Current Geriatric Diagnosis & Treatment, 1st Edition

Section III - Common Disorders in the Elderly

29. Common Skin Disorders

Daniel S. Loo MD

Barbara A. Gilchrest MD

SEBORRHEIC KERATOSIS

ESSENTIALS OF DIAGNOSIS

• Seborrheic keratosis is the most common benign epithelial tumor of adulthood.
• The trunk is affected more than the extremities, head, and neck.
• Primary lesions are 5-20 mm light brown to dark brown-black papules and plaques with a rough, warty surface (Figure 29-1).

Differential Diagnosis

Solar lentigo, melanocytic nevus, and verruca vulgaris are included in the differential diagnosis. If the diagnosis is uncertain, histopathological examination is strongly recommended.

Complications

Friction, pressure, and trauma to these lesions may cause irritation or inflammation.

Treatment

Irritated or inflamed lesions can be treated with cryotherapy (Box 29-1), curettage, or shave removal.

EPIDERMAL INCLUSION CYST

ESSENTIALS OF DIAGNOSIS

• This cutaneous cyst is an epithelium-lined sac filled with keratin and located within the dermis.
• Distribution is more common on the trunk than the face and extremities.
• Primary lesions are 0.5-4 cm flesh-colored to yellow dermal to subcutaneous nodules (Figure 29-2).
• Cysts are freely mobile on palpation. With pressure, cheese-like keratin can often be expressed through a central punctum.
• Differential diagnosis includes lipoma.

Complications

Rupture of the cyst wall leads to extrusion of keratin debris into the dermis and a foreign body inflammatory response. The area becomes tense, tender, and painful.

Treatment

These cysts do not resolve spontaneously. Permanent removal can be achieved only by excising the entire cyst wall. Incision and drainage (I) may temporarily relieve pressure but is not curative. In the case of a ruptured cyst, the use of antibiotics is controversial because this is not a true infection (abscess) but rather an inflammatory reaction to foreign material. However, tetracycline has an anti-inflammatory effect, and a dosage of 500 mg twice daily may be helpful. If there is no improvement within 1 week, I followed by infiltration of the area with triamcinolone acetonide, 10 mg/mL, will provide relief. Surgery of inflamed tissue is not recommended. If any portion of the cyst wall remains after treatment, recurrence is likely.

WARTS (VERRUCA VULGARIS & VERRUCA PLANTARIS)

ESSENTIALS OF DIAGNOSIS

• These human papillomavirus-induced growths are found most frequently on the hands and feet followed by the extremities and the trunk.
• Primary lesions are 5-15 mm flesh-colored papules and plaques with a verrucous or filiform surface. Reddish-brown punctate dots (thrombosed capillary loops) are diagnostic (Figure 29-3).

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The lesion may require paring with a no. 15 blade to visualize the capillary loops.

Figure 29-1 Seborrheic keratoses. Waxy, stuck-on papules and plaques, with varying shades of brown and a verrucous surface. Courtesy Neill Peters, MD.

Differential Diagnosis

The differential diagnosis of verruca vulgaris includes flat warts and seborrheic keratosis. The differential diagnosis of verruca plantaris includes callus and clavus (corn).

Treatment

Multiple plantar warts are often stubborn regardless of the treatment modality. Several treatments may be needed before significant improvement occurs. Immunocompromised patients may have widespread involvement and are refractory to standard treatment modalities.

1. CRYOTHERAPY (SEE BOX 29-1)

Two to 3 freeze-thaw cycles are recommended to induce blistering. Treatment is repeated every 3-4 weeks. Plantar warts are thicker and often require paring with a no. 15 blade before freezing.

1. CANTHARADIN

Cantharadin 0.7% (Cantharone) can be used in the office setting. It is applied to the wart, allowed to dry, and covered for 8-12 h. A blister develops within 1-2 days. Treatment is repeated every 3-4 weeks.

1. SALICYLIC ACID

Salicylic acid 40% plasters can be used at home. The plaster is cut to fit over the wart and left in place for 24 h. This is repeated daily. Between treatments, the superficial macerated debris can be removed with a pumice stone or emery board.

Box 29-1. CRYOTHERAPY

1. Indications

o Liquid nitrogen can be used to treat

o Actinic keratosis

o Seborrheic keratosis (irritated)

o Warts

1. Dipstick technique
2. Roll extra cotton over the tip of the cotton applicator.
3. Dip tip into liquid nitrogen.
4. Apply tip of applicator to lesion until 1-2 mm of normal surrounding skin turns white.
5. Wait until lesion completely thaws back to normal color.
6. Repeat (number of freeze-thaw cycles depends on the lesion being treated).
7. Open-spray technique

(Requires hand-held nitrogen unit and C-tip aperture)

1. Nozzle should be 1-2 cm from target lesion and perpendicular to it.
2. Squeeze trigger to emit continuous burst of spray.
3. The lesion and not more than 1-2 mm of surrounding normal skin should be frosted.
4. Wait until lesion completely thaws back to normal color.
5. Repeat (number of freeze-thaw cycles depends on the lesion being treated).
6. Adverse effects

Patients must be informed that

1. During application treated area will sting or burn followed by throbbing.
2. Treated area will become erythematous and edematous and will vesiculate or blister within hours.
3. Hypopigmentation is common in darkly pigmented individuals.

