Dermatologic Presentations

Perspective

Cutaneous eruptions can be manifestations of primary dermatologic disease or signal underlying systemic illness. In addition to medical and family history, three factors are particularly important: onset and evolution of the skin problem, associated symptoms, and prior treatment.

With adequate lighting available, the physical examination is performed with the patient undressed. In general, the dermatologic evaluation includes a thorough evaluation of the scalp, mouth, and nails. Although the examination depends largely on inspection of the skin, palpation helps assess the texture, consistency, and tenderness of the lesions.

Skin lesions are divided into growths and rashes. Growths are subdivided into epidermal, pigmented, and dermal or subcutaneous proliferative processes. Rashes are divided into two groups, depending on whether the epidermis is involved. Lesions and rashes with epidermal involvement are described as being eczematous, scaling, vesicular, papular, pustular, or hypopigmented. Rashes without epidermal involvement are described as being erythematous, purpuric, or indurated.

The diagnosis is aided by the configuration of the lesions and distribution on the body’s surface. On occasion, a configuration is specific for a disease; however, the morphologic appearance of the primary lesion is usually given more diagnostic weight (Table 120-1). Finally, many skin diseases have preferential areas of involvement, so the location of the eruption may aid in diagnosis. Several serious dermatologic disorders, such as Stevens-Johnson syndrome, may be manifested initially with lesions on mucous membranes only, thus making an examination of the mucous membranes an important part of a dermatologic evaluation.

Table 120-1

Definitions of Skin Lesions

LESION	APPEARANCE
Macule	Flat; color differs from surrounding skin
Patch	A macule with surface changes (i.e., scale or wrinkling)
Papule	Elevated skin lesion <0.5 cm in diameter
Plaque	Elevated skin lesion >0.5 cm in diameter; without substantial depth
Nodule	Elevated skin lesion >0.5 cm in diameter and depth
Cyst	Nodule filled with expressible material
Vesicle	Blisters <0.5 cm in diameter filled with clear fluid
Bullae	Blisters >0.5 cm in diameter filled with clear fluid
Pustule	Vesicle filled with cloudy or purulent fluid
Crust	Liquid debris that has dried on the skin surface; usually moist and yellowish brown
Scale	Visibly thickened stratum corneum; usually white
Lichenification	Epidermal thickening characterized by visible and palpable skin thickening and accentuated skin markings
Induration	Dermal thickening that feels thick and firm
Wheal	Papule or plaque of dermal edema; often with central pallor and irregular borders
Erythema	Red appearance of skin caused by vasodilation of dermal blood vessels; blanchable
Purpura	Red appearance of skin caused by blood extravasated from disrupted dermal blood vessels; nonblanchable
Macular purpura	Flat, nonpalpable
Papular purpura	Elevated, palpable

Modified from Lookingbill DP, Marks JG: Principles of Dermatology, 3rd ed. Philadelphia, Saunders, 1993.

Emergency department (ED) management focuses on stabilization (e.g., toxic epidermal necrolysis), symptom control (e.g., acute urticaria and pruritus), flare control (e.g., eczema), and treatment (e.g., skin infections or infestations). A variety of treatment options are available for dermatologic problems, including topical, oral, and intravenous preparations. Vehicles for topical preparations include soaks, creams, ointments, foams, gels, and lotions; use of the proper vehicle is a key component of successful treatment.

Aluminum acetate (Burow’s solution), aluminum sulfate–calcium acetate (Domeboro), or oatmeal soaks may provide symptomatic relief of pruritus in patients with conditions with crusting or weeping. Saline wet soaks provide a moist environment and may be used to promote epithelialization of denuded areas; wet-to-dry dressings can be used for lesions requiring débridement. When wet occlusive dressings are applied, the normal skin is protected from maceration by the creation of a lipophilic barrier with an ointment. If a wet dressing is allowed to dry, it can stick to a wound and thus negate its benefit when it is removed.

Creams are a mixture of oil, water, and preservatives that penetrate the skin on application. Creams may cause drying of the skin and are best used for acute conditions. Lotions are a mixture of powder and water and may require shaking before application. Lotions may be used on any body surface, especially hair-bearing areas. Ointments are emulsions of water and oil that do not penetrate the skin on application; ointments are not usually applied to hairy areas or in natural folds. Ointments are especially useful for treatment of dry lesions. Occlusive dressings are used to increase potency by promoting absorption. Gels and foams liquefy when they are applied to the skin. They are frequently used for scalp lesions as they penetrate the hair barrier easier than other formulations do. Whenever a potent topical medication is prescribed, patients and caregivers are advised not to use their fingers for application; a cotton-tipped applicator or a plastic spatula is recommended instead.

