentation: Irritant contact dermatitis characterized by erythematous eruption on buttocks and genital areas with exclusion of other potential causes. Rarely associated with diaper candidiasis, characterized by a red, raised papular rash with small pustules at the periphery. Tends to involve the skin creases.19
  2. 2. Treatment: Frequent diaper changes, air exposure, adequate drying, gentle cleaning, and judicious use of topical barrier preparations. If persistent, can use low-potency topical steroid until cleared. For candidiasis, treatment with topical nystatin, miconazole, or clotrimazole is sufficient. Combination steroid/antifungal creams should be avoided due to steroid-related side effects and association with persistent fungal infections.20

VII. Autoimmune and Allergic Dermatologic Conditions

A. Contact Dermatitis

  1. 1. Irritant dermatitis: Exposure to physical, chemical, or mechanical irritants to the skin. Common irritants include frequent hand washing, hot water, lip-licking, thumb-sucking, and exposure to chemicals, paints, or certain foods like citrus fruits.
  2. 2. Allergic dermatitis (see Fig. 8.31, Color Plates):
    1. a. Pathogenesis: Immune reaction to an environmental trigger that comes into contact with the skin. After initial sensitization period of 7 to 10 days in susceptible individuals, an allergic response occurs with subsequent exposures.
    2. b. Common allergens: Toxicodendron spp. (poison ivy, oak, sumac), nickel, cobalt, gold, dyes, fragrances, formaldehyde, and latex.
    3. c. Clinical presentation: Pruritic erythematous dermatitis that can progress to chronic scaling, lichenification, and pigment changes. Poison ivy (see Fig. 8.32, Color Plates): Exposure to urushiol causes streaks of erythematous papules, pustules, and vesicles. Highly pruritic, can become edematous, especially if rash is on face or genitals. In extreme cases, anaphylaxis can occur.
    4. d. Diagnosis: Careful history taking and recognition of unusual shapes and locations suggesting an “outside job” allow for clinical diagnosis. Patch testing may also be helpful when trigger cannot be identified.
    5. e. Treatment:
      1. (1) Remove causative agent. Moisturize with ointment like Vaseline or Aquaphor twice per day. Use antihistamine and/or oatmeal baths as needed for itching, sedation, and sleeping, though they do not directly impact the rash.
      2. (2) Mild/moderate: Topical steroids twice a day for 1 week, then daily for 1 to 2 weeks.
      3. (3) Widespread/severe: Systemic steroids for 2 to 3 weeks, with taper. There is no role for short courses of steroids because eruption will flare when drug is stopped.
      4. (4) For poison ivy contact, remove clothing and wash skin with mild soap and water as soon as possible.
B. Atopic Dermatitis (Eczema) (See Figs. 8.33–8.37, Color Plates)
  1. 1. Pathogenesis: Due to inadequate skin barrier function from combination of genetic and environmental factors, resulting in transepidermal water loss. Can be associated with elevated serum IgE.
  2. 2. Epidemiology21 : Affects up to 20% of children in the United States, the vast majority with onset before age 5 years. Other comorbidities may follow including asthma, allergic rhinitis, and food allergies. Eczema resolves or improves in over 75% of patients by adulthood.
  3. 3. Clinical presentation: Dry, pruritic skin with acute changes, including erythema, vesicles, crusting, and chronic changes, including scaling, postinflammatory hypo- or hyperpigmentation (see Figures EC 8.P and EC 8.S), and lichenification.
    1. a. Infantile form: Erythematous, scaly lesions on the cheeks, scalp, and extensor surfaces. Covered areas (especially the diaper area) are usually spared.
    2. b. Childhood form: Lichenified plaques in flexural areas.
    3. c. Adolescence: More localized and lichenified skin changes. Predominantly on skin flexures, hands, and feet.
  4. 4. Treatment21 : See Chapter 15
    1. a. Lifestyle: Avoiding triggers (products with alcohol, fragrances, astringents, sweat, allergens, and excessive bathing). Avoid scratching (eczema is the “itch that rashes”).
    2. b. Bathing: Should be less than 5 minutes in lukewarm water with a gentle bar soap and no washcloth or scrubbing. Skin should be patted dry (not rubbed) and followed by rapid application of an emollient (“soak and smear”).
    3. c. Consider diluted bleach baths once or twice a week (mix 1/4 cup of bleach in full tub of lukewarm water and soak for 10 minutes, then rinse off with fresh water).
    4. d. Skin hydration: Frequent use of bland emollients with minimal water content (Vaseline or Aquaphor). Avoid lotions, as they have high water and low oil content, which worsens dry skin.
    5. e. Oral antihistamines: There is little evidence that antihistamines improve skin lesions in atopic dermatitis. Non-sedating antihistamines can be used for environmental allergies and hives. Sedating antihistamines may be of transient benefit for sedation at bedtime.
    6. f. Treatment for inflammation:
      1. (1) Mild disease: Topical steroids22 ( Table 8.3 ): Low and medium potency steroid ointments once or twice daily for 7 days during a flare. Severe flares may require a high-potency steroid for a longer duration of therapy, followed by a taper to a low-potency steroid. Use of topical steroids in areas where skin is thin (groin, axilla, face, under breasts) should generally be avoided. Short durations of low-potency steroids may be used as needed in these areas. Ointments can be applied over steroid.