ONYCHOMYCOSIS

ESSENTIALS OF DIAGNOSIS

• Characteristic features include distal thickening of the nail plate, yellow discoloration, and subungual debris (Figure 29-4).

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• Because visual appearance is insufficient to make a diagnosis, microscopy is necessary.
• Differential diagnosis includes pincer nails, onychogryphosis, psoriasis, lichen planus, and repeated trauma.

Figure 29-2 Epidermal inclusion cyst. This large 4 × 5-cm cyst on the left shoulder is tense but freely mobile over underlying tissues.

General Considerations

Yeast or dermatophyte infection of the nail plate requires laboratory confirmation. Nail dystrophy alone is not sensitive or specific for onychomycosis. The average cost of systemic antifungal therapy is $400-$600. Thus, treating all patients with nail dystrophy for presumed onychomycosis is expensive. There are 3 diagnostic tests.

Figure 29-3 Plantar wart. The 2- to 3-mm punctate brown papules are thrombosed capillary loops.

Figure 29-4 Onychomycosis. This fingernail demonstrates the characteristic thick subungual hyperkeratosis and debris.

1. DIRECT MICROSCOPY

Trim back the distal edge of the involved nail. Use a small 1-mm curet or no. 15 blade to scrape the undersurface of the nail plate and nail bed. Place the sample on a glass slide and add 1 drop of potassium hydroxide (KOH) 20% with dimethylsulfoxide (DMSO). Demon stration of hyphae after a few minutes confirms the diagnosis. Sensitivity is highly variable and dependent on experience.

1. CULTURE

Obtain sample as just described and place on Sabouraud's dextrose agar containing chloramphenicol and cycloheximide (Mycosel or Mycobiotic agar). Nail clippings are poor specimens for culture. If there is no growth within 3weeks, the test is negative. Sensitivity is 50-60%.

1. PATHOLOGY

Send a nail clipping in a formalin container for periodic acid-Schiff (PAS) stain. Sensitivity is < 90%.

Pathogenesis

Public exercise facilities and pools are common sites for transmission of dermatophytes, usually via the feet. Tinea pedis can spread to the adjacent nail and often precedes onychomycosis. Toenails are affected more often than fingernails.

Prevention

Treatment of tinea pedis with topical antifungals can prevent onychomycosis and decrease risk of recurrence.

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Treatment

Before initiating therapy, patients should be informed that toenails grow very slowly, approximately 1 mm/mo. Thus, if half of the nail is involved, it will take 6-9 mo to clear. If the entire nail is involved, it will take 12-15 mo to clear. Systemic antifungals maintain an effective concentration in the nail matrix for 6-9 mo after therapy is discontinued.

1. SYSTEMIC ANTIFUNGALS

See Table 29-1 for comparison of dosing regimens, mycological cure, and cost.

Terbinafine—This is the treatment of choice for dermatophyte onychomycosis, providing superior long-term clinical efficacy and lower rates of relapse compared with pulse itraconazole. Terbinafine may increase levels of theophylline, nortriptyline, and caffeine and decrease the level of cyclosporine. Rifampin, cimetidine, and terfenadine may alter serum levels of terbinafine. Terbinafine is best avoided in patients with active hepatitis B or C, cirrhosis, or other chronic hepatic disorders. In healthy individuals, baseline liver function tests are optional.

Itraconazole—This is the treatment of choice for onychomycosis caused by yeast (Candida) or molds. Itraconazole is contraindicated in patients taking astemizole, terfenadine, triazolam, midazolam, cisapride, lovastatin, and simvastatin. Itraconazole may increase drug levels of oral hypoglycemic agents, immunosuppressants, HIV-1 protease inhibitors, and anticoagulants. Anticonvulsants, antituberculosis agents, revirapine, H₂ antihistamines, proton pump inhibitors, and didanosine may alter serum levels of itraconazole. Itraconazole is best avoided in patients with active hepatitis B or C, cirrhosis, or other chronic hepatic disorders. In healthy individuals, baseline liver function tests are optional.

1. CICLOPIROX NAIL LACQUER SOLUTION

Ciclopirox nail lacquer solution 8% may be effective in patients with only 1-2 nails affected and minimal involvement of the distal nail plate. It is brushed onto affected nails daily for 6 mo. Nails should be trimmed, with regular removal of the unattached infected nail.

Prognosis

With the use of systemic antifungals, relapse rates range from 20-50%. Prophylactic weekend application of topical antifungals may prevent recurrences.

Sigurgeirsson B et al: Long-term effectiveness of treatment with terbinafine vs itraconazole in onychomycosis. Arch Dermatol 2002;138:353. [PMID: 11902986]

DRY SKIN, PRURITUS, & ASTEATOTIC DERMATITIS

ESSENTIALS OF DIAGNOSIS

• Dry skin is a common problem and manifests itself predominantly as pruritus.
• More than 80% of elderly persons have symptoms related to skin problems; the most frequent complaint is pruritus from dry skin.
• Symptoms are more common in the winter.
• Indoor heat and low humidity combined with hot showers and overuse of soaps result in dryness and cracking of the skin.
• Dry skin may lead to asteatotic dermatitis, with erythematous patches and slightly raised plaques on the anterior shins and extensor surfaces of the arms and less involvement of the trunk. Cracking and dry scaling may also be seen.

