Background

The ability to concisely characterize lesions is important for communicating w/ colleagues & formulating Ddx

A complete exam includes skin, mucosal surfaces, nails, hair, & LN (when appropriate)

History: Duration, timing, sx, where/how did lesion(s) start, PMHx, meds (esp new)

Approach to Describing Skin Lesions

Every description must include

• Color (if applicable)

(2)  Primary lesion

• Secondary characteristics (if applicable)
• Distribution
• Grouping (if applicable)

Example: “Ms.        is a 46-year-old woman w/ well-demarcated erythematous plaques w/ silvery scale on her extensor surfaces, scalp, & gluteal cleft” (psoriasis)

Color

White (milium), yellow (sebaceous hyperplasia), gray (argyria), blue (blue nevus), green (pseudomonas), violaceous (Kaposi sarcoma), red or erythematous (psoriasis)

If erythematous, consider quality: Violaceous erythema (EM), beefy red erythema (candidiasis), bright red erythema (drug eruptions), dusky erythema (SJS–TEN)

Primary Lesions

 

 

 

 

Macule: Flat, nonpalpable lesion <1 cm diameter (⊕ color or min textural change)

Patch: Flat, nonpalpable lesion >1 cm

Papule: Palpable, solid lesion <1 cm

Plaque: Elevated or depressed, often flat, palpable lesion >1 cm Nodule: Palpable rounded lesion that usually denotes deep dermal or SC process >1 cm

Tumor: Palpable solid lesion either above or beneath skin’s surface, usually >2 cm

Vesicle: Elevated lesion containing clear fluid <0.5 cm Pustule: An elevated lesion that contains purulent fluid <1 cm Bulla: A lesion that contains clear fluid >0.5 cm

Secondary Lesion(s)—What are Other Components/Descriptors?

Scale: Quality (e.g., silvery: psoriasis, greasy: seb derm) Lichenification: Thickening of epidermis due to persistent scratching or rubbing, characterized by hyperpigmentation & marked hyperlinearity; implies chronicity

Erosion: Loss of epidermis ± superficial dermis → dyspigmentation

Ulcer: Loss of significant dermis or SC tissue → scar

Other: Excoriations, fissures, exudate/crust, desquamation or “peeling”

Distribution—Where are the Lesions?

 

Generalized, flexural (AD), extensor (psoriasis), chest, scalp, upper back (tinea versicolor), acral (2° syphilis, RMSF, EM), dermatomal (VZV), photoexposed (cutaneous lupus), follicular (folliculitis), bilateral LE (stasis dermatitis) vs. unilateral (cellulitis)

Consider areas of sparing (e.g., contact dermatitis spares intertriginous folds)

Grouping—What is their Relationship to Each Other?

Linear (contact dermatitis), herpetiform (herpes simplex, zoster), annular: Ring-like w/ central clearing (tinea corporis, granuloma annulare), polycyclic: Coalescing annular lesions (urticaria)

Morphologic Warning Signs

Dusky (grayish to violaceous) erythema: Impending necrosis esp of lesions w/ stellate or sharp borders (i.e., SJS/TEN, calciphylaxis, angioinvasive fungi)

Purple or violaceous nodules: Leukemia, lymphoma, malignant vascular tumors, Merkel cell, melanoma

Black lesions: Cutaneous necrosis, melanoma, eschar (anthrax)

The ABCs of Dermatology: A List of Additional Terms

Atrophy: Thinned epidermis = cigarette paper-like skin (e.g., chronic corticosteroid use)

Blaschkoid: Lesions that follow the “lines of Blaschko” or migration of embryonic cells; often represent genetic mosaicism

“Collarette of scale”: Thready ring of scale around a lesion implying previous pustule (e.g., folliculitis) or vesicle

Comedo: Plugged follicular units; “open” or “closed” (the defining lesion of acne)

Dermal: Denotes papules or nodules w/o surface change or scale Dermatographism: Linear, erythematous edematous plaques in places where skin is firmly stroked or scratched (form of mechanical urticaria)

Depigmented: Absence of pigment (e.g., vitiligo) vs. hypopigmented “Eczematous”: Definition of a clinical reaction pattern but also implies characteristic pathologic features (spongiosis); aka “dermatitis”; poorly defined erythematous patches w/ xerotic or waxy scale

Ephelides: “Freckle”; small brown macule in sun-exposed areas in pts

 

w/ fair skin; caused by ↑ melanogenesis

Erythroderma: Generalized, occasionally confluent redness ± scaling of the skin; often w/ systemic sx

Folliculitis: Inflammation of hair follicle, often manifesting as a pustule (e.g., Staph folliculitis)

Hyperkeratotic: Hypertrophy of the stratum corneum marked by thickened scale, in skin cancers, often firm

Induration: Palpation reveals firm skin caused by inflammation of dermis ± fat

Impetigo: Superficial skin infection caused by S. aureus toxin manifesting as honey-colored crusting or as bullae (“bullous impetigo”) Keloid: Elevated, irregular (often “claw-like”) firm scar, often pruritic or painful

Koebner phenomenon: Skin trauma that induces new lesions (e.g., psoriasis)

Morbilliform: Generalized, often blanchable & coalescing erythematous macules or thin plaques, w/o scale (classically viral exanthems or hypersensitivity drug eruptions); more specific/preferable to “maculopapular”

Nevus: Lesion characterized by proliferation of melanocytes—benign, atypical

Onychodystrophy: Broad term to describe dystrophy of nail plate

Onycholysis: Separation of nail bed from nail plate

Petechiae: Pinpoint nonblanchable erythematous macules caused by extravasation of RBCs into the skin (thrombocytopenia) Pedunculated: Lesion on a thin stalk (neurofibroma)

Poikiloderma: Hyperpigmentation + hypopigmentation + atrophy + telangiectasias – primarily due to chronic UV exposure, less often autoimmune disease

Purpura: Nonblanchable; macular (RBC extravasation w/o inflammation → traumatic or hematologic issue) vs. palpable (inflammation of blood vessels → vasculitis)

Reticulate: “Net-like” (livedo reticularis)

Sebaceous: Denotes involvement of sebaceous glands (palms & soles lack them); all sebaceous glands (except ectopic glands) are assoc w/ hair follicles (“pilosebaceous”)

Solar lentigo: Sun spots; brown macule in sun-exposed areas caused

 

by melanocytic proliferation

Target lesion: Erythematous round plaque w/ 3 zones of color Δ, center of lesion can be deeply erythematous or bullous (erythema multiforme)

Targetoid plaques: Erythematous round plaque w/ 2 zones of color Δ Telangiectasia: Small dilated blood vessels (rosacea, CTD) Verrucous: Wart-like architecture (seborrheic keratosis, verruca vulgaris)

Xerosis: Dry skin

 

Seborrheic Keratosis (Br J Dermatol 1997;137:411)

Benign cutaneous growth in >80% of adults aged 35–76; incidence ↑ w/ age, ♂ = ♀; ↑ frequency in areas of sun exposure; unknown trigger → keratinocyte proliferation, altered EGFR distribution, FGF3 mutation; no assoc w/ HPV

S/sx: Skin-colored or brown macules or papules, often w/ “warty” & “stuck on” appearance; can be pigmented; horn cysts (keratin-filled depressions) can be helpful feature; often multiple lesions; spares palms, soles, & mucosa

Dx: Clinical; referral to dermatology or excisional bx if uncertain; Ddx includes melanoma, verruca vulgaris (wart), squamous cell carcinoma, lentigo

Tx: Reassurance; electrodessication & curettage or cryotherapy for irritated lesion

Verucca Vulgaris (Common Wart) (JAAD 1990;22:547)

Caused by various HPV subtypes; prevalence ↓ w/ age; spread by skin- to-skin contact, fomites (nongenital lesions), sexual contact, autoinoculation; ↑ in areas of skin trauma, incl shaving; ↑ severity/incidence in meat handlers, atopic dermatitis, immunosuppressed

S/sx: Varies by subtype: Common wart: <1 cm, skin- colored/pink/brown hyperkeratotic papule w/ punctate hemorrhage; Flat wart: Sessile, skin-colored, smooth, <3 mm papules; often multiple

 

lesions; Plantar wart: Scaly, rough papule on sole w/ punctate hemorrhage; Genital wart: Skin-colored/brown, macerated; sometimes polypoid smooth papules

Dx: Clinical; biopsy for definitive dx/large lesions to exclude malignancy; Ddx includes SCC, verrucous CA, AK

Tx: Warts difficult to treat & often spontaneously resolve; consider reassurance; First line: Salicylic acid + cryotherapy > salicylic acid alone > cryotherapy alone (AFP 2011;84:288)

Cryotherapy: Tx should be q3wk; limit to 3 treatments & if no improvement → dermatology referral Salicylic acid: May be used as adjuvant (btw visits) for cryotherapy; instruct pt to soak area × 5 min, gently exfoliate w/ pumice/file, then apply QHS; S/e: Irritation (d/c if severe), maceration Second line: Other destructive modalities (curettage, electrodessication), duct tape

Secondary prevention: HPV transmission from tx items possible; have pts reserve home pumice/files for this purpose alone, avoid shaving directly over lesions

When to refer: Extensive/painful lesions, failure to improve w/ tx, dx uncertain—biopsy may be needed, periungual location (assoc w/ SCC) (JAAD 2011;64:1147), consideration of advanced tx (immunomodulators: imiquimod, intralesional Candida Ag; immunotx: squaric acid, DNCB; podophyllin toxin, topical 5-FU (Br J Dermatol

2011;165:432)

Angioma (JAAD 1997;37:887)

Most common acquired cutaneous vascular neoplasm, benign, present in most by age 60; ↑ in number & size w/ age; unknown etiology (hormonal influences); ↑ blood vessels seen on bx

S/sx: <5-mm bright red macules, dome-shaped papules; multiple on trunk & proximal extremities

Dx: Clinical; bx for definitive dx; Ddx incl petechiae, Kaposi sarcoma (larger), pyogenic granuloma (solitary, friable), bacillary angiomatosis Tx: If symptomatic, can be electrocauterized ± shave bx

Epidermal Inclusion Cyst (EIC)

Most common cutaneous cyst; ↑ in hair-bearing areas (posterior neck of ♂), filled w/ keratinaceous debris

 

S/sx: SC, soft, mobile nodule often w/ punctum, yellow/blue appearance; cyst rupture can → inflamed (sterile or bacterial)

Dx: Clinical; Ddx includes pilar cyst (scalp), dermoid cyst (eyebrow), lipoma, dermal tumor

Tx: Inflamed: intralesional steroids → refer to dermatology for future excision for definitive tx; Infected: I&D, oral antibiotics; avoid manipulation and extraction of contents unless I&D needed for superinfection

Lipoma

Subcutaneous tumor composed of adipocytes; ♂ > ♀

S/sx: Often solitary, mobile, soft nodules w/ predilection for trunk, arms, buttocks, & proximal lower extremities; can have multiple lesions

Dx: Clinical; excisional bx for definitive dx; Ddx incl EIC, angiolipoma (painful), liposarcoma (malignant variant, often >10 cm, proximal extremities, rapidly growing), spindle cell lipoma (large, often found on neck of ♂)

Tx: Referral for excisional bx if sx or dx uncertain; many lipomas deep, w/ fascial component; if large or over a joint, consider referral to plastic surgery

Fibromas

Angiofibroma: “Fibrous papule,” dermal tumor composed of fibroblasts & blood vessels; solitary (often on nose) or grouped, <5-mm dome- shaped, skin-colored papule(s); variant: Pearly penile papules (translucent papules on penile corona, often misdiagnosed as genital warts); Dx: Clinical, bx for definitive dx; Ddx: Intradermal nevus, BCC

(JAAD 1998;38:143)

Dermatofibroma: Composed of proliferation of fibroblasts & histiocytes; idiopathic or 2/2 arthropod bite, local trauma; usually solitary, often on lower extremities of ♀; multiple eruptions can be seen in SLE, HIV; Dx: Clinical—often upper outer arms, ⊕ dimple sign (dimple w/ lateral compression), bx for definitive dx; Ddx: Melanocytic nevus, melanoma, seborrheic keratosis, dermatofibrosarcoma protuberans (malignant variant, often >2 cm); Tx: Reassurance, excisional bx if symptomatic (e.g., pruritus) or large (J Eur Acad Dematol Venereol 2009;23:371)

Neurofibroma: Composed of neural mesenchymal tissue; 0.2–2 cm

 

skin-colored to pale pink pedunculated papules, soft, often on a broad base; solitary lesions common; Dx: Clinical ± “buttonhole sign” (easily invaginates w/ pressure); Ddx: Dermal nevus, acrochordon, neuromas, intradermal nevus, nevus lipomatosis; multiple lesions → consider type 1 neurofibromatosis

