Scaling conditions include psoriasis, seborrheic dermatitis, tinea corporis, pityriasis ("tinea") versicolor, eczema/atopic dermatitis, lichen planus, secondary syphilis, and scabies. Table 251-1 lists common features distinguishing these eruptions.
TABLE 251-1Comparison Features of Common Papulosquamous Eruptions ||Download (.pdf) TABLE 251-1 Comparison Features of Common Papulosquamous Eruptions
|Condition ||Distinguishing Clinical Features ||Location ||Special Signs ||Comments |
|Psoriasis ||Erythematous, well-marginated papules and plaques with silvery scale ||Trunk, extensor surfaces, scalp ||Auspitz sign; Koebner phenomenon, nail pitting ||Hereditary predilection; onset in early 20s |
|Seborrheic dermatitis ||Greasy, yellow scales ||Midchest, suprapubic, scalp, facial creases ||Can overlap with psoriasis, "sebopsoriasis" ||Debilitated, elderly, or infants (cradle cap) |
|Atopic dermatitis ||Ill-defined vesicles forming plaques with scale; chronic lesions lichenified ||Flexures > trunk ||Spares the nose ||Pruritus "itch that rashes"; atopic individuals |
|Lichen planus ||5 P's: purple, pruritic, polygonal, planar papules ||Any skin, mucous membranes, hair follicles ||Wickham striae; Koebner phenomenon ||Age 20–60 y old |
|Pityriasis rosea ||Lines of skin tension, collarette of scale ||Trunk, in Christmas tree pattern following skin lines ||Herald patch 1–2 wk before general eruption ||Spring and fall, age 15–40 y old; viral exanthem, herpes 6 and 7 |
|Tinea corporis ||Sharply demarcated, erythematous, scaly annular plaques; may coalesce into gyrate patterns ||Trunk, legs, arm, neck ||May need KOH/culture to diagnose; septate branching hyphae on KOH ||All ages; from pets, soil, or autoinoculation from hands/feet; incubation days or months |
|Pityriasis (tinea) versicolor ||Versicolored—red, salmon, light brown, dark brown, hypopigmented; well-demarcated scaly patches ||Central upper chest and back ||Spaghetti and meatballs on KOH; nonseptate pseudohyphae and budding yeast ||Young adults, summer, hot humid environments |
|Secondary syphilis ||At 2–10 wk, macular erythema on trunk, abdomen, inner extremities; followed by papular or papulosquamous lesions ||Palms, soles, trunk ||Serology ||Great masquerader—can take any form; can be confused with pityriasis rosea |
|Scabies ||Pruritic papules and burrows with crusting ||Finger webs, wrists, axillae, areolae, umbilicus, abdomen, waistband, genitals ||Scrapings show mites, feces, eggs ||Can be chronic "7-year itch"; intensely pruritic, especially at night |
Psoriasis is discussed in detail in chapter 253, "Skin Disorders: Extremities." Stress or alcohol ingestion can be associated with a flare of psoriasis. The following medications can also be related to an exacerbation: steroid withdrawal, lithium, β-blockers, interferon, and antimalarials.1 The differential diagnosis is listed in Table 251-1.
Diagnosis is clinical. The disorder is characterized by well-demarcated erythematous papules and plaques with a silvery white scale (Figure 251-1). Removal of the scale typically reveals minute bleeding points referred to as Auspitz sign. Chronic plaque psoriasis is the most common variety, and localization to the sacrum, gluteal cleft, or umbilicus can occur. In the skin folds, psoriasis often lacks the characteristic silvery scale and is present only as well-demarcated, red- to salmon-colored plaques. Involvement of the scalp and nails is not uncommon. Lesions of psoriasis tend to be symmetric with a predilection for the extensor surfaces. Localized physical trauma can cause new lesions to form (Koebner phenomenon—scratching causes new lesions to form in linear distribution of the scratch). Scattered discrete lesions, like water droplets, represent a distinctive form of psoriasis called guttate psoriasis (Figure 251-2). This can be seen on the trunk as an abrupt eruption following an infection such as streptococcal pharyngitis. Generalized pustular psoriasis (Figure 251-3) should be included in the differential diagnosis of the acutely ill patient.
