Dermatologic problems encountered in the emergency department

Review

Dermatologic Problems Encountered in the Emergency Department PETER C. FERRERA, MD,* MARSHA L. DUPREE, MD,I" VINCENT P. VERDILE, MD* Emergency physicians are often the first to encounter patients with dermatologic problems. A wide variety of dermatoses may be either the primary reason for presentation to the emergency department (ED) or an incidental finding on physical examination for a seemingly unrelated complaint. Often these skin conditions are benign and self-limited or easily treatable. The emergency physician, however, must be aware of potentially serious dermatoses that may represent more serious underlying disease or may be life-threatening. In addition, many patients already under the care of a dermatologist are undergoing medical or ultraviolet radiation treatments that may ca0se adverse reactions, which require visitation to the ED. Early consultation with a dermatologic specialist can be important for the definitive diagnosis and long-term care of most acute and chronic conditions. The purpose of this review is to highlight commonly encountered or potentially serious dermatoses and their management. The cutaneous diseases are grouped as follows: atopic dermatitis, contact dermatitis, papulosquamous lesions (pityriasis rosea, psoriasis), rosacea, infectious (fungal, viral, bacterial, scabies), erythema multiforme, basal cell carcinoma, granuloma annulare, hidradenitis suppurativa, and venous stasis dermatitis.

ATOPIC ECZEMA (ATOPIC DERMATITIS) Atopic eczema is a common chronic skin disorder, especially in children, with an increasing prevalence. ~,2 Patients often have a family or personal history of atopy, with conditions such as asthma or allergic rhinitis. Onset is most often within the first year of life, and 85% to 90% of

From the *Department of Emergency Medicine and 1-Division of Dermatology and Dermatopathology, Albany Medical College, Albany, NY. Manuscript received February 15, 1995, returned March 16, 1995; revision receivedApril 28, 1995, accepted May 5, 1995. Address reprint requests to Dr Ferrera, Department of Emergency MedicineA-139, Albany Medical Center, Albany, NY 12208. Key Words: Atopic dermatitis, atopic eczema, basal cell carcinoma, candidiasis, contact dermatitis, dermatophytoses, erythema multiforme, generalized pustular psoriasis, granuloma annulare, herpes zoster, hidradenitis suppurativa, impetigo, molluscum contagiosum, necrotizing fasciitis, pityriasis rosea, psoriasis, rosacea, scabies, seborrheic dermatitis, tinea infections, tinea versicolor, varicelia, venous stasis ulcers, warts. Copyright © 1996 by W.B. Saunders Company 0735-6757/96/1406-001555.00/0 588

affected individuals have the onset of the disease by the age of 5 years; all races are affected.2,3 The natural history of the disease tends towards eventual resolution as the patient ages, but more severely affected persons tend to have persistent lesions? The pathogenesis of atopic eczema is unclear, but immunoglobulin E (IgE) overproduction and decreased cell-mediated immunity are involved, z3 Histamine does not appear to be the mediator of the associated pruritis in this disease. 4 Lesions are erythematous, papular, and extremely pruritic, with a predilection for extensor surfaces of the arms and legs during infancy and early childhood? The face, neck, hands, and feet are also commonly involved. The diaper area is usually spared because of the increased moisture in this region. 3 Flexural involvement of the antecubital and popliteal fossae are more characteristic in older patients. Irritation of the lesions by scratching or rubbing leads to erosions, abrasions, and lichenification. The skin may appear pebbled in darker pigmented patients owing to perifollicular involvement. Lesions may become either depigmented or hyperpigmented. 2 Patients almost always have dry skin. Cheilitis is often an associated feature. The differential diagnosis includes seborrheic dermatitis, scabies, nummular eczema, allergic contact dermatitis, dermatophytoses, hyper-IgE syndrome, and Wiskott-Aldrich syndrome.2, 3 Potential complications associated with atopic eczema include superinfection with Staphylococcus aureus, increased susceptibility to localized or generalized herpes simplex cutaneous infections (eczema herpeticum), dry skin (xerosis), extensive and difficult-to-treat molluscum contagiosum and wart infections, and irritant contact dermatitis, z3 Factors that have been proposed to exacerbate atopic dermatitis include S aureus infection, overbathing with subsequent xerosis, emotional stress, sweating, and irritants such as woolen clothing, hot water, and detergent soaps.l-3 The role of certain foods (particularly eggs, seafood, nuts, milk, wheat, and soy) and aeroallergens such as dust in exacerbation of atopic dermatitis is controversial.l-3 Measures to prevent exacerbations include application of effective moisturizers and avoidance of known triggering factors. Application of a hydrophilic cream is useful for severe inflammatory lesions. 1 Nondetergent soaps are preferred for bathing (eg, Dove [Lever Brothers Co, NY, NY]). Short-term courses of topical corticosteroids, such as triamcinolone 0.1%, and a 10- to 14-day course of oral antistaphy-

FERRERA ET AL [] DERMATOLOGIC PROBLEMS

lococcal drugs such as erythromycin or dicloxacillin, are used for flare-ups, v3 Chronic lesions may respond well to tar-containing preparations. 1 Mupirocin ointment may be used for impetiginized lesions. Psoralen ultraviolet light therapy (PUVA) is also an effective treatment modality. 5,6 Lesions will usually resolve within 10 days to 2 weeks after the initiation of treatment.

CONTACT DERMATITIS Contact dermatitis is inflammation of the skin caused by exposure to one of many antigens or irritants. Several classifications of contact dermatitis exist, including allergic, irritant, photodermatitis, and contact urticaria. Allergic contact dermatitis (ACD) is a type IV hypersensitivity reaction (ie, non-IgE, cell-mediated delayed hypersensitivity) caused by many different agents, the most common of which are plants of the Rhus (Toxicodendron) genus (poison ivy, poison oak, poison sumac), 7 nickel, potassium dichromate, and paraphenylenediamine. 8 In elderly patients, the most common offending agents are topical medications. 9 Appearance of lesions occurs within 24 to 96 hours after exposure to the allergen. 1° When the etiologic agent of ACD is unknown, patch testing can be helpful for identification.l° Irritant contact dermatitis (ICD) is caused by direct local epidermal cytotoxic effect of the irritant and is also caused by various agents, including acids, alkalis, solvents, and oxidants. 8 The severity of the skin reaction in ICD is usually relative to the amount of agent and to the total contact time.~° Patients at the extremes of age are generally more susceptible to ICD. 11 The chief complaint in ICD is usually pain and burning, whereas in ACD pruritis predominates.l° Most forms of contact dermatitis appear similarly. Acutely, the area of skin contact develops a well-localized area of vesicles filled with clear fluid on an erythematous base. 8 Oozing and eroding skin develops as vesicles break open. Elderly patients usually have an intensely pruritic scaling rather than a vesiculating pattern, with lichenification and hyperpigmentation presenting early on. 9 In contrast to acute dermatitis, subacute dermatitis is seen as multiple papules with less associated edema. Chronic dermatitis presents as minimally swollen, scaly, and occasionally lichenified lesions. 8 In most instances, contact dermatitis resolves within 3 to 4 weeks after removal of the inciting agent. 8 In phototoxic and photoallergic contact dermatitis, irradiation with ultraviolet or visible light converts certain substances into irritants or allergens. Phototoxic reactions are nonimmunologically mediated, appearing as first-degree burns with patients complaining of burning. In contrast, photoallergic reactions are type IV hypersensitivity reactions that require prior sensitization; pruritis is the chief complaint. Agents implicated in photodermatitis include certain dyes, tars, plant products (eg, psoralens), and drugs (eg, sulfonamides, sulfonylureas, tetracyclines, griseofulvin, and thiazides), m,ll Lesions may persist for years and lichenification and hyperpigmentation may result. H The term contact urticaria comprises several different clinical forms, all of which share the onset of symptoms within several minutes to an hour after skin is exposed to rapidly absorbable agents.12 Contact urticaria may be classified mechanistically into the following groups: (1) immuno-

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logically mediated, (2) nonimmunologically mediated, and (3) uncertain mechanism mediated. Immunological contact urticaria is characterized by a wheal-and-flare response at the site of skin contact with an inciting agent. Organs other than the skin may be involved and anaphylactic shock is a possible outcome. 1°,12 Atopic patients have a higher incidence of immunologically mediated urticaria than patients without atopy. As in other forms of immediate hypersensitivity, immunological contact urticaria is an IgE-mediated process, which ultimately results in the release of inflammatory mediators such as histamine. 12 This form of urticaria requires prior exposure to the specific agent. Food is a very common inciting agent, and patients often present within 30 minutes of handling food, with symptoms ranging from itching to erythema and urticarial swelling. Recently, latex has been implicated in immunologically mediated contact urticaria, and has been seen frequently in health care workers who require the use of rubber gloves.13-~5 Nonimmunological contact urticaria is seen more commonly than immunological urticaria. Local erythema and edema results when the skin comes into contact with common agents such as benzoic acid, sorbic acid, cinnamic acid, and nicotinic acid esters. These urticants are found in ice cream, soft drinks, chewing gum, shampoos, perfumes, mouthwashes, creams, and ointments. Patients may complain of burning and itching alone or in combination with erythema, or may present with erythema without pruritis. Other organ systems are uninvolved. Because immune mechanisms are not involved, symptoms may appear on first exposure to the agent. Non-antibody-mediated release of prostaglandins or leukotrienes may be a possible mechanism of nonimmunologic urticaria. 12 Agents that cause contact urticaria that is not clearly immunologically related are classified as having an uncertain mechanism. Three examples of this type of urticaria are ammonium persulfate, solar, and aquagenic urticaria. 1J,12 Ammonium persulfate, a hair bleaching agent, can cause first-exposure urticaria but also may lead to systemic involvement. Solar urticaria may occur within 5 to 30 minutes of sun exposure, and may represent a hypersensitivity to a normal photoproduct. Hives appear around hair follicles in aquagenic urticaria after exposure to water, saline, or the patient's own sweat or sebum; a toxic mast cell degranulating agent found in sebum may be the causative agent. The differential diagnosis of contact dermatitis includes atopic dermatitis, dyshidrotic eczema, psoriasis, herpes simplex and herpes zoster, insect bites, drug eruptions, erythema multiforme, pustular lesions on the palms and soles, scabies, erysipelas, and lichen planus. 10.~1 Treatment of contact dermatitis consists of avoidance of irritants, Burow's solution (aluminum acetate) in combination with wet compresses for 15 to 20 minutes at a time several times daily, and topical corticosteroids for acute cases. 8,1°,11 Topical corticosteroids without the use of compresses are used to treat subacute and chronic dermatitis. Systemic corticosteroids are occasionally required for severe cases or patients with more than 30% body involvement. 7,8 Antihistamines may also be given to relieve itching. Restriction of sunlight exposure and the use of protective

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clothing may limit the development of lesions in patients with photodermatitis. In addition to avoidance of the offending agents, the use of chlorpheniramine-like antihistamines is useful in the treatment of contact urticaria; terfenadine and astemizole are less efficacious antihistamines.11 Nonsteroidal anti-inflammatory agents (NSAIDs) may be useful for nonimmunological contact urticaria via inhibition of prostaglandin and leukotriene release? 1 Anaphylactic reactions are treated in the usual manner, ie, epinephrine, intravenous fluids, steroids, antihistamines, and vasopressors if required.

