Disorders exhibiting papules and scale.
A chronic, recurrent disorder. Classic lesion is a well-marginated, erythematous plaque with silvery-white surface scale. Distribution includes extensor surfaces (i.e., knees, elbows, and buttocks); may also involve palms and scalp (particularly anterior scalp margin). Associated findings include psoriatic arthritis (Chap. 172) and nail changes (onycholysis, pitting or thickening of nail plate with accumulation of subungual debris).
Maintain cutaneous hydration; topical glucocorticoids; topical vitamin D analogue (calcipotriol) and retinoid (tazarotene); UV light (PUVA when UV used in combination with psoralens); for severe disease methotrexate or cyclosporine; acitretin can also be used but is teratogenic. Alefacept (dimeric fusion protein: LFA-3/Fc human IgG1), or ustekinumab (human monoclonal antibody that blocks IL-12 and IL-23) can be considered for chronic, moderate to severe plaque psoriasis. Etanercept (dimeric fusion protein: TNF receptor/Fc human IgG1), infliximab, and adalimumab (monoclonal antibodies directed against TNF) are approved for psoriatic arthritis and psoriasis.
A self-limited condition lasting 3–8 weeks. Initially, there is a single 2- to 6-cm annular salmon-colored patch (herald patch) with a peripheral rim of scale, followed in days to weeks by a generalized eruption involving the trunk and proximal extremities. Individual lesions are similar to but smaller than the herald patch and are arranged in symmetric fashion with long axis of each individual lesion along skin lines of cleavage. Appearance may be similar to that of secondary syphilis.
TREATMENT Pityriasis Rosea
Disorder is self-limited, so treatment is directed at symptoms; oral anti-histamines for pruritus; topical glucocorticoids; UV-B phototherapy in some cases.
Disorder of unknown cause; can follow administration of certain drugs and in chronic graft-versus-host disease; lesions are pruritic, polygonal, flat-topped, and violaceous. Course is variable, but most pts have spontaneous remissions 6–24 months after onset of disease.
TREATMENT Lichen Planus
Eczema, or dermatitis, is a reaction pattern that presents with variable clinical and histologic findings; it is the final common expression for a number of disorders.
One aspect of atopic triad of hayfever, asthma, and eczema. Usually an intermittent, chronic, severely pruritic, eczematous dermatitis with scaly erythematous patches, vesiculation, crusting, and fissuring. Lesions are most commonly on flexures, with prominent involvement of antecubital and popliteal fossae; generalized erythroderma in severe cases.
TREATMENT Eczema and Atopic Dermatitis
Avoidance of irritants; cutaneous hydration; topical glucocorticoids; treatment of infected lesions [often with Staphylococcus aureus (SA)—consider community-acquired methicillin-resistant strains (CA-MRSA)]. Systemic glucocorticoids only for severe exacerbations unresponsive to topical conservative therapy.
ALLERGIC CONTACT DERMATITIS
A delayed hypersensitivity reaction that occurs after cutaneous exposure to an antigenic substance. Lesions occur at site of contact and are vesicular, weeping, crusting; linear arrangement of vesicles is common. Most frequent allergens are resin from plants of the genus Toxicodendron (poison ivy, oak, sumac), nickel, rubber, and cosmetics.
TREATMENT Allergic Contact Dermatitis
Avoidance of sensitizing agent; topical glucocorticoids; consideration of systemic glucocorticoids over 2–3 weeks for widespread disease.
IRRITANT CONTACT DERMATITIS
Inflammation of the skin due to direct injury by an exogenous agent. The most common area of involvement is the hands, where dermatitis is initiated or aggravated by chronic exposure to water and detergents. Features may include skin dryness, cracking, erythema, edema.
TREATMENT Irritant Contact Dermatitis
Avoidance of irritants; barriers (use of protective gloves); topical glucocorticoids; treatment of secondary bacterial or dermatophyte infection.
A chronic noninfectious process characterized by erythematous patches with greasy yellowish scale. Lesions are generally on scalp, eyebrows, nasolabial folds, axillae, central chest, and posterior auricular area.
TREATMENT Seborrheic Dermatitis
Nonfluorinated topical glucocorticoids; shampoos containing coal tar, salicylic acid, or selenium sulfide.
A superficial infection of skin secondary to either S. aureus or group A β-hemolytic streptococci. The primary lesion is a superficial pustule that ruptures and forms a “honey-colored” crust. Tense bullae are associated with S. aureusinfections (bullous impetigo). Lesions may occur anywhere but commonly involve the face. Impetigo and furunculosis (painful erythematous nodule, or boil) have gained prominence because of increasing incidence of CA-MRSA.