      2. (2) Moderate disease: Crisaborole is a topical PDE4 inhibitor approved for mild to moderate eczema with preliminary studies of the 2% ointment showing improvement in the majority of clinical signs and symptoms, particularly pruritus.23 Topical calcineurin inhibitors ( tacrolimus ointment, pimecrolimus cream) are second-line therapies which should only be used in consultation with a dermatologist due to FDA “black box” warnings on these medications for theoretical increased risk of cancer, although there are no data to confirm and long-term safety studies are pending.24,25
      3. (3) Severe disease: Phototherapy with narrowband UVB light is a treatment option for older children and adolescents. Low-dose methotrexate is a consideration before cyclosporine. For many dermatologists, low-dose oral methotrexate is the first oral option for severe disease unresponsive to aggressive topical therapy. Oral cyclosporine is only used in severe cases of older children and adolescents who have failed other treatments due to concern for renal compromise. Dupilumab is an IL-4 receptor alpha antagonist prescribed for refractory cases, currently with FDA approval only for treatment in adults.
  5. 5. Complications26 :
    1. a. Bacterial superinfection: Usually S. aureus , sometimes Group A Streptococcus. Depending on extent of infection, treat with topical mupirocin or systemic antibiotics.
    2. b. Eczema herpeticum superinfection with herpes simplex virus can cause severe systemic infection. Presents as vesiculopustular lesions with central punched-out erosions that do not respond to oral antibiotics. Must be treated systemically with acyclovir or valacyclovir. Should be evaluated by ophthalmologist if there is concern for eye involvement.
C. Papular Urticaria (See Fig. 8.38, Color Plates)
  1. 1. Pathogenesis: Type IV hypersensitivity reaction to fleas, mosquitos, or bedbugs; also known as insect bite–induced hypersensitivity (IBIH).
  2. 2. Clinical presentation/epidemiology: Summarized by the SCRATCH principles27
    1. a. Symmetric eruption: Exposed areas and scalp commonly affected. Spares diaper region, palms, and soles.
    2. b. Cluster: Appear as “meal clusters” or “breakfast, lunch, and dinner” which are linear or triangular groupings of lesions. Associated with bedbugs and fleas.
    3. c. Rover not required: A remote animal exposure or lack of pet at home does not rule out IBIH.
    4. d. Age: Tends to peak by age 2. Not seen in newborn period. Most tend to develop tolerance by age 10.
    5. e. Target lesions: Especially in darkly pigmented patients. Time: Emphasize chronic nature of eruption and need for patience and watchful waiting.
    6. f. Confused pediatrician/parent: Diagnosis often met with disbelief by parent and/or referring pediatrician.
    7. g. Household: Because of the nature of the hypersensitivity, usually only affects one family member in the household.
  3. 3. Management (3 Ps):
    1. a. Prevention: Wear protective clothing, use insect repellent when outside (AAP guidelines recommend up to 30% DEET or 12% picaridin containing repellents), launder bedding and mattress pads for bedbugs, and maximize flea control for pets.
    2. b. Pruritis control: Topical steroids or antihistamines may be of some benefit.
    3. c. Patience: Can be frustrating because of its persistent, recurrent nature. Ensure patients that their symptoms will resolve and they will eventually develop tolerance.
D. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis
  1. 1. Pathogenesis: Severe mucocutaneous reaction with partial to full epidermal necrosis due to keratinocyte necrosis. Stevens-Johnson syndrome (SJS) has less than 10% involvement of body surface area (BSA), whereas toxic epidermal necrolysis (TEN) has greater than 30% BSA involvement. SJS/TEN defines the gap of 10% to 30% involvement. Overall mortality for pediatric patients is less than 8%. Commonly caused by medications initiated in previous 8 weeks including sulfonamide antibiotics, lamotrigine, carbamazepine, phenobarbital, and several oncologic drugs. May also be caused by Mycoplasma pneumonia infections. Nearly one third of cases have no identified trigger.
  2. 2. Clinical presentation: Fever and flu-like prodrome for 1 to 3 days prior to mucocutaneous lesions. Ophthalmologic and oropharyngeal symptoms are often first sites of mucosal involvement. Urogenital mucosal involvement seen in two-thirds of patients may lead to urinary retention and have significant long-term anatomic changes in female patients. Epidermal lesions are described as exquisitely tender (with pain out of proportion), ill-defined, coalescing macules and patches of erythema with central purple-to-black areas. Lesions typically start on face and trunk then spread in a symmetric distribution sparing the scalp, palms, and soles. Bullae form with disease progression. Then, the epidermis sloughs with positive Nikolsky and Asboe-Hansen (lateral expansion of bullae with pressure) signs. Acute phase may last 8 to 12 days with reepithelization requiring up to four weeks.
  3. 3. Diagnosis: Although usually not necessary, clinical diagnosis may be confirmed with a skin biopsy. Additional work up includes CBC, CMP, ESR, CRP, bacterial and fungal cultures, M. pneumoniae PCR, and CXR.
  4. 4. Treatment: Remove offending agent, supportive care, and close monitoring of all organ systems in the inpatient/ICU setting. There is controversy regarding IVIG and single dose of TNF-alpha inhibitor early in course. Systemic steroids probably should not be used.
  5. 5. Complications: At risk for serious complications including secondary bacterial infections ( Staphylococcus aureus and Pseudomonas aeruginosa ), septic shock, pneumonia, acute respiratory distress syndrome (ARDS), and epithelial necrosis of the GI tract. Most common complication in children is corneal scarring and dry eye.
E. Autoimmune Bullous Diseases: See Section X, Online Content.
VIII. Nail Disorders 28 : see Section X , Online Content
IX. Disorders of Pigmentation: see Section X , Online Content

