Benjamin Bogucki and Milan J. Anadkat
OVERVIEW
· Compromise to the skin and its functions can lead to disfigurement, discomfort, and disability. In the United States, one in three visits to a primary care physician involves at least one skin complaint.1 Cutaneous findings may be valuable diagnostic and prognostic markers of internal disease that often precede other signs.2
· Skin disorders can cause significant psychological and emotional distress.3 Support foundations for patients with skin disorders can be accessed through the American Academy of Dermatology (http://www.aad.org).
· Skin cancer is the most common type of cancer. The American Cancer Society recommends that everyone practice monthly skin checks and have regular total body skin examinations performed by a physician every 3 years from age 20 to 40 and yearly after age 40 (http://cancer.org).
Dermatologic History and Physical Examination
The elements of the dermatologic history are presented in Table 41-1.
TABLE 41-1 Elements of the Dermatologic History
MEDICAL HISTORY
· Many conditions may be associated with skin disease:
o Autoimmune disease (lupus, dermatomyositis)
o Endocrinopathy (diabetes mellitus, thyroid disease)
o Hepatic dysfunction
o Genetic disorders (neurofibromatosis, Down syndrome)
o Immunosuppression (HIV/AIDS, transplant recipients)
o Malignancy
o Renal dysfunction
· Systemic medications are a frequent cause of rash and other skin complaints. All oral medications (especially new medications and antibiotics, antihypertensives, and antiepileptics), herbal supplements, and topical medications should be noted.
· Family history of primary skin diseases such as psoriasis, eczema, and skin cancer should be noted. Family history of autoimmune disorders or allergies may also be important.
· Occupational exposures, living conditions, and sexual history can be contributory.
PHYSICAL EXAMINATION
· Examine the entire skin surface as well as the palms and soles, genitals, oropharynx, and eyes. If there is a concern for or history of melanoma, examine the neck, axillae, and groin for lymphadenopathy.
· If a lesion is identified, classify it (see Table 41-2).
TABLE 41-2 Classification of Lesions
Dermatologic Therapies
Skin disorders are characterized by pruritus, inflammation, alterations in hydration, and pain. Identification and treatment of specific underlying conditions should always be attempted.
DRY SKIN CARE
· Almost all itchy skin conditions are improved by the following regimen:
· Take short, cool baths or showers (<5 minutes).
· Use mild, nondrying soaps (e.g., Dove, Oil of Olay, or Cetaphil). Scrubbing or the use of washcloths and loofahs should be discouraged. Limiting the use of soap to the axilla and groin may be necessary.
· After bathing, pat dry and apply thick moisturizers such as petroleum jelly or other thick lubricants (e.g., Eucerin or Cetaphil creams). In general, ointments and creams are more effective than lotions. Patients may be instructed that moisturizers that come in a jar are generally more effective than those that come in a pump dispenser. Moisturizers should be applied while the skin is still damp and may be safely reapplied as often as needed.
WET SKIN CARE
Excessive moisture in intertriginous areas can lead to bacterial or yeast overgrowth and infection.
· Dry the affected area and apply powder or dry dressing of absorptive material. Use of a fan or hair dryer may be helpful prior to application of powder.
· Separate skin surfaces with absorptive materials.
ANTIPRURITICS
· Pruritus and burning can lead to uncontrolled scratching and can perpetuate an underlying condition.
· Topical agents can be used to control symptoms.
o Camphor 1% to 3% and menthol provide a cooling sensation and may be stored in the refrigerator.
o Phenol 0.25% to 2% causes local hypoesthesia but should not be used on raw or ulcerated skin.
o Topical anesthetics (benzocaine), antihistamines (diphenhydramine), and neomycin are best avoided because of a high rate of contact dermatitis.
· Systemic antihistamines (H1 receptor antagonists) are most useful in the treatment of urticaria but are also helpful in other pruritic skin disorders. First-generation antihistamines (diphenhydramine, hydroxyzine) are particularly useful in the evening due to their sedative effect. Second-generation antihistamines (cetirizine, loratadine) may be easier to tolerate during the day as they are nonsedating.4
· Gabapentin and other neuroleptic medications have shown efficacy in neuropathic pruritus as well as idiopathic itch.5
PROTECTION
· Cotton and rubber gloves can be used to avoid excessive contact with water or chemical irritants. Cotton absorbs palmar sweat and should be cleaned or changed frequently.
· Barrier creams and ointments may prevent contact with irritating chemicals but are not substitutes for mechanical barriers.
TOPICAL STEROIDS
· Topical steroids are first-line therapy for many dermatologic conditions (Table 41-3). Topical steroids are effective, but can have significant side effects including skin atrophy, striae, acne, infection, and even suppression of the pituitary-adrenal axis.6 Side effects tend to occur with repeated application or application to the face, thin-skinned areas (neck, antecubital/popliteal fossae), or occluded areas (axillae, groin, inframammary folds). Patients should be reminded that a topical steroid should not be used as if it were a moisturizer. Topical steroids should be used on the affected areas of skin and never on normal skin.
· Several factors are important in determining the optimal steroid for a particular condition. Accurate diagnosis obviates the need for combination agents such as a weak azole antifungal and a high-strength topical steroid.
· Base or vehicle:
o Ointments are more lubricating as well as more occlusive, making them more potent. A lubricating ointment is best for dry dermatitis.
o Creams are less lubricating than ointments, but more so than gels, lotions, and solutions. A cream would be more appropriate for a weeping dermatitis. Creams are more likely than ointments to have additives that may irritate skin. If a patient complains of burning or stinging with a cream, it may be appropriate to switch to a comparable ointment.
o Lotions, gels, foams, and solutions are easier to use in hair-bearing areas and are most often used in dermatitis of the scalp. Gels may also be appropriate for the oropharynx.
· Strength:
o Higher-strength (classes 1 and 2) topical steroids are used for palmar/plantar areas or for severe or resistant lesions. They should never be used on the face.
o Midstrength (classes 3 through 5) topical steroids may be used on most parts of the body, but should generally be avoided on the face, genital areas, or skin folds.
o Lower-strength (classes 6 and 7) topical steroids may be safely used intermittently on the face.
· Dosage: Applications should generally be performed twice daily. When a cream or ointment is used, 1 g covers the face and 30 g covers the body of an adult (for 1 day).
· Occlusion: Occlusion with plastic wrap or gloves increases the potency of the steroid but should be reserved for severe, resistant lesions. A limited time course for occlusion should be specified. Occlusion increases both potency and risk of side effects.
TABLE 41-3 Topical Steroids
Note: Classes 6 and 7 are indicated for intermittent facial use. Classes 1 and 2 are indicated for palmar/plantar areas or severe/resistant lesions.
SKIN NEOPLASMS
Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) of the skin, which are sometimes grouped together as nonmelanoma skin cancer (NMSC), are the most common types of cancer diagnosed in the United States.7Melanoma is much less common than NMSC, but the incidence of melanoma has been on the rise for several decades, especially among younger patients.8
SKIN CANCER PREVENTION
· Patients should be advised to avoid sun exposure between 10 AM and 3 PM.
· Clothing (including hats and swimwear) with sun protection factor (SPF) can be purchased online and in many activewear stores.
· Sunscreens are useful adjuncts to long sleeves and wide-brimmed hats for fair-skinned people or patients with dermatoses induced by ultraviolet light. A daily moisturizer with broad-spectrum (ultraviolet A [UVA] and ultraviolet B [UVB]) coverage, preferably with at least SPF 30, is appropriate for most fair-skinned individuals.
o For certain light-sensitive disorders (e.g., systemic lupus erythematosus [SLE]) and photosensitizing drugs (e.g., tetracycline, sulfonamides, thiazides, quinolones), broad-spectrum sunscreens are necessary.
o All sunscreens should be applied 30 minutes before exposure and should be reapplied at least every 90 minutes and after bathing, swimming, or excessive sweating.
o Allergic and photosensitivity reactions occur to paraaminobenzoic acid, especially in patients who are sensitive to benzocaine, procaine, thiazides, and sulfonamides.
o Titanium dioxide and zinc oxide are opaque sunscreens that shield against UVA and UVB by providing a physical block. They are particularly useful on the nose and lips.