Topical corticosteroids are commonly used for a variety of inflammatory skin conditions. They induce topical vasoconstriction, depress local immunity, and cause skin thinning with prolonged use. Systemic absorption and side effects are possible. A variety of formulations are available (Table 120-2). The potency of steroids depends on the specific drug, its concentration, and the method of delivery (i.e., whether cream or ointment is used, how often it is applied, whether an occlusive dressing is placed). It is wise for clinicians to familiarize themselves with one or two high-, medium-, and low-potency steroids to limit possible errors. So-called mega potency topical steroids are generally not initiated without consulting a dermatologist. The lowest potency medication available should be used around natural orifices to minimize systemic absorption.

Table 120-2

Potency of Topical Steroids

Modified with permission from National Psoriasis Foundation: Topical steroids potency chart. Available at http://www.psoriasis.org/page.aspx?pid=469. Accessed August 16, 2011.

Scales, Plaques, and Patches

Fungal Infection

Principles of Disease

The dermatophytoses are superficial fungal infections that are limited to the skin.¹ A variety of lesions may occur, but the most common are scaling, erythematous papules, plaques, and patches, which often have a serpiginous or wormlike border. Dermatophytes generally grow best in excessive heat and moisture and grow only in the keratin or outer layer of the skin, nails, and hair. Keratin tends to accumulate in body folds, such as between toes and in the inguinal area, the axilla, and the inframammary areas. With the exception of tinea capitis, dermatophyte infections are not markedly contagious.

Any eruption thought to be a dermatophyte infection can be examined under the microscope in a potassium hydroxide (KOH) preparation. The specimen is examined for the characteristic branching hyphae of the dermatophytes or the short, thick hyphae and clustered spores of tinea versicolor. Affected hair, nail, or scales may be cultured on Sabouraud agar incubated at room temperature for 2 or 3 weeks.

Tinea Capitis

Clinical Features.: Tinea capitis is a fungal infection of the scalp. Although it is primarily regarded as a disease of preschool children, tinea capitis is increasingly recognized in adults, infants, and neonates. It is more common among African Americans, although the reasons for this are unknown.² Nosocomial transmission of dermatophyte infections, such as Trichophyton tonsurans, has also been reported.³ Recent outbreaks in the United States caused by T. tonsurans differ from epidemics of the 1940s and 1950s caused by Microsporum audouinii in that many patients have seborrheic-like scaling in the absence of alopecia.² Black dots, representing hair broken off near the scalp, may be noted clinically. Hair loss is the result of hyphae growing within the shaft, rendering it fragile, so that the hair strands break off 1 to 2 mm above the scalp. Circular patches of partial baldness may result. The disease may be transmitted by close child-to-child contact and contact with household pets, hats, combs, barber’s shears, and similar items. Complications include lymphadenitis, bacterial pyoderma, tinea corporis, pigmenting pityriasis alba, id reaction after treatment, secondary bacterial infection, and scarring alopecia.²

Differential Considerations.: The differential diagnosis of tinea capitis includes alopecia areata, atopic dermatitis, nummular eczema, bacterial infection, psoriasis, seborrheic dermatitis, “tinea” amiantacea, trichotillomania (hair pulling), and Langerhans cell histiocytosis.

Diagnostic Strategies.: A KOH preparation is not helpful in the presence of a kerion or in the absence of alopecia, in which case a fungal culture specimen should be obtained.

Management.: Systemic therapy is required for tinea capitis. Treatment usually begins with griseofulvin 20 mg/kg/day, usually not to exceed 1000 mg/day, taken as a single dose with a fat-containing food for a minimum of 6 weeks or 2 weeks after clinical resolution of inflammation. Higher doses may be needed. Griseofulvin can cause sun sensitivity. If treatment is initiated in the ED, refer the patient for a monthly follow-up evaluation. Alternative therapy includes fluconazole 200 mg/day (adults) or 3 to 5 mg/kg/day (children), itraconazole 200 mg daily (adults) or 3 to 5 mg/kg/day (children) for 4 to 6 weeks, oral terbinafine 3 to 6 mg/kg/day (children) or 250 mg/day (adults) for 4 to 6 weeks, and terbinafine cream once a day for 8 weeks. T. tonsurans species appear to be more sensitive to newer treatment modalities and require a shorter course of treatment than for Microsporum species. Selenium sulfide shampoo, 250 mg twice weekly, decreases shedding of spores. Family members should be evaluated.

