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Dermatologic Disorders Dermatolog ic Disorders General internists are called upon to evaluate dermatologic problems on a regular basis. A thorough understanding of the skin and its associated structures is required (Figure 31). Of note, most topical therapies for dermato- logic conditions are used off label because they are not FDA approved for the specific condition in r,t'hich they are t t G U R E 2 9. Red and swollen gingival tissue (b/ue arow) that typically bleeds commonly utilized. with brushing or flossing is characteristic of gingivitis. Also seen is abundant yellow dental plaque atthe gum line and between teeth (green anow). Reproduced from Wikimedia Commons. Gingivitis before trealmenl. Dlgital image https://commons.wikimedia Approach to the Patient With 0rg/wiki/Category:Gingivitis#/media/File:Gingivitisbefore.JPG.AugustS,20l3 AccessedJune26,2021. Dermatologic Disease Morphology Morphology of skin lesions can be categorized as primary or secondary. Primary skin lesion morphology is the appearance of a rash or growth in its initial or unaltered state. Over time, with itching or rubbing, secondary skin changes may occur. Table 62 lists primary and secondary skin lesions. Other important characteristics of skin lesions { include color, distribution, and configuration. Dermatologic s I conditions can also be categorized as neoplastic or inflam matory. Neoplasms manifest as localized areas of abnormal skin, whereas inflammatory conditions are usually more widespread. A differential diagnosis should be initially developed on the basis of morphologic features of the primary rash rather t I G U R E 3 0. Necrotizing ulcerative gingivitis, previously known as Vincent than focusing on identification of specific rashes and their angina (trench mouth), is an acute and painful oral conditi0n characterized by fetid characteristics. breath, loss or diminution of the interdental papilla, and necrotic sloughing of the gingiva. Necrotizing periodontal disease is a term that encompasses necrotizing ulcerative gingivitis and necrotizing ulcerative periodontitis. Physical Examination No standardized method has been developed for how to best perform a total-body skin examination, but experts agree that and necrotic areas of the tonsils and gingiva with red irregular patients should be fully undressed. A systematic approach is edges that may create a grayish pseudomembrane that bleeds recommended to decrease the possibility of overlooking any if scraped (Figure 3O). Lymph nodes may be enlarged and ten area of the body during examination. One method is to start der. This is usually seen in patients with poor oral hygiene or malnutrition, orwho smoke. Treatment includes oral antibiot- ics; twice-daily chlorhexidine rinses for 2 weeks: and, if severe, $rtt m fplll.rry oatmll cotnatlln debridement. Rcdculer Dental fracture is an emergency because a tooth becomes drrmlr nonviable t hour after fracture. Patients should handle the tooth by the crown, wash it in cold water, reposition it in the socket, and bite gently on a washcloth to help keep the tooth in place until seen by a dental professional. If immediate repo sitioning is not possible, the tooth should be placed in cold pasteurized milk while seeking immediate care by a dental professional.

Dermatolog ic Disorders General internists are called upon to evaluate dermatologic problems on a regular basis. A thorough understanding of the skin and its associated structures is required (Figure 31). Of note, most topical therapies for dermato- logic conditions are used off label because they are not FDA approved for the specific condition in r,t'hich they are t t G U R E 2 9. Red and swollen gingival tissue (b/ue arow) that typically bleeds commonly utilized. with brushing or flossing is characteristic of gingivitis. Also seen is abundant yellow dental plaque atthe gum line and between teeth (green anow). Reproduced from Wikimedia Commons. Gingivitis before trealmenl. Dlgital image https://commons.wikimedia Approach to the Patient With 0rg/wiki/Category:Gingivitis#/media/File:Gingivitisbefore.JPG.AugustS,20l3 AccessedJune26,2021. Dermatologic Disease Morphology Morphology of skin lesions can be categorized as primary or secondary. Primary skin lesion morphology is the appearance of a rash or growth in its initial or unaltered state. Over time, with itching or rubbing, secondary skin changes may occur. Table 62 lists primary and secondary skin lesions. Other important characteristics of skin lesions { include color, distribution, and configuration. Dermatologic s I conditions can also be categorized as neoplastic or inflam matory. Neoplasms manifest as localized areas of abnormal skin, whereas inflammatory conditions are usually more widespread. A differential diagnosis should be initially developed on the basis of morphologic features of the primary rash rather t I G U R E 3 0. Necrotizing ulcerative gingivitis, previously known as Vincent than focusing on identification of specific rashes and their angina (trench mouth), is an acute and painful oral conditi0n characterized by fetid characteristics. breath, loss or diminution of the interdental papilla, and necrotic sloughing of the gingiva. Necrotizing periodontal disease is a term that encompasses necrotizing ulcerative gingivitis and necrotizing ulcerative periodontitis. Physical Examination No standardized method has been developed for how to best perform a total-body skin examination, but experts agree that and necrotic areas of the tonsils and gingiva with red irregular patients should be fully undressed. A systematic approach is edges that may create a grayish pseudomembrane that bleeds recommended to decrease the possibility of overlooking any if scraped (Figure 3O). Lymph nodes may be enlarged and ten area of the body during examination. One method is to start der. This is usually seen in patients with poor oral hygiene or malnutrition, orwho smoke. Treatment includes oral antibiot- ics; twice-daily chlorhexidine rinses for 2 weeks: and, if severe, $rtt m fplll.rry oatmll cotnatlln debridement. Rcdculer Dental fracture is an emergency because a tooth becomes drrmlr nonviable t hour after fracture. Patients should handle the tooth by the crown, wash it in cold water, reposition it in the socket, and bite gently on a washcloth to help keep the tooth in place until seen by a dental professional. If immediate repo sitioning is not possible, the tooth should be placed in cold pasteurized milk while seeking immediate care by a dental professional. TEY POITT o Gingivitis is reversible with routine dental visits and cleanings, brushing with fluoride toothpaste, flossing, fluoride varnish anticavity treatment, and use of chlo- rhexidine oral rinses. tIGURE 31. Structureoftheskinshowing thestratum corneum, basal cell layer, papillary dermis, and reticular dermis.

TEY POITT o Gingivitis is reversible with routine dental visits and cleanings, brushing with fluoride toothpaste, flossing, fluoride varnish anticavity treatment, and use of chlo- rhexidine oral rinses. tIGURE 31. Structureoftheskinshowing thestratum corneum, basal cell layer, papillary dermis, and reticular dermis. a2

Dermatologic Disorders TA$LE e3. Dermatologic Emergencies Primary Skin Characteristics Widespread erythema or erythroderma (drug eruption, Lesions bacterial toxin-mediated disease, severe psoriasis) Macule Small flat discoloration of the skin, High fever and widespread rash (severe drug eruptions, typically <1 cm in diameter rickettsial diseases) Patch Flat discoloration of the skin >1 cm in Diffuse peeling or sloughing of skin (toxic epidermal necrolysis, diameter, often with surface change, such infection) as scale Dark, dusky, purple areas of painful skin (impending skin loss Papule Small(<1 cm) elevation of the skin; solid from infection or severe drug eruption) in nature Mucosal inflammation, erosions, or ulceration (severe drug Plaque Flat-topped "plateau-like" elevation of the eruption, autoimmune blistering disease with high risk for skin >1 cm in diameter morbid scarring) Nodule Space-occupying lesion within the dermis; Widespread blistering (autoimmune blistering disease, largerthan a papule and located deeper infection, severe drug eruption) Cyst Fluid-filled nodule containing fluid that is Purpura, particularly "retiform" or lacey, patterned purpura expressible (vasculitis, vasculopathy, infection, autoimmune disease)

TA$LE e3. Dermatologic Emergencies Primary Skin Characteristics Widespread erythema or erythroderma (drug eruption, Lesions bacterial toxin-mediated disease, severe psoriasis) Macule Small flat discoloration of the skin, High fever and widespread rash (severe drug eruptions, typically <1 cm in diameter rickettsial diseases) Patch Flat discoloration of the skin >1 cm in Diffuse peeling or sloughing of skin (toxic epidermal necrolysis, diameter, often with surface change, such infection) as scale Dark, dusky, purple areas of painful skin (impending skin loss Papule Small(<1 cm) elevation of the skin; solid from infection or severe drug eruption) in nature Mucosal inflammation, erosions, or ulceration (severe drug Plaque Flat-topped "plateau-like" elevation of the eruption, autoimmune blistering disease with high risk for skin >1 cm in diameter morbid scarring) Nodule Space-occupying lesion within the dermis; Widespread blistering (autoimmune blistering disease, largerthan a papule and located deeper infection, severe drug eruption) Cyst Fluid-filled nodule containing fluid that is Purpura, particularly "retiform" or lacey, patterned purpura expressible (vasculitis, vasculopathy, infection, autoimmune disease) Vesicle Small clear fluid-filled blister <1 cm Broad areas of exquisitely painful skin disproportionate to clinical examination findings (necrotizing fasciitis) Bulla Larger clear fluid-filled blister >1 cm Angulated purpura of the distal extremities (sepsis, Pustule Vesicle filled with purulent material autoimmune phenomena) Atrophy Loss of one or more portions of the skin Palpable purpura (small-vessel vasculitis from infection Burrow Serpiginous epidermal streaking/ medications, or autoimmune reactions) disruption caused by scabies mite lmmunosuppressed patients (particularly those with neutropenia) Comedo Noninflammatory lesion caused by keratin with skin lesions of unknown cause in the setting of fever, debris within the sebaceous gland/hair particularly red or purple nodules (skin signs of infeaion in follicle orifice; can be open or closed immunosuppressed hosts) Telangiectasia Visibly dilated, but not palpable, blood Purple or necrotic skin lesions in immunosuppressed hosts vessel in the epidermis (angioinvasive fungal infection)

Vesicle Small clear fluid-filled blister <1 cm Broad areas of exquisitely painful skin disproportionate to clinical examination findings (necrotizing fasciitis) Bulla Larger clear fluid-filled blister >1 cm Angulated purpura of the distal extremities (sepsis, Pustule Vesicle filled with purulent material autoimmune phenomena) Atrophy Loss of one or more portions of the skin Palpable purpura (small-vessel vasculitis from infection Burrow Serpiginous epidermal streaking/ medications, or autoimmune reactions) disruption caused by scabies mite lmmunosuppressed patients (particularly those with neutropenia) Comedo Noninflammatory lesion caused by keratin with skin lesions of unknown cause in the setting of fever, debris within the sebaceous gland/hair particularly red or purple nodules (skin signs of infeaion in follicle orifice; can be open or closed immunosuppressed hosts) Telangiectasia Visibly dilated, but not palpable, blood Purple or necrotic skin lesions in immunosuppressed hosts vessel in the epidermis (angioinvasive fungal infection) Wheal/hive Tra nsient, edematous, e rythematous Rapidly growing lesions in immunosuppressed hosts (infection, papule or plaque malignancy)

Vesicle Small clear fluid-filled blister <1 cm Broad areas of exquisitely painful skin disproportionate to clinical examination findings (necrotizing fasciitis) Bulla Larger clear fluid-filled blister >1 cm Angulated purpura of the distal extremities (sepsis, Pustule Vesicle filled with purulent material autoimmune phenomena) Atrophy Loss of one or more portions of the skin Palpable purpura (small-vessel vasculitis from infection Burrow Serpiginous epidermal streaking/ medications, or autoimmune reactions) disruption caused by scabies mite lmmunosuppressed patients (particularly those with neutropenia) Comedo Noninflammatory lesion caused by keratin with skin lesions of unknown cause in the setting of fever, debris within the sebaceous gland/hair particularly red or purple nodules (skin signs of infeaion in follicle orifice; can be open or closed immunosuppressed hosts) Telangiectasia Visibly dilated, but not palpable, blood Purple or necrotic skin lesions in immunosuppressed hosts vessel in the epidermis (angioinvasive fungal infection) Wheal/hive Tra nsient, edematous, e rythematous Rapidly growing lesions in immunosuppressed hosts (infection, papule or plaque malignancy) Secondary Skin Characteristics Lesiong Crust Dried serous fluid commonly derived hypopigmentation. Bug bites and acne often heal with from blisters or pustules; often moist and hyperpigmentation. yellow or brown Several dermatologic conditions constitute emergencies Excoriation Defect in the epidermis often caused by or warrant urgent attention and require immediate interven scratching tion or referral to a specialist (Table 63). Worrisome pigmented F!ssure Linear break in the epidermis, usually lesions (for example, suspected melanoma) also warrant along skin lines on the palms or soles urgent referral. Lichenification Visible thickening of the stratum corneum, The 2016 U.S. Preventive Services Task Force (USPSTF) resulting in accentuation of the normal skin lines statement found insufficient evidence to screen adults for skin

Secondary Skin Characteristics Lesiong Crust Dried serous fluid commonly derived hypopigmentation. Bug bites and acne often heal with from blisters or pustules; often moist and hyperpigmentation. yellow or brown Several dermatologic conditions constitute emergencies Excoriation Defect in the epidermis often caused by or warrant urgent attention and require immediate interven scratching tion or referral to a specialist (Table 63). Worrisome pigmented F!ssure Linear break in the epidermis, usually lesions (for example, suspected melanoma) also warrant along skin lines on the palms or soles urgent referral. Lichenification Visible thickening of the stratum corneum, The 2016 U.S. Preventive Services Task Force (USPSTF) resulting in accentuation of the normal skin lines statement found insufficient evidence to screen adults for skin Scale Thickened stratum corneum; often dry cancer, including persons with increased risk for skin cancer. and white or gray The USPSTF does recommend counseling young adults with Ulcer Full-thickness destruction of the fair skin types about minimizing exposure to ultraviolet (UV) epidermis into the underlying dermis radiation to reduce their risk for skin cancer.

Scale Thickened stratum corneum; often dry cancer, including persons with increased risk for skin cancer. and white or gray The USPSTF does recommend counseling young adults with Ulcer Full-thickness destruction of the fair skin types about minimizing exposure to ultraviolet (UV) epidermis into the underlying dermis radiation to reduce their risk for skin cancer. Diagnostic Tests with the head and neck, working down to the torso, upper Diagnostic tests and tools that may augment the physical extremities, and lower extremities. The routine skin examina examination include microscopic examination of skin scrap tion may also be incorporated into the physical examination ings, examination with Wood lamp, and skin biopsy. Skin by assessing the trunk when auscultating the heart and lungs, scrapings should be viewed on a microscope slide with potas the arms when checking blood pressure and pulse, and the sium hydroxide if tinea is suspected or mineral oil if scabies is legs when checking pulses and joints. a consideration. Rashes in persons with darker skin color may be more A Wood lamp is an inexpensive UV light that can be used difficult to detect because the erythema may be more to evaluate the depigmentation seen in vitiligo and the fluores- subtle. Areas of active inflammation develop hyper or cence seen in erythrasma. 83

Dermatologic Disorders TABLE 64. Types of Skin Biopsies Technique Description Lesion Types AssociatedConditions Comments Shave biopsy Razor blade skimmed Superficial lesions Seborrheic keratosis, Rapid removal of underthe target lesion involving the epidermis acrochordons sam ple/lesion; requires or dermal-epidermal least amount time of unction; elevated biopsytechniques; no esions closure required Scoop (saucerization) Deeper shave biopsy Pigmented lesions Basal or squamous cell Provides entire lesion tech n ique scooping under the carcinomas for histologic lesion, leaving a saucer- exam i nation like defect Dysplastic nevi or melanoma Punch biopsy Circular knife pushed lnflammatory lesions Sarcoidosis, vascu litis, Rapid sampling of around the lesion, involving the dermis or bullous disorders, epidermis and dermis; removing a plug of subcutaneous tissue; adnexaltumors preferred technique for tissu e tumors most inflammatory conditions lncisional biopsy Wedge of lesion Larger tumors or Large squamous cell Provides a larger removed with a scalpel deeper infiltrating carcrnomas, sample of tissue for diseases calciphylaxis histologic examination when it is difficult to biopsy the entire lesion Excisional biopsy Removal of entire Neoplasms Dysplastic nevi, Provides entire lesion neoplasm, usually with melanoma for histologic sca pel I examination; biopsy potentially prov des definitive treatment

TABLE 64. Types of Skin Biopsies Technique Description Lesion Types AssociatedConditions Comments Shave biopsy Razor blade skimmed Superficial lesions Seborrheic keratosis, Rapid removal of underthe target lesion involving the epidermis acrochordons sam ple/lesion; requires or dermal-epidermal least amount time of unction; elevated biopsytechniques; no esions closure required Scoop (saucerization) Deeper shave biopsy Pigmented lesions Basal or squamous cell Provides entire lesion tech n ique scooping under the carcinomas for histologic lesion, leaving a saucer- exam i nation like defect Dysplastic nevi or melanoma Punch biopsy Circular knife pushed lnflammatory lesions Sarcoidosis, vascu litis, Rapid sampling of around the lesion, involving the dermis or bullous disorders, epidermis and dermis; removing a plug of subcutaneous tissue; adnexaltumors preferred technique for tissu e tumors most inflammatory conditions lncisional biopsy Wedge of lesion Larger tumors or Large squamous cell Provides a larger removed with a scalpel deeper infiltrating carcrnomas, sample of tissue for diseases calciphylaxis histologic examination when it is difficult to biopsy the entire lesion Excisional biopsy Removal of entire Neoplasms Dysplastic nevi, Provides entire lesion neoplasm, usually with melanoma for histologic sca pel I examination; biopsy potentially prov des definitive treatment The skin biopsy is the gold standard test used to diagnose many cutaneous conditions and allours Therapeutic Principles correlation of histologic and clinical findings. Table 6,1 in Dermatology describes the types of skir.r biopsies. Shave (Figure 32) and Genera I Considerations punch (Figure 33) biopsies are the llost conlmonlv usecl '['he effectireness of a topical n.redication depends largell, on techniques. its abilitl, to be absorbed through the skin. Absrtrption is

The skin biopsy is the gold standard test used to diagnose many cutaneous conditions and allours Therapeutic Principles correlation of histologic and clinical findings. Table 6,1 in Dermatology describes the types of skir.r biopsies. Shave (Figure 32) and Genera I Considerations punch (Figure 33) biopsies are the llost conlmonlv usecl '['he effectireness of a topical n.redication depends largell, on techniques. its abilitl, to be absorbed through the skin. Absrtrption is ; t I G U R E 3 3. Punch biopsy is performed to remove a small nevus surrounded FIGURE 32. Shave biopsyof a lesion onthescalp. by purple skin markings. 84

Dermatologic Disorders dependent on the chemical structure, concentration, and TABLE 66. Frequently Used Topical Dermatologic delivery vehicle of the medication as well as skin hydration Medications and thickness. Medication lndications In general, ointments have a higher potency than creams, Topical glucocorticoids lnflammatory dermatoses which in turn have a higher potency than solutions or suspen- sions. The various vehicles available for topical medications Topicalantifungals Cutaneous fungal infections are listed in Table 65. Patients tend to favor creams because Terbinafine, nystatin, econazole, miconazole, they rub in, leaving minimal residue. An occlusive vehicle, ciclopirox, clotrimazole such as an ointment, increases penetration, but adherence Topical retinoids may be low because of its greasy feel. The alcohol content Tretinoin, adapalene Acne and drying nature of gels can cause burning and stinging on damaged skin. Tazarotene Psoriasis Topicalantibiotics

are listed in Table 65. Patients tend to favor creams because Terbinafine, nystatin, econazole, miconazole, they rub in, leaving minimal residue. An occlusive vehicle, ciclopirox, clotrimazole such as an ointment, increases penetration, but adherence Topical retinoids may be low because of its greasy feel. The alcohol content Tretinoin, adapalene Acne and drying nature of gels can cause burning and stinging on damaged skin. Tazarotene Psoriasis Topicalantibiotics TABLE 65. Vehicles forTopical Dermatologic Medications Mupirocin, neomycin, Superficial bacterial bacitracin infections Vehicle Characteristics Erythromycin, clindamycin Acne Cream Equal mixture of oil and watel with a smooth Metronidazole Rosacea texture and whitish in color Topical chemotherapy Easily rubs in and leaves minimal residue 5-Fluorouracil Actinic keratosis Highly prefened by patients because of aesthetic feel and appearance Topicalantiparasitic Foam Preparation that merges a gas (propane or Permethrin Scabies butane) with the medication Vitamin D analogues Allows the medication to be dispersed within a field of minute bubbles Calcipotriene Psoriasis

TABLE 65. Vehicles forTopical Dermatologic Medications Mupirocin, neomycin, Superficial bacterial bacitracin infections Vehicle Characteristics Erythromycin, clindamycin Acne Cream Equal mixture of oil and watel with a smooth Metronidazole Rosacea texture and whitish in color Topical chemotherapy Easily rubs in and leaves minimal residue 5-Fluorouracil Actinic keratosis Highly prefened by patients because of aesthetic feel and appearance Topicalantiparasitic Foam Preparation that merges a gas (propane or Permethrin Scabies butane) with the medication Vitamin D analogues Allows the medication to be dispersed within a field of minute bubbles Calcipotriene Psoriasis Used predominantly in terminal hair-bearing ski n Table 66 outlines categories of topical medications, Gel Semi-solid vehicle with alcohol base including those most frequently used and their indications. Drying in nature lrritating to broken skin owing to alcohol Topical Glucocorticoids content Topical glucocorticoids are used fbr their anti inflammatory Lotion Thicker than a solution owing to its increased effects. Because they are applied directly to the area ofinvolve- emollient properties ment, systemic adverse effects are minimized. Topical gluco Typically water based corticoids are classified by their potency level. There is a Easy to apply on large areas generic equivalent in each class, allowing for a cost-effective Ointment Oil-in-water mixture with a transparent clear approach (Table 67). appearance and greasy/oily texture A rule of thumb lor administration of topical glucocorti Most occlusive of the vehicles coids is that 30 grams of a topical glucocorticoid is enough to Highest viscosity cover the entire surface of a 70 kg (15a lb) adult, once. Proportionately less is needed for smaller areas. Difficult to use under clothing or on the hands/fingers of an active person Topical glucocorticoids may cause striae, easy bruising, atrophy, and telangiectasia. Side effects are most frequently Patch Unique vehicle that is applied to skin seen when using higher potencies for longer periods, in areas Standardized method of releasing medication over time of thin skin (such as the face), or in skin folds, or when used under occlusion. Use of glucocorticoids around the eyes can Powder Solid particulate preparation exacerbate glaucoma and cause cataracts. Typically used in skin folds to aid in moisture control and to reduce skin-on-skin friction Topical Antifungal Agents Soluti on The active medication is suspended in a water Topical antifungal agents are used for superficial fungal infec- or alcohol base tions. Topical azole antifungal agents are suitable for treatment Viscosity of water; easy to apply to scal p/hair- of localized infection, whereas oral agents are used to treat bearing areas recurrent, recalcitrant, or widespread disease. Suspension Oil and water mixture that separates when Topical glucocorticoids are frequently commercially allowed to sit combined with topical antifungal agents (clotrimazole- Must be shaken thoroughly before use betamethasone). These combinations should be avoided

Used predominantly in terminal hair-bearing ski n Table 66 outlines categories of topical medications, Gel Semi-solid vehicle with alcohol base including those most frequently used and their indications. Drying in nature lrritating to broken skin owing to alcohol Topical Glucocorticoids content Topical glucocorticoids are used fbr their anti inflammatory Lotion Thicker than a solution owing to its increased effects. Because they are applied directly to the area ofinvolve- emollient properties ment, systemic adverse effects are minimized. Topical gluco Typically water based corticoids are classified by their potency level. There is a Easy to apply on large areas generic equivalent in each class, allowing for a cost-effective Ointment Oil-in-water mixture with a transparent clear approach (Table 67). appearance and greasy/oily texture A rule of thumb lor administration of topical glucocorti Most occlusive of the vehicles coids is that 30 grams of a topical glucocorticoid is enough to Highest viscosity cover the entire surface of a 70 kg (15a lb) adult, once. Proportionately less is needed for smaller areas. Difficult to use under clothing or on the hands/fingers of an active person Topical glucocorticoids may cause striae, easy bruising, atrophy, and telangiectasia. Side effects are most frequently Patch Unique vehicle that is applied to skin seen when using higher potencies for longer periods, in areas Standardized method of releasing medication over time of thin skin (such as the face), or in skin folds, or when used under occlusion. Use of glucocorticoids around the eyes can Powder Solid particulate preparation exacerbate glaucoma and cause cataracts. Typically used in skin folds to aid in moisture control and to reduce skin-on-skin friction Topical Antifungal Agents Soluti on The active medication is suspended in a water Topical antifungal agents are used for superficial fungal infec- or alcohol base tions. Topical azole antifungal agents are suitable for treatment Viscosity of water; easy to apply to scal p/hair- of localized infection, whereas oral agents are used to treat bearing areas recurrent, recalcitrant, or widespread disease. Suspension Oil and water mixture that separates when Topical glucocorticoids are frequently commercially allowed to sit combined with topical antifungal agents (clotrimazole- Must be shaken thoroughly before use betamethasone). These combinations should be avoided 85

Dermatologic Disorders , Potency and Exarnples of Topical bacitracin) are used frequently. The most frequent side effect is Glucocorticoids allergic contact dermatitis, which limits their utility. Potency Glucocorticoid Weak Hydrocortisone 1 .0% or 2.5% o Topical glucocorticoids can avoid the adverse effects of Low Desonide 0.05% systemic glucocorticoid therapy but can cause striae, Triamcinolone acetonide 0.025a/" easy bruising, atrophy, and telangiectasia. Fluocinolone acetonide 0.01 % . There is a generic equivalent in each class oftopical glu- HVC Medium Triamcinolone acetonide 0.1 % cocorticoids, allowing for a cost-effective approach.

, Potency and Exarnples of Topical bacitracin) are used frequently. The most frequent side effect is Glucocorticoids allergic contact dermatitis, which limits their utility. Potency Glucocorticoid Weak Hydrocortisone 1 .0% or 2.5% o Topical glucocorticoids can avoid the adverse effects of Low Desonide 0.05% systemic glucocorticoid therapy but can cause striae, Triamcinolone acetonide 0.025a/" easy bruising, atrophy, and telangiectasia. Fluocinolone acetonide 0.01 % . There is a generic equivalent in each class oftopical glu- HVC Medium Triamcinolone acetonide 0.1 % cocorticoids, allowing for a cost-effective approach. Fluocinolone acetonide 0.025% o Combined topical glucocorticoids and antifungal agents HVC should be avoided because th€y can worsen some tinee Betamethasone valerate 0.1 % infections and, when used in the groin area, have a high Fluticasone propionate 0.05% risk for causing striae. Hydrocortisone butyrate 0.1 % Hydrocortisone valerate 0.02% High Betamethasone dipropionate 0.05% Dermatitis Fluocinonide 0.05% Atopic Dermatitis Halcinonide 0.1% Atopic dermatitis is a pruritic inflammatory condition that Amcinonide 0.1% commonly presents on the face and flexural surfaces, such as Desoxi m etason e 0.25"/" the popliteal and antecubital fossae (Figure 34). Excoriations and thickening (lichenification) ofthe skin caused by scratch- Triamcinolone acetonide 0.5% ing often accompany other signs of the atopic triad (allergic Ultra Augmented betamethasone dipropionate 0.05% rhinitis, asthma, and eczema). Pathogenesis is multifactorial Clobeasol propionate 0.05% and related to compromised skin barrier and an underlying Halobetasol propionate 0.05% immune response. Treatment is directed toward improving Diflorasone diacetate 0.05% skin barrier function and decreasing pro-inflammatory Flurandrenolide tape rytokines. Affected skin is often secondarily infected by S. oureus owing to a decrease in antimicrobial peptides. The use offragrance-free, synthetic detergent and non- because they can worsen some tinea infections and, when soap-based cleansers and moisturizers is the primary treat- used in the groin area, have a high risk for causing striae. ment. Application of moisturizers immediately afterbathing is recommended to improve skin hydration. Topical glucocorti- Topical I m m u nomodu lators coids are firstline anti-inflammatory medications used in Topical immunomodulators (tacrolimus ointment and pime- crolimus cream) can be used in place of topical glucocorticoids for an extended period without the development of atrophy or striae. These medications have a black-box warning for the rare development of skin cancer and cutaneous lymphoma.

Fluocinolone acetonide 0.025% o Combined topical glucocorticoids and antifungal agents HVC should be avoided because th€y can worsen some tinee Betamethasone valerate 0.1 % infections and, when used in the groin area, have a high Fluticasone propionate 0.05% risk for causing striae. Hydrocortisone butyrate 0.1 % Hydrocortisone valerate 0.02% High Betamethasone dipropionate 0.05% Dermatitis Fluocinonide 0.05% Atopic Dermatitis Halcinonide 0.1% Atopic dermatitis is a pruritic inflammatory condition that Amcinonide 0.1% commonly presents on the face and flexural surfaces, such as Desoxi m etason e 0.25"/" the popliteal and antecubital fossae (Figure 34). Excoriations and thickening (lichenification) ofthe skin caused by scratch- Triamcinolone acetonide 0.5% ing often accompany other signs of the atopic triad (allergic Ultra Augmented betamethasone dipropionate 0.05% rhinitis, asthma, and eczema). Pathogenesis is multifactorial Clobeasol propionate 0.05% and related to compromised skin barrier and an underlying Halobetasol propionate 0.05% immune response. Treatment is directed toward improving Diflorasone diacetate 0.05% skin barrier function and decreasing pro-inflammatory Flurandrenolide tape rytokines. Affected skin is often secondarily infected by S. oureus owing to a decrease in antimicrobial peptides. The use offragrance-free, synthetic detergent and non- because they can worsen some tinea infections and, when soap-based cleansers and moisturizers is the primary treat- used in the groin area, have a high risk for causing striae. ment. Application of moisturizers immediately afterbathing is recommended to improve skin hydration. Topical glucocorti- Topical I m m u nomodu lators coids are firstline anti-inflammatory medications used in Topical immunomodulators (tacrolimus ointment and pime- crolimus cream) can be used in place of topical glucocorticoids for an extended period without the development of atrophy or striae. These medications have a black-box warning for the rare development of skin cancer and cutaneous lymphoma. Topical Retinoids Topical retinoids are used frequently in the treatment of acne and psoriasis. They are vitamin A analogues that affect keratinocyte proliferation and differentiation. Use of these medications should be avoided in pregnancy owing to the risk for teratogenicity.

Fluocinolone acetonide 0.025% o Combined topical glucocorticoids and antifungal agents HVC should be avoided because th€y can worsen some tinee Betamethasone valerate 0.1 % infections and, when used in the groin area, have a high Fluticasone propionate 0.05% risk for causing striae. Hydrocortisone butyrate 0.1 % Hydrocortisone valerate 0.02% High Betamethasone dipropionate 0.05% Dermatitis Fluocinonide 0.05% Atopic Dermatitis Halcinonide 0.1% Atopic dermatitis is a pruritic inflammatory condition that Amcinonide 0.1% commonly presents on the face and flexural surfaces, such as Desoxi m etason e 0.25"/" the popliteal and antecubital fossae (Figure 34). Excoriations and thickening (lichenification) ofthe skin caused by scratch- Triamcinolone acetonide 0.5% ing often accompany other signs of the atopic triad (allergic Ultra Augmented betamethasone dipropionate 0.05% rhinitis, asthma, and eczema). Pathogenesis is multifactorial Clobeasol propionate 0.05% and related to compromised skin barrier and an underlying Halobetasol propionate 0.05% immune response. Treatment is directed toward improving Diflorasone diacetate 0.05% skin barrier function and decreasing pro-inflammatory Flurandrenolide tape rytokines. Affected skin is often secondarily infected by S. oureus owing to a decrease in antimicrobial peptides. The use offragrance-free, synthetic detergent and non- because they can worsen some tinea infections and, when soap-based cleansers and moisturizers is the primary treat- used in the groin area, have a high risk for causing striae. ment. Application of moisturizers immediately afterbathing is recommended to improve skin hydration. Topical glucocorti- Topical I m m u nomodu lators coids are firstline anti-inflammatory medications used in Topical immunomodulators (tacrolimus ointment and pime- crolimus cream) can be used in place of topical glucocorticoids for an extended period without the development of atrophy or striae. These medications have a black-box warning for the rare development of skin cancer and cutaneous lymphoma. Topical Retinoids Topical retinoids are used frequently in the treatment of acne and psoriasis. They are vitamin A analogues that affect keratinocyte proliferation and differentiation. Use of these medications should be avoided in pregnancy owing to the risk for teratogenicity. Topical Antibiotics Clindamycin and erythromycin are topical antibiotics used in the treatment of acne. They are well tolerated and have few to no side effects, although bacterial resistance with monotherapy has been inereasing over the past several decades. Mupirocin is a topical antibiotic ointment commonly used to treat skin infections caused by Stophylococcus oureus, such as impetigo. tIGURE 34. Atopicdermatitis,showingskinthickening(lichenification)dueto Over-the-counter combination antibiotics (neomycin and scratching and dry scaling in the popliteal flexure.