Prevention

A humidifier in the bedroom is helpful. Daily use of moisturizers, especially those containing lactic acid or urea, is recommended to heal dry skin. Moisturizers should be used after bathing while the skin is still slightly moist. Use of bath oils should be avoided because of the risk of slipping.

Table 29-1. Systemic antifungal treatment of toenails.

Drug Dosing regimen Mycological cure (18 mo) Cost Terbinafine Continuous: 250 mg/day × 3-4 mo 75-80% $510-$680 Itraconazole Continuous: 200 mg/day × 3 mo 70% $1000 Pulse: 400 mg/day × 1 week/mo × 3-4 mo 40-50% $470-$630 Fluconazole 150 mg × 1 day/week × 6 mo 50% $260

Figure 29-5 Asteatotic dermatitis. This plaque on the left lateral shin demonstrates fine crackling or fissuring.

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Differential Diagnosis

Atopic dermatitis, contact dermatitis, and irritant dermatitis can resemble dry skin or asteatosis. Dry skin and asteatotic dermatitis (Figure 29-5) may also coexist with these conditions. Pruritus in the elderly can be caused by a variety of dermatological and systemic conditions, but the most common cause is dry skin.

Treatment

Patient education about preventing dry skin includes

• Reducing use of soaps and rinsing well.
• Application of hydrophilic petrolatum or urea 10% cream to moist skin immediately after bath or shower.
• Reducing vigorous rubbing of the skin with towels, which may exacerbate pruritus.
• In asteatotic dermatitis, in addition to measures used for dry skin, applying a class 4 topical steroid ointment to eczematous patches twice daily for 2-3 weeks or until inflammation and pruritus have resolved. (See Table 29-2 for topical steroid potency rating.)

SEBORRHEIC DERMATITIS

ESSENTIALS OF DIAGNOSIS

• The face (especially between the eyebrows and nasolabial folds), scalp, and chest are affected (Figure 29-6).
• Primary lesions are erythematous patches and plaques with secondary changes of greasy scales.
• Rosacea, eczema, lupus, and photosensitivity disorders must be considered in the differential diagnosis.

Table 29-2. Steroid cream potency rating.

Class Trade name Generic 1 Temovate 0.05% Clobetasol proprionate Ultravate 0.05% Halobetasol proprionate 2 Lidex 0.05% Fluocinonide Psorcon 0.05% Diflorasone diacetate 3 Aristocort A 0.5% Triamcinolone acetonide Topicort LP 0.05% Desoximetasone 4 Elocon 0.1% Mometasone furoate Kenalog 0.1% Triamcinolone acetonide 5 Westcort 0.2% Hydrocortisone valerate Dermatop 0.1% Prednicarbate 6 Desowen 0.05% Desonide Aristocort A 0.025% Triamcinolone acetonide 7 Hytone 1% Hydrocortisone Hytone 2.5% Hydrocortisone 1. Steroid ranking from Class 1 (strongest) → class 7 (weakest) 1. Most steroids come in both a cream and ointment. For the same concentration, the ointment is slightly more potent than the cream (fluocinonide .05% ointment is stronger than fluocinonide .05% cream). 2. Most topical steroids are applied twice daily. 3. Class 1 steroids should be used in severe inflammatory or pruritic skin conditions (psoriasis, contact dermatitis, scabies). 2. Adverse effects 1. Atrophy, telangiectasias, and striae may occur with prolonged use of potent topical steroids (classes 1 and 2). For instance, clobetasol cream applied twice daily for > 1 mo may result in atrophy. The FDA limits the duration of use of all class 1 steroids to 2 weeks. 2. The face, genitals, intertriginous areas, and mucosal surfaces absorb steroids more readily and are more prone to these side effects. Potent topical steroids should not be used < 2 weeks on the face, genitals, intertriginous areas, and mucosal surfaces. 3. Potent topical steroids applied to < 50% total body surface area may have systemic effects. FDA, Food and Drug Administration.

General Considerations

Overgrowth of a commensal yeast, Malassezia furfur, results in this common dermatitis.

Figure 29-6 Seborrheic dermatitis. Abundant scale distributed over the medial eyebrows, nasolabial folds, mustache, and beard.

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Treatment

1. ANTIDANDRUFF SHAMPOOS

Over-the-counter zinc pyrithione 1%, selenium sulfide 1%, or ketoconazole 1% shampoo can be applied to the scalp every day for 1 week and then tapered to once or twice weekly to prevent recurrence. The lather should be massaged on the face for a few minutes before rinsing. Ketoconazole 2% shampoo may be more effective.

1. TOPICAL TREATMENT

Topical treatment may be needed for patients unresponsive to shampoos alone.

1. Facial involvement—Apply ketoconazole 2% cream twice daily for 2-3 weeks or class 6 steroid cream twice daily for 2-3 weeks.
2. Scalp pruritus—A class 5 steroid solution can be applied daily as needed.

STASIS DERMATITIS

ESSENTIALS OF DIAGNOSIS

• Chronic venous insufficiency results from pooling of venous blood in the lower extremities and increased capillary pressure.
• Chronic venous insufficiency is most commonly associated with varicose veins.
• Anterior shins are affected most, followed by calves, dorsal feet, and ankles.
• Primary lesions are red-brown to brown hyperpigmented macules and patches (Figure 29-7), often with pedal edema.
• Erythematous patches with fine crackling and scales can be seen as secondary changes.
• Ulceration may occur in up to 30% of patients.
• Pigmented purpuric dermatosis, minocycline hyperpigmentation, and contact dermatitis are included in the differential diagnosis.

