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52 COMMON SKIN CONDITIONS

52 COMMON SKIN CONDITIONS
Harrison’s Manual of Medicine

52

COMMON SKIN CONDITIONS

Papulosquamous Disorders
Eczematous Disorders
Infections and Infestations
Acne
Vascular Disorders
Cutaneous Drug Reactions
Bibliography

PAPULOSQUAMOUS DISORDERS
Disorders exhibiting papules and scale.
PSORIASIS   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. 164) and nail changes (onycholysis, pitting or thickening of nail plate with accumulation of subungual debris).

TREATMENT
Maintain cutaneous hydration; topical glucocorticoids; coal tar ointment; topical vitamin D analogue (calcipotriol); UV light (PUVA when UV used in combination with psoralens); methotrexate or cyclosporine for severe advanced disease.

PITYRIASIS ROSEA   A self-limited condition lasting 3–8 weeks. Initially, there is a single 2–6 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
Disorder is self-limited, so treatment is directed at symptoms; oral antihistamines for pruritus; topical glucocorticoids; UV-B phototherapy in some cases.

LICHEN PLANUS   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
Topical glucocorticoids.

ECZEMATOUS DISORDERS
ECZEMA   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.
ATOPIC DERMATITIS   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. Most pts with atopic dermatitis are chronic carriers of Staphylococcus aureus in anterior nares and on skin.

TREATMENT
Avoidance of irritants; cutaneous hydration; topical glucocorticoids; treatment of infected lesions. 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 Rhus (or Toxicodendron) genus (poison ivy, oak, sumac), nickel, rubber, and cosmetics.

TREATMENT
Avoidance of sensitizing agent; topical glucocorticoids; consideration of systemic glucocorticoids over 2–3 weeks for widespread disease or involvement of face or genitals.

IRRITANT CONTACT DERMATITIS   Inflammation of the skin due to direct injury by an exogenous agent. The most frequent cause of hand eczema, where dermatitis is initiated or aggravated by chronic exposure to water and detergents. Features may include skin dryness, cracking, erythema, edema.

TREATMENT
Avoidance of irritants; barriers (use of vinyl gloves); topical glucocorticoids; treatment of secondary bacterial or dermatophyte infection.

SEBORRHEIC DERMATITIS   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
Nonfluorinated topical glucocorticoids; shampoos containing coal tar, salicylic acid, or selenium sulfide.

INFECTIONS AND INFESTATIONS
IMPETIGO   A superficial infection of skin secondary to either S. aureus or group A b-hemolytic streptococci. The primary lesion is a superficial pustule that ruptures and forms a “honey-colored” crust. Tense bullae are associated with S. aureus infections (bullous impetigo). Lesions may occur anywhere but commonly involve the face.

TREATMENT
Gentle debridement of adherent crusts with soaks and topical antibiotics; appropriate oral antibiotics depending on organism (Chap. 78).

ERYSIPELAS   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 b-hemolytic streptococci, occurring at sites of trauma or other breaks in skin.

TREATMENT
Appropriate antibiotics depending on organism (Chap. 78).

SCABIES   A common infestation of children and adults due to the mite Sarcoptes scabiei. Often presents as pruritus, commonly worse at night. Typical lesions include burrows (short linear lesions often in web spaces of fingers) and small vesiculopapular lesions in intertriginous areas. Excoriations, often with bleeding, may be prominent.

TREATMENT
Topical permethrin; topical lindane (penetrates skin and has potential for CNS toxicity; should not be used in pregnant women or infants). To prevent reinfestation, clothing should be washed in hot water and close contacts treated simultaneously.

HERPES SIMPLEX (See also Chap. 102)   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 multinucleate giant cells.

TREATMENT
Will differ based on disease manifestations and level of immune competence (Chap. 102); appropriate antibiotics for secondary infections, depending on organism.

HERPES ZOSTER (See also Chap. 102)   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 multinucleate giant cells; indistinguishable from herpes simplex except by culture. Postherpetic neuralgia, lasting months to years, may occur, especially in elderly.

TREATMENT
Will differ based on disease manifestations and level of immune competence (Chap. 102)

DERMATOPHYTE INFECTION   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
Depends on affected site and type of infection. Topical imidazoles, triazoles, and allylamines may be effective. Haloprogin, undecylenic acid, ciclopiroxolamine, and tolnaftate are also effective, but nystatin is not active against dermatophytes. Griseofulvin, 500 mg/d, if systemic therapy required. Itraconazole may be effective for nail infections.

CANDIDIASIS   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. 86). 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.

TREATMENT
(See also Chap. 108) Removal of predisposing factors; topical nystatin or azoles; systemic therapy reserved for immunosuppressed patients, unresponsive chronic or recurrent disease; vulvovaginal candidiasis may respond to a single dose of fluconazole, 150 mg.

WARTS   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 neoplasia of the uterine cervix and external genitalia in females (Chap. 83).

TREATMENT
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.

ACNE
ACNE VULGARIS   Usually a self-limited disorder of teenagers and young adults. Comedones (small cyst formed in hair follicle) are clinical hallmark; often accompanied by inflammatory lesions of papules, pustules, or nodules. May scar in severe cases.

TREATMENT
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 (teratogenic—all females must be screened for pregnancy prior to drug initiation and maintain effective contraception during treatment course).

ACNE ROSACEA   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
Oral tetracycline, 250–1500 mg/d; topical metronidazole and topical nonfluorinated glucocorticoids may be useful.

VASCULAR DISORDERS
ERYTHEMA NODOSUM   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, treatment with some drugs (esp. sulfonamides, oral contraceptives, and estrogens), and a wide range of infections including streptococcal and tubercular; may be idiopathic.

TREATMENT
Identification and treatment/removal of underlying cause. NSAID for severe or recurrent lesions; systemic glucocorticoids are effective but dangerous if underlying infection is not appreciated.

ERYTHEMA MULTIFORME   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
Provocative agent should be sought and eliminated if drug-related. In mild cases limited to skin, only symptomatic treatment is needed (antihistamines, NSAID). For Stevens-Johnson, systemic glucocorticoids are controversial but often used; prevention of secondary infection and maintenance of nutrition and fluid/electrolyte balance are critical.

URTICARIA   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.

TREATMENT
See Chap. 157.

VASCULITIS   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, drugs (esp. thiazides), and inflammatory bowel disease. May occur as an idiopathic, predominantly cutaneous vasculitis.

TREATMENT
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. 160). 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, and toxic epidermal necrolysis (TEN). Diagnosis is usually made by appearance and careful medication history.

TREATMENT
Withdrawal of the medication. Treatment based on nature and severity of cutaneous pathology.

Bibliography

For a more detailed discussion, see Swerlick RA, Lawley TJ: Eczema, Psoriasis, Cutaneous Infections, Acne, and Other Common Skin Disorders, Chap. 56, p. 309; Stern RS, Chosidow OM, Wintroub BU: Cutaneous Drug Reactions, Chap. 59, p. 336; and Bologna JL, Braverman IM: Skin Manifestations of Internal Disease, Chap. 57, p. 315, in HPIM-15.

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