· Patients should perform skin self-examinations monthly. Encourage patients to use the ABCDEs when examining their own skin. Lesions with the following traits are more likely to be malignant and should be evaluated by a physician.9
o Asymmetry: If a line is drawn through the lesion, the two sides do not match.
o Border: Irregular, notched, or scalloped borders are worrisome for melanoma.
o Colors: Melanoma may have different shades of brown, tan, or black within one lesion. Red, blue, and white areas may also be present.
o Diameter: A diameter of >6 mm is concerning for melanoma.
o Evolution: Any change in size, shape, color, or other characteristic is more likely to be present in a malignant lesion, and this factor is often the most significant of the five when considering the likelihood of malignancy. Development of pain, pruritus, or bleeding of the lesion is also concerning for skin cancer.
SEBORRHEIC KERATOSIS
· Seborrheic keratoses are hyperkeratotic epidermal papules commonly found in middle-aged and elderly patients.
· Seborrheic keratoses are benign skin neoplasms that can be confused with skin cancer. They have no malignant potential.
· On exam, they have a waxy, stuck-on appearance and may be tan, yellow, dark brown, or black in color. White horn cysts may be visible on close inspection. There is always a well-defined border. They usually appear on the face, chest, and back.
· Stucco keratoses are a variant consisting of small white papules on the lower legs.
· Dermatosis papulosa nigra is a form of seborrheic keratosis that appears as multiple small, darkly pigmented, possibly pedunculated papules on the cheeks and periorbital areas of Black, Hispanic, and Asian patients.
· If symptomatic, seborrheic keratoses may be removed using laser, cryosurgery (liquid nitrogen), curettage, or excision. Most seborrheic keratoses, however, do not require treatment or are treated for cosmetic reasons. If a clinician is not certain of the diagnosis, manipulation must be avoided as the differential of pigmented lesions includes melanoma.
ACROCHORDON
Also called acrochordons, skin tags are pedunculated skin-colored to brown papules commonly occurring on skin experiencing friction, specifically the neck, axillae, and groin. Treatment options for irritated or cosmetically troubling lesions include snipping with scissors and, less commonly, electrodessication or cryosurgery.
KERATINOUS CYST
Cysts on the skin present as firm subcutaneous nodules often with a central black punctum. They are freely mobile. Pilar cysts frequently occur on the scalp. Inflamed cysts may be treated with corticosteroid injection or, if necessary, incision and drainage. Once inflammation has subsided, definitive treatment consists of excision. The entire epithelial lining surrounding the cyst must be removed to prevent recurrence.
LIPOMA
Lipomas present as rubbery subcutaneous tumors. They are freely mobile. Lipomas are benign lesions. Treatment consists of excision, but is generally reserved for changing, symptomatic, or cosmetically undesirable lesions.
MELANOCYTIC NEVUS
· By definition, a melanocytic nevus is a benign skin neoplasm. Nevi are common growths and usually appear from birth through ages 35 to 40.
· Melanocytic nevi present as circumscribed papules or macules and may be flesh colored or darkly pigmented. They present on any area of the skin but often are concentrated in sun-exposed areas.
· Unlike melanoma, nevi are symmetric with well-defined borders and uniform color. They are usually <6 mm in diameter.
· Dysplastic nevi may have many of the characteristics of melanoma. Dysplastic nevi are controversial, but it is generally agreed that patients with a large number of nevi, particularly irregular or dysplastic nevi, are at higher risk for developing melanoma and should be examined more frequently.
SOLAR LENTIGO
Solar lentigines are benign pigmented lesions caused by chronic sun exposure. On examination, they appear as tan to dark brown macules often on the face and dorsal hands. Special attention should be paid to lesions that violate the ABCDEs as the differential includes lentiginous-type melanoma. Biopsy of the entire clinical lesion is preferred to avoid sampling bias.
CHERRY ANGIOMA
Cherry angiomas are benign collections of blood vessels appearing as round, red papules. No treatment is necessary unless lesions become irritated or bleed.
ACTINIC KERATOSIS
· Actinic keratosis (AK) is a premalignant lesion caused by chronic sun exposure. If left untreated, a small percentage of AKs may develop into SCC.10
· On examination, AKs appear as erythematous, raised papules with a firm scaly texture. On palpation, they have a sandpaper feel and are often easier to palpate than see.
· Typically, actinic keratoses are treated with cryosurgery. Other therapeutic options for patients with persistent or widespread lesions include curettage, topical 5-fluorouracil, topical imiquimod, or photodynamic therapy.
Basal Cell Carcinoma
GENERAL PRINCIPLES
· BCC is common and associated with chronic sun exposure. Fair-skinned individuals are at the highest risk.
· Patients with a history of one BCC have a 50% risk of developing a second primary within 5 years.11 There is a very low metastatic potential, but BCCs can cause significant local tissue destruction.
· Patients with a history of BCC should be examined every 6 to 12 months.
DIAGNOSIS
· BCC presents most commonly as a pearly, telangiectatic papule on the face or trunk.
· Superficial BCC may occur on the trunk and extremities and appear as a scaly plaque with raised borders. Ulceration is common.
· Diagnosis is made by shave or punch biopsy.
TREATMENT
· Surgical options include excision, electrodessication and curettage, or Mohs micrographic surgery if the BCC is located in a functionally or cosmetically sensitive area.
· Medical therapies include imiquimod and 5-fluorouracil for superficial BCCs.
· Radiation may be used to treat BCC in some instances when surgery is not an option.
· Vismodegib, a hedgehog inhibitor, has recently been approved by the FDA in the treatment of metastatic or locally advanced BCC.12
Squamous Cell Carcinoma
· SCC is caused by chronic sun exposure. SCC may also arise in chronic ulcers (Marjolin ulcer) or other chronic skin lesions.
· People with fair skin and a history of actinic keratoses are at higher risk of developing SCC. The risk of SCC is significantly increased in patients who are being treated with immunosuppressive medications, including patients with solid organ or allogeneic stem cell transplantation, inflammatory bowel disease, HIV, connective tissue disease, and myelodysplasia.13
· Patients with a history of one SCC are at higher risk of developing a second primary lesion. Metastasis is possible but uncommon, occurring in <5% of cases. Risk factors for metastasis include location (e.g., lips, ears, and genitalia), immunosuppression, and carcinomas arising from non-UV causes (e.g., long-standing discoid lupus or burns).14
· Patients with a history of SCC should be followed closely, and lymph node examination is recommended.
· SCC is characterized by a red scaly papule, plaque, or nodule, more commonly in a sun-exposed area. Lesions may have a verrucous appearance.
· Diagnosis is made by shave or punch biopsy.
· Surgical options include excision with at least 4-mm margins, Mohs micrographic surgery, or possibly electrodessication and curettage if histology is not aggressive.
Melanoma
GENERAL PRINCIPLES
· Melanoma can develop anywhere on the body. In Caucasian men, the back is the most common location, whereas in Caucasian women, the legs are most common.15 Melanomas occur more often on the palms, soles, and nail beds in Asians, Hispanics, and African Americans.
· People with a family history of melanoma are at increased risk for developing melanoma; however, most melanomas are diagnosed in patients with no family history of melanoma.
· Unlike BCC and SCC, melanoma has a high potential for metastasis.
· Patients with melanoma should be examined for lymphadenopathy. Sentinel node biopsy may also be performed for cancer staging.
DIAGNOSIS
· On examination, asymmetry, irregular borders, multiple colors, and a diameter >6 mm are worrisome signs for a malignant lesion.
· Excisional biopsy should be performed on any concerning or changing lesion. It is preferable not to sample a portion of the lesion but to provide the entire clinical lesion for pathologic examination, as the melanoma may be present in only a portion of the clinical lesion. Additionally, the tumor thickness (Breslow thickness), which provides important prognostic information, may be lost if only a portion of a lesion is removed.
TREATMENT
· Wide local excision is the definitive treatment for melanoma. Excisional margins and need for sentinel lymph node biopsy are based on the Breslow thickness of the lesion.