 

Figure 3-1. Diagnostic algorithm for common benign growths

 

 

 

 

Background (JAAD 2009;60:S1; JAMA 2016;316:1329)

Definition: Chronic disease of pilosebaceous follicle, characterized by comedo formation & assoc inflammatory lesions

Epidemiology: Affects 50 million people, 85% of adolescents; can persist into adulthood, particularly in ♀ (affects 12% of adult ♀);

 

severity ♂ > ♀ in adolescence; ♀ > ♂ postpubertal

Pathogenesis: Multifactorial; includes aberrant follicular keratinization, hormonal influences, ↑ sebum production, colonization w/ Propionibacterium acnes → follicle rupture → inflammatory host response

Severe disease has significant psychosocial impact: Similar to epilepsy, asthma, DM, can → 2–3x ↑ in suicidal ideation (Br J Dermatol

1999;140:672; J Invest Derm 2011;131:363)

Evaluation (JAMA 2004;292:726)

Diagnosis: Clinical, w/ wide range in severity of presentation

History: Eval for triggers (below); role of diet controversial

 

Acne Triggers (NEJM 2005;352:1463)
Cosmetic	Occlusive creams/makeup/pomades, “anti-frizz” serums
Mechanical	Friction/pressure (e.g., helmets) → “acne mechanica”
Drug- induced	Glucocorticoids (monomorphic papules & pustules), phenytoin, lithium, INH, iodides, bromides, androgens, vits B2, B6, & B12, AZA, CsA, disulfiram, psoralens, thiourea, & EGFR inhibitors
Hormonal	Flares w/ menses, significant jawline/chin acne → eval for signs of hyperandrogenism (see “Polycystic Ovary Syndrome”)
Occupational	Insoluble cutting oils (machinery), coal tar, chlorinated hydrocarbons (e.g., dry cleaning)
Radiation	Radiation acne

Exam: Morphology: Closed (“whiteheads”) & open (“blackheads”) comedones; erythematous papules, pustules, nodules, & cysts Healed lesions: Postinflammatory hyperpigmentation ± “ice-pick” (deep, punctate) & “boxcar” (wider/shallower) scarring Distribution: Face, back, chest

 

Differential diagnosis: Rosacea, including perioral dermatitis (no comedones), sebaceous hyperplasia (yellowish papules w/o comedones), folliculitis, gram ⊖ folliculitis (after prolonged oral abx), keratosis pilaris (on trunk/extremities), pseudofolliculitis barbae/acne keloidalis nuchae (“razor bumps” on shaved areas, ↑ prevalence African-American ♂), Favre–Racouchot (comedones from photodamage)

 

Classification
Severity	Description
Mild	Primarily open & closed comedones; <10 papules & pustules
Moderate	Comedonal & inflammatory lesions present; mild disease of the trunk
Moderate– severe	Numerous papules & pustules (>40), occasional tender nodules & cysts; ⊕ truncal involvement, ± scarring
Severe	Many large, painful nodules & cysts, significant scarring +/– systemic sx

Treatment (NEJM 2005;352:1463; JAAD 2016; 74:945; JAMA Dermatol 2016;152:655)

Aimed at correcting follicular keratinization, ↓ sebum production, ↓ bacterial colonization, & ↓ inflammation

Treatment algorithm largely divided into topical ± systemic tx based on severity; algorithm-based initiation of tx by PCPs ↓ need for dermatology referral by 72%

 

Common Acne Treatments
Class	Example Medication Rx	Side Effects/Notes
Topical Tx: 1st-line for pts w/ Mild Disease
Retinoids	Tretinoin 0.025–0.1% (C,G, microsphere gel vehicle) QHS	Irritation, photosensitivity
Topical antimicrobialsa	Benzoyl peroxide 2.5–10% (C,G,L,W) QD–BID	Irritation, bleaches clothing/linens
	Clindamycin 1% (preferred)	bacterial resistance
Other agents	Azelaic acid 15–20% (C,G) QD–BID	Irritation
	Salicylic acid OTC QD–BID	Irritation, dryness
Systemic Therapy
Oral antibiotics (1st line)a	Doxycycline 50–100 mg QD–BID	GI upset, photosensitivity; more effective than tetracycline
Oral antibiotics (2nd line)a	TMP–SMX DS BID	Hypersensitivity, photosensitivity, TEN
	Macrolides (azithromycin, erythromycin)	Erythromycin—antibiotic resistance, GI s/e
Hormonal agents (♀ only)	Spironolactone 50–200 mg	Menstrual irregularities, breast tenderness, teratogenicity, hyperkalemia, gynecomastia
	Estrogen-containing OCP	See “Contraception”
Oral retinoids	Isotretinoin 0.5–1 mg/kg/d	Usually Rx’ed by dermatologist; teratogen, xerosis, ↑ LFTs, visual changes

 

Formulations: C, cream; G, gel; L, lotion; S, soln; W, wash; F, foam (Data from NEJM

2005;352:1463)

aShould be used in combination w/benzoyl peroxide or retinoid to limit incidence of abx resistance.

Combination therapy with topical retinoid + antimicrobial agents preferred approach for almost all pts w/ acne, especially for ≥ moderate acne; many add’l combination agents available beyond those in above table

Topical or oral antibiotics should be combined w/ benzoyl peroxide or retinoid to limit incidence of abx resistance; monotherapy w/ systemic antibiotics not recommended

Limit oral abx to shortest duration possible (<3 mo); ideal use as to bridge until topical tx becomes effective

Oral isotretinoin most effective acne medication; federally mandated Rx regulation program (ipledgeprogam.com) due to ↑risk of teratogenicity Adjunctive treatments: no dietary modifications definitively improve acne, but some evidence low glycemic load diets may be beneficial

When to Refer to Dermatology Scarring, severe disease

Treatment-refractory: If fail 3-mo course of oral antibiotics +

topicals

For consideration of additional adjunctive tx: oral retinoids, extractions/peels, & laser/light-based therapies (e.g., photodynamic Rx); intralesional steroids for cystic, tender lesions (caution: can → permanent atrophy even at low dose)

Systemic/severe variants: Especially, acne fulminans (usually adolescent ♂ w/ fever, arthralgias, large inflamm nodules, ↑ WBC, ↑ ESR, proteinuria, osteolytic lesions); acne conglobata (usually adolescent ♂ w/ severe nodular acne, draining lesions, & sinus tracts) Rare disorders: SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, osteitis); PAPA syndrome (sterile pyogenic arthritis, pyoderma gangrenosum, acne), PAPA-HS (+ hidradenitis suppurativa)

 

Background (J Invest Dermatol Symp Proc 2011;15:1; JAMA Dermatol 2015;151:1213)

Chronic relapsing/remitting d/o; 2.7–10% prevalence among pts w/ N. European ancestry

Epidemiology: Onset btw 30–50 y; ↑ in ♀ & fair-skinned individuals; often ⊕ FHx

Pathogenesis: Uncertain – genetics + environment; may involve dysregulated innate immunity, inflammatory reaction to cutaneous microbes, ↑ angiogenesis & VEGF expression in response to UV light, matrix metalloproteinases (MMPs)

Diagnosis (NEJM 2005;352:793)

Clinical diagnosis: 4 major subtypes; features may overlap; bx used only to r/o other dx; use Hx to distinguish from other causes of flushing (e.g., menopause, anxiety, carcinoid, mastocytosis, pheo) & assess ocular sx

 

Rosacea Subtypes (NEJM 2005;352:793)
Subtype	Morphology/Characteristic
Erythematotelangiectatic (most common)	Persistent centrofacial erythema, flushing, telangiectasias, ↑ cutaneous Se; classically spares periocular skin
Papulopustular	Centrofacial erythema; small dome-shaped erythematous papules & pustules; variant: Perioral dermatitis (unlike acne, pruritic & no comedones)
Phymatous	Rhinophyma (sebaceous gland hypertrophy w/ dilated pores, tissue hypertrophy if severe) occurring predominantly in ♂ on nose; may also involve chin, forehead, ears, eyelids
Ocular	May be seen w/ other subtypes; nonspecific ocular itching, gritty sensation, dryness, conjunctival injection, recurrent chalazion or hordeolum, blepharitis; rarely can → keratitis, uveitis, scleritis, or episcleritis

Triggers: Sun exposure, temperature extremes, EtOH, hot liquids, spicy foods, exercise, topical irritants

Differential dx for erythematotelangiectatic & papulopustular subtypes: Dermatoheliosis (photoaging), SLE (sparing of nasolabial folds, no pustules); seb derm (can occur simultaneously but has greasy yellow scale & occurs on facial creases/eyebrows), acne vulgaris (no comedones or scarring w/ rosacea), steroid-induced dermatitis (can be periorificial), & Demodex mite folliculitis

 

Treatment (NEJM 2005;352:793)

General approach: Aimed at ↓ bacterial burden & inflammation, ↓ trigger exposure

Nonpharmacologic treatment: Sunscreen w/ UVA/UVB protection is essential tx for all types; use physical barriers (titanium dioxide or zinc oxide) given chemical sunscreen may ↑ rosacea; moisturizers, avoid harsh cleansers w/ acetone & vasodilating drugs (e.g., CCBs or niacin), trigger avoidance

Medical/surgical treatment: Inflammatory lesions generally responsive to medication; telangiectasias or phymatous changes require lasers or surgery

Erythematotelangiectatic: Difficult to treat; focus on behavioral modification & trigger avoidance; evidence for light-based or laser therapies—intensed pulsed light (IPL), pulsed-dye laser (PDL) → refer to dermatology; topical tx to consider; brimonidine gel 0.33%QD (caution with s/e: rebound erythema, burning), oxymetazoline hydrochloride cream 1% QD

Papulopustular (Cochrane Database Syst Rev 2011;3:CD003262)

Topical tx: MNZ 0.75% gel or cream QD–BID (1st-line); 10% Na sulfacetamide/5% sulfur BID crm or lotion or cleanser; azelaic acid 15% gel or foam BID (↑ effective but ↑ irritating, less with foam); benzoyl peroxide 2.5–10% gel, crm, or lotion QD–TID; ivermectin 1% cream QD

Systemic tx: If mod/severe, doxycycline 50–100 mg QD or BID × 6– 12 wk; minocycline 50–100 mg BID × 6–12 wk; or MNZ 200 mg QD or BID × 4–6 wk; consider adjunct topical maintenance Rx

Phymatous: Surgical excision or laser ablation

Ocular: Eyelid hygiene (flush lids w/ water BID), artificial tears for mild sx; refer promptly to ophthalmology for serious or persistent sx; CsA 0.5% ophthalmic emulsion may be more effective than artificial tears, & systemic abx may be used if local Rx fails (Cochrane Database Syst Rev 2011;3:CD003262)

 

Background (JAMA 2016;316:436)

Nonmelanoma skin cancer accounts for 98% of US skin cancers; includes BCC, SCC, MCC; precursors to SCC include AKs & SCC in situ

Sun exposure is primary cause of melanoma & nonmelanoma skin cancer; cumulative risk of BCC/SCC linked to cumulative sun exposure UVB excites DNA → pyrimidine dimers (esp TT dimers) which are carcinogenic, esp in the basal layer of the epidermis; p53 mutations → resistant to apoptosis

Epidemiology and Risk Factors (AFP 2012;86:161; JAMA 2016;316:436)

Highest incidence in older, fair-skinned pts w/ long-term sun exposure;

♂ > ♀, pts with hx sunburn

Other risk factors: Tanning beds (1.5× ↑ risk of BCC, 2.5× ↑ risk of SCC), Prior nonmelanotic skin CA (risk of 2nd nonmelanotic skin CA 35% at 3 y, 50% at 5 y), solid organ tx (10x ↑ risk of BCC, 65x ↑ risk of SCC: Heart/lung >> kidney >> liver, esp those on AZA, CsA (JAAD 2011;64:981), chronic voriconazole, vemurafenib, photosensitizing meds such as HCTZ assoc w/ ↑ risk of SCC; hx ionizing radiation (esp as child) (Dermatol Surg 2016;42(9): 1107)

SCC-specific associations: CLL, burns (Marjolin ulcers), chronic wounds, HPV (subtypes 16, 18, 33), smoking (Arch Dermatol 2012;148:939) Prevention: Photoprotection is foundation of prevention: Daily sunscreen use for 4.5 y ↓ risk SCC by 35% (Cancer Epi Bio Prev 2006;25:46); see Prevention section of “Melanoma”