PITYRIASIS ROSEA Pityriasis rosea (PR) is a common, acute, self-limited exanthem occurring worldwide, predominantly affecting adolescents and young adults during the fall and winter months. 16 The etiology is uncertain, although presumed to be virally induced. 16,17The disease is first manifested by an erythematous, mildly pruritic, ovoid, sharply bordered macular lesion (herald patch) approximately 2 to 5 cm in diameter. 16Several days later, a fine scale appears within the herald patch. Within 7 to 14 days after the appearance of the herald patch, the trunk, neck, and proximal extremities begin to develop pale red oval macular or papular lesions, which may also involve the face, scalp, and distal extremities of young children (Figure 1).16,17These subsequent lesions can average 1 cm in diameter. The exanthem takes on a characteristic distribution of a Christmas tree, following the course of the ribs, with the long axes of the lesions running within the cleavage lines of the skin. 16,17The lesions develop scales within several days, but new lesions may continue to appear for up to 2 weeks, and may involve the oral mucosa and gingiva. ~s The herald patch may be absent in 10% to 15% of patients. 16Atypical presentations of the rash include pure papules, hemorrhagic lesions, involvement of the palms and soles, or lesions on the face and extremities with sparing of the trunk (inverse pityriasis rosea). 16,17 The differential diagnosis includes secondary syphilis, tinea corporis, drug eruption, nonspecific viral exanthem, and guttate psoriasis. 16,17 Serologic testing for syphilis may be indicated to distinguish PR from secondary syphilis. The lesions usually last for 4 to 6 weeks. No specific treatment is required, but symptomatic treatment of pruritis may be necessary. 16.17Recurrences are rare. 17

PSORIASIS Psoriasis is a common dermatosis characterized by erythematous papules and scaly plaques of varying sizes, predominantly occurring on the scalp, intertriginous regions, and on extensor surfaces such as the elbows and knees. 19,2° Pruritis is a variable complaint, and lesions undergo periods of exacerbation and resolution, but spontaneous remission seldom occurs. The prevalence of this disease in the United States ranges from 0.5% to 1.5%, more commonly seen in Caucasians of northern European descent. 19A family history of psoriasis occurs in one third of those affected. 19The mean age of onset in the United States is 28 years. 19Three factors that are implicated as disease triggers are psychological stress, skin injury, and infection? 9 The Koebner reaction is the development of localized psoriasis after injury to the

skin and may occur in 30% to 50% of patients. 19 Upper respiratory infections and streptococcal pharyngitis have been associated with psoriasis exacerbations.19,2° Arthritis is seen in 5% to 7% of patients with psoriasis, and as many as 25% to 40% of patients with severe psoriasis have arthritis. 19 Nail abnormalities are also seen in up to 50% of patients. 19,20 The first step in treatment of psoriasis is to prevent dehydration of the skin by application of an emollient. Topical corticosteroids and crude coal tar can be used for less severe disease, z° Extensive psoriasis is generally treated with psoralen plus ultraviolet-A (PUVA) radiation therapy, which is believed to work by inhibition of epidermal DNA synthesis. 2~ Potential serious chronic problems associated with use of PUVA include squamous cell carcinoma, basal cell carcinoma, and cataract formation. Acute complications of PUVA therapy include sunburn reactions, nausea, pruritus, headache, and vesiculation. Methotrexate or cyclospofine may be used for severe disease. 2° An uncommon but potentially serious form of psoriasis is the generalized pustular form (GPP), characterized by fever and the presence of many sterile pustules. 22Adenopathy and leukocytosis may also occur. 22Factors known to induce GPP include a tapering in the dose of systemic corticosteroids, withdrawal of potent topical steroids, nonsteroidal antiinflammatory agents (NSAIDs), pregnancy, viral upper respiratory tract infections (URIs), and [3-hemolytic streptococcal infections. 2224 Histologically, a perivascular lymphohistiocytic infiltration occurs in the papillary dermis, followed by neutrophil migration into the epidermis; thinned keratinocytes separate individual neutrophils. 22,25The differential diagnosis includes widespread folliculitis, subcorneal pustular dermatosis, and pustular drug hypersensitivity to such agents as ampicillin, diltiazem, co-trimoxazole, furosemide, isoniazid, imipenem/cilastatin and some of the cephalosporins. 25 Pustular drug eruptions are distinguished from GPP in that there is often no personal or family history of psoriasis and the lesions quickly resolve without treatment after discontinuance of the inciting agent, and by the presence of eosinophils in the lesion. 25 GPP is difficult to treat and methotrexate, corticosteroids, retinoids, hydroxyurea, and other antimetabolites may be required for severe cases. 22,25The prognosis is guarded, because a large number of deaths have occurred in patients with GPP, attributable to either the disease, eg, cardiac failure or respiratory infection during a flare-up, or its treatment. 23

ROSACEA Rosacea is a common cutaneous vascular disorder of the face characterized by episodes of facial flushing which progresses to fixed erythema and pustule formation (Figure 2). 26,27 Blepharitis and conjunctivitis may be associated ocular findings. 26 Rhinophyma, a bulbous distortion of the nose representing connective tissue hypertrophy and fibroplasia, is an uncommon but possible end-stage complication. 26 Aggravating factors may include the ingestion of alcoholic beverages, certain cheeses, tea, coffee, and spicy foods, in addition to stress and embarrassment? 6 Patients may complain of pain or soreness in the region of erythema. With disease progression, the erythema becomes more permanent and telangiectasia develops within the affected

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FIGURE 4.

FIGURE 1.

Erythema multiforme on arms.

Pityriasis rosea.

FIGURE 5.

FIGURE 2.

FIGURE 3.

Granuloma annulare.

Rosacea.

Tinea versicolor of upper back.

FIGURE 6.

Axillary hidradenitis suppurativa.

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region. 26'27 The chin, forehead, and midface are the most common areas of involvement. 26 The differential diagnosis may include systemic lupus erythematosus, carcinoid syndrome, seborrheic dermatitis, and acne vulgaris. 26 The latter two conditions may occur in combination with rosacea. Treatment for mild cases consists of topical metronidazole or clindamycin. 26,27 Long-term use of systemic tetracyclines and erythromycin are required for severe cases or treatment failures of mild rosacea. 26 Dapsone has also been used for severe cases. 26 Argon lasers are used to treat disfiguring facial teiangiectasias. 26,27 Plastic surgery may be required if rhinophyma develops. 26

FUNGAL INFECTIONS

Dermatophytoses (Tinea ) Dermatophytes are a group of fungi that cause superficial infections of the skin collectively referred to as tinea. These infections are not highly contagious, and the resultant inflammation is secondary to the host's allergic response to the fungal antigens. 2s The organisms responsible for tinea include species of Trichophyton, Microsporum, and Epidermophyton. The appearance of tinea infections mimics that of eczema, superficial bacterial infection, and contact dermatitis. Vesicles may appear at the wound edge when significant inflammation is present. 2s A quick test that should be performed in the ED involves scraping the lesion and placing the scrapings onto a microscope slide. One drop of 10% or 20% potassium hydroxide (KOH) solution is then added. After a coverslide is placed, the slide is either gently heated over a low flame or allowed to dry for 5 minutes. The slide is then examined for hyphae with septae. The overall sensitivity of the KOH technique is 88%, but is less than 50% for tinea capitis. 2s Fungal cultures could be performed if the suspicion for fungal infection is high despite a negative KOH examination. Tinea pedis ("athlete's foot"). Tinea pedis is an extremely common infection presenting as variably severe prnritis and maceration between the toes, especially the fourth and fifth, and on the soles of the feet. 2s,29 Tinea corporis ("ringworm"). Tinea corporis is a common infection of the glabrous skin of the trunk and extremities. The involved area initially is flat and scaly, but ultimately becomes raised. 2s Hypopigmentation occurs in the center of the lesion and the wound edges become scaly or vesicular. Scrapings for KOH examination should be taken from the lesion edges. Tinea capitis. Tinea capitis is a common scalp infection in children, beginning as a round patch of scaling associated with a small region of alopecia. 28 Multiple areas of the scalp may be involved. A boggy, inflammatory mass called a kerion may develop in severe cases, resulting in possible permanent alopecia. 28'3° Tinea cruris ('Jock itch"). Tinea cruris is a common groin infection more often seen in men than women. Severe maceration may lead to subsequent bacterial superinfection. If the penis or scrotum are involved, the infection is probably due to candidiasis rather than tinea. 29 Tinea unguium. Tinea unguium represents a dermatophytic infection of the nails. The toenails are more often