Psoriasis. Large, well-marginated scaling plaques. [Photo contributed by University of North Carolina Department of Dermatology.]
Guttate psoriasis. Note discrete erythematous scaly papules resembling raindrops on the trunk. [Photo contributed by University of North Carolina Department of Dermatology.]
Pustular psoriasis. [Photo contributed by University of North Carolina Department of Dermatology.]
Topical treatment for localized plaques includes moisturization with plain petroleum jelly or topical steroids. Ointment-based products have the highest hydration efficacy. High-potency steroids, such as clobetasol foam, spray, ointment, or cream, can be used on the trunk. Prolonged use may result in atrophy, steroid acne, pyoderma, or rebound with abrupt discontinuation. Do not prescribe systemic steroids due to the great risk of rebound or induction of pustular psoriasis.
Seborrheic dermatitis is a chronic inflammatory disease with a predilection for areas of increased sebaceous gland activity. Incidence increases with age and in specific disease states.2 Erythema with a greasy yellowish scale is seen in the sebum-producing areas, such as the scalp, eyebrows, ears, beard, midchest, and groin (Figure 251-4). The lesions are often well marginated and symmetric. Weeping and crusting may occur, especially in the body folds and ears. Pruritus may be present. Severe involvement may occur in debilitated patients such as those with Parkinson's disease, Down's syndrome, or acquired immunodeficiency disease.
Seborrheic dermatitis. [Reproduced with permission from Wolff KL, Johnson R, Suurmond R: Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology, 5th ed. © 2005, McGraw-Hill, New York.]
The presternal area, axillae, and groin are common sites for truncal involvement. The axillary involvement typically starts in the apices, similar to a contact dermatitis to deodorants, whereas clothing dermatitis involves the periphery but spares the axillary vault. The inframammary regions and umbilicus may also be involved. The differential diagnosis is presented in Table 251-1.
Treatment is aimed at controlling disease. Mild cases may respond to over-the-counter shampoos containing ketoconazole 1%, selenium sulfide, zinc pyrithione, or salicylic acid. These can be lathered into any affected area on the scalp or body. Prescription-strength ketoconazole 2% shampoo can be used several times weekly, or ketoconazole cream for the face can be used twice daily. Hydrocortisone 1% cream or lotion, or 2.5% cream or lotion for more difficult cases, can be used twice daily in combination with antifungals.
Pityriasis rosea is a viral exanthema associated with herpesvirus 6 and 7. It may be a reactivation of the latent herpesvirus that triggers a viremia and subsequent eruption.3 It most frequently affects those between 15 and 40 years old, most often in spring and fall. Pityriasis typically begins with a single, or "herald," patch, which is a fine scaling, erythematous- to salmon-colored discrete oval patch 2 to 5 cm in size (Figure 251-5). In 1 to 2 weeks, a generalized eruption occurs on the trunk and proximal arms, with a characteristic "Christmas tree" pattern of macules and plaques, with the long axis of the lesions oriented along skin tension lines (Figure 251-6). A collarette of scale with the open edge of scale on the inside of the lesion is a helpful diagnostic finding. Rarely, the face, palms, soles, or oral cavity can be involved. Pruritus can be moderate to severe. Mild constitutional symptoms may also occur at the onset of the eruption. Spontaneous resolution occurs within 4 to 16 weeks. Relapses or recurrences are uncommon.
Herald patch in pityriasis rosea (arrow). [Courtesy of the Centers for Disease Control and Prevention.]
Pityriasis rosea. Fine scaly plaques along skin tension lines. [Photo contributed by University of North Carolina Department of Dermatology.]
Table 251-1 lists the major differential diagnoses. In addition, several medications can cause a pityriasis-like eruption: captopril, barbiturates, lisinopril, ketotifen, arsenicals, interferon, imatinib mesylate, gold, and clonidine. Guttate psoriasis can mimic pityriasis rosea but does not have the characteristic collarette of scale.