· The role of complete lymphadenectomy in the surgical treatment of patients with positive sentinel nodes remains controversial.
· Metastatic melanoma may be treated with immunotherapy (interferon, IL-2, ipilimumab, vaccine therapy), chemotherapy, and the recently introduced targeted agent, vemurafenib, but prognosis remains generally poor.16
DERMATITIDES
Contact Dermatitis
GENERAL PRINCIPLES
· Irritant contact dermatitis is a nonallergic reaction of the skin to chemical or physical agents. Mild irritants require repeated or prolonged contact to cause dermatitis (e.g., soaps, detergents, and solvents). Strong irritants can cause dermatitis following a single exposure (e.g., strong acids or alkali).
· Allergic contact dermatitis is a form of delayed hypersensitivity (type IV reaction) that develops only in previously sensitized individuals. The distribution and pattern of the dermatitis may suggest a specific allergen. Patch testing may be necessary to identify the offending allergen. Common allergens include the following:
o Plants (e.g., Rhus dermatitis, otherwise known as poison ivy, oak, and sumac): characterized by linear, vesicular lesions
o Metals (e.g., nickel, chrome): commonly diagnosed on skin that touches jewelry and fasteners, especially the earlobes and the periumbilical area
o Rubber/latex: affects skin in contact with gloves, condoms, and elastic
o Topical medications: specifically neomycin, benzocaine, additives in creams, and other vehicles
o Cosmetics: preservatives in makeup, perfume, and hair dye
DIAGNOSIS
· Acute dermatitis is characterized by erythema, weeping/oozing, crusting, and vesiculation. Poison ivy often produces linear vesicles. Severe lesions may demonstrate edema, ulceration, and large bullae.
· Chronic dermatitis is characterized by scale, dryness, and eventually thickening and hyperlinearity (lichenification) of the skin.
· The diagnosis is made largely by history of exposure to irritants or allergens.
· Skin examination may reveal a particular pattern associated with a type of dermatitis.
TREATMENT
· Mild dermatitis is treated with topical steroids, topical or systemic antipruritics, and avoidance of the offending agent.
· Severe blistering reactions are treated with oral prednisone, 0.5 to 1 mg/kg tapered over 14 to 21 days; antipruritics; and drying agents.
Atopic Dermatitis (Eczema)
· In contrast to contact dermatitis, atopic dermatitis is not caused by a specific irritant or allergen, although irritants and allergens can exacerbate eczema.
· Atopic dermatitis presents as erythematous, scaly plaques that may demonstrate lichenification and pigment alteration (hyper- or hypopigmentation).
· Dyshidrotic eczema is characterized by vesiculation. Scratching or rubbing worsens the condition.
· Commonly affected areas include skin flexures, hands, and feet.
· Effective therapy includes emollients, dry skin care, topical steroids, and antihistamines for reduction of pruritus. Choice of topical steroid depends on the location and severity of the lesion as well as the age of the patient.
· Recalcitrant cases may be treated with UV light therapy or immunosuppressants.
· Superinfection is common and should be treated with antibiotics targeting staph and strep.
Stasis Dermatitis
Stasis dermatitis is characterized by bilateral erythema, hyperpigmentation, and scaling that is most prominent on the lower legs. It may be mistaken for cellulitis, which is almost always unilateral. Successful treatment of stasis dermatitis requires reduction of lower extremity edema with compression stockings. Triamcinolone 0.1% ointment applied bid is an appropriate topical steroid.
Keratosis Pilaris
Keratosis pilaris is a common chronic papular eruption that occurs on the proximal extensor surfaces of the extremities and cheeks throughout life. The rash is characterized by scaly follicular papules and is usually asymptomatic. Treatment is often unsatisfactory and includes emollients, keratolytics, and topical retinoids.
Seborrheic Dermatitis
· Seborrheic dermatitis is a very common, usually mild dermatitis in adults. However, it can be quite severe in patients with HIV or Parkinson disease.17
· In adults, erythema with fine white or greasy scale is seen on the scalp (dandruff), eyebrows, eyelids, nasolabial folds, ears, sternal area, axillae, inframammary folds, and perineum.
· Antiseborrheic shampoos, such as selenium sulfide, zinc pyrithione, tar, or 2% ketoconazole are used at least every other day for 10 to 15 minutes. For the face or trunk, ketoconazole cream or 1% to 2.5% hydrocortisone cream bid is used.
Psoriasis
GENERAL PRINCIPLES
· Psoriasis is a chronic recurring condition with varying degrees of severity. While some patients suffer from widespread disease, others may have only a few small patches of involvement. Psoriatic arthritis involves the joints and may cause significant disfigurement and disability. Ten to twenty percent of patients with psoriasis will develop psoriatic arthritis.
· Psoriasis has been associated with high rates of cardiovascular disease.18
· Psoriasis is frequently associated with significant emotional distress and depression.19
· Stress, smoking, alcohol consumption, and certain medications (e.g., lithium, beta-blockers) can aggravate the disease. There may also be severe worsening of psoriasis after treatment with systemic steroids, and for this reason, systemic steroids should not be used to treat psoriasis.
DIAGNOSIS
· Examination reveals erythematous plaques with silvery scale on the elbows, knees, scalp, and trunk. Nail changes including pitting and “oil spots” may also be present. Psoriasis can progress to generalized erythroderma (psoriasis involving >90% body surface area [BSA]).
· Guttate (“drop-like”) psoriasis is characterized by small, erythematous papules on the trunk and may be associated with streptococcal pharyngitis.
TREATMENT
· Mild-to-moderate psoriasis is treated topically with topical steroids, vitamin D3 analogs (calcipotriene), retinoids (tazarotene), tar derivatives, natural sunlight, or narrow-band UVB radiation. Calcipotriene and tazarotene are more expensive than topical steroids but less likely to cause skin atrophy. Calcipotriene can cause hypercalcemia if it is used on >10% of the body. Tazarotene can cause burning, erythema, and desquamation. Sunlight and UVB radiation can cause burning and increase the long-term risk of skin cancer.
· Severe psoriasis (>30% BSA) may require phototherapy or systemic agents (e.g., methotrexate, acitretin, cyclosporine, etanercept, adalimumab, infliximab, ustekinumab). These therapies must be closely monitored. Some biologic agents increase the risk of infection, especially reactivation of tuberculosis. Tuberculosis tests (purified protein derivative [PPD] or interferon-gamma release assay) must be checked yearly. Systemic therapies are for patients who are incapacitated by their disease and resistant to less toxic forms of treatment. They are the only therapies effective for psoriatic arthritis.
· Scalp psoriasis is treated topically with tar shampoo and steroid solutions. Prominent scale must be removed before topical treatments will work.
· Guttate psoriasis may respond to penicillin or amoxicillin if there is an underlying streptococcal infection. Phototherapy is also particularly effective for guttate psoriasis.
· Inverse psoriasis affects the axillae, inframammary folds, and groin. Topical steroids, often in combination with topical antifungals, are appropriate for these locations.
Pityriasis Rosea
· Pityriasis rosea is characterized by pink, oval papules with minimal peripheral scale. The papules align parallel to lines of skin cleavage, often resulting in a Christmas tree distribution on the trunk. The herald patch is a larger pink plaque that precedes the more diffuse rash.
· Pityriasis rosea may be mildly pruritic and is self-limiting, usually resolving in 6 to 12 weeks.
· Treatment is often frustrating, but sunlight, phototherapy, topical steroids, erythromycin, and antipruritics have all been reported to be effective.
· The rash of secondary syphilis can closely mimic pityriasis rosea. If there is any clinical suspicion, serologic testing for syphilis should be pursued.
Lichen Planus
· Lichen planus is characterized by pruritic, purple, polygonal papules that favor the volar wrists, ankles, and genitals. Lesions have lacy white scale (Wickham striae). Oral lesions are common and appear as lacy white plaques or erosions, often on the buccal mucosa.
· Lichen planus has been associated with chronic hepatitis, particularly in populations with a high incidence of hepatitis C.20 Lichen planus may also be induced by systemic medications, most commonly ACE inhibitors and thiazide diuretics.