X. Online Content

A. Autoimmune and Allergic Lesions

  1. 1. Autoimmune bullous diseases
    1. a. Very rare in children but should be considered if bullous lesions do not respond to standard therapy. Suspicion for any of the following should warrant referral to a dermatologist for diagnosis and management.
    2. b. Pemphigus vulgaris (Figure EC 8.A):
      1. (1) Pathogenesis: IgG autoantibodies to epidermal adhesion molecules, which interrupt integrity of epidermis and/or mucosa and result in extensive blister formation.
      2. (2) Clinical presentation: Flaccid bullae that start in the mouth and spread to face, scalp, trunk, extremities, and other mucosal membranes. Positive Nikolsky sign. Ruptured blisters are painful and prone to secondary infection. Can lead to impaired oral intake if there is significant oral mucosal involvement.
      3. (3) Treatment: Systemic glucocorticoids, rituximab, and/or intravenous immunoglobulin.
    3. c. Pemphigus foliaceus:
      1. (1) Pathogenesis: IgG autoantibodies bind to the same antigen as in bullous impetigo and staphylococcal scalded skin syndrome; thus lesions are superficial and rupture easily. Can be triggered by certain drugs, including thiol compounds and penicillins.
      2. (2) Clinical presentation: Scaling, crusting erosions on erythematous base that appear on face, scalp, trunk, and back. No mucosal involvement. Lesions are more superficial than in pemphigus vulgaris.
      3. (3) Treatment: Systemic glucocorticoids or rituximab. There is currently a move away from systemic steroids due to good efficacy and safety data on rituximab.
    4. d. Bullous pemphigoid:
      1. (1) Pathogenesis: Autoantibodies to the epithelial basement membrane that results in an inflammatory cascade and causes separation of epidermis from dermis and epithelium from subepithelium.
      2. (2) Clinical presentation: Prodrome of inflammatory lesions that progresses into large (1 to 3 cm), tense, extremely pruritic bullae on trunk, flexural regions, and intertriginous areas. Few patients have oral mucosal lesions. Negative Nikolsky sign.
      3. (3) Treatment: Immunosuppression (topical glucocorticoids, systemic glucocorticoids, glucocorticoid-sparing agents like methotrexate, mycophenolate, or azathioprine).
    5. e. Dermatitis herpetiformis:
      1. (1) Pathogenesis: Strong genetic predisposition and link to gluten intolerance/celiac disease. IgA deposits found in dermal papillae.
      2. (2) Clinical presentation: Symmetric, intensely pruritic papulovesicles clustered on extensor surfaces.
      3. (3) Treatment: Dapsone, strict gluten-free diet.

Descriptive text is not available for this image

Figure EC 8.A
Pemphigus vulgaris.
From Cohen BA. Dermatology Image Atlas; 2001. http://www.dermatlas.org/.

B. Nail Disorders28
  1. 1. Acquired nail disorders
    1. a. Paronychia: Red, tender swelling of proximal or lateral nail folds ([Figure EC 8.B Figure EC 8.C])
      1. (1) Acute form: Caused by bacterial invasion after trauma to cuticle
        1. (a) Clinical features: Exquisite pain, sudden swelling, and abscess formation around one nail.
        2. (b) Treatment: Responds quickly to drainage of abscess and warm tap-water soaks; occasionally anti-staphylococcal antibiotics required.
      2. (2) Chronic form: May involve one or several nails, history of frequent exposure to water or thumb-sucking; causative organisms Candida species, usually C. albicans.
        1. (a) Clinical features: Mild tenderness, minimal purulence, nail may be discolored or dystrophic.
        2. (b) Treatment: Resolves with topical antifungal agents and water avoidance; heals without scarring when thumb-sucking ends.
    2. b. Nail dystrophy: Distortion and discoloration of normal nail-plate structure; often traumatic or inflammatory causes ([Figure EC 8.D Figure EC 8.E Figure EC 8.F Figure EC 8.G Figure EC 8.H Figure EC 8.I]).
      1. (1) Onychomycosis: A result of dermatophyte fungal infection, unusual before puberty. Oral and topical antifungals (terbinafine, itraconazole, ciclopirox) are used off-label with high cure rates and few adverse effects.29
      2. (2) Subungual hematoma: Brown-black nail discoloration following crush injury. Usually resolves without treatment; large, painful blood collections may be drained. Must differentiate from melanoma and melanonychia.
    3. c. Nail changes and systemic disease ([Figure EC 8.J Figure EC 8.K])
      1. (1) Clubbing: Complication of chronic lung or heart disease.
      2. (2) Beau lines: Transverse, white lines/grooves that move distally with nail growth; due to growth arrest from systemic illness, medications, or toxins.
      3. (3) Onychomadesis: Accentuated Beau lines often with separation of the nail from base of nail. Usually self-limited and very common following Coxsackie A6 hand, foot, and mouth disease.
  2. 2. Congenital/hereditary nail disorders
    1. a. Isolated nail disorders ([Figure EC 8.L Figure EC 8.M])
      1. (1) Congenital nail dystrophy: Clubbing and spooning (koilonychia), may be autosomal dominant with no other anomalies.
      2. (2) Congenital ingrown toenails: Most self-limiting.
    2. b. Genodermatosis and systemic disease ([Figure EC 8.N Figure EC 8.O])
      1. (1) Periungual fibromas: Arise in proximal nail groove, common finding in tuberous sclerosis.
      2. (2) Congenital nail hypoplasia: Can occur with intrauterine exposure to anticonvulsants, alcohol, and warfarin.