Kerion

A kerion is a fungal infection affecting hair follicles that is characterized by intense inflammation with erythematous, boggy lesions often with frank pus. The inflammation is generally uniform and does not display satellite lesions. It usually affects the scalp and is more common in children and in African Americans. Local alopecia and scarring can ensue. Accurate differentiation of lesions with and without superinfection can be challenging, and a bacterial culture may be useful when there is doubt. Kerions tend to be less tense and less tender than bacterial abscesses; however, with superinfection or existing drainage, the distinction becomes less pronounced. A toothbrush, Papanicolaou smear cytology brush, or moistened cotton swab is helpful for quick, painless sampling of large areas of the scalp.

Kerions are treated the same as tinea capitis, with the addition of prednisone 1 mg/kg/day for 1 or 2 weeks to help decrease the inflammatory reaction and subsequent alopecia and scarring. If bacterial superinfection exists, an antibiotic is added. Antibiotic options include oral cephalexin, 500 mg every 6 hours for adults or 50 mg/kg/day divided in four doses not to exceed 500 mg per dose for children, for 1 week; dicloxacillin 100 mg twice a day; and clindamycin 300 mg orally every 6 hours for adults or 8 to 25 mg/kg/day as palmitate in three or four divided doses for children. If intravenous clindamycin is used, the dose is 600 to 900 mg every 6 to 8 hours for adults or 40 mg/kg/day divided three or four times a day for children not to exceed 600 mg per dose. Clindamycin is recommended when community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is a concern, that is, in those cases in which purulent drainage is present. Surgical drainage of kerions is not helpful and should be avoided.

Tinea Corporis

Clinical Features.: Tinea corporis is the classic “ringworm” infection. Its characteristic presentation is a sharply marginated, annular lesion with raised or vesicular margins and central clearing (Fig. 120-1). Lesions may be single or multiple; multiple lesions are occasionally concentric. Tinea cruris, which involves the groin, is similar in appearance and may also include the perineum, thighs, and buttocks, but the scrotum is characteristically spared.

Figure 120-1 Tinea corporis. (Courtesy David Effron, MD.)

Differential Considerations.: The differential diagnosis of tinea cruris includes granuloma annulare, psoriasis, intertrigo with secondary candidiasis, and erythrasma.

Management.: Infections of the body, groin, and extremities usually respond to topical measures alone. A number of effective topical antifungal agents are available, including clotrimazole (Lotrimin), haloprogin (Halotex), miconazole (Micatin), tolnaftate (Tinactin), terbinafine, naftifine, and griseofulvin 1%. Two or three daily applications of the cream form of any of these preparations result in healing of most superficial lesions in 1 to 3 weeks.⁴ Acute inflammatory lesions displaying oozing or blisters are treated additionally (four times a day) with open, wet compresses of Burow’s solution, an aluminum acetate solution that is useful as a soothing wet dressing for inflammatory skin conditions.

Tinea Pedis

Tinea pedis, or athlete’s foot, appears with scaling, maceration, vesiculation, and fissuring between the toes and on the plantar surface of the foot. In extensive cases, the entire sole may be involved. A secondary bacterial infection may occur. The vesicular pustular form of tinea pedis should be considered when vesicles and pustules on the instep are noted. The differential diagnosis includes contact dermatitis and dyshidrotic eczema. A KOH preparation is helpful to differentiate between these processes. Interdigital lesions may cause minimal symptoms and serve as a portal of entry for bacterial cellulitis. Treatment options include terbinafine 1% cream twice daily for 2 to 4 weeks; miconazole 2% cream, powder, or spray twice daily for 2 to 4 weeks; and clotrimazole 1% cream, solution, or lotion twice daily for 2 to 4 weeks.⁵ For severe disease or if topical treatment has failed, use terbinafine 250 mg orally daily for 2 weeks, fluconazole 150 mg orally weekly for 2 to 4 weeks, or griseofulvin 500 mg orally daily for 2 weeks.

