Primary Lesions

Secondary Lesions

Lesions that arise from alteration of a primary lesion, sometimes as a result of manipulation of the skin through scratching, picking, or rubbing.

Clinical Presentation

Acne vulgaris primarily involves the face, chest, and upper back. Lesions include open (blackheads) and closed (whiteheads) comedones, papules, pustules, nodules, and cysts. Neonatal acne presents within the first few weeks of life on the forehead and cheeks and resolves usually by two months, requiring no treatment. The typical lesions of steroid acne are small erythematous papules and pustules, without comedones, primarily located on the back and chest.

Diagnosis

The diagnosis of acne vulgaris is usually straightforward, although a number of conditions may have a similar appearance. The differential diagnosis includes adenoma sebaceum, which appears as pink papules on the face of prepubertal patients with tuberous sclerosis (TS). Other cutaneous manifestations differentiate TS, including ash leaf spots, Shagreen patch, and periungual fibromas. In an infant, seborrheic dermatitis is often misdiagnosed as neonatal acne. Associated cradle cap and retroauricular scaling distinguish seborrhea.

Although comedones can be found in children as young as 6–7 years of age, consider androgen excess (gonadal or adrenal tumors, congenital adrenal hyperplasia) if there is inflammatory acne (papules and pustules) in a prepubertal child.

ED Management

Acne vulgaris is a chronic disease. To help prevent permanent scarring, initiate treatment in the ED, but refer the patient to a primary care setting for ongoing care. Daily anti-acne medication, the use of very gentle cleansers, and the avoidance of sunburns are critical to therapy. Defer the initiation of medications such as isotretinoin and oral contraceptives to the primary care provider.

Topical retinoids and topical and oral antibiotics are the mainstays of treatment. For a patient ≥12 years of age, start with adapalene (0.1% gel; over-the-counter), applied in a thin layer nightly to the affected area. Add topical benzoyl peroxide and clindamycin gel combination, also applied in a thin layer to the affected area, but in the morning.

Add oral antibiotics, either doxycycline 50 to 100 mg bid or 100 mg q day. As an alternative, prescribe minocycline 50 mg q day, bid, or tid. An extended-release form of minocycline has very good compliance and is given as a single daily dose based on weight: 45–49 kg: 45 mg; 50–59 kg: 55 mg; 60–71 kg: 65 mg; 72–84 kg: 80 mg; 85–96 kg: 90 mg; 97–110 kg: 105 mg; 111–125 kg: 115 mg; 126–136 kg: 135 mg.

Treat steroid acne with topical benzoyl peroxide (2.5–10%), a topical antibiotic (as described above), and discontinuation of the steroids, if possible. The management of acne associated with PCOS includes either a combination oral contraceptive or progestin with topical therapies (described above). No therapy, other than reassurance, is required for neonatal acne.

Follow-up

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  Primary care follow-up 2–3 days for patients requiring oral therapy, otherwise routine

ED Management

Most cases of alopecia require no immediate treatment. Refer the patient to a dermatologist or primary care physician for follow-up, especially when the diagnosis is in doubt, or the alopecia is worsening or failing treatment, or there is chronic or scarring alopecia. See p. 139 for the treatment of a kerion.

Clinical Presentation

Pruritic, dry, chronic, relapsing, eczematous lesions are major hallmarks of the disease. Infantile eczema occurs between birth and three years and is characterized by dry skin, erythema, papules, vesicles, oozing, and scales on the face, neck, chest, and extensor surfaces of the extremities. In older children subacute and chronic papular, scaly, and lichenified (thickened, leathery skin with accentuation of the normal skin markings) lesions occur, often in well-circumscribed plaques on the flexor aspects of the neck, arms, and legs. The antecubital and popliteal fossae are classically involved, and the periorbital and perioral regions may also be affected. The adolescent and adult forms demonstrate marked lichenification and flexural, hand, and foot involvement.

Other manifestations in children and adolescents may include nummular eczema (well-demarcated papular coin lesions) and pityriasis alba (discrete hypopigmented macules).

At any age the severe pruritus causes scratching which can lead to secondary bacterial infection. The superimposed pyoderma can confuse the clinical picture. Secondary herpesvirus infection (eczema herpeticum, pp. 125–126) can also occur and become generalized in atopic patients.

Atopic individuals can have a number of associated findings, including accentuated palmar creases, white dermatographism (blanching of the skin when stroked), and Dennie–Morgan folds or pleats (an extra groove of the lower eyelid). Keratosis pilaris (follicular hyperkeratosis) presents with scaly perifollicular papules on cheeks, upper arms, thighs, and buttocks.

Factors that can exacerbate symptoms in patients with AD include temperature, humidity, irritants, infections, foods, inhalant and contact allergens, and emotional stress.

Diagnosis

The diagnosis of atopic dermatitis is suggested by a family history of atopy, a personal history of allergies or asthma, dry and pruritic skin, and the typical location of the lesions that blend into the surrounding normal skin.