Descriptive text is not available for this image

Figure EC 8.B
Acute paronychia.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.C
Chronic paronychia.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.D
Onychomycosis.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.E
Traumatic subungual hemorrhage.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.F
Acral melanoma.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.G
Melanonychia.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.H
Nail psoriasis.
From Cohen BA. Disorders of the Hair and Nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.I
Atopic nails.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.J
Nail clubbing.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.K
Beau lines.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.L
Koilonychia.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.M
Congenital ingrown nails.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.N
Periungual fibromas.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.


Descriptive text is not available for this image

Figure EC 8.O
Fetal alcohol syndrome with congenital hypoplastic and dysplastic nails.
From Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:211–239.

C. Disorders of Pigmentation30
  1. 1. Hyperpigmentation
    1. a. Congenital melanocytic nevi (CMN): Melanocytic nevi that are either present at birth or appear within the first few months of life in 1% to 3% of neonates.31
      1. (1) Appearance: Black or tan in color with irregular borders and often dark terminal hairs.
      2. (2) Risks:
        1. (a) Melanoma—At least 5% of large CMN greater than 20 cm with 70% of this cohort having cancerous transformation by 10 years of age.32 The presence of approximately 20 satellite nevi (smaller congenital nevi) also increases risk of melanoma.
        2. (b) Neurocutaneous melanosis—Children with large, multiple, satellite nevi, or lesions over the spine are at risk for leptomeningeal involvement with symptoms that may include hydrocephalus and seizures that may require evaluation by gadolinium contrast MRI.33,34
    2. b. Epidermal melanosis: Most lesions appear tan or light brown
      1. (1) Café au lait spots (Figure EC 8.P): Discrete tan macules that appear at birth or during childhood in 10% to 20% of normal individuals, sizes vary from freckles to patches, may involve any site on skin. May be diagnostic marker for Neurofibromatosis type 1 (≥6 lesions, each greater than 5 mm in diameter in prepubertal, or greater than 15 mm in postpubertal child) or other syndromes.
      2. (2) Freckles (ephelides): Reddish-tan and brown macules on sun-exposed surfaces, usually 2 to 3 mm in diameter. Serve as an independent risk factor for skin cancers in adulthood and can be an added sign of the importance of photoprotection which may decrease additional lesions.
      3. (3) Acanthosis nigricans ([Figure EC 8.Q Figure EC 8.R]): Brown-to-black hyperpigmentation with velvety or warty skin in intertriginous areas, typically found in the skin folds of the neck and axilla. Most commonly occur in obese individuals with insulin resistance at risk for type II diabetes. Finding may decrease after puberty with weight reduction.
    3. c. Dermal melanosis: Slate-gray, dark brown, or bluish-green lesions.
      1. (1) Post-inflammatory hyperpigmentation (Figure EC 8.S): Most common cause of increased pigmentation.
        1. (a) Pathogenesis: Follows inflammatory processes in the skin (e.g., diaper dermatitis, insect bites, drug reactions, traumatic injuries).
        2. (b) Clinical features: Localized lesions, follow distribution of resolving disorder. More prominent in darkly pigmented children.
        3. (c) Treatment: Lesions typically fade over several months. Photoprotection is critical with protective clothing and sunscreen of at least SPF 30. Individuals should also avoid physical trauma to areas as well as medications that may worsen hyperpigmentation. Intervention with medication is not always required; however, when it is, hydroquinone is first-line therapy.35
      2. (2) Acquired nevomelanocytic nevi (aka pigmented nevi or moles) (Figure EC 8.T)
        1. (a) Pathogenesis: Develop in early childhood as flat lesions called junctional nevi, then develop into compound nevi when nevus cells migrate into the dermis and lesions enlarge and become papular.
        2. (b) Clinical features: Increase in darkness, size, and number during puberty; generally do not exceed 5 mm and retain regularity in color, texture, and symmetry; on sun-exposed areas.
        3. (c) Treatment: Excision unnecessary, unless cosmetic concern.
        4. (d) Changes associated with development of melanoma: See ABCDEs of Melanoma as well as burning, itching, or redness.
      3. (3) Melanomas (Figure EC 8.U)
        1. (a) Pathogenesis: May occur de novo or within acquired or congenital nevi.
        2. (b) Epidemiology: High lifetime risk in those with presence of multiple, large, and irregularly pigmented, bordered, textured nevi and family history of malignant melanomas.
        3. (c) Management: Children in high-risk families must be carefully observed for atypical nevi development especially in adolescence. Changing nevi with unusual appearance or an “ugly duckling” (mole that is different from all other moles) must be considered for biopsy.
        4. (d) ABCDEs of Melanoma: Criteria for older children and adults is as follows: Asymmetric shape, Borders that are irregular, Color that is variable throughout lesion, Diameter greater than the size of a pencil eraser (>6 mm), Evolution (change is the most important factor in melanoma diagnosis).36 Pediatric patients up to age 20 have their own ABCD criteria: Amelanotic, Bleeding, Bump, Color uniformity, De novo, any Diameter.37
      4. (4) Melanonychia (see Figure EC 8.G): Darkened nail pigment that most commonly is caused by melanin or hemosiderin deposits in the nail plate. Regular, organized longitudinal lines tend to be benign whereas irregularities are associated with nail melanoma in adults. However, nail matrix nevi in children often have features that would be considered red flags in the adult population; thus, these criteria may not be applied to children. There are no pediatric specific guidelines for management. Typically, this clinical finding is due to nail matric nevi. Nail melanomas are very rare though children with this clinical finding warrant close follow up.38,39
      5. (5) Spitz nevus (aka spindle and epithelial cell nevus) (Figure EC 8.V): Innocent nevomelanocytic nevus often confused with malignant melanoma.
        1. (a) Clinical features: Rapidly growing, dome-shaped, red or reddish-brown papules or nodules on face or lower extremities that reach full size quickly.
        2. (b) Management: Observe if features of innocent acquired nevus are present. Consider referral to pediatric dermatology if unusual atypical features present.
  2. 2. Hypopigmentation and depigmentation
    1. a. Localized hypopigmentation
      1. (1) Hypopigmented macules (Figure EC 8.W)
        1. (a) Epidemiology: 0.1% to 0.5% of normal newborns have a single hypopigmented macule but it may be a marker for tuberous sclerosis as 70% to 90% of those affected have such macules on the trunk at birth.
        2. (b) Clinical features: Trunk involvement is most common. Majority are lancet or ash-leaf shaped, but may be round, oval, dermatomal, segmental, or irregularly shaped. Vary from pinpoint confetti spots to large patches (>10 cm).
        3. (c) Diagnosis: Wood lamp helpful in lightly pigmented children.
        4. (d) Management: In those where systemic disease is suspected, close observation for other cutaneous findings and systemic symptoms is indicated.
      2. (2) Post-inflammatory hypopigmentation (Figure EC 8.X)
        1. (a) Pathogenesis: May appear after an inflammatory skin condition.
        2. (b) Clinical features: Seen in association with primary lesions of underlying disorder (such as atopic dermatitis). Patches usually variable in size and irregularly shaped. Concomitant hyperpigmentation is common.
    2. b. Diffuse hypopigmentation
      • (1) Albinism: Heterogeneous group of inherited disorders manifested by generalized hypopigmentation or depigmentation of skin, eyes, and hair. These individuals should undergo ophthalmologic examination to evaluate for various associated conditions. Sun protection is important as well as regular skin exams.