Red Flags

Any lesion w/ rapid growth, ulceration, spontaneous bleeding, tenderness (concern for perineural invasion)

Any nonhealing or enlarging lesion in an immunosuppressed pt Persistent hyperkeratotic or eroded lesions on the lip, ear, or “H” zone of the face

Any lesion >2 cm on the extremities or trunk

Actinic Keratoses (Br J Dermatol 2007;157:S18; JAAD 2013;68:S2)

Epidemiology: Prevalence in US 16–25%; incidence ↑ w/ age

In patients w/ 7–8 AKs, risk of developing invasive disease is 6.1– 10.2% over 10 y

 

Diagnosis/morphology: Skin-colored, pink, or erythematous macules w/ gritty scale (no papule); easier to feel than to see; cutaneous horns (15% w/ SCC at base); commonly distributed on head, neck, forearms Treatment: Individual lesion destruction or field Rx (5-FU 0.5% or 5% crm, diclofenac 3% gel, imiquimod 5% crm, ingenol mebutate gel, photodynamic Rx); caution w/ cryotherapy unless confident of dx (SCCs, SKs, melanomas can mimic AK)

Basal Cell Carcinoma

Epidemiology: Most common skin cancer; rarely metastasize but locally invasive & destructive; recurrence risk is 30% (JAAD 1990;22:413) Morphology: Pearly translucent papule or plaque w/ telangiectasias, often eroded; can have globules of pigment; rolled border

Superficial variant: Poorly defined pink patches w/ scale (Ddx: SCC- IS, eczema)

Distribution: Can occur anywhere (∼33% in areas w/o direct sun exposure), but most often on head/neck (85%), 25% of all lesions occur on nose (AFP 2012;86:161)

Diagnosis: Shave or punch bx

Treatment: Excision or electrodessication and curettage (ED&C) if superficial; topicals if superficial (imiquimod 5% crm or 5-FU 5% crm)

>> cryotherapy; XRT considered for poor surgical candidates, debulking, or ↑-risk subtypes

Squamous Cell Carcinoma In Situ (Bowen Disease)

Risk of transformation to SCC is 3–5% (Dermatol Surg 2011;37:1394) Morphology: Ill-defined pink scaly patches in sun exposed areas (Ddx eczema)

Treatment: ED&C, excision, topicals (imiquimod 5% crm or 5-FU 5% crm)

Squamous Cell Carcinoma (JAAD 2013;1:S019)

Epidemiology: >700,000 new cases/y in US; 0.3–16% risk of metastatic disease; incidence est 32–270/100,000 annually (no nat’l cancer registry); most pts >50 y

Morphology: Eroded, friable, hyperkeratotic papules, plaques, nodules; pain can = perineural invasion (↑ risk)

Distribution: Usually photodistributed; forearms/dorsum of hands most

 

common

High-risk lesions: (1) Histopathology: tumor thickness >2 mm, perineural invasion; (2) Clinical location: lips, genitals, ear; immunosuppression; recurrent tumors

Diagnosis: Shave bx (must get lesion base) or punch bx

Treatment: Refer to dermatology; low-risk lesions on the trunk, extremities → excision w/ appropriate margins; lesions on head/neck, large lesions on trunk or extremities, or high-risk lesions → Mohs micrographic surgery by a fellowship-trained Mohs surgeon (advantages include tissue preservation, margin-controlled, local anesthesia) (Mohs Surgery Appropriate Use Criteria (JAAD 2012;67:531)); XRT considered for poor surgical candidates or for debulking

Merkel Cell Carcinoma (JAAD 2008;58:375)

Most lethal of all skin cancers including melanoma; mortality is 33% Most lesions presumed benign at time of dx (can resemble BCCs, asx, nontender, red or pink violaceous papules & nodules)

Acronym: AEIOU (Asx; Expanding rapidly, Immunosuppressed,

Older than 50 y, UV exposed site on fair skin) Workup/treatment: Sentinel LN bx, surgery & radiation

When to Refer

Clinically suspicious lesion for BCC, SCC, or MCC; red flags (above); thick (hypertrophic) AKs or many lesions that require field tx; bx shows atypical nevus or melanoma

High-risk individuals: Prior skin CA, solid-organ transplant pts

(should be seen q3–6mo), CLL

 

Background (SEER, seer.cancer.gov/statfacts/html/melan.html; JAMA 2016;316:436)

Epidemiology: Lifetime risk 2.2% in US; incidence ↑ w/ age, but relatively common type of cancer in the young; median age at dx: 64 y 75% of melanomas develop de novo, not from pre-existing nevi; high- risk sites: trunk/back of ♂, lower legs of ♀; 50% of all melanomas initially discovered by pt (JAAD 1992;26:914)

 

Strongest risk factors: Personal hx melanoma (∼8% risk of 2nd melanoma at 2 y), family (1st-degree relative) hx of melanoma, multiple dysplastic nevi (if 5 atypical moles, 10x ↑ risk of melanoma), congenital nevus >20 cm, familial dysplastic nevi syndrome (NEJM 2004;351:998; JAAD 2005;52:197)

Additional risk factors: Inability to tan (only burn), freckles, blonde or red hair, blue eyes, tanning bed use, blistering sunburns, intermittent sun exposure (Clin Dermatol 1998;16:67)

Role of screening: Cure rates much higher w/ earlier stage lesions (5- y survival 98% w/ localized disease) → theoretical, if unproven benefit, which is likely ↑ in high-risk population; currently insufficient evidence per USPSTF (Ann Intern Med 2009;150:188)

PCP detection: Se 43–100%/Sp 93%; be alert for malignant features esp in ↑ risk groups

Definitions (NEJM 2004;351:998)

Dysplastic nevi (graded mild/moderate/severe atypia): Considered benign, but for lesions w/ severe (+/- moderate) atypia, re-excision should be considered; low rates of clinical recurrence for benign to moderate atypical dysplastic nevi (JAAD 2010;62:591)

Melanoma types:

Melanoma in situ: No invasive component; includes lentigo maligna Superficial spreading melanoma: (70% of melanomas); median age: 50s, most common type to arise from pre-existing nevi, no preference for sun-damaged skin Lentigo maligna melanoma (5–15%); irregular brown macules initially, often on head & neck; elderly pts w/ significant sun damage Acral lentiginous melanoma (2–3%); C-KIT mutation; most common sites thumb & toe; more common in Asians, African-Americans; may present at later stages (Arch Dermatol 2009;145:427) Nodular melanoma: 10–15%; most arise de novo; more common in ♂

Other: Polypoid, mucosal, desmoplastic (↑ risk of local recurrence), uveal, amelanotic (erythematous eroded papule/nodule, often confused w/ BCC or pyogenic granuloma)

Evaluation (JAMA 2004;292:2771)

History: PMHx or FHx of dysplastic nevi/melanoma? Blistering sunburns? Tanning bed use? Changing moles? Sx moles?

 

Exam: Entire skin, nails, hair; LN exam (if hx of invasive melanoma); attention to: Fitzpatrick skin type/phototype, extent of photodamage, nevi density, atypical moles, “ugly duckling” nevi—moles that stand out from others, scars from prior melanoma/atypical nevus excision (risk of local recurrence)

ABCDEs of pigmented lesions: Increased likelihood of malignancy

Asymmetry (of pigment or shape) Border irregularity (Jagged or notched borders) Color variegation (≥3 colors concerning—in particular, blue/gray/white, light brown, dark brown, black, red) Diameter (>6 mm), especially growing in diameter Evolving (or symptomatic—pain, pruritus, bleeding)

Diagnosis: Suspicious lesions → timely referral to dermatology for eval and biopsy

Biopsy: if unable to obtain prompt referral to derm, may biopsy in office

Margins: Avoid partial bx; capture entire breadth of lesion w/ 1–2 mm clinical margins; capture entire depth (critical for staging) Technique: Elliptical, punch excision w/ sutures or shave removal as needed for depth Interpretation: Path should be read by dermatopathologist

Prevention & Treatment (NEJM 2004;351:998; Crit Rev Oncol Hematol 2010;74:27;

JAAD 2011;65:1032)

Sun protection: Avoid or seek shade during peak hours of sunlight (10 am–3 pm); ∼80% of UV rays can pass through clouds; wear sun- protective clothing esp during water sports (clothing w/ UPF), UVA protective sunglasses, hat w/ >4 in brim

Sunscreen pearls:

1. SPF ≥30; daily use of SPF assoc w/ 50% ↓ in melanoma, 73% ↓ in invasive melanoma
2. Use products labeled “broad-spectrum” covering UVA & UVB— physical blockers w/ zinc, titanium, ecamsule, oxy-or avobenzone
3. Use enough—1 tsp to head & neck; “underdosing” of sunscreen common
4. Reapply at least every 2 h
5. Use cream   or   lotion;   sprays   likely   less   effective   (Br   J    Dermatol

2007;156:716)

Monthly self-skin checks: Educate pts about ABCDEs, ugly duckling

 

nevi

When to refer to dermatology

Clinically suspicious lesions or bx with atypical nevus Personal hx of melanoma or otherwise high risk; risk of

recurrence highest in first 2 y after initial dx (Int J Cancer 1997;73:198; Cancer 2003;97:639) All new melanoma diagnoses (may also need surgical oncology or medical oncology)

Pt information: aad.org/media-resources/stats-and-facts/prevention- and-care/sunscreens

 

Animal Bites (Clin Infect Dis 2005;41:1373)

Background: Only 20% brought to medical attention; dog bites more common; cat bites often deeper & ↑ risk of infection

Microbiology: Wound infections usually polymicrobial; pathogens reflect flora of animal oral cavity (Pasteurella spp, Capnocytophaga canimorsus, anaerobes) & human skin (staph, strep)

Evaluation: History: Timing of bite, location, depth, immunization hx

PMHx: Immunocompromised, s/p splenectomy, sickle cell (functional asplenia) Exam: Wound severity, signs of local & systemic infection (fever, erythema, edema, drainage, LAD), distal neurovascular exam Workup: If severe, ✓ CBC, BCx, U/S; consider radiograph

Management: Irrigate, assess for foreign body, consider superficial debridement; 1° closure for simple superficial lacs <12 h old w/o sx of infection; do not close cat bites or hand/foot wounds; referral to surgery for complex wounds & any bite affecting hands or joints; consider plastic surgery referral for facial wounds

Antibiotics: Tx for clinical infection or Ppx if deep puncture, on hand, near joints, or compromised host; Choice of abx: Amoxicillin/clavulanate “Dogmentin” (875/125 mg BID × 3–5 d for Ppx, longer for clinical infection); alternatively doxycycline, TMP–SMX, or FQ + clindamycin (for anaerobic coverage); consider MRSA coverage if ↑ risk (e.g., known MRSA carrier, immunosuppressed), or if

 

⊕ purulent drainage/surrounding cellulitis

Immunization: Tetanus toxoid IM if out-of-date (>5 y or <3 lifetime doses) or uncertain, tetanus Ig if vaccine hx unknown for severe wounds (>6 h old & >1 cm deep, & signs of infection or debris); rabies postexposure Ppx (human diploid cell vaccine ASAP [day 0] + HRIg [day 0, 3, 7, 14, & 28 if no prior vaccine; days 0 & 3 if prior complete cell culture vaccine]) for all wild animal bites (incl raccoons, etc); for domestic animals, observe animal × 10 d → if nl behavior, no rabies PEP, if animal ill → sacrificed & tissue tested

Human Bites (CID 2005;41:1373)

Background: Risk of infection ↑ compared to other animal bites Microbiology: Pathogens = oral & skin flora; strep, staph, haemophilus, eikenella most common; anaerobes often ⊕ in mixed cultures

Management: Same as above for dog & cat bites; no 1° closure for human bite; all pts should receive prophylactic abx; clenched-fist bites (injury from striking teeth) often require IV abx & consultation w/ hand surgeon

Bloodborne pathogens: HCV, HIV transmission risk very low; however, if there is blood in saliva → counseling about HIV PEP warranted; HBV transmission possible; unvaccinated or undetectable anti-HBs should receive HBIg & HBV series

Insect Bites and Stings (J Allergy Clin Immunol 2011;127:852)

Usually self-limited local reaction, rarely can → systemic reaction/anaphylaxis

Local reaction: Remove stinger, apply cold compresses, nonsedating antihistamines; for severe edema, consider oral steroids; expectant mgmt regarding infection

Systemic reaction: Inpt eval, at d/c prescribe epinephrine auto- injector, refer to allergy for skin testing & consideration of immunotherapy

Lice (NEJM 2002;346:1645; JAAD 2004;50:1; CID 2007;44:S153;

cdc.gov/parasites/lice.index.html)

