Chapter 93: Dermatitis

• Atopic dermatitis affects 10% to 20% of children and 60% to 70% of cases remit by 15 years of age.

• Typical patterns of eczematous rash occur based on the age of the patient—extensor surfaces of the extremities, cheeks, and scalp for young children; flexor surfaces of the extremities for older children.

• Nickel allergy is the most common identifiable cause of allergic contact dermatitis.

• Irritant diaper dermatitis occurs on the convex surfaces of skin in the diaper area, while fungal diaper dermatitis occurs in the concave surfaces with satellite papules on the adjacent skin.

• Most cases of dermatitis, regardless of cause, respond to topical steroids and removal of causative agent. Rarely, systemic steroids are needed to bring inflammation under control.

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 are not well defined enough 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, scalp, trunk, and flexor and extensor surfaces of extremities. Scratching can lead to weeping lesions, lichenification, or crusted erosions (Figs. 93-1 and 93-2). 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. 93-3). 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. 93-4). 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 tacrolimus or pimecrolimus, approved for use in children older than 2 years), or systemic steroids in severe flares. Use only low-potency steroids on the face or other areas of thin skin. Referral to a dermatologist is indicated if the patient requires a steroid stronger than intermediate strength. Table 93-1 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. Cephalexin (50 mg/kg divided TID or QID) or clindamycin (30 mg/kg divided TID) are reasonable antibiotic choices. 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. Antiviral agents (Acyclovir 30 mg/kg divided TID) active against HSV should be given systemically (along with anti-staphlycoccal antibiotics) when eczema herpeticum is identified. Inpatient treatment with IV antiviral agents is sometimes necessary with severe infections.³

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.⁴ 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 bed bugs (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.

Recognition

Lesions start as pruritic papules, vesicles, and/or wheals are usually seen as linear, grouped clusters (so-called “breakfast–lunch–dinner”) on exposed areas of skin sparing the groin and axillary regions. Urticarial papules develop a central vesicle within 1 to 3 days. Central crusting followed by residual hypo- or hyperpigmented lesions completes the process.⁵ Secondary bacterial infection can occur through scratching of lesions. Diagnosis is usually made through thorough 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.⁶

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.⁷

Recognition

Asymptomatic hypopigmented, scaly patches are commonly seen on the face, but can be present on any part of the body. 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 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.⁸

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.⁹

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. Similar 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.¹⁰ 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.

Ancillary Studies

Diagnosis is usually made clinically in the ED, but patch testing can be done by a dermatologist to confirm the diagnosis (and distinguish it from a contact allergic dermatitis) as an outpatient.

Etiology

Juvenile plantar dermatosis (JPD) is a condition that affects school-age children, generally self-resolving by puberty. The exact cause is unclear, but is associated with AD and the wearing of tight, poorly ventilated shoes. Friction of shoes on the feet may also play a role. Incidence of JPD has been on the decline, possibly due to more cases being identified as allergic contact dermatitis (ACD).¹¹

Pathophysiology

Histologic examination reveals acanthosis with hyperkeratosis, lymphocytic infiltrate in the dermis around the sweat ducts, and inflammation in the epidermis.¹²

Recognition

JPD features include redness of the plantar foot surface, especially the anterior heel and plantar toe surface. Chronic JPD patients demonstrate fissuring of the plantar surface of toes sparing the interdigital spaces (which helps to differentiate it from tinea pedis), cracking and dryness of the plantar surface of the foot with pain and burning.

Management

Topical emollients, steroids, and changing footwear are recommended but often are not curative. Case reports describing improvement with use of calcineurin inhibitors have been described.¹³

Ancillary Studies

In the ED, diagnosis is usually made by history and clinical appearance. Patch testing can be done in the dermatologist office as an outpatient.

Etiology

The cause of lichen striatus (LS) is unknown. This dermatosis affects children from ages 6 months to 15 years, and is caused possibly by a viral illness, trauma, or hypersensitivity. Atopy may be a predisposing factor in developing LS.

Pathophysiology

T-cell mediated autoimmune inflammation in the epidermis leads to keratinocyte death and typical appearance. Histopathology changes over time as lesions progress from red–brown to hypopigmented.¹⁴

Recognition

LS presents with erythematous or brownish papules that are scaly with occasional vesicles. Lesions are usually solitary, linear, and unilateral with distribution on the extremities, and less commonly on the trunk. The onset is abrupt, progressing over weeks with resolution in 6 months to 2 years leaving a temporary hypopigmented area. Lesions are nonpruritic and not painful.¹⁵ Diagnosis is usually based on clinical appearance of lesions.