· Treatment is with topical steroids, emolliation, and antipruritics. Severe, generalized cases may require oral prednisone or phototherapy.
Thermal Burns
· Dermatitis of varying intensity may be caused by excessive heat on the skin.
· First-degree burns congest superficial blood vessels, causing erythema that may be followed by desquamation (e.g., sunburn). Treatment includes prompt cold application and emolliation.
· Second-degree burns cause edema, vesicles, and severe pain. Treatment includes prompt cold application and emolliation. Vesicles should not be opened unless they are tense and painful. When required, drainage under aseptic technique is recommended.
· Third-degree burns cause full-thickness necrosis of the skin and anesthesia. Severe second- and third-degree burns benefit from specialized teams of physicians.
ACNE
Acne Vulgaris
GENERAL PRINCIPLES
· Acne vulgaris often develops around puberty and persists long into adulthood.
· Acne is an inflammatory condition with an infectious component and is characterized by open comedones (blackheads) and closed comedones (whiteheads).
· Treatments require at least 2 months of regular use to show significant improvement. Therapies should be continued for at least this long before changing treatment course.
· Acne may be improved by the use of oral contraceptives (OCPs) but is often worsened by medroxyprogesterone (Depo-Provera).
· Inflammatory acne is characterized by erythematous papules and pustules.
· Nodulocystic acne is characterized by larger nodules and results in scarring and should be treated aggressively.
TREATMENT
· Comedolytics are the first-line therapy for acne.
o Benzoyl peroxide, 2.5%, 5%, or 10%, is available as a wash or gel. Higher concentrations and gels may be used in patients with oily skin. Unlike topical antibiotics, benzoyl peroxide does not promote antibiotic resistance. Patients should be warned that benzoyl peroxide bleaches clothes.
o Topical retinoids (tretinoin, adapalene, tazarotene) are available in creams and gels. They should be used in small quantities (a pea-sized amount covers the entire face) on clean, dry skin. Higher-concentration creams and gels can be drying and can predispose to photosensitivity. Less frequent application may be necessary if irritation is significant.
· Topical antibiotics can be used in inflammatory acne and are most helpful when used in combination with benzoyl peroxide or a topical retinoid.
o Clindamycin solution, lotion, or pledget one to two times daily
o Erythromycin solution or pledget one to two times daily
· Systemic antibiotics are often used in moderate-to-severe inflammatory acne and in nodulocystic acne. They should be tapered after several months of therapy. An inability to discontinue oral antibiotics without acne flare may be an indication for referral to a dermatologist for oral isotretinoin therapy.
o Doxycycline, tetracycline, and minocycline are most commonly prescribed. Side effects include stomach upset and photosensitivity. Blue discoloration of the skin has been described with chronic use of minocycline.
o Erythromycin may also be used. Allergies and side effects may limit antibiotic choices in a given patient.
· Oral isotretinoin is used in severe nodulocystic acne or acne vulgaris unresponsive to the therapies listed above. Isotretinoin, 1 mg/kg/day, is prescribed for 5 to 6 months. All other acne therapies should be discontinued prior to starting isotretinoin.
o Because of the teratogenicity of the drug, isotretinoin is regulated by the government. Patients must register through an online monitoring system (iPLEDGE) and answer questions before filling a prescription. Furthermore, women of childbearing potential on isotretinoin are required to use two forms of birth control and have monthly pregnancy tests.
o Isotretinoin is generally well tolerated, but side effects include liver function abnormalities, elevated triglycerides, photosensitivity, and severe dryness of the lips and skin. There is also a controversial association with depression and suicidality.
o For patient safety and medicolegal reasons, isotretinoin should only be prescribed by a physician familiar with its use.
Hidradenitis Suppurativa
· Hidradenitis suppurativa presents as recurrent painful cysts and nodules of the axillae, groin, and buttocks. Sinus tract formation is common.
· While secondary infection may complicate hidradenitis, it is not a primarily infectious condition.
· Treatment ranges from topical and systemic antibiotics to intralesional corticosteroid injection to systemic retinoids and biologics. Surgical excision is the definitive therapy in the axillae, but is not always possible in the groin.
Acne Rosacea
GENERAL PRINCIPLES
· Acne rosacea usually affects patients between 30 and 60 years of age. It is more common in fair-skinned individuals.
· Rosacea is a chronic condition with intermittent exacerbations and remissions.
· There are several subtypes: erythematotelangiectatic, papulopustular, phymatous, glandular, and ocular.
DIAGNOSIS
· On examination, erythema and telangiectasias on the cheeks and nose are the most common findings. Inflammatory papules and pustules may be present on the face, particularly in a perioral distribution.
· Rhinophyma may be present in long-standing rosacea and is more common in men.
· Ocular changes, including dryness, irritation, conjunctivitis, blepharitis, and rarely keratitis may occur.
· Flushing of the cheeks is common and may be exacerbated by alcohol, heat, sun exposure, strenuous exercise, stress, medications, and certain foods (e.g., spicy, hot beverages, red wine).
TREATMENT
· Rosacea typically does not respond to comedolytics.
· Sunscreen is a first-line therapy for all patients. Sunlight, spicy foods, and hot beverages should be minimized if they are triggers.
· Topical antibiotics such as metronidazole gel or lotion and clindamycin are commonly used for papules and pustules.
· Sodium sulfacetamide wash or lotion may also be effective.
· Systemic antibiotics (doxycycline, 50 to 100 mg bid) may be effective for moderate-to-severe papulopustular rosacea.
· Laser therapy can be particularly effective for the redness and telangiectasias of rosacea, which typically does not respond well to medical treatments.
ULCERS
· Ninety percent of lower extremity ulcers are due to venous insufficiency, 5% result from arterial disease, and 5% are due to miscellaneous causes, including diabetic microangiopathy, pyoderma gangrenosum (PG), malignancy, vasculitis, and infection.
· Definitive diagnosis is often made by skin biopsy, but biopsy sites on the legs often heal poorly over a period of weeks to months, so they should be avoided if possible.
· Venous ulcers tend to occur on the lower medial aspect of the legs in areas of stasis dermatitis. Treatment aims to improve venous return with compression hose. Wet-to-dry dressings provide excellent debridement for 2 to 3 days, but longer use can interfere with wound healing. Most wounds improve if kept covered and moist. This is best achieved with occlusive dressings. Unna wraps may be particularly effective in severe cases. Surgery to correct venous return may be employed for patients with extensive venous hypertension or venous reflux disease.
· Pyoderma gangrenosum (PG) is a neutrophilic dermatosis that typically presents as an eroded nodule or pustule on the lower extremities, although it may occur anywhere on the body. PG is frequently associated with an underlying medical condition, most commonly inflammatory bowel disease.21 Infection must be ruled out prior to making the diagnosis of PG, often necessitating a biopsy and culture. Treatment is typically initiated with topical and systemic steroids, with gradual transition to steroid-sparing agents.
BLISTERING DISORDERS
Pemphigus Vulgaris
· Pemphigus vulgaris is characterized by flaccid bullae that break easily, leaving denuded areas that increase in size with progressive peripheral detachment. Oral lesions are common.
· Prior to the introduction of systemic corticosteroids, the mortality of pemphigus was very high.
· Pemphigus foliaceus is characterized by more superficial flaccid bullae that may accumulate thick scale. Oral lesions are uncommon. Pemphigus foliaceus has a better prognosis than pemphigus vulgaris.
· Physical examination reveals flaccid bullae and erosions. Nikolsky sign (creation of blister with application of horizontal, tangential pressure to the skin) is present.
· Diagnosis is confirmed by skin biopsy with routine histologic examination and direct immunofluorescence. Patient serum can also be submitted for indirect immunofluorescence to follow autoantibody titers.
· High-dose prednisone, 1 to 2 mg/kg/day, is effective in controlling the disease. There is mounting evidence that early use of rituximab can decrease the need for systemic steroids and lead to long-term remission.22
· Supportive care in a hospital setting may be required if large areas of skin are denuded or mucosal involvement is severe.