Treatment is symptomatic. Oral antihistamines by mouth and topical steroid creams (triamcinolone 0.1% in adults or hydrocortisone 1% in children) with emollients (petroleum jelly–based preparations) can help the pruritus. Ultraviolet B phototherapy from a dermatologist or natural sunlight may speed the resolution of the lesions. Macrolides are not indicated.4,5
All superficial dermatophyte infections of the trunk, neck, arms, and legs are referred to as tinea corporis. Specific names are used for eruptions involving the groin (tinea cruris), feet (tinea pedis), hands (tinea manuum), face (tinea faciei), and scalp (tinea capitis); see associated chapters in this book for more detailed information about these specific locations. All ages can be affected, and lesions can spread by autoinoculation from other parts of the body. Trichophyton rubrum and Trichophyton mentagrophytes are the most common organisms that can spread from involvement of the feet. Occupational or recreational exposure (gyms, locker rooms) occurs from contaminated clothing, furniture, and/or equipment. Exposure to animals or contaminated soil may also cause tinea corporis. Pets may harbor Trichophyton verrucosum or Microsporum canis, whereas T. mentagrophytes from Southeast Asia bamboo rats can cause a very inflamed and highly contagious widespread eruption. The incubation period is variable and may be days or months after exposure.6 The eruption may be chronic with mild pruritus as the only symptom. Tinea corporis is characterized by one or more sharply demarcated, mildly erythematous, annular scaling plaques (Figure 251-7). Central clearing gives the name "ringworm." The advancing scaling border is a characteristic finding, and the border is an excellent area to demonstrate long branching hyphae with a potassium hydroxide preparation (see Figure 248-1 and Table 248-6). Abrupt onset of widespread tinea may be associated with acquired immunodeficiency syndrome or other immunosuppressive disorders or use of topical steroids. Occlusion, shaving, or topical steroid use may result in a deep, purulent, boggy folliculitis. The differential diagnosis is provided in Table 251-1.
Tinea versicolor. Hypopigmented macules with fine scale. [Photo contributed by University of North Carolina Department of Dermatology.]
Treatment of limited lesions is with topical antifungal preparations (Table 251-2). Apply twice a day and extend the application to at least 3 cm beyond the advancing margin. Treat for at least 4 weeks and continue for 1 week after resolution. If tinea pedis or unguium is also present, apply the antifungal to the feet and nails. Widespread tinea corporis or involvement of the follicles warrants oral therapy (Table 251-2).6 Oral agents may be expensive and can have interactions and contraindications in specific patient populations. Refer to a drug reference manual for specific details. Terbinafine requires baseline liver function tests before administration. Itraconazole is contraindicated in congestive heart failure and in patients taking lovastatin or simvastatin. Griseofulvin will cause a disulfiram (Antabuse®)-like effect with alcohol consumption in some patients and can be photosensitizing (caution patients to avoid intense light). Safety profiles in children are similar to adults.7 Provide scheduled follow-up to assess treatment response.
TABLE 251-2Treatment of Tinea Corporis
"TINEA" PITYRIASIS VERSICOLOR
Pityriasis versicolor is caused by the overgrowth of the yeasts Malassezia furfur (previously Pityrosporum ovale) and Malassezia globosa. Malassezia species are part of the normal cutaneous flora and reside in keratin of skin and hair follicles. They require oil to grow, so the disease is more prevalent in young adults when sebaceous gland activity is highest. Predisposing factors include high temperature/humidity, oily skin, and steroid treatment.
Asymptomatic, hypo- or hyperpigmented, and coalescing scaly macules are seen on the trunk or proximal extremities. The central upper chest and back are the most common areas of involvement (Figure 251-7). Facial lesions may be present in infants and the immunocompromised. The "versicolor" refers to the varying shades of erythema and pigmentation. In untanned individuals, the lesions may be salmon or light brown. On darkly pigmented skin, the lesions may be hypopigmented. The fine scale is best appreciated by gently abrading the lesions with a glass slide or blade. The condition may be present for months or years and is usually asymptomatic. Patients usually present due to cosmetic concerns regarding the inconsistent pigmentation.
The hyperpigmented, scaling pink macules of pityriasis versicolor may appear similar to those found in tinea corporis, psoriasis, pityriasis rosea, seborrheic dermatitis, or nummular eczema. Hypopigmented lesions should be differentiated from pityriasis alba, leprosy, or postinflammatory conditions. A potassium hydroxide preparation obtained by gently scraping the surface of the lesion and examining under the microscope (see Table 248-6) will reveal the characteristic short chopped hyphae and yeast forms termed "spaghetti and meatballs" (Figure 251-8).