affected than the fingernails, and tinea pedis is almost always present. 28,3° The infected nails become opaque yellow and thickened and the distal portions become brittle. Treatment regimens may consist of the application of topical agents (Table 1). 28 More severe infections that are not responding well to topical treatment and tinea capitis both require oral antifungal agents. 2s In addition, tinea capitis complicated by kerion formation may benefit from the use of prednisone therapy for two weeks. 3° Available oral agents include ketoconazole (Nizoral; Janssen Pharmaceutica, Titusville, NJ), griseofulvin, itraconazole, and fluconazole (Diflucan; Roerig Division, Pfizer Inc, New York, NY). Hepatotoxicity is the main potential concern with use of ketoconazole if therapy is to last beyond 2 weeks? 8 Prolongation of the QT interval and torsades de pointes have been reported with concomitant use of ketoconazole and terfenadine. 31 Griseofuivin causes fewer serious adverse reactions than ketoconazole and should be used as the first-line oral agent. Care must be used when griseofulvin is administered to patients taking oral contraceptives or warfarin, because griseofulvin enhances the metabolism of these agents. 28 Absorption of griseofulvin is enhanced by administration with food. 32 Early dermatological follow-up is necessary for the long-term management of patients with serious fungal infections or for patients who are placed on oral agents. In general, steroids are contraindicated in the treatment of fungal infections because the fungus may undergo more rapid growth. 33 However, the use of the combination antifungal and steroid agent betamethasone dipropionate/clotrimazole (Lotrisone; Schering Corp, Kenilworth, NJ) has been said to more rapidly reduce the symptoms of fungal infections than use of antifungals alone if used for less than 2 weeks. 33 Prolonged use of Lotrisone has been reported to cause a Majocchi granuloma, which is a fungal dermal abscess resembling a kerion. 34 In addition to prolonging the fungal infection, extended use of Lotrisone cream can lead to the development of striae, a well-known potential complication of steroid use. 35 It is probably safest to treat simple fungal infections with topical antifungals without the addition of steroids.

Tinea Versicolor (Pityriasis Versicolor) Infection of the stratum corneum by Malassezia furfur (Pityrosporum orbiculare) leads to tinea versicolor, which presents as small round or oval macular areas of hyperpigmentation or hypopigmentation (Figure 3). 30,32 The back, chest, and shoulders are commonly affected; in tropical climates the face is also often affected. 3z36 High temperature and humidity are predisposing factors. 29 The most frequent patient complaints are cosmesis and mild pruritis. 36 The differential diagnosis includes pityriasis alba, secondary syphilis, seborrheic dermatitis, and vitiligo. 3°,32,36Treatment usually consists of 2.5% selenium sulfide shampoo (eg, Selsun [Ross Products Division, Abbott Laboratories, Columbus, OH], Exsel [Allergan Inc, Irvine, CA]) for l to 2 weeks, but topical imidazoles may also be used. 32 A single 400-rag dose of ketoconazole is also effective.36 Elimination of fungal colonization occurs well before pigmentation abnormalities resolve. 3°,32

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Candidiasis TABLE1, Treatment Regimens for Dermatophytoses (Tinea) Antimicrobial Agents Tinea Infection Tinea capitis

Generic

Brand Name

Oral Fluconazole GriseofUlvin

Diflucan Grisactin, Grifulvin Ketoconazole Nizoral Itraconaz01e Sporanox

Tinea pedis, tinea cruris, and tinea corporis

Topical Undecylenic acid Ciclopirox Tolnaftate Miconazole

Cruex, Desenex

Loprox Tinactin Micatin, Monistat Clotrimazole Lotrimin Econazole Spectazole Oxiconazole Oxistat Ketoconazole Nizoral Naftifine Naftin Terbinafine Lamisil

Tinea unguium Topical Ciclopirox Terbinafine

Oral Griseofulvin

Loprox Lamisil

Grisactin, Grifulvin

Regimen Griseofulvin 10 to 20 mg/kg/d (max I g/d) or ketoconazole 3 to 4 mg/kg/d (max 1.6 g/d) Orally. For kerion formation, add prednisone 1 mg/kg/d for 2 weeks. Topical agents twice daily (except ketoconazole, which is once daily) for 4 weeks for tinea pedis, or 2 to 3 weeks for tinea cruris or corporis. Oral regimens may be required for severe infection. Topical agents twice daily for 6 to 9 months for fingernails, 9to 12 months for toenails. Griseofulvin 10 mg/kg/d for fingernails and 15 mg/kg/d for toenails for same duration as topical regimen.

NOTE: Manufacturers of brand name products: Diflucan, Roerig Division, Pfizer Inc, New York, NY; Grisactin, Wyeth-Ayerst Laboratories, Philadelphia, PA; Grifulvin, Micatin, Monistat, Spectazole, Ortho Pharmaceutical Corp, Dermatological Division, Raritan, NJ; Nizoral, Sporanox, Janssen Pharmaceutica Inc, Titusville, NJ; Loprox, Hoechst-Roussel Pharmaceuticals Inc, Somerville, NJ; Tinactin, Lotrimin, Schering-Plough Corp, Kenilworth, NJ; Oxistat, Glaxo Dermatology, Division of Glaxo Wellcome Inc, Research Triangle Park, NC; Naftin, Allergan Inc, Irvine, CA; Lamisil, Sandoz Pharmaceuticals Corp, East Hanover, NJ.

Cutaneous infection with Candida albicans occurs in all age groups, but is most commonly seen in infants as diaper dermatitis) ° Affected areas appear as bright red, welldemarcated patches, often associated with satellite lesions. Infection at the corners of the mouth, known as perleche or candidal angular cheititis, may be seen in individuals who wear dental braces. 3° Treatment for both diaper dermatitis and perleche usually consists of topical antifungals such as nystatin, clotrimoxazole, or miconazole for 7 to 10 days. 3°

Seborrheic Dermatitis Seborrhea is a very common disorder that appears to be either caused or exacerbated by infection with Pityrosporum orbiculare (P ovale or Malassezia furfur), a fungus considered to be part of the normal skin flora. 32,37,38 Seborrhea presents as papulosquamous lesions of the scalp, eyebrows, ears, perinasal and periorbital region, and the chest. Treatment consists of ketoconazole (Nizoral) or flucanozole shampoo applied twice weekly until lesions resolve. 3~,37-4°

VIRAL INFECTIONS

Warts Warts are caused by human papillomaviruses (HPV), with an incidence of 7% to 10%. 41 Two thirds resolve spontaneously within 2 yearsY Warts are capable of spreading from one body site to another and can be transmitted to susceptible close contacts. 41 Commonly affected sites are the hands, feet, face, and genitalia. Genital warts are primarily sexually transmitted, but nonsexual transmission can also occur. 42 Common warts (verrucae vulgaris) are mostly found on the hands and feet, whereas flat warts most often affect the face. 42 Treatment is aimed at eradication of the wart and not the HPV. Cryosurgery, electrocautery, surgical removal, or application of topical solutions containing salicylic acid, podophyllin, and trichloroacetic acid are the most commonly used methods to destroy warts. 41,42 Recurrence rates are high despite initial complete response rates of 50% to 75%. 42

Molluscum Contagiosum Molluscum contagiosum is a common disease, especially in children, caused by a poxviridae virus. Lesions appear as small umbilicated papules anywhere on the body, but rarely involve the palms and soles. 42,43 Erythema and scaling may surround the lesion. Infection occurs after contact with an affected individual, and genital involvement should be thought of as a sexually transmitted infection. 42 In otherwise healthy patients the disease is self-limited and resolves spontaneously over several months without scarring. 42,43 However, in patients with the acquired immunodeficiency syndrome (AIDS), lesions tend to persist and are refractory to standard treatment.42, 43 Treatment is aimed at reducing infectivity and to prevent transmission. Available treatments include curettage, cryotherapy, and topical trichloroacetic acid.42,43

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Chickenpox and Herpes Zoster Varicella zoster virus (VZV) is a ubiquitous herpesvirus which causes primary varicella (chickenpox) and herpes zoster (shingles). VZV is acquired via the respiratory route or by direct contact with cutaneous lesions. 44 The virus replicates within regional lymph nodes, and viremia ensues within 4 to 6 days of initial exposure. Replication then reoccurs within the liver and spleen. A second viremia occurs, and the virus spreads to the epidermis by 14 to 16 days after exposure. Patients are infectious from 4 days before until at least 5 days after the appearance of the rash, ie, when the lesions crust over. 45 VZV occurs endemically throughout the year, but epidemics occur during late winter and early spring. Ninety percent of cases involve children younger than 10 years old. Varicella usually begins with the concomitant onset of general malaise, low-grade fever, and the rash in young children. 45 Prodromal flulike symptoms often precede the exanthem in older children and adults by 1 to 3 days. 45 The exanthem appears initially on the face and trunk as small red macules, which progress rapidly to pruritic clear vesicles. These vesicles contain infective virus until infiltration of neutrophils and monocytes occurs and decreases the viral count. The lesions then crust over as edema fluid is resorbed and desquamated epidermal cells accumulate. Lesions are characteristically present in various stages of development, The lesions usually heal without scarring within 2 weeks unless secondary bacterial infection occurs? 5 Adults tend to be affected more severely than children, with more lesions and prolonged constitutional symptoms. 45 The differential diagnosis of VZV includes other viral exanthems, insect bites, erythema multiforme, and drug eruptions. 45 Although generally a mild and self-limiting disease, chickenpox is occasionally associated with serious complications. Bacterial superinfection of the skin lesions is the most common complication. 45 Central nervous system involvement may manifest as Reye syndrome with acute cerebellar ataxia, encephalitis, and myelitis. 45 VZV pneumonitis, manifested by fever, cough, dyspnea, chest pain, and hemoptysis, is a potentially lethal complication, with a mortality of 10% in immunocompetent adults and 30% in immunocompromised hostsY '46VZV during pregnancy can lead to congenital malformations or fetal death. 45 Immunocompromised patients, such as those undergoing chemotherapy for neoplasms or those with AIDS, have higher mortality and more extracutaneous lesions. 45 VZV travels from the skin into the nerve endings of sensory nerve fibers and remains latent for an extended period within the sensory ganglion. The virus may reactivate at a later time after a decrease in VZV-specific cell-mediated immunity (CMI). 45 Reactivation of VZV, ie, herpes zoster, causes pain as the virus travels down the sensory nerve before reaching the epidermis. 45 Patients without prior infection with VZV can develop primary varicella after direct contact with a patient with herpes zoster. 45 Herpes zoster can afflict all age groups but tends to affect older individuals and the immunocompromised. 44 Zoster recurs in approximately 5% of patients. 45 Pain or pruritus in the region of the involved dermatome are the initial symptoms of zoster, usually preceding the