Tinea Versicolor

Clinical Features.: Tinea versicolor is a superficial yeast infection caused by Pityrosporum ovale. Superficial scaling patches occur mainly on the chest and trunk but may extend to the head and limbs. As the name implies, lesions can be a variety of colors, including pink, tan, and white. The disease may be associated with pruritus, but medical care is often sought because the spots do not tan. On physical examination, a fine subtle scale is noted that may appear hypopigmented (Fig. 120-2). Pale yellow or orange fluorescence under Wood’s light is sometimes present. The differential diagnosis includes vitiligo and seborrheic dermatitis. A KOH preparation reveals short hyphae mixed with spores (“chopped spaghetti and meatballs”).

Figure 120-2 Tinea versicolor. (Courtesy David Effron, MD.)

Management.: Tinea versicolor may be treated with 2.5% selenium sulfide shampoo, imidazole creams, ketoconazole cream or foam, or oral ketoconazole as a single 400-mg dose or 200 mg daily for 5 to 10 days.⁶ Fluconazole 150 to 300 mg weekly for 2 to 4 weeks may also be used. Recurrence rates vary from 15 to 50%, and recurrence is considered the rule rather than the exception. Monthly prophylaxis with propylene glycol and water, selenium shampoo, or azole creams can help prevent recurrences. Pigmentation may not return to normal for months. Propylene glycol is inexpensive and effective.

Tinea Unguium (Onychomycosis)

Clinical Features.: Tinea unguium results in nails that are opaque, thickened, cracked, and crumbled. Subungual debris is present, and the nail may contain yellowish longitudinal streaks. The nail of the great toe is most commonly involved. Involvement of all of the nails of the hands and feet is rare.

Management.: Topical therapy of the nails alone rarely results in a cure because penetration into the nail keratin is poor. Fingernails typically respond more rapidly to therapy than toenails do. Oral griseofulvin and ketoconazole require prolonged courses, with high relapse rates and numerous side effects.⁷ Newer agents such as itraconazole, fluconazole, and terbinafine are safer and more effective. They also offer shorter treatment periods, thus improving compliance.⁷ The infection may be resistant to this regimen as well, however, and surgical removal of the nail is occasionally required. The choice of specific agent may be best left to a consultant or patient’s primary physician, given the long course of treatment and frequency of treatment failure. If therapy is started in the ED, reliable follow-up is needed. Griseofulvin ultramicrosize 375 mg twice daily or ketoconazole 400 mg daily is given for 4 to 6 months. Newer agents are preferred by dermatologists: terbinafine 250 mg/day for 6 to 12 weeks (a longer course is given for toenail involvement) is considered first-line therapy. Recurrence is common.⁸

Scaly Papules

Fungal lesions are typically scaly, as are lesions of secondary syphilis. Additional scaly diseases are discussed in this section.

Pityriasis Rosea

Pityriasis rosea is a mild skin eruption predominantly found in children and young adults. The lesions are multiple pink or pigmented oval papules or plaques 1 to 2 cm in diameter on the trunk and proximal extremities. Mild scaling may be present. The lesions are parallel to the ribs, forming a Christmas tree–like distribution on the trunk. Oral lesions are rare. In children, papular or vesicular variants of the disease may occur.

In half the cases, the generalized eruption is preceded by the appearance of a herald patch. This is a larger lesion, 2 to 6 cm in diameter, that resembles the smaller lesions in other respects. The eruption is usually asymptomatic, although pruritus may be present.

Pityriasis rosea is self-limited, resolving in 8 to 12 weeks. Its cause is unknown, although a virus is suspected. The differential diagnosis includes tinea corporis, guttate psoriasis, lichen planus, drug eruption, Lyme disease, and secondary syphilis. Recurrences are rare. Treatment is usually unnecessary, except for symptomatic alleviation of bothersome pruritus. Direct sun exposure or, alternatively, ultraviolet B therapy to severely affected areas has been recommended; the application of moderately potent topical steroids to severely pruritic areas also has its proponents. The benefits of these treatments are questionable,¹¹ and ED interventions are usually limited to simple reassurance and close follow-up.

Atopic Dermatitis

Principles of Disease

Atopic dermatitis is a common dermatologic condition often referred to as eczema or chronic dermatitis. Atopic dermatitis is the cutaneous manifestation of an atopic state, and although it is not an allergic disorder, it is associated with allergic diseases such as asthma and allergic rhinitis. Patients with atopic dermatitis are known to have abnormalities of both humoral and cell-mediated immunity.¹² The exact mechanism is unclear, but eosinophil, mast cell, and lymphocyte activation triggered by increased production of interleukin-4 by specific T helper cells seems to be involved. Increased immunoglobulin E levels are found in most but not all patients with atopic dermatitis, but there is a poor correlation between the severity of the dermatitis and the serum immunoglobulin E level. The course of atopic dermatitis involves remissions and exacerbations. More than 90% of patients have the onset of atopic dermatitis before 5 years of age. New-onset atopic dermatitis in older children or adults should suggest other diagnoses.