Potassium hydroxide preparation with pseudohyphae, showing "spaghetti and meatballs" pattern. [Photo contributed by University of North Carolina Department of Dermatology.]
Treat with ketoconazole 2% shampoo, applied daily for a week, washing off after 10 to 15 minutes. Other topical options include econazole, miconazole, clotrimazole, or ketoconazole cream (Table 251-2). Widespread involvement usually makes these less cost effective and more difficult to apply. Extensive or refractory pityriasis versicolor can be treated with oral ketoconazole, 400 milligrams, itraconazole, 400 milligrams, or fluconazole, 300 milligrams, in weekly doses.6,8
Discoloration may take months to resolve after treatment and is not a sign of treatment failure. Relapses are frequent, and instructions on prophylactic regimens should be given to include once-weekly selenium sulfide 2.5% or ketoconazole 2% shampoo.
The terms eczema and atopic dermatitis are often used interchangeably and have a variety of presentations. This section focuses on truncal involvement. In chronic eczema, the hallmark is the "itch that rashes," in which an itch–scratch cycle perpetuates the condition. Itching is common and often worse at night and is aggravated by heat and sweat. Atopic individuals have a personal or family history of asthma, allergic rhinitis, nasal polyps, or "sensitive" skin. The acute stage demonstrates erythematous plaques that may be edematous and with miniature vesicles. Subacute lesions have more scale. The chronic stage presents with thickened (lichenified) skin showing accentuation of the normal skin markings caused by chronic rubbing (Figure 251-9). Scratching causes excoriations.
Atopic dermatitis. Lichenification, excoriations, and ill-defined scaling erythema. [Photo contributed by University of North Carolina Department of Dermatology.]
Chronic contact dermatitis may be misdiagnosed as eczema or atopic dermatitis (Table 251-1) or may actually be a factor in the flare of eczema. See chapter 253 for further discussion. The acute stage is typically limited to the area of contact with well-marginated erythema and edema. Papules and vesicles may be present, and bullae may occur in severe reactions with secondary crusting and erosions. Linear (such as from poison ivy) or geographic lesions (such as nickel allergy; Figure 251-10) are typical. Pruritus can be severe. Subacute lesions have mild erythema, dry scale, and fine papules. Chronic eruptions will be lichenified with accentuation of the skin markings and show postinflammatory pigmentary changes. The subacute and chronic stages are frequently confused with endogenous eczema. The distribution is initially confined to the site of exposure but later can spread to sites beyond.
Allergic contact dermatitis. Erythematous scaly papules and lichenified plaques on the lower abdomen (contact with belt buckles). [Photo contributed by University of North Carolina Department of Dermatology.]
Treatment is directed at disease control.9 Avoid harsh soaps and other irritants or contactants. Moisturize within 2 minutes of bathing with plain petroleum jelly, Aquaphor®, or Eucerin® cream. Use topical steroids, such as 1% hydrocortisone ointment, for mild disease or intertriginous sites; medium-potency preparations, such as triamcinolone 0.1%, for moderate involvement; or higher potency steroids, such as clobetasol, for more severe eruptions. Ointments are the most effective vehicle, but foam delivery systems are effective and more cosmetically elegant. Severe contact reactions may require an oral prednisone taper over 3 weeks. The usual dose in a child is prednisone, 1 to 2 milligrams/kg PO, up to 40 milligrams/d. Adults respond well to a tapering dose of prednisone, 40 to 60 milligrams/d PO each morning. Oral antihistamines, such as diphenhydramine or hydroxyzine, can control nighttime pruritus and scratching. Staphylococcal or streptococcal superinfections typically present with crusting and exudates. Prescribe cephalexin or dicloxacillin because antibiotic resistance is common with erythromycin. Treat for community-acquired methicillin-resistant Staphylococcus aureus based on cultures or local patterns of bacterial resistance.