Topical Antibiotics Clindamycin and erythromycin are topical antibiotics used in the treatment of acne. They are well tolerated and have few to no side effects, although bacterial resistance with monotherapy has been inereasing over the past several decades. Mupirocin is a topical antibiotic ointment commonly used to treat skin infections caused by Stophylococcus oureus, such as impetigo. tIGURE 34. Atopicdermatitis,showingskinthickening(lichenification)dueto Over-the-counter combination antibiotics (neomycin and scratching and dry scaling in the popliteal flexure. 86 .t

Dermatologic Disorders addition to cleansers and moisturizers; glucocorticoid treat- ment is typically applied twice daily until lesions are cleared. Proactive maintenance therapy using topical glucocorticoids once to twice weekly in areas that commonly flare can be con sidered to prevent relapses. Topical calcineurin inhibitors, such as tacrolimus and pimecrolimus, are steroid-sparing agents useful for such areas as the face and skin folds, where permanent atrophy caused by long-term or potent topical glucocorticoid use is a concern. $ystemic glucocorticoids should be avoided, if possible, owing to flares after discontinuation; these agents should only be considered in severe exacerbations or when bridging to another systemic therapy. Steroid-sparing therapies, such as cyclosporine, methotrexate, azathioprine, and mycophenolate mofetil, are systemic treatment options. Dupilumab is effective in decreasing pruritus and disease activity in adults with mod- erate to severe atopic dermatitis that is recalcitrant to topical agents.

addition to cleansers and moisturizers; glucocorticoid treat- ment is typically applied twice daily until lesions are cleared. Proactive maintenance therapy using topical glucocorticoids once to twice weekly in areas that commonly flare can be con sidered to prevent relapses. Topical calcineurin inhibitors, such as tacrolimus and pimecrolimus, are steroid-sparing agents useful for such areas as the face and skin folds, where permanent atrophy caused by long-term or potent topical glucocorticoid use is a concern. $ystemic glucocorticoids should be avoided, if possible, owing to flares after discontinuation; these agents should only be considered in severe exacerbations or when bridging to another systemic therapy. Steroid-sparing therapies, such as cyclosporine, methotrexate, azathioprine, and mycophenolate mofetil, are systemic treatment options. Dupilumab is effective in decreasing pruritus and disease activity in adults with mod- erate to severe atopic dermatitis that is recalcitrant to topical agents. Contact Dermatitis Pathophysiolory and Evaluation There are two types of contact dermatitis: allergic and irritant. Allergic contact dermatitis is a tlpe IV delayed hypersensitivity reaction that results in an eczematous eruption at the site of contact. Irritant contact dermatitis is more common than allergic contact dermatitis and results from direct damage to the skin caused by chemicals, soaps, or detergents; it is not immune mediated. Discovering the cause of contact dermatitis is essential to its treatment and prevention. A detailed history can help iden t I G U R E 3 5. Epicutaneous patch testing is commonly applied to the back (top) to evaluate for allerg ic contact dermatitis. The erythematous patch identified 48 hours tiff the cause, but often epicutaneous patch testing is needed after epicutaneous patch testing (bottom) indicates a positive reaction to a specific to identiSz the source (Figure 35). Because allergies can develop allergen. over time, a lengthy history of using a skin product without a reaction does not exclude that product as a potential trigger. Common contact allergens are described in Table 68. Urushiol, the allergen found in plants, such as poison ivy, T&mi..il &6. Common ContactAllergens poison oak, and poison sumac, is a common cause of allergic Contact Allergens Occupations/Exposures contact dermatitis. Clinically, it presents with intensely pru Benzophenones Sunscreens (contact and ritic, often linear, vesicular papules, plaques, and vesicles photocontact dermatitis) (Figure 36). In sensitized patients, lesions can present at differ- Balsam of Peru Common fragrance in personal ent locations at different times for up to 14 days after exposure. care products and foods Fluid from blisters is not antigenic. After exposure, patients Methacrylate Dental flllings, cement for joint should remove contaminated clothing and gently wash the replacement (orthopedic surgeons and dentists) skin with soap and water. Nickel is another common allergen and is found in every- Methylisothiazolinone Baby wipes, personal care products day items, such as jewelry zippers, and cell phones. Paraphenylenediamine Permanent hair dye Eczematous dermatitis of the lower abdomen is a common presentation of a nickel allergr caused by a clothing snap or Formaldehyde and Cosmetics and personal care formaldehyde-releasing products belt buckle. Patients may use a commercially available nickel preservatives test kit to identifiz items that contain nickel. (quaternium-15) Neomycin and bacitracin are commonly used for wound Rubber accelerators Shoe and glove dermatitis; care. They can cause an allergic contact derrnatitis that mimics (carba mix, thiurams, common in health care workers a wound infection. Given the prevalence of sensitivity to these benzothiazoles) products, patients should use plain petrolatum in place of Cocamidopropyl Personal care products betaine (shampoos) topical antibiotics to aid healing of clean wounds.

Contact Dermatitis Pathophysiolory and Evaluation There are two types of contact dermatitis: allergic and irritant. Allergic contact dermatitis is a tlpe IV delayed hypersensitivity reaction that results in an eczematous eruption at the site of contact. Irritant contact dermatitis is more common than allergic contact dermatitis and results from direct damage to the skin caused by chemicals, soaps, or detergents; it is not immune mediated. Discovering the cause of contact dermatitis is essential to its treatment and prevention. A detailed history can help iden t I G U R E 3 5. Epicutaneous patch testing is commonly applied to the back (top) to evaluate for allerg ic contact dermatitis. The erythematous patch identified 48 hours tiff the cause, but often epicutaneous patch testing is needed after epicutaneous patch testing (bottom) indicates a positive reaction to a specific to identiSz the source (Figure 35). Because allergies can develop allergen. over time, a lengthy history of using a skin product without a reaction does not exclude that product as a potential trigger. Common contact allergens are described in Table 68. Urushiol, the allergen found in plants, such as poison ivy, T&mi..il &6. Common ContactAllergens poison oak, and poison sumac, is a common cause of allergic Contact Allergens Occupations/Exposures contact dermatitis. Clinically, it presents with intensely pru Benzophenones Sunscreens (contact and ritic, often linear, vesicular papules, plaques, and vesicles photocontact dermatitis) (Figure 36). In sensitized patients, lesions can present at differ- Balsam of Peru Common fragrance in personal ent locations at different times for up to 14 days after exposure. care products and foods Fluid from blisters is not antigenic. After exposure, patients Methacrylate Dental flllings, cement for joint should remove contaminated clothing and gently wash the replacement (orthopedic surgeons and dentists) skin with soap and water. Nickel is another common allergen and is found in every- Methylisothiazolinone Baby wipes, personal care products day items, such as jewelry zippers, and cell phones. Paraphenylenediamine Permanent hair dye Eczematous dermatitis of the lower abdomen is a common presentation of a nickel allergr caused by a clothing snap or Formaldehyde and Cosmetics and personal care formaldehyde-releasing products belt buckle. Patients may use a commercially available nickel preservatives test kit to identifiz items that contain nickel. (quaternium-15) Neomycin and bacitracin are commonly used for wound Rubber accelerators Shoe and glove dermatitis; care. They can cause an allergic contact derrnatitis that mimics (carba mix, thiurams, common in health care workers a wound infection. Given the prevalence of sensitivity to these benzothiazoles) products, patients should use plain petrolatum in place of Cocamidopropyl Personal care products betaine (shampoos) topical antibiotics to aid healing of clean wounds. 87

Dermatologic Disorders -*\r. * ',! F lG U R E 3 7. Hand dermatitis, with findings of palmar edema, erythema, desquamation, and fissuring. t I G U R E 3 6. Linear erythematous plaques and vesicles are commonly seen in allergic contact dermatitis caused by poison ivy. Fragrances are common allergens fbund in many cos- metic products, moisturizers, and detergents. They may also be present as flavoring agents of toothpastes, mouthwashes, and fbod and beverages. Most household cleansers and personal hygiene products contain preservatives that can produce allergic contact derma- titis. Risk fbr allergic contact dermatitis is increased in some occupations, such as health care workers, who are exposed to rubber accelerators. Avoidance ofthe causative agent is preventive and cura- tive. 'fopical glucocorticoids are used while attempting to identify and eliminate the allergen source. Severe allergic contact eruptions may necessitate a 2 to 3-week taper of sys FIGU RE 3 8. Ihe typical physical findings of dyshidrotic eczema are multiple temic glucocorticoids. Because of the risk fbr rebound derma small vesicles on the palmar or plantar skin, especially along the lateral aspects o{ the fingers and toes. The diagnosis is supported by a history of recurrent episodes of titis, shorter courses of systemic glucocorticoids are not intense pruritus on the palms and/or soles, followed by the development of reconrnrended. multiple small vesicles.Ihe vesicles will desquamate, leaving erosions and fissures.

Fragrances are common allergens fbund in many cos- metic products, moisturizers, and detergents. They may also be present as flavoring agents of toothpastes, mouthwashes, and fbod and beverages. Most household cleansers and personal hygiene products contain preservatives that can produce allergic contact derma- titis. Risk fbr allergic contact dermatitis is increased in some occupations, such as health care workers, who are exposed to rubber accelerators. Avoidance ofthe causative agent is preventive and cura- tive. 'fopical glucocorticoids are used while attempting to identify and eliminate the allergen source. Severe allergic contact eruptions may necessitate a 2 to 3-week taper of sys FIGU RE 3 8. Ihe typical physical findings of dyshidrotic eczema are multiple temic glucocorticoids. Because of the risk fbr rebound derma small vesicles on the palmar or plantar skin, especially along the lateral aspects o{ the fingers and toes. The diagnosis is supported by a history of recurrent episodes of titis, shorter courses of systemic glucocorticoids are not intense pruritus on the palms and/or soles, followed by the development of reconrnrended. multiple small vesicles.Ihe vesicles will desquamate, leaving erosions and fissures. Hand Dermatitis Treatment includes topical emollients, such as petrola Iland dermatitis often results from a combination of causes, tum. A potent topical glucocorticoid ma1'be necessary during such as excessive hand washing. contact dermatitis, atopic flares. Triggers should be identif'ied and avoided. Placing dermatitis, or dyshidrotic eczenra. It is most commonly seen in lvhite cotton glore liners inside ol rubber glores is recom patients who hold jobs iruolving prolonged exposure to water, mended lbr patients when lvorking with chemicals and u'ater. chemicals, and occlusive gloves (health care, house cieaning, lbod preparation, hairstyling). It is characterized by pruritic, Seborrheic Dermatitis erythematous plaques on the palmar and dorsal hands, which Seborrheic dermatitis is a common condition characterized b1' can lead to fissuring and lichenification over time (see Table 62 greasy. yellow, sca1y, erythematous patches in seborrheic and Figure 37). Dyshidrotic eczema presents with vesicles on areas (scaip, face, ears, upper chest. axillae. and inguinal folds) the palms and sides of the fingers (Figure 38). (Figure 39). On the face. specific areas of inrolr,-ement include The differential diagnosis of hand dermatitis includes the eyebrows, medial aspects of the cheeks. intereyebro$' tinea, psoriasis, and scabies. The patient's entire body should region, and nasal ala. This disease is beliered to be caused b1'a be examined for other rashes that may help differentiate hand heightened sensitivi0T to )'easts. such as Malossezia. It is more dermatitis from these other causes. If tinea is suspected. the prevalent in patients who are immunocompromised, such as fbet should be examined for tinea pedis and onychomycosis patients with HIV/AIDS or organ transplant recipients. Patients (two f'eet one hand syndrome). with Parkinson disease or Down syndrome also have a higher

Dermatologic Disorders Fl G U RE 39. Seborrheic dermatitis, with fine, oily scale around the medial eyebrows. prevalence of seborrheic dermatitis. Diagnosis is made clinically on the basis ofthe distribution and appearance ofthe patches. Treatment includes over-the-counter medications, such as selenium sulfide or zinc pyrithione shampoos. Ketoconazole shampoo and cream are also effective. Patients should apply the shampoo on the skin and allow it to sit for 5 minutes before rinsing it off. Low-potency topical glucocorticoids can be used in combination with antifungal treatments when severe t I G U R E 4 0. Ihese coinrhaped erythematous plaques are characteristic of inflammation is present. Oral ketoconazole is not recom- nummular dermatitis. mended owing to the risk for liver and adrenal toxicity, although other oral antifungal agents may be used for severe or refractory disease. Ifconventional therapies are not effective, other diagnoses must be considered, including rosacea, lupus erythematosus, and contact dermatitis. Nummular Dermatitis Nummular dermatitis is characterized by coin-shaped, pruritic, scaly plaques commonly found on the extremities (Figure O). It is more common in men and elderly persons. The round plaques may be mistaken for other conditions, such as tinea corporis, psoriasis, or contact dermatitis. Potent topical gluco- corticoids and emollients are the preferred treatment.

Nummular Dermatitis Nummular dermatitis is characterized by coin-shaped, pruritic, scaly plaques commonly found on the extremities (Figure O). It is more common in men and elderly persons. The round plaques may be mistaken for other conditions, such as tinea corporis, psoriasis, or contact dermatitis. Potent topical gluco- corticoids and emollients are the preferred treatment. lntertrigo Intertrigo is dermatitis involving adjacent skin folds (axillary infoamammarfr abdominal, and inguinaD Gigure 41). Predisposing conditions include obesity, friction, occlusion, and factors that interfere with immune response, such as diabetes mellitus. Intertrigo presents with erythematous, macerated plaques. Secondary infection with Candido is common and may be sus pected by the presence of multiple small red papules and pus tules that surround the main rash (satellite pustules). Treatment of intertrigo consists of drying the area and use of agents (such as drying powder) to reduce moisture and maceration and to prevent secondary yeast infection. Short F IG U R E 4 1 . lntertrigo, a chronic recurrent skin condition that is often seen in patients with obesity, is caused by moist conditions in skin fold areas and is courses of low-potency topical glucocorticoids may be added worsened by heat and exercise. The rash is confined to the intertriginous areas and to treat the associated inflammation. If secondary Candida does not extend beyond these boundaries. Secondary infection with Candida may infection is suspected, concomitant treatment with topical occur, as in this patient. lndicators ol Candida infection include small red papules antifungal agents can be added. on the periphery of the rash. 89

Dermatologic Disorders XtY POIf,TS ((o,itinaedl . Venous stasis dermatitis may be misdiagnosed as cellu- HVC litis; however, cellulitis is usually unilateral, more acute in onset, and often associated with pain, leukocytosis, and occasionallY fever.

XtY POIf,TS ((o,itinaedl . Venous stasis dermatitis may be misdiagnosed as cellu- HVC litis; however, cellulitis is usually unilateral, more acute in onset, and often associated with pain, leukocytosis, and occasionallY fever. Urticaria Urticaria (hives) represent localized edema caused by mast cell degranulation releasing histamine, leukotrienes, complement, and prostaglandins. Urticaria are characterized by well demarcated 1- to B cm plaques that appear quickly and resolve in a matter of hours . Individual lesions may be pink or white, often surrounded by a red flare, and may manifest as round, oval, annular, arciform, or serpiginous. Urticaria are extremely pruritic and tend to appear on body sites that receive repetitive FIGU RE 42. Venous stasis dermatitis, characterized by edema, bilateral pressure or rubbing, such as the waistline and posterior neck. erythematous patches, weeping vesicles, ankle varic0sities, and hyperpigmentation. Although individual urticaria resolve in less than 24 hours, recurrent crops of hives may last for weeks. In most cases, Venous Stasis Dermatitis urticaria resolve spontaneously and the cause is never deter mined. If the episodes last for longer than 6 weeks, the condi Venous stasis dermatitis is common in patients with chronic lower extremig edema, most commonly secondary to venous tion is classified as chronic. Ifthe individual urticarial lesions persist longer lhan 24 hours, or if they are accompanied by stasis (Figure 42). Venous stasis dermatitis can be very pruritic and erythematous, and symptoms are often bilateral with systemic symptoms (joint pain, fever), urticarial vasculitis (a medial distal leg predominance. Dependent edema, hyperpig form of small vessel vasculitis) must be considered. Food allergz, viral infection, and medication reaction are mentation, and dilated veins are common associated findings. Symptoms can be managed topically with glucocorticoids and the most common causes of acute urticaria (Figure 43). Food emollients, but the condition will not significantly improve induced allergic reactions most commonly result from shell until the edema is addressed with leg elevation and compres- fish, peanuts, and tree nuts. Infrequent but important causes sion. Because of a similar clinical presentation, venous stasis of urticaria include autoimmune thyroid disease and malig- dermatitis may be misdiagnosed as cellulitis; however, celluli nancies, particularly lymphoma. Physical urticaria are induced tis is usually unilateral, more acute in onset, and often associ by physical stimuli, such as sunlight, sweating, physical pres- ated with pain, leukocl.tosis, and occasionally fever. sure, vibration, water, or cold temperature. Urticaria is a clinical diagnosis. Physical maneuvers that (tr Polf,It can help with diagnosis include circling lesions with a marker . Allergic contact dermatitis is a type IV delayed hyper- to see whether they resolve within 24 hours and gently sensitivity reaction and is best diagnosed with epicuta- scratching uninvolved skin with the end ofa tongue depressor neous patch testing. to see whether urticaria (not just redness) can be induced o Hand dermatitis is characterized by pruritic, erythema- tous plaques on the hands and results from a combina- tion ofcauses, such as excessive hand washing, contact dermatitis, atopic dermatitis, or dyshidrotic eczema. HVC o Inexpensive treatment of seborrheic dermatitis includes over-the counter medications, such as selenium sulfide or zinc pyrithione shampoos. o Treatment of intertrigo (dermatitis involving adjacent skin folds) consists of drying the affected area, using drying powder to reduce moisture, and in some cases using short courses of low potency topical glucocorti- coids to treat the associated inflammation; concomitant treatment with topical antifungal agents can be added if secondary candidainfection is suspected. FIG U RE 43, Urticarial lesions on the waist, characterized by small and large (continued) edematous and erythematous plaques of various shapes.

Urticaria Urticaria (hives) represent localized edema caused by mast cell degranulation releasing histamine, leukotrienes, complement, and prostaglandins. Urticaria are characterized by well demarcated 1- to B cm plaques that appear quickly and resolve in a matter of hours . Individual lesions may be pink or white, often surrounded by a red flare, and may manifest as round, oval, annular, arciform, or serpiginous. Urticaria are extremely pruritic and tend to appear on body sites that receive repetitive FIGU RE 42. Venous stasis dermatitis, characterized by edema, bilateral pressure or rubbing, such as the waistline and posterior neck. erythematous patches, weeping vesicles, ankle varic0sities, and hyperpigmentation. Although individual urticaria resolve in less than 24 hours, recurrent crops of hives may last for weeks. In most cases, Venous Stasis Dermatitis urticaria resolve spontaneously and the cause is never deter mined. If the episodes last for longer than 6 weeks, the condi Venous stasis dermatitis is common in patients with chronic lower extremig edema, most commonly secondary to venous tion is classified as chronic. Ifthe individual urticarial lesions persist longer lhan 24 hours, or if they are accompanied by stasis (Figure 42). Venous stasis dermatitis can be very pruritic and erythematous, and symptoms are often bilateral with systemic symptoms (joint pain, fever), urticarial vasculitis (a medial distal leg predominance. Dependent edema, hyperpig form of small vessel vasculitis) must be considered. Food allergz, viral infection, and medication reaction are mentation, and dilated veins are common associated findings. Symptoms can be managed topically with glucocorticoids and the most common causes of acute urticaria (Figure 43). Food emollients, but the condition will not significantly improve induced allergic reactions most commonly result from shell until the edema is addressed with leg elevation and compres- fish, peanuts, and tree nuts. Infrequent but important causes sion. Because of a similar clinical presentation, venous stasis of urticaria include autoimmune thyroid disease and malig- dermatitis may be misdiagnosed as cellulitis; however, celluli nancies, particularly lymphoma. Physical urticaria are induced tis is usually unilateral, more acute in onset, and often associ by physical stimuli, such as sunlight, sweating, physical pres- ated with pain, leukocl.tosis, and occasionally fever. sure, vibration, water, or cold temperature. Urticaria is a clinical diagnosis. Physical maneuvers that (tr Polf,It can help with diagnosis include circling lesions with a marker . Allergic contact dermatitis is a type IV delayed hyper- to see whether they resolve within 24 hours and gently sensitivity reaction and is best diagnosed with epicuta- scratching uninvolved skin with the end ofa tongue depressor neous patch testing. to see whether urticaria (not just redness) can be induced o Hand dermatitis is characterized by pruritic, erythema- tous plaques on the hands and results from a combina- tion ofcauses, such as excessive hand washing, contact dermatitis, atopic dermatitis, or dyshidrotic eczema. HVC o Inexpensive treatment of seborrheic dermatitis includes over-the counter medications, such as selenium sulfide or zinc pyrithione shampoos. o Treatment of intertrigo (dermatitis involving adjacent skin folds) consists of drying the affected area, using drying powder to reduce moisture, and in some cases using short courses of low potency topical glucocorti- coids to treat the associated inflammation; concomitant treatment with topical antifungal agents can be added if secondary candidainfection is suspected. FIG U RE 43, Urticarial lesions on the waist, characterized by small and large (continued) edematous and erythematous plaques of various shapes. 90

Urticaria Urticaria (hives) represent localized edema caused by mast cell degranulation releasing histamine, leukotrienes, complement, and prostaglandins. Urticaria are characterized by well demarcated 1- to B cm plaques that appear quickly and resolve in a matter of hours . Individual lesions may be pink or white, often surrounded by a red flare, and may manifest as round, oval, annular, arciform, or serpiginous. Urticaria are extremely pruritic and tend to appear on body sites that receive repetitive FIGU RE 42. Venous stasis dermatitis, characterized by edema, bilateral pressure or rubbing, such as the waistline and posterior neck. erythematous patches, weeping vesicles, ankle varic0sities, and hyperpigmentation. Although individual urticaria resolve in less than 24 hours, recurrent crops of hives may last for weeks. In most cases, Venous Stasis Dermatitis urticaria resolve spontaneously and the cause is never deter mined. If the episodes last for longer than 6 weeks, the condi Venous stasis dermatitis is common in patients with chronic lower extremig edema, most commonly secondary to venous tion is classified as chronic. Ifthe individual urticarial lesions persist longer lhan 24 hours, or if they are accompanied by stasis (Figure 42). Venous stasis dermatitis can be very pruritic and erythematous, and symptoms are often bilateral with systemic symptoms (joint pain, fever), urticarial vasculitis (a medial distal leg predominance. Dependent edema, hyperpig form of small vessel vasculitis) must be considered. Food allergz, viral infection, and medication reaction are mentation, and dilated veins are common associated findings. Symptoms can be managed topically with glucocorticoids and the most common causes of acute urticaria (Figure 43). Food emollients, but the condition will not significantly improve induced allergic reactions most commonly result from shell until the edema is addressed with leg elevation and compres- fish, peanuts, and tree nuts. Infrequent but important causes sion. Because of a similar clinical presentation, venous stasis of urticaria include autoimmune thyroid disease and malig- dermatitis may be misdiagnosed as cellulitis; however, celluli nancies, particularly lymphoma. Physical urticaria are induced tis is usually unilateral, more acute in onset, and often associ by physical stimuli, such as sunlight, sweating, physical pres- ated with pain, leukocl.tosis, and occasionally fever. sure, vibration, water, or cold temperature. Urticaria is a clinical diagnosis. Physical maneuvers that (tr Polf,It can help with diagnosis include circling lesions with a marker . Allergic contact dermatitis is a type IV delayed hyper- to see whether they resolve within 24 hours and gently sensitivity reaction and is best diagnosed with epicuta- scratching uninvolved skin with the end ofa tongue depressor neous patch testing. to see whether urticaria (not just redness) can be induced o Hand dermatitis is characterized by pruritic, erythema- tous plaques on the hands and results from a combina- tion ofcauses, such as excessive hand washing, contact dermatitis, atopic dermatitis, or dyshidrotic eczema. HVC o Inexpensive treatment of seborrheic dermatitis includes over-the counter medications, such as selenium sulfide or zinc pyrithione shampoos. o Treatment of intertrigo (dermatitis involving adjacent skin folds) consists of drying the affected area, using drying powder to reduce moisture, and in some cases using short courses of low potency topical glucocorti- coids to treat the associated inflammation; concomitant treatment with topical antifungal agents can be added if secondary candidainfection is suspected. FIG U RE 43, Urticarial lesions on the waist, characterized by small and large (continued) edematous and erythematous plaques of various shapes. 90 I

Dermatologic Disorders cutaneous adverse reactions Stevens-Johnson syndrome and toxic epidermal necrolysis. Table 69 describes patterns of drug reactions. Medications can also induce an array of specific diseases, including psoriasis, bullous pemphigoid, and cuta- neous lupus erythematosus. Discontinuing the causative drug is the first step in treating drug reactions.

cutaneous adverse reactions Stevens-Johnson syndrome and toxic epidermal necrolysis. Table 69 describes patterns of drug reactions. Medications can also induce an array of specific diseases, including psoriasis, bullous pemphigoid, and cuta- neous lupus erythematosus. Discontinuing the causative drug is the first step in treating drug reactions. Exanthematous (Morbilliform) Exanthematous, or morbilliform (measles-like), drug erup tions are the most common drug reactions, most likely repre- senting a type IV delayed hypersensitivity reaction. As such, the rash appears during the first or second week after drug exposure, although subsequent exposures can produce a reac- tion much more quickly. Patients develop erythematous pap ules and macules that coalesce symmetrically to form plaques. tl G U RE 44. Tongue'blade-stroke-induced dermographism (dermatographism). The papules are often dense and monomorphic and accompa- A wheal appears within a few minutes in the area subjected to a light scratch. nied by varying degrees of pruritus, beginning on the trunk and progressing distally across the limbs (Figure 45). Palms (dermatographism) (Figure 44). The cause of urticaria is and soles are usually spared. This type of reaction is classically induced with the use of ampicillin or amoxicillin in patients investigated primarily by history and physical examination. Diagnostic evaluation for urticaria is not recommended with acute Epstein Barr virus infection. Treatment involves cessation of the causative agent, and unless the history suggests a specific cause. If symptoms per- the use of systemic and/or topical glucocorticoids and oral H, sist, laboratory tests, including a complete blood count with antihistamines. Patients should be counseled to contact their differential, urinalysis, erythrocyte sedimentation rate or clinician ifthey develop fever, skin pain, blisters, pustules, or C reactive protein, thyroid stimulating hormone, and liver mucous membrane involvement, indicating a more serious chemistry tests, can be considered. If associated with systemic and potentially Iife-threating condition. symptoms or suspicion of urticarial vasculitis, skin biopsy is helpful. Nonsedating, long-acting antihistamines are the treatment of choice for urticaria; topical antihistamines have Fixed Drug Eruption not been found to be effective and may lead to allergic contact Fixed drug eruptions recur at the same sites on the skin with dermatitis. each exposure. Pink-to-purple circinate plaques with central Angioedema, both acquired and hereditary is discussed dusky discoloration or vesiculation appear most commonly on in MKSAP 19 Pulmonary and Critical Care Medicine. the lips, face, fingers, and genitals (Figure 46). The first expo sure typically generates one plaque that recurs in the same TIY POIilTS location with each repeated exposure. Additional plaques HVC . Urticaria is characterized by well-demarcated, erythe- may develop with subsequent exposures. Lesions typically matous, pruritic plaques that appear quickly and resolve with postinflammatory hyperpigmentation. Treatment resolve in a matter of hours; diagnostic evaluation for involves cessation of the causative agent, and, if symptoms are urticaria is not recommended unless the history sug- significant, systemic and/or topical glucocorticoids and oral H, gests a specific cause. antihistamines. HVC o Nonsedating, long-acting antihistamines are the treat- ment of choice for urticaria; topical antihistamines have Drug-lnduced Hypersensitivity not been found to be effective and may lead to allergic Syndrome (DRESS Syndrome) contact dermatitis. Drug-induced hypersensitivity syndrome (DIHS) and drug reaction with eosinophilia and systemic symptoms (DRESS) are synonymous and represent a severe life-threatening medi- Drug Eruptions cation reaction. DRESS is increasingly being referred to as Drug reactions are an important consideration in the differen- DIHS to emphasize the fact that eosinophilia is not always tial diagnosis fbr any rash because medications can produce present. almost any pattern of skin disease. The most common types of The most common medications that cause DIHS include cutaneous adverse reactions are exanthematous (morbilli sulfonamide antibiotics, allopurinol, and anticonvulsants, but form), urticarial, fixed drug, photosensitivity, drug-induced many other medications have been implicated (Table 7o). hypersensitivity syndrome, hypersensitivity vasculitis, acute Unlike other se'uere medication reactions, the onset of symp generalized exanthematous pustulosis, and the severe toms is delayed, often 2 to 6 weeks after exposure. Symptoms

Exanthematous (Morbilliform) Exanthematous, or morbilliform (measles-like), drug erup tions are the most common drug reactions, most likely repre- senting a type IV delayed hypersensitivity reaction. As such, the rash appears during the first or second week after drug exposure, although subsequent exposures can produce a reac- tion much more quickly. Patients develop erythematous pap ules and macules that coalesce symmetrically to form plaques. tl G U RE 44. Tongue'blade-stroke-induced dermographism (dermatographism). The papules are often dense and monomorphic and accompa- A wheal appears within a few minutes in the area subjected to a light scratch. nied by varying degrees of pruritus, beginning on the trunk and progressing distally across the limbs (Figure 45). Palms (dermatographism) (Figure 44). The cause of urticaria is and soles are usually spared. This type of reaction is classically induced with the use of ampicillin or amoxicillin in patients investigated primarily by history and physical examination. Diagnostic evaluation for urticaria is not recommended with acute Epstein Barr virus infection. Treatment involves cessation of the causative agent, and unless the history suggests a specific cause. If symptoms per- the use of systemic and/or topical glucocorticoids and oral H, sist, laboratory tests, including a complete blood count with antihistamines. Patients should be counseled to contact their differential, urinalysis, erythrocyte sedimentation rate or clinician ifthey develop fever, skin pain, blisters, pustules, or C reactive protein, thyroid stimulating hormone, and liver mucous membrane involvement, indicating a more serious chemistry tests, can be considered. If associated with systemic and potentially Iife-threating condition. symptoms or suspicion of urticarial vasculitis, skin biopsy is helpful. Nonsedating, long-acting antihistamines are the treatment of choice for urticaria; topical antihistamines have Fixed Drug Eruption not been found to be effective and may lead to allergic contact Fixed drug eruptions recur at the same sites on the skin with dermatitis. each exposure. Pink-to-purple circinate plaques with central Angioedema, both acquired and hereditary is discussed dusky discoloration or vesiculation appear most commonly on in MKSAP 19 Pulmonary and Critical Care Medicine. the lips, face, fingers, and genitals (Figure 46). The first expo sure typically generates one plaque that recurs in the same TIY POIilTS location with each repeated exposure. Additional plaques HVC . Urticaria is characterized by well-demarcated, erythe- may develop with subsequent exposures. Lesions typically matous, pruritic plaques that appear quickly and resolve with postinflammatory hyperpigmentation. Treatment resolve in a matter of hours; diagnostic evaluation for involves cessation of the causative agent, and, if symptoms are urticaria is not recommended unless the history sug- significant, systemic and/or topical glucocorticoids and oral H, gests a specific cause. antihistamines. HVC o Nonsedating, long-acting antihistamines are the treat- ment of choice for urticaria; topical antihistamines have Drug-lnduced Hypersensitivity not been found to be effective and may lead to allergic Syndrome (DRESS Syndrome) contact dermatitis. Drug-induced hypersensitivity syndrome (DIHS) and drug reaction with eosinophilia and systemic symptoms (DRESS) are synonymous and represent a severe life-threatening medi- Drug Eruptions cation reaction. DRESS is increasingly being referred to as Drug reactions are an important consideration in the differen- DIHS to emphasize the fact that eosinophilia is not always tial diagnosis fbr any rash because medications can produce present. almost any pattern of skin disease. The most common types of The most common medications that cause DIHS include cutaneous adverse reactions are exanthematous (morbilli sulfonamide antibiotics, allopurinol, and anticonvulsants, but form), urticarial, fixed drug, photosensitivity, drug-induced many other medications have been implicated (Table 7o). hypersensitivity syndrome, hypersensitivity vasculitis, acute Unlike other se'uere medication reactions, the onset of symp generalized exanthematous pustulosis, and the severe toms is delayed, often 2 to 6 weeks after exposure. Symptoms 91

Dermatologic Disorders TABLE 69. Patterns of Drug and Chemical Reactions Reaction Type Classic Agents Time to Onset Additional Features Exanthematous Antibiotics (penicillins, sulfonamides, 4-14 d No effective test for causation; gold (morbilliform) cephalosporins), NSAlDs, allopurinol, standard to determine causation is antiepileptic agents rechallenge (not recommended) U rtica rial

TABLE 69. Patterns of Drug and Chemical Reactions Reaction Type Classic Agents Time to Onset Additional Features Exanthematous Antibiotics (penicillins, sulfonamides, 4-14 d No effective test for causation; gold (morbilliform) cephalosporins), NSAlDs, allopurinol, standard to determine causation is antiepileptic agents rechallenge (not recommended) U rtica rial lmmunologic Penicillin, anesthetic agents, ACE Minutes to a few hours Most chronic urticaria cases are not inhibitors drug related, but aspirin may cause or exacerbate chronic cases of urticaria Nonimmunologic Vancomycin, rifampicin, acetylcysteine, Minutes to a few hours Red person syndrome is related to the opioids, radiocontrast agents infusion rate of vancomycin Photosensitivity Phototoxic Voriconazole, demeclorycline, Hours Voriconazole phototoxicity can cause doxycycline, NSAlDs, skin cancer within a few years of fluoroquinolones, amiodarone treatment May result in fingernail shedding Photoallergic Hydrochlorothiazide, sulfonamide 7-1 0 d for first exposure; May persist after ultraviolet light antibiotics; sulfonylureas; tricyclic hours for subsequent exposure (fall or winter months) antidepressants; sunscreens; exPosures fragrances containing { 6-methylcou mari n, musk am brette, or sandalwood oil Pigmentation Minocycl ine, amiodarone, Variable Most appear on sun-exposed areas hydroxychloroquine, antiretroviral Bleomycin may cause flagellate therapy, bleomycin, gold salts pigmented macules on the back Zidovudine may cause pig mentatron or pigmented streaking of the fingernails Minocycline may cause hyperpigmentation on sun-exposed areas and on acne scars Fixed d rug Sulfonamides, NSAlDs, antiepileptic 1-2 wk after initial Pseudoephedrine-related reactions agents, tetracyclines exposure;24hfor may not pigment subsequent exposures Va scu liti NSAlDs, antibiotics, 1-3 wk, within 3 d of Levamisole is used to add bulk and hyd roch lorothiazide, fu rosem ide, rechallenge weight to cocaine; drug-induced minocycline, TNF inhibitors, vasculitis is often ANCA positive, with propylthiouracil, G M-CSF, levamisole both p- and c-ANCA patterns Stevens-Johnson Allopurinol aminopenicillins 1-3 wk after exposure Systemic manifestations are common syndrome/toxic (ampicillin, amoxicillin), epidermal necrolysis carbamazepine, lamotrigine, t nevirapine, phenytoin, sulfamethoxazole-trimethoprim, sulfasalazine

lmmunologic Penicillin, anesthetic agents, ACE Minutes to a few hours Most chronic urticaria cases are not inhibitors drug related, but aspirin may cause or exacerbate chronic cases of urticaria Nonimmunologic Vancomycin, rifampicin, acetylcysteine, Minutes to a few hours Red person syndrome is related to the opioids, radiocontrast agents infusion rate of vancomycin Photosensitivity Phototoxic Voriconazole, demeclorycline, Hours Voriconazole phototoxicity can cause doxycycline, NSAlDs, skin cancer within a few years of fluoroquinolones, amiodarone treatment May result in fingernail shedding Photoallergic Hydrochlorothiazide, sulfonamide 7-1 0 d for first exposure; May persist after ultraviolet light antibiotics; sulfonylureas; tricyclic hours for subsequent exposure (fall or winter months) antidepressants; sunscreens; exPosures fragrances containing { 6-methylcou mari n, musk am brette, or sandalwood oil Pigmentation Minocycl ine, amiodarone, Variable Most appear on sun-exposed areas hydroxychloroquine, antiretroviral Bleomycin may cause flagellate therapy, bleomycin, gold salts pigmented macules on the back Zidovudine may cause pig mentatron or pigmented streaking of the fingernails Minocycline may cause hyperpigmentation on sun-exposed areas and on acne scars Fixed d rug Sulfonamides, NSAlDs, antiepileptic 1-2 wk after initial Pseudoephedrine-related reactions agents, tetracyclines exposure;24hfor may not pigment subsequent exposures Va scu liti NSAlDs, antibiotics, 1-3 wk, within 3 d of Levamisole is used to add bulk and hyd roch lorothiazide, fu rosem ide, rechallenge weight to cocaine; drug-induced minocycline, TNF inhibitors, vasculitis is often ANCA positive, with propylthiouracil, G M-CSF, levamisole both p- and c-ANCA patterns Stevens-Johnson Allopurinol aminopenicillins 1-3 wk after exposure Systemic manifestations are common syndrome/toxic (ampicillin, amoxicillin), epidermal necrolysis carbamazepine, lamotrigine, t nevirapine, phenytoin, sulfamethoxazole-trimethoprim, sulfasalazine GM-CSF = granulocyte-macrophage colony-stimulating factor; TNF = tumor necrosis factor.