Management

Topical low- to medium-potency steroids do not seem to help shorten the duration of this condition.

Etiology

ACD is much less common that irritant contact dermatitis (ICD), accounting for a minority (20%) of cases of contact dermatitis. Plants (poison ivy, sumac, oak), nickel, thimerosal, perfumes, variety of synthetic chemicals in rubber, metals, dyes, and preservatives can cause ACD. Nickel allergy is the most common cause of ACD.¹⁶

Pathophysiology

ACD is a type IV T-cell mediated hypersensitivity reaction. The allergen penetrates skin and activates Langerhans cell within skin, which presents the antigen to T-cells (sensitization). Upon re-exposure to allergen, memory T-cells activate the allergic response leading to skin findings.

Recognition

ACD skin findings include red, edematous, areas in discrete patterns matching distribution of causative agent exposure (e.g., a button-shaped area over the area where a button on jeans makes contact with the skin), but unlike irritant contact dermatitis, these patients can have vesicles and papules present. Rhus dermatitis is a specific ACD appearing as a linear, pruritic, vesicobullous eruption after exposure to poison ivy, sumac, or oak. Shoe dermatitis is an ACD affecting dorsa of feet, sparing the skin between the toes that clinically is indistinguishable from JPD (an irritant contact dermatitis-–see section on Juvenile Plantar Dermatosis for more information).

Management

Topical moisturizers, systemic antihistamines, and topical steroids are the mainstay of treatment of ACD. Oral steroid course lasting 5 to 7 days can be used for severe flares. In rhus dermatitis, a 14-day course (7 days 1 mg/kg/d followed by a 7-day taper) is sometimes used. Topical calcineurin inhibitors may be used as second-line therapy.¹⁷

Ancillary Studies

Diagnosis is usually made by history and clinical appearance of lesions. Refractory cases of ACD or those involving the face/hands should have patch testing done against various allergens by a dermatologist or allergist.

Etiology

ICD accounts for approximately 80% of contact dermatitis cases. Irritants leading to ICD include but are not limited to: saliva, feces, urine, foods, detergents, soaps, wipes, bubble baths, nickel, and cobalt. Nickel is the most common identifiable cause of ICD.¹⁸ Ask about exposures to hygiene products, new clothing/diapers, footwear, jewelry, cosmetics, fragrances, deodorants, medicines (systemic and topical), and nonprescription medicinal supplements. Inquire about products used by parents and siblings, as children often will experiment with these substances on their own skin leading to ICD.¹⁹

Pathophysiology

ICD is a nonimmunologic inflammatory reaction to any substance irritating the skin.

Recognition

ICD physical reveals red patches in discrete patterns matching distribution of causative agent exposure (Fig. 93-5). Lip licker's dermatitis is a unique perioral ICD seen after excessive licking around lips, usually in toddlers. Contact diaper dermatitis is a commonly seen form of ICD (see section on Diaper Dermatitis for more information).

Management

Allergen avoidance is most important treatment in ICD. Topical moisturizers, systemic antihistamines, and topical steroids are the mainstay of treatment of ICD. Resistant cases may require topical calcineurin inhibitors or even systemic steroids for a short (5 days) course. Barrier creams (zinc oxide) are useful in treating diaper ICD, and should be applied with every diaper change.

Ancillary Studies

ICD is usually a clinical diagnosis. Confirmation via patch testing can be done as an outpatient in consultation with a dermatologist.

Etiology

This group of inflammatory conditions in the groin area is the most common dermatologic problem of infancy. Overhydration of skin, skin-on-skin friction, presence of urine, feces, and microorganisms all play a role in the development of diaper dermatitis. Less commonly, diaper rash can be a symptom of nutritional deficiency or more severe systemic illness (e.g., Kawasaki disease, histiocytosis).

Pathophysiology

Enzymes and alterations in pH in stool and urine break down skin. Friction from skin-on-skin movement leads to irritation. Once skin integrity is interrupted from overhydration and irritation, fungi and bacteria, and occasionally viruses (such as HSV) may invade skin, leading to infection.