Descriptive text is not available for this image

Figure EC 8.P
Café-au-lait spot.
From Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:48–68.


Descriptive text is not available for this image

Figure EC 8.Q
Acanthosis nigricans, axilla.
From Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:48–68.


Descriptive text is not available for this image

Figure EC 8.R
Acanthosis nigricans, neck.
From Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:48–68.


Descriptive text is not available for this image

Figure EC 8.S
Postinflammatory hyperpigmentation.
From Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:48–68.


Descriptive text is not available for this image

Figure EC 8.T
Compound nevomelanocytic nevus.
From Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:48–68.


Descriptive text is not available for this image

Figure EC 8.U
Melanoma.
From Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:48–68.


Descriptive text is not available for this image

Figure EC 8.V
Pigmented spitz nevus.
From Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:48–68.


Descriptive text is not available for this image

Figure EC 8.W
Congenital hypopigmented macule.
From Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:48–68.


Descriptive text is not available for this image

Figure EC 8.X
Postinflammatory hypopigmentation.
From Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:48–68.

  1. 3. Dyspigmentation
    1. a. Blaschkoid dyspigmentation40: Congenital hypopigmentation and hyperpigmentation along the lines of Blaschko (Figure EC 8.Y).
      1. (1) Patterns of hyper- or hypopigmentation: Whorl shape on trunk, V-shape on the back, waves on the vertex scalp.
      2. (2) Pathogenesis: Blaschko lines occur due to genetic mosaicism.
      3. (3) Children unlikely to have or develop serious extracutaneous involvement.

Descriptive text is not available for this image

Figure EC 8.Y
Blaschkoid dyspigmentation.
From Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. China: Saunders Elsevier; 2013:48–68.