In infants, seborrheic dermatitis (pp. 132–133) causes a nonpruritic yellowish or salmon-colored, greasy eruption of the face, scalp, and intertriginous areas. The eruption of a contact dermatitis (pp. 111–113) has a sharp border with the uninvolved skin, and the history may suggest the offending agent. The lesions of tinea corporis (pp. 138–140) usually have central clearing and a raised scaly annular border. Bacterial infections (pp. 107–109) are not preceded by pruritus and are generally more localized than atopic rashes. Psoriatic lesions are usually well-demarcated with a silvery scale and are found on extensor surfaces, gluteal creases, scalp, and genital regions. The eruption of scabies (p. 130) does not follow the usual sites of predilection of AD, and the family or personal history of atopy may be negative. A secondary autoeczematization process may occur with scabies that makes differentiation between eczema and scabies difficult. To differentiate scabies, look for lesions in the interdigital spaces, on the areola, wrists, waist, and groin, and in infants on the palmo-plantar surfaces.

ED Management

Atopic dermatitis is a chronic condition that is best managed in the primary care setting, but therapy can be initiated in the ED. The goals are to hydrate the skin, prevent itching, and treat inflammation. Instruct the patient to avoid excessive bathing, harsh detergents, and fragrances, and to use moisturizers and emollients as first-line therapy (Cetaphil, Eucerin, Aquaphor, Vaseline). Use a low-potency corticosteroid for maintenance therapy, whereas intermediate- and high-potency corticosteroids are indicated for the treatment of clinical exacerbation over short periods of time (see Table 5.3).

Treat pruritus with diphenhydramine (5 mg/kg/day div qid) or hydroxyzine (2 mg/kg/day div qid).

Prescribe a mid-potency topical corticosteroid (0.1% triamcinolone ointment, 0.05% fluticasone cream, 0.1% mometasone cream) for the body and extremities and a low-potency one (1–2.5% hydrocortisone ointment, 0.05% aclometasone, cream or ointment) for the face, neck, and other delicate areas. Limit the course to two weeks and do not use under occlusion in delicate areas.

Do not use oral steroids without consulting a dermatologist. Defer initiating topical nonsteroidal immunomodulator therapy (tacrolimus, opimecrolimus) to the primary care or dermatology office setting.

Reserve the use of wet wraps for severe flares and use only for a few days at a time, because they are time-consuming and children often are resistant to their application. Instruct the family to apply a mild- to moderate-potency topical steroid in a thin layer to the affected area, follow with emollient, cover with slightly damp Kerlix or cotton pajamas, and then place a dry Kerlix or dry pajamas over the treated sites, nightly for 3–5 nights.

If there is a secondary bacterial infection, use topical mupirocin tid on localized areas of involvement, but treat more extensive infections as a cellulitis (pp. 107–109) with oral antibiotics and arrange careful follow-up to document adequate response to treatment.

Follow-up

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  Primary care follow-up in 1–2 weeks

Indications for Admission

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  Severe involvement in a patient who cannot be adequately treated at home or shows signs of secondary infection that would be best treated with intravenous antibiotics

  
  
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  Evidence of eczema herpeticum (pp. 125–126)

Clinical Presentation and Diagnosis

ED Management

Knowing the local community MRSA pattern is critical for choosing the most appropriate empiric treatment. If there is a significant concern, use either clindamycin or trimethoprim-sulfamethoxazole plus a first-generation cephalosporin.

Follow-up

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  Impetigo: primary care follow-up in 2–3 days, if no improvement

  
  
• 
  

  Folliculitis: primary care follow-up in 1–2 weeks

  
  
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  Furunculosis, cellulitis, and erysipelas: primary care follow-up in 2–3 days

Indications for Admission

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  Furunculosis or cellulitis in a patient with an immune deficiency

  
  
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  Fever, proximal lymphadenopathy, and lymphangitic streaking in association with cellulitis or other deep skin infection

  
  
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  Inadequate response to outpatient management

  
  
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  Suspected staphylococcal scalded skin syndrome

  
  
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  Hemodynamic instability

Clinical Presentation

Diagnosis

The typical intense erythema, scaly border, and satellite lesions suggest the diagnosis of cutaneous candidiasis. See diaper dermatitis for differential diagnosis (pp. 113–115). When the diagnosis is in doubt, prepare a KOH prep from a skin scraping or send a fungal culture, but do not delay treatment.

Thrush is often confused with milk in the oral cavity, although milk can easily be scraped from the oral mucosa without causing any bleeding.

ED Management

Prescribe topical nystatin ointment, or miconazole, clotrimazole, or econazole cream. Apply bid or tid to cutaneous eruptions, such as intertrigo, for 2–3 weeks or two days past clearing. Avoid combination products containing neomycin, which can be irritating, as well as topical steroid combination preparations due to the risk of adverse effects from long-term use, especially in areas of occlusion. If the eruption is markedly inflamed, use a low-potency topical corticosteroid such as hydrocortisone 1–2.5% bid for 2–3 days, in addition to a topical antifungal. Instruct the parents to keep these areas clean and dry, if possible, and to use hypoallergenic, gentle cleansers. The additional use of a barrier product containing zinc oxide is often helpful.