Head lice (pediculosis capitis): Children > adults, spread through shared items, infestation

 

S/sx: Scalp pruritis or asx; dx by visualization of louse ± nit w/ fine- toothed comb Environment tx: wash sheets/clothes on hot + hot dryer x 10 min (delicate items which cannot be washed in hot water → hot dryer x 30 min); helmets, headphones, hats → freezer o/n or sealed plastic bag x 2 wk; inspect household members and tx if ⊕

Head tx: topical permethrin 1% (OTC), 2 applications 1 wk apart (alt: Malathion, benzyl EtOH, 0.5% ivermectin lotion); TMP–SMX w/ permethrin or PO ivermectin for tx failure

Body lice (pediculosis corporis): Vector for typhus, trench, & recurrent fever; ↑ prevalence in crowded living quarters (shelters, prisons, SNFs), poor hygiene; S/sx: Waist, axillae, nuchal pruritic/excoriated papules; visualize louse or nit on clothes (often in seams)

Ddx: Scabies, allergic dermatitis; skin scraping useful if dx unclear Tx: Primary treatment is improved hygiene (cannot survive >24 h away from human host); heat-wash linens/clothes and regular change of clothes; may tx with pediculocide if unable to arrange this/add’l tx desired (o/n application of permethrin to body; see Scabies treatment)

Genital lice (pediculosis pubis, “crabs”): Transmitted during sexual activity, screen for co-infection w/ other STIs; S/sx: Pubic & axillae pruritus, louse or nits on hair

Ddx: Scabies, trichomycosis axillaris, white piedra

Tx: 1% permethrin (OTC), return in 1 wk, re-treat PRN; tx partner/notify partners from last 30 d, heat-wash lines/clothes; eval for other STIs

Spider Bite (Lancet 2011;378:2039; NEJM 2005;352:700)

Most spiders are not toxic to humans; severe reaction should prompt consideration of differential; often misdiagnosed soft-tissue MRSA infection

Black widow, brown widow (southern US), & false black widow (worldwide) usually cause unremarkable local reaction (papules, pustules) ± local pain; recluse spider (US) bites rarely can → local necrosis, systemic sx & hemolytic anemia; supportive care

Bedbugs (Cimex Lectularius) (JAMA 2009;301:1358)

 

Background: ↑ Prevalence of infestations worldwide; 5 mm in size → visible w/ naked eye; yellow/reddish color; feed at night; live close to host in furniture, mattresses, floorboards; can live 1 y w/o feeding; no evidence that insect serves as disease vector

Signs and symptoms: Usually no reaction to bite; most rashes brought to attention are 2–5 mm pruritic, maculopapular, erythematous; excoriation can → superinfection; case reports of more severe reaction (hypersensitivity, complex rashes)

Treatment: If sx, consider topical corticosteroids; if superinfected → abx (see “SSTI”)

Eradication: Very difficult; requires systematic effort; usually professional assistance; prevention advised (inspect hotel rooms, items purchased 2nd-hand, library books)

SCABIES

 

Background (NEJM 2010;362:717; Lancet 2006;367:1767; Ann Intern Med 2014;161:5)

Infestation by mite Sarcoptes scabiei affects ∼300 million worldwide; more common in debilitated pts or hx neuro d/o (crusted scabes), impoverished communities, homeless, group/crowded housing facilities; ↑ in winter mo 2/2 crowding

Transmission: Close personal contact (including sexual), contaminated clothing (rare)

Pathogenesis: Fertilized ♀ mite burrows into the stratum corneum → lays eggs → adult mites; affected individual typically has 10–15 mites at any given time; mites can live 24–36 h away from human host; skin eruption corresponds to degree of type IV hypersensitivity to mite, which begins ∼2–4 wk after initial infestation

Clinical Manifestations and Diagnosis (NEJM 2006;354:1718; BMJ

2005;331:619)

History: Risk factors as identified above; itching ↑ at night, nipples in

♀, genitalia in ♂, pruritus out of proportion to exam, ask if household contacts have itching

Exam findings: Erythematous papules, linear burrows (thread-like 5 mm gray-white ridges, representing tunneling of the mite), vesicles &

 

pustules, penile & scrotal nodules; 2° characteristics: Excoriations, sanguineous crust, lichenification (chronic cases)

Distribution: In adults, usually spares face & scalp; flexural: finger webs, volar wrists, axillae, inframammary; periareolar, periumbilical, genital

Differential diagnosis: Tinea, atomic dermatitis, drug eruption, dyshidrotic eczema, bullous pemphigoid, seb derm, psoriasis, Langerhans cell histiocytosis

Ancillary studies: Mineral oil prep: Most accurate on burrow on hands or wrists → no. 15 blade to scrape skin/stratum corneum → add a drop of mineral oil to slide → observe under microscope, dx made by identifying intact mite and/or eggs/feces; skin bx: Low Se for mite, shows only hypersensitivity reaction

Treatment (Lancet 2006;367:1767; Cochrane Database Syst Rev 2007;CD000320)

First-line: Permethrin 5% cream; most widely used & effective topical agent; apply to skin from neck down for 8–10 h (before bedtime → wash off in the am); repeat in 1 wk to tx newly hatched mites Alternatives: Ivermectin (1st line for crusted scabies [see below] & large outbreaks): not FDA approved; 200 μg/kg (dispensed in 3- & 6- mg tablets) in single dose, repeat in 1 wk; similar efficacy to permethrin, but better compliance

Lindane 1% lotion: 2nd line; organochlorine pesticide, can → neurotoxicity (numbness of skin, tremor); should not be used in pts

≤110 lb (MMWR 2005;54:533–535)

Decontamination: Mites cannot survive w/o human host for >3 d; linens & clothing should be placed in sealed plastic bags for 3 d → machine-washed & dried in hot dryer (>50°C)

Prophylaxis in close contacts: Single application of topical permethrin as above

Complications (Lancet 2006;367:1767; Lancet Infect Dis 2006;6:769)

Crusted scabies: Hyperinfection w/ hundreds of mites 2/2 host immunosuppression (i.e., AIDS, post transplant), also seen in trisomy 21 or neuro impairment; S/sx: Heavy hyperkeratotic scale & powdery crust due to high mite carriage; Tx: Oral ivermectin ± permethrin ± keratolytic agent (NEJM 1995;333:26; 1995;332:612; JAAD 2004;50:819)

Postscabetic hypersensitivity: Most common sequela; eczematous

 

& pruritic; may persist for 1–2 wk after successful tx; tx w/ topical corticosteroids and/or antihistamines

Secondary infection: S. aureus: Impetigo, furunculosis; S. pyogenes:

Soft-tissue infections; can rarely → poststrep GN

Patient information: http://cdc.gov/parasites/scabies

 

Background (BMJ 2012;344:e4380)

Dermatophytes: Fungi that infect superficial epidermis (stratum corneum), hair, & nails → “tinea”; distinguished from deep mycoses, which have ↑ ability to disseminate

Dermatophytoses largely characterized by site of infection Microbiology: 3 dermatophyte genera: Trichophyton (most common), Epidermophyton, & Microsporum; those w/ animal reservoirs (e.g., M. canis) tend to be more inflammatory

Transmission: Person–person, autoinoculation, or via fomite (floor, gym mat, shower stall)

Epidemiology and Risk Factors (Clin Dermatol 2010;28:197)

20% of world’s population is affected; T. rubrum most common Risk factors: Hot, humid climates; local immunosuppression of the skin (topical corticosteroids), systemic immunosuppression (AIDS, transplant pts), animal contact, use of communal bathing facilities & occlusive footwear (onychomycosis)

Extensive disease in adults should raise question of immunosuppression (e.g., HIV)

Clinical Presentation

 

Superficial Mycoses
Dermatophytoses
Subtype	Presentation
Tinea pedis (“athlete’s foot”)	Range from asx to intensely pruritic, usually bilateral; gradually progressive, duration of months to years Interdigitary skin: (Most common/initial site) white maceration/fissuring or dry scale Soles/lateral feet: Well-demarcated erythema w/ powdery or

 

	hyperkeratotic, occasionally peeling “moccasin scale” Often w/ simultaneous tinea cruris or onychomycosis (check groin &   buttocks if feet involved) Ddx: Psoriasis, AD, pityriasis rosea, 2° syphilis
Tinea unguium (onychomycosis)	Common w/ ↑ age, DM, tinea pedis, occlusive footwear Yellow, thickened nail plate, subungual hyperkeratotic debris, nail plate lifting off nail bed (onycholysis) Types: Distal plate (most common), also white superficial (spots which coalesce at nail plate), proximal subungual (HIV) Ddx: Candida, other yeast (esp in tropical climates & in pts w/ DM or immunosupp); psoriasis
Tinea corporis “ringworm”	Common in younger adults; ⊕ pruritus, on legs, arms, or torso Erythematous pinpoint papules initially → slowly enlarging annular patches w/ central clearing & enhanced border; trailing scale Ddx: Allergic contact dermatitis, atopic dermatitis psoriasis
Tinea cruris (“jock itch”)	More common w/ ♂ gender, obesity Well-demarcated dull red/tan plaques w/ overlying scale on thighs, inguinal region (scrotal involvement rare) Ddx: Candida, erythrasma (coral-red fluorescence w/ Wood lamp) (Br J Dermatol 2003;149:S65:1)

Other tinea subtypes (BMJ 2012;344:e4380)

Tinea barbae: Unilateral, tender boggy papules & plaques over bearded area Tinea manuum: Dry, scaly erythematous, burning patches on hand, often unilateral

Tinea faciei: Asymmetric annular plaques often w/ trailing scale on face; Ddx seb derm Tinea capitis: Typically immunocompromised; “black dots” (broken-off hairs) in round patches of alopecia; Ddx: Seb derm, trichotillomania, cutaneous lupus (scarring)

Tinea incognito: any tinea presentation where scale is obliterated by use of emollients (usually steroids); key to dx is annular morphology, leading edge

Dermatophyte-related eruptions

Dermatophytids: “Id reaction”; widespread hypersensitivity most common w/inflammatory tinea capitis; pinpoint monomorphic pruritic papules on palms/soles Majocchi granuloma: Fungal folliculitis: Tinea invades dermis/follicle; T. rubrum most common; erythematous to violaceous papules → annular boggy plaque; shins of women is classic (often due to shaving); ↑ risk w/ topical corticosteroid

Diagnostic Tools

Microscopy: Use in all pts in whom tinea is suspected (modest

 

Se/high Sp)

• Use 15 blade or 2nd slide to scrape scale onto slide
• Apply coverslip & 1–2 drops of 10–20% KOH w/ DMSO or Swartz Lamkins
• View on low & high power to confirm septate hyphae

Culture: Scale or nail clipping sent in saline or w/o medium (depending on lab); only definitive means of fungal speciation

Nail clippings: Used to dx onychomycosis, most often to confirm infection before starting PO Rx; send for culture or in formalin for PAS stain

Wood lamp (365 nm): Useful to identify certain subtypes of tinea capitis that fluoresce blue-green (most commonly M. canis) or dx erythrasma (coral-red)

Treatment

General approach: Esp important to Rx tinea pedis in all immunocompromised or DM pts due to ↑ risk of SSTI (from breakdown of skin barrier); if tinea pedis occurs in presence of onychomycosis, it can recur unless onychomycosis treated

Counseling: Use ventilated shoes if possible; wear socks (cotton) w/ shoes; completing full tx course important for effectiveness; in recurrent diseases, assess for pet exposure; wash contaminated clothes, towels, socks, footwear

Topical: Indicated for initial tx of tinea pedis, corporis, cruris; avoid combination antifungal/steroid products as can worsen tinea and → fungal folliculitis (above); nystatin not effective against tinea Systemic: Consider in severe/refractory cases or immunocompromised pts, also for onychomycosis (or tinea pedis in presence of onychomycosis), tinea capitis, or Majocchi granuloma (fungal folliculitis)

 

Tinea Treatment by Location
Type	Treatment
Tinea pedis	Terbinafine 1% crm topical daily × 4–6 wk (OTC) Topical azole (e.g., econazole 1% crm) daily × 4–6 wk Ciclopirox gel/crm 0.77% BID × 1–4 wk (BMJ 1999;319:79; Cochrane Database System Rev 2007;3: CD00143)
Tinea	Terbinafine 250 mg PO daily × 6 wk for fingernails, 12 wk for toenails—most