Author(s)

Jennifer Reed DiBiagio, MD, M. Cooper Lloyd, MD, MPH

References

  1. ISSVA classification for vascular anomalies. International society for the study of vascular anomalies. http://www.issva.org/UserFiles/file/ISSVA-Classification-2018.pdf. . ISSVA classification for vascular anomalies. international society for the study of vascular anomalies. Available at: http://www.issva.org/UserFiles/file/ISSVA-Classification-2018.pdf. Accessed September 2018.
  2. D. Darrow, A. Greene, A. Mancini, A. Nopper Diagnosis and management of infantile hemangioma. Pediatrics. 2015;136:e1060. Darrow D, Greene A, Mancini A, Nopper A. Diagnosis and management of infantile hemangioma. Pediatrics. 2015;136: e1060  [PMID:26416931]
  3. D. Krowchuk, et al. Clinical practice guideline for the management of infantile hemangiomas. Pediatrics. 2019;143(1):1-28. Krowchuk D et al. Clinical practice guideline for the management of infantile hemangiomas. Pediatrics. 2019;143(1):1-28  [PMID:30584062]
  4. D.A. Hartemink, Y.E. Chiu, B.A. Drolet, et al. PHACES syndrome: a review. Int J Pediatr Otorhinolaryngol. 2009;73:181-187. Hartemink DA, Chiu YE, Drolet BA, et al. PHACES syndrome: a review. Int J Pediatr Otorhinolaryngol. 2009;73:181-187.  [PMID:19101041]
  5. FDA, pierre fabre pharmaceuticals. hemangeol. 2014;.http://www.accessdata.fda.gov/drugsatfda_docs/label/2014/205410s000lbl.pdf. FDA, pierre fabre pharmaceuticals. hemangeol. March 2014. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2014/205410s000lbl.pdf. Accessed September 2018.
  6. E. Baselga, B. Dembowska-Baginska, P. Przewratil, et al. Efficacy of propranolol between 6 and 12 months of age in high-risk infantile hemangioma. Pediatrics. 2018;142(3):e20173866. Baselga E, Dembowska-Baginska B, Przewratil P, et al. Efficacy of propranolol between 6 and 12 months of age in high-risk infantile hemangioma. Pediatrics. 2018;142(3):e20173866.  [PMID:30082451]
  7. N.M. Bauman, R.J. McCarter, P.C. Guzzetta, et al. Propranolol vs prednisolone for symptomatic proliferating infantile hemangiomas: a randomized clinical trial. JAMA Otolaryngol Head Neck Surg. 2014;140(4):323-330. Bauman NM, McCarter RJ, Guzzetta PC, et al. Propranolol vs prednisolone for symptomatic proliferating infantile hemangiomas: a randomized clinical trial. JAMA Otolaryngol Head Neck Surg. 2014;140(4):323-330
  [PMID:24526257]
  8. B.A. Cohen, L. Rozell-Shannon Early diagnosis and intervention of vascular anomalies (infantile hemangiomas and malformations). Pediatric Care Online. http://pediatriccare.solutions.aap.org. . Cohen BA, Rozell-Shannon L. Early diagnosis and intervention of vascular anomalies (infantile hemangiomas and malformations). pediatric care online. Available at: http://pediatriccare.solutions.aap.org. Accessed September 2018.
  9. C.S. Kwok, S. Gibbs, C. Bennett Topical treatment for cutaneous warts. Cochrane Database Syst Rev. 2012;9:CD001781. Kwok CS, Gibbs S, Bennett C. Topical treatment for cutaneous warts. Cochrane Database Syst Rev. 2012;(9):CD001781.  [PMID:22972052]
  10. M.I. Hicks, D.M. Elston Scabies. Dermatol Ther. 2009;22:279-292. Hicks MI, Elston DM. Scabies. Dermatol Ther. 2009;22:279-292.  [PMID:19580575]
  11. M.D. Andrews, M. Burns Common tinea infections in children. Am Fam Physician. 2008;77:1415-1420. Andrews MD, Burns M. Common tinea infections in children. Am Fam Physician. 2008;77:1415-1420.  [PMID:18533375]
  12. Tinea Capitis. In: The Red Book. 31st ed. Itasca: American Academy of Pediatrics; 798-801.
  13. A. Alkhalifah, A. Alsantali, E. Wang, et al. Alopecia areata update: part II. Treatment. J Am Acad Dermatol. 2010;62:191-202. Alkhalifah A, Alsantali A, Wang E, et al. Alopecia areata update: part II. Treatment. J Am Acad Dermatol. 2010;62:191-202.  [PMID:20115946]
  14. A.L. Zaenglein, D.M. Thiboutot Expert committee recommendations for acne management. Pediatrics. 2006;118:1188-1199. Zaenglein AL, Thiboutot DM. Expert committee recommendations for acne management. Pediatrics. 2006;118:1188-1199.  [PMID:16951015]
  15. C.B. Archer, S.N. Cohen, S.E. Baron Guidance on the diagnosis and clinical management of acne. Clin Exp Dermatol. 2012;37(suppl 1):1-6. Archer CB, Cohen SN, Baron SE. Guidance on the diagnosis and clinical management of acne. Clin Exp Dermatol. 2012;37(suppl 1):1-6.  [PMID:22486762]
  16. L.F. Eichenfield, A.C. Krakowski, C. Piggott, et al. Evidence-based recommendations for the diagnosis and treatment of pediatric acne. Pediatrics. 2013;131(suppl 3):S163-S186. Eichenfield LF, Krakowski AC, Piggott C, et al. Evidence-based recommendations for the diagnosis and treatment of pediatric acne. Pediatrics. 2013;131(suppl 3):S163-S186.  [PMID:23637225]