exanthem by several days. Constitutional symptoms such as fever and malaise occur in about 5% of patients. In some individuals, skin lesions never erupt despite the presence of the dermatomal pain, a condition called "zoster sine herpete."45,47 Cutaneous lesions resemble primary varicella, but in zoster the lesions are often grouped and develop more slowlyY The lesions crust over within 7 to 10 days, and as the crusts fall off, areas of scarring may occur. 47 The differential diagnosis includes herpes simplex virus (HSV) infections, contact dermatitis, burns, and localized skin infections. 45 Zoster most commonly affects the thoracic region (55%) and the fifth cranial nerve (CN V) (15%). 47 Visual loss can occur when the ophthalmic division of CN V is affected, and zoster involvement of this nerve occurs in 7% to 18% of cases. 48 Otalgia, tinnitus, deafness, vertigo, and Bell's palsy can occur by zoster involvement of the facial and auditory nerves. 45 Paralysis occurs in 1% to 5% of patients with zoster, due to extension of the virus from sensory ganglia to anterior horn cells45; paralysis can continue for several weeks. Postherpetic neuralgia (PHN) is the most common complication of zoster. PHN affects 10% to 15% of patients with zoster and is characterized by continued pain 1 to 2 months after the crusted lesions have resolvedY ,47 PHN rarely occurs before the age of 50 years, but the risk increases markedly after age 60 years. 49 PHN may result from an imbalance of sensory input as nociceptive fibers regenerate more rapidly than large myelinated (inhibitory) nerve fibers after destruction by zoster. 47 Dissemination of zoster occurs via infected monocytes and lymphocytes, and immunocompromised patients have a 40% risk of developing disseminated diseaseY Fatal pneumonitis, hepatitis, or encephalitis may result from dissemination. 49 Isolated vesicles found at a distance to the affected dermatome are probably the result of hematogenous spread and are seen in up to 35% of immunocompetent patients. 45 The presence of a herpesvirus in a lesion is revealed by the presence of multinucleated giant cells and intranuclear inclusion bodies by Tzanck smear. However, to distinguish VZV from HSV, culture, serology, direct immunofluorescence staining of lesions, or molecular techniques (eg, polymerase chain reaction) are required. 45 Treatment of ophthalmic herpes zoster includes hospitalization for patients with severe disease or suppressed immune systems, and for elderly patients. 48 Immediate ophthalmological consultation is mandatory. Systemic corticosteroids are recommended by some authors for patients with large hemorrhagic skin bullae, optic neuritis, progressive proptosis with total ophthalmoplegia, and cerebral angiitis. 48 Nonsteroidal anti-inflammatory agents such as flurbiprofen have been helpful in patients with episcleritis, scleritis, and sclerokeratitis. 48 Acyclovir, 800 mg orally five times daily for 7 to 10 days, has shown some efficacy in acute herpetic neuralgia and in decreasing the duration and spread of the rash in immunocompromised patients if therapy is initiated within 48 to 72 hours of onset. 47'48 Therapies for PHN include amitriptyline, capsaicin cream, and possibly carbamazepine. 47 Neither acyclovir or prednisolone have been shown to decrease the risk of PHN. 5° Both acyclovir, 10 mg/kg every 8 hours, or vidarabine, 10 mg/kg/day, are

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efficacious in the treatment of disseminated zoster, but the duration of hospitalization is shorter in patients treated with acyclovir.51 Intravenous acyclovir is the recommended treatment for varicella pneumonitis in doses of 30 mg/kg/day divided every 8 hours in adults or 1,500 mg/mZ/day divided every 8 hours for children? 6 Although the use of acyclovir for the treatment of typical varicella in otherwise healthy individuals is controversial, there are several benefits to initiating treatment within 24 hours of the onset of the rash. Acyclovir may reduce the total number of lesions, expedite time to healing, and decrease the duration of fever,s2 The dosage of acyclovir in immunocompetent patients is 800 mg five times daily in adults and 10 to 20 mg/kg/day in 4 divided doses in children. 52 Although acyclovir is associated with few adverse reactions, there is a small risk of nephrotoxicity because intravenous administration can lead to precipitation of the drug in nephrons. 53 Renal failure is usually reversible with discontinuance of the drug. To lessen the risk of nephrotoxicity, the patient should be well hydrated and the drug should be given over a 1-hour period9 Immunocompromised patients without prior history of primary varicella should receive varicella-zoster immune globulin (VZIG) if exposed to a case of active varicella. 54 VZIG is only prophylactic if administered within 4 days of exposure. 54 The issue of varicella in pregnancy is important because both the mother and fetus or newborn are at risk for potentially serious complications. Varicella embryopathy, which may include central nervous system and eye damage, limb deformities, and epidermal scarring, is associated with infection during the first 2 trimesters. 55 Varicella of the newborn occurs in 10% to 20% of neonates whose mothers have contracted the infection perinatally, with a mortality rate as high as 20% to 30%. 56 Susceptible pregnant women exposed to varicella should be given VZIG within 4 days after exposure at a dose of 125 U per 10 kg, up to a maximum of 625 U. 56 Women in whom clinical varicella develops should receive intravenous acyclovir, 10 to 15 mg/kg every 8 hours for 7 days. 5~,56Neonates at risk should be given 125 U of VZIG. If the neonate develops varicella, acyclovir is the recommended treatment at a dose of 30 mg/kg/day. As of March 17, 1995, the live attenuated varicella virus vaccine was approved for use in individuals older than 12 months in the United States. The vaccine has shown efficacy in preventing the development of varicella in both healthy and immunocompromised hosts in trials conducted over the past 20 years. 57 In addition, the vaccine may also be used to prevent the development of zoster in older individuals with history of varicella58 and in leukemic children. 59 Breakthrough varicella has occurred in vaccinated patients, but these episodes have been associated with mild clinical features. 57 Although the VZV antibody response was found to decrease after 1 year postvaccination in elderly patients, CMI persists for at least 4 years in most subjects. 58 However, as Nader et al demonstrated, VZV CMI responses are not as persistent in adults when compared to children receiving the vaccine, suggesting that adults may require booster vaccinations to maintain immunity. 6o

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BACTERIAL INFECTIONS Impetigo

Impetigo represents the most common pediatric cutaneous infection. 61,6z The lesions are contagious. Impetigo is divided into two forms, bullous and nonbullous. Bullous impetigo is the less prevalent form and is caused by Staphylococcus aureus. The patient will have small blisters (bullae) appearing on previously uninjured skin, usually on the face, buttocks, trunk, and perineum. 61The bullae spontaneously rupture within 1 to 2 days. The differential diagnosis of bullous disorders includes thermal burns, pemphigus vulgaris, Stevens-Johnson syndrome, and allergic reactions. The nonbullous form begins in a traumatized area, usually on the face and/or extremities. The infection begins as an erythematous papule, progressing to a thick honey-colored crusted lesion. Constitutional symptoms are usually absent, but regional lymphadenopathy is often found. Spontaneous healing usually occurs over several weeks, but lesions may become chronic and ulcerated, and complications such as cellulitis and septicemia may develop. Group A streptococci, S aureus, or both may be the causative agents. The differential diagnosis may include herpes simplex, varicella zoster, tinea corporis, scabies, and pediculosis capitis. Disease occurs primarily in the summer, and predisposing factors include humidity, crowding, and poor hygiene. 6~ Treatment should consist of a [3-1actamase-resistant agent effective against both group A streptococci and S aureus, such as cephalexin, amoxicillin/clavulanate, or erythromycin, for widespread disease. 61,62 Mupirocin (Bactroban; SmithKline Beecham Pharmaceuticals, Philadelphia, PA) is a topical antibiotic ointment active against both S aureus and group A streptococci and may be used when the disease is not widespread. 63,64Treatment for 7 days is usually adequate for either the oral or topical regimen. 61 Necrotizing Fasciitis

Unlike the majority of dermatologic processes evaluated in the ED, necrotizing fasciitis (NF) is an uncommon disorder. However, NF is associated with substantial morbidity and mortality even when promptly recognized and treated. Although one of the first reports was over a century ago, 65 the terminology and bacteriology associated with NF have been somewhat confusing until recent improvements in isolation and culture techniques helped to clarify the polymicrobial nature of this infection. NF is a precipitous infection of the skin that involves the dermis, subcutaneous tissues, and the fascia. The hallmark of the infection is that it migrates along fascial planes, sometimes in the absence of overlying skin manifestations, and characteristically spares muscles. 66,67 Patients may first present with what appears to be a common superficial cellulitis. Early on, the skin may appear erythematous and edematous but soon develops crepitus, cutaneous ulceration, necrosis, bullae, and abscesses. 67,6sAlthough any body part can be affected, the extremities are most often involved. 66,68 To date, anecdotal reports have identified risk factors predisposing to NF, including trauma, diabetes mellitus, another infectious process (eg, varicella), previous surgery, arteriosclerosis, advanced age, intravenous drug abuse,