 

unguium	effective (about 80%) (Br J Dermatol 2004;150:537) Itraconazole 200 mg daily × 3 mo; or 400 mg/d for 1 wk, monthly for 3–4 mo (latter regimen is not FDA approved) Nail avulsion (podiatry, dermatology)
Tinea corporis Tinea cruris	Topical azole (e.g., econazole 1% crm) daily × 4–6 wk Terbinafine 1% crm topical daily × 4–6 wk (OTC) Ciclopirox gel/crm 0.77% BID × 1–4 wk (BMJ 1999;319:79; Cochrane Database System Rev 2014;8:CD009992)

(BMJ 2012;344:e4380)

When to refer: Consider derm referral if skin infections fail to improve w/in 1 mo, nail infections fail to improve w/in 3 mo, or either clinically worsens with tx

NONDERMATOPHYTIC CUTANEOUS FUNGAL INFECTIONS

 

 

Selected Nondermatophytoses
Organism	Presentation	Treatment
Tinea versicolor (Malassezia furfur)	Salmon-colored, hypopigmented, or hyperpigmented patches w/ brawny scale on V-chest, shoulders, upper back “Spaghetti & meatballs”— hyphal & round yeast forms on KOH	Selenium sulfide lotion QD × 1 wk (leave on for 10 min); ketoconazole crm or shampoo used as body wash QD × 2 wk (JAAD 1986;15:500)
Cutaneous candidiasis (C. albicans)	Intertrigo: Macerated, erythematous (“beefy red”), fissured, eroded plaques, w/ satellite papules or pustules in folds; ⊕ burning or skin pain Risk factors: Warmth, moisture, oral abx	Topical azole, nystatin cream (for dry areas) or powder (for wet/intertriginous areas; cream there can → maceration) consider fluconazole 150 mg PO × 1

 

Background (J Invest Dermatol 2011;131:67; Lancet 2001;357:1076; NEJM 2008;358:1483)

Definition: Common, chronic relapsing dermatitis, assoc w/ xerosis & IgE-mediated sensitivities; often called eczema (due to classic “eczematous” pattern of dermatitis)

Epidemiology: Prevalence 11% in US; childhood onset (90% by age 5); sx often improve w/ age (JACI 2004;113:832); “Atopy”: 30% of pts w/ AD

 

also have asthma, 35% have allergic rhinitis

Pathophysiology: Thought to be combination of environmental exposures & genetic predisposition; epidermal barrier dysfunction 2/2 filaggrin mutation → ↑ transepidermal water loss → dry skin

Risk factors: smoking (JAAD 2016; 75:1119); IgE dysregulation in subset of pts; “Hygiene hypothesis”: ↑ Atopy assoc w/ ↓ microbial exposure early in life, esp in developed countries; assoc w/ food allergies but causal relationship not established

Complications:

Mental health: ↓ health-related QOL on par w/psoriasis (JAAD 2017;77:274) Ocular: keratoconus, anterior subcapsular cataracts

Infectious: secondary infection common: esp S. aureus: Pts w/ AD have ↓ human defensin-2 →↑ S. aureus colonization → inflammation → ↑ flares HSV: “Eczema herpeticum” (punched-out hemorrhagic erosions; see “Herpes”)

Evaluation (JAAD 2014;70:338)

General approach: AD is a clinical diagnosis made w/ exam findings

History: Location, duration, severity of itch (incl sleep disturbance), past tx, personal or ⊕ FHx of atopy (AR, asthma); triggers: foods, emotional stress, environmental factors (season/temperature; often ↑ in winter); skin irritants such as wool, solvents, & sweat Exam: Acute: Poorly defined, excoriated erythematous patches, vesicles, serous exudates, & crusts; chronic: Lichenified (↑ skin markings) & hyperpigmented plaques, prurigo nodules; 2° characteristics: Excoriations, punctate erosions, ± impetigo

Labs: Low threshold to culture crust or punctate erosions

 

American Academy of Dermatology Diagnostic Criteria (JAAD 2014;70:338)
Essential Criteria (necessary for dx)	1.  Pruritus 2.  Typical morphology & age-specific patterns –  Current or previous flexural lesions (in adults) –  Sparing of the groin and axillary regions 3.  Chronic or relapsing history
Important Features (seen in most cases)	1.  Early age of onset 2.  Personal or family hx of atopy and/or IgE reactivity 3.  Xerosis

 

Assoc Features (support dx but ↓ Se)	Atypical vascular responses: Facial pallor or erythema, delayed blanch response, white dermatographism Ocular/ periorbital changes   Keratosis pilaris, hyperlinear palms, Ichthyosis, pityriasis alba Perifollicular accentuation, lichenification, prurigo lesions

Differential diagnosis (must exclude): Infections/infestations:

Scabies, HIV, tinea

Inflammatory: Seborrheic derm, irritant/ACD, psoriasis, hypersensitivity drug reaction

Malignancy: Cutaneous T-cell lymphoma, Langerhans cell histiocytosis

Immunologic: GVHD, connective tissue disease

Dishydrotic eczema (aka dishydrosis or pompholyx): related to but distinct from AD; affects palms of hands > soles of feet; erythematous patches studded with small, skin-colored, pinpoint fluid-filled blisters (“tapioca ball”-like); assoc w/ water exposure, may have burning sensation; can co-occur w/ AD or can be assoc w/ exposure to allergen or irritant; tx is removing/avoiding irritants, drying thoroughly, wearing work gloves, and ↑ potency steroids; refer to dermatology if behavioral measures and short trial of ↑ potency steroids insufficient → consideration of systemic tx (Am J Clin Dermatol 2010;11:30)

Treatment (NEJM 2005;352:2314; Pediatr Dermatol 1997;14:321; JAAD 2014;70:338)

Moisturizers: Mainstay of tx and preventing flares; proper hydration of skin å need for topical steroid by ~50%; many types available; consider ceramide-containing creams, petrolatum-based ointments (hydrolatum, Aquaphor, petroleum jelly; lotions generally inadequate if significant xerosis); restore epidermal barrier function;

Proper technique: “Soak & seal” use of moisturizers soon after bathing → ↓ skin dryness, ↓ itching, protects from irritants, improves appearance; daily lukewarm (not hot) bath 15–20 min, cleanser only where/when necessary (pH-neutral, nonsoap preferred), followed by application of ceramide-containing moisturizer or petrolatum-based emollient

Topical corticosteroids: 1st-line topical tx for mod/severe AD, rec BID dosing (see “Topical Corticosteroids”); use lowest effective potency at lowest frequency possible to prevent s/e; ointments preferred (most hydrating); intermittent maintenance use (BIW) can ↓ potential for

 

relapse (Br J Dermatol 2002;147:528); s/e: Irreversible atrophy, striae, hypopigmentation if used improperly

Antipruritics: Antihistamines PRN day (nonsedating) ± night, esp if significant sleep disruption, allergic dermatographism, or AR (see “Allergic Rhinitis”) (JAAD 2004;50:391;404)

↓ Staph colonization: For severe cases, twice-weekly dilute bleach baths (0.5 cup of 6% bleach to full bathtub, immerse × 5–10 min, then rinse, pat dry, emollients) plus intranasal mupirocin oint 5 consecutive d/mo; oral abx not recommended for routine use

Elimination diets not recommended for AD tx; severe food allergies co- exist in subset of patients, esp children, but no clear causal relationship; consider review with allergist

When to Refer

Severe or refractory disease (e.g., not controlled after 2–3 mo of topical steroid use), consideration of PO corticosteroids; erythroderma, skin pain, ? of concomitant contact dermatitis

Consideration of topical calcineurin inhibitors (pimecrolimus, tacrolimus), other nonsteroidal treatments (crisaborole) phototherapy, immunomodulators (CsA, MMF, MTX)

If suspect widespread viral or bacterial superinfection—e.g., eczema herpeticum—dermatologic emergency: Prompt tx w/ abx or antivirals; may need ED/hospitalization

 

SEBORRHEIC DERMATITIS (NEJM 2009;360:387)

 

Background

Definition: Chronic, relapsing inflammatory disease affecting sebaceous gland-dense skin (scalp, nasolabial fold) Pathophysiology: Unclear; suspected abnl immune response to

Malassezia yeast (part of nl flora, but likely ↑ colony burden in seb derm pts)

Epidemiology: 7–12% incidence in adults; most common in healthy 30–60 yo, ♂ > ♀ (AFP 2006;74:125)

 

Risk factors: Parkinson disease and other neuro d/o assoc w/ severe/refractory disease, trisomy 21, HIV/AIDS (in up to 85% of patients w/ CD4 <400); disease often ↑ w/ stress; certain medications (interferon, lithium, psoralen)

Clinical Manifestations

Scalp: Most commonly affected; ranges from fine scaling (“dandruff”) to more inflammatory disease w/ erythema, pruritus

Face/neck: Erythematous, greasy, ± pruritic patch w/ yellowish scale involving forehead, glabella, eyebrows, lateral nose/nasolabial fold, retroauricular fossa, external auditory canal (ddx discoid lupus, psoriasis), & other hair-bearing skin of head & neck (e.g., beard) Other: Blepharitis (eyelids); otitis externa; involvement of central chest (can be psoriasiform, pityriasiform, “petaloid” variant resembles flower petals), umbilicus, intertriginous areas of trunk

Evaluation

Clinical diagnosis: KOH scraping can r/o tinea; consider HIV testing if severe/refractory

Differential diagnosis: Psoriasis, tinea, AD, contact dermatitis, impetigo, rosacea (⊕ telangiectasia), candidiasis, erythrasma, DM, & SLE (malar rash spares nasolabial folds)

Treatment (Arch Dermatol 2005;141:47; Cochrane Database Syst Rev 2015;5:CD008138)

Reactions may have antifungal, keratolytic, and/or immunomodulatory effects

Scalp: Ketoconazole 2% shampoo 2×/wk until clearance, then 1×/wk to 1×/every other wk for Ppx; may also use ciclopirox 1% shampoo w/similar dosing schedule; OTC selenium sulfide, zinc pyrithione, coal tar, & salicylic acid shampoos also used solo or as adjuvant; topical corticosteroids may be useful for short-term control of sx but ↑ risk of adverse effects (e.g., atrophy, telangiectasia) & similar efficacy to the antifungals

Face/nonscalp areas: 1st-line ketoconazole 2% crm or foam BID for at least 4 wk (J Drugs Dermatol 2007;6:1001); consider ciclopirox 1% crm BID as 2nd line (Br J Dermatol 2001;144:1033); topical corticosteroids & immunomodulators if unresponsive to antifungals

When to refer: if not responding to ketoconazole or OTCs →

 

dermatology

 

ALLERGIC CONTACT DERMATITIS (ACD)

 

Background (Dermatol Clin 2012;30:87)

T-cell–mediated, delayed (type IV) hypersensitivity reaction; time interval to sensitization may be weeks to years; subsequent rechallenge may cause ACD w/in hours to days

Epidemiology: Prevalence ↑ w/ age (highest at age 60–69), ♀ > ♂ Over 3000 chemicals assoc w/ ACD: Nickel, neomycin, bacitracin among most common

 

Most Common Contact Allergens (J Clin Aesthet Dermatol 2010;3:36; JAAD 2004;51:S60)
Class	Examples
Plant (“Phyto-ACD”)	Urushiol in poison oak/ivy/sumac
Metals	Nickel, gold (also can include nickel as alloy), cobalt
Preservatives	Formaldehyde, quaternium-15, parabens, MCI/MI
Cosmetics	Balsam of Peru, fragrance mix, p-phenylenediamine
Antibiotics	Neomycin, bacitracin
Textiles	Potassium dichromate, disperse blue

Clinical Manifestations

Acute: Well-demarcated, erythematous papules & plaques ± vesicles/bullae/exudate w/ prominent pruritus; often linear pattern from transfer of allergen (e.g., band from ring or watch); allergen can be aerosolized presenting as facial/eyelid erythema & edema

Chronic: Lichenified papules & plaques, scaling, erythema, excoriations, & pigment Δ

Often difficult to distinguish from Irritant Contact Dermatitis (ICD) (see below); ACD may be superimposed on ICD

Evaluation

Hx/PE: Hx of exposure to & withdrawal from allergens w/ emphasis on cosmetic/hygiene products, topical meds, jewelry, clothing, hobbies, plant contact, & occupation (hairdressers, construction workers,

 

metalworkers); ask about “wet wipes” esp in persistent anogenital dermatitis

Ddx: ICD, AD, tinea, psoriasis, dyshidrotic eczema, scabies (esp if on hands), stasis dermatitis, & cellulitis

Dx: Refer to Dermatology/Allergy for patch testing, which is the gold standard; Thin-layer Rapid Use Epicutaneous (TRUE) test commonly used & FDA-approved; customized patch testing also available including a wider spectrum of allergens