  17. M. Kawshima, S. Harada, C. Loesche, Y. Miyachi Adapalene gel 0.1% is effective and safe for Japanese patients with acne vulgaris: a randomized, multicenter, investigator-blinded controlled study. J Dermatol Sci. 2008;49(3):241. Kawshima M, Harada S, Loesche C, Miyachi Y. Adapalene gel 0.1% is effective and safe for Japanese patients with acne vulgaris: a randomized, multicenter, investigator-blinded controlled study. J Dermatol Sci. 2008;49(3):241.
  18. K. Graupe, W.J. Cunliffe, H.P. Gollnick, R.P. Zaumseil Efficacy and safety of topical azelaic acid (20 percent cream): an overview of results from European clinical trials and experimental reports. Cutis. 1996;57(suppl 1):20. Graupe K, Cunliffe WJ, Gollnick HP, Zaumseil RP. Efficacy and safety of topical azelaic acid (20 percent cream): an overview of results from European clinical trials and experimental reports. Cutis. 1996:57(suppl 1):20.  [PMID:8654128]
  19. M.S. Pogacar, U. Maver, N.M. Varda, D. Micetc-Turk Diagnosis and management of diaper dermatitis in infants with emphasis on skin microbiota in the diaper area. Int J Dermatol. 2018;57:265-275. Pogacar MS, Maver U, Varda NM, Micetc-Turk D. Diagnosis and management of diaper dermatitis in infants with emphasis on skin microbiota in the diaper area. Int J Dermatol. 2018;57:265-275.
  20. S. Alston, B. Cohen, M. Braun Persistent and recurrent tinea corporis in children treated with combination antifungal/corticosteroid agents. Pediatrics. 2003;111:201. Alston S, Cohen B, Braun M. Persistent and recurrent tinea corporis in children treated with combination antifungal/corticosteroid agents. Pediatrics. 2003;111;201.  [PMID:12509578]
  21. M.A. McAleer, C. Flohr, A.D. Irvine Management of difficult and severe eczema in childhood. BMJ. 2012;345:e4770. McAleer MA, Flohr C, Irvine AD. Management of difficult and severe eczema in childhood. BMJ. 2012;345:e4770.  [PMID:22826585]
  22. L.F. Eichenfield, W.L. Tom, T.G. Berger, et al. Guidelines of care for the management of atopic dermatitis. Section 2. Management and treatment of atopic dermatitis with topical therapies. J Am Acad Dernatol. 2014;71(1):116-132. Eichenfield LF, Tom WL, Berger TG, et al. Guidelines of care for the management of atopic dermatitis. Section 2. Management and treatment of atopic dermatitis with topical therapies. J Am Acad Dernatol. 2014;71(1):116-132.
  23. L.F. Stein Gold, L. Spelman, M.C. Spellman, M.H. Hughes, L.T. Zane A phase 2, randomized, controlled, dose-ranging study evaluating crisaborole topical ointment, 0.5% and 2% in adolescents with mild to moderate atopic dermatitis. J Drugs Dermatol. 2015;14(12):1394. Stein Gold LF, Spelman L, Spellman MC, Hughes MH, Zane LT. A phase 2, randomized, controlled, dose-ranging study evaluating crisaborole topical ointment, 0.5% and 2% in adolescents with mild to moderate atopic dermatitis. J Drugs Dermatol. 2015;14(12):1394.  [PMID:26659931]
  24. T.S. Patel, S.C. Greer, R.B. Skinner Jr. Cancer concerns with topical immunomodulators in atopic dermatitis: overview of data and recommendations to clinicians. Am J Clin Dermatol. 2007;8:189-194. Patel TS, Greer SC, Skinner RB Jr. Cancer concerns with topical immunomodulators in atopic dermatitis: overview of data and recommendations to clinicians. Am J Clin Dermatol. 2007;8:189-194.  [PMID:17645374]
  25. T.G. Berger, M. Duvic, A.S. Van Voorhees, M.J. VanBeek, I.J. Frieden, American Academy of Dermatology Association Task Force The use of topical calcineurin inhibitors in dermatology: safety concerns. Report of the American academy of dermatology association task force. J Am Acad Dermatol. 2006;54(5):818. Berger TG, Duvic M, Van Voorhees AS, VanBeek MJ, Frieden IJ, American Academy of Dermatology Association Task Force. The use of topical calcineurin inhibitors indermatology: safety concerns. report of the american academy of dermatology association task force. J Am Acad Dermatol. 2006;54(5):818.  [PMID:16635663]
  26. M. Boquniewicz, D.Y. Leung Recent insights into atopic dermatitis and implications for management of infectious complications. J Allergy Clin Immunol. 2010;125:4-13. Boquniewicz M, Leung DY. Recent insights into atopic dermatitis and implications for management of infectious complications. J Allergy Clin Immunol. 2010;125:4-13.
  27. R.G. Hernandez, B.A. Cohen Insect bite-induced hypersensitivity and the SCRATCH principles: a new approach to papular urticaria. Pediatrics. 2006;118:e189-e196. Hernandez RG, Cohen BA. Insect bite-induced hypersensitivity and the SCRATCH p16. rinciples: a new approach to papular urticaria. Pediatrics. 2006;118:e189-e196.  [PMID:16751615]