Gentle debridement of adherent crusts with soaks and topical antibiotics; appropriate oral antibiotics depending on organism (Chap. 86).
Superficial cellulitis, most commonly on face, characterized by a bright red, sharply demarcated, intensely painful, warm plaque. Because of superficial location of infection and associated edema, surface of plaque may exhibit a peau d’orange (orange peel) appearance. Most commonly due to infection with group A β-hemolytic streptococci, occurring at sites of trauma or other breaks in skin.
Appropriate antibiotics depending on organism (Chap. 86).
HERPES SIMPLEX (SEE ALSO CHAP. 108)
Recurrent eruption characterized by grouped vesicles on an erythematous base that progress to erosions; often secondarily infected with staphylococci or streptococci. Infections frequently involve mucocutaneous surfaces around the oral cavity, genitals, or anus. Can also cause severe visceral disease including esophagitis, pneumonitis, encephalitis, and disseminated herpes simplex virus infection. Tzanck preparation of an unroofed early vesicle reveals multinucleated giant cells.
TREATMENT Herpes Simplex
Will differ based on disease manifestations and level of immune competence (Chap. 108); appropriate antibiotics for secondary infections, depending on organism.
HERPES ZOSTER (SEE ALSO CHAP. 108)
Eruption of grouped vesicles on an erythematous base usually limited to a single dermatome (“shingles”); disseminated lesions can also occur, especially in immunocompromised pts. Tzanck preparation reveals multinucleated giant cells; indistinguishable from herpes simplex except by culture. Postherpetic neuralgia, lasting months to years, may occur, especially in the elderly.
TREATMENT Herpes Zoster
Will differ based on disease manifestations and level of immune competence (Chap. 108).
Skin fungus, may involve any area of body; due to infection of stratum corneum, nail plate, or hair. Appearance may vary from mild scaliness to florid inflammatory dermatitis. Common sites of infection include the foot (tinea pedis), nails (tinea unguium), groin (tinea cruris), or scalp (tinea capitis). Classic lesion of tinea corporis (“ringworm”) is an erythematous papulosquamous patch, often with central clearing and scale along peripheral advancing border. Hyphae are often seen on KOH preparation, although tinea capitis and tinea corporis may require culture or biopsy.
TREATMENT Dermatophyte Infection
Depends on affected site and type of infection. Topical imidazoles, triazoles, and allylamines may be effective. Haloprogin, undecylenic acid, ciclopirox olamine, and tolnaftate are also effective, but nystatin is not active against dermatophytes. Griseofulvin, 500 mg/d, if systemic therapy required. Itraconazole or terbinafine may be effective for nail infections.
Fungal infection caused by a related group of yeasts. Manifestations may be localized to the skin or rarely systemic and life-threatening. Predisposing factors include diabetes mellitus, cellular immune deficiencies, and HIV (Chap. 114). Frequent sites include the oral cavity, chronically wet macerated areas, around nails, intertriginous areas. Diagnosed by clinical pattern and demonstration of yeast on KOH preparation or culture.
(See also Chap. 115) Removal of predisposing factors; topical nystatin or azoles; systemic therapy reserved for immunosuppressed pts, unresponsive chronic or recurrent disease; vulvovaginal candidiasis may respond to a single dose of fluconazole, 150 mg.
Cutaneous neoplasms caused by human papilloma viruses (HPVs). Typically dome-shaped lesions with irregular filamentous surface. Propensity for the face, arms, and legs; often spread by shaving. HPVs are also associated with genital or perianal lesions and play a role in the development of cancer of the uterine cervix and external genitalia in females (Chap. 92).
Cryotherapy with liquid nitrogen, keratinolytic agents (salicylic acid). For genital warts, application of podophyllin solution is effective but can be associated with marked local reactions; topical imiquimod also has been used.
Usually a self-limited disorder of teenagers and young adults. Comedones (small cysts formed in hair follicles) are clinical hallmark; often accompanied by inflammatory lesions of papules, pustules, or nodules. May scar in severe cases.
TREATMENT Acne Vulgaris
Careful cleaning and removal of oils; oral tetracycline or erythromycin; topical antibacterials (e.g., benzoyl peroxide), topical retinoic acid. Systemic isotretinoin only for unresponsive severe nodulocystic acne (risk of severe adverse events including teratogenicity and possible association with depression).