Treatment (AFP 2010;82:249; JAAD 2005;53:845)

Avoidance of allergen; 1st-line tx is mid-to-high potency topical steroids (see “Topical Corticosteroids”)

Severe disease: Prednisone taper over ∼2 wk (short “dose pack” may

→ rebound flare)

Wet dressings, oatmeal baths, & oral antihistamines for sx relief

IRRITANT CONTACT DERMATITIS (ICD)

 

Background

Nonimmune-mediated physical/chemical damage to epidermis → inflammation

Most common (>>ACD) cause of occupational skin disease; highest prevalence in cosmeticians, also seen in health care, agricultural, custodial workers (Dermatol Clin 2012;30:87)

May occur after single exposure to harsh chemical or chronic exposure to milder irritant (e.g., solvents, acids/bases, & detergents)

Clinical Manifestations

Acute: Well-demarcated erythematous papules & plaques, often w/ evolving vesicles/bullae & possible necrotic ulceration; usually painful, ± pruritus; commonly involves hands, also face (esp thin eyelid skin) or any other area of contact w/ irritant

Chronic: Poorly demarcated lichenified papules & plaques w/ scaling, crusting, & fissures; often painful & pruritic; typically involves hands

Evaluation

Hx/PE: Hx of exposure to & withdrawal from possible irritants, esp at

 

home (e.g., laundry or dishwasher detergent) & workplace (hand sanitizer, occupational chemicals)

Dx: Usually clinical, Ddx same as ACD; consider patch testing if concern of superimposed ACD

Treatment (JAAD 2005;53:845)

Avoidance of suspected irritant; short-term topical steroids ± occlusion, esp for severe disease, but data lacking; restoring dermal barrier: ↓ freq of exposure to water (e.g., handwashing) when feasible; lipid-rich moisturizers (JAAD 2005;53:845)

Prevention: Barrier creams, lipid-rich moisturizers, & softened fabrics; nonlatex gloves w/ cotton liners & regular glove removal, substitution w/ nonirritant agents (Br J Dermatol 2009;160:946)

 

Background (NEJM 2012;366:2492; JAAD 2008;59:995)

Case reports for nearly all medications, rates up to 10 cases/1000 new users

Clinical presentation: Majority of cases mild, but can be severe w/ systemic involvement; morbilliform (aka “exanthematous”) most common (80%) followed by urticarial (5–10%)

Risk factors: HIV, HSCT, connective tissue disease, autoimmune or viral hepatitis (Br J Dermatol 2003;149:1018)

Evaluation (NEJM 2012;366:2492)

History: Assess all pts for systemic, ocular, mucosal sx; obtain detailed med hx

Onset after starting new med: <36 h (urticarial) 4–14 d (exanthem); 4–21 d (TEN/SJS) ∼21 d (DRESS) Course: Peak w/in 2 d of stopping offending med; often fades by 1 wk after stopping

Exam: Complete skin exam; evaluate mucosa in all pts

 

Cutaneous Drug Eruptions
Reaction Type	Presentation	Classic “Culprit” Meds
Morbilliform	Erythematous macules & papules coalescing	PCNs (amoxicillin w/

 

“Exanthematous” (most common) Type IV hypersensitivity	into plaques; symmetric, widely distributed; ± pruritus Often w/ superficial exfoliation in resolution phase; mucous membranes spared	acute mononucleosis) TMP–SMX (↑ risk w/ HIV) FQs, anticonvulsants Allopurinol
Urticarial Type I hypersensitivity	Pink-to-erythematous edematous plaques ± soft-tissue edema of lips, upper airway, eyelids, genitalia (angioedema); see “Urticaria”	ASA, NSAIDs, PCN
Fixed drug eruption Occurs in same place each time	Usually multiple, sometimes solitary, red/violaceous hyperpigmented plaques, often on acral surfaces, mucosa, or genitalia (glans penis)	NSAIDs, TMP–SMX Tetracyclines, pseudoephedrine
Drug reaction w/ eosinophilia and systemic symptoms (DRESS) (JAAD 2013;146:1373)	Most common presentation is morbilliform rash (incl face, trunk, UE) 2–6 wk after starting new Rx; facial edema, LAN Systemic sx may include fever (often precedes rash for days–wk), pruritis; organ dysfunction (hepatic > renal, pulm, CV); derm emergency → ED (mortality up to 10%)	Anticonvulsants (carbamazepine, lamotrigine, phenytoin) Sulfonamides (dapsone, sulfasalazine) Allopurinol NSAIDs (celecoxib, ibuprofen) Antivirals (Nevirapine) Antidepressants (buproprion, fluoxetine)
SJS/TEN (NEJM 1995;333:1600; JAAD 2008;58:25)	Fever, malaise, erythroderma, skin pain, dysphagia, dysuria, blisters, mucosal involvement = dermatologic emergency → ED	Allopurinol, TMP–SMX Carbamazepine β-lactam abx NSAIDs

Labs: If systemic sx, CBC w/ diff, LFTs, Cr

Differential diagnosis: Viral exanthem (usually children), GVHD (in appropriate clinical setting), toxic shock syndrome

Treatment

Identify and discontinue offending agent; if simple morbilliform eruption (no systemic sx) & if drug necessary & temporary (e.g., chemotherapy), can consider “treating through” rash w/ close clinical & lab monitoring

Therapy: Antihistamines for sx relief (nonsedating during the day, sedating at night); topical or systemic corticosteroids for sx relief, though little empiric evidence

Rechallenge should generally be avoided as subsequent eruptions on

 

re-exposure may be more severe (NEJM 2012;366:2492)

If patient has allergy to one aromatic anticonvulsant, must also avoid others in same class (phenytoin, phenobarbital, carbamazepine)

When to Refer

Immediate referral to emergency department: Pustular lesions (acute generalized exanthematous pustulosis), duskiness, skin pain, blisters/epidermal desquamation, ocular/mucosal involvement (SJS/TEN) systemic involvement (e.g., DRESS)

 

Background (Allergy 2009;64:1427; 2011;66:317; J Allergy Clin Immunol 2014;133:1270)

Urticaria: Type 1 (IgE-mediated) hypersensitivity reaction, characterized by the appearance of wheals: Pruritic, pink/erythematous edematous plaques, can be arcuate or polycyclic w/ central clearing, no scale; each individual lesion must resolve in 24 h → migratory appearance (a circled lesion “disappears”) Pathophysiology: IgE → mast cell degranulation → histamine release

→ plasma leakage into skin → wheals

Classification: Acute: <6 wks’ duration of recurrent or continuous lesions; lifetime prevalence 20% (AFP 2011;83:1078)

Chronic: ≥6 wk’ duration; lifetime prevalence 1%, peak age 20–40 y,

♀ > ♂; often idiopathic; majority of cases will resolve w/in 1 y

Associated syndromes

Angioedema: soft-tissue edema of lips, upper airway, eyelids, genitalia; occurs in 40% of pts w/acute urticaria (NEJM 2002;346:175); can also occur w/o urticaria (e.g., ACEI s/e) Anaphylaxis: Urticaria or angioedema + extraderm manifestations (resp, CV, GI sx) = emergency requiring epinephrine; must be ruled out

Epidemiology & risk factors

Acute: 50% idiopathic; most commonly 2/2 infection (viral URI, GAS), medications (PCN, ASA, NSAIDs), food (strawberries, peanuts, shellfish, tomatoes, eggs, milk, in pts w/ latex allergy: Chestnuts, banana, passion fruit, kiwi, avocados)

 

Evaluation (Allergy 2009;64:1417; 2009;64:1427; 2011;66:317; NEJM 2002;346:175)

History:

• Obtain hx of lesions (duration of lesions, frequency of attacks, pruritis) (2) Assess for s/sx of angioedema or anaphylaxis: wheezing, facial swelling, vomiting (3) Evaluate for potential triggers: PMHx, systemic health changes, allergies and ask about: Acute: Infection: URIs, strep; Medications: PCN, ASA, NSAIDs Food: strawberries, peanuts, shellfish, tomatoes, eggs, milk (in pts w/ latex allergy, chestnuts, banana, passion fruit, kiwi, & avocado all identified triggers) Chronic: Idiopathic most common (J Allergy Clin Immunol 2012;129:1307); Autoimmune: SLE, Sjögren’s, RA, anti-IgE receptor IgG antibodies, thyroid disease Food additives: Yeast, azo dyes, benzoic acid, sulfites, nickel Infections: HBV, HCV, pylori, parasitosis

Hematologic malignancy (rare) (Arch Dermatol 2012;148:103) Physical:

Exercise, cold weather, dermatographism (“skin writing”)

Exam: if lesions present, confirm blanching (r/o vasculitis)

Labs: Acute: none needed unless dictated by hx/PE to r/o a chronic illness; skin testing can help confirm specific allergic cause if suggested by hx

Chronic: AAAAI “Choosing Wisely” recommends against routine testing for chronic urticaria, given frequently idiopathic; targeted testing as dictated by hx/PE may include CBC w/diff, ESR, thyroid eval, H. pylori, HBV/HCV testing

Differential diagnosis: Urticarial vasculitis (painful), bullous pemphigoid (esp in elderly; lesions not migratory), Sweet syndrome, mastocytosis, erythema multiforme (targetoid, not migratory), serum sickness; hereditary or ACEI-induced angioedema (no wheals)

Treatment (Allergy 2009;64:1427; 2011;66:317; NEJM 2002;346:175)

General approach: Treat underlying cause whenever possible; topical agents typically have no role in mgmt; anyone w/ s/sx suspicious for anaphylaxis needs IM epinephrine (0.3 mL of 1:1000 dilution) & → to ED

 

Type	Interventions
Acute	1st line: Avoid trigger; add nonsedating H1 antihistamines 2nd line: Consider oral corticosteroids (for 3–5 d, if no response to antihistamines; rebound may occur)
Chronic	“Stepped” approach; start w/ step appropriate for level of severity Step 1: avoid triggers; nonsedating antihistamine Step 2: add one of the following: dose increase of nonsedating antihistamine 4× standard dose (Allergy 2011;66:317; 2002;346:175); second nonsedating antihistamine; H2 antagonist, leukotriene receptor antagonist, sedating antihistamine QHS ————–make derm/allergy referral, if have not already done so————– Step 3: add/increase potent antihistamine (doxepin, hydroxyzine) as tolerated Step 4: omalizumab SC (NEJM 2013;368:2527), CyA, other immunologics/biologics

(Cochrane Database Syst Rev 2012;14:CD008596; J Allergy Clin Immunol 2014;133:1270)

When to Refer

Dermatology: Individual lesions persist for >24 h, assoc w/ postinflammatory purpura or pigmentation, bullae, skin pain; chronic urticarial for further mgmt

Allergy: If ↑ suspicion for environmental, food, or med hypersensitivity

→ serologic (RAST) or prick testing; for consideration of newer generation antihistamines or omalizumab

 

Background (JAAD 2008;58:826; Ann Intern Med 2011;155:ITC 2–1; JAAD 1999;41:401)

Definition: Chronic inflammatory condition affecting skin, nails, & joints; assoc w/ multiple medical & psychiatric comorbidities; effect on quality of life ≈ major medical diseases

Pathophysiology: Immune dysregulation (↑ Th1 & Th17 cytokines), keratinocyte hyperproliferation (↑ epidermal cycle, ↑ mitotic activity), & genetics (many associations)

Epidemiology: Prevalence is 2% (US), onset 15–25 y, affects ♀ & ♂ equally; 80% of patients have mild–moderate disease; risk factors: Tob, EtOH, obesity, ⊕ FHx (1st-degree relative in 1/3 of psoriasis pts); also assoc w/ IBD, depression, NAFLD, CAD, SCC, lymphoma; disease severity may be ↑ in pts w/HIV

Classification: Multiple subtypes; plaque most common (80–90%), then guttate

 

Psoriasis Subtype Classification (Ann Intern Med 2011;155:ITC2-1)
Subtype	Distribution & Morphology	Notes
Plaque	Symmetric, extensor surfaces (elbows, knees), scalp, penis, umbilicus, intergluteal cleft	Most common Ddx: AD, tinea, cutaneous lupus, mycosis fungoides
Guttate	Droplet-sized lesions on extremities & trunk, spares palms/soles	Abrupt onset, often younger pts after GAS infection (eval for s/sx) Ddx: Pityriasis rosea
Palmar- Plantar	Thick-fissured plaques + scale on palms/soles, or solitary pustules coalescing	Assoc w/ tob Ddx: Eczematous dermatitis, tinea manuum, reactive arthritis
Inverse	Well-demarcated, erythematous thin plaques w/ min scale, inframammary, axillary, intergluteal	Ddx: Intertrigo, tinea, erythrasma
Erythrodermic	Confluent erythematous plaques/scale on >75% BSA ± systemic sx	Can be triggered by PO steroid withdrawal → urgent derm referral vs. ED
Pustular	Individual or coalescing sterile pustules —generalized or near existing plaques	Assoc ↓ Ca → urgent derm referral vs. ED