Recognition

Contact or irritant diaper dermatitis appears as redness and scaling of convex areas of skin (“mountain peaks”) that come into contact with the diaper that usually spares skin folds.²⁰ Candidal diaper dermatitis features beefy erythema in intertriginous areas (“valleys”) with papular “satellite” lesions. Infants may have oral thrush present.

Bacterial diaper dermatitis is typified by the presence of bullae or impetiginous lesions (honey crust). In folliculitis, small red papules and pustules are present on the buttocks, thighs and low abdomen HSV can occur in the diaper area, with vesicles or bullae noted during first few weeks of life progressing to punched-out blisters. A severe form of diaper dermatitis called Jacquet dermatitis features severe erosions with punched-out lesions.

Management

The following actions can help prevent diaper rash: frequent changing of diapers (q3 to 4 hours or ASAP when stool or urine is present), using barrier cream skin protection (e.g., zinc oxide, petrolatum), using nonocclusive diapers, using superabsorbent diapers, and avoiding cloth diapers and scented wipes.

For contact (irritant) dermatitis a topical barrier paste, ointment, or cream (e.g., zinc oxide, petrolatum, lanolin) should be liberally applied every diaper change. For severe cases, a low-potency steroid cream (hydrocortisone 1%) can be applied topically BID for maximum of 2 weeks. Stomahesive powder is reserved for severe cases refractory to steroids and barrier creams. Cornstarch powder applied topically to the diaper area (and taking special care to avoid the infant's face where aspiration may occur) daily can help reduce friction on skin. This is especially useful for contact dermatitis associated with prolonged wetness. Irritant diaper dermatitis present for >3 days usually has a component of Candida infection, even if the typical candidal appearance is not yet present. Treat these cases with an antifungal cream.²¹

For fungal dermatitis a topical antifungal (miconazole, clotrimazole, nystatin creams) should be applied directly to skin every diaper change until clear for 7 days. Some advocate additional application of a layer of a barrier cream. For bacterial infections topical mupirocin 2% cream applied TID can be used until clear for 7 days. Mupirocin has antifungal properties, so if you are treating a presumed bacterial infection, it may obviate the need to also apply an antifungal cream.²²

Ancillary Studies

Clinical appearance alone is usually sufficient to make the diagnosis. If diagnosis is in question, a skin scraping will show pseudohyphae when potassium hydroxide (KOH) preparation is done in cases of Candida diaper dermatitis. Culture of bullae or lesions may yield definitive diagnosis In rare cases of refractory dermatitis with other systemic symptoms (e.g., failure to thrive in nutritional deficiencies, hepatosplenomegaly, and chronic otorrhea in histiocytosis) other studies including nutrient levels or biopsies are warranted.

Etiology

No exact mechanism is clearly responsible for seborrheic dermatitis (SD), though an interaction between increased sebum production, yeast colonization and immune-mediated inflammation is suspected.²³

Pathophysiology

An unclear link between fungal colonization, immune-mediated inflammatory reaction and hyperproliferation of keratinocytes is suspected to result in the lesions of SD. In infants, Candida and Malassezia have been cultured from lesions.²⁴

Recognition

SD presents in infants usually by the second month of life as greasy, yellow or white, scales on a red base over the scalp, face, chest, diaper area, and/or ears. When isolated to the scalp in infants, it is termed “cradle cap.” A second peak in adolescence occurs presenting as scaly plaques over the eyebrows, scalp (“dandruff”), ears, nasolabial folds, and eyelids. Peaks of exacerbations occur in the winter months. Diagnosis is usually made based on clinical appearance of lesions.

Management

Most cases are benign, asymptomatic, and self-resolving (usually by age 1 to 2 years in the infant form. In infants, topical mineral oil or nonprescription shampoos will loosen the scale enough to be gently brushed away with a soft toothbrush. Safety of selenium containing shampoos has not been established in infants, and is not recommended until after age 2 years. Low-potency topical steroids can be used for SD present in locations outside the scalp. Teenagers can use topical ketoconazole 2% topical preparation for facial lesions along with a low-potency steroid or calcineurin inhibitor for inflammatory lesions. Medicated shampoos (selenium sulfide, tar, salicylic acid, zinc pyrithione, or ketoconazole) are effective for scalp involvement.²⁵

Etiology

Friction of skin-on-skin on intertriginous surfaces leads to primary inflammation and can be a setup for invasion of bacterial or fungal infections. Cutaneous erythrasma, caused by Corynebacterium minutissimum, is a bacterial infection complication of intertrigo that presents as small, reddish-brown macules that may coalesce into larger patches with sharp borders.²⁵ Intertrigo is common in the obese and babies.