Lichen planus may affect the skin, mucous membranes, and hair follicles. It is idiopathic in most cases, although cell-mediated immunity and human leukocyte antigen genetic susceptibility probably play a role. Age of onset is usually between 20 and 60 years old, and there is a 1% to 2% familial incidence.10
The hallmark of lichen planus is the constellation of the "5 P's": purple, polygonal, pruritic, planar papules. The onset may be abrupt or over several weeks. The course is variable and may last months to years. Spontaneous resolution may occur, but recurrences are also common. The violaceous flat-topped papules may be discrete or generalized (Figure 251-11). Common sites of involvement include the lumbar region, flexor wrists, pretibia, scalp, and penis. Koebner phenomenon, caused by scratching, may result in a linear array of papules. In pigmented skin, a deep brown hyperpigmentation may occur. Wickham striae are fine white lacy reticulate lines that adhere to the papules and are pathognomonic for this condition (Figure 251-12). Involvement of the mucous membranes occurs in approximately half of those with the disease, and it is not uncommon to have only oral involvement. The posterior buccal mucosa is most commonly affected; however, gingiva, tongue, and lips may also be involved. Painful erosions may be present, and these patients have a 2% to 3% lifetime risk of squamous cell carcinoma developing in these areas. About 70% of patients with mucosal vulvovaginal lichen planus also have oral involvement, so it is important to ask about genital symptoms.10
Lichen planus. Violaceous, flat-topped polygonal papules on the back. [Photo contributed by University of North Carolina Department of Dermatology.]
Wickham striae, lace-like striations. [Photo contributed by University of North Carolina Department of Dermatology.]
There are many other variants of lichen planus, with the most common being hypertrophic, which presents with thick, hyperkeratotic plaques on the shins. Annular lichen planus is more common in men and typically involves the axillae, penis, or groin. This variant presents with asymptomatic ringed lesions approximately 1 cm in diameter. Follicular involvement of the scalp can result in a scarring alopecia. Nail changes can result in destruction of the nail fold and nail bed, with longitudinal splintering (pterygia).
Other papulosquamous diseases are included in the differential diagnosis of lichen planus (Table 251-1). The oral mucosal involvement and Wickham striae are helpful in distinguishing lichen planus from psoriasis. Chronic discoid lupus and fungal infections may have similar cutaneous findings.
Lichenoid drug eruptions can be identical to lichen planus, except they tend to be more generalized and photodistributed and there is a history of drug ingestion. The latent period can be months to years, with an average of 12 months, and it may take years to resolve after withdrawal of the offending agent. Common medications are listed in Table 251-3 in the later section "Drug Reactions." Chronic graft-versus-host disease, dermatomyositis, and malignant lymphomas may also have lichenoid eruptions.
TABLE 251-3Drug Reactions and Common Causative Agents ||Download (.pdf) TABLE 251-3 Drug Reactions and Common Causative Agents
|Type of Reaction ||Common Drugs ||Comments |
|Morbilliform exanthem ||Penicillins/cephalosporins, sulfonamides, minocycline, anticonvulsants ||Usually <14 d of exposure, resolves within 2 wk; trunk first then extremities |
|Urticaria or angioedema ||Aspirin, NSAIDs, opiates, iodinated contrast material ||Usually <36 h since exposure, or within minutes of exposure |
|Photosensitivity eruption || |
Toxic: tetracyclines, NSAIDs, fluoroquinolones, amiodarone, psoralens, phenothiazides
Allergic: thiazides, sulfonamides, antimalarials, quinidine, quinine, tricyclic antidepressants, NSAIDs
|Sun-exposed areas; exaggerated sunburn responses |
|Lupus erythematosus–like ||Procainamide, phenytoin, minocycline, hydralazine, penicillamine ||Photodistributed eruption |
|Acneiform eruption ||β-Lactam antibiotics, steroids, contraceptives, phenytoin, halogens, lithium, phenobarbital, haloperidol, ethambutol, isoniazid ||No comedones; monomorphic papules and pustules on back, shoulders, and chest; within 5 d of exposure |
|Pigmentation ||Zidovudine, heavy metals, phenytoin, oral contraceptives, minocycline, amiodarone, clofazimine, antimalarials ||Chronic drug ingestion |
|Fixed drug eruption ||Tetracyclines, sulfas, NSAIDs, barbiturates, phenolphthalein ||Reexposure causes recurrence in same location |
|Vesiculobullous eruption ||Penicillamine, captopril, sulfas, thiols ||Hard to distinguish from bullous disorder |