Prevention

Compression stockings and leg elevation in patients with varicose veins may help prevent stasis changes.

Figure 29-7 Stasis dermatitis. Hyperpigmented macules and patches involving the left medial malleolus. Courtesy of Neill Peters, MD.

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Treatment

Compression stockings at 20-30 mm Hg can be applied. Elevation of the legs above the level of the heart whenever sitting or lying down will reduce venous pooling. Class 5 steroid ointment applied twice daily will relieve any eczematous patches or plaques.

PSORIASIS

ESSENTIALS OF DIAGNOSIS

• This is a hereditable T cell-mediated inflammatory dermatosis; 33% of those affected have a positive family history.
• Psoriasis may be precipitated by streptococcal pharyngitis (guttate psoriasis).
• There is symmetric involvement of extensor surfaces (elbows, knees, lumbosacral) and scalp. The flexures and genitals may also be involved (inverse psoriasis).
• Primary lesions are erythematous papules and plaques with secondary changes of thick micaceous scale (Figure 29-8).
• Nails may demonstrate yellow-brown oil spots, pitting (Figure 29-9), and onycholysis.
• Differential diagnosis includes eczema, seborrheic dermatitis, and lichen planus.

Figure 29-8 Psoriasis. Plaques with thick micaceous scale on the lower back.

Figure 29-9 Nail psoriasis. This thumbnail demonstrates pitting and distal onycholysis.

Complications

Arthritis of the small and large joints may accompany psoriasis. Generalized pustular psoriasis and erythrodermic psoriasis may be life threatening and require hospitalization.

Treatment

Choice of therapy is dependent on disease severity. For individuals with < 30% total body surface area affected, topical therapies are generally effective.

1. TOPICAL CORTICOSTEROIDS
2. Trunk & extremities–Class 1 steroid ointment is applied to plaques twice daily for 2-3 weeks or until flattening of lesional skin occurs.
3. Face, intertriginous sites–Class 5 steroid cream is applied to plaques twice daily for 2-3 weeks or until flattening of lesional skin occurs.
4. CALCIPOTRIENE

Calcipotriene, .005% ointment applied twice daily, has a slower onset of action compared with topical steroids and is effective for moderate plaque psoriasis. Irritation is the most common side effect.

1. NATURAL SUNLIGHT

Natural sunlight, when practical, is often very helpful. Before 10 _am and after 2 _pm, the patient should lie flat for 15-20 min on each side 2-3 times a week. For those patients with < 30% total body surface area affected, referral to a dermatologist for phototherapy or systemic agents should be considered.

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Prognosis

Psoriasis is a chronic disease characterized by exacerbations and remissions. A positive family history, early onset, and extensive involvement are poor prognostic factors.

ROSACEA

ESSENTIALS OF DIAGNOSIS

• Sometimes referred to as adult acne, rosacea is most common in women aged 40 to 50 and is characterized by flushing.
• Lesions affect the central face (nose, cheeks, forehead, and chin).
• Primary lesions are erythematous papules and pustules(Figure 29-10).
• Secondary changes include confluent telangiectasias with erythema.
• Differential diagnosis includes acne, perioral dermatitis, and systemic lupus erythematosus.

Pathogenesis

Although the cause of rosacea is unknown, any stimulus that increases skin temperature of the head and neck can trigger flushing, including sunlight, hot showers, exercise, alcohol, hot beverages, and spicy foods.

Figure 29-10 Rosacea. Papules and pustules of the central face with enlarged nose and telangiectasias.

Complications

Some cases can progress to rhinophyma (enlarged bulbous nose). Ocular involvement (blepharitis, conjunctivitis) may occur in up to 50% of patients.

Treatment

1. SUNSCREEN

Patients may be able to reduce symptoms by avoiding triggers and applying sunscreen with a sun protection factor of ≥ 15 daily.

1. TOPICAL ANTIBIOTICS

Topical antibiotics include metronidazole, 0.75% cream or gel applied twice daily, and sodium sulfacetamide 10%/sulfur 5% lotion applied twice daily.

1. SYSTEMIC ANTIBIOTICS

Systemic antibiotics include tetracycline, 500 mg orally twice daily on an empty stomach, and doxycycline, 100mg orally twice daily.

1. LASER TREATMENT

For telangiectasias, the patient can be referred to a dermatologist for pulsed dye laser treatment. This is most effective, although it does not prevent development of new telangiectasias.

CONTACT DERMATITIS

ESSENTIALS OF DIAGNOSIS

• Contact dermatitis is a delayed-type hypersensitivity reaction to an antigen (allergen) that contacts the skin and causes severe pruritus.
• Symptoms can be acute or chronic.

Prevention

Patients should be advised to avoid sources of known allergens. Table 29-3 lists the most frequent contact allergens and their sources.

Differential Diagnosis

Acute contact dermatitis can be localized to 1 region or generalized and has linear or artificial patterns (Figure 29-11). Primary lesions include vesicles and erythematous,

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edematous plaques. Secondary changes include erosions, exudates, and crusts.

Table 29-3. Most frequent contact allergens & their sources.