Psoriatic arthritis classification: 5 patterns of joint involvement, individual pt’s pattern can change over time (NEJM 2017; 376:957; J Rheumatol 2003;30:1022); 30–50% of pts also have enthesitis, most commonly Achilles or plantar fascia (Arthritis Rheumatol 2016;68:312)

Asymmetric oligoarthritis (usually hands/wrists, esp DIPs) most common Other variants: Symmetric polyarthritis (RA-like), distal arthritis (DIPs only), sacroiliitis & spondylitis, or “arthritis mutilans” (severe, rapid joint destruction, & deformity)

Evaluation (JAAD 2008;58:851;1031; JAAD 2009;60:643; Lancet 2015;386:983)

History: Typical features: Pruritus, disease remits in summer (likely 2/2 UV exposure)

Triggers: Infection, including GAS (guttate “teardrop” psoriasis), meds (steroid withdrawal, βBs, lithium, antimalarials, ACEIs); provocation of lesions by skin trauma (scratching, piercing, tattoos, sunburn: Koebner phenomenon) or injury (sunburn, chemical irritants) Complications: up to 30% of pts w/ mod–severe disease develop psoriatic arthritis (see below); up to 60% have depression

 

Exam: Full cutaneous exam & joint exam (focusing on hands)

Skin: Subtype-specific morphology & distribution noted above; lesions are typically discrete erythematous plaques w/ adherent silvery scale; Distribution: Scalp commonly involved (Ddx: seb derm, tinea); lateral face, retroauricular areas; extensor surfaces (elbows, knees), back; Auspitz sign: scale removal → punctate bleeding Nails: 2/3 of pts w/ PsA have nail disease (Br J Rheumatol 1994;33:834); Pitting: Punctate depressions 2/2 nail matrix disease; Oil spots: Yellow-brown discoloration of nail bed Onycholysis: Separation of nail plate from bed (Ddx: onychomycosis) Joints: Hands/wrists most common (esp DIPs); tenosynovitis, enthesitis, dactylitis (“sausage digits”) w/ telescoping of digits in advanced disease

Studies: Psoriasis dx is clinical; psoriatic arthritis dx supported by imaging and should obtain radiograph of hands if acro-osteolysis suspected, “pencil in cup deformity” classic); no particular labs helpful; consider labs to r/o RA if on arthritis on Ddx

Treatment (JAAD 2009;60:643; 2010;62:114; 2009;61:451; JAAD 2009;60(4):643–59)

Initial management based on affected % of BSA (for BSA definition, see “Burns”)

Mild, limited disease (<3% BSA): Topical agents (below); note choice of vehicle (ointment, crm, gel, etc) very important to successful delivery of medication, should be tailored to individual pt; occlusion of any topical agent (e.g., saran wrap) ↑↑ potency; caution re: overuse, can → permanent atrophy/hypopigmentation; see “Topical Corticosteroids” for details of dosing & s/e

 

Topical Tx of Psoriasis
Class	Example/Initial Dosing	Notes/Safety Monitoring
Corticosteroids	See “Topical Corticosteroids” Class I/II for torso or extremities; Class VI/VII for face, axilla, groin BID	Limit high dose to 4 wk of continuous use; gradually ↓ use/potency to class IV for torso/extremities, then to PRN as tolerated; monitor for s/e; limit use as monotherapy when possible
Vitamin D	Calcipotriene	Transient irritation; inactivated by UVA; <100 g/wk to

 

analogs	0.005% oint, soln, crm BID Calcitriol 3 μg/g oint BID	avoid ↑ serum Ca; photosensitivity
Retinoids	Tazarotene 0.05% crm, gel QHS	Irritation (gel > crm), photosensitivity Pregnancy category X Best used in combination w/ topical steroids
Coal tar	Variety of preparations; apply QD; e.g., 5% liquor carbonis detergens	May stain skin & clothing; unpleasant odor; inexpensive
Misc	Topical tacrolimus/pimecrolimus; emollients; salicylic acid; anthralin

(Ann Intern Med 2011;155:ITC2–1; JAAD 2009;60:643; 2011;65:137; 2010;62:114; 2009;61:451)

Moderate to severe disease (incl PsA or disabling palmo-plantar): → Derm for consideration of phototherapy, systemic retinoids or immunomodulators; rheumatology for evaluation of joint disease; avoid systemic corticosteroids; risk of rebound, pustular, or erythrodermic flare that can → need for hospitalization

When to refer: Dx uncertain—cutaneous T-cell lymphoma and other more severe diseases can mimic psoriasis; refractory, or moderate–severe disease; inability to wean high-potency corticosteroids; consideration of systemic tx, phototherapy → Dermatology; erythrodermic or pustular subtypes → Dermatology (or ED if severe)

Pt information: National Psoriasis Foundation, www.psoriasis.org/about-psoriasis

 

Background (NEJM 1999;341:491; 2007;357:1620; Clin Exp Dermatol 2002;27:389)

3 phases in hair cycle: Anagen (growth phase, ∼2–6 y, ∼90–95%)

→ catagen (involutional phase, ∼2–3 wk, <1%) → telogen (resting phase, ∼2–3 mo, 5–10%)

Number of hairs on scalp: ∼100,000; nl scalp loss: ∼100 telogen

 

hairs/d

Hair loss: Abnormalities in cycling ± inflammation; thinning (c/w androgenetic alopecia) vs. shedding (c/w alopecia areata or telogen effluvium) vs. both

Categorized as nonscarring alopecia: Follicular openings visible on exam vs. scarring alopecia: Follicular ostia no longer visible (tissue architecture destroyed)

Evaluation (NEJM 2007;357:1620)

History: Med review, infections, stressors, surgeries, pregnancy, wt loss, use of hair straighteners, braids, rollers; ⊕ FHx of alopecia; duration/pattern; menstrual cycle irregularities

Exam: Scalp: ⊕ Scale, crust, pustules, erythema; Hair shaft: Note length, diameter, texture; distribution; hair breakage; ± follicular ostia intact; skin & nails, hair pull test

Labs: Consider CBC w/ diff, iron studies, TSH, free & total testosterone, DHEA-S, PRL, ANA, vit D, zinc

Biopsy: Refer to dermatology to ensure proper technique and accessioning by a dermatopathologist—4-mm punch bx is standard (J

Cutan Pathol 2008;35:82)

Etiologies (NEJM 2007;357:1620)

Male androgenetic alopecia: Most common; occurs after puberty

Causes: Genetic, hormonal (DHT); early-onset/vertex assoc w/ ↑ incidence CAD (J Cardiovasc Risk 2001;3:147; BMJ Open 2013;3:e002537) S/sx: Progressive follicular miniaturization & shortening of anagen phase Distribution: Frontotemporal & vertex of head

Tx: Must be used indefinitely or progression will resume; minoxidil 5% soln BID or 5% foam QD (s/e: facial hypertrichosis, irritant dermatitis, possible ↑ shedding in 1st 2–8 wk); finasteride 1 mg PO QD in men (s/e: sexual dysfunction) (JAAD 2012;67:379); emerging data on dutasteride; hair transplant; consideration of red light lasers, combs, devices

Female pattern hair loss (FPHL): typically 40s–60s, insidious onset Causes: Genetic, hormonal (postmenopausal, PCOS) etiologies S/sx: Widened part & “thinner ponytail”; affected areas similar to ♂:

progressive follicular miniaturization & shortening of anagen

 

phase Distribution: Crown/widened part; frontal hairline preserved; “Christmas tree/Ludwig pattern”

Tx: Consider derm referral to r/o other etiologies and mimickers that can → scarring; minoxidil 2% soln or 5% foam (s/e listed above); spironolactone; hair transplant; consideration of red light lasers, combs, devices

Telogen effluvium: Premature shift to telogen → diffuse shedding; starts 2–4 mo after trigger (J Invest Dermatol 2003;121:985)

Causes: Stress, wt loss, infection, fever, hypothyroidism, Fe deficiency, meds (minoxidil [1st 2–8 wk]; heparin, coumadin, ramipril, βB, lithium, IFN-α, TCAs, oral retinoids, terbinafine, VPA, OCPs, postpartum [2–5 mo postdelivery]) S/sx: Hair pull test → grab ∼60 hairs, tug the group of hairs proximally to distally, ⊕ if >6 hairs are released (NEJM 1999;341:491; Clin Exp Dermatol 2002;27:389) Tx: Reversal of trigger, if possible (Arch Dermatol 1993;129:356; JAAD 1996;35:899)

Traction alopecia: Nonscarring hair loss 2/2 persistent tension applied to hair strands; seen w/ specific hair styles (e.g., tight braids); may affect 1% of US persons of African ancestry (Arch Dermatol 2006;142:377) often frontotemporal distribution; Tx: Reduce tension on hairs via change in hair style or ↓ pulling (softer hair ties, etc); derm referral for severe/refractory disease

Anagen effluvium (NEJM 2007;357:1620; JAAD 2011;64:604); hair matrix arrest

→ tapered fractures of the hair shaft; starts 7–14 d after thallium or chemotherapy (cyclophosphamide, doxorubicin, taxanes); can → permanent alopecia (taxanes, busulfan, cyclophosphamide, tamoxifen)

Tx: Counseling before starting Rx; scalp cooling, minoxidil, wigs if pt preference

Alopecia areata (NEJM 2012;366:1515; JAAD 2009;60:85; 2010;62:177; 2010;62:191);

aberrant HLA expressed by hair bulb; lifetime incidence 1.7%; 16% of pts also have other autoimmune disease; chronic, relapsing course, but spontaneous remission possible; ↑ risk of severe disease if hx atopic dermatitis, juvenile onset, widespread, duration >5 y, onychodystrophy

S/sx: Discrete circular bald patches w/ “exclamation point” hairs (proximal narrowing); Totalis (scalp only) or Universalis (scalp + body); 60% w/ nail pitting; rarely lesions are inflammatory (w/

 

erythema) Tx: Refer to dermatology; intralesional corticosteroids (s/e: permanent dermal atrophy); topical immunotherapy; JAK inhibitor tofacitinib promising new tx (JAAD 2017;76:22) Pt information: www.naaf.org

Scarring (cicatricial) alopecia: Causes: Multiple etiologies; may be primary process (inflammatory follicular destruction; e.g., discoid lupus erythematosus, lichen planopilaris, dissecting cellulitis, folliculitis decalvans) or secondary process (indiscriminate follicular damage from another disease process; e.g., burns, sarcoid, malignancy); also characterized by type of cellular infiltrate (JAAD 2005;53:1); S/sx: No follicular ostia; tufted hairs (“doll’s hairs”); refer to derm if suspected Other: Trichotillomania: Often childhood onset, impulse-control d/o assoc w/ psychiatric disease (OCD); S/sx: Bizarre pattern of w/ incomplete clearing areas Tx: behavioral/psychiatric (AFP 2003;68:93); Tinea capitis: See “Tinea”; Hair shaft disorders: Acquired & congenital etiologies

When to Refer

Scarring alopecia or unclear etiology or if biopsy needed, consider for alopecia areata/androgenetic alopecia especially female pattern alopecia

 

Background

Definitions: Erosion: Epidermal injury; heals w/o scar;

Ulcer: dermal injury; scarring w/reduced tensile strength Primary intention: Wound edges are surgically approximated Secondary intention: Wound left to heal w/o approximation

Stages of wound healing (JAAD 2008;58:185; Adv Wound Care 2016;5:32)

Inflammatory phase: Platelets → PMNs → macrophages and fibroblasts; chronic wounds often stalled here; can mimic infection (red, warm) Proliferative phase: 1st week, angiogenesis, collagen production Remodeling phase: 2nd week; contraction via myofibroblasts; at 3 wk, at 20% of final tensile strength

 

Multiple factors adversely affect wound healing, including advanced age, malnutrition, medications (glucocorticoids, chemotherapy), inadequate arterial perfusion (PAD, Raynaud’s), smoking, immunosuppression, diabetes, hepatic or renal disease, poor self-care, venous insufficiency, allergic contact dermatitis (JAAD 2008;58:185)

Evaluation

History: Attempt to determine etiology of specific lesion (trauma), precipitating/exacerbating factors (diabetes, PAD, venous insufficiency, neuropathy; see above), prior wounds and their tx responses; pathergy (worsening w/ trauma), prior tx for this wound