lmmunologic Penicillin, anesthetic agents, ACE Minutes to a few hours Most chronic urticaria cases are not inhibitors drug related, but aspirin may cause or exacerbate chronic cases of urticaria Nonimmunologic Vancomycin, rifampicin, acetylcysteine, Minutes to a few hours Red person syndrome is related to the opioids, radiocontrast agents infusion rate of vancomycin Photosensitivity Phototoxic Voriconazole, demeclorycline, Hours Voriconazole phototoxicity can cause doxycycline, NSAlDs, skin cancer within a few years of fluoroquinolones, amiodarone treatment May result in fingernail shedding Photoallergic Hydrochlorothiazide, sulfonamide 7-1 0 d for first exposure; May persist after ultraviolet light antibiotics; sulfonylureas; tricyclic hours for subsequent exposure (fall or winter months) antidepressants; sunscreens; exPosures fragrances containing { 6-methylcou mari n, musk am brette, or sandalwood oil Pigmentation Minocycl ine, amiodarone, Variable Most appear on sun-exposed areas hydroxychloroquine, antiretroviral Bleomycin may cause flagellate therapy, bleomycin, gold salts pigmented macules on the back Zidovudine may cause pig mentatron or pigmented streaking of the fingernails Minocycline may cause hyperpigmentation on sun-exposed areas and on acne scars Fixed d rug Sulfonamides, NSAlDs, antiepileptic 1-2 wk after initial Pseudoephedrine-related reactions agents, tetracyclines exposure;24hfor may not pigment subsequent exposures Va scu liti NSAlDs, antibiotics, 1-3 wk, within 3 d of Levamisole is used to add bulk and hyd roch lorothiazide, fu rosem ide, rechallenge weight to cocaine; drug-induced minocycline, TNF inhibitors, vasculitis is often ANCA positive, with propylthiouracil, G M-CSF, levamisole both p- and c-ANCA patterns Stevens-Johnson Allopurinol aminopenicillins 1-3 wk after exposure Systemic manifestations are common syndrome/toxic (ampicillin, amoxicillin), epidermal necrolysis carbamazepine, lamotrigine, t nevirapine, phenytoin, sulfamethoxazole-trimethoprim, sulfasalazine GM-CSF = granulocyte-macrophage colony-stimulating factor; TNF = tumor necrosis factor. begin with fever and flulike symptoms, quickly followed by lymphocytosis and elevated aminotransferase levels. burning skin pain and rash. Patients typically develop a mor Hypotension, shock, and multisystem organ damage are pos billiform exanthem that starts on the face and upper trunk sible. Death occurs in approximately 10'1, of patients with and spreads distally (Figure 47). Eventually the patient devel- DIHS. Immediate discontinuation of the causative agent is ops striking facial edema and redness, a hallmark of DIHS. mandatory and systemic glucocorticoids tapered over weeks Oral mucosal involvement is common but is less severe than to months can be helpful. DIHS caused by an aromatic antiepi Stevens Johnson syndrome/toxic epidermal necrolysis or ery leptic agent can also pose a serious threat owing to cross- thema multiforme. reaction with other aromatic antiepileptics. For example, if Systemic involvement is necessary for the diagnosis of phen).toin causes DIHS, the patient may experience cross- DIHS and most commonly includes eosinophilia or an atypical reaction with phenobarbital or carbamazepine.

begin with fever and flulike symptoms, quickly followed by lymphocytosis and elevated aminotransferase levels. burning skin pain and rash. Patients typically develop a mor Hypotension, shock, and multisystem organ damage are pos billiform exanthem that starts on the face and upper trunk sible. Death occurs in approximately 10'1, of patients with and spreads distally (Figure 47). Eventually the patient devel- DIHS. Immediate discontinuation of the causative agent is ops striking facial edema and redness, a hallmark of DIHS. mandatory and systemic glucocorticoids tapered over weeks Oral mucosal involvement is common but is less severe than to months can be helpful. DIHS caused by an aromatic antiepi Stevens Johnson syndrome/toxic epidermal necrolysis or ery leptic agent can also pose a serious threat owing to cross- thema multiforme. reaction with other aromatic antiepileptics. For example, if Systemic involvement is necessary for the diagnosis of phen).toin causes DIHS, the patient may experience cross- DIHS and most commonly includes eosinophilia or an atypical reaction with phenobarbital or carbamazepine. 92

Dermatologic Disorders TABTE 70. Medications Most Commonly Causing Drug-lnduced Hypersensitivity Syndrome Abacavir (HLA-B 5701 allele testing recommended before use) Allopurinol (HLA-B*5801 allele testing in patients of Korean, Han Chinese, Thai, and African descent recommended before use) Aromatic antiepileptic drugs (carbamazepine, oxcarbazepine, phenytoin, and phenobarbital) (HLA-B*1 502 allele testing recommended before carbamazepine and oxcarbamazepine use in patients ofAsian descent) Minocycline Proton pump inhibitors Sulfasalazine FIGU RE 4 5. A morbilliform drug eruption consists of symmetrically arranged erythematous macules and papules, some discrete and others confluent. tl G U RE 47. Generalized morbilliform eruption in a patient with drug-induced hypersensitivity syndrome (also refened to as drug reaction with eosinophilia and systemic symptoms IDRESS] syndrome). Vesicles, blisters, and pustules may also be seen.

tl G U RE 47. Generalized morbilliform eruption in a patient with drug-induced hypersensitivity syndrome (also refened to as drug reaction with eosinophilia and systemic symptoms IDRESS] syndrome). Vesicles, blisters, and pustules may also be seen. Hypersensitivity Vascu litis Drugs are the most common cause of hypersensitivity vasculi- tis, a small-vessel vasculitis, which is discussed in MKSAP 19 Rheumatologz.

Hypersensitivity Vascu litis Drugs are the most common cause of hypersensitivity vasculi- tis, a small-vessel vasculitis, which is discussed in MKSAP 19 Rheumatologz. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis Stevens-Johnson syndrome (SJS) and toxic epidermal necroly- sis (TEN) are a spectrum of severe mucocutaneous reactions defined by the extent of affected body surface area (BSA) involved with immune-mediated cutaneous necrosis. They are the most severe and deadly of the cutaneous adverse drug reactions. SJS refers to patients with less than 10% BSA affected, and TEN refers to those with greater than 30% BSA affected. The term SJS/TEN overlap refers to patients with 10o/o to 30% BSA affected. Key features include full-thickness epi- dermal necrosis with involvement of mucous membranes F I G UR E 4 5. (A) A fixed drug reaction causing an intense, pink, oval plaque (Figure 48). Essentially all cases of TEN are temporally corre- with a dusky, vesiculated center. The patch will gradually fade, leaving lated with medications (see Table 70), whereas approximately postinflammatory hyperpigmentation (B) Fixed drug eruption on the posterior 25"/. of SJS cases are caused by infection or vaccination. HIV neck, appearing as a pink plaque with a dusky, edematous center. lnflammation appears starkly pink in lighter skin tones, and more subtly as violet to brown- infection, kidney disease, and uncontrolled autoimmune dis purple in darker skin tones. ease also contribute to increased risk.

Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis Stevens-Johnson syndrome (SJS) and toxic epidermal necroly- sis (TEN) are a spectrum of severe mucocutaneous reactions defined by the extent of affected body surface area (BSA) involved with immune-mediated cutaneous necrosis. They are the most severe and deadly of the cutaneous adverse drug reactions. SJS refers to patients with less than 10% BSA affected, and TEN refers to those with greater than 30% BSA affected. The term SJS/TEN overlap refers to patients with 10o/o to 30% BSA affected. Key features include full-thickness epi- dermal necrosis with involvement of mucous membranes F I G UR E 4 5. (A) A fixed drug reaction causing an intense, pink, oval plaque (Figure 48). Essentially all cases of TEN are temporally corre- with a dusky, vesiculated center. The patch will gradually fade, leaving lated with medications (see Table 70), whereas approximately postinflammatory hyperpigmentation (B) Fixed drug eruption on the posterior 25"/. of SJS cases are caused by infection or vaccination. HIV neck, appearing as a pink plaque with a dusky, edematous center. lnflammation appears starkly pink in lighter skin tones, and more subtly as violet to brown- infection, kidney disease, and uncontrolled autoimmune dis purple in darker skin tones. ease also contribute to increased risk. 93

Dermatologic Disorders F I G UR E 4 9 . Edema and vesicles on the lower lip and with erosions and mucosal sloughing on the upper lip secondary to Stevens-Johnson syndrome.

Dermatologic Disorders F I G UR E 4 9 . Edema and vesicles on the lower lip and with erosions and mucosal sloughing on the upper lip secondary to Stevens-Johnson syndrome. FIGU RE 48. Ihis patient has toxic epidermal necrolysis. Skin findings may vary erythema multiforme. The presence of extensive epidermal and include flat, atypical, purpuric, targetoid lesions that coalesce into dusky, sloughing and a positive Nikolsky sign (gentle traction pres poorly demarcated, confluent patches or confluent tender erythema without sure on intact skin causes shearing of intact epidermis away identifiable individual lesions. The involved epidermis blisters and sloughs, as from the dermis resulting in an erosion) further differentiate seen here, leaving behind denuded dermis. SJS/TEN from erythema multiforme major (Table 71). Systemic manifestations are common in patients Symptoms usually begin within I to 3 weeks of expo- with SJS/TEN. All patients experience fever and malaise. sure to the inciting agent. Patients may notice fever, malaise, Lymphadenopathy, elevated aminotransferase levels, and and symptoms of upper respiratory infections followed by cytopenias are common. Pneumonitis, nephritis, hepatitis, skin pain, grittiness of the eyes, and odynophagia. Within and myocarditis may occur. Hypovolemia and electrolyte several days, patients develop red or purple dusky macules imbalances due to loss of the skin barrier are common. on the trunk that progress to vesicles, erosions, and ulcera The acute phase ofthe disease lasts I to 2 weeks, and skin tion. Painful erosions develop in the mouth, eyes, or genitals reepithelization may take 2 to 4 weeks. Mortality is high, with 5'u, in as many as 95% of patients. Erythema multiforme may to 10% of SJS cases being fatal and up to 33'1, of patients with TEN also present with mucosal ulceration, malaise, and vesicular dying of disease complications, such as secondary infection, skin eruption, and thus distinguishing these entities is criti transcutaneous fluid loss, or respiratory complications. Early cally important (see Erythema Multiforme). Erythema mul- identification and withdrawal of the causative medication tiforme most commonly involves the extremities, whereas improve outcomes. The SCORTEN scale is a validated severity-of- SJS and TEN develop on the trunk and face (Figure 49). illness tool for TEN and SJS that can be applied early in the course Patients with SJS/TEN may exhibit atypical targetoid mac- of the disease and directly correlates with mortality (Iable 72). ules demonstrating one or two colored rings; when pre- Treatment of SJSiTEN is highly controversial. Intravenous sent. lesions with three colored zones are characteristic of glucocorticoids or intravenous immune globulins are probably

FIGU RE 48. Ihis patient has toxic epidermal necrolysis. Skin findings may vary erythema multiforme. The presence of extensive epidermal and include flat, atypical, purpuric, targetoid lesions that coalesce into dusky, sloughing and a positive Nikolsky sign (gentle traction pres poorly demarcated, confluent patches or confluent tender erythema without sure on intact skin causes shearing of intact epidermis away identifiable individual lesions. The involved epidermis blisters and sloughs, as from the dermis resulting in an erosion) further differentiate seen here, leaving behind denuded dermis. SJS/TEN from erythema multiforme major (Table 71). Systemic manifestations are common in patients Symptoms usually begin within I to 3 weeks of expo- with SJS/TEN. All patients experience fever and malaise. sure to the inciting agent. Patients may notice fever, malaise, Lymphadenopathy, elevated aminotransferase levels, and and symptoms of upper respiratory infections followed by cytopenias are common. Pneumonitis, nephritis, hepatitis, skin pain, grittiness of the eyes, and odynophagia. Within and myocarditis may occur. Hypovolemia and electrolyte several days, patients develop red or purple dusky macules imbalances due to loss of the skin barrier are common. on the trunk that progress to vesicles, erosions, and ulcera The acute phase ofthe disease lasts I to 2 weeks, and skin tion. Painful erosions develop in the mouth, eyes, or genitals reepithelization may take 2 to 4 weeks. Mortality is high, with 5'u, in as many as 95% of patients. Erythema multiforme may to 10% of SJS cases being fatal and up to 33'1, of patients with TEN also present with mucosal ulceration, malaise, and vesicular dying of disease complications, such as secondary infection, skin eruption, and thus distinguishing these entities is criti transcutaneous fluid loss, or respiratory complications. Early cally important (see Erythema Multiforme). Erythema mul- identification and withdrawal of the causative medication tiforme most commonly involves the extremities, whereas improve outcomes. The SCORTEN scale is a validated severity-of- SJS and TEN develop on the trunk and face (Figure 49). illness tool for TEN and SJS that can be applied early in the course Patients with SJS/TEN may exhibit atypical targetoid mac- of the disease and directly correlates with mortality (Iable 72). ules demonstrating one or two colored rings; when pre- Treatment of SJSiTEN is highly controversial. Intravenous sent. lesions with three colored zones are characteristic of glucocorticoids or intravenous immune globulins are probably TiaBLE 7''? . Comparison of Erythema Multiforme, Stevens-Johnson Syndrome, and Toxic Epidermal Necrolysis Characteristic Eryrthema Multiforme Stevens-JohnsonSyndrome ToxicEpidermalNecrolysis Morphology Typical three-zoned target (dark Atypical targets and confluent Extensive, confluent erythema central area or blister; a red erythema with sloughing with sloughing inflammatory ring; a ring of pale edema); lesions with onlytwo rings are common as well Distribution Favors extremities Trunk and extremities; <10% Trunk and extremities; >30% body surface area involvement" body surface area involvement" Mucosal disease One or two sites Two or more sites Two or more sites (oral, eye, genitourinary)

TiaBLE 7''? . Comparison of Erythema Multiforme, Stevens-Johnson Syndrome, and Toxic Epidermal Necrolysis Characteristic Eryrthema Multiforme Stevens-JohnsonSyndrome ToxicEpidermalNecrolysis Morphology Typical three-zoned target (dark Atypical targets and confluent Extensive, confluent erythema central area or blister; a red erythema with sloughing with sloughing inflammatory ring; a ring of pale edema); lesions with onlytwo rings are common as well Distribution Favors extremities Trunk and extremities; <10% Trunk and extremities; >30% body surface area involvement" body surface area involvement" Mucosal disease One or two sites Two or more sites Two or more sites (oral, eye, genitourinary) Constitutional symptoms + +-+/+++ # Etiology lnfection (%) 50 26 6 Drugs implicated (0,6) 50 74 94 Mortality rate (%) 0 5-13 25-39 ustevens'Johnson syndrome/toxic epidermal necrolysis overlap is defined as 1 OZo to 3Ool" body surface area involvement, with the remaining features the same as those of Stevens-Johnson syndrome. 94

Dermatologic Disorders TABLE 72. SCORTENToolValues Eighty percent of cases are caused by antibiotics. Most cases are self limited and resolve within 2 weeks. Treatment consists SCORTEN Features' Values Associated With Poor Prognosis ofcessation ofthe causative agent and supportive carei topical and systemic glucocorticoids may be helpful for symptomatic Age ,40 y relief. The condition carries a mortality rate of less than 5'/n. Malignancy Present Heart rate >120/min r(rY P0rilTs Body surface area >10"/" . Exanthematous, or morbilliform, drug eruptions are the most common drug reactions; treatment involves cessa- Plasma glucose >252 mg/dL(1 3.98 mmol/L) tion of the causative agent, and the use of systemic and/ Blood urea nitrogen >28 mg/dL(9.99 mmol/L) or topical glucocorticoids and oral H, antihistamines. Bicarbonate <20 mEq/L(20 mmol/L) o Fixed drug reactions recur at the same site or sites with SCORTEN = SCORe of Toxic Epidermal Necrosis. each exposure and consist of pink-to-purple circinate "The likelihood of death increases with each feature. Five or more features is plaques with central dusky discoloration or vesicula- associated wrth a 90o/o mortalrty rate. tion, most commonly on the lips, face, fingers, and Data from Bastuji Garin S, Fouchard N, Bertocchi M, et al. SCORTEN: a severity of illness score for toxic epidermal necrolysis. J lnvest Dermatol. 2000;1 1 5:1 49 53. genitals. lPlV lD: 1 09512291 d oi:101A46/j.1523 17 47 .2000.00061 .\ r Drug-induced hypersensitivity syndrome (also known HVC as drug reaction with eosinophilia and systemic symp- the most commonly used treatments, but neither is supported toms [DRESS]) develops 2 to 6 weeks after drug expo- by strong evidence. Supportive care in an ICU with experi sure; discontinuation of the causative drug is the first enced nursing staff is critical for wound care, and many step in treatment. patients are transferred to a burn center. A low threshold is . Key features of Stevens-Johnson syndrome and toxic recommended for performing cultures and initiation of epidermal necrolysis include full-thickness epidermal empiric antibiotics; however, use of prophylactic antibiotics is necrosis with involvement of mucous membranes, not recommended. Ophthalmologic and urologic consulta which is potentially fatal owing to secondary infection, tions are mandatory if ocular or genital involvement is present transcutaneous fluid loss, or respiratory complications. because destructive scarring may occur in these systems.

TABLE 72. SCORTENToolValues Eighty percent of cases are caused by antibiotics. Most cases are self limited and resolve within 2 weeks. Treatment consists SCORTEN Features' Values Associated With Poor Prognosis ofcessation ofthe causative agent and supportive carei topical and systemic glucocorticoids may be helpful for symptomatic Age ,40 y relief. The condition carries a mortality rate of less than 5'/n. Malignancy Present Heart rate >120/min r(rY P0rilTs Body surface area >10"/" . Exanthematous, or morbilliform, drug eruptions are the most common drug reactions; treatment involves cessa- Plasma glucose >252 mg/dL(1 3.98 mmol/L) tion of the causative agent, and the use of systemic and/ Blood urea nitrogen >28 mg/dL(9.99 mmol/L) or topical glucocorticoids and oral H, antihistamines. Bicarbonate <20 mEq/L(20 mmol/L) o Fixed drug reactions recur at the same site or sites with SCORTEN = SCORe of Toxic Epidermal Necrosis. each exposure and consist of pink-to-purple circinate "The likelihood of death increases with each feature. Five or more features is plaques with central dusky discoloration or vesicula- associated wrth a 90o/o mortalrty rate. tion, most commonly on the lips, face, fingers, and Data from Bastuji Garin S, Fouchard N, Bertocchi M, et al. SCORTEN: a severity of illness score for toxic epidermal necrolysis. J lnvest Dermatol. 2000;1 1 5:1 49 53. genitals. lPlV lD: 1 09512291 d oi:101A46/j.1523 17 47 .2000.00061 .\ r Drug-induced hypersensitivity syndrome (also known HVC as drug reaction with eosinophilia and systemic symp- the most commonly used treatments, but neither is supported toms [DRESS]) develops 2 to 6 weeks after drug expo- by strong evidence. Supportive care in an ICU with experi sure; discontinuation of the causative drug is the first enced nursing staff is critical for wound care, and many step in treatment. patients are transferred to a burn center. A low threshold is . Key features of Stevens-Johnson syndrome and toxic recommended for performing cultures and initiation of epidermal necrolysis include full-thickness epidermal empiric antibiotics; however, use of prophylactic antibiotics is necrosis with involvement of mucous membranes, not recommended. Ophthalmologic and urologic consulta which is potentially fatal owing to secondary infection, tions are mandatory if ocular or genital involvement is present transcutaneous fluid loss, or respiratory complications. because destructive scarring may occur in these systems. Acute Generalized Exanthematous Pustulosis Pruritus Acute generalized exanthematous pustulosis is the rapid onset Pruritus is one of the most common symptoms in dermatol of pustular rash after a medication exposure in a patient with ogr. lt is commonly associated with a variety of skin diseases, out a history of pustular psoriasis. Onset occurs within several yet it may occur independent of skin pathologz. Inflammatory days of exposure. Patients present with fever and erythema skin diseases are often associated with pruritus, including and eventually develop myriad dense nonfolliculocentric pus atopic dermatitis, contact dermatitis, and urticaria. In elderly tules, primarily in skin folds and on the trunk (Figure 50). persons, xerotic, or dry skin, is a common cause of pmritus. When pruritus occurs in the absence of skin findings, medications and systemic diseases should be considered. Common medications that cause pruritus include opioids, calcium channel blockers, hydrochlorothiazide, and NSAIDs (Table 73). A variety of systemic conditions are associated with pruritus. Uremic pruritus is common in patients with advanced kidney disease. Pruritus can also be associated with

Acute Generalized Exanthematous Pustulosis Pruritus Acute generalized exanthematous pustulosis is the rapid onset Pruritus is one of the most common symptoms in dermatol of pustular rash after a medication exposure in a patient with ogr. lt is commonly associated with a variety of skin diseases, out a history of pustular psoriasis. Onset occurs within several yet it may occur independent of skin pathologz. Inflammatory days of exposure. Patients present with fever and erythema skin diseases are often associated with pruritus, including and eventually develop myriad dense nonfolliculocentric pus atopic dermatitis, contact dermatitis, and urticaria. In elderly tules, primarily in skin folds and on the trunk (Figure 50). persons, xerotic, or dry skin, is a common cause of pmritus. When pruritus occurs in the absence of skin findings, medications and systemic diseases should be considered. Common medications that cause pruritus include opioids, calcium channel blockers, hydrochlorothiazide, and NSAIDs (Table 73). A variety of systemic conditions are associated with pruritus. Uremic pruritus is common in patients with advanced kidney disease. Pruritus can also be associated with TABLE 73. Common MedicationsThat May Cause Pruritus Calcium channel blockers Hydrochlorothiazide Opioids/opiates NSAIDs ACE inhibitors Anticoagula nts Antibiotics (trimethoprim-sulfamethoxazole) FIGU RE 5 0. Pinpoint puslules on a background of erythema in a patient with Selective serotonin reuptake inhibitors acute generalized exanthematous pustulosis.

TABLE 73. Common MedicationsThat May Cause Pruritus Calcium channel blockers Hydrochlorothiazide Opioids/opiates NSAIDs ACE inhibitors Anticoagula nts Antibiotics (trimethoprim-sulfamethoxazole) FIGU RE 5 0. Pinpoint puslules on a background of erythema in a patient with Selective serotonin reuptake inhibitors acute generalized exanthematous pustulosis. 95

Dermatologic Disorders q." ra* F IG U R E 5 1 . Linear excoriations resulting irom pruritis in a patient with cholestatic liver disease. t I G U R E 5 3. Patients with psychogenic itch often report nonhealing sores, such { as those seen on this patient's arm. The lesions often have a linear or irregular shape from repeated manipulation. Scars lrom previous episodes are often seen among the active lesions.

t I G U R E 5 3. Patients with psychogenic itch often report nonhealing sores, such { as those seen on this patient's arm. The lesions often have a linear or irregular shape from repeated manipulation. Scars lrom previous episodes are often seen among the active lesions. Treatment of pruritus is directed at the underlying cause. The treatment of inflammatory skin conditions with topical glucocorticoids and emollients can help alleviate pruritus. Topical medications containing menthol can also be helpful. First-generation oral antihistamines may be helpful for noc -"--:Frft turnal pruritus. For older patients with xerotic skin, dry skin t I G U R E 5 2. A localized and persistent area of pruritus without associated care should be provided. primary skin lesions, usually on the back or forearms, suggests neuropathic itch. The area of hyperpigmentation seen on this patient is secondary to chronic scratching. rEY ?Orttt o When pruritus occurs in the absence of skin findings, cholestatic hepatobiliary diseases (Figure 51) as well as cirrho medications and a variety of systemic causes, including sis in the absence of cholestasis. Thyroid disease and poly- kidney or liver disease, thyroid disease, or HIV infection, cy,themia vera might present with itching, the latter often should be considered. occurring aflter a warm bath or shower. Generalized pruritus o Reactions to common medications, such as opioids, may be the presenting symptom in malignancies, such as calcium channel blockers, hydrochlorothiazide, and Hodgkin lymphoma. Certain infections, such as HIV may also NSAIDs, are frequent causes of pmritus. present with generalized itching. o Topical glucocorticoids and emollients are appropriate Neuropathic pruritus describes the itch that is caused by dysfunction of a peripheral or central nerve due to surgery treatment for pruritus associated with inllammatory trauma, neuropathy, or infection (postherpetic neuralgia). skin conditions. Neuropathic itch is often localized; examples include the fore- arm (brachioradial pruritus) and mid- to upper back (notalgia paresthetica) (Figure 52). Various psychiatric conditions can Acneiform Eruptions also manifest as itching (psychogenic itch) (Figure 53). Acne Vulgaris A complete blood count, thyroid function studies, kidney Acne vulgaris is a chronic inflammatory condition affecting function studies, liver chemistry tests, an HIV test, and chest the pilosebaceous unit (hair follicle and sebaceous gland). radiography are an appropriate initial evaluation. A review of Although most common during adolescence, acne can affect the patient's medications should also be performed. patients at any age. The clinical features of acne are open

Treatment of pruritus is directed at the underlying cause. The treatment of inflammatory skin conditions with topical glucocorticoids and emollients can help alleviate pruritus. Topical medications containing menthol can also be helpful. First-generation oral antihistamines may be helpful for noc -"--:Frft turnal pruritus. For older patients with xerotic skin, dry skin t I G U R E 5 2. A localized and persistent area of pruritus without associated care should be provided. primary skin lesions, usually on the back or forearms, suggests neuropathic itch. The area of hyperpigmentation seen on this patient is secondary to chronic scratching. rEY ?Orttt o When pruritus occurs in the absence of skin findings, cholestatic hepatobiliary diseases (Figure 51) as well as cirrho medications and a variety of systemic causes, including sis in the absence of cholestasis. Thyroid disease and poly- kidney or liver disease, thyroid disease, or HIV infection, cy,themia vera might present with itching, the latter often should be considered. occurring aflter a warm bath or shower. Generalized pruritus o Reactions to common medications, such as opioids, may be the presenting symptom in malignancies, such as calcium channel blockers, hydrochlorothiazide, and Hodgkin lymphoma. Certain infections, such as HIV may also NSAIDs, are frequent causes of pmritus. present with generalized itching. o Topical glucocorticoids and emollients are appropriate Neuropathic pruritus describes the itch that is caused by dysfunction of a peripheral or central nerve due to surgery treatment for pruritus associated with inllammatory trauma, neuropathy, or infection (postherpetic neuralgia). skin conditions. Neuropathic itch is often localized; examples include the fore- arm (brachioradial pruritus) and mid- to upper back (notalgia paresthetica) (Figure 52). Various psychiatric conditions can Acneiform Eruptions also manifest as itching (psychogenic itch) (Figure 53). Acne Vulgaris A complete blood count, thyroid function studies, kidney Acne vulgaris is a chronic inflammatory condition affecting function studies, liver chemistry tests, an HIV test, and chest the pilosebaceous unit (hair follicle and sebaceous gland). radiography are an appropriate initial evaluation. A review of Although most common during adolescence, acne can affect the patient's medications should also be performed. patients at any age. The clinical features of acne are open 96

Dermatologic Disorders comedones (blackheads); closed comedones (whiteheads); TABLE 74. Types of Acneiform Eruptions inflammatory papules and pustules; and nodulocystic lesions Acneiform Distinguishing Characteristics on the face, neck, chest, shoulders, and back (Figure 54 and Eruption Frgure 55,. Perioral/ Papules and pustules around mouth, Acneiform lesions are common, and the differential diag- periorificial eyelids, or nose; more common in nosis is broad. Variations in distribution and primary lesions dermatitis women; topical glucocorticoids may be may provide clues to help diflerentiate acne vulgaris from associated in some cases

comedones (blackheads); closed comedones (whiteheads); TABLE 74. Types of Acneiform Eruptions inflammatory papules and pustules; and nodulocystic lesions Acneiform Distinguishing Characteristics on the face, neck, chest, shoulders, and back (Figure 54 and Eruption Frgure 55,. Perioral/ Papules and pustules around mouth, Acneiform lesions are common, and the differential diag- periorificial eyelids, or nose; more common in nosis is broad. Variations in distribution and primary lesions dermatitis women; topical glucocorticoids may be may provide clues to help diflerentiate acne vulgaris from associated in some cases other diagnoses (Table 74). Finally, onset of acne combined Rosacea Flushing, telangiectasias; lack of with other signs of hyperandrogenism, such as hirsutism and comedones; pustules common on nose, cheeks, forehead, and chin oligomenorrhea, warrant consideration of polycystic ovary Folliculitis Follicular-based papules and pustules; syndrome, congenital adrenal hyperplasia, or an underlying often on the scalp or trunk; most adrenal or ovarian tumor. commonly caused by Staphylococcus The pathogenesis is attributed to abnormal keratinization aureus within the hair follicle, excess sebum production (stimulated Drug induced Monomorphic pustules and papules; by androgens), colonization of the follicle by Cutibacterium common inciting medications include glucocorticoids, lithium, anticonvulsants, ocnes (formerly Propionibacterium acnes), and the release of and epidermal growth factor receptor inhibitors Chloracne Appears in the scrotal region and the postauricular scalp; history of exposure to halogenated aromatic compounds (dioxin) Pseudofollicu litis Common in the beard area; skin-colored barbae or erythematous papules at hair-bearing sites; more common in Black men

other diagnoses (Table 74). Finally, onset of acne combined Rosacea Flushing, telangiectasias; lack of with other signs of hyperandrogenism, such as hirsutism and comedones; pustules common on nose, cheeks, forehead, and chin oligomenorrhea, warrant consideration of polycystic ovary Folliculitis Follicular-based papules and pustules; syndrome, congenital adrenal hyperplasia, or an underlying often on the scalp or trunk; most adrenal or ovarian tumor. commonly caused by Staphylococcus The pathogenesis is attributed to abnormal keratinization aureus within the hair follicle, excess sebum production (stimulated Drug induced Monomorphic pustules and papules; by androgens), colonization of the follicle by Cutibacterium common inciting medications include glucocorticoids, lithium, anticonvulsants, ocnes (formerly Propionibacterium acnes), and the release of and epidermal growth factor receptor inhibitors Chloracne Appears in the scrotal region and the postauricular scalp; history of exposure to halogenated aromatic compounds (dioxin) Pseudofollicu litis Common in the beard area; skin-colored barbae or erythematous papules at hair-bearing sites; more common in Black men intlammatory cytokines. Treatments are directed at all four mechanisms (Figure 56). No universally accepted schema exists, but a common grading system is to classi$z acne as mild, moderate, and severe. Mild acne consists of primarily comedones with few inflammatory papules and no nodules or cysts. Moderate acne involves several comedones and inflammatory papules; a few nodules may be present as well. Severe acne is characterized by large lesion counts involving comedones and inflammatory pustules along with several cysts. Topical retinoids (tretinoin primarily, but also adapalene tl GU RE 54. Acnevulgaris. Note the conspicuous papules and pustules (<5 mm), large open comedones on the nose, and one nodule (5 mm) at the lateral eyebrow and tazarotene) are first line treatments for all types of acne area (arrow\. because they are effective for both comedonal and inflamma- tory acne. Retinoids help normalize the keratinization of the hair follicle and are comedolytic, thus reducing follicular plugging. They also decrease inflammatory cytokines that are activated by C. ccnes and reduce postinflammatory hyperpig- mentation. Topical retinoids may cause erythema, burning, and dryness. A11 topical retinoids are contraindicated in pregnancy. Topical antibiotics, such as erythromycin or clindamy cin, are helpful in inflammatory acne because they target C. ocnes and have anti-inflammatory effects. Clindamycin, azelaic acid, and erythromycin are the only acne treat rf ments that are demonstrated to be safe in pregnancy. Because of increased antibiotic resistance, topical antibiot- ics should not be used as monotherapy and should be com bined with topical benzoyl peroxide in treatment for mild, tIGURE 55. Extensiveacne involvementof the upperand mid-back,with moderate, or severe acne. Topical benzoyl peroxide has papules, pustules, nodules, granulation tissue, postinflammatory erythema, bactericidal properties and is not known to promote the hyperpigmentation, and scaning. development of resistant bacteria. Benzoyl peroxide may

intlammatory cytokines. Treatments are directed at all four mechanisms (Figure 56). No universally accepted schema exists, but a common grading system is to classi$z acne as mild, moderate, and severe. Mild acne consists of primarily comedones with few inflammatory papules and no nodules or cysts. Moderate acne involves several comedones and inflammatory papules; a few nodules may be present as well. Severe acne is characterized by large lesion counts involving comedones and inflammatory pustules along with several cysts. Topical retinoids (tretinoin primarily, but also adapalene tl GU RE 54. Acnevulgaris. Note the conspicuous papules and pustules (<5 mm), large open comedones on the nose, and one nodule (5 mm) at the lateral eyebrow and tazarotene) are first line treatments for all types of acne area (arrow\. because they are effective for both comedonal and inflamma- tory acne. Retinoids help normalize the keratinization of the hair follicle and are comedolytic, thus reducing follicular plugging. They also decrease inflammatory cytokines that are activated by C. ccnes and reduce postinflammatory hyperpig- mentation. Topical retinoids may cause erythema, burning, and dryness. A11 topical retinoids are contraindicated in pregnancy. Topical antibiotics, such as erythromycin or clindamy cin, are helpful in inflammatory acne because they target C. ocnes and have anti-inflammatory effects. Clindamycin, azelaic acid, and erythromycin are the only acne treat rf ments that are demonstrated to be safe in pregnancy. Because of increased antibiotic resistance, topical antibiot- ics should not be used as monotherapy and should be com bined with topical benzoyl peroxide in treatment for mild, tIGURE 55. Extensiveacne involvementof the upperand mid-back,with moderate, or severe acne. Topical benzoyl peroxide has papules, pustules, nodules, granulation tissue, postinflammatory erythema, bactericidal properties and is not known to promote the hyperpigmentation, and scaning. development of resistant bacteria. Benzoyl peroxide may 97

Dermatologic Disorders FIRST LINE SECOND LINE BP or topical retinoid Add topical retinoid or BP (ii not on already) -oR- -oR- Topical combination therapf Mild acne Consider alternate retinoid BP + antibiotic or -oR- Retinoid + BP or Consider topical dapsone Retinoid + BP + antibiotic Topical combination therapf Consider alternate combination therapy BP + antibiotic or -oR- Retinoid + BP or Consider change in oral antibiotic Retinoid + BP + antibiotic -oR- Moderate acne -oR- Add combined oral contraceptive or Oral antibiotic + topical retinoid + BP oral spironolactone (females) -oR- -oR- Oral antibiotic + topical retinoid + BP + Consider oral isotretinoin topical antibiotic

Topical combination therapf Consider alternate combination therapy BP + antibiotic or -oR- Retinoid + BP or Consider change in oral antibiotic Retinoid + BP + antibiotic -oR- Moderate acne -oR- Add combined oral contraceptive or Oral antibiotic + topical retinoid + BP oral spironolactone (females) -oR- -oR- Oral antibiotic + topical retinoid + BP + Consider oral isotretinoin topical antibiotic Consider change in oral antibiotic Oral antibiotic + topical combination therapf -oR- BP + antibiotic or Add combined oral contraceptive or Severe acne Retinoid + BP + antibiotic oral spironolactone (females) -oR- -oR- Oral isotretinoin Consider oral isotretinoin FIGU RE 5 6. Treatment algorithm for the management of acne vulgaris in adolescents and young adults. BP= benzoyl peroxide. 'Thedrug may be prescribed asafix€d combination productorasa separate component.