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malnutrition, neoplasm, and obesity. 66-69Previously healthy patients have also been affected. 69,7° If there is a delay by the patient in seeking medical attention, the first presentation in the ED may be that of frank shock with obvious skin involvement. Otherwise, the patient may present with mental status changes, fever, and a tender, hot, and erythematous lesion. The classic findings of dusky, blue-gray skin with crepitus and anesthesia (due to superficial nerve destruction) over the area does not occur until 2 to 4 days after the onset of infection. 66 Hemorrhagic bullae and systemic manifestations of shock may develop shortly thereafter as organisms and toxins become bloodborne. Gangrenous skin becomes apparent in 4 to 5 days, with sloughing of necrotic skin occurring at 8 to 10 days. 67 The necrosis of the skin is believed to result from thrombosis of subcutaneous blood vessels. 66-69 A toxic shock-like syndrome of NF has also been reported with group A streptococcal infections. 70 The organisms most often cultured from the blood and wounds of patients with NF include Clostridium spp, group A [3-hemolytic streptococci (GABHS), Staphylococcus aureus, Staphylococcus epidermidis, Pseudomonas aeruginosa, Escherichia coli, Bacteroides spp, Peptostreptococcus, group D streptococci, Proteus mirabilis and Candida spp. 68 Although it was once believed that the majority of cases of NF were caused by GABHS, it has become apparent with better culturing techniques that these infections are polymicrobial, including both aerobic and anaerobic organisms. 68 The recent reports of highly virulent GABHS infections (eg, "flesh-eating bacteria") may be due in part to the expression of the M antigens of the organism, to which the population has little immunity. 69 The ED diagnosis can be made rather expeditiously by several available methods. First, aspiration of the edges of the lesion and subsequent Gram staining of the aspirate can readily identify an organism. 69 Second, plain film radiography can be used to detect the presence or absence of soft tissue air under the area of skin involvement. 71 Computed tomography (CT) and magnetic resonance imaging (MRI) may also be useful adjuncts. 67 Although a leukocytosis is usually present and laboratory evidence of organ failure may be evident, no single laboratory test is helpful in establishing the diagnosis. The differential diagnosis includes erysipelas, cellulitis, and clostridial gas gangrene. Both erysipelas and cellulitis have associated lymphangitis and lymphadenopathy, features that rarely occur with NE 66 Erysipelas tends to be sharply demarcated, whereas in NF the lesion tends not to be clearly delineated. 69Although NF often presents similarly to cellulitis, its progression is much more rapid. Clostridial gangrene is characterized by muscle involvement. 66 Treatment begins with a high index of suspicion for the diagnosis of NF, followed by the administration of intravenous broad-spectrum antibiotics; the combination of clindamycin with either an aminoglycoside or a third-generation cephalosporin will cover anaerobic, gram-negative and gram-positive organisms. 69 Prompt surgical consultation is mandatory, because debridement and fasciotomies are necessary66,67; amputation may occasionally be required to halt the spread of infection. Hyperbaric oxygen therapy may be considered an adjunctive treatment measure, but should

never delay surgical debridement. 71 Despite aggressive treatment, mortality ranges from 8% to 67% for these patients. 7J and death is usually secondary to sepsis, respiratory or renal failure, or multi-organ failure.66

SCABIES Scabies is a contagious dermatosis caused by the Sarcoptes scabiei mite. Transmission is primarily by person-toperson contact? Patients typically complain of pruritis, often worse at night. 72,73The number of mites commonly found in typical infestations averages 10 to 15. 74 Burrows are the classic lesions, which are serpiginous gray-white papules most often seen in the interdigital webs of the hand, the flexor surfaces of the wrist and elbows, the beltline, breasts. axillae, and genitalia. 72-74 Burrows contain the mite, eggs, and stool (scybala). The dermatosls may present atypically as in Norwegian scabies, which is seen in immunocompromised and institutionalized patients. 7z73 In Norwegian scabies, lesions are crusted and scaly and may appear on the head, neck, buttocks, and perianal area. Hundreds of thousands of mites may be found on an individual afflicted with Norwegian scabies. 72 Infants may also present atypically with red crusted lesions and burrows, and lesions may involve the face. 72 The diagnosis of scabies is made by microscopic evidence of mites or eggs. A drop of mineral oil is placed on a no. 15 blade and several nonexcoriated burrows are scraped onto a microscope slide. The differential diagnosis includes other insect infestations (fleas, dog and cat parasites), atopic dermatitis, dermatitis herpetiformis, folliculitis, and syphilis.72,73 Treatment consists of a single application of 5% permethrin (Elimite; Allergan, Inc, Irvine, CA) cream to the entire external body surface. 72,73The cream is applied at night and washed off the following morning, 8 to 12 hours after application. Household members and sexual contacts should also receive treatment. Lindane (Kwell; Reedco, Inc, Humacat, Puerto Rico) was once a common treatment, but the concern of neurotoxicity has lessened its u s e . TMAlthough the mites and eggs will be destroyed after one application of permethrin, pruritis may continue for several weeks because of an allergic reaction to mite body parts, and symptomatic treatment is frequently necessary. 72,73 Clothes and bedding should be washed with hot water within 48 hours after treatment. Superinfection with S aureus or group A streptococci is the primary complication of scabies, and oral antibiotics may be necessary for treatment. 7z73

ERYTHEMAMULTIFORME(EM) EM is a skin reaction classically characterized by symmetric well-demarcated plaques found most often on the extensor surface of the extremities (Figure 4). Other regions of the body such as the palms, soles, neck, face, flexor surfaces of the extremities, and mucosal surfaces may also be affected. 75 Young adults between the ages of 20 to 40 years are most often affected, but children may also be affected. 75 Incidence is believed to be less than 1%. 75 Classification schemes for EM have been controversial, and there has been debate about whether EM, Stevens-

FERRERA ET AL • DERMATOLOGIC PROBLEMS

Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN) represent discrete disease processes or form a continuum of the same process. 76 EM has commonly been classified into two subsets: the mild variant EM minor, and the more severe disease EM major or SJS. 75 Although confluent mucous membrane erosions of the eyes and mouth are characteristic of SJS, genital, pharyngeal, and upper respiratory mucosa may also be involved. Patients may complain of flulike symptoms such as malaise, headache, fever, cough, rhinorrhea, and sore throat the week prior to outbreak of cutaneous lesions, but this prodrome may be due to the disease process that caused EM rather than being a characteristic of EM. 75,77 Once skin eruptions form, complaints of itching and burning skin and painful mucosal erosions are common in EM minor. 7s Constitutional symptoms may be profound in patients with SJS.75 Patients with EM may have several types of lesions at one time. The classic skin lesion is the "target" lesion, named for its two concentric rings of color changes with a well-defined border surrounding a central grayish blister or region of necrosis. 7s-77 Lesions may also appear as atypical "targets," either being raised or flat but with poorly defined borders and only one concentric ring, or as irregularly shaped macules with or without blisters. 76 With healing some scaling may result and hyperpigmentation is common. In EM minor, healing occurs within 4 weeks, but the course of SJS runs about 6 weeks. Recurrences are more common in EM minor than in SJS. 75 Although no significant complications occur with EM minor, visual impairment, esophagitis, and pneumonia may complicate SJS. If widespread epidermal denudation occurs, ie, greater than 30% body surface area, leading to TEN, mortality may be as high as 50% secondary to fluid losses and sepsis. 75 Herpes simplex virus (HSV) infection, Mycoplasma infections, and drugs are the three best documented etiologies of EM; numerous other infections, neoplastic processes, and collagen vascular diseases have also been implicated but less well proven. 75,77HSV may be responsible for the majority of cases, and recurrences of EM secondary to HSV are not uncommon. EM from Mycoplasma infection may involve multiple mucosal surfaces and form large bullae, leading to EM major; recurrences are uncommon. Drugs such as sulfonamides, penicillins, diphenylhydantoin, and methotrexate can lead to SJS or TEN. v5,77 Sulfonamides are the prototypical drug that can lead to SJS, usually appearing 1 to 2 weeks after initiation of therapy, but occasionally occurring within hours in previously sensitized patients. 7s The differential diagnosis includes urticaria, pityriasis rosea, tinea corporis, lupus erythematosus, Kawasaki syndrome, and syphilis when lesions are annular; bullous pemphigoid, dermatitis herpetiformis, pemphigus, and bullous contact dermatitis when bullous lesions are present; and herpetic gingivostomatitis, Behcet's disease, and Reiter's syndrome when the oral mucosa is involved. 75,77 Treatment consists of cessation of medications if permissible, fluid replacement, and topical antibiotics to prevent secondary bacterial infections. Some authors recommend the use of prednisone, at least 1 mg/kg/day, or equivalent intravenous steroid therapy for SJS.78 Acyclovir prophylaxis may prevent recurrent HSV-associated EM. 78

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BASAL CELL CARCINOMA Cancer of the skin is the most prevalent malignancy in the United States and Australia, with basal cell carcinoma (BCC) representing the most common type. 79 In the United Kingdom the incidence of BCC has increased by 235% since 1978. 8o An estimated 900,000 to 1.2 million people in the United States will develop a nonmelanoma skin cancer in 1994, exceeding the combined total of cancers of the lung, breast, colon, rectum, prostate, and bladder and all lymphomas. 81 The median age at presentation is 68 to 70 years. Sun-exposed areas of lightly pigmented individuals are the most common sites. Several forms of BCC are recognized. 79 The most frequent form is nodular BCC, seen as an indurated translucent papule with a distinct border, often with telangiectasias within the growth. The cystic type of BCC is similar to nodular BCC except that cystic areas are seen within the lesion. Sclerosing BCC has an indistinct border and lacks the characteristics of the nodular and cystic forms, making this form more difficult to diagnose. Superficial multicentric BCC appears as a red scaly patch and may be misdiagnosed as inflammatory dermatitis or psoriasis. Pigmented BCC contains melanin but otherwise appears and behaves as nodular BCC. Although most skin cancer deaths are caused by malignant melanoma, fatalities have also been reported with invasive BCC. Metastatic lesions are seen more frequently in men, and the mean life expectancy is 8 months once metastases are identified. 82 The most frequent sites of metastases are to regional lymph nodes, lung, bone, and skin. 82 There is a 2% incidence of metastasis with tumors larger than 3 cm in diameter. 82 Individuals with numerous or changing moles, those with a family history of skin cancer, people with heavy sun exposure, and fair-skinned individuals over the age of 50 years should be routinely referred for screening by a dermatologist. 80 Treatment options for the removal of BCC include curettage and electrodessication, scalpel excision and suture closure, Mohs' micrographic surgery, cryosurgery, and radiotherapy. 79 Chemotherapy with 5-fluorouracil is effective for treating superficial multicentric BCC. Regardless of the treatment modality, patients should be followed up at 6 weeks, 3 months, and then at least once yearly.