Contact allergens Common sources Nickel Jewelry Fragrance mix Skin or hair care products Thimerosal Vaccines, eye and nasal medications Quaternium-15 Cosmetics Neomycin Antibiotic ointment Formaldehyde Nail polish, cosmetics Bacitracin Antibiotic ointment Thiuram Latex gloves, shoes (rubber products) Balsam of Peru Fragrance in cosmetics Cobalt Metal-plated objects (buckles, button, zippers) P-paraphenylenediamine Hair dye Carba mix Rubber elastic of underwear

Chronic contact dermatitis can be localized to 1 region or generalized and occurs in linear or artificial patterns (indicative of external contact). Primary lesions appear as lichenified plaques. Secondary changes include hyperpigmentation.

Atopic dermatitis, scabies, and irritant dermatitis must be considered in the differential diagnosis.

Figure 29-11 Contact dermatitis. These square-shaped, itchy plaques resulted from electrode adhesive pads from a transcutaneous electrical nerve stimulation unit.

Complications

Left untreated, dermatitis may spread, causing debilitating pruritus.

Treatment

If < 10% of the surface area is involved, a class 1 steroid ointment can be applied 3 times a day for 2-3 weeks or until the dermatitis and pruritus resolves. If < 10% of body surface area is affected, a prednisone taper is appropriate (Box 29-2).

DRUG ERUPTION (MORBILLIFORM)

ESSENTIALS OF DIAGNOSIS

• Maculopapular eruptions, the most common type of drug eruption, usually occur during the first 2weeks of a new medication.
• The most common drugs implicated in drug eruptions are penicillins (ampicillin, amoxicillin), sulfonamides (trimethoprim-sulfamethoxazole), nonsteroidal anti-inflammatory drugs (naproxen,

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piroxicam), anticonvulsants (carbamazepine, phenytoin), and antihypertensives (captopril, diltiazem).

• Distribution of drug eruptions is bilateral and symmetric, usually beginning on the head and neck or upper trunk and progressing down the limbs.
• Primary lesions are erythematous macules and papules with areas of confluence(Figure 29-12).
• Pruritus is occasionally present.
• Differential diagnosis includes viral exanthem, bacterial infection, and collagen vascular disease.

BOX 29-2. PREDNISONE TAPER

1. Indications

(severe pruritus from a variety of conditions)

1. Contact dermatitis > 10% surface area
2. Scabies
3. Severe eczema
4. Drug eruption
5. Dosing

start with 1 mg/kg and then taper by 5 mg each consecutive day.

1. For 130-lb patient, start with 60 mg and taper by 5 mg each day for 12-day course.
2. Severe cases may require a higher starting dose or a prolonged taper over 2-3 weeks.
3. Medrol dosepaks are inadequate for most adults.
4. Side effects

(review patient's history for hypertension, diabetes, glaucoma)

1. Water retention
2. Weight gain
3. Increased appetite
4. Mood swings
5. Restlessness

Complications

Drug hypersensitivity syndrome is potentially life threatening and presents as a triad of fever, skin eruption (80% morbilliform), and internal organ involvement (hepatitis, nephritis, lymphadenopathy). This occurs on first exposure to the drug, with symptoms starting 1-6 weeks after exposure. Laboratory tests to evaluate potential asymptomatic internal organ involvement include transaminases, complete blood cell count, urinalysis, and serum creatinine.

Treatment

The drug most likely to have caused the eruption should be stopped along with any unnecessary medications.

Topical and oral steroids provide symptomatic relief. Regimens include class 1 steroid cream twice daily for 2-3 weeks or prednisone taper (see Box 29-2) if creams are ineffective. Resolution usually occurs within 1-2 weeks.

Figure 29-12 Morbilliform drug eruption. Macules and papules of the right flank and back with areas of confluence. Courtesy Melvin Lu, MD.

Sullivan JR, Shear NH: Drug eruptions and other adverse drug effects in aged skin. Clin Geriatr Med 2002:18;21. [PMID: 11913737]

HERPES ZOSTER (see also Chapter 34: Common Infections)

ESSENTIALS OF DIAGNOSIS

• Herpes zoster is caused by reactivation of varicella-zoster virus in the dorsal root ganglion.
• Distribution of grouped vesicular lesions is unilateral(Figure 29-13) and within 1-2 adjacent dermatomes (ophthalmic branch of trigeminal nerve, thoracic, and cervical are most commonly affected).
• Primary lesions are vesicles(Figure 29-14) on an erythematous base. Secondary changes consist of pustules and crusts.
• Immunosuppression, especially hematological malignancy and HIV infection, substantially increase the risk for herpes zoster as well as dissemination.

Figure 29-13 Herpes zoster. Unilateral S1 and S2 distribution.

Figure 29-14 Herpes zoster. The same patient as in Figure 29-13 has grouped vesicles on an erythematous base.

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General Considerations

Pain precedes the eruption in < 90% of cases. Rarely, the eruption does not develop, and neuralgia is the only manifestation of zoster (zoster sine herpete). In most cases, grouped vesicles in a dermatomal distribution are enough to establish the diagnosis. A positive Tzanck smear cannot distinguish between herpes simplex and varicella-zoster virus. Viral cultures identify herpes simplex within 2-3 days; however, varicella-zoster culture can take 1-2 weeks with frequent false-negative results.

Differential Diagnosis

Herpes simplex, eczema herpeticum, varicella, and acute contact dermatitis are included in the differential diagnosis.