Clinical Features

Atopic dermatitis has no pathognomonic skin lesions or unique laboratory parameters. Diagnostic criteria include itchy skin plus three or more of the following: history of flexural involvement, generalized dry skin, history of asthma or hay fever, onset of rash before 2 years of age, and flexural dermatitis.¹³ These criteria are sensitive (85%) and specific (96%).

Skin lesions generally appear as inflammatory thickened, papular, or papulovesicular lichenification and hyperpigmentation. The skin is typically dry and may be scaly, but in the acute phase, it may also be vesicular, weeping, or oozing. The distribution of lesions varies with the age of the patient. In infants, inflammatory exudative plaques are seen on the cheeks, on the extensor surfaces, and in the diaper area. Older children and adults have lesions in the antecubital and popliteal flexion areas, neck, face, and upper chest. Infantile atopic dermatitis usually begins in the fourth to sixth month of life and improves by the third to fifth year of life. The childhood form occurs between 3 and 6 years of age and resolves spontaneously or continues into the adult form.

Intense pruritus is a hallmark of atopic dermatitis. During flares, patients may present with complaints of intense itching and failure of routine treatments to control their symptoms. Patients may also present with secondary infections. The itching may be focal or generalized, is worse during the winter, and is triggered by increased body temperature and emotional stress. It may be particularly annoying at night. Excoriations may be prominent, and secondary bacterial infection of excoriated lesions is common. Repeated scratching and rubbing produce lichenification, a condition of hyperpigmentation, thickening of the skin, and accentuation of skin furrows. Lichenification is a common feature of chronic atopic dermatitis.

Differential Considerations

The differential diagnosis of infantile atopic dermatitis includes histiocytosis X, Wiskott-Aldrich syndrome, chronic seborrheic dermatitis, phenylketonuria, Bruton’s X-linked agammaglobulinemia, psoriasis, and scabies. Fixed drug eruptions and contact dermatitis round out the differential diagnosis regardless of age. Complications of atopic dermatitis include pyogenic skin infections, otitis externa, cataracts, keratoconus, retinal detachment, and cutaneous viral infections.

Management

The optimal protocol for management in children has not been established. Treatment should be aimed at control of inflammation, dryness, and itching. The use of sedating antihistamines at bedtime can be beneficial in patients with atopic dermatitis who have comorbid allergic conditions and sleep disturbances.

Management includes a careful review of daily skin care with patients or caregivers. General recommendations for all patients include avoidance of nonspecific skin irritants, wool, nonessential toiletries, and detergents and use of cotton clothing as much as possible. Patients should take daily warm baths or showers for approximately 10 to 15 minutes to hydrate the skin, followed by gentle pat drying and immediate application of a topical anti-inflammatory medication on the affected areas and a ceramide-based moisturizer such as Cetaphil, EpiCeram, or CeraVe on the asymptomatic areas. Medium-potency topical corticosteroids may be sufficient to treat moderate flares. Ointment-based medications are usually better tolerated by most patients during an acute flare.

Skin dryness is treated with lubricating ointments such as Vaseline or 10% urea in Eucerin cream (not lotion). Treatment of exudative areas includes the application of wet dressings, which are useful for their moisturizing, anti-inflammatory, and antipruritic actions. Two or three layers of gauze soaked in Burow’s solution should be applied for 15 to 20 minutes four times a day for exudative lesions. Antihistamines may be helpful in reducing the pruritus and are also useful for their sedative and soporific effects, although there is no convincing evidence that H₁ antihistamines decrease itching in patients with atopic eczema.

Topical corticosteroids are the cornerstone of therapy and are prescribed in ointment form. When the dermatitis is severe, the application of a fluorinated corticosteroid ointment such as half-strength betamethasone valerate is recommended to affected areas three times a day. Fluorinated corticosteroids should not be used on the face because they can produce permanent cutaneous atrophy. Milder corticosteroid preparations, such as 0.025% triamcinolone ointment, may be used on the face and intertriginous areas. Patients with extremely severe disease may require systemic steroids. Ultraviolet B treatment is moderately effective, although its mechanism of action is not well understood.