  28. B.A. Cohen Disorders of the hair and nails. Pediatric Dermatology. Philadelphia: Elsevier; 2013. Cohen BA. Disorders of the hair and nails. In: Pediatric Dermatology. 4th ed. Philadelphia: Elsevier; 2013:211-239.
  29. A.K. Gupta, R.R. Mays, S.G. Versteeg, N.H. Shear, S.F. Frielander Onychomycosis in children: safety and efficacy of antifungal agents. Pediatric Dermatology. 2018;35:552-559. Gupta AK, Mays RR, Versteeg SG, Shear NH, Frielander SF. Onychomycosis in children: Safety and efficacy of antifungal agents. Pediatric Dermatology. 2018;35:552-559.  [PMID:29943838]
  30. B.A. Cohen Disorders in pigmentation. Pediatric Dermatology. Philadelphia: Elsevier; 2013. Cohen BA. Disorders in pigmentation. In: Pediatric Dermatology. 4th ed. Philadelphia: Elsevier; 2013:48-68.
  31. K.N. Kanada, M.R. Merin, A. Munden, S.F. Friedlander A prospective study of cutaneous findings in newborns in the United States: correlation with race, ethnicity, and gestation status using updated classification and nomenclature. J Pediatr. 2012;161(2):240-245. Kanada KN, Merin MR, Munden A, Friedlander SF. A prospective study of cutaneous findings in newborns in the United States: correlation with race, ethnicity, and gestation status using updated classification and nomenclature. J Pediatr. 2012 Aug; 161 (2): 240-245.  [PMID:22497908]
  32. A.A. Marghoob Congenital melanocytic nevi. Evaluation and management. Dermatol Clin. 2002;20:607. Marghoob AA. Congenital melanocytic nevi. Evaluation and management. Dermatol Clin 2002; 20:607.  [PMID:12380048]
  33. Marghoob AA. Number of satellite nevi as a correlate for neurocutaneous melanocytosis in patients with large congenital melanocytic nevi. Journal A.MA. Archives of Dermatology (1960-2012). Vols 140. 2. 171–175.
  34. F. Di Rocco, G. Sabatino, M. Koutzoglou, D. Battaglia, M. Caldarelli, G. Tamburrini Neurocutaneous melanosis. Childs Nerv Syst. 2004;20(1):23. Di Rocco F, Sabatino G, Koutzoglou M, Battaglia D, Caldarelli M, Tamburrini G. Neurocutaneous melanosis. Childs Nerv Syst. 2004; 20(1):23.  [PMID:14576958]
  35. V.D. Callender, S. St Surin-Lord, E.C. Davis, M. Maclin Postinflammatory hyperpigmentation: etiologic and therapeutic considerations. Am J Clin Dermatol. 2011;12(2):87. Callender VD, St Surin-Lord S, Davis EC, Maclin M. Postinflammatory hyperpigmentation: etiologic and therapeutic considerations. Am J Clin Dermatol. 2011;12(2)2:87.  [PMID:21348540]
  36. American Academy of Dermatology. https://www.aad.org/public/spot-skin-cancer/learn-about-skin-cancer/detect.... . American Academy of Dermatology. Available at: https://www.aad.org/public/spot-skin-cancer/learn-about-skin-cancer/detect/what-to-look-for. Accessed September 2018.
  37. K.M. Cordoro, D. Gupta, I.J. Frieden, T. McCalmont, M. Kashani-Sabet Pediatric melanoma: results of a large cohort study and proposal for modified ABCD detection criteria for children. J Am Acad Dermatol. 2013;68(6):913-925. Cordoro KM, Gupta D, Frieden IJ, McCalmont T, Kashani-Sabet M. Pediatric melanoma: results of a large cohort study and proposal for modified ABCD detection criteria for children. J Am Acad Dermatol. 2013 Jun; 68(6):913-925.  [PMID:23395590]
  38. L. Thomas, S. Dalle Dermoscopy provides useful information for the management of melanonychia striata. Dermatol Ther. 2007;20(1):3-10. Thomas L, Dalle S. Dermoscopy provides useful information for the management of melanonychia striata. Dermatol Ther. 2007 Jan;20(1):3-10.  [PMID:17403255]
  39. B.M. Piraccini, E. Dika, P.A. Fanti Tips for diagnosis and treatment of nail pigmentation with practical algorithm. Dermatol Clin. 2015;33(2):185-195. Piraccini BM, Dika E, Fanti PA. Tips for diagnosis and treatment of nail pigmentation with practical algorithm. Dermatol Clin. 2015 Apr; 33(2):185-195.  [PMID:25828711]
  40. J. Cohen, K. Shahrokh, B. Cohen Analysis of 36 cases of blaschkoid dyspigmentation: reading between the lines of Blaschko. Pediatr Dermatol. 2014;31(4):471-476. Cohen J, Shahrokh K, Cohen B. Analysis of 36 Cases of Blaschkoid dyspigmentation: reading between the lines of Blaschko. Pediatr Dermatol. 2014;31(4):471-476.  [PMID:25039703]

Dermatology is a sample topic from the Harriet Lane Handbook.

To view other topics, please or .

The Harriet Lane Handbook app and website provides pediatric diagnosis and treatment, pediatric management algorithms, and pediatric drug formulary from experts at Johns Hopkins University. .