For thrush, instill 1 mL of a nystatin oral suspension in each side of the mouth qid, after feedings, until at least two days past clearing. Advise the parent to rub persistent lesions with a gauze pad soaked with nystatin suspension and to discard any old pacifiers, nipples, or teething toys that may be contaminated. Sterilize nipples and pacifiers after use during the treatment phase and encourage treatment of Candida breast colonization and/or infection in lactating mothers. Suspect an underlying immunodeficiency or re-exposure to contaminated items as listed above in a patient with persistent or recurrent thrush in the absence of antibiotic use. For such a patient, or one who has failed to clear on nystatin, prescribe oral fluconazole (6 mg/kg once, then 3 mg/kg/day for 14 days) or clotrimazole troches for a patient >3 years of age (10 mg qid for 7–14 days, dissolve slowly in mouth, do not chew or swallow whole).

Follow-up

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  Primary care follow-up in 1–2 weeks

Clinical Presentation

Irritant contact dermatitis presents within minutes to hours of the contact as an acute eczematous reaction, with erythema, scaling, swelling, vesicles, and erosions of varying severity at the site of the contact. Lesions may be linear and have a sharp demarcation between the involved and uninvolved skin.

Allergic contact dermatitis presents within hours or days with erythema, edema, bullae, and vesicles, most commonly on the hands and face, but also seen on the feet, eyelids, ears, neck, axillae, and periumbilical area. Once again, the lesions may be linear and have a sharp demarcation between the involved and uninvolved skin. Rhus dermatitis presents within 1–3 days of exposure and persists for 1–3 weeks. If aerosolized, there may be severe facial edema presenting in a similar fashion as angioedema, but with fine vesiculation.

Phytophotodermatitis reactions may be eczematous and erythematous, with prominent vesicles and bullae, located in areas of psoralen contact. The cutaneous reaction may assume bizarre digitate, linear or drip patterns. The rash often resolves with subsequent hyperpigmentation. Photoxic reactions can easily be confused with child abuse, burns, or herpes simplex infection.

Diagnosis

The diagnosis is purely clinical, based on appearance and history of exposure. Inquire about exposure to possible offending agents (new soap, detergent, shoes, or foods, or playing in the woods) and whether there has been previous similar episodes or a known sensitivity to a substance. On examination, look for an eczematoid eruption either in nontypical locations or in a linear pattern, with sharp demarcations between involved and normal skin.

ED Management

Avoidance of the offending agent or allergen is critical. Treat an acute dermatitis with open wet dressings (tap water, normal saline, 5% Burrow’s solution) PRN, calamine lotion, daily soothing baths (Aveeno, oatmeal), and antihistamines (hydroxyzine 2 mg/kg/day div tid or diphenhydramine 5 mg/kg/day div qid). For intense inflammation or pruritus, prescribe a low- to medium-potency topical corticosteroid (see Table 5.3) bid for two weeks.

Use a systemic corticosteroid for a dermatitis that is widespread or involves the mucous membranes or eye lids. Start with 0.5–1.5 mg/kg/day (40 mg/day maximum) of prednisone or prednisolone for 4–5 days, then taper over 4–6 days to prevent a rebound in the eruption.

For a chronic contact dermatitis the above modalities may be effective, but refer the patient to a dermatologist for definitive diagnosis and treatment.

Follow-up

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  As needed based on severity; if on systemic steroids follow in two weeks

Indications for Admission

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  Severe reactions with extensive involvement involving mucous membranes or threatening the eyes or upper respiratory tract

Bibliography

Bernstein DI. contact dermatitis for the practicing allergist. J Allergy Clin Immunol Pract. 2015;3(5):652–628; quiz 659–660.

Goldenberg A, Silverberg N, Silverberg JI, Treat J, Jacob SE. Pediatric allergic contact dermatitis: lessons for better care. J Allergy Clin Immunol Pract. 2015;3(5):661–667.

Jacob SE, Goldenberg A, Pelletier JL, et al. Nickel allergy and our children’s health: a review of indexed cases and a view of future prevention. Pediatr Dermatol. 2015;32(6):779–785.

Paller AS, Mancini AJ: Contact dermatitis. In Hurwitz S, Paller A, Mancini A (eds.) Hurwitz’s Textbook of Clinical Pediatric Dermatology (4th edn.). Philadelphia, PA: WB Saunders, 2011; 61–70.

Pelletier JL, Perez C, Jacob SE. Contact dermatitis in pediatrics. Pediatr Ann. 2016;45(8):e287–292.

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Chapter 1 – Resuscitation Chapter 4 – Dental Emergencies Chapter 11 – Gynecologic Emergencies Chapter 9 – Gastrointestinal Emergencies Chapter 19 – Psychological and Social Emergencies Chapter 17 – Orthopedic Emergencies