Physical exam: Vitals (systemic infection); for extremity wounds, do full extremity exam (color, edema, symmetry w/other limb, warmth, distal pulses, capillary refill, sensation, tenderness, LAN)

Wound assessment: Consider the “ABCDE”s of each wound; being able to concisely describe complex wounds invaluable for future visits to determine progress; consider including photograph in medical record (BMJ 2006;332:285) Area: wound size, depth (full vs. partial thickness) & location on body Base: viable: granulation/beefy red vs. nonviable: fibrinous (gray-yellow), necrotic (black), % viable/nonviable tissue Circumference: Describe periwound skin—erythematous, warm, dusky, black, callus Drainage: Serous, sanguinous, purulent, malodorous, minimal/moderate/copious Edge: Smooth, punched out, undermining, tunneling, rolled borders (chronic wound)

Labs: Routine labs not recommended; for wounds w/ delayed healing, investigation for etiologies which can delay wound healing above; all wounds colonized so routine culture unhelpful; (see “Skin and Soft- Tissue Infections”)

Management (BMJ 2006;332:777; Adv Wound Care 2016;5:32; JAAD 2008;58:185)

Initial wound management: Irrigation: Clean w/ normal saline, high pressure if significant contamination; Tetanus vaccine: PRN (see “Immunizations”)

 

General Approach to Chronic/Complex Wounds
Keep wound moist, but not wet Debride nonviable tissue (except for arterial ulcers) Gently	Manage modifiable factors which may delay healing

 

 

 

 

Moisture: If wound dry, petrolatum generally preferred over topical abx

— ↓ infection rate & ↓ contact allergy; topical abx preferred in trauma, burns (Ann Emerg Med 2013;61:86)

Debridement: Necrotic tissue on wound base impairs healing and should be removed if adequate arterial flow (confirm pulses, do NOT debride wounds in setting if concern for arterial insufficiency at site); many different mechanisms available; sharp mechanical debridement (scalpel; if sensate, premedicate with topical lidocaine or prilocaine 2.5% covered by plastic wrap x 30 min prior to debridement), enzymatic (collagenase), osmotic (Medihoney), autolytic (hydrogels such as Aquaform)

“Fill” wound: Do not pack, gently fill; fill/partially fill if there is a potential space/depth left by the wound; can use sterile gauze or petrolatum-impregnated gauze (change gauze daily), calcium alginate (good for ↑ exudate), Medihoney, Aquacel; silver dressings (Aquacel Ag) can ↓ bacterial load in colonized/infected wounds; avoid iodine as can affect thyroid function and → tissue damage in acute wounds (J Hosp Infection 2010;76:191); if wound stable, alginate dressings can stay in for up to 1 wk

Cover wound: This layer should be determined by need for managing exudate; consider skin protectant (e.g., Cavilon) to protect periwound skin and help bandages adhere

 

Commonly Used Wound Dressings (BMJ 2006;332:777; JAAD 2013;68:e117)
Class/Example	Type of Wound	Function (Moisture, Debride, Fill, Cover)	Notes
Film (Tegaderm)	Superficial, dry- min exudate	C	Caution w/ fragile skin (e.g., elderly) Flexible; good for joints
Telfa	Dry-min exudate	M, C
Hydrocolloids (DuoDERM)	Dry-min exudate	Sheet: M, D, C Gel: M, D, F	↑ACD risk, “gel and smell”—produces malodorous d/c which can mimic infection Can be worn for several days
Hydrogels (Aquaform)	Low-med exudate,	Sheet: M, D (autolytic),	Flat wounds, cavities, and sinuses May be left in place several days

 

	slough/escar	F, C Gel: M, D, F	Can soften eschar for mechanical debridement; caution re: maceration of periwound skin
Alginates	High exudate	M, D (autolytic), F	May be left in place for several days Caution re: maceration of periwound skin
Hydrofibers Aquacel)	High exudate	M, D (autolytic), F	Highly absorbent, nonadherent
Foams (Mepilex)	Variable exudate (depends on foam)	M, F, ±C	Offer cushioning for wound May be left in place for up to 7 d on stable wounds

Venous stasis ulcers (see “Lower Extremity Edema”); any pt w/ possible PAD should have ABI/TBI eval prior to initiating pressure wrap to avoid inducing ischemia in vulnerable limb

When to Refer

Failure of wound healing, complex wound mgmt, consideration for topical growth factors, vacuum-assisted closure devices

BURNS

 

Background: 450,000 people seek medical care for burns annually in US; majority of cases mild; most commonly 2/2 flame exposure, most commonly at home NEJM 2009;360:893; ameriburn.org)

General approach:

• Evaluate mechanism of burn
• Determine burn size, location, and depth
• Determine if   emergency   treatment   warranted   (high-risk wounds)
• If appropriate   for   outpatient   management,   provide   pain control and wound care
• Reassess frequently to ensure wound healing

Burn mechanism: Can be thermal, electrical (often deeper than suggested by cutaneous findings, can → compartment syndrome), chemical (acids, alkali, solvents), radiation (fluoroscopy or XRT)

 

Sunburn: If severity >expected or focal/geometric distribution, consider: topical phototoxic reaction: Phytophoto dermatitis (lime, lemon), topical retinoids systemic phototoxic agents: Doxycycline, FQs, amiodarone, thiazides, naproxen, furosemide, some antimalarials

Burn size: Calculated by body surface area (BSA): Reference is one palm = 1% BSA; less accurate in obese pts

Burn location: high-risk locations include face, neck (assess airway regardless of burn size), hands, feet, genitals, or over major joints (risk contractures)

Burn depth: determines severity & prognosis (NEJM 1996;335:1581)

Superficial (epidermis only): erythema, dry, painful; e.g., sunburn; heals w/o scarring Partial thickness (epidermis & superficial-full dermis): bullae, erythema, intense pain, ↓sensation → heals w/significant scarring Full thickness (epidermis, dermis, and below): Whitish, charred or translucent, no pinprick sensation in burned area

High-risk wounds (need referral to burn center): concomitant trauma (e.g., fracture), electrical or chemical burn, partial thickness >10% BSA, full-thickness burns, high-risk location (see above) or concern for inhalation injury; If in doubt, call a burn center for phone triage; list at www.ameriburn.org

Outpatient management:

Superficial burn: Analgesia as needed (NSAIDs); soothing gel/ointment (aloe vera) Partial thickness: Analagesia as needed; tetanus immunization if not current; ensure wound clean (sterile water irrigation); larger blisters/those over joints may need debridement, but should also be considering referral if considering debridement; cover wound with antibiotic ointment or silver sulfadiazine, then cover by occlusive dressing; larger wounds may require more dressing, such as Aquacel Ag (silver-impregnated absorptive dressing) (J Burn Care Res 2009;30:380) Larger partial- thickness or full-thickness wounds: Referral for early surgical management

 

                 TOPICAL CORTICOSTEROIDS

 

 

Background (JAAD 2009;60:643)

Topical corticosteroids have anti-inflammatory, antimitotic, vasconstrictive and immunosuppressive properties that make them effective in treating a variety of dermatologic processes, but improper use can → permanent s/e

Mechanism of action: pass through cell membrane to react with receptor proteins → into nucleus, alter transcription of genes that are involved in inflammatory pathways (e.g., ↓ phospholipase A2 release) Class/potency assoc w/ drug’s ability to produce vasoconstriction & determined by:

• Drug structure (individual molecule)
• Drug concentration (for individual drug; e.g., hydrocortisone 2.5% more potent than hydrocortisone 1%, but not more potent than desonide 05%)
• Vehicle of application (determines absorption)

General Approach (www.aad.org)

Steps in prescribing topical corticosteroids

• Determine an appropriate vehicle
• Determine potency required
• Determine appropriate amount to dispense
• Select appropriate Rx given above; note certain topical steroids can be very expensive/not covered by insurance; table below includes only generics
• Counsel pts on appropriate use: amount, duration, & s/e (see below)

Vehicle (www.aad.org)

Vehicle choice should be determined by location & patient preference Vehicle also dictates potency (oint [most potent] > crm > lotion) Ointment: Lipophilic base (often petrolatum); occludes epidermis, “traps” Rx next to skin, most hydrating; best for hyperkeratotic lesions & nonhair bearing skin (palms/soles, trunk ok); avoid in intertriginous areas (too potent & can → maceration)

Cream: Base includes water, less “greasy” & nonocclusive; often preferred by pts, good on trunk, face, neck

 

Lotion: Includes water & ± EtOH; more drying, good for hair-bearing areas (e.g., genitalia); can sting when applied

Solution, foam: Preferred for scalp

Gel: Jelly-like, consider use for exudative lesions (i.e., acute contact dermatitis)

Potency

Use class to determine potency; cannot compare strengths of concentration across different agents

Consider location of lesion, etiology of lesion, & its severity Location: Thicker skin (palms, soles) require ↑ potency; thinner skin (face, genitalia) require ↓ potency

Etiology: Certain dermatoses require higher potency (psoriasis w/ thick plaques/scale); some more responsive & respond to lower-potency agents (seb derm)

Severity: Not all lesions are created equal; trial of lower potency appropriate for milder disease; can up titrate as necessary

Reserve high-potency steroids for thick skin (e.g., acral skin, lichenified lesions) or lesions refractory to lower potency steroids; avoid use in intertriginous areas (e.g., axilla, groin)

 

Selected Topical Corticosteroids (AFP 2009;79:135; www.aad.org)
Class/Potency	Name & Concentration	Formulation
I (ultra-high)	Betamethasone dipropionate 0.05%	O
	Clobetasol propionate 0.05%	C, G, O, L, So, F
II (high)	Fluocinonide 0.05%	C, G, O
III (high)	Fluticasone propionate 0.005%	O
IV (mid)	Triamcinolone acetonide 0.1%	C, O
V (low-mid)	Fluocinolone acetonide 0.025%	C
VI (low)	Desonide 0.05%	C
	Fluocinolone acetonide 0.01%	So
VII (least potent)	Hydrocortisone 2.5% Hydrocortisone 1% (OTC)	C, L

 

Vehicle and Potency by Site
Site	Suggested Steroid Class
Scalp	Consider starting w/ Class VI → okay to escalate

 

Palms/soles	Class I or II
Periorbital	Class VII
Face/neck, Intertriginous areas	Class VI or VII
Trunk/extremities	Moderate inflammation: Class III–V
	Severe inflammation or thick plaques on extensor surfaces: Class I—II
Genitalia/Groin	Class V–VII

(Adapted from Schalock PC (ed.). Primary Care Dermatology. 2010)

C, cream; F, foam; G, gel; L, lotion; O, ointment; So, solution

Application (AFP 2009;79:135; www.aad.org; JAAD 2009;60:643)

Common causes of treatment failure: Nonadherence, underapplication, tachyphylaxis (↓ response to one steroid over time), messiness/dislike of vehicle

Quantity: Consider % body surface area involved; inadequate amount Rx’ed → underapplication; excessive amount Rx’ed can → extended duration of use w/o follow-up (e.g., avoid Rx’ing >15 g for facial lesion)

Single application: 2% BSA (2 palms) requires 0.5 g; covering entire avg adult → 30 g 1 wk’s worth of BID application: covering entire avg adult → 400 g 1 mo’s worth of BID application: Face → 30 g; extensor surfaces of both arms → 120–150 g; widespread on trunk, legs, arms: → 1–2 lb (454 g = 1 lb)

May use occlusive dressing on acral surfaces to ↑↑ potency, but → ↑ risk of s/e

Counseling (JAAD 2009;60(4):643–59)

Duration: ≤4 wk of consecutive use advised, stop tx when condition resolves (taper by ↓ freq and/or potency q2wk to avoid rebound); ≤3 wk of consecutive use for face, intertriginous areas, or class I (ultra-high potency): If recurrent issue, use for 1–2 wk intervals to avoid s/e, consider derm referral

Side effects: ↑ Potency & duration → ↑ risk; should be discussed w/ all pts; write on all higher-potency Rx: “Not for face, armpit, or groin”; many s/e are permanent include atrophy (striae, telangiectasias, ↑ fragility); infection (can worsen/mask); hypopigmentation; systemic s/e (if ↑ potency/duration/BSA; weekly clobetasol or halobetasol dosing should be ≤50 g; glaucoma/cataracts in chronic periocular use; flare

 

rosacea or perioral dermatitis

When to Refer

Patients who are not responsive despite above recommendations → refer to dermatology, regardless of etiology; consider referral in pregnant/breastfeeding pts