Consider change in oral antibiotic Oral antibiotic + topical combination therapf -oR- BP + antibiotic or Add combined oral contraceptive or Severe acne Retinoid + BP + antibiotic oral spironolactone (females) -oR- -oR- Oral isotretinoin Consider oral isotretinoin FIGU RE 5 6. Treatment algorithm for the management of acne vulgaris in adolescents and young adults. BP= benzoyl peroxide. 'Thedrug may be prescribed asafix€d combination productorasa separate component. cause irritation and allergic contact dermatitis in rare Rosacea patients. Rosacea is an inflammatory condition appearing in the third Oral antibiotics are frequently used for moderate to to sixth decades of life. Rosacea is most common among severe inflammatory acne and acne that is resistant to topi patients of Irish and English descent who have Iight cal treatment alone. Oral antibiotics inhibit C. ccnes and complexions. It is defined by chronic inflammation of the can also decrease inflammation. Tetracycline-based antibi- pilosebaceous units, with increased vascular reactivity. The otics are often used because they exhibit both of these pathogenesis is undetermined. There are a variety of clinical desirable properties. When possible, oral antibiotics should presentations of rosacea, including erythrotelangiectatic, be limited to 3 months to decrease the risk for antibiotic papulopustular, phymatous, and ocular rosacea. resistance. The papulopustular variant of rosacea can be confused In severe nodulocystic or recalcitrant acne, oral isotreti- with acne, but rosacea does not present with comedonal lesions noin should be considered. Owing to teratogenicity, isotreti- (Figure 57). Telangiectasias are seen in the erythrotelangiectatic noin prescribers must be enrolled in the FDA required regulatory program iPLEDGE. Adult acne is more common in women and is related to androgenic hormones. It typically presents along the jawline and often flares with the menstrual cycle. Although consid- ered second-line therapy, oral contraceptives or spironolac- tone (aldosterone receptor blocker with antiandrogen activity) can be added to other treatments in women with moderate to severe acne. Combined estrogen-progesterone oral contraceptives are effective for inflammatory acne in women and girls older than 14 years without evidence of hyperandrogenism. When counseling patients with acne, it is important to stress the importance of adherence to treatment and the time course for improvement, which is often several weeks to months. In addition to prescribed medications, only non- FIGU RE 57. Papulopustular rosacea causes erythema and pink papules of the comedogenic cosmetics and moisturizers should be used. convexities of the face, namely, the forehead, nose, cheeks, and chin.

cause irritation and allergic contact dermatitis in rare Rosacea patients. Rosacea is an inflammatory condition appearing in the third Oral antibiotics are frequently used for moderate to to sixth decades of life. Rosacea is most common among severe inflammatory acne and acne that is resistant to topi patients of Irish and English descent who have Iight cal treatment alone. Oral antibiotics inhibit C. ccnes and complexions. It is defined by chronic inflammation of the can also decrease inflammation. Tetracycline-based antibi- pilosebaceous units, with increased vascular reactivity. The otics are often used because they exhibit both of these pathogenesis is undetermined. There are a variety of clinical desirable properties. When possible, oral antibiotics should presentations of rosacea, including erythrotelangiectatic, be limited to 3 months to decrease the risk for antibiotic papulopustular, phymatous, and ocular rosacea. resistance. The papulopustular variant of rosacea can be confused In severe nodulocystic or recalcitrant acne, oral isotreti- with acne, but rosacea does not present with comedonal lesions noin should be considered. Owing to teratogenicity, isotreti- (Figure 57). Telangiectasias are seen in the erythrotelangiectatic noin prescribers must be enrolled in the FDA required regulatory program iPLEDGE. Adult acne is more common in women and is related to androgenic hormones. It typically presents along the jawline and often flares with the menstrual cycle. Although consid- ered second-line therapy, oral contraceptives or spironolac- tone (aldosterone receptor blocker with antiandrogen activity) can be added to other treatments in women with moderate to severe acne. Combined estrogen-progesterone oral contraceptives are effective for inflammatory acne in women and girls older than 14 years without evidence of hyperandrogenism. When counseling patients with acne, it is important to stress the importance of adherence to treatment and the time course for improvement, which is often several weeks to months. In addition to prescribed medications, only non- FIGU RE 57. Papulopustular rosacea causes erythema and pink papules of the comedogenic cosmetics and moisturizers should be used. convexities of the face, namely, the forehead, nose, cheeks, and chin. 98

t t Dermatologic Disorders I IL is{f;i-r :r!, Managementof Rosacea t h lnterventions Avoidance Sun protection (sunscreen or sun-protective t clothing) ( I Triggers: foods (spicy, warm), alcohol, warm environments L Topical Metronidazole, Q.7 5% or 1%

IL is{f;i-r :r!, Managementof Rosacea t h lnterventions Avoidance Sun protection (sunscreen or sun-protective t clothing) ( I Triggers: foods (spicy, warm), alcohol, warm environments L Topical Metronidazole, Q.7 5% or 1% t Sodium sulfacetamide/sulfur i Azelaic acid, 15%-20% I Calcineurin inhibitors (pimecrolimus, t tacrolimus) Permethrin t Systemic Tetracycline antibiotics (doxycycline, 40 mg) t Macrolide antibiotics (erythromyci n, azithromycin, clarithromycin) L Lasel li ght, and Lasers (PDL, Nd:YAG, CO2, and others) L surgica I lntense pulsed light

t Sodium sulfacetamide/sulfur i Azelaic acid, 15%-20% I Calcineurin inhibitors (pimecrolimus, t tacrolimus) Permethrin t Systemic Tetracycline antibiotics (doxycycline, 40 mg) t Macrolide antibiotics (erythromyci n, azithromycin, clarithromycin) L Lasel li ght, and Lasers (PDL, Nd:YAG, CO2, and others) L surgica I lntense pulsed light L Electrosurgery t I Nd:YAG = neodymium-doped yttrium aluminum garnet; PDL = pulsed dye laser i tIGURE 58. Erythrotelangiectaticrosaceapresentspredominantlywithpatches t of erythema and telangiectasia.

L Electrosurgery t I Nd:YAG = neodymium-doped yttrium aluminum garnet; PDL = pulsed dye laser i tIGURE 58. Erythrotelangiectaticrosaceapresentspredominantlywithpatches t of erythema and telangiectasia. topical metronidazole, an azelaic acid formulation, and topical L ivermectin. Topical glucocorticoids should be avoided. Oral L antibiotics, such as low-dose doxycycline, have been shown to help control inflammation in papulopustular and ocular rosa- t t cea; use oflow dosing decreases side effects and reduces the t prevalence ofbacterial resistance. Pulsed dye laser therapy is also effective for er5rthema and telangiectasias. For patients i with severe rhinophyma, surgery is the treatment of choice.

topical metronidazole, an azelaic acid formulation, and topical L ivermectin. Topical glucocorticoids should be avoided. Oral L antibiotics, such as low-dose doxycycline, have been shown to help control inflammation in papulopustular and ocular rosa- t t cea; use oflow dosing decreases side effects and reduces the t prevalence ofbacterial resistance. Pulsed dye laser therapy is also effective for er5rthema and telangiectasias. For patients i with severe rhinophyma, surgery is the treatment of choice. Hidradenitis Suppurativa Hidradenitis suppurativa is an inflammatory skin disorder of the apocrine glands. This disease occurs more commonly in women and typically begins after puberty. Areas frequently affected are intertriginous areas, such as the axillae, groin, and FIGU RE 5 9. Rhinophyma, characterized by hyperplastic sebaceous glands and underneath the breasts. The condition is characterized by enlargement of the nose, in a patient with long*tanding, uncontrolled rosacea. comedones, painful nodules, abscesses, draining sinuses, and scarring (Figure 6O). Risk factors include obesity, family his- subtype (Figure 58). Most patients also have frequent flushing in tory and cigarette smoking. For this reason, weight loss and response to triggers, such as stress, alcohol consumption, heat, smoking cessation are encouraged. and excessive sunlight. Ocular rosacea may present with Hidradenitis suppurativa is extremely difficult to treat. injected conjunctiva and "gritfy sensation" alone, or with asso- No single treatment has been effective for all patients; how- ciated skin findings. In phymatous rosacea, severe sebaceous eveq several are options available (Table 76). Decolonization hyperplasia and chronic inflammation lead to fibrous over- with dilute bleach baths and chlorhexidine washes may be $owth of the skin, creating a nodular, tumor-like deformation used in addition to topical clindamycin. Common systemic of the facial stmctures, most commonly the nose (rhinophyma) treatments include oral antibiotics, such as tetracyclines or (Figure 59). the combination of clindamycin and rifampin. Adalimumab, Treatment for rosacea is targeted toward the most promi- a tumor necrosis factor o inhibitor, is an FDA-approved nent signs and symptoms in each patient (Table 75). Treatment treatment for moderate to severe hidradenitis suppurativa. of erythrotelangiectatic rosacea focuses primarily on behavio- Moderate to severe disease is defined by the presence of ral modiflcations, such as avoidance of identified triggers of multiple recurring nodules or abscesses and scarring. flushing, proper use ofsun protection, and use ofgentle skin Surgery may be required for chronic hidradenitis suppu- cleansers. Treatment for papulopustular rosacea includes rativa. This may involve incision and drainage or deroofing of

Hidradenitis Suppurativa Hidradenitis suppurativa is an inflammatory skin disorder of the apocrine glands. This disease occurs more commonly in women and typically begins after puberty. Areas frequently affected are intertriginous areas, such as the axillae, groin, and FIGU RE 5 9. Rhinophyma, characterized by hyperplastic sebaceous glands and underneath the breasts. The condition is characterized by enlargement of the nose, in a patient with long*tanding, uncontrolled rosacea. comedones, painful nodules, abscesses, draining sinuses, and scarring (Figure 6O). Risk factors include obesity, family his- subtype (Figure 58). Most patients also have frequent flushing in tory and cigarette smoking. For this reason, weight loss and response to triggers, such as stress, alcohol consumption, heat, smoking cessation are encouraged. and excessive sunlight. Ocular rosacea may present with Hidradenitis suppurativa is extremely difficult to treat. injected conjunctiva and "gritfy sensation" alone, or with asso- No single treatment has been effective for all patients; how- ciated skin findings. In phymatous rosacea, severe sebaceous eveq several are options available (Table 76). Decolonization hyperplasia and chronic inflammation lead to fibrous over- with dilute bleach baths and chlorhexidine washes may be $owth of the skin, creating a nodular, tumor-like deformation used in addition to topical clindamycin. Common systemic of the facial stmctures, most commonly the nose (rhinophyma) treatments include oral antibiotics, such as tetracyclines or (Figure 59). the combination of clindamycin and rifampin. Adalimumab, Treatment for rosacea is targeted toward the most promi- a tumor necrosis factor o inhibitor, is an FDA-approved nent signs and symptoms in each patient (Table 75). Treatment treatment for moderate to severe hidradenitis suppurativa. of erythrotelangiectatic rosacea focuses primarily on behavio- Moderate to severe disease is defined by the presence of ral modiflcations, such as avoidance of identified triggers of multiple recurring nodules or abscesses and scarring. flushing, proper use ofsun protection, and use ofgentle skin Surgery may be required for chronic hidradenitis suppu- cleansers. Treatment for papulopustular rosacea includes rativa. This may involve incision and drainage or deroofing of 99

Dermatologi< Disorders f EY POIXTS (ominued) o Oral antibiotics are frequently used for moderate to severe inflammatory acne and acne resistant to topical treatment alone; courses of oral antibiotics should be limited to 3 months to decrease the risk for antibiotic resistance. . Isotretinoin is indicated for severe nodulocystic and recalcitrant acne; it is associated with severe birth defects and must be administered through the federal I

f EY POIXTS (ominued) o Oral antibiotics are frequently used for moderate to severe inflammatory acne and acne resistant to topical treatment alone; courses of oral antibiotics should be limited to 3 months to decrease the risk for antibiotic resistance. . Isotretinoin is indicated for severe nodulocystic and recalcitrant acne; it is associated with severe birth defects and must be administered through the federal I regulatory program iPLEDGE. . Treatment for papulopustular rosacea includes topical metronidazole, azelaic acid, and topical ivermectin; oral antibiotics, such as low-dose doxycycline, have been shown to help control inflammation in ocular and pap- ulopustular rosacea. t I G U R E 6 0. Hidradenitis suppurativa often presents with tender subcutaneous nod u les. The nodu les may sponta neously ru ptu re or coalesce, forming pai nful, deep . Hidradenitis suppurativa is an inflammatory skin disor- dermal abscesses. der of the apocrine glands that affects the intertriginous areas, such as the axillae, groin, and underneath the TABLE 76. Treatment Options for Hidradenitis breasts; clinical findings include comedones, painful Suppurativa nodules, abscesses, draining sinuses, and scarring. Disease Severity Treatment Options and Considerations Mild Pigment Disorders Predominantly Antibacterial washes, topical Vitiligo comedones, small antibiotics, analgesics, warm Vitiligo is a common acquired autoimmune condition charac papules or pustules, compresses solitary nodules terized by the loss of function or absence of melanocytes, Smoking cessation and weight resulting in patchy depigmentation oflthe skin. Affecting both lossu sexes equally, vitiligo can occur at any age and can have a sig Moderate nificant impact on quality of life. Clinically, it appears as com Multiple nodules, Oral antibiotics with antibacterial pletely depigmented, well-demarcated symmetric macules or abscesses, or cysts; washes and/or topical antibiotics, scarring analgesics, adalimumab, wide patches with no scale (Figure 61). Its onset is insidious and local excision asymptomatic, starting as smaller macules that gradually For women: oral contraceptives, enlarge. It tends to be more visible in persons with darker skin spironolactone types (Figure 62) or in sun exposed areas, as the surrounding Severe skin will become darker with sun exposure. The most Multiple nodules, sinus Referral to dermatologist or tracts; scarring surgeon for consideration of wide local excision, adalimumab, or clinical trial uRecommended for all disease severity categories.

regulatory program iPLEDGE. . Treatment for papulopustular rosacea includes topical metronidazole, azelaic acid, and topical ivermectin; oral antibiotics, such as low-dose doxycycline, have been shown to help control inflammation in ocular and pap- ulopustular rosacea. t I G U R E 6 0. Hidradenitis suppurativa often presents with tender subcutaneous nod u les. The nodu les may sponta neously ru ptu re or coalesce, forming pai nful, deep . Hidradenitis suppurativa is an inflammatory skin disor- dermal abscesses. der of the apocrine glands that affects the intertriginous areas, such as the axillae, groin, and underneath the TABLE 76. Treatment Options for Hidradenitis breasts; clinical findings include comedones, painful Suppurativa nodules, abscesses, draining sinuses, and scarring. Disease Severity Treatment Options and Considerations Mild Pigment Disorders Predominantly Antibacterial washes, topical Vitiligo comedones, small antibiotics, analgesics, warm Vitiligo is a common acquired autoimmune condition charac papules or pustules, compresses solitary nodules terized by the loss of function or absence of melanocytes, Smoking cessation and weight resulting in patchy depigmentation oflthe skin. Affecting both lossu sexes equally, vitiligo can occur at any age and can have a sig Moderate nificant impact on quality of life. Clinically, it appears as com Multiple nodules, Oral antibiotics with antibacterial pletely depigmented, well-demarcated symmetric macules or abscesses, or cysts; washes and/or topical antibiotics, scarring analgesics, adalimumab, wide patches with no scale (Figure 61). Its onset is insidious and local excision asymptomatic, starting as smaller macules that gradually For women: oral contraceptives, enlarge. It tends to be more visible in persons with darker skin spironolactone types (Figure 62) or in sun exposed areas, as the surrounding Severe skin will become darker with sun exposure. The most Multiple nodules, sinus Referral to dermatologist or tracts; scarring surgeon for consideration of wide local excision, adalimumab, or clinical trial uRecommended for all disease severity categories. painful abscesses and sinus tracts. Radical wide excision may also be used for refractory cases after other therapeutic options have been exhausted. Even after successful surgical treatment, recurrence is common.

regulatory program iPLEDGE. . Treatment for papulopustular rosacea includes topical metronidazole, azelaic acid, and topical ivermectin; oral antibiotics, such as low-dose doxycycline, have been shown to help control inflammation in ocular and pap- ulopustular rosacea. t I G U R E 6 0. Hidradenitis suppurativa often presents with tender subcutaneous nod u les. The nodu les may sponta neously ru ptu re or coalesce, forming pai nful, deep . Hidradenitis suppurativa is an inflammatory skin disor- dermal abscesses. der of the apocrine glands that affects the intertriginous areas, such as the axillae, groin, and underneath the TABLE 76. Treatment Options for Hidradenitis breasts; clinical findings include comedones, painful Suppurativa nodules, abscesses, draining sinuses, and scarring. Disease Severity Treatment Options and Considerations Mild Pigment Disorders Predominantly Antibacterial washes, topical Vitiligo comedones, small antibiotics, analgesics, warm Vitiligo is a common acquired autoimmune condition charac papules or pustules, compresses solitary nodules terized by the loss of function or absence of melanocytes, Smoking cessation and weight resulting in patchy depigmentation oflthe skin. Affecting both lossu sexes equally, vitiligo can occur at any age and can have a sig Moderate nificant impact on quality of life. Clinically, it appears as com Multiple nodules, Oral antibiotics with antibacterial pletely depigmented, well-demarcated symmetric macules or abscesses, or cysts; washes and/or topical antibiotics, scarring analgesics, adalimumab, wide patches with no scale (Figure 61). Its onset is insidious and local excision asymptomatic, starting as smaller macules that gradually For women: oral contraceptives, enlarge. It tends to be more visible in persons with darker skin spironolactone types (Figure 62) or in sun exposed areas, as the surrounding Severe skin will become darker with sun exposure. The most Multiple nodules, sinus Referral to dermatologist or tracts; scarring surgeon for consideration of wide local excision, adalimumab, or clinical trial uRecommended for all disease severity categories. painful abscesses and sinus tracts. Radical wide excision may also be used for refractory cases after other therapeutic options have been exhausted. Even after successful surgical treatment, recurrence is common. XEY POIXII HVC o Treatment of comedonal and inflammatory acne includes topical retinoids, benzoyl peroxide, and topical antibiotics; because of increased antibiotic resistance, topical antibiotics should not be used as monotherapy. (Continued) ttGURE 61. Well-demarcated symmetric patches of depigmented skin with no scale and accentuation of normal, sun-exposed skin, typical of vitiligo.

XEY POIXII HVC o Treatment of comedonal and inflammatory acne includes topical retinoids, benzoyl peroxide, and topical antibiotics; because of increased antibiotic resistance, topical antibiotics should not be used as monotherapy. (Continued) ttGURE 61. Well-demarcated symmetric patches of depigmented skin with no scale and accentuation of normal, sun-exposed skin, typical of vitiligo. 100

Dermatologic Disorders Melasma Melasma, also known as chloasma or the mask of pregnancy, is a common acquired condition resulting in patchy hyperpig- mentation of the skin on the face. It can also be seen on the upper extremities. In this condition, melanocltes overproduce melanin owing to a multitude of factors, including UV radia- tion, genetic predisposition, and hormonal influence (preg- nancy, use of oral contraceptives). Women and individuals with darker skin types are more commonly predisposed. Clinically, it presents as ill-defined, tan to dark brown reticu- Iated patches, mostly on the sun-exposed areas of the face (malar, mandibular, and centrofacial regions) (Figure 63). It worsens with sun exposure. The main differential diagnoses include postinflammatory hyperpigmentation, freckles, and lentigines. Melasma often fades during the postparhrm period, t I G U R E 6 2. Vitiligo, with well-demarcated symmetric patches of depigmented with sun protection, and upon discontinuation oforal contra- skin with no scale in a darkly pigmented person. ceptives. It may take months to years for pigmentation to normalize. Treatment can be challenging. The mainstay of treatment commonly affected areas involve the extensor surfaces, such as is strict sun protection, avoidance or discontinuation of the the dorsal hands and feet, elbows, and knees, and the perior- causative factors, and use of lightening agents. ificial areas, such as around the mouth, eyes, rectum, and genitals. It can be associated with other autoimmune condi- tions, such as type 1 diabetes and thyroid disease. It may be challenging to distinguish vitiligo from other conditions that cause depigmentation, such as postinflam- matory hypopigmentation, tinea versicolor, and pityriasis alba. The diagnosis of postinflammatory hypopigmentation is based on recognition of hypomelanotic or amelanotic macules or patches that correspond to previous inflamma- tory lesions. If the diagnosis is in doubt, a skin biopsy may assist in identifying the responsible inflammatory lesion. The diagnosis of tinea versicolor can be confirmed with a potassium hydroxide preparation that shows hyphae and yeast cells. Pityriasis alba occurs in children and adolescents. Defi ning characteristics include patches of hypopigmentation on the face, neck, upper trunk, and proximal extremities. Lesions typically manifest some border irregularity and are associated with a fine scale. History and physical examination, including a Wood lamp examination to help accentuate the depigmentation and the distribution ofthe lesions, helps confirm the diagnosis of vitiligo. Lesions appear bright white and sharply delineated when examined with a Wood lamp. Treatment for depigmented skin can be challenging, pro- longed, and suboptimal. Topical therapies include high- potency glucocorticoids or immunomodulators (tacrolimus, pimecrolimus). Phototherapy with UV light is also an option and can be the treatment of choice for widespread involve- ment. Repigmentation occurs first around hair follicles as they are thought to be the reservoirs for melanocytes. As a result, repigmented skin will initially have a speckled appearance. Depigmentation therapy can also be considered if the vitiligo t t G U R E 63. lll-defined, reticulated hyperpigmented patches on the malar is widespread (>50% BSA). cheeks, typical of melasma.

Melasma Melasma, also known as chloasma or the mask of pregnancy, is a common acquired condition resulting in patchy hyperpig- mentation of the skin on the face. It can also be seen on the upper extremities. In this condition, melanocltes overproduce melanin owing to a multitude of factors, including UV radia- tion, genetic predisposition, and hormonal influence (preg- nancy, use of oral contraceptives). Women and individuals with darker skin types are more commonly predisposed. Clinically, it presents as ill-defined, tan to dark brown reticu- Iated patches, mostly on the sun-exposed areas of the face (malar, mandibular, and centrofacial regions) (Figure 63). It worsens with sun exposure. The main differential diagnoses include postinflammatory hyperpigmentation, freckles, and lentigines. Melasma often fades during the postparhrm period, t I G U R E 6 2. Vitiligo, with well-demarcated symmetric patches of depigmented with sun protection, and upon discontinuation oforal contra- skin with no scale in a darkly pigmented person. ceptives. It may take months to years for pigmentation to normalize. Treatment can be challenging. The mainstay of treatment commonly affected areas involve the extensor surfaces, such as is strict sun protection, avoidance or discontinuation of the the dorsal hands and feet, elbows, and knees, and the perior- causative factors, and use of lightening agents. ificial areas, such as around the mouth, eyes, rectum, and genitals. It can be associated with other autoimmune condi- tions, such as type 1 diabetes and thyroid disease. It may be challenging to distinguish vitiligo from other conditions that cause depigmentation, such as postinflam- matory hypopigmentation, tinea versicolor, and pityriasis alba. The diagnosis of postinflammatory hypopigmentation is based on recognition of hypomelanotic or amelanotic macules or patches that correspond to previous inflamma- tory lesions. If the diagnosis is in doubt, a skin biopsy may assist in identifying the responsible inflammatory lesion. The diagnosis of tinea versicolor can be confirmed with a potassium hydroxide preparation that shows hyphae and yeast cells. Pityriasis alba occurs in children and adolescents. Defi ning characteristics include patches of hypopigmentation on the face, neck, upper trunk, and proximal extremities. Lesions typically manifest some border irregularity and are associated with a fine scale. History and physical examination, including a Wood lamp examination to help accentuate the depigmentation and the distribution ofthe lesions, helps confirm the diagnosis of vitiligo. Lesions appear bright white and sharply delineated when examined with a Wood lamp. Treatment for depigmented skin can be challenging, pro- longed, and suboptimal. Topical therapies include high- potency glucocorticoids or immunomodulators (tacrolimus, pimecrolimus). Phototherapy with UV light is also an option and can be the treatment of choice for widespread involve- ment. Repigmentation occurs first around hair follicles as they are thought to be the reservoirs for melanocytes. As a result, repigmented skin will initially have a speckled appearance. Depigmentation therapy can also be considered if the vitiligo t t G U R E 63. lll-defined, reticulated hyperpigmented patches on the malar is widespread (>50% BSA). cheeks, typical of melasma. 101

Dermatologic Disorders T EY PO I IITS o Vitiligo is an acquired autoimmune condition that causes loss of melanocytes and subsequent depigmen- tation of the skin; it can be associated with other auto- immune conditions, such as gpe 1 diabetes and thyroid disease. . Treatment of depigmented skin includes topical thera pies, such as high potency glucocorticoids or immu- nomodulators, and phototherapy with ultraviolet light for widespread involvement. o Melasma, which results in patchy hyperpigmentation on the face during pregnancy or with oral contraceptive use, is treated with strict sun protection, avoidance or discontinuation of causative factors, and lightening F I G UR E 6 5. Bullous pemphigoid is characterized by subepidermal bullae blisters that are tense and do not rupture easily. lt predominantly involves agents. nonmucosal surfaces. Sites ol predilection are the lower abdomen, inner thighs groin, axillae, and flexural aspects of the arms and legs.

o Vitiligo is an acquired autoimmune condition that causes loss of melanocytes and subsequent depigmen- tation of the skin; it can be associated with other auto- immune conditions, such as gpe 1 diabetes and thyroid disease. . Treatment of depigmented skin includes topical thera pies, such as high potency glucocorticoids or immu- nomodulators, and phototherapy with ultraviolet light for widespread involvement. o Melasma, which results in patchy hyperpigmentation on the face during pregnancy or with oral contraceptive use, is treated with strict sun protection, avoidance or discontinuation of causative factors, and lightening F I G UR E 6 5. Bullous pemphigoid is characterized by subepidermal bullae blisters that are tense and do not rupture easily. lt predominantly involves agents. nonmucosal surfaces. Sites ol predilection are the lower abdomen, inner thighs groin, axillae, and flexural aspects of the arms and legs. Autoimmune Bullous Diseases that progress to tense bullae (Figure 65). Oral involvement is Autoimmune bullous diseases (ABDs) vary from primary cuta- present in approximately 20'7, of patients. There are varying neous disorders to manifestations of underlying systemic dis- degrees of pruritus with bullous pemphigoid. Bullae heal ease (Table 77). with pigment change but otherwise do not scar. It typically has a protracted course, with exacerbations and remission. Pemphigus Vulgaris The use of steroid sparing agents significantly decreases Pemphigus vulgaris is the most common intraepidermal ABD, mortality. and its incidence increases with age. It presents with flaccid oral or other mucosal bullae that rupture easily and leave ero XEY POITIS sions (Figure 64). Pemphigus vulgaris has a positive Nikolsky . Pemphigus vulgaris is the most common intraepider sign. Lesions heal with pigment change but otherwise do not mal autoimmune bullous disease and is characterized scar. Before the use of oral glucocorticoids and steroid-sparing by flaccid oral or other mucosal bullae that rupture eas- agents, mortality was high. ily and leave erosions; treatment is oral glucocorticoids and steroid sparing agents. Bullous Pemphigoid . Bullous pemphigoid is the most common subepidermal Bullous pemphigoid is the most common subepidermal ABD autoimmune bullous disease and is characterized by and overall the most common ABD. Onset is usually in adults variably pruritic urticarial and eczematous lesions that aged 60 years or older and presents with urticarial plaques progress to tense bullae.

Autoimmune Bullous Diseases that progress to tense bullae (Figure 65). Oral involvement is Autoimmune bullous diseases (ABDs) vary from primary cuta- present in approximately 20'7, of patients. There are varying neous disorders to manifestations of underlying systemic dis- degrees of pruritus with bullous pemphigoid. Bullae heal ease (Table 77). with pigment change but otherwise do not scar. It typically has a protracted course, with exacerbations and remission. Pemphigus Vulgaris The use of steroid sparing agents significantly decreases Pemphigus vulgaris is the most common intraepidermal ABD, mortality. and its incidence increases with age. It presents with flaccid oral or other mucosal bullae that rupture easily and leave ero XEY POITIS sions (Figure 64). Pemphigus vulgaris has a positive Nikolsky . Pemphigus vulgaris is the most common intraepider sign. Lesions heal with pigment change but otherwise do not mal autoimmune bullous disease and is characterized scar. Before the use of oral glucocorticoids and steroid-sparing by flaccid oral or other mucosal bullae that rupture eas- agents, mortality was high. ily and leave erosions; treatment is oral glucocorticoids and steroid sparing agents. Bullous Pemphigoid . Bullous pemphigoid is the most common subepidermal Bullous pemphigoid is the most common subepidermal ABD autoimmune bullous disease and is characterized by and overall the most common ABD. Onset is usually in adults variably pruritic urticarial and eczematous lesions that aged 60 years or older and presents with urticarial plaques progress to tense bullae. Photo- or Light-lnduced ",* t Dermatoses Photo and light-sensitive conditions may be secondary to systemic diseases, such as systemic lupus erythematosus and porphyria cutanea tarda, or conditions limited to the skin, including phototoxic/photoallergic conditions and polymor phous light eruption. Diagnosis of the disorders limited to the skin is usually clinical, but skin biopsy is often per formed to support the clinical diagnosis and rule out other dermatoses.

Photo- or Light-lnduced ",* t Dermatoses Photo and light-sensitive conditions may be secondary to systemic diseases, such as systemic lupus erythematosus and porphyria cutanea tarda, or conditions limited to the skin, including phototoxic/photoallergic conditions and polymor phous light eruption. Diagnosis of the disorders limited to the skin is usually clinical, but skin biopsy is often per formed to support the clinical diagnosis and rule out other dermatoses. Porphyria Cutanea Tarda Porphyria cutanea tarda is the most prevalent gpe of porphyria t I G U R E 6 4. The flaccid intraepidermal vesirles of pemphigus vulgaris are readily and presents with skin fragility and bullae or erosions on sun- broken, leaving behind weeping erosions. exposed areas. most frequently the dorsal hands (Figure 66). 102

Dermatologic Disorders TABLE 77. Characteristics of Autoimmune Blistering Diseases Disease Clinical Characteristics Pathology Comments Pe mphi gus Tender, fragile blisters and erosions Suprabasilar clefting compared lncidence varies by country and VU lgaris seen in oral mucosa and skin; with subepidermal clefting seen in ethnicity and is estimated to be 0.5 mucous membrane lesions much bullous pemphigoid to 3.2 cases per 1 00,000 persons more common than in bullous per year DIF/llF: intercellular pattern within pemphigoid; Nikolsky sign (rubbing of the skin resulting in the epidermis blister formation) is positive Pe m ph s US Scaling and crusted lesions on face High granular or subcorneal clefting lncidence varies by country with {oliaceu s and uppertrunk, and erythroderma compared with suprabasal clefting estimated occurrence of 0.5 to 6.6 with no mucosal involvement; seen in pemphigus vulgaris cases per million persons per year Nikolsky sign is positive DIF/llF: intercellular pattern within the epidermis Paraneoplastic Painful oral, conjunctival, Mixed pattern of both suprabasal High mortality rate (up to 90%) and pemphigus esophageal, and laryngeal erosions acantholysis and interface dermatitis association with underlying accompany a polymorphous skin neoplasms: non-Hodgkin eruption marked by con{luent DIF/llF: lgG binds in an intercellular lymphoma (427"), chronic pattern within the epidermis; erythema, bullae, erosions, and lymphocytic leukemia (29%), reactants at the dermal-epidermal intractable stomatitis; patients also Castleman disease ( 1 0%) junction. The combination of have respiratory problems that may intercellular and subepidermal be fatal deposition o{ immunoreactants is a clue to the diagnosis lgA pemphigus A vesicopustular eruption with clear Subcorneal collection of Unknown {requency blisters that rapidly transform into neutrophils pustules; trunk and proximal DIF shows deposition of extremities are most commonly involved, with relative sparing of the intercellular lgA at the epidermal mucous membranes surfaces

TABLE 77. Characteristics of Autoimmune Blistering Diseases Disease Clinical Characteristics Pathology Comments Pe mphi gus Tender, fragile blisters and erosions Suprabasilar clefting compared lncidence varies by country and VU lgaris seen in oral mucosa and skin; with subepidermal clefting seen in ethnicity and is estimated to be 0.5 mucous membrane lesions much bullous pemphigoid to 3.2 cases per 1 00,000 persons more common than in bullous per year DIF/llF: intercellular pattern within pemphigoid; Nikolsky sign (rubbing of the skin resulting in the epidermis blister formation) is positive Pe m ph s US Scaling and crusted lesions on face High granular or subcorneal clefting lncidence varies by country with {oliaceu s and uppertrunk, and erythroderma compared with suprabasal clefting estimated occurrence of 0.5 to 6.6 with no mucosal involvement; seen in pemphigus vulgaris cases per million persons per year Nikolsky sign is positive DIF/llF: intercellular pattern within the epidermis Paraneoplastic Painful oral, conjunctival, Mixed pattern of both suprabasal High mortality rate (up to 90%) and pemphigus esophageal, and laryngeal erosions acantholysis and interface dermatitis association with underlying accompany a polymorphous skin neoplasms: non-Hodgkin eruption marked by con{luent DIF/llF: lgG binds in an intercellular lymphoma (427"), chronic pattern within the epidermis; erythema, bullae, erosions, and lymphocytic leukemia (29%), reactants at the dermal-epidermal intractable stomatitis; patients also Castleman disease ( 1 0%) junction. The combination of have respiratory problems that may intercellular and subepidermal be fatal deposition o{ immunoreactants is a clue to the diagnosis lgA pemphigus A vesicopustular eruption with clear Subcorneal collection of Unknown {requency blisters that rapidly transform into neutrophils pustules; trunk and proximal DIF shows deposition of extremities are most commonly involved, with relative sparing of the intercellular lgA at the epidermal mucous membranes surfaces Bullous Tense blisters preceded by intense Subepidermal bullae without One of most common autoimmune pemphigoid pruritus or urticarial lesions most acantholysis and with prominent blistering diseases, with up to 4.3 commonly seen in elderly persons eosinophils cases per 1 00,000 persons per year on the trunk, limbs, and flexures; DIF shows linear lgG deposition at does not usually present with oral lesions the basement membrane zone

Bullous Tense blisters preceded by intense Subepidermal bullae without One of most common autoimmune pemphigoid pruritus or urticarial lesions most acantholysis and with prominent blistering diseases, with up to 4.3 commonly seen in elderly persons eosinophils cases per 1 00,000 persons per year on the trunk, limbs, and flexures; DIF shows linear lgG deposition at does not usually present with oral lesions the basement membrane zone Epidermolysis Bullae and erosions mostly on Subepidermal cleavage without Rare disease with unknown bullosa acquisita extensor areas that may mimic acantholysis frequency bullous pemphigoid, or heal with DIF shows lgG deposition at the Can be associated with scarring and milia basement membrane zone that inflammatory bowel disease localizes to the base on salt-split skin Cicatricial Presents with bullae, erosions, milia, Histology is similarto bullous Rare disease, with estimated pemphigoid and scarring on the mucous pemphigoid incidence of 0.9 to 1.1 cases per membranes and conjunctivae of million persons per year DIF may reveal patterns similar to middle-aged to elderly persons; oral mucosa is almost always bullous pemphigoid, linear lgA lncreased risk for malignancy in bullous dermatosis, or some patients involved; conjunctival lesions are also common epidermolysis bullosa acquisita Prompt treatment should be initiated to avoid permanent ocular and oral scarring Dermatitis Severely pruritic grouped vesicles Histology shows neutrophilic Common blistering disease, with 10 herpetiformis or erosions on elbows, knees, back, infiltrate atthe tips of the dermal to 1 'l cases per 100,000 persons scalp, and buttocks; lesions occur papillae causing subepidermal per year in crops and are symmetrically separation Nearly all patients with dermatitis distributed; often the vesicles are DIF shows granular lgA deposition herpetiformis will have celiac not seen because the process is disease so itchy that they are almost immediately broken Linear lgA Pruritic, discrete, or clustered bullae Subepidermal bullae with ln adults, the estimated incidence is bullous in a herpetiform pattern ("cluster of neutrophils 0.6 case per 1 00,000 persons per dermatosis jewels"); annular or polycyclic year DIF shows linear lgA deposition lesions with vesicles and bullae at Ocular involvement can occur the periphery are common DIF = direct immunofluorescence; llF = indirect immunofluorescence.