Pathophysiology

Moisture and heat leads to friction of skin-on-skin surfaces causing inflammation and irritation deep in the folds of the skin. Superinfections usually occur with Staphylococcus, Group A Streptoccocus, Pseudomonas, Proteus, dermatophytes, and yeasts.²⁶

Recognition

Erythema and inflammation in “mirror image” patterns of the inguinal, axillary, and inframammary folds are seen in intertrigo. Patients may complain of pruritis or pain in the affected area. Sometimes, it involves neck folds, toe webs, antecubital fossae, umbilical, perineal, and intergluteal folds.

Management

Patients should minimize moisture and friction by using cornstarch or barrier creams (zinc oxide). Caution should be taken to avoid aspiration of powder if used near an infant's face. Avoid wool and synthetic fiber clothing. Intertriginous areas should be dried well after bathing and light, absorbent clothing should be worn. Open toe shoes are advised for interdigital web intertrigo. Concomitant bacterial and fungal infections should be treated with antibiotics or antifungal agents as appropriate.

Ancillary Studies

Diagnosis is usually clinical, though culture of an affected area for bacteria or fungus can be performed if the diagnosis is unclear. Wood lamp can help to identify pseudomonal infections (fluoresces green) or erythrasma (fluoresces red).

Etiology

Phytophotodermatitis (PPD) is a phototoxic inflammatory reaction that occurs when a chemical (psoralen) usually from a plant sap or juice, reacts with sun's UVA light (wavelength 320–380 nm) to cause blistering and erythema of the skin, followed by hyperpigmentation. Some cases have only the hyperpigmentation component present.

Pathophysiology

PPD is a type of phototoxic dermatitis. Exposure to the plant chemical psoralen followed by UVA light exposure results in a blistering, erythematous, or hyperpigmented dermatitis. Psoralens come from four plant families: Umbelliferae (hogweed, cow parsley, wild parsnip, celery, wild carrots), Rutucae (rue bergamot, citrus fruits), Moraceae (figs), and Leguminosae (scurf pea).²⁷

Recognition

Obtaining a history of exposure to psoralen and sunlight along with typical linear streaky lesions that are inflamed or hyperpigmented in a light- or sun-exposed area are key to making the diagnosis (Fig. 93-6). PPD has been recognized as a child abuse mimic.²⁸

Management

Removal of the offending agent is sometimes sufficient to treat this self-limiting condition. Use of UVA blocking sunscreen can minimize the effects of PPD. Mild-to-intermediate potency topical steroids and analgesics (acetaminophen or ibuprofen) can be used for more severe cases.

Ancillary Studies

In the ED, diagnosis is usually made by history and clinical appearance. Photopatch testing can be done in the dermatologist office as an outpatient.

Etiology

Oral and topical chemicals, most commonly in drugs, plants, or lotions, can trigger skin reactions on exposure to UV light. Photoallergic reactions are immunologically mediated, require prior sensitization and clinically resemble ACD. Phototoxic reactions do not require prior sensitization and present with intense erythroderma over light-exposed areas. A wide variety of topical and systemic drugs (NSAIDs, sulfas, phenothiazines, antimalarials) can cause either condition. Phototoxic reactions are more common than photoallergic reactions.²⁹

Pathophysiology

Although the exact mechanism is not fully understood, it is postulated that an exogenous compound combines with a skin or circulating protein that reacts with UVA light to create an antigenic conjugate, eliciting a delayed type hypersensitivity reaction leading to the clinically apparent dermatitis

Recognition

The presence of dermatitis or erythroderma is typically seen in sun- or light-exposed areas only. The rash typically spares shadow sites within scalp, under chin and nose. If the diagnosis is unclear, skin biopsy can be performed and typically reveal patterns of histopathological injury. Photopatch testing in the dermatologist's office may be helpful to make the diagnosis as an outpatient.

Management

Removal of the offending agent is critical to management of these patients. Cool compresses, topical steroids, and systemic antihistamines can be used for symptomatic care.