GRANULOMAANNULARE(GA) GA is considered a benign papular dermatosis with 4 recognized subtypes: localized (LGA), generalized (GGA), perforating (PGA), and subcutaneous (SGA). 83,84The etiology of this condition is unclear, although tuberculosis, trauma, and preceding infections have been proposed. 83,85 Histologically, lesions reside in the dermis and are composed of necrotic collagen surrounded by palisading histiocytes, lymphocytes, and fibroblasts. 8s LGA usually presents as asymptomatic flesh-colored or red papules arranged in a ringed pattern (Figure 5). 85 Lesions occur on the upper extremity in 60% of patients, on the lower extremity in 20%, on both upper and lower extremities in 7%, and on the trunk in 5%; LGA may occasionally be found on the face as well. 85 Women are more often affected than men, and patients tend to be younger than 40 years

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TABLE2. Summary of Features, Etiologies, and Treatments of Dermatological Conditions

Disease

Clinical Findings

Etiology

Treatment

Atopic D e r m a t i t i s

Erythematous, papular, pruritic lesions on extensor surfaces of arms and legs; face, neck, hands, and feet also involved. Flexor surfaces are involved in older patients.

IgE overproduction, decreased cell-mediated immunity

Hydropbilio cream, topicar steroids, topical antibiotios, PUVA

Contact Dermatitis

Well-localized area of vesicles on erythematous base. Wheal-and-flare response in urticaria. Itching in allergic form; burning in irhtant form. Erythematous, prudtic, sharply bordered patch, followed by smaller macules or papules in Christmas tree distribution.

Rhus genus, nickel, potassium dichromate, paraphenylenediamine, topical medications, phototoxicity Presumed virally induced

Avoidance of irritants, Burow's soaks, topical steroids; may require systemic steroids for severe cases; NSAIDs for nonimmune contact urticaria Symptomatic relief of pruritis

Psoriasis

Erythematous papules and scaly plaques, predominantly on scalp, intertriginous areas, and extensor surfaces. Arthritis in 5% to 7%.

Genetic predisposition, stress, skin trauma, and infection are disease triggers.

Prevent dehydration of skin. Topical steroids and crude coal tar. PUVA, methotrexate, or cyclosporine for severe cases.

Generalized Pustular Psoriasis

Fever, many sterile pustules, adenopathy, leukocytosis

Tapering of systemic steroids, withdrawal of topical steroids, NSAIDs, pregnancy, 13-streptococcal infection, viral URI

Methotrexate, steroids, retinoids, hydroxyurea

Rosacea

Facial flushing, pustule formation. Blepharitis and conjunctivitis can occur. Rhinophyma is endstage complication

Alcohol, cheeses, tea, coffee, spicy foods, stress, embarassment

Topical metronidazele or clindamycin. Systemic tatracyclines, erythromycin, and dapsone for severe cases. Argon laser for telangiectasias

Dermatophytoses (Tinea)

Pruritic maceration of toes and groin. Flat, scaly, and hypopigmented areas with vesicular edges on body. Kerion may develop on scalp. Brittle nails

Trichophyton, Microsporum, and Epidermophyton.

See Table 1.

Tinea Versicolor

Oval macular areas of hyperpigmentation or hypopigmentation on back, chest, and shoulders; mild pruritus

Pityrosporum orbiculare (Malassezia furfur)

Ketoconazole 400 mg once. 2.5% selenium sulfide for 1 to 2 weeks

Candidiasis

Red, well-demarcated patches often with satellite lesions

Candidaalbicans

Nystatin, clotrimoxazole, miconazole

Seborrheic Dermatitis

PapuIosquamous lesions of scalp, eyebrows, ears, perinasal and periorbital areas, and chest

P orbiculare either causes or exacerbates

Ketoconazole or fluconazole shampoo twice weekly; mild topical steroids

Warts

Verrucae vulgads affects hands and feet, flat warts affect face

Human papillomavirus

Cryosurgery, electrocautery, surgery, topical chemicals

Pitydasis Rosea

Molluscum Contagiosum

Umbilicated papules

Molluscum poxvirus

Cryotherapy, curettage, topical trichloroacetic acid.

Chickenpox (Primary varicella)

Small red macules, progressing to pruritic clear vesicles; lesions crust over; lesions present in various stages of development; pneumonitis, encephalitis, and Reye's syndrome

Varicella zoster virus

Acyclovir 30 mg/kg/d divided every 8 h (adults) or 1,500 mg/m2/d divided every 8 h (children) for pneumonitis; 800 mg 5 times daily (adults) or 10 to 20 mg/kg/d in 4 divided doses (children) for typical vadcella; VZlG to immunocompromJsed or susceptible pregnant women postexposure; 10 to 15 mg/kg every 8 h times 7 d for varicella in pregnancy

Herpes zoster

Pain or pruritus in area of involved dermatome; lesions crust over in 7 to 10 d; visual loss when CN V is involved; otalgia, tinnitus, deafness, vertigo, Bell's palsy may occur; paralysis rarely occurs; PHN is most common complication, dissemination often occurs in immunocompromised

Varicella zoster virus

Hospitalization, systemic steroids, NSAIDs for ophthalmic zoster; acyclovir 800 mg 5 times daily for 7 to 10 d for acute neuralgia; capsaicin cream 3 to 4 times daily, amitriptyline, and carbamazepine for PHN; acyclovir 10 mg/kg/d every 8 h for disseminated zoster.

Bullous Impetigo

Small blisters on face, buttocks, trunk and perineum, which rupture after 1 to 2 days

S aureus

Mupirocin for local disease. Oral antistaphylococcal agents for widespread disease

Nonbullous Impetigo

Erythematous papule, progressing to honey-colored crust

Gp A Streptococcus S aureus

Same as for bullous form

Necrotizing fasciitis

Tender, red, warm lesion which develops into dusky skin with crepitus and anesthesia; bullae and gangrene follow; shock may be present.

Polymicrobiai

Scabies

Pruritis, worse at night. Burrows found on hands, wrist, elbows, beltline, breasts, axillae, genitalia

Sarcoptes scabiei mite

Intravenous cUndamycin with either aminoglycoside or third-generation cephalosporin; early surgical debridement and fasciotomies; hyperbaric oxygen 5% permethrin cream to entire body for 8 to 12 hours. Wash bedding and clothes.

Erythema Multiforme

Symmetric, well-demarcated plaques most often on extensor surfaces of extremities. Target lesions.

Herpes simplex virus, Mycoplasma, and drugs are best documented.

Basal Cell Carcinoma

Nodular, cystic, sclerosing, and pigmented forms

Sun exposure

Granuloma Annulare

Localized, generalized, perforating and subcutaneous forms. Localized and generalized forms are flesh-colored or red papules in a ringed pattern. Perforating form has umbilicating papules

Unclea5 buttrauma, tubercolosis, andinfections have been proposed.

Hidradenitis Suppurativa

Tender ulceration and fibrosis of skin. Foul-smelling drainage Edematous red lesions which progress to ulceration on lower leg

Occlusion ofapocnne ducts orhairfollicles has beenproposed Incompetence of perforating veinsleadingto venous hypertension

Venous Stasis

Cessation of medications, fluid replacement, topical antibiotics. Acyclovir prophylaxis for Herpes simplex virus Mohs' surgery, curettage, cryosurgery, scalpel excision Usually undergoes spontaneous regression. Cryosurgery and intralesional steroids may be used for localized form. Potassium iodide, isotretinoin, and etretinate may be used for generalized form Erythromycin, metronidazole, topical antibacterials. Surgery for advanced cases Elevation and compression. Systemic steroids for severe cases. Sclerotherapy and surgery may be required

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old. 85 Although the lesions regress spontaneously in half of patients within 2 years, 40% of patients will have recurrent lesions; these recurrent lesions most often resolve within 2 yearsY The differential diagnosis includes, but is not limited to, tinea corporis, necrobiosis lipoidica diabeticorum (NLD), annular lichen planus, urticaria pigmentosa, arthropod bites, and sarcoidosis. 85,86 GGA is present in approximately 10% to 15% of patients with GA. 85,87The lesions appear similar to those in LGA but number in the hundreds and in one third of cases will be nonannular. 87 In contrast to LGA, GGA tends to affect older patients, has a more protracted course with less chance of spontaneous regression, and generally responds poorly to therapy. 87 Lesions are usually symmetrically located on the extremities and trunk, but almost any body area may also be involved. 87 The average duration of the lesions is 3 to 4 years, 85 but up to 25% of patients have durations of 5 years or longer. 87 Diabetes mellitus was found to be an associated disease in 21% of patients in one study, but may represent referral bias. 87 Intralesional corticosteroids and alkylating agents such as oral chlorambucil show success in treatment. 87 SGA is found exclusively in children and has no association with other rheumatologic or connective tissue diseases, s3 Others have referred to this condition as benign rheumatoid nodule, pseudorheumatoid nodule, isolated subcutaneous nodule, subcutaneous palisading granuloma, and palisading granuloma nodosum. 83 Patients present with a history of several months of rapidly growing, painless, soft-tissue swelling of the extremities or scalp. Histologically, there is a central area of necrotic collagen with a surrounding region of palisading histiocytes and a peripheral zone of inflammatory cells. Treatment is not usually required because most lesions undergo spontaneous resolution; however, most patients develop recurrences either at the biopsy site or another locationY Some patients consequently develop the localized form of GA (LGA). s3 PGA is characterized by umbilicated papules 1 to 4 mm in diameter that are found on the extremities. 86 Children are most often affected. Larger and more ulcerated plaques are more often seen in older patients and may have an association with diabetes mellitus. Spontaneous regression is the usual course for PGA. 86 The differential diagnosis of umbilicated lesions includes molluscum contagiosum, perforating collagenosis, perforating folliculitis, and sarcoidosisY Treatment is generally not required for LGA, SGA, and PGA because spontaneous regression of the lesions is the usual course. Recently, however, cryosurgery with nitrous oxide has been found to be a safe and efficacious treatment modality for LGA. s4 Various treatment regimens have been used with variable results for patients with GGA, recently including oral potassium iodide, sS,s9 isotretinoin, 90 and etretin a t e . 91