Complications

Patients with cutaneous involvement of the V₁ branch of the trigeminal nerve may experience ocular complications (keratitis, acute retinal necrosis) and need to undergo immediate slit-lamp examination by an ophthalmologist, particularly if skin lesions involve the side and tip of the nose (Hutchinson's sign). Immunocompromised patients are at risk for dissemination, defined as < 20 vesicles outside the primary and immediately adjacent dermatomes. Cutaneous dissemination may be followed by visceral involvement (lung, liver, brain) in 10% of these high-risk patients.

Postherpetic neuralgia is pain that persists after resolution of the cutaneous eruption. This most common complication is age dependent, affecting at least 50% of patients older than 60, and most frequently involves the face.

Treatment

The systemic antiviral drugs (acyclovir, famciclovir, valacyclovir) are effective in the acute phase of zoster and should be used within 48-72 h of rash onset. These drugs have been shown to reduce acute pain, accelerate healing, prevent scarring, and reduce the incidence of postherpetic neuralgia. Systemic corticosteroids (prednisone) may help to reduce acute pain but have no effect on incidence or severity of postherpetic neuralgia. Although the safety profile for the antiviral drugs is excellent, headache, nausea, diarrhea, and central nervous system (CNS), renal, and hepatic dysfunction can occur. In more severe cases, especially in disseminated zoster, initial intravenous acyclovir should be considered. Studies indicate that oral therapy is as effective as intravenous therapy in ophthalmic zoster.

Prognosis

The affected dermatome usually heals within 3-4 weeks and occasionally may scar. Postherpetic neuralgia is the major cause of morbidity.

SCABIES

ESSENTIALS OF DIAGNOSIS

• The Sarcoptes scabiei mite inhabits the human stratum corneum. Characteristic initial lesions are 3–8 mm linear or serpiginous ridges (burrows;Figure 29-15), often with a gray dot at one end (mite).

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• The interdigital web spaces of the hands, volar wrists, penis shaft, and areolae are commonly involved.
• Secondary changes include papules and nodules (nodular scabies), diffuse eczematous dermatitis, thick hyperkeratotic crusted plaques (crusted or Norwegian scabies), and vesicles or bullae (bullous scabies).
• Pruritus is intractable and debilitating.

Figure 29-15 Scabies. Serpiginous 3- to 8-mm burrows above a linear excoriation.

General Considerations

Close body contact is the most common mode of transmission. Fomite transmission is rare because the female mite cannot survive away from the host for < 24-36 h. Risk factors include nursing home residence, HIV and AIDS, and crowded living conditions.

Clinical Findings

Diagnosis is confirmed (finding mites, eggs [Figure 29-16], or feces) using direct microscopy in a simple bedside test.

1. Specimen collection—Place a drop of mineral oil on the center of a glass slide. Touch the sharp part of a no. 15 blade to the drop (so that the specimen will adhere to the blade). Holding the blade perpendicular to the skin, scrape an epidermal burrow to remove the stratum corneum. Pinpoint bleeding indicates the correct depth. Wipe contents onto the center of the glass slide. Choose 2 other burrows, and repeat steps 2-4 to increase the yield. Place coverslip over specimen and gently press down.
2. Microscope settings—Use × 4 objective to scan the slide.

Figure 29-16 Direct microscopy. Scabies mite hatched from an egg. Courtesy Neill Peters, MD.

Differential Diagnosis

The differential diagnosis includes atopic dermatitis, contact dermatitis, drug eruption, and urticarial bullous pemphigoid.

Complications

Nodular scabies is a pruritic hypersensitivity reaction to remnants of the mite. The lesions are firm erythematous to red-brown nodules occurring on the genitals and the axillae. Patients who are immunocompromised may develop crusted or Norwegian scabies with extensive yellow crusting. Norwegian scabies is extremely contagious because each crust contains hundreds of mites. Epidemics of scabies in nursing homes are relatively common and often go undetected for long periods.

Treatment

Goals of therapy include mite eradication, alleviation of pruritus, and prevention of transmission.

1. SCABICIDE

The patient and all close contacts should be treated simultaneously, including those who are asymptomatic.

1. Permethrin—Permethrin 5% cream is the most effective topical treatment. A 60-g tube is prescribed for whole-body application. Patients can be instructed to take a bath or shower and completely dry before application. Cream should be applied to the entire skin surface (from the neck down), with particular attention to finger web spaces, feet, genitals, and intertriginous sites. The cream should be washed off in 8 h. This regimen is repeated in 1 week. Compliance will result in < 90% cure rate.
2. Lindane—Lindane 1% lotion application instructions are identical to those for permethrin. Lindane is safe if used appropriately. Overexposure to lindane (excessive cutaneous applications, ingestion, application to excoriated or infected skin) can cause CNS toxicity, convulsions, and rarely death. Thus, patients with extensively eroded skin or crusted scabies should not be treated with lindane.
3. Ivermectin—Ivermectin, 0.2 mg/kg as an oral dose and repeated at 10-14 days, should be considered in cases resistant to topical treatment, crusted scabies, and the immunocompromised host (eg, HIV patients). Although

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more research is needed to determine the safety and efficacy of ivermectin compared with topical scabicides, this is a practical option for nursing home epidemics in which proper application of permethrin or lindane may be difficult to achieve.

1. PRURITUS

Even after successful mite eradication, severe pruritus can persist for 3-4 weeks. This often debilitating symptom is frequently overlooked and leads to unnecessary discomfort and suffering. Patients may receive repeated treatment for scabies in the mistaken belief that infestation persists.