Epidermolysis Bullae and erosions mostly on Subepidermal cleavage without Rare disease with unknown bullosa acquisita extensor areas that may mimic acantholysis frequency bullous pemphigoid, or heal with DIF shows lgG deposition at the Can be associated with scarring and milia basement membrane zone that inflammatory bowel disease localizes to the base on salt-split skin Cicatricial Presents with bullae, erosions, milia, Histology is similarto bullous Rare disease, with estimated pemphigoid and scarring on the mucous pemphigoid incidence of 0.9 to 1.1 cases per membranes and conjunctivae of million persons per year DIF may reveal patterns similar to middle-aged to elderly persons; oral mucosa is almost always bullous pemphigoid, linear lgA lncreased risk for malignancy in bullous dermatosis, or some patients involved; conjunctival lesions are also common epidermolysis bullosa acquisita Prompt treatment should be initiated to avoid permanent ocular and oral scarring Dermatitis Severely pruritic grouped vesicles Histology shows neutrophilic Common blistering disease, with 10 herpetiformis or erosions on elbows, knees, back, infiltrate atthe tips of the dermal to 1 'l cases per 100,000 persons scalp, and buttocks; lesions occur papillae causing subepidermal per year in crops and are symmetrically separation Nearly all patients with dermatitis distributed; often the vesicles are DIF shows granular lgA deposition herpetiformis will have celiac not seen because the process is disease so itchy that they are almost immediately broken Linear lgA Pruritic, discrete, or clustered bullae Subepidermal bullae with ln adults, the estimated incidence is bullous in a herpetiform pattern ("cluster of neutrophils 0.6 case per 1 00,000 persons per dermatosis jewels"); annular or polycyclic year DIF shows linear lgA deposition lesions with vesicles and bullae at Ocular involvement can occur the periphery are common DIF = direct immunofluorescence; llF = indirect immunofluorescence. 103

Dermatologic Disorders radiation. Photosensitivity reactions related to exogenous agents are either phototoxic or photoallergic. Exogenous agents include systemic drugs, certain plants. or topical applications. Phototoxicity can occur in anyone u'ith a threshold con centration of the responsible chemical or drug and is more common than photoallergr. Phototoxic reactions present as an exaggerated sunburn within minutes to hours of sun expo sure. Photoallergr is a cell-mediated immune response lound in previously sensitized individuals that can be elicited by small amounts of offending agent. Photoallergic reactions occur more commonly after topical exposure of a sensitizing agent and present as pruritic, eczematous eruptions rvithin 2'1 to 48 hours after sun exposure on sun-exposed body parts (Figure 67). Common causes of phototoxic and photoallergic reactions are listed in Table 78. Treatment of photosensitivity disorders includes avoidance of photosensitizing drugs and allergens and broad spectrum sunscreens.

radiation. Photosensitivity reactions related to exogenous agents are either phototoxic or photoallergic. Exogenous agents include systemic drugs, certain plants. or topical applications. Phototoxicity can occur in anyone u'ith a threshold con centration of the responsible chemical or drug and is more common than photoallergr. Phototoxic reactions present as an exaggerated sunburn within minutes to hours of sun expo sure. Photoallergr is a cell-mediated immune response lound in previously sensitized individuals that can be elicited by small amounts of offending agent. Photoallergic reactions occur more commonly after topical exposure of a sensitizing agent and present as pruritic, eczematous eruptions rvithin 2'1 to 48 hours after sun exposure on sun-exposed body parts (Figure 67). Common causes of phototoxic and photoallergic reactions are listed in Table 78. Treatment of photosensitivity disorders includes avoidance of photosensitizing drugs and allergens and broad spectrum sunscreens. Polymorphous Light Eruption Polymorphous light eruption is the most common idiopathic photosensitivity disorder. It typically manifests before age 30 years and is most common in fair skinned rtomen. first

Polymorphous Light Eruption Polymorphous light eruption is the most common idiopathic photosensitivity disorder. It typically manifests before age 30 years and is most common in fair skinned rtomen. first FIGU RE 66. Porphyria cutanea tarda manifests as a chronic blistering disease on sun-exposed skin, especially the back ol the hands. Hyperpigmentation of the skin and hypertrichosis of the fore head and temples are commonly seen. Porphyria cutanea tarda is most commonly caused by an acquired defect of hepatic uroporphyrinogen decarboxylase enzyme, which results in an excess of circulating porphyrins. Accumulated porphyrins in the skin are photosensitizing and cause phototoxicity upon light exposure. Chronic hepatitis C virus (HCV) infection is the most common cause, followed by alcohol-induced liver damage and hemochromatosis. The diagnosis is confirmed by increased plasma or urine porphy rin levels. Treatment is aimed at decreasing iron overload. In addi tion to treatment of the underlying condition, phlebotomy is the mainstay of therapy. Twice weekly hydroxychloroquine is an effective alternative to phlebotomy. Treatment of chronic HCV infection may be effective for treatment of porphyria cuta nea tarda, but the evidence is limited regarding this approach. t I G U R E 6 7. Pink, scaly, eczematous plaques on the arms ol a patient with a Phototoxic and Photoallergic Conditions photoallergic drug reaction caused by hydrochlorothiazide. Note sparing of the Photosensitivity disorders are a collection ofconditions char- area that was protected from light by a wristwatch. Phototoxic reactions (not acterized by an abnormal skin response after exposure to UV pictured) result in pink edematous macules or blistering, much like a sunburn. 104

5 I b I t Dermatologic Disorders I L TABLE 78. Common Causes of Phototoxic and t Photoallergic Reactions b Phototoxic Causes I b Topical Tar compounds l L Lime I Celery L Parsley I t Fig f Systemic St. John's wort I Voriconazole t Doxycycline I L Amiodarone I I Hydrochlorothiazide I Ouinolones Photoallergic Causes t Topical Sunscreens (benzophenones) I L Ketoprofen I Diclofenac D Fragrance (musk ambrette) I Chlorhexidine Systemic Griseofulvin Ouinolones : Ouinine I Sulfonamides appearing in the spring and early summer. The rash persists for weeks and resolves without scarring even with continued sun exposure. Lesions appear on sun-exposed skin within tIGURE 68. Polymorphous lighteruption maytaketheform olany light- induced, pruritic eruption, particularly after intense light exposure. lt is diagnosed hours of exposure. Although different types of eruptions may only after other light-induced eruptions (systemic lupus erythematosus, photodrug occur (polymorphous), the most common are pmritic erythe- reaction, and porphyria cutanea tarda, among others) have been excluded.The most matous papules (Figure 68). The type of lesion remains con common variant of polymorphous light eruption is pruritic, pink to red papules or sistent in an individual with each occurrence. The diagnosis is papules and vesicles as seen here; less common variants are plaques and urticaria.

appearing in the spring and early summer. The rash persists for weeks and resolves without scarring even with continued sun exposure. Lesions appear on sun-exposed skin within tIGURE 68. Polymorphous lighteruption maytaketheform olany light- induced, pruritic eruption, particularly after intense light exposure. lt is diagnosed hours of exposure. Although different types of eruptions may only after other light-induced eruptions (systemic lupus erythematosus, photodrug occur (polymorphous), the most common are pmritic erythe- reaction, and porphyria cutanea tarda, among others) have been excluded.The most matous papules (Figure 68). The type of lesion remains con common variant of polymorphous light eruption is pruritic, pink to red papules or sistent in an individual with each occurrence. The diagnosis is papules and vesicles as seen here; less common variants are plaques and urticaria. made clinically. Management centers on avoidance of sun exposure and use of sunscreens; when significant symptoms LEY'''',P0lt{T3r,{qdnrcdL, ,,.1,,., ':iii,. are present, topical glucocorticoids are an option, although . Polymorphous light eruption is an idiopathic photosensi- evidence ofefficacy is lacking. tivity disorder chamcterized by a rash (most commonly (tY P0rf,Tl pruritic e4rthematous papules) that persists for weeks o Porphyria cutanea tarda is the most prevalent type of and resolves without scarring. porphyria and presents with skin fragility and bullae or erosions on sun-exposed areas, most frequently the dorsal hands. Superficial Skin lnfections . Treatment of porphyria cutanea tarda includes treating Bacterial Skin lnfections the underlying condition and phlebotomy; twice- Impetigo and Ecthyma weekly hydroxychloroquine is an effective alternative to Impetigo is a superficial infection of the epidermis most com- phlebotomy. monly caused by S. aureus or group A streptococci. Impetigo . Photosensitivitydisorders (phototoxic orphotoallergic) is classified as bullous or nonbullous; ecthyma is a deeper ulcerative form. Impetigo is most commonly seen in children are a collection ofconditions characterized by an abnor- but can present in adults. mal skin response after exposure to ultraviolet radiation. Bullous impetigo is usually caused by S. oureus, which (Continued) produces exfoliative toxins targeting the adhesion molecule

made clinically. Management centers on avoidance of sun exposure and use of sunscreens; when significant symptoms LEY'''',P0lt{T3r,{qdnrcdL, ,,.1,,., ':iii,. are present, topical glucocorticoids are an option, although . Polymorphous light eruption is an idiopathic photosensi- evidence ofefficacy is lacking. tivity disorder chamcterized by a rash (most commonly (tY P0rf,Tl pruritic e4rthematous papules) that persists for weeks o Porphyria cutanea tarda is the most prevalent type of and resolves without scarring. porphyria and presents with skin fragility and bullae or erosions on sun-exposed areas, most frequently the dorsal hands. Superficial Skin lnfections . Treatment of porphyria cutanea tarda includes treating Bacterial Skin lnfections the underlying condition and phlebotomy; twice- Impetigo and Ecthyma weekly hydroxychloroquine is an effective alternative to Impetigo is a superficial infection of the epidermis most com- phlebotomy. monly caused by S. aureus or group A streptococci. Impetigo . Photosensitivitydisorders (phototoxic orphotoallergic) is classified as bullous or nonbullous; ecthyma is a deeper ulcerative form. Impetigo is most commonly seen in children are a collection ofconditions characterized by an abnor- but can present in adults. mal skin response after exposure to ultraviolet radiation. Bullous impetigo is usually caused by S. oureus, which (Continued) produces exfoliative toxins targeting the adhesion molecule 105

I Dermatologic Disorders l '1 I '] I F IG U R E 7 I . Superficial, saucer-shaped ulcers with overlying cruss are the I classic findings of ecthyma. Ihey almost always occur on the legs or feet and are i usually caused by streptococci. F I G UR E 6 9 . Sharply demarcated erosions with crusting on the arms and chest of a patient with bullous impetigo. r Diagrrosis is typically made on the basis of clinical appear- i

usually caused by streptococci. F I G UR E 6 9 . Sharply demarcated erosions with crusting on the arms and chest of a patient with bullous impetigo. r Diagrrosis is typically made on the basis of clinical appear- i ance, but bacterial culture can be obtained from the blister desmoglein-l between keratinocytes. This results in localized fluid or exudative crust to identiff the pathogen. Treatment blister formation (Figure Oe). This same toxin is responsible for consists of washing with soap and water and removal of the the more extensive exfoliation seen in staphylococcal scalded crust. Topical antibiotic treatment with mupirocin or retapa- skin qmdrome. Bullous impetigo presents as small vesicles that mulin is effective in most cases of impettgo. Oral antibiotics evolve into flaccid blisters. These blisters often ruptue, leaving are recommended for patients with widespread infection if a collarette of scale and honey-colored crusted erosions. outbreaks occur involving multiple people as well as in cases Nonbullous impetigo is more common and can be caused by S. aureus or group A streptococci, or both organisms. of ecthyma. Recommended antibiotics are cephalexin or dicloxacillin, unless methicillin-resistant S. oureus is sus- Nonbullous impetigo is characterized by erythematous pap- pected or confirmed. ules or plaques with honey-colored crust (Figure 7O). Satellite lesions are common. Nonbullous impetigo occurs on normal Erythrasma skin but can appear at areas of inflammatory conditions, such Erythrasma is a benign superficial bacterial infection of the as atopic dermatitis. skin manifesting as thin, pink-brown plaques in the groin, Ecthyma is a variant of impetigo characterized by an gluteal folds, or axillae, or less commonly in the interdigital or ulcerative lesion with an overlying eschar that extends into the inframammary regions (Figure 72). The skin often has a thin, dermis and may be associated with lymphadenitis Gigure n ). wrinkled appearance similar to cigarette paper. Symptoms are minimal and limited to mild pruritus. The causative organism is most commonly C-orynebacterium minutissimum. A Wood lamp examination will reveal a coral-red fluorescence. Clinical appearance and fluorescence are the best means ofdiagnosis; histopatholory and skin scrapings are not helpfirl. Treatment is with oral or topical erythromycin.

ance, but bacterial culture can be obtained from the blister desmoglein-l between keratinocytes. This results in localized fluid or exudative crust to identiff the pathogen. Treatment blister formation (Figure Oe). This same toxin is responsible for consists of washing with soap and water and removal of the the more extensive exfoliation seen in staphylococcal scalded crust. Topical antibiotic treatment with mupirocin or retapa- skin qmdrome. Bullous impetigo presents as small vesicles that mulin is effective in most cases of impettgo. Oral antibiotics evolve into flaccid blisters. These blisters often ruptue, leaving are recommended for patients with widespread infection if a collarette of scale and honey-colored crusted erosions. outbreaks occur involving multiple people as well as in cases Nonbullous impetigo is more common and can be caused by S. aureus or group A streptococci, or both organisms. of ecthyma. Recommended antibiotics are cephalexin or dicloxacillin, unless methicillin-resistant S. oureus is sus- Nonbullous impetigo is characterized by erythematous pap- pected or confirmed. ules or plaques with honey-colored crust (Figure 7O). Satellite lesions are common. Nonbullous impetigo occurs on normal Erythrasma skin but can appear at areas of inflammatory conditions, such Erythrasma is a benign superficial bacterial infection of the as atopic dermatitis. skin manifesting as thin, pink-brown plaques in the groin, Ecthyma is a variant of impetigo characterized by an gluteal folds, or axillae, or less commonly in the interdigital or ulcerative lesion with an overlying eschar that extends into the inframammary regions (Figure 72). The skin often has a thin, dermis and may be associated with lymphadenitis Gigure n ). wrinkled appearance similar to cigarette paper. Symptoms are minimal and limited to mild pruritus. The causative organism is most commonly C-orynebacterium minutissimum. A Wood lamp examination will reveal a coral-red fluorescence. Clinical appearance and fluorescence are the best means ofdiagnosis; histopatholory and skin scrapings are not helpfirl. Treatment is with oral or topical erythromycin. Dermatophlrtes Tinea (dermatophytosis) is classified according to the body site that is involved: tinea pedis (athlete's foot) (FigtrI€ 73), tinea manuum (hand) , tinea cruris (perineum or jock itch) (ti8we 7a) , tinea capitis (scalp) (Figure 75), tinea faciei (face), and tinea corporis (the body, excluding the genital area or inguinal folds) (Figure 76). Three genera of fungi account for most dermato- phytosis: Epidermophyton, Microsporum, and Trichophyton. Trichophyton rubrum is the most common causative species. Infection is more prevalent in hot and humid climates and in patients who are immunocompromised, particularly F I G Un E 7 0, Nonbullous impetigo is a superficial infection characterized by a those using chronic glucocorticoid therapy. Infection is yellowish, crusted surface that may be caused by staphylococci or streptococci. acquired from other humans, animals, or fomites.

Dermatophlrtes Tinea (dermatophytosis) is classified according to the body site that is involved: tinea pedis (athlete's foot) (FigtrI€ 73), tinea manuum (hand) , tinea cruris (perineum or jock itch) (ti8we 7a) , tinea capitis (scalp) (Figure 75), tinea faciei (face), and tinea corporis (the body, excluding the genital area or inguinal folds) (Figure 76). Three genera of fungi account for most dermato- phytosis: Epidermophyton, Microsporum, and Trichophyton. Trichophyton rubrum is the most common causative species. Infection is more prevalent in hot and humid climates and in patients who are immunocompromised, particularly F I G Un E 7 0, Nonbullous impetigo is a superficial infection characterized by a those using chronic glucocorticoid therapy. Infection is yellowish, crusted surface that may be caused by staphylococci or streptococci. acquired from other humans, animals, or fomites. t06

t t t Dermatologic Disorders t t t t I I t L I t t I I t L t t I G U R E 7 2. Erythrasma presents with sharply demarcated fine, pink-to-brown L scaling patches that are typically found in skin fold areas.The rash will fluoresce a i coral red with Wood lamp illumination. L F I G U R E 7 5. Kerion can be a result of tinea capitis infection and presents as t painful, boggy erythematous plaques with folliculitis and abscess formation. t I L t I i FIGURE 73. Erythematous patcheswith peripheral scale and associated onychomycosis (onychodystrophy with subungual debris of nails) in tinea pedis. t I G U R E 7 6. Tinea corporis on a patient's stomach, with characteristic presentation of annular, centrifugally growing erythematous patches with a raised rim of peripheral scale.

FIGURE 73. Erythematous patcheswith peripheral scale and associated onychomycosis (onychodystrophy with subungual debris of nails) in tinea pedis. t I G U R E 7 6. Tinea corporis on a patient's stomach, with characteristic presentation of annular, centrifugally growing erythematous patches with a raised rim of peripheral scale. The characteristic clinical presentation of tinea corporis, cruris, and faciei is annular/serpiginous scaly patches with central clearing and varying degrees of inflammation. Tinea cmris spares the scrotum, in contrast to intertrigo, which is in the differential diagnosis. Concomitant tinea pedis and cruris are common. In tinea capitis, invasion of the hair follicle leads to small broken hairs, with the surrounding scalp showing erythematous scaly patches with varying degrees of crust and numbers of pustules. Occipital adenopathy is common. The chronic form of tinea pedis and tinea manuum presents as mildly pruritic scaly patches involving most of the palms and soles in a "moccasin" or'glove" distribution (Figure 77).Two F I G UR E 7 4 . Tinea cruris, a dermatophyte infection of the groin, pubic region, and thighs, presents as erythematous annularto serpiginous lesions with peripheral feet-one hand is a characteristic pattern of involvement in scale and central clearing. tinea. Tinea pedis can have a more acute form, with 1- to

The characteristic clinical presentation of tinea corporis, cruris, and faciei is annular/serpiginous scaly patches with central clearing and varying degrees of inflammation. Tinea cmris spares the scrotum, in contrast to intertrigo, which is in the differential diagnosis. Concomitant tinea pedis and cruris are common. In tinea capitis, invasion of the hair follicle leads to small broken hairs, with the surrounding scalp showing erythematous scaly patches with varying degrees of crust and numbers of pustules. Occipital adenopathy is common. The chronic form of tinea pedis and tinea manuum presents as mildly pruritic scaly patches involving most of the palms and soles in a "moccasin" or'glove" distribution (Figure 77).Two F I G UR E 7 4 . Tinea cruris, a dermatophyte infection of the groin, pubic region, and thighs, presents as erythematous annularto serpiginous lesions with peripheral feet-one hand is a characteristic pattern of involvement in scale and central clearing. tinea. Tinea pedis can have a more acute form, with 1- to 107

Dermatologic Disorders F I GU R E T T. "Moccasin" type tinea pedis, characterized by mildly erythematous patches with fine scale that are well demarcated and are confined to the lateral foot, heel, and sole. tIGURE 78. Braght red patchesand plaqueswith satellite papules and pustules in the intertriginous area beneath the breasts that are characteristic of ca nd idiasis.

F I GU R E T T. "Moccasin" type tinea pedis, characterized by mildly erythematous patches with fine scale that are well demarcated and are confined to the lateral foot, heel, and sole. tIGURE 78. Braght red patchesand plaqueswith satellite papules and pustules in the intertriginous area beneath the breasts that are characteristic of ca nd idiasis. 2 mm vesicles, and can be extremely pruritic. The interdigital variant of tinea pedis shows fissures and maceration in the folds. Tinea incognito refers to tinea that has been erroneously invasive disease in immunocompromised and hospitalized treated with topical glucocorticoids, which initially decreases patients (see MKSAP 19 Infectious Disease). Antibacterial ther pruritus and leads to a clinical presentation that is less inflam- apy is a predisposing factor because it increases the number of matory than typical. Some patients, particularly those who are colonizing yeast present in skin and mucous membranes. immunosuppressed, may develop an uncommon condition in Intertrigo is an inflammatory skin disease that involves which the dermatophyte invades the dermis or subcutaneous the axillae and inframammary and inguinal folds, resulting tissue (Majocchi granuloma), causing the development of ery from moisture and friction (Figure 78). Candido is the most thematous or hyperpigmented perifollicular papules or small common secondary infection in intertrigo, with obesity being nodules indicating fungal infiltration of the hair follicles. an important risk factor. Most cases of intertrigo are not com- Tinea can be suspected on the basis of clinical presenta- plicated by candidal infection. When present, candidal inter tion and pruritus; however, diagnosis is based on visualization trigo presents as erythematous patches with satellite pustules of branching hyphae on microscopic examination of scrapings that are often macerated. Diagnosis is frequently made on using a potassium hydroxide preparation. Fungal culture, clinical grounds alone, but a potassium hydroxide preparation which provides species identification, can confirm the diagno can show spores and pseudohyphae. For successful treatment, sis. Culture is the preferred method for diagnosing tinea capi the area should be dry and use ofabsorbent powers and zinc tis; hair shafts should be included in the specimen. oxide paste can be helpful. Topical imidazoles and nystatin are Tinea should be treated to prevent skin breakdown, which generally effective, but recurrences are common. For wide- can be an entry port for bacterial infection. Dermatophltosis spread infection, oral fluconazole can be added. of non-hair bearing skin with limited involvement can be Chronic paronychia is associated with irritants or aller treated topically with the use of topical terbinaflne or gens and is caused by frequent exposure to water. Exacerbations imidazole creams, such as miconazole, clotrimazole, and keto can be caused by Candida (see Nail Disorders). conazole, applied once to tlvice daily for 2 to 4 weeks, ensuring that the application extends a few centimeters beyond the Pitlriasis Versicolor advancing border. Unlike superficial fungal infections caused Pityriasis versicolor, or tinea versicolor, is caused by Molassezia by Candida, dermatophy.tes do not respond to topical nystatin. furfur, a commensal fungus that lives in hair follicles and the Combined antifungals and topical glucocorticoids should be stratum corneum. Pityriasis versicolor is one of the most com avoided because they can lead to increased recurrences and mon chronic superficial lungal infections and is typically treatment failures. Dermatophytosis of hair-bearing skin, found in young adults, particularly in warm, humid environ including tinea capitis, or those with recurrent or extensive ments. It presents as asymptomatic, oval to round, minimally skin involvement should be treated with oral antifungal agents, scaly, hyper- or hypopigmented macules that can coalesce into such as terbinafine or itraconazole. patches on the trunk and upper extremities (Figure 79). The diagnosis of pityriasis versicolor can often be made by Yeast clinical presentation but may be confirmed by visualization of Candidiasis short rod shaped hyphae and round yeast ("spaghetti and meat- Candida species, in particular C. albicons, can cause superfi- balls") on microscopic examination of skin scrapings using a cial infections in moist occluded skin, such as the intertrigi potassium hydroxide preparation. Topical treatment using nous areas, oropharyngeal mucosa, and genitals, as well as ketoconazole 2ol, shampoo or selenium sulfide suspension is

2 mm vesicles, and can be extremely pruritic. The interdigital variant of tinea pedis shows fissures and maceration in the folds. Tinea incognito refers to tinea that has been erroneously invasive disease in immunocompromised and hospitalized treated with topical glucocorticoids, which initially decreases patients (see MKSAP 19 Infectious Disease). Antibacterial ther pruritus and leads to a clinical presentation that is less inflam- apy is a predisposing factor because it increases the number of matory than typical. Some patients, particularly those who are colonizing yeast present in skin and mucous membranes. immunosuppressed, may develop an uncommon condition in Intertrigo is an inflammatory skin disease that involves which the dermatophyte invades the dermis or subcutaneous the axillae and inframammary and inguinal folds, resulting tissue (Majocchi granuloma), causing the development of ery from moisture and friction (Figure 78). Candido is the most thematous or hyperpigmented perifollicular papules or small common secondary infection in intertrigo, with obesity being nodules indicating fungal infiltration of the hair follicles. an important risk factor. Most cases of intertrigo are not com- Tinea can be suspected on the basis of clinical presenta- plicated by candidal infection. When present, candidal inter tion and pruritus; however, diagnosis is based on visualization trigo presents as erythematous patches with satellite pustules of branching hyphae on microscopic examination of scrapings that are often macerated. Diagnosis is frequently made on using a potassium hydroxide preparation. Fungal culture, clinical grounds alone, but a potassium hydroxide preparation which provides species identification, can confirm the diagno can show spores and pseudohyphae. For successful treatment, sis. Culture is the preferred method for diagnosing tinea capi the area should be dry and use ofabsorbent powers and zinc tis; hair shafts should be included in the specimen. oxide paste can be helpful. Topical imidazoles and nystatin are Tinea should be treated to prevent skin breakdown, which generally effective, but recurrences are common. For wide- can be an entry port for bacterial infection. Dermatophltosis spread infection, oral fluconazole can be added. of non-hair bearing skin with limited involvement can be Chronic paronychia is associated with irritants or aller treated topically with the use of topical terbinaflne or gens and is caused by frequent exposure to water. Exacerbations imidazole creams, such as miconazole, clotrimazole, and keto can be caused by Candida (see Nail Disorders). conazole, applied once to tlvice daily for 2 to 4 weeks, ensuring that the application extends a few centimeters beyond the Pitlriasis Versicolor advancing border. Unlike superficial fungal infections caused Pityriasis versicolor, or tinea versicolor, is caused by Molassezia by Candida, dermatophy.tes do not respond to topical nystatin. furfur, a commensal fungus that lives in hair follicles and the Combined antifungals and topical glucocorticoids should be stratum corneum. Pityriasis versicolor is one of the most com avoided because they can lead to increased recurrences and mon chronic superficial lungal infections and is typically treatment failures. Dermatophytosis of hair-bearing skin, found in young adults, particularly in warm, humid environ including tinea capitis, or those with recurrent or extensive ments. It presents as asymptomatic, oval to round, minimally skin involvement should be treated with oral antifungal agents, scaly, hyper- or hypopigmented macules that can coalesce into such as terbinafine or itraconazole. patches on the trunk and upper extremities (Figure 79). The diagnosis of pityriasis versicolor can often be made by Yeast clinical presentation but may be confirmed by visualization of Candidiasis short rod shaped hyphae and round yeast ("spaghetti and meat- Candida species, in particular C. albicons, can cause superfi- balls") on microscopic examination of skin scrapings using a cial infections in moist occluded skin, such as the intertrigi potassium hydroxide preparation. Topical treatment using nous areas, oropharyngeal mucosa, and genitals, as well as ketoconazole 2ol, shampoo or selenium sulfide suspension is 108

Dermatologic Disorders I I FIGU RE 7 9. This patient exhibits classic findings of tinea versicolor, with tIGURE 81. Typical chickenpox(primaryvaricella-zostervirus infection) lesions hypopigmented and faintly scaly macules coalescing into patches on the upper develop in crops, such that lesions in different slages of development (macules, back. papules, vesicles, pustules, crusted erosions) are present simultaneously on any one part of the body; lesions are most prominent on the trunk rather than lhe effective. Either treatment should be applied from the upper extremities. Chickenpox is characterized by the simultaneous onset of fever and a cutaneous eruption. neck to the thighs and used to wash the scalp. Oral itraconazole can be used fbr patients with extensive disease or frequent recurrences. Because recurrences are frequent, weekly use of Diagnosis is based on clinical appearance. Molluscum topical treatments can be preventive. contagiosum is usually self-limited. However, in patients with severe cases or a protracted course, or in immunocompro Viral Skin lnfections and Exanthems mised persons, destructive modalities (cryotherapy, curettage, podophyllin) or topical medications (tretinoin, imiquimod) Molluscum Contagiosum Molluscum contagiosum is caused by a poxvirus. Infection can be used. Any of these treatments can be associated with occurs norrnally in children, in adults as a sexually transmitted scarring and pigment change. disease, and in patients with AIDS. The lesions are white to, yellow smooth papules with umbilicated centers (Figure 80). Varicella / Herpes Zoster Many patients develop a surrounding eczematous host Varicella zoster virus is a DNA virus that causes varicella (chick response. Papules can be located anpvhere on the skin, but in enpox), an acute illness characterized by fever and an eruption adults the genital area is typically involved. In patients with of vesicles on an ery.thematous base that is transmitted by res- piratory droplets (Figure 81). After primary infection, the virus AIDS, the most common area of infection is the face and the lesions tend to be larger. Transmission is by direct contact or remains latent in the dorsal root or cranial ganglia. Reactivation causes herpes zoster, or shingles (Figure 82). Prodromal symp- by fomites. toms, such as burning, stinging, or tingling, often occur in a ;#' dermatome, followed by eruption of grouped vesicles or pus tules on an erythematous base. The most common dermatomes

I FIGU RE 7 9. This patient exhibits classic findings of tinea versicolor, with tIGURE 81. Typical chickenpox(primaryvaricella-zostervirus infection) lesions hypopigmented and faintly scaly macules coalescing into patches on the upper develop in crops, such that lesions in different slages of development (macules, back. papules, vesicles, pustules, crusted erosions) are present simultaneously on any one part of the body; lesions are most prominent on the trunk rather than lhe effective. Either treatment should be applied from the upper extremities. Chickenpox is characterized by the simultaneous onset of fever and a cutaneous eruption. neck to the thighs and used to wash the scalp. Oral itraconazole can be used fbr patients with extensive disease or frequent recurrences. Because recurrences are frequent, weekly use of Diagnosis is based on clinical appearance. Molluscum topical treatments can be preventive. contagiosum is usually self-limited. However, in patients with severe cases or a protracted course, or in immunocompro Viral Skin lnfections and Exanthems mised persons, destructive modalities (cryotherapy, curettage, podophyllin) or topical medications (tretinoin, imiquimod) Molluscum Contagiosum Molluscum contagiosum is caused by a poxvirus. Infection can be used. Any of these treatments can be associated with occurs norrnally in children, in adults as a sexually transmitted scarring and pigment change. disease, and in patients with AIDS. The lesions are white to, yellow smooth papules with umbilicated centers (Figure 80). Varicella / Herpes Zoster Many patients develop a surrounding eczematous host Varicella zoster virus is a DNA virus that causes varicella (chick response. Papules can be located anpvhere on the skin, but in enpox), an acute illness characterized by fever and an eruption adults the genital area is typically involved. In patients with of vesicles on an ery.thematous base that is transmitted by res- piratory droplets (Figure 81). After primary infection, the virus AIDS, the most common area of infection is the face and the lesions tend to be larger. Transmission is by direct contact or remains latent in the dorsal root or cranial ganglia. Reactivation causes herpes zoster, or shingles (Figure 82). Prodromal symp- by fomites. toms, such as burning, stinging, or tingling, often occur in a ;#' dermatome, followed by eruption of grouped vesicles or pus tules on an erythematous base. The most common dermatomes tIGURE 80. Molluscum contagiosum is a common culaneous infection resulting Irom poxvirus infection. lt occurs in young children and sexually active Fl G U RE 82. Typical presentation ol herpes zoster (shingles) o{ the trunk, adults. lt presents as firm, umbilicated whiteto'yellow papules with varying characterized by painful grouped vesicles on an erythematous base in a dermatomal degrees of surrounding erythema. d istri bution.

tIGURE 80. Molluscum contagiosum is a common culaneous infection resulting Irom poxvirus infection. lt occurs in young children and sexually active Fl G U RE 82. Typical presentation ol herpes zoster (shingles) o{ the trunk, adults. lt presents as firm, umbilicated whiteto'yellow papules with varying characterized by painful grouped vesicles on an erythematous base in a dermatomal degrees of surrounding erythema. d istri bution. 109