Bullous Pemphigoid
· Bullous pemphigoid (BP) is characterized by large tense bullae on an erythematous base. It is most commonly seen in elderly patients.
· BP has a better prognosis than pemphigus.
· Physical examination reveals tense bullae. At its earliest stage, BP presents as urticarial plaques. It is less commonly seen on mucosal surfaces.
· Diagnosis is confirmed by biopsy for routine histologic examination and direct immunofluorescence.
· Localized disease may be treated with high-potency topical steroids.
· Generalized or persistent BP is treated with high-dose prednisone, 1 to 2 mg/kg/day, or steroid-sparing immunosuppressants such as gold, cyclophosphamide, azathioprine, or mycophenolate mofetil.
Dermatitis Herpetiformis
· Dermatitis herpetiformis usually presents in the second or third decade of life.
· It may be associated with gluten-sensitive enteropathy (celiac disease), but many patients deny gastrointestinal symptoms.
· Physical examination reveals eroded and crusted papules and rare vesicles that are symmetrically distributed on the extensor elbows, knees, and buttocks.
· Patients usually complain of intense pruritus.
· Diagnosis is confirmed by skin biopsy of lesional skin for routine histologic examination and perilesional skin for direct immunofluorescence. Laboratory tests for markers of celiac disease may also be useful in the diagnosis.
· Gluten-free diet is often helpful, but strict adherence is required.
· Dapsone, 50 to 150 mg/day, is highly effective.
· Antipruritics can be prescribed for symptomatic relief of the intense pruritus.
Erythema Multiforme
· Erythema multiforme is an acute, self-limited, often recurrent eruption characterized by “targetoid” lesions. The degree of severity varies widely.
· Lesions on the palms and soles are characteristic, but they may become more generalized.
· Erythema multiforme minor is localized to the skin, does not involve the mucosa, and has minimal to no prodromal symptoms.
· Erythema multiforme major is often preceded by a prodromal phase, and mucosal involvement is notable and may be severe.
· The clinical distinction between erythema multiforme major and Stevens-Johnson syndrome (SJS) may be challenging.
· Erythema multiforme is strongly associated with herpes simplex infection. Other infectious agents, such as Streptococcus and Mycoplasma, have also been reported as causes.23
Stevens-Johnson Syndrome and Toxic Epidermolysis Necrosis
GENERAL PRINCIPLES
· SJS and toxic epidermolysis necrosis (TEN) both present with a febrile, flu-like prodrome that rapidly progresses to skin pain, exanthem or targetoid lesions, and skin sloughing.
· Mucous membranes are always involved and consist of erosions of the mouth, eyes, genitalia, and lips with hemorrhagic crusts.
· SJS and TEN are a spectrum of disease; categorization depends on the BSA involved. SJS involves <10% BSA, TEN involves >30% BSA, and SJS/TEN overlap involves 10% to 30% BSA.
· Medications are the most common cause of SJS/TEN, most significantly penicillins, sulfonamides (e.g., trimethoprim-sulfamethoxazole), anticonvulsants (e.g., phenytoin, carbamazepine, lamotrigine), allopurinol, and nonsteroidal anti-inflammatory drugs (NSAIDs, e.g., piroxicam). However, up to 50% of cases are idiopathic.24
· Mortality of SJS is 1% to 5%, whereas mortality of TEN can be as high as 35%.
DIAGNOSIS
· Generalized skin sloughing is often seen on examination. The oral and genital mucosa should be examined; mucosal involvement presents with erosions and hemorrhagic crusts.
· Painful skin should be considered a serious warning sign.
· The Nikolsky sign is usually present.
· Diagnosis is confirmed by skin biopsy for routine histologic examination.
TREATMENT
· Treatment largely consists of symptomatic and supportive care. Admission to an intensive care unit, preferably a burn unit, is necessary if a significant area of skin is denuded. Intubation may be necessary. Any unnecessary medications should be held.
· Intravenous immunoglobulin (IVIG) is emerging as the treatment of choice in SJS/TEN. Systemic steroids are controversial and should probably be avoided unless they are administered before significant skin sloughing has occurred.25
· Antimicrobial silver impregnated dressings can be used to prevent secondary infection and can help limit painful dressing changes.
Drug Reaction with Eosinophilia and Systemic Symptoms
· Drug reactions in general and urticarial are covered in more detail in Chapter 39, Allergy and Immunology.
· Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a serious hypersensitivity syndrome that causes rash with fever and multiorgan involvement.
· The rash associated with DRESS is frequently maculopapular or morbilliform and usually resembles a typical drug rash. However, in contrast to a less serious drug eruption, patients with DRESS present with fever, lethargy, and lymphadenopathy, which may be confused with infection.
· Patients with DRESS frequently have abnormal liver function tests and peripheral eosinophilia or atypical lymphocytosis on complete blood count.26 Less commonly, there can be lung involvement or myocarditis.
· A large number of medications have been reported to cause DRESS. The most commonly implicated are carbamazepine, allopurinol, phenobarbital, and minocycline.
· Early recognition of DRESS and discontinuation of all possible inciting medications are the key to treatment. Systemic steroids are usually necessary in serious cases of DRESS and should be slowly tapered off over several weeks. End-organ damage may present several months after the initial onset of DRESS, so patients should be followed closely, with particular attention to thyroid function.27
ARTHROPOD BITES/STINGS
GENERAL PRINCIPLES
Reactions to insect bites are usually triggered by a toxin or an allergen injected into skin by the offending arthropod.
DIAGNOSIS
· Elements of the history that may be helpful include history of working in a basement, activity in densely wooded areas, and recent travel.
· Diagnosis is largely based on examination of the bite. If a tick bite is suspected, inspect the skin for presence of the tick, which often goes unnoticed by the patient.
o Bee, wasp, and yellow jacket stings consist of a painful red wheal with central punctum; the wheal fades in hours. A persistent local reaction with intense swelling around the sting area may arise and does not indicate a systemic allergy. In individuals with immediate systemic allergy, anaphylaxis may develop. Rarely, affected persons may manifest a delayed systemic allergic reaction that presents as urticaria, polyarthritis, and lymphadenopathy.
o Fire ant stings produce wheals with two hemorrhagic puncta. These usually evolve into pustules within hours.
o Mosquito bites appear as pruritic wheals developing within hours. Patients with blood dyscrasias or malignancies may display exuberant bullous reactions to bites.
o Flea bites produce grouped urticarial papules, some with puncta, frequently on the legs.
o Tick bites usually do not produce a wheal on the skin but may result in fevers, migratory rashes, joint pain, and other systemic symptoms.
o Spider bites are usually not serious. However, brown recluse bites may cause painful necrotic ulcers, and black widow bites can cause systemic sequelae.
TREATMENT
· If insects are attached to the skin, they should be flicked or carefully removed (not squeezed) from the skin.
· Ticks are best removed with a steady upward pull after grasping them as close to the skin as possible with forceps. It is important to confirm that the head has been removed. Clean the wound with soap, water, or mild disinfectant solution.
· Ice, cold compresses, and phenolated calamine lotion are soothing agents. Topical steroids and oral antihistamines may be useful for itching and inflammation.
· Necrotic spider bites from a brown recluse or black widow may become superinfected and require antibiotics. Surgical debridement is generally contraindicated.
· Anaphylactic reactions require emergency treatment (see Chapter 39).
ALOPECIA
Alopecias are divided into two major categories: nonscarring and scarring. Careful examination of the scalp for areas of regrowth and presence of follicular openings is important in distinguishing nonscarring from scarring alopecia. Nonscarring alopecia has the potential for regrowth, whereas scarring alopecia does not.
Nonscarring Alopecia
· Androgenetic alopecia has a genetic predisposition and is caused by circulating androgens interacting with androgen receptors in hair follicles. In men, androgenetic alopecia affects 25% of men >25 years of age and 50% of men >50 years of age.28 Male pattern usually begins with bitemporal recession. Female pattern is usually more diffuse, with sparing of the frontal hairline. Men can be treated with 5% minoxidil bid or 1 mg finasteride daily. These agents cause some hair regrowth but are more effective at preventing further hair loss. Finasteride is not indicated for women, but minoxidil bid may be of benefit.