Inflammatory disorder affecting predominantly the central face, rarely affecting pts <30 years of age. Tendency toward exaggerated flushing, with eventual superimposition of papules, pustules, and telangiectases. May lead to rhinophyma and ocular problems.
TREATMENT Acne Rosacea
Oral tetracycline, 250–1000 mg/d; topical metronidazole and topical nonfluorinated glucocorticoids may be useful.
Septal panniculitis characterized by erythematous, warm, tender subcutaneous nodular lesions typically over anterior tibia. Lesions are usually flush with skin surface but are indurated and have appearance of an erythematous/violaceous bruise. Lesions usually resolve spontaneously in 3–6 weeks without scarring. Commonly seen in sarcoidosis, administration of certain drugs (esp. sulfonamides, oral contraceptives, and estrogens), and a wide range of infections including streptococcal and tubercular; may be idiopathic.
TREATMENT Erythema Nodosum
Identification and treatment/removal of underlying cause. NSAIDs for severe or recurrent lesions; systemic glucocorticoids are effective but dangerous if underlying infection is not appreciated.
A reaction pattern of skin consisting of a variety of lesions but most commonly erythematous papules and bullae. “Target” or “iris” lesion is characteristic and consists of concentric circles of erythema and normal flesh-colored skin, often with a central vesicle or bulla.
Distribution of lesions classically acral, esp. palms and soles. Three most common causes are drug reaction (particularly penicillins and sulfonamides) or concurrent herpetic or Mycoplasma infection. Can rarely affect mucosal surfaces and internal organs (erythema multiforme major or Stevens-Johnson syndrome).
TREATMENT Erythema Multiforme
Provocative agent should be sought and eliminated if drug-related. In mild cases limited to skin, only symptomatic treatment is needed (anti-histamines, NSAID). For Stevens-Johnson, systemic glucocorticoids have been used but are controversial; prevention of secondary infection and maintenance of nutrition and fluid/electrolyte balance are critical.
A common disorder, either acute or chronic, characterized by evanescent (individual lesions lasting <24 h), pruritic, edematous, pink to erythematous plaques with a whitish halo around margin of individual lesions. Lesions range in size from papules to giant coalescent lesions (10–20 cm in diameter). Often due to drugs, systemic infection, or foods (esp. shellfish). Food additives such as tartrazine dye (FD&C yellow no. 5), benzoate, or salicylates have also been implicated. If individual lesions last >24 h, consider diagnosis of urticarial vasculitis.
See Chap. 167.
Palpable purpura (nonblanching, elevated lesions) is the cutaneous hallmark of vasculitis. Other lesions include petechiae (esp. early lesions), necrosis with ulceration, bullae, and urticarial lesions (urticarial vasculitis). Lesions usually most prominent on lower extremities. Associations include infections, collagen-vascular disease, primary systemic vasculitides, malignancy, hepatitis B and C, drugs (esp. thiazides), and inflammatory bowel disease. May occur as an idiopathic, predominantly cutaneous vasculitis.
Will differ based on cause. Pursue identification and treatment/elimination of an exogenous cause or underlying disease. If part of a systemic vasculitis, treat based on major organ-threatening features (Chap. 170). Immunosuppressive therapy should be avoided in idiopathic, predominantly cutaneous vasculitis as disease frequently does not respond and rarely causes irreversible organ system dysfunction.
CUTANEOUS DRUG REACTIONS
Cutaneous reactions are among the most frequent medication toxicities. These can have a wide range of severity and manifestations including urticaria, photosensitivity, erythema multiforme, fixed drug reactions, erythema nodosum, vasculitis, lichenoid reactions, bullous drug reactions, Stevens-Johnson syndrome, and toxic epidermal necrolysis (TEN). Diagnosis is usually made by appearance and careful medication history.
TREATMENT Cutaneous Drug Reactions
Withdrawal of the medication. Treatment based on nature and severity of cutaneous pathology.
For a more detailed discussion, see Lawley LP, McCall CO, Lawley TJ: Eczema, Psoriasis, Cutaneous Infections, Acne, and Other Common Skin Disorders, Chap. 52, p. 395; Shinkai K, Stern RS, Wintroub BU: Cutaneous Drug Reactions, Chap. 55, p. 432; and Bolognia JL, Braverman IM: Skin Manifestations of Internal Disease, Chap. 53, p. 405, in HPIM-18.