HIDRADENITIS SUPPURATIVA Hidradenitis suppurativa represents an idiopathic disorder of skin containing apocrine glands, such as the axillae, anogenital region, and female breast. 92 The disease usually begins after onset of puberty and before the age of 40 years. 92 The pathogenesis is classically believed to begin

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with blocking of apocrine ducts by keratin, leading to glandular dilatation and subsequent bacterial infection. 92 However, other authors believe this disease results from occlusion of hair follicles rather than of apocrine ducts; Carmen et a193found that hair shaft-containing sinuses lined by squamous epithelium were a more common histologic finding than apocrine gland inflammation. 93 Regardless of pathogenesis, the overlying skin becomes ulcerated and healing occurs by fibrosis. Epithelialized sinus tracts form within the fibrotic dermis. 94 The lesions present as tender swellings, and recurrent infections lead to foul-smelling drainage from the lesions (Figure 6). 94 Obesity and ache are frequent associations. 92 Potential complications include lymphedema or decreased mobility of a limb because of scarring, anal or urethral fistulae, and squamous cell carcinoma. 92 The differential diagnosis of sinus tract-producing disorders includes tuberculosis, actinomycosis, Crohn's disease, lymphogranuloma venereum, granuloma inguinale, cat-scratch disease, tularemia, and nocardiosis. 92 Treatment consists of oral antibiotics such as erythromycin and metronidazole, topical antibacterials, and surgery for advanced cases.92, 94

VENOUS STASIS DERMATITIS/ULCERS Among the causes of lower extremity ulcerations, including neuropathies, arterial insufficiency, and sickle cell disease, venous hypertension accounts for approximately half of the cases. 95 Hypertension in the venous system is caused by incompetence of the one-way valves of the perforating veins or long saphenous vein; retrograde flow can occur, which is then transmitted as elevated pressures to the subcutaneous tissues, resulting in dermatitis. 95,96 Although venous stasis tends to affect elderly patients more commonly, ulcerations appear in 40% of patients before the age of 50 years. 95 Some of the factors predisposing to venous hypertension include trauma, thrombophlebitis, and a genetic propensity. 96 Edema, deposition of fibrin around capillaries, microvascular abnormalities, ischemia, and the formation of free radicals may all contribute to venous hypertension and subsequent stasis ulceration. 96 Stasis dermatitis presents as edematous, red, and occasionally oozing lesions on the lower extremities which may progress to ulceration. 9 Although the medial portion of the leg is most often affected, many ulcers will appear laterally and posteriorly. 95 Varicosities and hyperpigmentation often are associated with the ulcers. 95 Lipodermatosclerosis, representing induration of the skin surrounding the ulcer, may also be seen. 95 Arterial insufficiency must be ruled out as the cause of the ulcer, as treatment methods are markedly different. Ulcers of diminished arterial inflow usually present as punched out lesions which may extend down to tendons and muscle beds and often have black eschars. 95 Treatment modalities for stasis dermatitis include elevation of the affected leg and compression bandages to reduce the edema.9,95 Although topical antibiotics and steroids have been used in the past, Falanga 95 cautions against the use of such agents because of the potential for exacerbating the dermatitis; the use of systemic corticosteroids tapered over a 6-week period is preferable to topical therapy for severe

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dermatitis. 95 Sclerotherapy and surgery may also be required. Some authors have reported very good results of ligation and division of incompetent perforating veins for patients with ulcers refractory to conservative measures. 9v Infected ulcers are treated with antibiotics, but often it is difficult to differentiate colonization from true infection. 95,97 The patient and physician must expect that the healing process may take many months, and many ulcers may still not resolve after 1 year of treatment. 95 Table 2 summarizes the important clinical features, presumed etiologies, and current treatment regimens for the dermatologic conditions discussed in this article.

REFERENCES 1. Przybilla B, Eberlein-Konig B, Rueff F: Practical management of atopic eczema. Lancet 1994;343:1342-1346 2. Lapidus CS, Honig PJ: Atopic dermatitis. Pediatr Rev 1994;15: 327-332 3. Hanifin JM: Atopic dermatitis in infants and children. Pediatr Clin North Am 1991 ;38:763-789 4. Wahigren CF: Pathophysiology of itching in urticaria and atopic dermatitis. Allergy 1992;47:65-75. 5. Krutmann J, Czech W, Diepgen T, et al: High-dose UVA1 therapy in the treatment of patients with atopic dermatitis. J Am Acad Dermatol 1992;26:225-230 6. Atherton DJ, Carabott F, Glover MT, et al: The role of psoralen photochemotherapy (PUVA) in the treatment of severe atopic eczema in adolescents. Br J Dermatol 1988;118:791-795 7. Millikan LE, Shrum JP: An update on common skin diseases. Postgrad Med 1992;91:96-115 8. Klaus MV, Wieselthier JS: Contact dermatitis. Am Fam Physician 1993;48:629-632 9. Beacham BE: Common dermatoses in the elderly. Am Fam Physician 1993;47:1445-1450 10. Krasteva M: Contact dermatitis. Int J Dermatol 1993;32:547560 11. Agency for Toxic Substances and Disease Registry: Contact dermatitis and urticaria from environmental exposures. Am Fam Physician 1993;48:773-780 12. Harvell J, Bason M, Maibach H: Contact urticaria and its mechanisms. Food Chem Toxico11994;32:103-112 13. Pecquet C, Leynadier F, Dry J: Contact urticaria and anaphylaxis to natural latex. J Am Acad Dermatol 1990;22:631-633 14. Taylor JS, Cassettari J, Wagner W, et al: Contact urticaria and anaphylaxis to latex. J Am Acad Dermatol 1989;21:874-877 15. Maso MJ, Goldberg DJ: Contact dermatoses from disposable glove use: a review. J Am Acad Dermatol 1990;23:733-737 16. Ginsburg CM: Pityriasis rosea. Pediatr Infect Dis J 1991 ;10:858859 17. Tunnessen WW, Jr: Picture of the month: Pityriasis rosea. Am J Dis Child 1991 ;145:1441-1442 18. Vidimos AT, Camisa C: Tongue and cheek: Oral lesions in pityriasis rosea. Cutis 1992;50:276-280 19. Krueger GG, Duvic M: Epidemiology of psoriasis: Clinical issues. J Invest Dermato11994;102:14S-18S. 20. Das UN, Vijaykumar K, Madhavi N, et al: Psoriasis: Current concepts and new approaches to therapy. Med Hyp 1992;38:56-62. 21. Helm TN, Dijkstra JWE, Ferrara RJ, et al: PUVA therapy. Am Fam Physician 1991 ;43:908-912. 22. Lyons JH: Generalized pustular psoriasis. Int J Dermatol 1987;26:409-418 23. Ryan T J, Baker H: The prognosis of generalized pustular psoriasis. Br J Dermatol 1971 ;85:407-411 24. Ostlere LS, Akhras F, Langtry JAA, et al: Generalized pustular psoriasis associated with bacterial endocarditis of the anterior papillary muscle. Br J Dermatol 1992;127:187-188 25. Spencer JM, Silvers DN, Grossman ME: Pustular eruption after drug exposure: Is it pustular psoriasis or a pustular drug reaction? Br J Dermatol 1994; 130:514-519 26. Chu T: Treatment of rosacea. Practitioner 1993;237;941-945