· Alopecia areata is characterized by rapid, complete hair loss in one or more oval patches. The scalp is most often affected, but any hair-bearing area may be involved. Alopecia areata totalis and alopecia areata universalis involve all the hair of the head or entire body, respectively. Alopecia areata is considered to be an autoimmune disorder and may occasionally be associated with other autoimmune disorders, most commonly thyroid disease. Spontaneous regrowth often occurs within 6 months, but recurrence is common. Intralesional triamcinolone is used for persistent or rapidly enlarging patches.
· Telogen effluvium is characterized by abrupt, diffuse hair loss over the entire scalp that results in decreased hair density. Anagen hairs (growing phase) are prematurely pushed into the telogen phase (resting) of the hair cycle, usually 2 to 4 months after the inciting event. Hair loss can continue for a subsequent 4 months prior to regrowth occurring. Inciting events include pregnancy, febrile illness, surgery, crash diets, systemic anticoagulant therapy, or any stressful life episode. Treatment consists of reassurance and should be directed at eliminating the underlying cause.
· Anagen effluvium is a widespread loss of anagen hair from actively growing follicles due to arrest of cell division. It manifests as acute, severe hair loss. Causes include cytotoxic agents for cancer chemotherapy, thallium, boron, and radiation therapy.
· Trichotillomania is excessive and repeated manipulation of hair by the patient that results in hair breakage. It typically produces a well-circumscribed area of broken hairs and alopecia. Treatment should be directed at discussing the nature of the problem with the patient, who may unknowingly persist in manipulating his or her hair. Recalcitrant cases may require psychiatric evaluation and medication. Excessive traction on hair in certain hairstyles can cause hair loss through a similar mechanism. Although trichotillomania and traction alopecia are considered nonscarring, prolonged trauma to hair follicles may lead to permanent hair loss.
· Other causes of nonscarring alopecia include the following:
o Endocrinologic abnormalities, most commonly thyroid disease.
o OCPs may initiate androgenic alopecia in predisposed women, and telogen effluvium may develop 2 to 4 months after anovulatory agents are discontinued.
o Nutritional causes include kwashiorkor, marasmus, zinc deficiency, essential fatty acid deficiency, and malabsorption.
Scarring Alopecia
· When hair follicles are scarred, hair loss is permanent. On physical examination, the follicular openings are no longer seen.
· Causes:
o Long-standing infections, either bacterial and fungal (e.g., tinea capitis)
o Neoplasm, either primary or metastatic
o Physical and chemical agents
o Autoimmune disorders, including discoid lupus erythematosus (DLE) and lichen planopilaris
o Neutrophilic scalp dermatoses (dissecting scalp cellulitis and folliculitis decalvans)
NAIL DISORDERS
· Nail disorders are associated with systemic disease or congenital conditions or can be the result of infection, injury, or trauma.
· Beau lines are characterized by a transverse depression spanning the nail plate that is associated with any systemic stressor (e.g., chemotherapy, sepsis) that causes a temporary cessation of nail growth. The insult can be dated by measuring the distance between the proximal nail fold and the leading edge of the depression (fingernails grow 0.1 to 0.15 mm/day).
· Onycholysis is distal separation of the nail plate from the nail bed. Common causes include trauma, drug reactions, contact dermatitis, and psoriasis.
· Onychomycosis is discussed under the section “Fungal Skin Infections.”
· Paronychia is localized infection at the nail margin. It may be acute (usually following trauma) or chronic (through occupational exposure). Cultures are frequently positive for Staphylococcus aureus in cases of acute paronychia. Treatment is based on the underlying cause. In acute paronychia, saline soaks and topical antibiotics can be prescribed. If an abscess is present, drainage and antibiotic treatment are indicated. In the case of chronic paronychia, steroid ointment is usually required, sometimes with the addition of a topical antifungal cream.29
PIGMENT DISORDERS
· Any inflammation of the skin may result in postinflammatory pigment alteration. Postinflammatory hyperpigmentation is especially common in darker skin types. Treatment is not necessary, and pigment will often revert to baseline over weeks to months. Areas of pigment alteration should not be treated as primary lesions. For example, patients treating eczematous rashes should be advised to taper topical steroids when redness, scale, and itching have resolved, not when pigment has normalized.
· Vitiligo is characterized by depigmented patches, often symmetric, around the eyes, nose, mouth, ears, genitals, and dorsal hands. It can be segmental or become generalized. It often has significant psychosocial effects, particularly in patients with darker skin. It is rarely associated with other autoimmune diseases. Recommendations include broad-spectrum sunscreens and observation for cutaneous malignancies in depigmented patches. Treatment is often difficult and includes topical steroids, phototherapy, and controlled exposure to sunlight. In severe cases, permanent depigmentation may be considered.
· Melasma is characterized by pigmented patches on the forehead, cheeks, lips, and extensor forearms. It is commonly seen with OCP use and pregnancy. Changing OCPs has little effect on disease course. Regular use of broad-spectrum sunscreen and vigorous photoprotection are most important in halting the progression of melasma. Topical hydroquinones, tretinoin, and laser may be used to treat existing melasma.
FUNGAL SKIN INFECTIONS
Candidiasis
Candidiasis is discussed in detail in Chapter 26, General Infectious Diseases.
Tinea Versicolor
· Tinea versicolor is a superficial cutaneous infection caused by the dimorphic organism Malassezia. In yeast form, these are normal skin flora, but conversion to the hyphal form is associated with the clinical condition. The rash is frequently seasonal, as high heat and humidity seem to facilitate the transformation to hyphal form.
· In immunocompromised patients, Malassezia may cause more serious infections including folliculitis, catheter-related fungemia, and focal infections.
· On physical examination, there are thin scaly papules and plaques on the trunk, extremities, and face. Papules and plaques may be hypo- or hyperpigmented. Lesions often are more pronounced after sun exposure.
· KOH examination reveals spores and pseudohyphae (macaroni and meatballs). Tinea versicolor is not amenable to culture.
· Selenium sulfide 2.5% shampoo is used every day for 15 minutes for 7 days, weekly thereafter, and more often if needed. Over-the-counter dandruff shampoos contain less selenium sulfide and require more frequent use. Any topical azole antifungal cream can be used twice daily for 2 weeks.
· Systemic antifungal therapy: a single dose of fluconazole 400 mg is effective, although the rate of relapse may be as high as 35%.30
Tinea Capitis
· Tinea capitis (scalp ringworm) is very rarely seen in patients >15 years of age. It is most often caused by Trichophyton tonsurans. It may be confused with other more common scalp dermatoses in adults, such as psoriasis or seborrheic dermatitis.
· Physical examination reveals scaling alopecia with broken hairs. Posterior cervical lymphadenopathy often develops.
· Differential diagnosis includes alopecia areata and seborrheic dermatitis. However, alopecia areata has no scaling, and seborrheic dermatitis has no alopecia.
· KOH examination of scale reveals hyphae; microscopic examination of broken hairs reveals endospores or ectospores. Fungal culture should be performed.
· Griseofulvin, 5 to 20 mg/kg/day for 4 to 8 weeks. It should be taken with a fatty meal and may cause photosensitivity. Terbinafine, itraconazole, and fluconazole have also been used successfully. Systemic therapy is required but can be supplemented with topical therapy to decrease the chance of spreading the disease; 2.5% selenium sulfide or 2% ketoconazole shampoo every other day is recommended.
· Children are no longer infectious once on treatment and can return to school.
Onychomycosis
· Onychomycosis refers to any fungal infection of the nail, with toenail infection much more common than fingernail. Tinea unguium specifically refers to nail infections caused by dermatophytes. Onychomycosis of the fingernail is more often due to the yeast Candida albicans. Onychomycosis is often of significant cosmetic concern to patients.
· Onychomycosis is typified by flaky, thickened, yellow finger or toenails. There are several patterns of onychomycosis: distal/lateral subungual (the most common type), proximal subungual (uncommon and characteristically occurring in immunocompromised patients), and white superficial.
· Examination of subungual debris or fragments of the thickened nail plate with KOH preparation should reveal hyphae. Culture and biopsy may also be used to confirm the diagnosis if necessary.
