ETIOLOGY

Atopic dermatitis (AD), also known as eczema, is a very common inflammatory skin condition affecting approximately 10% to 20% of children. It usually presents in the first 6 months of life, and 60% to 70% of cases remit by 15 years of age.¹ Over 50% of children with AD have been shown to have sensitization to a food or aeroallergen. However, the clinical relevance of these food allergens is not well-enough defined to recommend elimination diets.² Children with AD are also at risk of developing asthma and allergic rhinitis.

PATHOPHYSIOLOGY

AD results from the primary problem of dry skin, perhaps arising from a defective skin barrier in the stratum corneum. This defect in skin integrity places the child at risk for skin infection with bacteria, fungi, and viruses. Furthermore, dry skin becomes pruritic, and inflammation results after persistent itching.

RECOGNITION

Clinical manifestations vary with the age of the patient. Infants may present with symmetric dry red patches or vesicles on the cheeks (Fig. 94-1), scalp, trunk, and flexor and extensor surfaces of extremities. Scratching can lead to weeping lesions, lichenification, or crusted erosions (Figs. 94-2 and 94-3). Older children tend to have lesions on the flexural areas of the extremities, face, neck, and dorsum of hands and feet. Nummular (“coin shaped”) eczema usually manifests as round, extremely pruritic lesions on the extremities (Fig. 94-4). Eczema herpeticum is a condition that occurs when Herpes simplex virus (HSV) infection penetrates the skin through the already impaired barrier affected by an eczematous lesion (Fig. 94-5). It is commonly coinfected with Staphylococcus aureus. AD is usually a clinical diagnosis made by typical patterns of lesions and symptoms.

MANAGEMENT

Dry skin requires liberal use (five times per day) of emollients. Systemic antihistamines relieve itchy skin. Inflamed skin is improved by the use of topical steroids, calcineurin inhibitors (such as 0.3% tacrolimus or pimecrolimus for children younger than 16 years, approved for use in children older than 2 years), or systemic steroids in severe flares. Use only low-potency steroids or calcineurin inhibitors on the face or other areas of thin skin to avoid skin atrophy. Referral to a dermatologist is indicated if the patient requires a steroid stronger than intermediate strength. Table 94-1 shows a list of topical steroids along with their potencies. Nummular eczema responds well to topical medium-strength steroids and systemic antihistamines. Antibiotics covering S. aureus and Streptococcus should be given when lesions appear infected. For localized lesions, topical mupirocin or fusidic acid may be applied (BID or TID to affected area for 7–10 days).³ Cephalexin (50 mg/kg divided TID or QID) or clindamycin (30 mg/kg divided TID) are reasonable antibiotic choices when lesions are more widespread. Consider coverage of methicillin-resistant Staphylococcus aureus (MRSA) in areas where it is highly prevalent, with antibiotic choices based on local patterns of susceptibility of the organism. Cleansing the skin in a bath containing dilute sodium hypochlorite may help when superinfection is present, as well as to prevent recurrence of infection.⁴ Antiviral agents (acyclovir 30 mg/kg divided TID) active against HSV should be given systemically (along with antistaphylococcal antibiotics) when eczema herpeticum is identified. Inpatient treatment with IV antiviral agents is sometimes necessary with severe infections.⁵

ETIOLOGY

Papular urticaria, also known as insect bite–induced hypersensitivity reaction, is a condition in which chronic or recurrent eruptions of usually symmetric pruritic papules, vesicles, and wheals result from a hypersensitivity reaction to biting or stinging insects.⁶ Although it can be seen at any age, the peak age is from 2 to 10 years. Common inciting insects include dog and cat fleas, mosquitoes, scabies, lice, ticks, and an increasing incidence of bedbugs (Cimex lectularius).

PATHOPHYSIOLOGY

Sensitization to the causative agent is required to develop papular urticaria, and is the reason this condition is not seen frequently in the very young. A delayed type hypersensitivity develops and leads to increasing reaction with each exposure in children.

RECOGNITION

Lesions start as pruritic papules, vesicles, and/or wheals that are usually seen as linear, grouped clusters (so-called “breakfast–lunch–dinner”) on exposed areas of skin, sparing the groin and axillary regions, and sometimes concentrated at sock lines and the waistband area.⁷ Urticarial papules develop a central vesicle within 1 to 3 days. Central crusting followed by residual hypo- or hyperpigmented lesions completes the process.⁸ Secondary bacterial infection can occur through scratching of lesions. Diagnosis is usually made through history and physical examination.

MANAGEMENT

Systemic antihistamines and topical steroids can provide symptomatic relief. Antibiotics should be used to treat bacterial superinfections. Environmental control of the source of the pests (treating pets for infestations, new mattresses if bed bugs are identified, washing clothing, and bedding in hot water) is key to preventing further outbreaks.⁹

ETIOLOGY

There are no confirmed causative agents, though various fungi (Pityrosporum, Aspergillus) and bacteria (Staphylococcus and Streptococcus) have been suggested. Atopy is a common coincident condition.

PATHOPHYSIOLOGY

Reduced melanin pigment in the presence of variable number of melanocytes is present in histopathological examination of pityriasis alba (PA) biopsies, suggesting possible abnormal degradation of melanosomes.¹⁰

RECOGNITION

Lesions start as erythematous, well-demarcated macular lesions with scaly edges that transform to asymptomatic hypopigmented, scaly patches that are commonly seen on the face (Fig. 94-6), but can be present on any part of the body.¹¹ PA differs from vitiligo in that some pigment is present in PA, and the borders of skin affected are much less distinct than in vitiligo. In the emergency department (ED), diagnosis is usually made by history and clinical appearance alone, and ancillary studies are not typically necessary for diagnostic purposes.

MANAGEMENT

Topical emollients are routinely used with topical steroids and calcineurin inhibitors reserved for severe cases.¹²

ETIOLOGY

Pompholyx, also known as dyshidrotic eczema, is a chronic relapsing vesicobullous inflammatory disease of the hands and feet in the same family as AD.

In two-thirds of cases, pompholyx is triggered most commonly by contact allergy. Mycoses, drugs, and food allergies account for many of the other known causative agents.¹³

PATHOPHYSIOLOGY

Pompholyx is an eczematous reaction of the palmar and plantar surfaces with edema and thickening of the epidermis and overlying horny layer of epithelium.

RECOGNITION

Symmetrically distributed palmar and/or plantar surface “weepy” lesions characterized by itching and burning are typical presenting symptoms. Symptoms are exacerbated by sweaty hands/feet, occlusive covering of hands/feet, working in wet environments, and smoking.

MANAGEMENT

Pompholyx is a difficult condition to treat effectively. Control inflammation and blister formation by using topical steroids or calcineurin inhibitors (tacrolimus or pimecrolimus). Systemic therapy with steroids is used for severe flares. Alitretinoin, a systemic retinoid, has been studied, with dose-dependent improvement in pompholyx flares in up to 33% of adults receiving the highest (30 mg) dose studied compared to 16% with placebo. Studies in children are lacking. Topical therapy with bexarotene (a retinoid X receptor agonist) and intracutaneous botulinum toxin is being studied but is not yet approved for children or adults with pompholyx at this time.¹⁴ Phototherapy with UVA light is a therapeutic option in an outpatient dermatology clinic. Systemic antihistamines can be used to control pruritis. Antibiotics should be used if bacterial superinfection occurs.