|Lichenoid eruption ||ACE inhibitors (captopril enalapril), β-blockers (labetalol, propranolol), methyldopa, antimalarials, quinidine, TNF inhibitors (etanercept, infliximab), hydrochlorothiazide, gold and other metals, penicillamine, NSAIDs ||May occur months after exposure, oral lesions, slow resolution up to 2 y |
|Anticoagulant necrosis ||Coumadin, heparin ||Onset in 3–5 d, well-demarcated painful area of fatty tissue |
Treatment is with topical or intralesional steroids. Mid- to high-potency preparations, such as triamcinolone 0.1% ointment or fluocinonide 0.05% ointment twice a day, are helpful, although treatment does not cure the disease. Intralesional triamcinolone, 3 milligrams/mL, can be used for very symptomatic cutaneous or mucous membrane lesions. Fluocinonide, 0.05% gel four times a day, can be used in the mouth. Oral analgesics, such as lidocaine jelly 2%, can be applied to the erosions three times a day before meals. Severe erosions or oral involvement may require PO prednisone, 40 to 60 milligrams every morning for 1 to 2 weeks. Other systemic treatments include cyclosporine, retinoids, azathioprine, methotrexate, and mycophenolate mofetil.
Although the lesions are transient and often clinically unimpressive, the inclusion of secondary syphilis in the differential diagnosis of papulosquamous conditions in the ED is important.
Secondary syphilis exhibits skin manifestations in most patients and consists of early and later manifestations. The early eruption appears 2 to 10 weeks after the appearance of the primary chancre and is an evanescent macular rash lasting only a few hours or days. The macular erythema commonly appears on the sides of the trunk, midabdomen, and inner extremities. The discrete round macules are of varying shades from light pink to rose or even brownish red. It may be faint and difficult to appreciate on darkly pigmented skin. This phase of the disease is often asymptomatic, although associated symptoms can include fever, sore throat, fatigue, headache, meningismus, and shotty, firm, nontender lymphadenopathy of the posterior cervical, axillary, and epitrochlear regions. Pruritus may be present. The macular eruption resolves spontaneously and may leave postinflammatory hyperpigmentation.11
Later eruptions may present in a variety of forms, hence the referral to syphilis as the great imitator. This phase typically lasts 2 to 6 weeks and resolves spontaneously. Multiple recurrences over a period of 1 year can occur before infection enters the latent stage. The later eruptions of secondary syphilis are often papular lesions 2 to 5 mm in size, may be generalized, and are reddish to copper in color. The papules may be subtle or deeply infiltrated and firm. The surface may be smooth and shiny or have a thick, adherent scale (Figure 251-13). Palmar-plantar involvement is a helpful finding and is characterized by tender copper-colored discrete macules with a collarette of scale. Postinflammatory hyperpigmentation can be prominent and persist for weeks to months. Psoriasiform, follicular, lichenoid, or acneiform lesions can occur. Vesiculobullous lesions of the palms and soles are seen in neonatal syphilis. Patients with human immunodeficiency virus may have atypical presentations, including very large infiltrated, scaling, and crusted plaques. Annular lesions may occur, most frequently around the mouth, and may mimic sarcoidosis. Patchy nonscarring "moth eaten" alopecia may be present. Split papules at the corners of the mouth, asymptomatic white plaques on mucous membranes, and condyloma lata in the genitals are highly infectious stigmata.
Secondary syphilis. Papulosquamous eruption. [Photo contributed by University of North Carolina Department of Dermatology.]
In secondary syphilis, the nontreponemal serologic tests are strongly reactive. Exceptions include the prozone phenomenon, in which a false-negative result occurs with high antibody titers, and rarely, in patients with acquired immunodeficiency syndrome, seronegative syphilis may occur. Histologic stains of affected tissues can be performed to confirm the diagnosis in seronegative patients.
The various cutaneous manifestations of syphilis may resemble many other cutaneous diseases (Table 251-1). Pityriasis rosea is the most common condition to consider and can have very similar cutaneous findings. However, the lesions of syphilis tend to be more circular and randomly arranged on the trunk, not with the oval "Christmas tree" distributed findings in pityriasis rosea. Pityriasis rosea also lacks palmoplantar and mucous membrane lesions and lymphadenopathy.