· Topical treatment (topical azoles, ciclopirox 8% solution) is usually not curative as monotherapy but may be of some benefit in mild onychomycosis that does not involve the lunula.
· Terbinafine, 250 mg PO daily, is often effective. Fingernail infections should be treated for 6 weeks and toenails for 12 weeks. Liver function tests must be monitored during therapy. Recurrence is common after cessation of therapy.31
· Patients should be reminded that nails will not look “normal” during or immediately after treatment. It takes several months (6 to 12 for fingernails, 12 to 18 for toenails) after initiation of therapy before a healthy appearing nail is seen.
Other Tinea Infections
GENERAL PRINCIPLES
· Tinea corporis (ringworm) is a dermatophytic infection of the skin, excluding the scalp, hands, feet, nails, and groin. It is most often caused by Trichophyton rubrum.
· Tinea pedis (athletes’ foot) is usually caused by Trichophyton mentagrophytes in the acute form; the chronic form is commonly caused by T. rubrum. Both are contagious.
· Tinea cruris (jock itch) is most often caused by T. rubrum. It is much more common in men than in women. Obesity, perspiration, humidity, and autoinoculation from other sites of dermatophytic infection (e.g., tinea pedis, unguium) are contributing factors.
DIAGNOSIS
· In tinea corporis, examination reveals scaly, annular, slightly raised erythematous plaques. The plaques may be pustular at the margins and hypopigmented centrally.
· Tinea pedis is characterized by interdigital scaling and maceration. If soles are involved, the scaling is often in a “moccasin” distribution. Localized blisters can develop on the arch of the foot.
· Tinea cruris resembles tinea corporis and presents in the groin folds and bilateral buttocks, but never involves the penis or scrotum. Differential diagnosis includes intertrigo, candidiasis, and erythrasma. Candidiasis often involves the scrotum and presents with satellite pustules and bright red plaques. Erythrasma, a rare condition, is characterized by a hyperpigmented patch with fine scale and exhibits coral red fluorescence on Wood lamp examination.
· In all forms of tinea, skin scraping with KOH preparation shows branched hyphae.
TREATMENT
· In all forms of tinea, involved areas should be kept clean and dry, with use of drying powders as needed (particularly in the case of tinea cruris).
· Initial topical therapy includes antifungal creams such as ketoconazole 1% bid for up to 1 month. In severe cases, treatment with an oral antifungal agent may be required.
· For patients with recurrent, severe, or unresolving tinea infection, referral to a dermatologist may be necessary. Consider diabetes mellitus, HIV, or other immunocompromising condition in an adult with this diagnosis.
BACTERIAL SKIN INFECTIONS
Bacterial skin infections are discussed in detail in Chapter 26, General Infectious Diseases.
VIRAL SKIN INFECTIONS
Varicella-zoster virus and herpes simplex virus are discussed in Chapters 26 (General infectious Diseases) and 27 (Human Immunodeficiency Virus Infection and Sexually Transmitted Diseases), respectively.
Warts
· Warts are intraepidermal tumors caused by infection with the human papillomavirus.
· Verruca vulgaris, or common warts, are flesh- to brown-colored hyperkeratotic papules. Acral areas are most frequently affected, but any skin or mucous membrane may be involved.
· Filiform warts are finger-like slender projections that arise particularly on the face or neck.
· Flat warts (verruca plana) are small, 1- to 3-mm flesh- to tan-colored papules on the face, neck, extensor upper extremities, and extensor lower extremities.
· Plantar warts are common warts that involve the thick skin of the sole.
· Condyloma acuminata are anogenital warts and are the most common sexually transmitted infection.
· Warts may resolve spontaneously or recur after apparent cure. Treatments often need to be repeated.
· Topical agents include keratolytic preparations, such as salicylic acid as well as tretinoin or podophyllum. Imiquimod is effective for genital warts.32
· Surgical destruction involves cryosurgery using liquid nitrogen, electrodessication and curettage, excision, or laser therapy.
Molluscum Contagiosum
· Mollusca are grouped umbilicated papules caused by the molluscum contagiosum virus.
· They are very common in children and spread easily through physical contact. Mollusca can be transmitted through sexual contact and is most often seen as a sexually transmitted infection in adults. If widespread mollusca are seen in adults, HIV should be suspected.
· Mollusca appear as small (1 to 5 mm), discrete flesh-colored or pearly white waxy papules with central umbilication. They are commonly found on the face and flexures in children and on the genital area, lower abdomen, and thighs in adults. Lesions may become inflamed in children who pick or scratch them.
· Spontaneous resolution usually occurs in immunocompetent individuals.
· If treatment is desired, cryotherapy or topical cantharidin can be used.
· HIV patients often require more aggressive therapy, and referral to a dermatologist is appropriate.
SKIN INFESTATIONS
Scabies
· The causative agent is the mite Sarcoptes scabiei.
· Patients give a history of intense pruritus on the hands, feet, and genitalia. Multiple family members are often afflicted.
· Immunosuppressed or debilitated patients may develop crusted scabies, where mites are so numerous that the skin takes on a crusted appearance.
· Careful examination of the web spaces of the hands will often reveal the characteristic burrow made by a female mite. Scraping these burrows will produce the highest yield on KOH preparations.
· Permethrin 5% cream is applied over the entire body from the neck down and left on overnight. All persons living in the home should also be treated. The treatment should be repeated in 1 week.
· Bedding and exposed clothing must be washed, and items that cannot be easily washed should be placed in a sealed bag for 1 week.
Pediculosis
· The causative agent is the louse (Pediculus spp.). Different varieties infest different areas of the body.
· Commonly affected areas include the scalp (including eyelashes in children), body hair, and pubic hair.
· Lice lay eggs on hair shafts that can be seen as white ovals (nits).
· Some diseases, such as epidemic typhus, are transmitted between humans via louse vectors.
· Infestations may be asymptomatic or cause pruritus.
· Permethrin 1% rinse is the first-line therapy. Resistant cases may require permethrin 5% cream or lindane shampoo. Removal of all nits with a fine comb is essential to treatment success. Family members are often treated as well.
SKIN SIGNS OF AUTOIMMUNE DISEASE
Lupus Erythematosus
· LE is a multisystem disorder. It can range from a relatively benign but bothersome cutaneous eruption with no internal involvement to a severe systemic disease that is potentially fatal (see Chapter 33, Rheumatologic Diseases).
· Chronic cutaneous lupus erythematosus is also known as DLE. It is characterized by erythema, scaling, hypopigmentation, follicular plugging, scarring, and telangiectasias. DLE may be localized or widespread. Widespread discoid lesions occur above and below the neck. Systemic LE will develop in only 5% of DLE patients.33
· Subacute cutaneous lupus erythematosus is nonscarring with prominent photosensitivity. Most patients are antinuclear antibody positive and anti-Ro/SS-A positive. Of patients with subacute cutaneous lupus erythematosus, 50% meet clinical criteria for SLE, although they usually have a mild systemic disease if present.34
· Acute cutaneous lupus erythematosus is characterized by malar rash, DLE lesions, photosensitivity, and oral ulcers.
· Diagnosis can often be made from clinical exam. Distribution of lesions and presence of scars should be noted. History of worsening of symptoms with sun exposure is important.
· Biopsy of active lesions is helpful in confirming the diagnosis. Biopsy for direct immunofluorescence (lupus band) has largely been supplanted by serologic testing in SLE. Direct immunofluorescence may be beneficial in cases of suspected DLE.
· Serum tests for common markers of autoimmune disease, such as antinuclear antibody and anti-Ro/SS-A antibodies, may be useful.
· Cutaneous lupus often responds to antimalarials (e.g., hydroxychloroquine) and topical steroids. Sun protection is important, even in darker skin types.
Dermatomyositis
· Dermatomyositis combines an inflammatory myopathy with characteristic cutaneous findings (see Chapter 33, Rheumatologic Diseases). Dermatomyositis sine myositis has characteristic skin findings without evidence of myopathy.