Class 1 steroid ointment can be applied 2-3 times daily for 2-4 weeks or until complete resolution of pruritus. Prednisone taper (see Box 29-2) may be needed.

1. TRANSMISSION PREVENTION

All clothes worn within 2 days of treatment, towels, and bed sheets should be machine washed in hot water or dry cleaned. Management of nursing home outbreaks requires clinical and epidemiological expertise and possibly involvement of public health experts.

Prognosis

Immunocompetent individuals do well with standard therapy. Crusted scabies, usually in the immunosuppressed, may require < 2 applications of topical scabicides or ivermectin or a combination.

Meinking TL, Elgart GW: Scabies therapy for the millennium. Pediatr Dermatol 2000;17:154. [PMID: 10792811]

Walker GJ, Johnstone PW: Interventions for treating scabies. Cochrane Database Syst Rev 2000;2:CD000320. [PMID: 10796527]

ACTINIC KERATOSIS

ESSENTIALS OF DIAGNOSIS

• Actinic keratosis is a precursor lesion to squamous cell carcinoma.
• Distribution of lesions includes the face, lips, ears, dorsal hands, and forearms (photodistribution).
• Primary lesions are 3-10 mm rough, adherent, scaly white papules and plaques(Figure 29-17), often on an erythematous base.
• Palpation reveals a gritty, sandpaper-like texture. Lesions are often more readily palpated than visualized.
• Differential diagnosis includes dry seborrheic keratosis and retention hyperkeratosis.

Figure 29-17 Actinic keratosis. This is a rough, adherent, scaly papule on the right nasal bridge.

General Considerations

Actinic keratoses are more common in whites and are directly related to cumulative lifetime sun exposure. Immunosuppressed patients, particularly transplant recipients, are at higher risk for actinic keratoses. Daily sunscreen, long-sleeve shirts, broad-brimmed hats, and avoidance of sun can prevent these lesions.

Complications

Various studies cite a < 1-20% risk of transformation to squamous cell carcinoma (SCC) for an individual lesion over the course of a year.

Treatment

Cryotherapy (see Box 29-1) with 2 freeze-thaw cycles is recommended for actinic keratoses. 5-Fluorouracil 5% cream can be applied to affected areas twice daily for 3 weeks. Patients must be informed that treated areas will become severely irritated, inflamed, and eroded.

The patient should return in 1-2 weeks for assessment of side effects. Compliance may be improved by dividing the affected area into smaller subunits and treating 1 subunit at a time to minimize the inflammatory reaction.

Patients with actinic keratoses should be examined annually and are also at risk for basal cell carcinoma (BCC), SCC, and melanoma.

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BASAL CELL CARCINOMA

ESSENTIALS OF DIAGNOSIS

• Basal cell carcinoma is the most common skin cancer (~75%) and is related to chronic ultraviolet light exposure.
• Basal cell carcinoma is derived from stem cells in the basal layer of the epidermis.
• The head and neck are most frequently involved; the nose is the most common site.
• Primary lesions are translucent or pearly papules or nodules(Figure 29-18), often with visible telangiectasias. Secondary changes include central ulceration or crusting.
• The lesion may break down or bleed and does not heal.
• Biopsy (rolled shave or punch technique) is required to confirm the diagnosis.
• Squamous cell carcinoma, keratoacanthoma, and sebaceous hyperplasia are included in the differential diagnosis.

Complications

Although BCC rarely metastasizes, if left untreated, it may become locally invasive and extend to underlying cartilage, fascia, muscle, and bone.

Figure 29-18 Basal cell carcinoma. A 1.5-cm shiny nodule with telangiectasias adjacent to the right nasalala.

Treatment

Electrodesiccation and curettage (ED & C) and excision have comparable cure rates of 90% for low-risk tumors.

Mohs' surgery is the most effective technique (98-100% cure rate) and is indicated for high-risk tumors.

Prognosis

BCC patients determined to be at high risk for recurrence and metastasis have ≥ 1 of the following: recurrent tumor, tumor on the trunk and extremities < 2 cm, tumor on the head and neck < 1 cm, tumor with poorly defined borders, tumor with immunosuppressed host, and tumor occurring at a site of prior radiation. Recurrence rate with standard modalities (ED & C or excision) is < 10%.

For patients with a prior BCC, the 3-year cumulative risk for BCC recurrence is ~44%. For most patients, an annual skin exam is sufficient for detecting new BCCs. Because the number of previous skin cancers is a strong risk factor for subsequent skin cancers, patients with multiple BCCs should be seen more frequently.

Marcil I, Stern RS: Risk of developing a subsequent nonmelanoma skin cancer in patients with a history of nonmelanoma skin cancer. Arch Dermatol 2000;136:1524. [PMID: 11115165]

Miller SJ: The National Comprehensive Cancer Network (NCCN) guidelines of care for nonmelanoma skin cancers. Dermatol Surg 2000;26:289. [PMID: 10759812]

SQUAMOUS CELL CARCINOMA

ESSENTIALS OF DIAGNOSIS

• SCC is derived from keratinocytes above the basal layer of the epidermis, often with actinic keratoses as precursor lesions.
• The head, neck, dorsal hands, and forearms are affected.
• Primary lesions are firm indurated papules, plaques, or nodules(Figure 29-19). Secondary changes include rough adherent scale, central erosion, or ulceration with crust.
• The lesion does not heal and breaks down or bleeds.
• Biopsy with rolled shave or punch technique is required to confirm the diagnosis.
• Differential diagnosis includes basal cell carcinoma and keratoacanthoma.