Treatment is benzathine penicillin G (single dose of 2.4 million units IM, 1.2 million units in each buttock). Doxycycline, 100 milligrams PO twice a day for 2 weeks, can be used in penicillin-allergic patients. Further discussion is provided in chapter 149, "Sexually Transmitted Infections."
Scabies is infestation by the Sarcoptes scabiei mite and should be considered in any patient with complaints of severe generalized pruritus. The mite burrows and multiplies within the upper layer of the skin. In classic scabies, there are 6 to 10 live mites present on the skin. In immunocompromised patients, there may be more than 1 million mites present.
Scabies is usually spread by skin-to-skin contact and can occur in any age group. The mite can also remain alive for >48 hours on inanimate objects, such as clothing and linens. The eruption can vary, ranging from minimal findings to extensive secondary excoriations and eczematous lesions. Hypersensitivity to the mite occurs before the development of symptoms. The initial exposure may not produce symptoms for several weeks. Reinfestation may produce pruritus within 1 to 3 days. Previous sensitization, inadequate treatment, and the host's immune status can alter the appearance of the condition. Chronic, undiagnosed scabies is referred to as the 7-year itch.
Intense pruritus is common, especially at night, although immunosuppressed patients may be asymptomatic. Women frequently complain of nipple itching, whereas men most frequently note the penile or scrotal pruritic lesions. Pruritic papules, secondary excoriations, and burrows are the classic findings. Secondary infection with crusting may occur. The head and neck are typically spared, although they may be involved in infants and the immunocompromised. Common sites of involvement include the finger webs, wrists, axillae, areolae, umbilicus, lower abdomen, waistband, and genitals (Figure 251-14, A and B).
A and B. Scabies. Erythematous scaling papules with excoriation. [Photos contributed by University of North Carolina Department of Dermatology.]
Red-brown papules and nodules may occur on the penis and scrotum. Crusted scabies occurs in immunosuppressed or debilitated patients. The lesions can be generalized and include the face and scalp, with marked crusting and heavy scaling. Pressure-bearing sites, such as the buttocks, elbows, and feet, are common areas of hyperkeratotic lesions. The tips of the fingers can be swollen, crusted, and have a psoriasiform scaling under the nails.
Atypical lesions can be seen in infants with involvement of the face and scalp, as well as vesicles or pustules on the palms and soles. An autosensitization-type reaction ("id") can occur with widespread urticarial papules predominantly on the trunk and proximal extremities. Other pruritic disorders, including eczema, atopic dermatitis, contact dermatitis, urticarias, dermatitis herpetiformis, pediculosis infestation, lichen planus, and metabolic disorders such as uremia or hypo- or hyperparathyroidism, should be considered in the evaluation. The presence of pruritus in other family members or close contacts is a helpful clue to scabies. A #15 blade can be gently scraped across a typical burrow and placed on a slide with mineral oil for microscopic confirmation. Diagnosis is made by the presence of the mite, feces, or ova (Figure 251-15).
Scabies eggs and feces. [Photo contributed by University of North Carolina Department of Dermatology.]
Treat with permethrin 5% cream applied overnight to the patient and all family members and close contacts. It should be applied from the neck down, covering all areas of the body, including under the nails, in the umbilicus, around the nipples, and the genitals. The face and scalp should be treated in affected infants and young children. It is washed off in 8 to 12 hours. A second application administered 1 week after the first is recommended. Lindane® is no longer recommended because of potential neurotoxicity and resistance.12
Ivermectin, 200 micrograms/kg PO single dose, is a very effective therapy for common and crusted scabies. Once-a-week dosage for two treatments is recommended. Three or more treatments may be required in the heavily infested or immunocompromised patient. This is also a convenient treatment for institutions or large groups.
Equally important in the treatment is the decontamination of the clothing, bed linens, and towels by hot water washing and machine drying. Items that cannot be washed should be sealed in plastic bags for 10 days. Itching may last for several weeks after treatment and is a sensitivity reaction to the remaining dead mites and mite products in the skin. Cortisone creams, such as triamcinolone 0.1%, or oral antihistamines can be given for the pruritus.