Dermatologic Disorders affected are in the thoracic region. With involvement of the first division of the trigeminal nerve (forehead extending over upper eyelid, or nasal tip involvement), ophthalmologic evaluation is mandatory because herpes zoster ophthalmicus with possible blindness can result. If vesicles are noted in the extemal ear canal, peripheral facial para$sis and auditory/vestibular symp toms can occur (Ramsay Hunt syndrome). Herpes zoster can be complicated by postherpetic neural- gia and has been associated with an increased risk for cerebro vascular disease. Postherpetic neuralgia is defined as chronic neuropathic pain that persists lor 3 months or more alter the initial onset of herpes zoster. The risk, severity, and complica tions ofherpes zoster, in particular postherpetic neuralgia, are increased in older patients, those with greater initial pain and more severe infection, and possibly in patients who are immu nosuppressed or on immunosuppressive or immunomodulat ing medications. t lGU R E 83. The oval-shaped patches of pityriasis rosea often follow skin Diagnosis of herpes zoster can usually be made on the cleavage lines. basis of characteristic dermatomal presentation. For unu sual cases or when the distinction between herpes simplex Vaccination is an effective means of decreasing the likeli virus and herpes zoster is required, ancillary studies are hood of herpes zoster. See Routine Care of the Healthy Patient available (Table 79). Oral acyclovir, valacyclovir, or famci for more information. clovir is effective fbr treating herpes zoster if initiated within 72 hours of presentation and can shorten the disease Pit5rriasis Rosea course as well as decrease the likelihood of postherpetic Pityriasis rosea is a common rash that may be related to reac neuralgia. Evidence is insufficient to support the addition of tivation of human herpesvirus 6 or 7. Pityriasis rosea begins as glucocorticoids to reduce the incidence of postherpetic a single annular patch or plaque with fine scaling (the herald neuralgia. patch), typically on the trunk, followed by numerous smaller, skin-colored to pink papules and plaques erupting along skin TABLE 79. Tests That Differentiate Between Varicella cleavage lines (Figure 83). This distribution on the posterior Zoster and Herpes Simplex Virus thorax can resemble a "fir tree" pattern. The herald patch is Method Sample Utility absent in up to 50'U, of patients. but when present it usually precedes the smaller plaques by several days up to 2 weeks. Hematoxylin and Skin biopsy Characteristic histologic eosin staining findings with Treatment is generally not necessary but topical glucocorti- immunohistochemistry to coids may be used for symptom relief. Secondary syphilis may differentiate VZVfrom have a similar appearance to pityriasis rosea but typically HSV involves the palms and soles and is usually associated with Direct Unroofed Discriminates among generalized lymphadenopathy. fluorescence vesicle HSV1, HSV2, and VZV antibody XIY POIXTS Polymerase chain reaction Unroofed vesicle Discriminates among HSV1, HSV2, and VZV r Tinea presents as annular scaly patches with central clearing and varying degrees of inflammation; diagnosis Serologies Peripheral Diagnosis of primary brlood in{ection with is made by demonstration of branching hyphae on seroconversion of virus- microscopic examination of scrapings using a potassium specific lgG antibodies hydroxide preparation. Tzanck preparation Unroofed vesicle Multinucleated keratinocytes and . Most dermatophytoses can be treated with topical terbi- cytopathic effect does not nafine or imidazole creams; if hair-bearing skin is differentiate VZVfrom affected or there is extensive or recurrent involvement, HSV technically difficult oral terbinafine or itraconazole should be used. Viral culture Unroofed vesicle Delay ol 48-72 h, but can discriminate among . Oral acyclovir, valacyclovir, or famciclovir is effective for HSV1, HSV2, and VZV; treating herpes zoster if initiated within 72 hours of useful for antiviral presentation; it can shorten the disease course and sensitivities decrease likelihood of postherpetic neuralgia. HSV = herpes slmplex vi rus; VZV = varicella zoster virus. (Continued)

affected are in the thoracic region. With involvement of the first division of the trigeminal nerve (forehead extending over upper eyelid, or nasal tip involvement), ophthalmologic evaluation is mandatory because herpes zoster ophthalmicus with possible blindness can result. If vesicles are noted in the extemal ear canal, peripheral facial para$sis and auditory/vestibular symp toms can occur (Ramsay Hunt syndrome). Herpes zoster can be complicated by postherpetic neural- gia and has been associated with an increased risk for cerebro vascular disease. Postherpetic neuralgia is defined as chronic neuropathic pain that persists lor 3 months or more alter the initial onset of herpes zoster. The risk, severity, and complica tions ofherpes zoster, in particular postherpetic neuralgia, are increased in older patients, those with greater initial pain and more severe infection, and possibly in patients who are immu nosuppressed or on immunosuppressive or immunomodulat ing medications. t lGU R E 83. The oval-shaped patches of pityriasis rosea often follow skin Diagnosis of herpes zoster can usually be made on the cleavage lines. basis of characteristic dermatomal presentation. For unu sual cases or when the distinction between herpes simplex Vaccination is an effective means of decreasing the likeli virus and herpes zoster is required, ancillary studies are hood of herpes zoster. See Routine Care of the Healthy Patient available (Table 79). Oral acyclovir, valacyclovir, or famci for more information. clovir is effective fbr treating herpes zoster if initiated within 72 hours of presentation and can shorten the disease Pit5rriasis Rosea course as well as decrease the likelihood of postherpetic Pityriasis rosea is a common rash that may be related to reac neuralgia. Evidence is insufficient to support the addition of tivation of human herpesvirus 6 or 7. Pityriasis rosea begins as glucocorticoids to reduce the incidence of postherpetic a single annular patch or plaque with fine scaling (the herald neuralgia. patch), typically on the trunk, followed by numerous smaller, skin-colored to pink papules and plaques erupting along skin TABLE 79. Tests That Differentiate Between Varicella cleavage lines (Figure 83). This distribution on the posterior Zoster and Herpes Simplex Virus thorax can resemble a "fir tree" pattern. The herald patch is Method Sample Utility absent in up to 50'U, of patients. but when present it usually precedes the smaller plaques by several days up to 2 weeks. Hematoxylin and Skin biopsy Characteristic histologic eosin staining findings with Treatment is generally not necessary but topical glucocorti- immunohistochemistry to coids may be used for symptom relief. Secondary syphilis may differentiate VZVfrom have a similar appearance to pityriasis rosea but typically HSV involves the palms and soles and is usually associated with Direct Unroofed Discriminates among generalized lymphadenopathy. fluorescence vesicle HSV1, HSV2, and VZV antibody XIY POIXTS Polymerase chain reaction Unroofed vesicle Discriminates among HSV1, HSV2, and VZV r Tinea presents as annular scaly patches with central clearing and varying degrees of inflammation; diagnosis Serologies Peripheral Diagnosis of primary brlood in{ection with is made by demonstration of branching hyphae on seroconversion of virus- microscopic examination of scrapings using a potassium specific lgG antibodies hydroxide preparation. Tzanck preparation Unroofed vesicle Multinucleated keratinocytes and . Most dermatophytoses can be treated with topical terbi- cytopathic effect does not nafine or imidazole creams; if hair-bearing skin is differentiate VZVfrom affected or there is extensive or recurrent involvement, HSV technically difficult oral terbinafine or itraconazole should be used. Viral culture Unroofed vesicle Delay ol 48-72 h, but can discriminate among . Oral acyclovir, valacyclovir, or famciclovir is effective for HSV1, HSV2, and VZV; treating herpes zoster if initiated within 72 hours of useful for antiviral presentation; it can shorten the disease course and sensitivities decrease likelihood of postherpetic neuralgia. HSV = herpes slmplex vi rus; VZV = varicella zoster virus. (Continued) 110

Dermatologic Disorders l(EY PO I ilTS (@ntr,tued, TAtsLE 80" Treatment of Ectoparasitic lnfestations . Pi@asis rosea begins as a single annular patch or plaque lnfestation Treatment with fine scaling (the herald patch), typically on the trunk, Pediculosis 1% permethrin cream rinse for first-line followed by numerous smaller, skin colored to pink pap- capitis (head lice) treatment; 0.5% malathion for resistance; topical or oral ivermectin" as alternative ules and plaques erupting along skin cleavage lines. Pthirus pubis treatments (pubic lice) Clear nits and eggs with fine-tooth comb

l(EY PO I ilTS (@ntr,tued, TAtsLE 80" Treatment of Ectoparasitic lnfestations . Pi@asis rosea begins as a single annular patch or plaque lnfestation Treatment with fine scaling (the herald patch), typically on the trunk, Pediculosis 1% permethrin cream rinse for first-line followed by numerous smaller, skin colored to pink pap- capitis (head lice) treatment; 0.5% malathion for resistance; topical or oral ivermectin" as alternative ules and plaques erupting along skin cleavage lines. Pthirus pubis treatments (pubic lice) Clear nits and eggs with fine-tooth comb Ectoparasites Use petrolatum ointment for eyelash i nfestation Lice Wash and dry clothing, bedding, and There are three Bpes of lice that infest humans: head (Pediculus linens in high heat humanus copitis), body (Pediculus humonus corporis), and Pediculosis Destroy clothing, bedding, and linens, or pubic (Pthirus pubis) lice. Head lice live on the scalp and attach corporis (body wash and drythese items on high heat lice ) eggs (nits) to the proximal hair shaft (Figure 84). Transmission occurs by close personal contact or by fomites, such as bed Scabiesb Topical 5% permethrin cream applied from neck down and repeat in 7 days or ding, clothing, or hairbrushes. oral ivermectin" on days 1 and 8 Body lice live in the seams of clothing, not on the skin, Wash and dry clothing, bedding, and and are associated with poor hygiene. Excoriations result in linens in high heat; repeat in 1 wk crusted papules or linear petechiae on the trunk, neck, and Bed bugs Professional exterm ination proximal arms. Body lice can transmit serious infections, Wash and dry clothing, bedding, and including trench fever (Bartonella quintana), louse-borne linens in high heat; repeat in 1 wk relapsing fever (Borrelia recurrentis), and epidemic typhus uContraindicated in pregnant women. (R ickettsio pro w azekii) . blreat all members of the househoid. Pubic lice (crab louse) are typically spread by sexual con- tact but may attach to other sites, such as eyebrows or eye lashes (Pediculosis cilioris). Screening for other sexually transmitted infections should be considered in patients diag nosed with pubic lice. Table 8o outlines treatment for lice.

Ectoparasites Use petrolatum ointment for eyelash i nfestation Lice Wash and dry clothing, bedding, and There are three Bpes of lice that infest humans: head (Pediculus linens in high heat humanus copitis), body (Pediculus humonus corporis), and Pediculosis Destroy clothing, bedding, and linens, or pubic (Pthirus pubis) lice. Head lice live on the scalp and attach corporis (body wash and drythese items on high heat lice ) eggs (nits) to the proximal hair shaft (Figure 84). Transmission occurs by close personal contact or by fomites, such as bed Scabiesb Topical 5% permethrin cream applied from neck down and repeat in 7 days or ding, clothing, or hairbrushes. oral ivermectin" on days 1 and 8 Body lice live in the seams of clothing, not on the skin, Wash and dry clothing, bedding, and and are associated with poor hygiene. Excoriations result in linens in high heat; repeat in 1 wk crusted papules or linear petechiae on the trunk, neck, and Bed bugs Professional exterm ination proximal arms. Body lice can transmit serious infections, Wash and dry clothing, bedding, and including trench fever (Bartonella quintana), louse-borne linens in high heat; repeat in 1 wk relapsing fever (Borrelia recurrentis), and epidemic typhus uContraindicated in pregnant women. (R ickettsio pro w azekii) . blreat all members of the househoid. Pubic lice (crab louse) are typically spread by sexual con- tact but may attach to other sites, such as eyebrows or eye lashes (Pediculosis cilioris). Screening for other sexually transmitted infections should be considered in patients diag nosed with pubic lice. Table 8o outlines treatment for lice. Scabies Scabies (Sarcoptes scobiei) infestation is characterized by intensely pruritic, crusted papules, nodules, and burrows that develop in the interdigital spaces, wrists, ankles, breasts, peri- umbilical area, and genitals (Figure 85). In patients who are immunocompromised, highly contagious crusted scabies occurs, with thick concrete like scale. Scabies is transmitted

Scabies Scabies (Sarcoptes scobiei) infestation is characterized by intensely pruritic, crusted papules, nodules, and burrows that develop in the interdigital spaces, wrists, ankles, breasts, peri- umbilical area, and genitals (Figure 85). In patients who are immunocompromised, highly contagious crusted scabies occurs, with thick concrete like scale. Scabies is transmitted F I G UR E 8 5, A burrow characteristic of scabies is present on the proximal hypothenar eminence (arow). Scrapings ol the proximal end of the burrow revealed the scabies mite (see tigute 86). by close personal contact, and diagnosis is confirmed by microscopic identification of mites, eggs, or scybala (feces) on a mineral oil preparation of skin scrapings (Figure 86). Outbreaks are common in settings such as nursing homes, prisons, and shelters. See Table 80 for treatment. Pruritus may FIGURE 84. Head lice. Multiple nitsappearaswhiteadhesionson the persist for weeks after eradication of scabies and does not patient s black hair. necessarily represent resistance or reinfection. "Postscabetic 111

Dermatologic Disorders TtY POIilIS . Body lice cause excoriations that result in crusted pap- ules or linear petechiae on the trunk, neck, and proxi mal arms, and can transmit serious infections. o Pruritus may persist for weeks after eradication of scabies HVC and does not necessarily represent resistance or reinfec- tion and does not require retreatment. . Bed bug bites are characteristically Iinearly arranged urticarial papules ("breakfast, lunch. and dinner' bites) on exposed skin and are painless and pruritic.

TtY POIilIS . Body lice cause excoriations that result in crusted pap- ules or linear petechiae on the trunk, neck, and proxi mal arms, and can transmit serious infections. o Pruritus may persist for weeks after eradication of scabies HVC and does not necessarily represent resistance or reinfec- tion and does not require retreatment. . Bed bug bites are characteristically Iinearly arranged urticarial papules ("breakfast, lunch. and dinner' bites) on exposed skin and are painless and pruritic. Burns Burns are the fourth most common type of traumatic injury and may be caused by a multitude of agents. including chemi cal. thermal, and electrical. as well as LIV light. Thermal burns are assessed based on the amount of BSA involvement. depth of burn, and specific area involved. Grading of burns is described in Table 81. Estimating the BSA involved is based on tlGU RE 86, Sarcoptesscableimite(arow) seen on mineral oil preparation of skin scrapings. the rule of 9s: The head and neck represent 9'X,, each arm is 9'X,. each leg is 18%, the anterior trunk is 18'),,. the posterior pruritus" can be treated with antihistamines; topical glucocor trunk is 1B'7,, and the genital region is 1'X, BSA. Treatment of ticoids; and, if severe, oral glucocorticoids. burns is based on the depth of the inlury Minor burns in areas of low risk for infection with a small BSA involvement can be Bed Bugs treated with gentle cleansing and application ofa sterile dress Bed bugs (Cimex lectulorius) live in floorboards, walls, vents, ing with petrolatum. Wounds prone to developing infection bedding, or furniture and crawl to the host to feed overnight. may be best treated lr,'ith a topical antibiotic in addition to the They do not live on the human body. Bites are characteristi sterile dressing. cally linearly arranged urticarial papules ("breakfast, lunch, and dinner" bites) on exposed skin (Figure 87). The lesions are painless and pruritic. See Table 80 for treatment. TABLE 81. Classification of Burns by Depth of lnjury Depth Degree Structures Signs and lnvolved Symptoms S uperficial First Epidermis Red and tender skin Su perficial Second Epidermis Blisters, pa rtia l-th ickn ess destroyed weeping, partial sloughed dermis skin, red; painfulto air and touch; bla nches

Burns Burns are the fourth most common type of traumatic injury and may be caused by a multitude of agents. including chemi cal. thermal, and electrical. as well as LIV light. Thermal burns are assessed based on the amount of BSA involvement. depth of burn, and specific area involved. Grading of burns is described in Table 81. Estimating the BSA involved is based on tlGU RE 86, Sarcoptesscableimite(arow) seen on mineral oil preparation of skin scrapings. the rule of 9s: The head and neck represent 9'X,, each arm is 9'X,. each leg is 18%, the anterior trunk is 18'),,. the posterior pruritus" can be treated with antihistamines; topical glucocor trunk is 1B'7,, and the genital region is 1'X, BSA. Treatment of ticoids; and, if severe, oral glucocorticoids. burns is based on the depth of the inlury Minor burns in areas of low risk for infection with a small BSA involvement can be Bed Bugs treated with gentle cleansing and application ofa sterile dress Bed bugs (Cimex lectulorius) live in floorboards, walls, vents, ing with petrolatum. Wounds prone to developing infection bedding, or furniture and crawl to the host to feed overnight. may be best treated lr,'ith a topical antibiotic in addition to the They do not live on the human body. Bites are characteristi sterile dressing. cally linearly arranged urticarial papules ("breakfast, lunch, and dinner" bites) on exposed skin (Figure 87). The lesions are painless and pruritic. See Table 80 for treatment. TABLE 81. Classification of Burns by Depth of lnjury Depth Degree Structures Signs and lnvolved Symptoms S uperficial First Epidermis Red and tender skin Su perficial Second Epidermis Blisters, pa rtia l-th ickn ess destroyed weeping, partial sloughed dermis skin, red; painfulto air and touch; bla nches Deep partial Second Epidermis Wet or dry, thickness and dermis white, destroyed yellow, or red; painful to pressure Full thickness Third Epidermis, Dry, white or dermis, and black; fat destroyed minimal pain Fou rth Epidermis, Dry, black; dermis, and minimal pain fat destroyed; also involves muscle and/ F IG U R E 87, Bedbug bites usually occur in a series ("breakfast, lunch, and or bone dinner").The lesions are painless, pruritic, urticarial papules.

Deep partial Second Epidermis Wet or dry, thickness and dermis white, destroyed yellow, or red; painful to pressure Full thickness Third Epidermis, Dry, white or dermis, and black; fat destroyed minimal pain Fou rth Epidermis, Dry, black; dermis, and minimal pain fat destroyed; also involves muscle and/ F IG U R E 87, Bedbug bites usually occur in a series ("breakfast, lunch, and or bone dinner").The lesions are painless, pruritic, urticarial papules. 112

Dermatologic Disorders unknown; however, an autoilrunune mechanism is postulated Alopecia owing to the high association with other autoimmune condi- Alopecia is the loss of hair and may be characterized as local tions, such as Bpe 1 diabetes mellitus and autoimmune thy- ized or generalized and scarring or nonscarring. Scarring alo roiditis. In some patients, there is complete loss of scalp hair pecia results in permanent hair loss, whereas nonscarring (alopecia totalis) and all body hair (alopecia universalis). Limited alopecia is potentially reversible. The diagnosis of most cases disease may undergo spontaneous remission. Intralesional or can be determined by history and physical examination and topical glucocorticoids are used to treat limited disease. Systemic confirmed with a punch biopsy. The area of the scalp with glucocorticoids may be used for refractory or extensive disease, active hair loss (not scar) should be chosen for biopsy. but relapse is common after discontinuing therapy. Treatment options for alopecia are described in Table 82. Traumatic alopecia includes traction alopecia (Figure 89), trichotillomania, and iatrogenic damage from chemicals and Nonscarring Localized and Generalized Alopecia heat. Traumatic alopecia can begin as nonscarring; however, Alopecia areata is characterized by well circumscribed round with continuing trauma, the alopecia can become permanent patches of nonscarring acute hair loss. The scalp is smooth and and scarring. scaleless (Figure 88). It affects both',.r,omen and men, and onset Androgenic alopecia is an androgen dependent nonscar- usually occurs before the age of 30 years. The exact cause is ring alopecia seen in both men and women. The onset begins

unknown; however, an autoilrunune mechanism is postulated Alopecia owing to the high association with other autoimmune condi- Alopecia is the loss of hair and may be characterized as local tions, such as Bpe 1 diabetes mellitus and autoimmune thy- ized or generalized and scarring or nonscarring. Scarring alo roiditis. In some patients, there is complete loss of scalp hair pecia results in permanent hair loss, whereas nonscarring (alopecia totalis) and all body hair (alopecia universalis). Limited alopecia is potentially reversible. The diagnosis of most cases disease may undergo spontaneous remission. Intralesional or can be determined by history and physical examination and topical glucocorticoids are used to treat limited disease. Systemic confirmed with a punch biopsy. The area of the scalp with glucocorticoids may be used for refractory or extensive disease, active hair loss (not scar) should be chosen for biopsy. but relapse is common after discontinuing therapy. Treatment options for alopecia are described in Table 82. Traumatic alopecia includes traction alopecia (Figure 89), trichotillomania, and iatrogenic damage from chemicals and Nonscarring Localized and Generalized Alopecia heat. Traumatic alopecia can begin as nonscarring; however, Alopecia areata is characterized by well circumscribed round with continuing trauma, the alopecia can become permanent patches of nonscarring acute hair loss. The scalp is smooth and and scarring. scaleless (Figure 88). It affects both',.r,omen and men, and onset Androgenic alopecia is an androgen dependent nonscar- usually occurs before the age of 30 years. The exact cause is ring alopecia seen in both men and women. The onset begins TABLE 82. Management of Selected Types of Alopecia Type Treatment Options Possible Associations Androgenetic alopecia Men: topical minoxidil 5%,' Sn-reductase inhibitors Men: increased rate of prostate cancer (if onset in (fi nasterid e," d utasteride) the 20s) Women:topical minoxidil 5% foam," Women: polycystic ovary syndrome spironolactoneb Both: hair transplant, cosmetic camouflage Alopecia areata <50% scalp involvement: watchful waiting, topical Autoimmune disease (hyperthyroidism, glucocorticoids + topical minoxidil, anthralin, hypothyroidism, vitiligo, pernicious anemia, type 1 intra lesional g ucocorticoid I diabetes mellitus) >50% scalp i nvolvement: topical immunotherapy Atopic eczema (squaric acid or DPCP); topical glucocorticoids for all patients; topical minoxidil, phototherapy, systemic immunosuppressants, wigs or other cosmetic camouflage, intralesional triamcinolone for brows, and bimatoprost for eyelashes may be used Telogen effluvium Remove or correct potential trigger Anemia, thyroid disease, significant weight loss, eating disorders, childbirth, high fever, major Watchful waiting surgery, blood loss, mental stress Medications: anabolic steroids or supplemental androgens, antithyroid medications, antiepileptics, p-blockers, oral retinoids, warfarin Discoid lupus Sunscreen or other sun protection Systemic lupus erythematosus (5%-1 0%) erythematosus G lucocorticoids:

TABLE 82. Management of Selected Types of Alopecia Type Treatment Options Possible Associations Androgenetic alopecia Men: topical minoxidil 5%,' Sn-reductase inhibitors Men: increased rate of prostate cancer (if onset in (fi nasterid e," d utasteride) the 20s) Women:topical minoxidil 5% foam," Women: polycystic ovary syndrome spironolactoneb Both: hair transplant, cosmetic camouflage Alopecia areata <50% scalp involvement: watchful waiting, topical Autoimmune disease (hyperthyroidism, glucocorticoids + topical minoxidil, anthralin, hypothyroidism, vitiligo, pernicious anemia, type 1 intra lesional g ucocorticoid I diabetes mellitus) >50% scalp i nvolvement: topical immunotherapy Atopic eczema (squaric acid or DPCP); topical glucocorticoids for all patients; topical minoxidil, phototherapy, systemic immunosuppressants, wigs or other cosmetic camouflage, intralesional triamcinolone for brows, and bimatoprost for eyelashes may be used Telogen effluvium Remove or correct potential trigger Anemia, thyroid disease, significant weight loss, eating disorders, childbirth, high fever, major Watchful waiting surgery, blood loss, mental stress Medications: anabolic steroids or supplemental androgens, antithyroid medications, antiepileptics, p-blockers, oral retinoids, warfarin Discoid lupus Sunscreen or other sun protection Systemic lupus erythematosus (5%-1 0%) erythematosus G lucocorticoids: Topical are first line lntralesional for recalcitrant or thick lesions Oral reserved for patients with rapid progression Antimalarial agents Retinoids: topical or oral if severe Traumatic alopecia Traction/styling alopecia: decrease tension from Concomitant psychiatric disorder is more common styling practices in adults than children Trichotillomania : cognitive behavioral therapy Consider referral to psychiatrist or psychologist Lichen planopilaris Topical, intralesional, or oral glucocorticoids; Lichen planus on the skin, nails, and oral and genital antimalarial agents; immunosuppressants mucosa

Topical are first line lntralesional for recalcitrant or thick lesions Oral reserved for patients with rapid progression Antimalarial agents Retinoids: topical or oral if severe Traumatic alopecia Traction/styling alopecia: decrease tension from Concomitant psychiatric disorder is more common styling practices in adults than children Trichotillomania : cognitive behavioral therapy Consider referral to psychiatrist or psychologist Lichen planopilaris Topical, intralesional, or oral glucocorticoids; Lichen planus on the skin, nails, and oral and genital antimalarial agents; immunosuppressants mucosa DPCP = d phenylcyclopropenone. "FDA-approved treatment for that condition or indication. bSpironolactone should not be administered during pregnancy and should be used with a highly effective contraceptive in premenopausal women. 113

Dermatologic Disorders t I G U R E 9 0. Iypical di$ribution of androgenic alopecia in a male. Note the bitemporal hairline recession and vertex hair loss. tl G U RE 88. Well-demarcated, smooth, oval patches of hair loss. Note the short hairs near the rim of the balding patch (arow). Closer examination of these hairs will reveal "exclamation point" hairs (hairs that narrow close to the skin surface). after puberty and can be gradual. In men, it presents as bitem- 1 poral hairline recession followed by vertex baldness (Figure 9O). In women, it often presents as generalized thinning and is often first recognized as widening of the part width on the crown (Figure 91). First-line treatment is topical minoxidil for FIGURE 91, Androgenicalopecia in afemale. Notethewidening ofthe part width at the crown.

after puberty and can be gradual. In men, it presents as bitem- 1 poral hairline recession followed by vertex baldness (Figure 9O). In women, it often presents as generalized thinning and is often first recognized as widening of the part width on the crown (Figure 91). First-line treatment is topical minoxidil for FIGURE 91, Androgenicalopecia in afemale. Notethewidening ofthe part width at the crown. both men and women. Oral finasteride is another approved treatment for men. Telogen effluvium is caused by a traumatic event (emo tionally or physiologically) that disrupts the natural hair cycle, resulting in diffuse hair shedding. After a traumatic event, the hairs in the anagen (growing) phase are prema turely converted into the telogen (resting) phase. Hair shed ding occurs about 3 months after the inciting event. This is commonly seen in women in the postpartum period. In most cases, telogen effluvium is self-limiting with resump tion of normal hair growth with resolution of the inciting factor.

both men and women. Oral finasteride is another approved treatment for men. Telogen effluvium is caused by a traumatic event (emo tionally or physiologically) that disrupts the natural hair cycle, resulting in diffuse hair shedding. After a traumatic event, the hairs in the anagen (growing) phase are prema turely converted into the telogen (resting) phase. Hair shed ding occurs about 3 months after the inciting event. This is commonly seen in women in the postpartum period. In most cases, telogen effluvium is self-limiting with resump tion of normal hair growth with resolution of the inciting factor. Scarring Localized and Generalized Alopecia Discoid lupus ery.thematous on the scalp can result in local ized scarring alopecia. It presents as multiple pink, scaling hypo- and hyperpigmented plaques (Figure 92). Treatment is topical and intralesional glucocorticoids and oral antimalarial t I G U R E 8 9. Iraction alopecia is a result of continuous pulling of the hair from agents. styling techniques, such as braids or ponytails. Hair los typically occurs along the frontal and temporal hairline and may be permanent if the cause of the tension Acne keloidalis nuchae is a chronic inflammatory disor- persists. der of the follicles that manifests as papules and pustules

Scarring Localized and Generalized Alopecia Discoid lupus ery.thematous on the scalp can result in local ized scarring alopecia. It presents as multiple pink, scaling hypo- and hyperpigmented plaques (Figure 92). Treatment is topical and intralesional glucocorticoids and oral antimalarial t I G U R E 8 9. Iraction alopecia is a result of continuous pulling of the hair from agents. styling techniques, such as braids or ponytails. Hair los typically occurs along the frontal and temporal hairline and may be permanent if the cause of the tension Acne keloidalis nuchae is a chronic inflammatory disor- persists. der of the follicles that manifests as papules and pustules 114

Dermatologic Disorders F I G UR E 94. Lichen planopilaris is a cause of scarring alopecia and often demonstrates rednes around the follicles. . Scarring alopecia results in permanent hair loss, whereas nonscarring alopecia may be reversible. o Alopecia areata, a nonscarring alopecia, is treated with intralesional or topical glucocorticoids for limited disease and systemic glucocorticoids for refractory or extensive disease. . First-line treatment of androgenic alopecia is topical minoxidil for both men and women; oral finasteride is another approved treatment for men. F IG U R E 9 2. Multiple pink scarring plaques of hair loss in discoid lupus erythematous. Nail Disorders The nail complex is composed of the nail plate, hyponych- ium, proximal and lateral nail folds, cuticle, nail bed, and matrix (Figure qS). The hyponychium is the skin underneath FIGURE 93. Multiple papulesand pustulesatthe napeof theneck characteristic of early acne keloidalis nuchae.

Nail Disorders The nail complex is composed of the nail plate, hyponych- ium, proximal and lateral nail folds, cuticle, nail bed, and matrix (Figure qS). The hyponychium is the skin underneath FIGURE 93. Multiple papulesand pustulesatthe napeof theneck characteristic of early acne keloidalis nuchae. causing an alopetic scar on the nape ofthe neck (Figure 93). It is more common in skin of color. Treatment includes topical glucocorticoids and topical or oral antibiotics. Large keloidal plaques may require surgical excision. Lichen planopilaris is a diffuse scarring alopecia that more commonly affects postmenopausal women. It presents as mild scaling and limited erythema surrounding the follicle (Figure 94). Treatment is difficult, but topical or intralesional FIGURE 95. Anatomy ofthe nail. Shown arethe nail plate(b/uearow), lateral corticosteroids and antimalarials may be used. nai I folds (red anows), and proxi mal nail fold (yellow arrow\. 115

Dermatologic Disorders TABLE 83. Nail Findings Associated With Systemic Conditions Nail Finding Description Associated Conditions Nail Plate Koilonychia (spoon nails) Thin curving-up nail with everted edges (spoon) lron disorders (Plummer-Vinson syndrome, hemochromatosis, iron deficiency anemia); chronic injury Trachyonychia Rough sandpaper nails on all 20 nails Lichen planus; psoriasis; eczema; idiopathic Onychogryphosis Curved, hypertrophic nails resembling claw Trauma; peripheral vascular disease; neglect Onychomadesis Periodic shedding of the nail beginning at its Severe systemic illness (high fever, toxic epidermal proximal end due to temporary arrest of the matrix necrosis, erythroderma, scarlet fever); surgery; medications Transverse indentations Transverse furrows beginning in the matrix Systemic illness or major trauma (childbirth, measles, (Beau lines) acute febrile illnesses, drug reaction) Pitted nails Tiny indentations on the nail plate due to abnormal Psoriasis; alopecia areata; lichen planus keratinization of the proximal nail matrix Nail Color Half-and-half (Lindsay) Proximal nail is white and the distal nail is red, pink, Chronic kidney disease nails and brown with a sharp line of demarcation Terry nails Distal 1-2 mm of nails have normal pink color, but Liver disease; chronic heart failure; diabetes mellitus; proximal end has abnormal white appearance normal aging Melanonychia Diffuse/partial brown-black Chemotherapeutic agents, antimalarial agents, minocycline, gold; common in persons with dark Longitudinal melanonychia (vertical brown band) skin types Nevus; lentigo; drugs; melanoma; trauma Green nailsyndrome Onycholytic toenails with green discoloration Prolonged immersion in fresh water and infection with Pseudomo nas aeruginosa Blue nails Blue lunulae Argyria, antimalarial agents, hepatolenticular degeneration 5-Fluorouracil and azidothymidine Yellow Yellow nail syndrome Aging; dermatophyte i nfection Lymphedema; chronic pulmonary disease Red lunulae Carbon monoxide poisoning; subungual digital myxoid cyst; heart failure Periungual/Cuticle Ragged cuticles (Samitz Dystrophic, ragged-appearing cuticles Dermatomyositis sign) Periungual erythema Alternating areas of capillary dilated, torturous Dermatomyositis; scleroderma; systemic lu pus vessels and capillary dropout; red cuticles erythematosus (less common)

TABLE 83. Nail Findings Associated With Systemic Conditions Nail Finding Description Associated Conditions Nail Plate Koilonychia (spoon nails) Thin curving-up nail with everted edges (spoon) lron disorders (Plummer-Vinson syndrome, hemochromatosis, iron deficiency anemia); chronic injury Trachyonychia Rough sandpaper nails on all 20 nails Lichen planus; psoriasis; eczema; idiopathic Onychogryphosis Curved, hypertrophic nails resembling claw Trauma; peripheral vascular disease; neglect Onychomadesis Periodic shedding of the nail beginning at its Severe systemic illness (high fever, toxic epidermal proximal end due to temporary arrest of the matrix necrosis, erythroderma, scarlet fever); surgery; medications Transverse indentations Transverse furrows beginning in the matrix Systemic illness or major trauma (childbirth, measles, (Beau lines) acute febrile illnesses, drug reaction) Pitted nails Tiny indentations on the nail plate due to abnormal Psoriasis; alopecia areata; lichen planus keratinization of the proximal nail matrix Nail Color Half-and-half (Lindsay) Proximal nail is white and the distal nail is red, pink, Chronic kidney disease nails and brown with a sharp line of demarcation Terry nails Distal 1-2 mm of nails have normal pink color, but Liver disease; chronic heart failure; diabetes mellitus; proximal end has abnormal white appearance normal aging Melanonychia Diffuse/partial brown-black Chemotherapeutic agents, antimalarial agents, minocycline, gold; common in persons with dark Longitudinal melanonychia (vertical brown band) skin types Nevus; lentigo; drugs; melanoma; trauma Green nailsyndrome Onycholytic toenails with green discoloration Prolonged immersion in fresh water and infection with Pseudomo nas aeruginosa Blue nails Blue lunulae Argyria, antimalarial agents, hepatolenticular degeneration 5-Fluorouracil and azidothymidine Yellow Yellow nail syndrome Aging; dermatophyte i nfection Lymphedema; chronic pulmonary disease Red lunulae Carbon monoxide poisoning; subungual digital myxoid cyst; heart failure Periungual/Cuticle Ragged cuticles (Samitz Dystrophic, ragged-appearing cuticles Dermatomyositis sign) Periungual erythema Alternating areas of capillary dilated, torturous Dermatomyositis; scleroderma; systemic lu pus vessels and capillary dropout; red cuticles erythematosus (less common) the distal free edge of the nail plate. It seals the junction The distal nail plate becomes discolored (yellow white, or between the distal nail plate and the nail bed. The nail fold brown) and thickened. Under the nail plate, there is an accu- protects the nail matrix and produces the cuticle. The nail mulation of subungual debris, resulting in separation of the bed is adherent to the bottom ofthe nail plate. Nail disorders nail plate from the nail bed (onycholysis) (Figure 96). Proximal can be caused by various diseases, infections, trauma, and subungual onychomycosis appears similar except that it starts drugs (Table 83). at the proximal nail fold. This pattem is rare and can be associ ated with HIV and immunosuppression. lnfection Onychomycosis is treated mostly for cosmetic reasons. Onychomycosis Confirmation of infection with potassium hydroxide prepa Onychomycosis is a dermatophytosis of the nail commonly ration, staining with periodic acid-Schifl or fungal culture seen in elderly persons, especially those with comorbidities, should be done before treatment to rule out psoriasis or such as diabetes mellitus, peripheral vascular disease, or traumatic nail changes. Topical antilungal agents are of immunosuppression. Toenails are most commonly affected. limited efficacy; oral therapy with terbinafine or itraconazole Distal subungual onychomycosis is the most common pattern. is more effective.

the distal free edge of the nail plate. It seals the junction The distal nail plate becomes discolored (yellow white, or between the distal nail plate and the nail bed. The nail fold brown) and thickened. Under the nail plate, there is an accu- protects the nail matrix and produces the cuticle. The nail mulation of subungual debris, resulting in separation of the bed is adherent to the bottom ofthe nail plate. Nail disorders nail plate from the nail bed (onycholysis) (Figure 96). Proximal can be caused by various diseases, infections, trauma, and subungual onychomycosis appears similar except that it starts drugs (Table 83). at the proximal nail fold. This pattem is rare and can be associ ated with HIV and immunosuppression. lnfection Onychomycosis is treated mostly for cosmetic reasons. Onychomycosis Confirmation of infection with potassium hydroxide prepa Onychomycosis is a dermatophytosis of the nail commonly ration, staining with periodic acid-Schifl or fungal culture seen in elderly persons, especially those with comorbidities, should be done before treatment to rule out psoriasis or such as diabetes mellitus, peripheral vascular disease, or traumatic nail changes. Topical antilungal agents are of immunosuppression. Toenails are most commonly affected. limited efficacy; oral therapy with terbinafine or itraconazole Distal subungual onychomycosis is the most common pattern. is more effective. 115

Dermatologic Disorders tlG URE 96. Yellow hypertrophic nail plate and subungual debris resulting from onychomycosis. FIGUnE 98. Nail pitting in a patientwith psoriasis. Paronychia Paronychia is an infection or irritation of the nail fold. Infection is caused bytrauma or chronic maceration leading to an incom- petent cuticle. Acute paronychia is painful swelling of the nail fold, most commonly caused by S. oureus. It typically affects only one nail. Chronic paronychia tends to be more insidious and involve multiple fingers. In adults, it is most often seen in those with frequent hand immersion in water. There is tender swelling in the nail folds with missing or dystrophic cuticles (Figure 97). Chronic paronychia can cause ridgrng of the nail plate. It is a multifactorial condition with several inciting fac- tors, including water, irritants, and possibly Condido species. Treatment of acute paronychia includes the use of warm compresses; incision and drainage; and, in severe cases, oral antibiotics. For chronic paronychia, minimizing inciting factors is ke5z Treatment includes topical glucocorticoids and antifungal agents to reduce inflammation and minimizing inciting factors.