Cyclosporine and other immunosuppressant agents are being used with some promising benefit. Further studies are needed to determine ideal dosing and safety profiles for these agents.¹³

Topical calcineurin inhibitors, including tacrolimus ointment and pimecrolimus cream, are nonsteroidal topical immunosuppressants approved in the United States for use on children 2 years or older; they are useful for treatment of lesions on the thinner skin areas (face, groin, and axillae) where repeated applications of topical corticosteroids may result in skin atrophy or striae.¹⁴ A burning sensation at the site of application may occur. Note that the Food and Drug Administration has issued a “black box” warning concerning long-term continuous treatment with topical calcineurin inhibitors and cancer, although there is currently no evidence for a causal link.¹⁵

Inpatient admission is a consideration for those patients who have generalized erythema and exfoliation (erythroderma) or intractable itching in that skin breakdown and severe secondary bacterial or viral skin infections may occur.

Skin Infections in Patients with Atopic Dermatitis

Patients with atopic dermatitis are susceptible to infection and colonization by a variety of organisms because of their defective skin barrier functions and local skin immunodeficiency. Widespread disseminated viral infections, such as eczema molluscatum, eczema vaccinatum, and eczema herpeticum, and recurrent staphylococcal pustulosis are especially concerning.

Eczema molluscatum is self-limited. Eczema vaccinatum results from exposure of patients to vaccinia virus either by intentional inoculation or through contact with someone recently immunized against smallpox. Therapy for eczema vaccinatum requires prompt administration of intravenous immune globulin, which can be obtained from the Centers for Disease Control and Prevention.¹⁶

Eczema herpeticum constitutes a medical emergency. Patients present with disseminated eruptions of dome-shaped vesicles that may or may not be superimposed on areas of eczematous rashes, with the head, neck, and trunk commonly affected. Fever, malaise, and local lymphadenopathy are variable, depending on the timing of presentation and host characteristics. Complications include keratoconjunctivitis, viremia, multiorgan involvement with meningitis, and encephalitis. Clinical suspicion of eczema herpeticum mandates initiation of intravenous acyclovir in conjunction with antistaphylococcal antibiotics for possible bacterial superinfection. Lumbar puncture should not be attempted if infected lesions are present over the lumbar area. Ophthalmology consultation is needed for patients with periocular or suspected eye involvement.

Pustules

Impetigo

Principles of Disease

Impetigo is a slowly evolving pustular eruption, most common in preschool children. Currently, Staphylococcus aureus is the most common pathogen, with group A streptococcus a distant second.¹⁷ Poor health and hygiene, malnutrition, and various antecedent dermatoses, especially atopic dermatitis, predispose individuals to impetigo.

Clinical Features

Streptococcal impetigo (ecthyma) is found most often on the face and other exposed areas. The eruption often begins as a single pustule but later develops multiple lesions. It begins as 1- to 2-mm vesicles with erythematous margins. When these break, they leave red erosions covered with a golden yellow crust. Lesions may be pruritic but usually are not painful. Regional lymphadenopathy is commonly present. Lesions are contagious among infants and young children and less so in older children and adults. Postpyodermal acute glomerulonephritis is a recognized complication of streptococcal impetigo.

Staphylococcal impetigo is differentiated from streptococcal impetigo in that it is more superficial, and there is little surrounding erythema. Other diagnostic considerations are herpes simplex virus (HSV) and inflammatory fungal infections. A Gram stain of the weepy erosion obtained after removal of the crust will reveal gram-positive cocci. MRSA impetigo is increasingly common. Risk factors include prior infection or colonization with MRSA.¹⁸

Bullous impetigo is caused by phage group 2 staphylococci. It is seen primarily in infants and young children. The initial skin lesions are thin-walled, 1- to 2-cm bullae. When these rupture, they leave a thin serous crust and collarette-like remnant of the blister roof at the rim of the crust. The face, neck, and extremities are most often affected. The differential diagnosis includes contact dermatitis, HSV infection, superficial fungal infections, and pemphigus vulgaris. A Gram stain of the fluid from a bulla reveals gram-positive cocci. Cultures are positive in 95% of cases.