Figure 29-19 Squamous cell carcinoma. This hard 2.5 × 2.5-cm nodule with overlying dry hemorrhagic crust is at risk for spread to cervical nodes. Courtesy Melvin Lu, MD.

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General Considerations

SCC comprises ~20% of all skin cancers and has the capacity to metastasize. If SCC is suspected, palpation of regional lymph nodes is recommended. SCC should be suspected in any persistent nodule, plaque, or ulcer, especially when occurring in sun-damaged skin, on the lower lip, in areas of prior radiation, in old burn scars, or on the genitals. Immunosuppressed patients (eg, transplant recipients) are at higher risk for SCC because of impaired cell-mediated immunity.

Complications

SCC on the lips or ears has a 10-15% risk of spread to cervical nodes. The overall rate of metastasis from all skin sites ranges from < 1-5%.

Treatment

ED & C and excision have comparable cure rates of 90% for low-risk tumors. Mohs' surgery is the most effective technique (98-100% cure rate) and is indicated for high-risk tumors.

Prognosis

SCC patients considered to be at high risk for recurrence and metastasis have 1 or more of the following: recurrent tumor; tumor on the trunk and extremities <2 cm; tumor on the head and neck < 1 cm; tumor occurring on the genitals, lips, ears, site of prior radiation, or scar; tumor with poorly defined borders; and tumor with immunosuppressed host. Recurrence rate with standard modalities (ED & C or excision) is < 10%.

For patients with a prior SCC, the 3-year cumulative risk for another SCC is ~18%. Annual follow-up examinations for at least 3 years is recommended. Because the number of previous skin cancers is a strong risk factor for subsequent skin cancers, patients with multiple SCCs should be seen more frequently.

Marcil I, Stern RS: Risk of developing a subsequent nonmelanoma skin cancer in patients with a history of nonmelanoma skin cancer. Arch Dermatol 2000;136:1524. [PMID: 1115165]

Miller SJ: The National Comprehensive Cancer Network (NCCN) guidelines of care for nonmelanoma skin cancers. Dermatol Surg 2000;26:289. [PMID: 10759812]

MELANOMA

ESSENTIALS OF DIAGNOSIS

• Melanoma, derived from melanocytes, has the greatest potential for metastasis.
• The trunk and legs are affected more than the face and neck, although the face and neck are more likely to be affected in the elderly.
• The primary lesion is a brown-black macule, papule, plaque, or nodule with ≥ 1 of the following features(Figure 29-20): asymmetry, border irregularity, color variegation, diameter < 6 mm.
• Patients may notice an increase in size (diameter) of a pigmented lesion and bleeding.

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• Lesions should be excised with a margin of clinically normal skin down to subcutaneous fat.

Figure 29-20 Melanoma. 2 × 2-cm plaque on the chest with varying shades of brown to black, asymmetry, and irregular borders.

General Considerations

The incidence of melanoma is increasing faster than any other cancer. The lifetime risk of melanoma in an individual in the United States born in 2001 is estimated at 1 in 71. Melanoma is the most common cancer in women aged 25-29 and the second most common, after breast cancer, for women aged 30-34.

Older men have the highest incidence of melanoma and the highest mortality rates from melanoma. In the United States, the incidence of thick tumors (> 4 mm) has continued to increase in men 60 years of age and older. Nearly 50% of all melanoma deaths involve white men 50 years of age and older.

Risk factors include light complexion (red-blond hair), blistering sunburns during childhood, tendency to tan poorly and sunburn easily, and a positive family history. Additional risk factors in the middle-aged population include age < 50 years, male sex, and a history of actinic keratoses or nonmelanoma skin cancers.

Differential Diagnosis

Seborrheic keratosis, solar lentigo, dysplastic nevus, and pigmented BCC are included in the differential diagnosis.

Complications

Untreated melanoma has a high risk of metastasis to lymph nodes, liver, lungs, and brain.

Treatment

Melanoma is treated by surgical excision with margins determined by histological tumor thickness (Breslow depth). Evaluation of nodal involvement with sentinel lymph node biopsy is recommended for primary melanomas deeper than 1.0 mm and for tumors £ 1 mm when histological ulceration is present. Frequency of follow-up, laboratory tests, and imaging studies depends on stage of disease.

Prognosis

Tumor thickness and presence or absence of histological ulceration are the most important prognostic factors. Patients with thin melanomas (< 1.0 mm) have the best prognosis (< 90% 5-year survival rate), whereas those with thick tumors (< 4 mm) have a 50% 5-year survival rate. For patients with nodal involvement, the number of affected nodes determines the overall prognosis.

Balch CM et al: Final version of the American Joint Committee on Cancer staging system for cutaneous melanoma. J Clin Oncol 2001;19:3635. [PMID: 11504745]

Jemal A et al: Recent trends in cutaneous melanoma incidence among whites in the United States. J Natl Cancer Inst 2001;93:678. [PMID: 11333289]

Sober AJ et al: Guidelines of care for primary cutaneous melanoma. J Am Acad Dermatol 2001;45:579. [PMID: 11568750]