Paronychia Paronychia is an infection or irritation of the nail fold. Infection is caused bytrauma or chronic maceration leading to an incom- petent cuticle. Acute paronychia is painful swelling of the nail fold, most commonly caused by S. oureus. It typically affects only one nail. Chronic paronychia tends to be more insidious and involve multiple fingers. In adults, it is most often seen in those with frequent hand immersion in water. There is tender swelling in the nail folds with missing or dystrophic cuticles (Figure 97). Chronic paronychia can cause ridgrng of the nail plate. It is a multifactorial condition with several inciting fac- tors, including water, irritants, and possibly Condido species. Treatment of acute paronychia includes the use of warm compresses; incision and drainage; and, in severe cases, oral antibiotics. For chronic paronychia, minimizing inciting factors is ke5z Treatment includes topical glucocorticoids and antifungal agents to reduce inflammation and minimizing inciting factors. lnflammatory Nail Disorders Psoriasis affects fingernails more commonly than toenails. If F I G Un E 9 9. Nail pitting, onycholysis, and yellow-red discololation ("oil stains") the nail matrix is affected, tiny multiple pits will be seen on are often present when the nails are involved in psoriasis. the nail plate (Figure 98). In cases of nail bed involvement, yellow-red discoloration ("oil stains") can occur (Figure 99). Other findings include nail plate thickening, separation of the nail plate from the nail bed, distal nail plate crumbling, and splinter hemorrhages (Figure fOO). Patients with psoriatic nail involvement are often affected by psoriatic arthritis. Lichen planus involves the nails in about 10% ofcases. It causes nail plate dystrophy, including thinning; red-streaking; and pterygium unguis formation, which is the scarring of the proximal nail fold and matrix (Figure fof).

lnflammatory Nail Disorders Psoriasis affects fingernails more commonly than toenails. If F I G Un E 9 9. Nail pitting, onycholysis, and yellow-red discololation ("oil stains") the nail matrix is affected, tiny multiple pits will be seen on are often present when the nails are involved in psoriasis. the nail plate (Figure 98). In cases of nail bed involvement, yellow-red discoloration ("oil stains") can occur (Figure 99). Other findings include nail plate thickening, separation of the nail plate from the nail bed, distal nail plate crumbling, and splinter hemorrhages (Figure fOO). Patients with psoriatic nail involvement are often affected by psoriatic arthritis. Lichen planus involves the nails in about 10% ofcases. It causes nail plate dystrophy, including thinning; red-streaking; and pterygium unguis formation, which is the scarring of the proximal nail fold and matrix (Figure fof). lngrown Toenail An ingrown toenail is the result of the nail plate growing into the lateral nail fold, causing an inflammatory response. Ingrown toenails of the great toe are most common, presenting t I G U R E 9 7. Tender, pink swelling of the proximal and lateral nail fold due to as painful swelling of the lateral nail fold (Figure 1O2). There chronic paronychia. Note the partially absent dystrophic cuticle (arows). may be some weeping granulation tissue.

lngrown Toenail An ingrown toenail is the result of the nail plate growing into the lateral nail fold, causing an inflammatory response. Ingrown toenails of the great toe are most common, presenting t I G U R E 9 7. Tender, pink swelling of the proximal and lateral nail fold due to as painful swelling of the lateral nail fold (Figure 1O2). There chronic paronychia. Note the partially absent dystrophic cuticle (arows). may be some weeping granulation tissue. 117

Dermatologic Disorders \ FIGURE 100. Characteristicfeaturesof nail psoriasisincludedistal onycholysis F I G U R E 1 0 2. Iender pink swelling of the lateral nail Iold of the great toe, with (separation of the nail plate from the underlying nail bed) [arrows] and splinter some pink granulation tissue growing on the lateral distal end suggesting an hemorrhages, which representthe Auspitz sign (punctuate bleeding) in the nail ingrown toenail. bed. ln addition, some patients may display the "oil-stain" sign (clrcle), which is characterized by a localized tan to brown discoloration of the nail. ln more severe forms of psoriatic involvement, there can be thickening and crumbling of the nails. tlGU RE 1 03. Melanonychia striata (benign). Longitudinal black pigmentation with transverse streaks on the nail plate are tharacleristic 0l melanonychia.

FIGURE 100. Characteristicfeaturesof nail psoriasisincludedistal onycholysis F I G U R E 1 0 2. Iender pink swelling of the lateral nail Iold of the great toe, with (separation of the nail plate from the underlying nail bed) [arrows] and splinter some pink granulation tissue growing on the lateral distal end suggesting an hemorrhages, which representthe Auspitz sign (punctuate bleeding) in the nail ingrown toenail. bed. ln addition, some patients may display the "oil-stain" sign (clrcle), which is characterized by a localized tan to brown discoloration of the nail. ln more severe forms of psoriatic involvement, there can be thickening and crumbling of the nails. tlGU RE 1 03. Melanonychia striata (benign). Longitudinal black pigmentation with transverse streaks on the nail plate are tharacleristic 0l melanonychia. Squamous Cell Carcinoma t I G U R E 1 0 1 . Lichen planus can cause pitting, onycholysis, and nail dystrophy. Squamous cell carcinoma of the nail unit often presents with Lichen planus is a common cause of 20 nail dystrophy (trachyonychia), characterized pain, swelling, and erythema. It commonly arises in the nail by roughness and longitudinal ridging of the nail plate on all 20 nails fold and appears as a hyperkeratotic papule and plaque similar to \,\'arts (Figure 104). If treatnlent of a \\'art does not progress Conservative treatment for milcl to moderate ingrown as expected, a biopsy is rnarranted to rule out squamous cell toenails involves wider shoes, trimming the nail plate straight carcinoma, which, in the nail. is strongly associated with across. antiseptic application. and inserting a cotton pledget human papillomavirus infection. under the nail edge. For severe cases, partial or complete nail avulsion with matricectomy may be necessary. rtY P0trrs . Onychomycosis is a dermatophyosis of the distal nail Melanonychia plate, which becomes discolored (yellow. white, or I\4elanonychia is a brown banded pigmentation of the nail brown) and thickened. plate that can bc caused by increased melanin production in o Treatment of onychomycosis is not necessary in most cases. HVC the nail matrix, benign hyperplasia. and melanoma (see o Acute paronychia is a painful swelling of the nail fold. Melanoma). Longitudinal melanonychia is benign (Figure 1O3) most commonly caused by Stophylococcus oureus. and is most commonly found on dark skinned patients on typically affecting one nail; chronic paronychia tends to multipte nails. l-ongitudinal. irregular melanonychia on a sin be more insidious and involve multiple fingers. gle nail can be a sign of melanoma.

Squamous Cell Carcinoma t I G U R E 1 0 1 . Lichen planus can cause pitting, onycholysis, and nail dystrophy. Squamous cell carcinoma of the nail unit often presents with Lichen planus is a common cause of 20 nail dystrophy (trachyonychia), characterized pain, swelling, and erythema. It commonly arises in the nail by roughness and longitudinal ridging of the nail plate on all 20 nails fold and appears as a hyperkeratotic papule and plaque similar to \,\'arts (Figure 104). If treatnlent of a \\'art does not progress Conservative treatment for milcl to moderate ingrown as expected, a biopsy is rnarranted to rule out squamous cell toenails involves wider shoes, trimming the nail plate straight carcinoma, which, in the nail. is strongly associated with across. antiseptic application. and inserting a cotton pledget human papillomavirus infection. under the nail edge. For severe cases, partial or complete nail avulsion with matricectomy may be necessary. rtY P0trrs . Onychomycosis is a dermatophyosis of the distal nail Melanonychia plate, which becomes discolored (yellow. white, or I\4elanonychia is a brown banded pigmentation of the nail brown) and thickened. plate that can bc caused by increased melanin production in o Treatment of onychomycosis is not necessary in most cases. HVC the nail matrix, benign hyperplasia. and melanoma (see o Acute paronychia is a painful swelling of the nail fold. Melanoma). Longitudinal melanonychia is benign (Figure 1O3) most commonly caused by Stophylococcus oureus. and is most commonly found on dark skinned patients on typically affecting one nail; chronic paronychia tends to multipte nails. l-ongitudinal. irregular melanonychia on a sin be more insidious and involve multiple fingers. gle nail can be a sign of melanoma. 118

Dermatologic Disorders Warts, Corns, and Skin Tags Warts Warts (verruca and condyloma) are caused by hun.ran papillo mavirus (HPV). HPV infbction can occur at any age but is gpi cally seen in children and young adults. Larger, more numerous lesions that are recalcitrant to treatment can be seen in persons who are immunocompromised. There are numerous HPV sub types, but certain subtypes are associated with specific clinical lesions and are more common at specific sites (Table 84). Verruca vulgaris (common warts) are skin col<,rred digitate pap ules with thrombosed capillaries (Figure 106). Vemrca plana (flat warts) are skin colored, llat topped papules. Condyloma acuminata (genital warts) are smooth to digitate papules that are skin-colored to tan (Figure 107). Verruca plantaris (plantar

Warts, Corns, and Skin Tags Warts Warts (verruca and condyloma) are caused by hun.ran papillo mavirus (HPV). HPV infbction can occur at any age but is gpi cally seen in children and young adults. Larger, more numerous lesions that are recalcitrant to treatment can be seen in persons who are immunocompromised. There are numerous HPV sub types, but certain subtypes are associated with specific clinical lesions and are more common at specific sites (Table 84). Verruca vulgaris (common warts) are skin col<,rred digitate pap ules with thrombosed capillaries (Figure 106). Vemrca plana (flat warts) are skin colored, llat topped papules. Condyloma acuminata (genital warts) are smooth to digitate papules that are skin-colored to tan (Figure 107). Verruca plantaris (plantar F I G UR E 1 04. Verruca plaque on the lateral nail Iold that looks like a wa(, but TABLE 84. Human Papillomavirus Subtypes biopsy demonstrated squamous cell carcinoma. 5u btype Clinical Lesion (Location) 1 Verruca plantaris/palmaris (soles/palms) Benign Nodules and Tumors )t Verruca vulgaris (fingers, knees, and elbows) Seborrheic Keratosis 3, 10 Verruca plana (face and legs; associated with shaving) Seborrheic keratoses are benign pigmented neoplasms of 6, 11 Condyloma acuminata keratinocyte origin that are common in older adults. They are 16,18, Condyloma acuminata (associated with high risk "stuck on" papules and plaques that occur anywhere on the 31, 33 for cervical, anal, and penile cancer) body. They most commonly occur on the trunk and spare the palms, soles, and mucous membranes. Seborrheic keratoses range in size lrom a few millimeters to several centimeters. Usually they are brorvn, but they can range in color lrom tan to black (Figure f05). They may become irritated or excoriated. Seborrheic keratosis can mimic melanoma and squamous cell carcinoma, but skin biopsy confirms the diagnosis. When seborrheic keratoses are symptomatic, they may be treated with cryotherapy or shave removal. The sign of Leser 'l'rdlat is the sudden eruption of numerous seborrheic keratosis and is associated with an internal malignancy.

F I G UR E 1 04. Verruca plaque on the lateral nail Iold that looks like a wa(, but TABLE 84. Human Papillomavirus Subtypes biopsy demonstrated squamous cell carcinoma. 5u btype Clinical Lesion (Location) 1 Verruca plantaris/palmaris (soles/palms) Benign Nodules and Tumors )t Verruca vulgaris (fingers, knees, and elbows) Seborrheic Keratosis 3, 10 Verruca plana (face and legs; associated with shaving) Seborrheic keratoses are benign pigmented neoplasms of 6, 11 Condyloma acuminata keratinocyte origin that are common in older adults. They are 16,18, Condyloma acuminata (associated with high risk "stuck on" papules and plaques that occur anywhere on the 31, 33 for cervical, anal, and penile cancer) body. They most commonly occur on the trunk and spare the palms, soles, and mucous membranes. Seborrheic keratoses range in size lrom a few millimeters to several centimeters. Usually they are brorvn, but they can range in color lrom tan to black (Figure f05). They may become irritated or excoriated. Seborrheic keratosis can mimic melanoma and squamous cell carcinoma, but skin biopsy confirms the diagnosis. When seborrheic keratoses are symptomatic, they may be treated with cryotherapy or shave removal. The sign of Leser 'l'rdlat is the sudden eruption of numerous seborrheic keratosis and is associated with an internal malignancy. tIGURE 1 06, Ihecommon wartisaverrucous papulethatiskeratoticand exophytic. #; .4:,1.'-. -

F I G UR E 1 04. Verruca plaque on the lateral nail Iold that looks like a wa(, but TABLE 84. Human Papillomavirus Subtypes biopsy demonstrated squamous cell carcinoma. 5u btype Clinical Lesion (Location) 1 Verruca plantaris/palmaris (soles/palms) Benign Nodules and Tumors )t Verruca vulgaris (fingers, knees, and elbows) Seborrheic Keratosis 3, 10 Verruca plana (face and legs; associated with shaving) Seborrheic keratoses are benign pigmented neoplasms of 6, 11 Condyloma acuminata keratinocyte origin that are common in older adults. They are 16,18, Condyloma acuminata (associated with high risk "stuck on" papules and plaques that occur anywhere on the 31, 33 for cervical, anal, and penile cancer) body. They most commonly occur on the trunk and spare the palms, soles, and mucous membranes. Seborrheic keratoses range in size lrom a few millimeters to several centimeters. Usually they are brorvn, but they can range in color lrom tan to black (Figure f05). They may become irritated or excoriated. Seborrheic keratosis can mimic melanoma and squamous cell carcinoma, but skin biopsy confirms the diagnosis. When seborrheic keratoses are symptomatic, they may be treated with cryotherapy or shave removal. The sign of Leser 'l'rdlat is the sudden eruption of numerous seborrheic keratosis and is associated with an internal malignancy. tIGURE 1 06, Ihecommon wartisaverrucous papulethatiskeratoticand exophytic. #; .4:,1.'-. - t I G U R E 1 0 5. Seborrheic keratoses are brown, scaly, waxy papules or plaques that commonly occur in older persons. They frequently have a "stuck-on" appearance and otten have verrucous (warty) surface changes as well. Seborrheic keratoses typically demonstrate horn cysts (epidermal cysts filled with keratin) on F I G UR E 1 0 7 . Anogenital warts (condyloma acuminatum) present as verrucous the surface that can best be visualized on dermoscopy. papules over the penile shaft and foreski n with adjacent erosions after imiquimod therapy.

t I G U R E 1 0 5. Seborrheic keratoses are brown, scaly, waxy papules or plaques that commonly occur in older persons. They frequently have a "stuck-on" appearance and otten have verrucous (warty) surface changes as well. Seborrheic keratoses typically demonstrate horn cysts (epidermal cysts filled with keratin) on F I G UR E 1 0 7 . Anogenital warts (condyloma acuminatum) present as verrucous the surface that can best be visualized on dermoscopy. papules over the penile shaft and foreski n with adjacent erosions after imiquimod therapy. 119

Dermatologic Disorders warts) and verruca palmaris (palmar warts) are exophytic and endophytic papules with thrombosed capillaries manifesting as black dots when the top of the wart is pared down. Diagnosis is clinical. Warts are uzually self-limited; how- ever, in severe cases, including those with a protracted course or in persons who are immunocompromised, destructive treatments can be used. Location of the lesions must be taken into account when selecting treatment, which can be associ- ated with pigment change or scarring. Numerous treatments (salicylic acid, cryotherapy, tricarboxylic acid, cantharidin, podophyllin, and laser) focused on destroying infected keratinocytes are available. Other treatments, such as imiqui- mod and intralesional Candido, elicit a local immune response F I G U R E I 09. Dermatofibromas appear as firm dermal nodules about the size of a pencil eraser. They are frequently hyperpig mented or may have pigment at the to eliminate the warts. periphery. HPV vaccination is recommended for young persons to prevent cervical and anal carcinoma and should also serve to during the second trimester of pregnancy and may regress decrease anogenital warts. See Routine Care of the Healthy postpartum. Perianal skin tags are common in patients with Patient for more information. Crohn disease. If lesions become necrotic or crusted, they may require removal with cryotherapy or snip excision. They Callus and Corns can be of cosmetic concern, especially when numerous. The A callus is a collection of thickened, hardened stratum cor- presence of numerous lesions, particularly in the setting of neum that presents as a flat papule or plaque at the site of obesity and acanthosis nigricans, is associated with insulin repetitive trauma, frequently under bones. Sometimes the resistance. term corn is used interchangeably with callus; however, corns have more distinct edges, are more rounded, and have a central Dermatofibroma core that can be soft or hard. Corns are typicaily seen on the Dermatofibrornas are benign, fibrohistiocytic lesions that are sides or tops of toes. Treatment involves mechanical or chemi- common on the extremities, particularly the legs of young cal paring with salirylic acid, but removing the pressure from women. They are tan-to-brown discrete papules that often the site is necessary to prevent repeated formation. have a slightly darker brown ring encircling the main part of the lesion (Figure lo9). Dermatofibromas are usually asymp- Acrochordon (Skin TagB) tomatic, and treatment is not necessary. Acrochordons (skin tags) are skin-colored, pedunculated papules (Figure 108). They are most commonly seen on the Nevi neck and skin folds in older adults and those with obesity and Melanorytic nevi are benigrr neoplasms composed of melano- diabetes mellitus. Skin tags appear with increased frequency cytes; they are commonly referred to as moles. They occur anywhere on the body, including the palms, soles, and mucous membranes. Melanocytic nevi can appear early in childhood and increase in number until middle age. They vary in clinical appearance depending on the location of melanocytes within the skin (Table S5 and Figure ilo). Clinically they can mimic melanoma, necessitating a biopsy for accurate diagnosis. Halo nevi are melanorytic nevi with an admixed chronic lymphocytic infiltrate that signffies regression of the nevus.

warts) and verruca palmaris (palmar warts) are exophytic and endophytic papules with thrombosed capillaries manifesting as black dots when the top of the wart is pared down. Diagnosis is clinical. Warts are uzually self-limited; how- ever, in severe cases, including those with a protracted course or in persons who are immunocompromised, destructive treatments can be used. Location of the lesions must be taken into account when selecting treatment, which can be associ- ated with pigment change or scarring. Numerous treatments (salicylic acid, cryotherapy, tricarboxylic acid, cantharidin, podophyllin, and laser) focused on destroying infected keratinocytes are available. Other treatments, such as imiqui- mod and intralesional Candido, elicit a local immune response F I G U R E I 09. Dermatofibromas appear as firm dermal nodules about the size of a pencil eraser. They are frequently hyperpig mented or may have pigment at the to eliminate the warts. periphery. HPV vaccination is recommended for young persons to prevent cervical and anal carcinoma and should also serve to during the second trimester of pregnancy and may regress decrease anogenital warts. See Routine Care of the Healthy postpartum. Perianal skin tags are common in patients with Patient for more information. Crohn disease. If lesions become necrotic or crusted, they may require removal with cryotherapy or snip excision. They Callus and Corns can be of cosmetic concern, especially when numerous. The A callus is a collection of thickened, hardened stratum cor- presence of numerous lesions, particularly in the setting of neum that presents as a flat papule or plaque at the site of obesity and acanthosis nigricans, is associated with insulin repetitive trauma, frequently under bones. Sometimes the resistance. term corn is used interchangeably with callus; however, corns have more distinct edges, are more rounded, and have a central Dermatofibroma core that can be soft or hard. Corns are typicaily seen on the Dermatofibrornas are benign, fibrohistiocytic lesions that are sides or tops of toes. Treatment involves mechanical or chemi- common on the extremities, particularly the legs of young cal paring with salirylic acid, but removing the pressure from women. They are tan-to-brown discrete papules that often the site is necessary to prevent repeated formation. have a slightly darker brown ring encircling the main part of the lesion (Figure lo9). Dermatofibromas are usually asymp- Acrochordon (Skin TagB) tomatic, and treatment is not necessary. Acrochordons (skin tags) are skin-colored, pedunculated papules (Figure 108). They are most commonly seen on the Nevi neck and skin folds in older adults and those with obesity and Melanorytic nevi are benigrr neoplasms composed of melano- diabetes mellitus. Skin tags appear with increased frequency cytes; they are commonly referred to as moles. They occur anywhere on the body, including the palms, soles, and mucous membranes. Melanocytic nevi can appear early in childhood and increase in number until middle age. They vary in clinical appearance depending on the location of melanocytes within the skin (Table S5 and Figure ilo). Clinically they can mimic melanoma, necessitating a biopsy for accurate diagnosis. Halo nevi are melanorytic nevi with an admixed chronic lymphocytic infiltrate that signffies regression of the nevus. Types of Melanocytic Nevi Type Location of Clinical Melanoclrte Appeatance Nests in Skin Junctional Dermal-epidermal Brown-to-black melanocytic nevus junction macules Compound Dermalepidermal Tan-to-brown melanocytic nevus junction and dermis papules or nodules lntradermal Dermis Tan-to-skin- F I G UR E 1 0 8. Acrochordons (skin tags) are skin-colored papules that arise on melanocytic nevus colored papules areas of friction, such as the neck, axillae, and groin.

Types of Melanocytic Nevi Type Location of Clinical Melanoclrte Appeatance Nests in Skin Junctional Dermal-epidermal Brown-to-black melanocytic nevus junction macules Compound Dermalepidermal Tan-to-brown melanocytic nevus junction and dermis papules or nodules lntradermal Dermis Tan-to-skin- F I G UR E 1 0 8. Acrochordons (skin tags) are skin-colored papules that arise on melanocytic nevus colored papules areas of friction, such as the neck, axillae, and groin. 120

Dermatologic Disorders FIGURE 1 I 0. Compound melanocytic nevi aretan-to-brown papules with regular borders and even color. FIGUnE 1 1 2. Dysplasticnevi arecommonlylargerthan6 mm and have irregular borders. Ihis patient has numerous dysplastic nevi and is at increased risk for melanoma.

FIGURE 1 I 0. Compound melanocytic nevi aretan-to-brown papules with regular borders and even color. FIGUnE 1 1 2. Dysplasticnevi arecommonlylargerthan6 mm and have irregular borders. Ihis patient has numerous dysplastic nevi and is at increased risk for melanoma. stand out from the patient's other nevi. Patients with multiple dysplastic nevi are at risk for developing melanoma and should be monitored closely (Figure 112). Some of these patients have dysplastic nevus syndrome. Criteria for this syndrome include a history of melanoma in one or more first- or second-degree relatives, the presence ofmore than 50 nevi, multiple nevi with atypical clinical features, and multiple nevi with atypical histologic features. These patients are at increased risk for melanoma and should have yearly total- body skin examinations. f IGURE I 1 1. Halo nevus,with a depigmented halosunounding a brown papule. . Warts are usually self-limited and treatment unneces- HVC Halo nevi are central tan-to-brown macules or papules with a sary; however, in severe cases, including those with a surrounding halo of hypopigmented or depigmented skin protracted course or in persons who are funmunocom- (Figure 111) . They most frequently present on the back of teen- promised, destructive treatments can be used. agers or young adults. Multiple halo nevi have been associated . Dysplastic nevi can display one or more of the identi$r- with melanoma; therefore, these patients should have a com- ing characteristics of melanoma; patients with multiple plete skin examination to assess for concurrent lesions. dysplastic nevi are at increased risk for melanoma and should be monitored closely. Dysplastic Nevi r Excisional biopsy of dysplastic nevi is reserved for HVC Dysplastic (or atypical) nevi are melanocytic nevi that are lesions that display features suggesting melanoma, are often asymmetric and irregularly bordered, have multiple changing in size and color, are symptomatic, or stand colors, and may be quite large in diameter. Dysplastic nevi are out from the patient's other nevi. most commonly found on the trunk and extremities. Many have a "fried egg" appearance with an eccentric, dark brown papular center and surrounding light brown ring. Dysplastic nevi can display one or more of the identiffing characteristics Premalignant and of melanoma, making an accurate clinical diagnosis impossi- Malignant Tumors ble (see Melanoma). In cases of uncertainty, biopsy of the Skin cancer is a major public health concem, and one in five lesion can typically exclude melanoma; however, it is impera- people in the United States will develop it. Most cases are tive to sample the entire lesion, including a 1- to 2-mm border caused by excessive UV light exposure. People ofall skin pig- of normal surrounding skin. mentation can develop skin cancer, but fair-skinned persons Although melanoma can arise within any melanocytic are more susceptible to the effects of UV light exposure. nevi, including dysplastic nevi, the risk for this occurring within any given lesion is quite small. Excisional biopsy is Actinic Keratosis reserved for lesions that display features suggesting mela- Actinic keratoses are precancerous lesions of the epidermis. noma, are changing in size and color, are symptomatic, or Approximately l% lo 5% of actinic keratoses will develop into

stand out from the patient's other nevi. Patients with multiple dysplastic nevi are at risk for developing melanoma and should be monitored closely (Figure 112). Some of these patients have dysplastic nevus syndrome. Criteria for this syndrome include a history of melanoma in one or more first- or second-degree relatives, the presence ofmore than 50 nevi, multiple nevi with atypical clinical features, and multiple nevi with atypical histologic features. These patients are at increased risk for melanoma and should have yearly total- body skin examinations. f IGURE I 1 1. Halo nevus,with a depigmented halosunounding a brown papule. . Warts are usually self-limited and treatment unneces- HVC Halo nevi are central tan-to-brown macules or papules with a sary; however, in severe cases, including those with a surrounding halo of hypopigmented or depigmented skin protracted course or in persons who are funmunocom- (Figure 111) . They most frequently present on the back of teen- promised, destructive treatments can be used. agers or young adults. Multiple halo nevi have been associated . Dysplastic nevi can display one or more of the identi$r- with melanoma; therefore, these patients should have a com- ing characteristics of melanoma; patients with multiple plete skin examination to assess for concurrent lesions. dysplastic nevi are at increased risk for melanoma and should be monitored closely. Dysplastic Nevi r Excisional biopsy of dysplastic nevi is reserved for HVC Dysplastic (or atypical) nevi are melanocytic nevi that are lesions that display features suggesting melanoma, are often asymmetric and irregularly bordered, have multiple changing in size and color, are symptomatic, or stand colors, and may be quite large in diameter. Dysplastic nevi are out from the patient's other nevi. most commonly found on the trunk and extremities. Many have a "fried egg" appearance with an eccentric, dark brown papular center and surrounding light brown ring. Dysplastic nevi can display one or more of the identiffing characteristics Premalignant and of melanoma, making an accurate clinical diagnosis impossi- Malignant Tumors ble (see Melanoma). In cases of uncertainty, biopsy of the Skin cancer is a major public health concem, and one in five lesion can typically exclude melanoma; however, it is impera- people in the United States will develop it. Most cases are tive to sample the entire lesion, including a 1- to 2-mm border caused by excessive UV light exposure. People ofall skin pig- of normal surrounding skin. mentation can develop skin cancer, but fair-skinned persons Although melanoma can arise within any melanocytic are more susceptible to the effects of UV light exposure. nevi, including dysplastic nevi, the risk for this occurring within any given lesion is quite small. Excisional biopsy is Actinic Keratosis reserved for lesions that display features suggesting mela- Actinic keratoses are precancerous lesions of the epidermis. noma, are changing in size and color, are symptomatic, or Approximately l% lo 5% of actinic keratoses will develop into 121

Dermatologic Disorders .z$. F I G UR E I I 3. Actinic keratoses are typically pink, thin papules or plaques that occur on sun-exposed areas, particularly the face and dorsal arms. Fl G U R E 1 1 5. Pink hyperkeratotic nodule on sun-exposed skin consistent with squamous cell tarcinoma. squamous cell skin cancers. Although the risk that an indi- vidual lesion will develop into a squamous cell carcinoma is pigmented patients, those with skin of darker pigment more low, many patients have multiple actinic keratoses, which often develop SCC in regions with chronic inflammation or increase their overall risk. Actinic keratoses present as ill- scarring. SCC can be locally invasive and has the potential to defined, pink, scaly papules or plaques, mostly in sun exposed metastasize. Histologically, it can range from well differenti areas (Figure 113). Individual lesions can be treated with cryo ated SCC to the more aggressive poorly differentiated SCC. therapy. [n patients with diffuse actinic damage, field treat High risk features in SCC are tumor diameter greater than ment with topical medications (5 fluorouracil, imiquimod, 2 cm, tumor thickness greater than 2 mm, poorly differenti- ingenol mebutate) or photodynamic therapy can be used. ated subtypes, perineural invasion, and tumor location on the Lesions that do not resolve with cryotherapy or are more indu ear or nonglabrous lip (Figure 116). rated will require biopsy to rule out an invasive neoplasm. With SCC in situ (Bowen disease), malignant keratino cytes are confined to the epidermis. It appears as large scaly Squamous Cell Carcinoma and Keratoacanthoma pink and tan plaques with well defined borders (Figure 117). Squamous cell carcinoma (SCC), the second most common Surgical excision, including Mohs micrographic surgery skin cancer, is a malignant neoplasm of keratinocytes. It pre is typically first line treatment lor high risk SCC given its sents as pink, scaly indurated plaques, papules, or nodules potentially aggressive behavior and risk for metastasis. If sur- that can ulcerate and bleed (Figure 114 and Figure 115). Risk gery is contraindicated. radiation therapy is an option. In cases factors are UV light exposure, ionizing radiation, chemical of metastasis, chemotherapy can also be considered. carcinogens (coal tar and arsenic), viruses (HPV), and immu Keratoacanthoma is considered to be a variant of SCC by nosuppression (organ transplant). SCC occurs in areas of sun some and a benign tumor by others. Histologicallyl it can exposure and areas of chronic injury (burn scars, irradiated resemble SCC. Keratoacanthoma has a distinct appearance and sites, discoid lupus erythematosus). Compared with lightly

F I G UR E I I 3. Actinic keratoses are typically pink, thin papules or plaques that occur on sun-exposed areas, particularly the face and dorsal arms. Fl G U R E 1 1 5. Pink hyperkeratotic nodule on sun-exposed skin consistent with squamous cell tarcinoma. squamous cell skin cancers. Although the risk that an indi- vidual lesion will develop into a squamous cell carcinoma is pigmented patients, those with skin of darker pigment more low, many patients have multiple actinic keratoses, which often develop SCC in regions with chronic inflammation or increase their overall risk. Actinic keratoses present as ill- scarring. SCC can be locally invasive and has the potential to defined, pink, scaly papules or plaques, mostly in sun exposed metastasize. Histologically, it can range from well differenti areas (Figure 113). Individual lesions can be treated with cryo ated SCC to the more aggressive poorly differentiated SCC. therapy. [n patients with diffuse actinic damage, field treat High risk features in SCC are tumor diameter greater than ment with topical medications (5 fluorouracil, imiquimod, 2 cm, tumor thickness greater than 2 mm, poorly differenti- ingenol mebutate) or photodynamic therapy can be used. ated subtypes, perineural invasion, and tumor location on the Lesions that do not resolve with cryotherapy or are more indu ear or nonglabrous lip (Figure 116). rated will require biopsy to rule out an invasive neoplasm. With SCC in situ (Bowen disease), malignant keratino cytes are confined to the epidermis. It appears as large scaly Squamous Cell Carcinoma and Keratoacanthoma pink and tan plaques with well defined borders (Figure 117). Squamous cell carcinoma (SCC), the second most common Surgical excision, including Mohs micrographic surgery skin cancer, is a malignant neoplasm of keratinocytes. It pre is typically first line treatment lor high risk SCC given its sents as pink, scaly indurated plaques, papules, or nodules potentially aggressive behavior and risk for metastasis. If sur- that can ulcerate and bleed (Figure 114 and Figure 115). Risk gery is contraindicated. radiation therapy is an option. In cases factors are UV light exposure, ionizing radiation, chemical of metastasis, chemotherapy can also be considered. carcinogens (coal tar and arsenic), viruses (HPV), and immu Keratoacanthoma is considered to be a variant of SCC by nosuppression (organ transplant). SCC occurs in areas of sun some and a benign tumor by others. Histologicallyl it can exposure and areas of chronic injury (burn scars, irradiated resemble SCC. Keratoacanthoma has a distinct appearance and sites, discoid lupus erythematosus). Compared with lightly t I G U R E I 1 6. Squamous cell carcinoma lesions on the lower lip most commonly F I G UR E I 1 4. Pink scaly plaque consistent with squamous cell carcinoma arise from sun damage, often in the setting o{ actinic cheilitis.