Management

Systemic and topical therapies are equally successful in treating impetigo.¹⁷ For more extensive lesions, systemic treatment is recommended. There is no evidence, however, that systemic antibiotics prevent the development of acute glomerulonephritis. The efficacy is similar for topical mupirocin 2% ointment three times a day, oral erythromycin ethylsuccinate 250 mg four times a day for 10 days in adults or 30 mg/kg/day in children, and cephalexin 50 mg/kg/day not exceed 500 mg per dose three times a day for 7 to 10 days.¹⁷ Mupirocin is avoided when there is concern about methicillin-resistant strains, and care should be taken that it does not get into the patient’s mouth.

Therapy for bullous impetigo consists of an oral penicillinase-resistant semisynthetic penicillin, such as dicloxacillin, 250 mg four times a day for 5 to 7 days for adults, or erythromycin ethylsuccinate, 250 mg four times a day in adults or 30 to 50 mg/kg/day in children. Azithromycin may also be used, dosed at 500 mg on the first day in adults, followed by 250 mg a day for 4 days; in children, it is dosed at 10 mg/kg given on the first day, followed by 5 mg/kg/day for 4 days more. If the infection is limited to a small area, mupirocin 2% ointment three times a day may be used. Without treatment, impetigo generally heals within 3 to 6 weeks.¹⁷

Folliculitis

Clinical Features

Folliculitis is an inflammation in the hair follicle, usually caused by S. aureus. It appears as a pustule with a central hair. The lesions are usually on the buttocks and thighs, occasionally in the beard or scalp, and may cause mild discomfort. The differential diagnosis includes acne, keratosis pilaris, and fungal infection. Gram-negative folliculitis with Pseudomonas aeruginosa can occur after exposure to infected hot tubs and swimming pools or in individuals taking antibiotics for acne; it can be differentiated from staphylococcal folliculitis by a Gram stain of the lesion.

Management

Treatment with an antiseptic cleanser such as povidone-iodine or chlorhexidine every day or every other day for several weeks is usually adequate. For patients with extensive involvement, a 7- to 10-day course of doxycycline 100 mg two times a day or dicloxacillin 500 mg four times a day may be added.

Hidradenitis Suppurativa

Hidradenitis suppurativa affects the apocrine sweat glands. Recurrent abscess formation in the axillae and groin resembles localized furunculosis. The condition tends to be recurrent and may be extremely resistant to therapy. Hidradenitis suppurativa may be treated with drainage of abscesses if they are fluctuant, painful, and large. Antistaphylococcal antibiotics are useful if they are administered early and for a prolonged period. Begin treatment for mild disease with topical clindamycin, 10 mg/mL twice daily, for 3 months. In patients with more severe or nonresponsive disease, begin clindamycin, 300 mg twice daily, combined with rifampin, 300 mg twice daily, for 3 to 6 months.¹⁹ Antiandrogen therapy may be considered if antibiotics do not produce improvement. Many cases do not respond, however, and eventually require local excision and skin grafting of the involved area. Sonography will help differentiate abscesses from vascular or lymphoid structures.

Carbuncle

A carbuncle is a large abscess that develops in the thick, inelastic skin of the back of the neck, back, or thighs and usually involves hair follicles. Carbuncles may produce severe pain and fever. Septicemia may accompany the lesions. The diagnosis of skin abscess, furuncle, or carbuncle is usually made clinically. Ultrasonography is often helpful in diagnosis of carbuncles or abscesses that may not appear fluctuant on examination.

Local heat should be applied to furuncles and carbuncles, which should be incised and drained when fluctuant. Antibiotics are unnecessary with incision and drainage unless cellulitis or septicemia is present.

Community-Associated Methicillin-Resistant Staphylococcus aureus

Principles of Disease

The incidence of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) has soared since the first report in 1993. In many major U.S. cities, CA-MRSA is now the most common pathogen cultured from ED patients presenting with skin and soft tissue infections.²⁰ Concern exists that CA-MRSA may be more virulent than methicillin-sensitive strains, and colonization with CA-MRSA may produce more overt infections.²⁰

Hospital-acquired MRSA isolates can survive on a variety of inanimate surfaces, sometimes for weeks. It is unclear whether this is also true for CA-MRSA isolates; if it is true, their presence on such items as clothing, towels, and athletic equipment might contribute to outbreaks. Pets (including dogs and cats), livestock, and birds have been identified as MRSA carriers; their role in MRSA transmission to humans requires further evaluation.²¹

Clinical Features

CA-MRSA infections are most often manifested as skin and soft tissue suppuration, such as an abscess, furuncle, or cellulitis. Lesions frequently exhibit central necrosis and are often confused with spider bites by patients.²² Clinical features cannot distinguish with certainty skin and soft tissue infections caused by MRSA from those caused by methicillin-susceptible S. aureus. Although rare, CA-MRSA infection can also be manifested as necrotizing fasciitis.²³ Recurrences of CA-MRSA cellulitis are common. Contagion among the close household contacts of patients as well as correctional facility, school, and sports team contacts is well recognized.