27. Wilkin JK: Rosacea: Pathophysiology and treatment. Arch Dermato11994;130:359-362 28. Bergus GR, Johnson JS: Superficial tinea infections. Am Fam Physician 1993;48:259-268 29. Odom R: Pathophysiology of dermatophyte infections. J Am Acad Dermatol 1993;28:$2-$7 30. Rezabek GH, Friedman AD: Superficial fungal infections of the skin: Diagnosis and current treatment recommendations. Drugs 1992;43:674-682 31. Nightingale SL: Warnings issued on nonsedating antihistamines terfenadine and astemizole. JAMA 1992;268:705 32. Goldgeier MH: Fungal infections of the skin, hair, and nails. Pediatr Ann 1993;22:253-259 33. Pariser DM: Topical steroids: A guide for use in the elderly patient. Geriatrics 1991 ;46:51-63 34. Reynolds RD, Boiko S, Lucky AW: Exacerbation of tinea corporis during treatment with 1% clotrimazole/0.05% betamethasone dipropionate (Lotrisone). Am J Dis Child 1991 ;145:1224-1225 35. Barkey WF: Striae and persistent tinea corporis related to prolonged use of betamethasone dipropionate 0.05% cream/ clotrimazole 1% cream (Lotrisone cream). J Am Acad Dermatol 1987;117:518-519 36. Borelli D, Jacobs PH, Nail L: Tinea versicolor: Epidemiologic, clinical, and therapeutic aspects. J Am Acad Dermato11991 ;25:300305 37. Rigopoulos D, Katsambas A, Antoniou C, et al: Facial seborrheic dermatitis treated with fluconazole 2% shampoo, int J Dermatol 1994;33:136-137 38. McGrath J, Murphy GM: The control of seborrheic dermatitis and dandruff by antipityrosporal drugs. Drugs 1991 ;41:178-184 39. Carr MM, Pryce DM, Ive FA: Treatment of seborrhoeic dermatitis with ketoconazole: I. Response of seborrhoeic dermatitis of the scalp to topical ketoconazole. Br J Dermatol 1987;116:213-216 40. Green CA, Farr PM, Shuster S: Treatment of seborrhoeic dermatitis with ketoconazole: I1. Response of seborrhoeic dermatitis of the face, scalp and trunk to topical ketoconazole. Br J Dermatol 1987;116:217-221 41. Janniger CK: Childhood warts. Cutis 1992;50:15-16 42. Beutner KR: Cutaneous viral infections. Pediatr Ann 1993;22: 247-252 43. Highet AS: Molluscum contagiosum. Arch Dis Child 1992;67: 1248-1249 44. Straus SE: Overview: The biology of varicella-zoster virus infection. Ann Neurol 1994;35:$4-$8 (suppl) 45. Rockley PF, Tyring SK: Pathophysiology and clinical manifestations of Varicella zoster virus infections. Int J Dermatol 1994;33:227232 46. Feldman S: Variceila-zoster virus pneumonitis. Chest 1994;106: 22S-27S 47. Mamdani FS: Pharmacologic management of herpes zoster and postherpetic neuralgia. Can Fam Physician 1994;40:321-332 48. Marsh RJ, Cooper M: Ophthalmic herpes zoster. Eye 1993;7: 350-370 49. Gilden DH: Herpes zoster with postherpetic neuralgia-persisting pain and frustration. N Engl J Med 1994;330:932-934 50. Wood MJ, Johnson RW, McKendrick MW, et al: A randomized trial of acyclovir for 7 days or 21 days with and without prednisolone for treatment of acute herpes zoster. N Engl J Med 1994;330:896-900 51. Whitley RJ, Gnann JW, Hinthorn D, et al: Disseminated herpes zoster in the immunocompromised host: a comparative trial of acyclovir and vidarabine. J Infect Dis 1992; 165:450-455 52. Wagstaff AJ, Faulds D, Goa KL: Aciclovir: A reappraisal of its antiviral activity, pharmacokinetic properties and therapeutic efficacy. Drugs 1994;47:153-205 53. Spangler JG, Kirk JK, Knudson MP: Uses and safety of acyclovir in pregnancy. J Fam Pract 1994;38:186-191 54. Gallant JE, Moore RD, Chaisson RE: Prophylaxis for opportunistic infections in patients with HIV infection. Ann Intern Med 1994; 120:932-944 55. Enders G, Miller E, Cradock-Wilson J, et al: Consequences of varicella and herpes zoster in pregnancy: Prospective study of 1739 cases. Lancet 1994;343:1548-1551 56. Chapman S, Duff P: Varicella in pregnancy. Semin Perinatol 1993; 17:403-409

FERRERA ET AL • DERMATOLOGIC PROBLEMS

57. Asano Y, Suga S, Yoshikawa T, et al: Experience and reason: Twenty-year follow-up of protective immunity of the Oka strain live varicella vaccine. Pediatrics 1994;94:524-526 58. Levin MJ, Murray M, Zerbe GO, et al: Immune responses of elderly persons 4 years after receiving a live attenuated varicella vaccine. J Infect Dis 1994;170:522-526 59. Hardy I, Gershon AA, Steinberg SP, et al: The incidence of zoster after immunization with live attenuated varicella vaccine: a study in children with leukemia. N Engl J Med 1991 ;325:1545-1550 60. Nader S, Bergen R, Sharp M, et al: Age-related differences in cell-mediated immunity to varicella-zoster virus among children and adults immunized with live attenuated varicella vaccine. J Infect Dis 1995;171:13-17 61. Dagan R: Impetigo in childhood: Changing epidemiology and new treatments. Pediatr Ann 1993;22:235-240 62. Demidovich CW, Wittier RR, Ruff ME, et al: Impetigo: Current etiology and comparison of penicillin, erythromycin, and cephalexin therapies. Am J Dis Child 1990; 144:1313-1315 63. Goldfarb J, Crenshaw D, O'Horo J, et al: Randomized clinical trial of topical mupirocin versus oral erythromycin for impetigo. Antimicrob Agents Chemother 1988;32:1780-1783 64. Britton JW, Fajardo JE, Krafte-Jacobs B: Comparison of mupirocin and erythromycin in the treatment of impetigo. J Pediatr 1990; 117:827-829 65. Jones J: Investigation upon the nature, causes, and treatment of hospital gangrene as it prevailed in the Confederate armies 1861-1865. New York: U.S. Sanitary Commission, Surgical Memoirs of the War of Rebellion, 1871 66. Janevicius RV, Hann SE, Batt MD: Necrotizing fasciitis. Surg Gynecol Obstet 1982; 154:97-102 67. Gannon T: Dermatologic emergencies. Postgrad Med 1994;96: 67-82 68. Umbert IJ, Winkelmann RK, Oliver GF, et al: Necrotizing fasciitis: A clinical, microbiologic, and histopathologic study of 14 patients. J Am Acad Dermatol 1989;20:774-781 69. Chelsom J, Halstensen A, Haga T, et al: Necrotising fasciitis due to group A streptococci in western Norway: Incidence and clinical features. Lancet 1994;344:1111-1115 70. Stevens DL, Tanner MH, Winship J, et al: Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A. N Engl J Med 1989;321:1-7 71. Atiyeh BC, Zaatari AM: Necrotizing fasciitis of the upper extremity. J Emerg Med 1994; 12:611-613 72. Sterling GB, Janniger CK, Kihiczak G, et al: Scabies. Am Fam Physician 1992;46:1237-1241 73. Pruksachatkunakorn C, Duarte AM, Schachner L: Scabies: How to find and stop the itch. Postgrad Med 1992;91:263-269 74. Haag ML, Brozena SJ, Fenske NA: Attack of the scabies: What to do when an outbreak occurs. Geriatrics 1993;48:45-53 75. Huff JC, Weston WL, Tonnesen MG: Erythema multiforme: A critical review of characteristics, diagnostic criteria, and causes. J Am Acad Dermato11983;8:763-775 76. Bastuji-Garin S, Rzany B, Stern RS, et al: Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme. Arch Dermato11993;129:92-96

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77. Stampien TM, Schwartz RA: Erythema multiforme. Am Fam Physician 1992;46:1171-1176 78. Patterson R, Dykewicz MS, Gonzalzles A, et al: Erythema multiforme and Stevens-Johnson syndrome: descriptive and therapeutic controversy. Chest 1990;98:331-336 79. Pariser DM, Phillips PK: Basal cell carcinoma: When to treat it yourself, and when to refer. Geriatrics 1994;49:39-44 80. Ko CB, Walton S, Keczkes K, et al: The emerging epidemic of skin cancer. Br J Dermato11994;130:269-272 81. Miller DL, Weinstock MA: Nonmelanoma skin cancer in the United States: incidence. J Am Acad Dermatol 1994;30:774-778 82. Snow SN, Sahl W, Lo JS, et al: Metastatic basal cell carcinoma. Cancer 1994;73:328-335 83. Davids JR, Kolman BH, Billman GF, et al: Subcutaneous granuloma annulare: Recognition and treatment. J Pediatr Orthop 1993; 13:582-586 84. Blume-Peytavi U, Zouboulis CC, Jacoby H, et al: Successful outcome of cryosurgery in patients with granuloma annulare. Br J Dermatol 1994; 130:494-497 85. Muhlbauer JE: Granuloma annutare. J Am Acad Dermatol 1980;3:217-230 86. Samlaska CP, Sandberg GD, Maggio KL, et al: Generalized perforating granuloma annulare. J Am Acad Dermatol 1992;27:319322 87. Dabski K, Winkelmann RK: Generalized granuloma annulare: Clinical and laboratory findings in 100 patients. J Am Acad Dermatol 1989;20:39-47 88. Smith JB, Hansen CD, Zone JJ: Potassium iodide in the treatment of disseminated granuloma annulare. J Am Acad Dermatol 1994;30:791-792 89. Caserio RJ, Eaglstein WH, Allen CM: Treatment of granuloma annulare with potassium iodide. J Am Acad Dermatol 1984;10:294 (letter) 90. Schleicher SM, Milstein HJ, Lim SJM, et al: Resolution of disseminated granuloma annulare with isotretinoin. Int J Dermatol 1992;31:371-372 91. Botella-Estrada R, Guillen C, Sanmartin O, et al: Disseminated granuloma annulare: Resolution with etretinate therapy. J Am Acad Dermatol 1992;26:777-778 92. Radcliffe KW: Hidradenitis suppurativa. Genitourin Med 1991; 67:58 93. Carmen C, Yu W, Cook MG: Hidradenitis suppurativa: A disease of follicular epithelium, rather than apocrine glands. Br J Dermatol 1990; 122:763-769 94. Edlich RF, Silloway KA, Rodeheaver GT, et al: Epidemiology, pathology, and treatment of axillary hidradenitis suppurativa. J Emerg Med 1986;4:369-378 95. Falanga V: Venous ulceration. J Dermatol Surg Onco11993;19: 764-771 96. Angel MF, Ramasastry SS, Swartz WM, et al: The causes of skin ulcerations associated with venous insufficiency: A unifying hypothesis. Plast Reconstr Surg 1987;79:289-297 97. Jamieson WG, DeRose G, Harris KA: Management of venous stasis ulcer: Long-term follow-up. Canad J Surg 1990;33:222-223