F I G UR E I I 3. Actinic keratoses are typically pink, thin papules or plaques that occur on sun-exposed areas, particularly the face and dorsal arms. Fl G U R E 1 1 5. Pink hyperkeratotic nodule on sun-exposed skin consistent with squamous cell tarcinoma. squamous cell skin cancers. Although the risk that an indi- vidual lesion will develop into a squamous cell carcinoma is pigmented patients, those with skin of darker pigment more low, many patients have multiple actinic keratoses, which often develop SCC in regions with chronic inflammation or increase their overall risk. Actinic keratoses present as ill- scarring. SCC can be locally invasive and has the potential to defined, pink, scaly papules or plaques, mostly in sun exposed metastasize. Histologically, it can range from well differenti areas (Figure 113). Individual lesions can be treated with cryo ated SCC to the more aggressive poorly differentiated SCC. therapy. [n patients with diffuse actinic damage, field treat High risk features in SCC are tumor diameter greater than ment with topical medications (5 fluorouracil, imiquimod, 2 cm, tumor thickness greater than 2 mm, poorly differenti- ingenol mebutate) or photodynamic therapy can be used. ated subtypes, perineural invasion, and tumor location on the Lesions that do not resolve with cryotherapy or are more indu ear or nonglabrous lip (Figure 116). rated will require biopsy to rule out an invasive neoplasm. With SCC in situ (Bowen disease), malignant keratino cytes are confined to the epidermis. It appears as large scaly Squamous Cell Carcinoma and Keratoacanthoma pink and tan plaques with well defined borders (Figure 117). Squamous cell carcinoma (SCC), the second most common Surgical excision, including Mohs micrographic surgery skin cancer, is a malignant neoplasm of keratinocytes. It pre is typically first line treatment lor high risk SCC given its sents as pink, scaly indurated plaques, papules, or nodules potentially aggressive behavior and risk for metastasis. If sur- that can ulcerate and bleed (Figure 114 and Figure 115). Risk gery is contraindicated. radiation therapy is an option. In cases factors are UV light exposure, ionizing radiation, chemical of metastasis, chemotherapy can also be considered. carcinogens (coal tar and arsenic), viruses (HPV), and immu Keratoacanthoma is considered to be a variant of SCC by nosuppression (organ transplant). SCC occurs in areas of sun some and a benign tumor by others. Histologicallyl it can exposure and areas of chronic injury (burn scars, irradiated resemble SCC. Keratoacanthoma has a distinct appearance and sites, discoid lupus erythematosus). Compared with lightly t I G U R E I 1 6. Squamous cell carcinoma lesions on the lower lip most commonly F I G UR E I 1 4. Pink scaly plaque consistent with squamous cell carcinoma arise from sun damage, often in the setting o{ actinic cheilitis. 122

Dermatologic Disorders F 1G U R E I 1 9 . Pearly nodule with arborizing telangiectasias (botto m left of nodule\ and ulceration characteristic of nodular basal cell carcinoma. Patients usually present with a new papule that is bleeding or not healing. They often have other signs of photodamage, such F lG U R E 1 1 7. Squamous cell carcinoma in situ (Bowen disease) typically as freckles and lentigines. presents as a gradually enlarging, well-demarcated erythematous plaque with an irregular border and surface crusting or scaling. Nodular basal cell carcinoma is the most common type of BCC. It presents as a pearly or translucent nodule or papule

Patients usually present with a new papule that is bleeding or not healing. They often have other signs of photodamage, such F lG U R E 1 1 7. Squamous cell carcinoma in situ (Bowen disease) typically as freckles and lentigines. presents as a gradually enlarging, well-demarcated erythematous plaque with an irregular border and surface crusting or scaling. Nodular basal cell carcinoma is the most common type of BCC. It presents as a pearly or translucent nodule or papule clinical course. It appears rapidly (within 4 to 6 weeks) as a with arborizing telangiectasias. It may have a central depres round pink nodule with a central, keratin-filled crater, giving sion or ulceration with a rolled waxy border (Figure 119). The it a "volcaniform" appearance (Figure 118). After its rapid term rodent ulcer is used to describe the ulceration. Nodular BCC is most commonly found on the face, especially the nose. growth, some keratoacanthomas tend to involute. Because it is difficult to differentiate flrom SCC, they are often treated with Histologically, nodular BCC is a low-risk subtype, whereas surgical excision. micronodular BCC is higher risk. The two subtypes can only be distinguished by histologic assessment. Basal Cell Carcinoma The superficial type of BCC appears as a pink red patch with or without scale. It may have a slight threadlike pearly Basal cell carcinoma (BCC) is a malignant neoplasm arising rolled border. lt can be mistaken for an actinic keratosis: SCC from the basal Iayer of the epidermis. It is the most common in situ; or a patch of dermatitis, such as psoriasis or nummular type of skin cancer. Metastasis rarely occurs; however, without dermatitis. Superficial BCC tends to be a persistent solitary treatment, it can cause significant local tissue destruction. The patch that does not respond to topical glucocorticoids. Biopsy most common causative factor is W light exposure. There are provides defi nitive diagnosis. different histologic subtypes, including superficial, pigmented, Pigmented BCC presents as shiny blue black papules, sclerotic, and nodular, that result in varying clinical appearance. nodules, or plaques that can appear translucent with blue- black speckles and a rolled border. It is more common in patients with darker skin. Sclerotic BCC, which includes morpheaform and infiltra tive subtypes, presents as atrophic plaques or papules that can resemble a scar. Although it is the least common BCC, it is a high-risk, aggressive histologic subtype. The diagnosis of BCC should be confirmed histologically with a shave or punch biopsy. The use of a dermatoscope to identiff dermatoscopic patterns of BCCs (such as arborizing vessels) can improve the accuracy ofpre biopsy diagnosis. Treatment ofBCC should be based on patient preference and health status, location ofthe lesion, histologic subtype, size, and primary versus recurrent nature. Therapeutic options include surgery (standard excision, Mohs micrographic surgery); elec- trodessication and curettage; cryosurgery; topical chemotherapy; F I G U R E 1 I 8. Rapidly growing, pink "volcaniform" nodule with central crust radiation therapy; and, for metastatic or inoperable lesions, oral that is characteristic of a keratoacanthoma. hedgehog pathway inhibitors (vismodegib, sonidegib).

clinical course. It appears rapidly (within 4 to 6 weeks) as a with arborizing telangiectasias. It may have a central depres round pink nodule with a central, keratin-filled crater, giving sion or ulceration with a rolled waxy border (Figure 119). The it a "volcaniform" appearance (Figure 118). After its rapid term rodent ulcer is used to describe the ulceration. Nodular BCC is most commonly found on the face, especially the nose. growth, some keratoacanthomas tend to involute. Because it is difficult to differentiate flrom SCC, they are often treated with Histologically, nodular BCC is a low-risk subtype, whereas surgical excision. micronodular BCC is higher risk. The two subtypes can only be distinguished by histologic assessment. Basal Cell Carcinoma The superficial type of BCC appears as a pink red patch with or without scale. It may have a slight threadlike pearly Basal cell carcinoma (BCC) is a malignant neoplasm arising rolled border. lt can be mistaken for an actinic keratosis: SCC from the basal Iayer of the epidermis. It is the most common in situ; or a patch of dermatitis, such as psoriasis or nummular type of skin cancer. Metastasis rarely occurs; however, without dermatitis. Superficial BCC tends to be a persistent solitary treatment, it can cause significant local tissue destruction. The patch that does not respond to topical glucocorticoids. Biopsy most common causative factor is W light exposure. There are provides defi nitive diagnosis. different histologic subtypes, including superficial, pigmented, Pigmented BCC presents as shiny blue black papules, sclerotic, and nodular, that result in varying clinical appearance. nodules, or plaques that can appear translucent with blue- black speckles and a rolled border. It is more common in patients with darker skin. Sclerotic BCC, which includes morpheaform and infiltra tive subtypes, presents as atrophic plaques or papules that can resemble a scar. Although it is the least common BCC, it is a high-risk, aggressive histologic subtype. The diagnosis of BCC should be confirmed histologically with a shave or punch biopsy. The use of a dermatoscope to identiff dermatoscopic patterns of BCCs (such as arborizing vessels) can improve the accuracy ofpre biopsy diagnosis. Treatment ofBCC should be based on patient preference and health status, location ofthe lesion, histologic subtype, size, and primary versus recurrent nature. Therapeutic options include surgery (standard excision, Mohs micrographic surgery); elec- trodessication and curettage; cryosurgery; topical chemotherapy; F I G U R E 1 I 8. Rapidly growing, pink "volcaniform" nodule with central crust radiation therapy; and, for metastatic or inoperable lesions, oral that is characteristic of a keratoacanthoma. hedgehog pathway inhibitors (vismodegib, sonidegib). 123

Dermatologic Disorders the incidence of melanoma is increasing faster than any other t cancer. The estimated Iifetime risk for melanoma is 1in 50. ft I tends to affect a younger population. There are four major clinical subtypes: zuperficial spreading, lentigo maligna, acral Ientiginous, and nodular melanoma. Risk factors include UV light exposure (both chronic and intermittent blistering sun- burns), genetics/family history large number of nevi, dysplas- I I tic nevi, and fair skin. Although melanoma can arise from a prior nevi, a majority develop de novo. 'l In general, the ABCDEs of identiffing characteristics can I

the incidence of melanoma is increasing faster than any other t cancer. The estimated Iifetime risk for melanoma is 1in 50. ft I tends to affect a younger population. There are four major clinical subtypes: zuperficial spreading, lentigo maligna, acral Ientiginous, and nodular melanoma. Risk factors include UV light exposure (both chronic and intermittent blistering sun- burns), genetics/family history large number of nevi, dysplas- I I tic nevi, and fair skin. Although melanoma can arise from a prior nevi, a majority develop de novo. 'l In general, the ABCDEs of identiffing characteristics can I help diagnose melanoma: Asymmetry irregular Border, mul- tiple Colors, Diameter greater than 6 mm, and Evolution or change over time. Not all melanomas follow all of these char- acteristics, and biopsy should be considered ifthere is a lesion I that is different from the patient's other nevi. t I G U n E I 2 0. Untreated basal cell carcinomas (BCC) over time can become Superficial spreading melanoma is the most common large and cause significant local tissue damage. BCC occuning in the mask area of type of melanoma (Figure 121). It can occur anywhere on the the face and BCC with certain histology not only expand in the skin but can also body. In men, the most common Iocation is the back, whereas invade deeper tissues, including the fascia, muscle, bone, and nerves. These tumors in women, it is more often found on the legs. are at high risk for recu nence after treatment, along with structural damage. Ientgo maligna is a melanoma more @uently found on the head and neck region. It is associated with frequent chronic Surgical excision is the most commonly used intervention W light exposure. It is uzually found in older patiefis, peaking in and results in the highest curc rate. Mohs micrographic sur- the seventh and eighth decades oflife. It presents as ill-defined, gery is a highly specialized surgical technique that combines asymmetric brown orblack macules orpatches, often reaching a patholory and surgery for complete margin control and tissue diameterof 5 to 7 cmbefore in'rasion (tigure Uf2). The change and conservation. It is appropriately used for cancers in the head darkening of the lesion can be very insidious and may be mis- and neck regron, those that are large or recurrent, or in areas taken for a solar lentigo or seborrheic keratoses. where tissue-sparing is critical for function. Figure 12O shows Acral lentiginous melanoma occurs on the palms, soles, BCC that would likely be managed with Mohs micrographic and distal fingers and toes. It is an ill-defined, black macule surgery. Curettage and electrodessication can be used for plaque, and it more frequenfly occurs in patients with darker superficial or nodular BCCs on the trunk. It should not be used skin (Figure 123). The average time to diagnosis is 2 years, and for tumors 2 cm or larger, those with poorly defined borders, it is often diagnosed at an advanced stage. recurrent or high-risk histologic subtypes, and those Melanoma of the nail matrix can occur on any nail but is appearing in certain anatomic locations (face, scalp, eyelids). most common on the nail of the thumb and great toe. It com- Cryosurgery for BCC differs from that for actinic keratosis; the monly presents as longitudinal melanonychia (tigure Ila). margin, depth, and temperature must be monitored to achieve Biopsy of the nail matrix should be performed if pigment cure. Topical chemotherapy with S-fluorouracil or imiquimod extends onto the nail folds (Hutchinson sign). See Nail can be used for superficial BCC; however, its cure rate is user Disorders for more information. dependent. The treatment course lasts for weeks and results in marked inflammation and irritation. Topical therapies are inappropriate for deep, recurrent, or sclerotic tumors. Radiation therapy is generally reserved for inoperable tumors or patients who decline surgical treatment. Follow-up skin examination every 6 to 12 months is rec- ommended because the risk for another BCC is increased. Prevention with sun protection, including routine use of sun- screen with sun protection factor greater than 35, protective clothing (wide-brimmed hats, long sleeves), and avoidance of midday sun (10:OO au to 2:00 rrr,t), is highly recommended.

help diagnose melanoma: Asymmetry irregular Border, mul- tiple Colors, Diameter greater than 6 mm, and Evolution or change over time. Not all melanomas follow all of these char- acteristics, and biopsy should be considered ifthere is a lesion I that is different from the patient's other nevi. t I G U n E I 2 0. Untreated basal cell carcinomas (BCC) over time can become Superficial spreading melanoma is the most common large and cause significant local tissue damage. BCC occuning in the mask area of type of melanoma (Figure 121). It can occur anywhere on the the face and BCC with certain histology not only expand in the skin but can also body. In men, the most common Iocation is the back, whereas invade deeper tissues, including the fascia, muscle, bone, and nerves. These tumors in women, it is more often found on the legs. are at high risk for recu nence after treatment, along with structural damage. Ientgo maligna is a melanoma more @uently found on the head and neck region. It is associated with frequent chronic Surgical excision is the most commonly used intervention W light exposure. It is uzually found in older patiefis, peaking in and results in the highest curc rate. Mohs micrographic sur- the seventh and eighth decades oflife. It presents as ill-defined, gery is a highly specialized surgical technique that combines asymmetric brown orblack macules orpatches, often reaching a patholory and surgery for complete margin control and tissue diameterof 5 to 7 cmbefore in'rasion (tigure Uf2). The change and conservation. It is appropriately used for cancers in the head darkening of the lesion can be very insidious and may be mis- and neck regron, those that are large or recurrent, or in areas taken for a solar lentigo or seborrheic keratoses. where tissue-sparing is critical for function. Figure 12O shows Acral lentiginous melanoma occurs on the palms, soles, BCC that would likely be managed with Mohs micrographic and distal fingers and toes. It is an ill-defined, black macule surgery. Curettage and electrodessication can be used for plaque, and it more frequenfly occurs in patients with darker superficial or nodular BCCs on the trunk. It should not be used skin (Figure 123). The average time to diagnosis is 2 years, and for tumors 2 cm or larger, those with poorly defined borders, it is often diagnosed at an advanced stage. recurrent or high-risk histologic subtypes, and those Melanoma of the nail matrix can occur on any nail but is appearing in certain anatomic locations (face, scalp, eyelids). most common on the nail of the thumb and great toe. It com- Cryosurgery for BCC differs from that for actinic keratosis; the monly presents as longitudinal melanonychia (tigure Ila). margin, depth, and temperature must be monitored to achieve Biopsy of the nail matrix should be performed if pigment cure. Topical chemotherapy with S-fluorouracil or imiquimod extends onto the nail folds (Hutchinson sign). See Nail can be used for superficial BCC; however, its cure rate is user Disorders for more information. dependent. The treatment course lasts for weeks and results in marked inflammation and irritation. Topical therapies are inappropriate for deep, recurrent, or sclerotic tumors. Radiation therapy is generally reserved for inoperable tumors or patients who decline surgical treatment. Follow-up skin examination every 6 to 12 months is rec- ommended because the risk for another BCC is increased. Prevention with sun protection, including routine use of sun- screen with sun protection factor greater than 35, protective clothing (wide-brimmed hats, long sleeves), and avoidance of midday sun (10:OO au to 2:00 rrr,t), is highly recommended. Melanoma Melanoma is a malignant neoplasm of the melanocytes. Although it is less common than BCC and SCC, it is histologi- cally aggressive and has a much higher rate of metastasis. It is FIGUnE 121. Asuperficial spreading melanoma with prominentABCD: responsible for most skin cancer deaths. In the United States, Asymmetry, inegular Borders, Color variation, and large size (Diameter).

Melanoma Melanoma is a malignant neoplasm of the melanocytes. Although it is less common than BCC and SCC, it is histologi- cally aggressive and has a much higher rate of metastasis. It is FIGUnE 121. Asuperficial spreading melanoma with prominentABCD: responsible for most skin cancer deaths. In the United States, Asymmetry, inegular Borders, Color variation, and large size (Diameter). 124

Dermatologic Disorders ** a i t lG U R E I 2 2. lll-defined asymmetric brown patch consistent with a lentigo maligna, which presents as a slowly enlarging, variegated, pigmented patch on sun-damaged skin. tIGURE I 24. Longitudinal melanonychia showing the hyperpigmentation at the proximal nail fold (Hutchinson sign), a clinical sign suggesting the presence of subungual melanoma. FIGURE 123.lll-delined,asymmetric,black-grayulceratedplaqueontheheel, typical of acral lentiginous melanoma. Nodular melanoma begins in the vertical growth phase and is more aggressive. It grows rapidly and presents as blue black, smooth, or eroded nodules occurring any,vhere on the body (Figure 12s). All suspicious pigmented lesions must be biopsied. The preferred biopsy method for a pigmented lesion is an exci- sional biopsy with a 1- to 2-mm margin to obtain the entire t lG U R E 1 2 5. Nodular melanomas typically present as uniformly dark blue or lesion and prevent sampling error. Shave biopsies should be black "berry-like" lesions that most commonly originate from normal skin. They can

Nodular melanoma begins in the vertical growth phase and is more aggressive. It grows rapidly and presents as blue black, smooth, or eroded nodules occurring any,vhere on the body (Figure 12s). All suspicious pigmented lesions must be biopsied. The preferred biopsy method for a pigmented lesion is an exci- sional biopsy with a 1- to 2-mm margin to obtain the entire t lG U R E 1 2 5. Nodular melanomas typically present as uniformly dark blue or lesion and prevent sampling error. Shave biopsies should be black "berry-like" lesions that most commonly originate from normal skin. They can avoided in most pigmented lesions because there is risk fbr also arise from preexisting nevi, as did this melanoma. Nodular melanomas grow vertically rather than horizontally. transecting a melanoma and preventing accurate staging of the lesion. A modified shave technique for pigmented lesions is scoop biopsy, in which the deep dermis or subcutaneous Poor prognostic factors include male gender, increasing tissue is removed to get underneath the lesion. In wide, ill- age, increased tumor thickness (Breslow depth), ulceration, defined lesions, it may be impossible to remove the entire increased tumor mitotic rate, and head/neck/trunk locations. lesion and thus an incisional biopsy is acceptable. Definitive Melanomas are staged with the tumor, nodal, and metastasis treatment cannot be determined until histologic confirmation (TNM) system (https'//cancerstaging.org/references tools/ and final staging of the tumor is completed. quickreferences/Documents/ MelanomaLarge.pdf ). 125

Dermatologic Disorders IE? POIIIS severe psoriasis also have a greater risk for cardiovascular dis- . Squamous cell carcinoma presents as pink, scaly indu- ease (leading cause of death among patients with psoriasis) and chronic kidney disease. Psoriasis is associated with multi- rated plaques, papules, or nodules that can ulcerate and ple cardiovascular risk factors, including obesity, hyperten- bleed. sion, diabetes, dyslipidemia, and the metabolic syndrome. o Nodular basal cell carcinoma is the most common type Tobacco smoking may worsen psoriasis, and all patients of basal cell carcinoma, typically presenting as a pearly should be counseled against smoking, especially because of or translucent nodule or papule with arborizing telan- the elevated risk for cardiovascular disease. The pharmaco giectasias; it may often have a central depression or logic treatment of psoriasis depends on the severity of the ulceration with a rolled waxy border. disease. Topical glucocorticoids are the mainstay of treatment o Identi$ing characteristics of melanoma are the ABCDEs: lor localized disease. Topical vitamin D analogues are also used Asymmetry irregular Border, multiple Colors, Diameter as monotherapy or in combination with topical glucocorti greater than 6 mm, and Evolution or change over time. coids. Systemic therapies, including phototherapy and oral o All suspicious pigmented lesions must be biopsied; the medications (e.g., methotrexate, acitretin, and cyclosporine), preferred method is an excisional biopsy with a 1- to should be considered in patients with skin involvement of 2-mm margin. greater than 10'X, BSA (severe psoriasis), psoriatic arthritis, psoriasis recalcitrant to topical treatments, or psoriasis in locations such as the scalp or groin.

. Squamous cell carcinoma presents as pink, scaly indu- ease (leading cause of death among patients with psoriasis) and chronic kidney disease. Psoriasis is associated with multi- rated plaques, papules, or nodules that can ulcerate and ple cardiovascular risk factors, including obesity, hyperten- bleed. sion, diabetes, dyslipidemia, and the metabolic syndrome. o Nodular basal cell carcinoma is the most common type Tobacco smoking may worsen psoriasis, and all patients of basal cell carcinoma, typically presenting as a pearly should be counseled against smoking, especially because of or translucent nodule or papule with arborizing telan- the elevated risk for cardiovascular disease. The pharmaco giectasias; it may often have a central depression or logic treatment of psoriasis depends on the severity of the ulceration with a rolled waxy border. disease. Topical glucocorticoids are the mainstay of treatment o Identi$ing characteristics of melanoma are the ABCDEs: lor localized disease. Topical vitamin D analogues are also used Asymmetry irregular Border, multiple Colors, Diameter as monotherapy or in combination with topical glucocorti greater than 6 mm, and Evolution or change over time. coids. Systemic therapies, including phototherapy and oral o All suspicious pigmented lesions must be biopsied; the medications (e.g., methotrexate, acitretin, and cyclosporine), preferred method is an excisional biopsy with a 1- to should be considered in patients with skin involvement of 2-mm margin. greater than 10'X, BSA (severe psoriasis), psoriatic arthritis, psoriasis recalcitrant to topical treatments, or psoriasis in locations such as the scalp or groin. I nfla mmatory Dermatoses Lichen Planus Psoriasis Lichen planus is a T-cell mediated disease classically present Psoriasis is a chronic inflammatory dermatosis, typically pre ing as pruritic, flat topped, violaceous papules, often on the senting with thick, well-demarcated red plaques with overly- flexural surfaces of the extremities (wrists and ankles) and ing silvery scale (Figure 126). It affects approximately 2"/,,1o 4"/,' mucous membranes (Figure 127). This disease is fairly com of the population. The incidence peaks at age 30 to 39 years mon. with an incidence of O.2% to 1'l, in adults. Other variants and again around age 60 years. Psoriasis has many clinical include nail, genital, bullous, atrophic, and hypertrophic presentations, the most common being plaque psoriasis, or Iichen planus. Mucosal lesions have lacy white streaks psoriasis lrrlgaris. Other less common subtypes include gut (Wickham striae) or erosions and ulcerations. tate psoriasis (commonly seen in pediatric patients), palmo Lichen planus tends to resolve over the course of 1 to plantar psoriasis (fiequently seen with pustules as the primary 2 years, although oral and nail lichen planus are more persis- lesion), and inverse psoriasis (often seen without scale in the tent. Some studies have shown an increased prevalence of HCV intertriginous areas). Inverse psoriasis is frequently misdiag infection in patients with lichen planus. Squamous cell carci- nosed because of lack of scale; location (flexural); and resem noma transformation has been reported most commonly in blance to such conditions as tinea, intertrigo, and allergic erosive oral lichen planus and hypertrophic lichen planus contact dermatitis. The severity of psoriasis can range drasti (Figure 128). cally, from a single plaque to an erythrodermic presentation Potent topical glucocorticoids are effective in most involving more than 90'X, BSA. patients. Systemic glucocorticoids, oral retinoids, sulfasalazine, Psoriasis is a systemic disease. Approximately 30% of patients have concurrent psoriatic arthritis. Patients with

I nfla mmatory Dermatoses Lichen Planus Psoriasis Lichen planus is a T-cell mediated disease classically present Psoriasis is a chronic inflammatory dermatosis, typically pre ing as pruritic, flat topped, violaceous papules, often on the senting with thick, well-demarcated red plaques with overly- flexural surfaces of the extremities (wrists and ankles) and ing silvery scale (Figure 126). It affects approximately 2"/,,1o 4"/,' mucous membranes (Figure 127). This disease is fairly com of the population. The incidence peaks at age 30 to 39 years mon. with an incidence of O.2% to 1'l, in adults. Other variants and again around age 60 years. Psoriasis has many clinical include nail, genital, bullous, atrophic, and hypertrophic presentations, the most common being plaque psoriasis, or Iichen planus. Mucosal lesions have lacy white streaks psoriasis lrrlgaris. Other less common subtypes include gut (Wickham striae) or erosions and ulcerations. tate psoriasis (commonly seen in pediatric patients), palmo Lichen planus tends to resolve over the course of 1 to plantar psoriasis (fiequently seen with pustules as the primary 2 years, although oral and nail lichen planus are more persis- lesion), and inverse psoriasis (often seen without scale in the tent. Some studies have shown an increased prevalence of HCV intertriginous areas). Inverse psoriasis is frequently misdiag infection in patients with lichen planus. Squamous cell carci- nosed because of lack of scale; location (flexural); and resem noma transformation has been reported most commonly in blance to such conditions as tinea, intertrigo, and allergic erosive oral lichen planus and hypertrophic lichen planus contact dermatitis. The severity of psoriasis can range drasti (Figure 128). cally, from a single plaque to an erythrodermic presentation Potent topical glucocorticoids are effective in most involving more than 90'X, BSA. patients. Systemic glucocorticoids, oral retinoids, sulfasalazine, Psoriasis is a systemic disease. Approximately 30% of patients have concurrent psoriatic arthritis. Patients with t I G U R E I 2 6 . Psoriasis presents as well-demarcated, erythematous, tl G U RE 1 2 7. Lichen planus presents as purple, flat-topped papules, most polymorphous plaques with silvery scale. commonly on the ankles and wrists.

I nfla mmatory Dermatoses Lichen Planus Psoriasis Lichen planus is a T-cell mediated disease classically present Psoriasis is a chronic inflammatory dermatosis, typically pre ing as pruritic, flat topped, violaceous papules, often on the senting with thick, well-demarcated red plaques with overly- flexural surfaces of the extremities (wrists and ankles) and ing silvery scale (Figure 126). It affects approximately 2"/,,1o 4"/,' mucous membranes (Figure 127). This disease is fairly com of the population. The incidence peaks at age 30 to 39 years mon. with an incidence of O.2% to 1'l, in adults. Other variants and again around age 60 years. Psoriasis has many clinical include nail, genital, bullous, atrophic, and hypertrophic presentations, the most common being plaque psoriasis, or Iichen planus. Mucosal lesions have lacy white streaks psoriasis lrrlgaris. Other less common subtypes include gut (Wickham striae) or erosions and ulcerations. tate psoriasis (commonly seen in pediatric patients), palmo Lichen planus tends to resolve over the course of 1 to plantar psoriasis (fiequently seen with pustules as the primary 2 years, although oral and nail lichen planus are more persis- lesion), and inverse psoriasis (often seen without scale in the tent. Some studies have shown an increased prevalence of HCV intertriginous areas). Inverse psoriasis is frequently misdiag infection in patients with lichen planus. Squamous cell carci- nosed because of lack of scale; location (flexural); and resem noma transformation has been reported most commonly in blance to such conditions as tinea, intertrigo, and allergic erosive oral lichen planus and hypertrophic lichen planus contact dermatitis. The severity of psoriasis can range drasti (Figure 128). cally, from a single plaque to an erythrodermic presentation Potent topical glucocorticoids are effective in most involving more than 90'X, BSA. patients. Systemic glucocorticoids, oral retinoids, sulfasalazine, Psoriasis is a systemic disease. Approximately 30% of patients have concurrent psoriatic arthritis. Patients with t I G U R E I 2 6 . Psoriasis presents as well-demarcated, erythematous, tl G U RE 1 2 7. Lichen planus presents as purple, flat-topped papules, most polymorphous plaques with silvery scale. commonly on the ankles and wrists. 126

Dermatologic Disorders F I G U R E I 2 9. Targetoid lesions of erythema multiforme, characterized by discrete and confluent annular lesions with pale or dusky centers surrounded by erythematous rings.

F I G U R E I 2 9. Targetoid lesions of erythema multiforme, characterized by discrete and confluent annular lesions with pale or dusky centers surrounded by erythematous rings. nasopharlmx, and genitals are less commonly affected. Fever and malaise may precede rash, and joint pain and swelling have been described. Intemal organ involvement, except as related to under- lying disorder, is unusual and should prompt reconsideration of the diagnosis. Skin biopsy can be helpflrl when the diagnosis is unclear, and direct immunofluorescence can be used to exclude the possibility of autoimmune bullous disease. EM can recur and, in approximate$ 70% of patients, recurence is associated with FIGU R E I 28. Hypertrophic lichen planus presenting with dark purple papules herpes simplex virus infection. These patients may benefit from that coalesce to thick, lichenified plaques, emphasized in areas subjected to frequent scratching and rubbing. suppressive antiviral therapy. Antimicrobial therapy is helpfrrl if M. pneumoniae is the trigger of EM. Systemic glucocorticoids are and phototherapy are reserved for severe cutaneous or persis highly effective for decreasing inflammation and pain, even if tent oral disease. patients have an infectious trigger, and short courses (g + weeks) should be considered early in the disease. Eryrthema Multiforme Ery.thema multiforme (EM) minor is an immune-mediated Erythema Nodosum condition that can be recognized by its classic targetoid plaques Erythema nodosum is the most common form ofpanniculitis, or with characteristic histopathologic features. The sharply inflammation of the subcutaneous fat. Erythema nodosurn man- defined circinate plaques feature two differently colored con- ifests as ill-deflned, tender, bilateral dermal red or violaceous centric rings (pale inner ring, red outer ring) surrounding a nodules, most commonly on the shins bilaterally (Figure 130). pale, dusky, vesiculated or crusted center (Figure 129). These plaques typically appear on the face and acral sites, such as the back of the hands, the arms, legs, or feet. The palms and soles may also be involved. Crops of lesions persist for approxi- mately 7 days and resolve without scarring. Most cases of EM minor are caused by infections, with herpes simplex virus types l and 2 beingthe most common followedby Mycoplasma pneumonioe, particularly in children. Drug-induced cases of EM minor are less frequent and typically result from NSAIDs, antiepileptic drugs, or sulfonamides. Mucosal involvement is rare, but ifpresent, is insignificant. EM major has severe mucosal involvement and systemic grmptoms in addition to typical skin findings foundin EM minor. Lesions in the mouth blister and become painftrl erosions. They are oftenpolycyclic and involve thebuccal mucosa and lips, where tl G U RE I 3 0. Erythema nodosum manifests as painful, red-brown nodules on the edges rnay suggest the concentric rings of EM. The eyes, the anterior shins.

nasopharlmx, and genitals are less commonly affected. Fever and malaise may precede rash, and joint pain and swelling have been described. Intemal organ involvement, except as related to under- lying disorder, is unusual and should prompt reconsideration of the diagnosis. Skin biopsy can be helpflrl when the diagnosis is unclear, and direct immunofluorescence can be used to exclude the possibility of autoimmune bullous disease. EM can recur and, in approximate$ 70% of patients, recurence is associated with FIGU R E I 28. Hypertrophic lichen planus presenting with dark purple papules herpes simplex virus infection. These patients may benefit from that coalesce to thick, lichenified plaques, emphasized in areas subjected to frequent scratching and rubbing. suppressive antiviral therapy. Antimicrobial therapy is helpfrrl if M. pneumoniae is the trigger of EM. Systemic glucocorticoids are and phototherapy are reserved for severe cutaneous or persis highly effective for decreasing inflammation and pain, even if tent oral disease. patients have an infectious trigger, and short courses (g + weeks) should be considered early in the disease. Eryrthema Multiforme Ery.thema multiforme (EM) minor is an immune-mediated Erythema Nodosum condition that can be recognized by its classic targetoid plaques Erythema nodosum is the most common form ofpanniculitis, or with characteristic histopathologic features. The sharply inflammation of the subcutaneous fat. Erythema nodosurn man- defined circinate plaques feature two differently colored con- ifests as ill-deflned, tender, bilateral dermal red or violaceous centric rings (pale inner ring, red outer ring) surrounding a nodules, most commonly on the shins bilaterally (Figure 130). pale, dusky, vesiculated or crusted center (Figure 129). These plaques typically appear on the face and acral sites, such as the back of the hands, the arms, legs, or feet. The palms and soles may also be involved. Crops of lesions persist for approxi- mately 7 days and resolve without scarring. Most cases of EM minor are caused by infections, with herpes simplex virus types l and 2 beingthe most common followedby Mycoplasma pneumonioe, particularly in children. Drug-induced cases of EM minor are less frequent and typically result from NSAIDs, antiepileptic drugs, or sulfonamides. Mucosal involvement is rare, but ifpresent, is insignificant. EM major has severe mucosal involvement and systemic grmptoms in addition to typical skin findings foundin EM minor. Lesions in the mouth blister and become painftrl erosions. They are oftenpolycyclic and involve thebuccal mucosa and lips, where tl G U RE I 3 0. Erythema nodosum manifests as painful, red-brown nodules on the edges rnay suggest the concentric rings of EM. The eyes, the anterior shins. 127

Dermatologic Disorders '':'*Ell S+. Conditions ferrrr,rorrly.Associated With TAEI-E S7, Causes of Acute and Chronic Ervthrodernra Erythenra Nodosum Causes ofAcute Causes of Chronic Streptococcal infection Erythroderma Erythroderma Pregnancy Atopic dermatitis (flare) Atopic dermatitis Oral contraceptive agent use Psoriasis (flare) Psoriasis Hormone replacement therapy use Medication reaction Cutaneous T-cell lymphoma lnflammatory bowel disease Autoimmune disease Graft-versus-host d isease Sarcoidosisu Staphylococcal scalded skin Pityriasis rubra pilaris Medication reaction syndrome Toxic shock syndrome "Erythema nodosum indicates a good prognosis for patients with sarcoidosis. Sdzary syndrome" "Will transition to chronic erythroderma. Erythema nodosum is a nonspecific reaction to a systemic process. Conditions that are commonly associated with ery- thema nodosum are listed in Table 86. Most cases of erythema nodosum resolve spontaneously over 4 to 6 weeks. Therapy is supportive and includes the use of NSAIDs and compression stockings.

"Will transition to chronic erythroderma. Erythema nodosum is a nonspecific reaction to a systemic process. Conditions that are commonly associated with ery- thema nodosum are listed in Table 86. Most cases of erythema nodosum resolve spontaneously over 4 to 6 weeks. Therapy is supportive and includes the use of NSAIDs and compression stockings. Erythroderma Erythroderma is defined as diffuse erythema covering 80% to 90o1, BSA that is commonly associated with pruritus, peripheral edema, erosions, scaling, and lymphadenopathy (Figure 131). Erythroderma may be acute or chronic in pres- entation. Up to 40% of cases are idiopathic with exacerba- tion of a preexisting rash and medication reaction being other common etiologies (Table 87). Erythroderma second- ary to drug reactions, staphylococcal scalded skin syn- drome, and autoimmune bullous diseases often have an acute onset without a long-standing history of preceding dermatosis. Atopic dermatitis or psoriasis can flare to eryth- roderma after injudicious use and abrupt cessation of sys- FIGURE I 32. Ihis patientwith cutaneousT-cell lymphoma hasclassicpatch' temic glucocorticoids. Alopecia, nail dystrophy, and thick- stage mycosis {ungoides with well-demarcated patches and thin overlying scale on the back. ln patients with skin o{ color, these patches are often hyperpigmented ening of the palms and soles are indicative of a long standing with less erythema and are usually pruritic. cause, such as cutaneous T-cell lymphoma (Figure 132), graft-versus-host disease, psoriasis, or pityriasis rubra pila- Management of erythroderma involves treatment of ris. Complications may result from heat and fluid loss across the inflamed skin. infection and managing fluid and electrolyte imbalance. Emollients will help to restore the skin barrier, and topical glucocorticoids and systemic antihistamines will improve pruritus.