Management

Several studies have demonstrated excellent outcomes for abscesses caused by CA-MRSA that are treated with incision and drainage alone.²⁴ If antibiotics are needed, information on local antibiotic resistance patterns can help clinicians assess the likelihood of CA-MRSA infection and guide decisions about empirical treatment. A specimen for culture and susceptibility testing, which was considered to be unnecessary in the pre–CA-MRSA era, may be useful in guiding therapy. Specimens are obtained at the time of incision and drainage of purulent lesions.

In patients with larger abscesses, associated areas of cellulitis, or systemic signs of infection, antimicrobial therapy is needed in addition to incision and drainage. The optimal oral antimicrobial regimen for the treatment of skin and soft tissue infections is not known. The type and route of therapy are guided by the severity of the clinical syndrome.

Clindamycin combines MRSA activity with effectiveness against the majority of other gram-positive organisms. Side effects include diarrhea, Clostridium difficile colitis, and increasing rates of clindamycin resistance.²⁵ Rifamycin has anti-MRSA activity, but resistance readily develops, so it should not be used alone. The advantage of rifamycin is its long half-life, which allows once-a-day administration, and it penetrates well into all tissues and body fluids; its disadvantages include a high potential for drug-drug interactions. Linezolid is active against almost all CA-MRSA isolates and group A streptococci. Disadvantages of its use include high cost, lack of routine availability, hematologic side effects, and potential for resistance among S. aureus strains. Prolonged linezolid administration increases the likelihood of resistance.²⁶

Trimethoprim-sulfamethoxazole or tetracycline is not recommended as sole empirical therapy for a nonpurulent cellulitis of unknown cause because of group A streptococci resistance to these agents. A β-lactam antibiotic may augment treatment. Cephalosporins and macrolides are ineffective against CA-MRSA. Fluoroquinolones should be avoided because S. aureus resistance develops readily.

Patients with large abscesses, abscesses in high-risk locations, fever, signs of systemic infection, young age, or immunodeficiency prompt consideration of hospitalization. Vancomycin is still considered the parenteral drug of choice for patients with invasive S. aureus infection, although clinical failures have been reported. It seems reasonable to combine vancomycin with another effective antistaphylococcal agent because many antibiotics have better bactericidal activity. In severely ill patients, carbapenems such as meropenem, panipenem, and ertapenem are recommended because they are active against CA-MRSA and synergistic with vancomycin.²⁷ Use of parenteral clindamycin (not recommended as monotherapy), trimethoprim-sulfamethoxazole, and linezolid has been described. In addition, daptomycin and tigecycline are now approved for the treatment of skin and soft tissue infections caused by MRSA.²⁸

Recurrent infections are generally treated like initial episodes. Some providers recommend “decolonization” strategies, although neither the indications for their use nor their effectiveness in reducing the risk of recurrences is established. Decolonization strategies include the use of intranasal mupirocin to reduce nasal carriage of MRSA; however, eradication of nasal colonization appears to be transient. The efficacy of attempts to eradicate CA-MRSA among household members has not been studied.

Prevention

Common antiseptics appear to retain reasonable activity against CA-MRSA, although the results of studies are somewhat conflicting. Good personal hygiene, including appropriate handwashing techniques, separation of infected patients from other types of patients, and routine cleaning of shared equipment, are essential to limiting CA-MRSA spread.²⁹

Gonococcal Dermatitis

Clinical Features

The arthritis-dermatitis syndrome is the most common presentation of disseminated gonococcal disease. It occurs in 1 or 2% of patients with gonorrhea, affecting women primarily.³⁰ Fever and migratory polyarthralgias commonly accompany the skin lesions. The lesions are often multiple and have a predilection for periarticular regions of the distal extremities. The lesions begin as erythematous or hemorrhagic papules that evolve into pustules and vesicles with an erythematous halo (Fig. 120-3). They closely resemble the lesions of meningococcemia at this stage. They may or may not be tender and may have a gray necrotic or hemorrhagic center. Healing with crust formation usually occurs within 4 or 5 days, although recurrent crops of lesions may appear even after antibiotics have been started.