· Dermatomyositis may be associated with an underlying malignancy, particularly ovarian cancer. Newly diagnosed patients should have all age-appropriate cancer screenings performed, and imaging may be considered in select cases.35
· Pathognomonic signs on examination include a heliotrope rash, which is a violaceous hue over the eyelids, and Gottron papules, which are erythematous papules over the knuckles.
· Other cutaneous findings include periungual telangiectasias, photosensitivity, rash on the neck and upper chest (shawl sign), calcinosis cutis (more common in children), cuticular hypertrophy, and splinter hemorrhages.
· Laboratory findings include elevated muscle enzymes, the presence of myositis antibodies, and a pauci-inflammatory interface dermatitis on biopsy.
· The cutaneous disease often responds to therapy for the systemic disease, such as antimalarials, systemic steroids, and methotrexate.
Scleroderma
· Scleroderma is characterized by thickening or hardening of the skin associated with increased dermal or subcutaneous sclerosis, or both. Localized cutaneous disease can occur, which includes morphea, linear scleroderma, and facial hemiatrophy.
· Systemic disease is further classified into two conditions:
o Limited scleroderma (CREST): calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia
o Diffuse scleroderma, or progressive systemic sclerosis
· Nephrogenic systemic fibrosis is a scleroderma-like illness that presents in patients with renal failure and has been strongly linked to use of specific gadolinium MRI contrast media.36 Typically, nephrogenic systemic fibrosis starts distally on the extremities and progresses proximally.
· Cutaneous manifestations include generalized sclerosis, acrosclerosis/sclerodactyly, calcinosis cutis, pruritus, nail fold capillary changes, mat-like telangiectasias, Raynaud phenomenon, taut facies, and salt-and-pepper dyspigmentation.
· Skin biopsy for routine histologic examination confirms the diagnosis.
· Cutaneous sclerosis and pruritus often responds to psoralen (a light sensitizer) combined with UVA therapy, though treatment is difficult and the disease is usually progressive.37
Vasculitis
GENERAL PRINCIPLES
· Cutaneous vasculitis most commonly presents as palpable purpura. Most cases are caused by skin-limited small vessel leukocytoclastic vasculitis, but cutaneous vasculitis may also be associated with the systemic vasculitides.
· Fifty percent of cases are idiopathic, but potential causes include the following:
o Infection: hepatitis, Streptococcus, upper respiratory viruses.
o Drugs: antibiotics, barbiturates, amphetamines, propylthiouracil.
o Autoimmune disease: SLE, rheumatoid arthritis.
o Other causes include cryoglobulinemia, Henoch-Schönlein purpura (IgA-related vasculitis), antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides, and Churg-Strauss syndrome.
DIAGNOSIS
· Screening for a history of autoimmune disorder, infection, or new medication is important.
· Skin biopsy for routine histologic examination confirms the diagnosis. Biopsy for direct immunofluorescence is useful in cases of suspected IgA-related vasculitis.
· Laboratory work to be considered in the appropriate clinical setting includes urinalysis, stool guaiac, complete blood count, erythrocyte sedimentation rate (ESR), chest radiography, hepatitis panel, antinuclear antibodies (ANA), ANCA, and cryoglobulins.
TREATMENT
· Most cases of cutaneous-only small-vessel leukocytoclastic vasculitis are self-limited. Treatment should be aimed at underlying causes.
· Prednisone improves the cutaneous disease but does not change the overall course.
· Appropriate treatment for most patients includes rest and NSAID medications.
Erythema Nodosum
GENERAL PRINCIPLES
· Erythema nodosum commonly presents in young women.
· Fifty percent of cases are idiopathic, but potential causes include the following:
o Streptococcal pharyngitis and other upper respiratory tract infections
o Medications: OCPs, sulfonamides, trimethoprim-sulfamethoxazole, salicylates, phenacetin, iodides, bromides
o Inflammatory bowel disease: ulcerative colitis, Crohn disease, infectious colitis
o Pulmonary disease: tuberculosis, sarcoidosis (Löfgren syndrome), coccidioidomycosis, histoplasmosis, blastomycosis, lymphoma
o Behçet disease
DIAGNOSIS
· Physical examination reveals tender subcutaneous nodules, commonly on the shins.
· Skin biopsy can confirm the diagnosis, but erythema nodosum is generally a clinical diagnosis.
· Appropriate evaluation includes complete blood count, PPD, and chest x-ray. If an obvious disease trigger is not apparent, effort should be made to identify the underlying cause.
TREATMENT
· Most cases are self-limited, lasting 3 to 6 weeks. Treatment is aimed at removing the offending agent or treating the underlying disease.
· Initial therapy is NSAIDs.
· Alternate therapies include oral potassium iodide, indomethacin, or colchicine. Steroids, intralesional, or systemic should only be considered once infections have been excluded or for recalcitrant cases.
SKIN SIGNS OF INTERNAL MALIGNANCY
Cutaneous Metastases
· The overall incidence of metastasis to skin is low.
· Metastatic carcinoma appears as firm subcutaneous nodules. The trunk and scalp are the most frequently affected sites.
· Melanoma is the most common cancer to metastasize to the skin. Solid organ cancers that may metastasize to the skin include the lung, breast, gastrointestinal tract, ovary, and kidney.
Lymphoreticular and Hematologic Malignancies
· Metastasis or paraneoplastic phenomena may affect the skin.
· Leukemia cutis or lymphoma cutis can resemble carcinomatous skin metastasis and appear as firm papules, nodules, or plaques. They are more likely to be hemorrhagic.
· Gingival hypertrophy and bleeding are common with leukemia.
· Sweet syndrome (acute febrile neutrophilic dermatosis) is associated with hematologic malignancies in at least 10% of cases, most commonly acute myelogenous leukemia.38 Sweet syndrome presents as a febrile illness with characteristic “juicy” red nodules and plaques. Biopsy for routine histologic examination and for tissue culture (to rule out infection) confirms the diagnosis.
· Cutaneous T-cell lymphoma is frequently referred to as its most common subtype, mycosis fungoides; cutaneous T-cell lymphoma may present with erythematous patches, plaques, nodules, tumors, generalized erythroderma, or its leukemic variant Sézary syndrome. Diagnosis is made with skin biopsy. Treatment is dictated by disease stage and may range from topical steroids and UV light treatment to chemotherapy.
SKIN SIGNS OF ENDOCRINOLOGIC DISORDERS
Thyroid Disorders
· Hyperthyroidism is associated with fine thin hair that may progress to diffuse alopecia, velvety skin with increased warmth and sweating, palmar erythema, and diffuse hyperpigmentation.
· Graves disease is associated with ophthalmopathy (exophthalmos, lid puffiness, and proptosis), pretibial myxedema, thyroid acropachy (characterized by digital clubbing), and soft tissue swelling of the hands and feet.
· Hypothyroidism is associated with congenital hypothyroidism, generalized myxedema, xerosis, keratoderma, cold pale skin, carotenemia, brittle hair that may progress to alopecia, loss of lateral third of eyebrows, and brittle, slow-growing nails.
Diabetes Mellitus
· Diabetic dermopathy appears as atrophic hyperpigmented patches on the shins.
· Necrobiosis lipoidica diabeticorum is characterized by well-circumscribed, yellow-brown, shiny plaques with pronounced epidermal atrophy and telangiectasia, commonly seen on the shins.
Lipoprotein Disorders
· Eruptive xanthomas arise in groups and exhibit an inflammatory acneiform appearance. They may be mistaken for pustules. Patients are at risk for acute pancreatitis. Plasma triglycerides are markedly increased, but cholesterol is often normal. Etiologic factors include genetic lipoprotein lipase deficiency, ethanol abuse, estrogens, or retinoids.
· Tendon xanthomas are subcutaneous nodules that affect the tendons with normal-appearing overlying skin. They may be mistaken for rheumatoid nodules. If plasma cholesterol is increased, the most likely cause is familial hypercholesterolemia. Patients are at risk for atherosclerosis and coronary disease.
· Xanthelasma is the most common but least specific type of xanthoma. It arises in the periocular area, especially on the eyelids; 50% of patients have increased serum cholesterol.39
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