Initial Evaluation

Although medical school teaches students to perform the history before doing the physical examination, this is not the most efficient way to approach the diagnosis of a skin condition. When the patient has a skin complaint, immediately look at the skin while asking your questions. Look carefully at the lesions and determine the lesion morphology. Table 33-1 provides definitions for the terms used to describe primary and secondary morphology. A magnifying glass and good lighting help to distinguish the morphology of many skin conditions. Next, touch the lesions, with gloves when appropriate. For some lesions, such as actinic keratosis with scaling or the sandpaper rash of scarlet fever, lightly feeling the skin provides much information. For deeper lesions, such as nodules and cysts, deep palpation is needed. Observe the distribution of the lesions. Try to determine if the primary lesions are arranged in groups, rings, lines, or merely scattered over the skin.

Table 33-1 Primary and Secondary Skin Lesions

Determine which parts of the skin are affected and which are spared. Be sure to look at the remainder of the skin, nails, hair, and mucous membranes. Patients often show only one small area and appear reluctant to expose the rest of their skin, especially their feet. With many skin conditions, it is essential to look beyond the most affected area because other areas may provide important clues (e.g., nail pitting when considering psoriasis). Patients may have lesions on their back or feet that they have not observed. For example, a patient may have a papular eruption on the hands or arms that represents an autosensitization reaction (id reaction) to a fungal infection on the feet; not looking for the fungus on the feet will lead to a missed diagnosis (Figs. 33-1 and 33-2). Some skin diseases have manifestations in the mouth; finding white patches on the buccal mucosa may lead to the correct diagnosis of lichen planus (Fig. 33-3).

Figure 33-1 Vesicular tinea pedis leading to autosensitization reaction.

(© Richard P. Usatine.)

Figure 33-2 Autosensitization reaction secondary to vesicular tinea pedis (id reaction).

(© Richard P. Usatine.)

Figure 33-3 Oral lichen planus showing Wickham’s striae.

(© Richard P. Usatine.)

Once the physician starts to look at the skin, the patient history will be more focused, directed toward finding the correct diagnosis. The following information assists in making a dermatologic diagnosis and planning treatment:

The most important in-office examinations of the skin are the following:

Topical Corticosteroids

The choice of a topical steroid involves maximizing benefit and minimizing adverse effects. Many skin conditions benefit greatly from topical steroids. However, local adverse effects of topical steroids are common with regular use over weeks to months. The most common adverse effect of topical steroids is skin atrophy, in which the epidermis becomes thin and the superficial capillaries dilate. Epidermal atrophy can be accompanied by hypopigmentation and telangiectasias. If atrophy involves the dermis, striae may occur. Although the epidermal atrophy may be reversible in months, striae are irreversible. When fluorinated steroids (the strongest steroids) are continuously applied to the face, perioral dermatitis, rosacea-like eruptions, and acneiform eruptions can occur.

Systemic adverse effects are rare and occur when large amounts of topical steroids are absorbed systemically. The risk of such absorption increases with stronger steroids, thinner skin, younger patients, longer duration of therapy, and the use of occlusion in therapy. Prescribing the minimum strength needed for the shortest duration required helps prevent adverse effects. In choosing the best topical steroid, consider the following factors:

Table 33-2 Potency of Topical Corticosteroids

Most skin preparations can be applied two times a day (bid), conveniently in the morning and evening. Try to estimate and prescribe an appropriate amount; many topical products are supplied in 15-gram, 30-g, 60-g, and 80-g sizes; 80 g is about the size of a tube of toothpaste. Based on common practice, it is accepted that 2 g of cream is required to cover the face or one hand, 3 g for an arm, 4 g for a leg, and 12 to 30 g for an entire body. To avoid adverse effects of steroid overuse, do not prescribe large quantities for small lesions, and specify duration of use. On the other end of the spectrum, prescribing only 15 g of steroid for a large area of involvement will be frustrating to the patient when the steroid is depleted before completing the prescribed treatment. Generic triamcinolone comes in 1-pound tubs (454 g), extremely helpful for patients with inflammatory conditions covering much of the body.

The duration of therapy is usually the time required for resolution of symptoms or lesions. To avoid adverse effects, the highest-potency steroids should not be used for longer than 2 to 4 weeks continuously. However, these can be used intermittently for chronic conditions such as psoriasis in a pulse-therapy mode (e.g., apply every weekend, with steroid-sparing medication on weekdays). For conditions with dry skin, liberal use of emollients between steroid applications can minimize steroid exposure while maximizing the benefits of therapy.

Management of Pruritus

Often, patients present because of the pruritus associated with a skin condition rather than the skin condition itself. Itching associated with visible lesions often responds to relatively nonspecific antipruritic treatments. If the itching is generalized, patients may obtain temporary relief from cool or tepid baths with the addition of colloidal oatmeal (Aveeno). Soap should be avoided. Oral antihistamines can be given every 6 to 8 hours, especially at bedtime to promote sleep. Diphenhydramine (Benadryl) and hydroxyzine (Atarax, Vistaril) are first-generation antihistamines that are relatively safe and effective, although caution should be used in older adult patients. Second-generation antihistamines are similarly effective for reducing pruritus in the daytime, and are less sedating for some patients. These include fexofenadine (Allegra), loratadine (Claritin), and cetirizine (Zyrtec). Usually, second-generation antihistamines are given once daily.

Atopic Dermatitis (Eczema)

Key Points

Atopic dermatitis (AD) is a potentially debilitating condition that can compromise quality of life. Its most frequent symptom is pruritus. Pruritus leads to scratching, resulting in secondary skin changes such as lichenification, excoriation, and breakdown of the skin barrier. Consequently, atopic dermatitis has been referred to as “the itch that rashes.”

Atopic dermatitis is a common problem affecting up to 15% of all children. In most cases, AD occurs before 5 years of age, frequently on the face in the first year of life (Fig. 33-4). As children grow, the antecubital and popliteal fossae are often involved (Fig. 33-5). The disease may occur intermittently between periods of complete remission. By adulthood, the incidence becomes less than 1%. Treatment should be directed at limiting itching, repairing the skin, and decreasing inflammation. Lubricants and topical corticosteroids are the mainstays of therapy. Topical pimecrolimus or tacrolimus are considered steroid-sparing agents and are effective for short-term use or in cases unresponsive to topical corticosteroids. These agents are only approved for second-line treatment in patients over 2 years of age. When required for severe cases, oral corticosteroids can be used. If pruritus does not respond to treatment, other diagnoses, such as bacterial overgrowth or viral infections, should be considered.

Figure 33-4 Atopic dermatitis.

(© Richard P. Usatine.)

Figure 33-5 Atopic dermatitis in antecubital fossa.

(© Richard P. Usatine.)

Always look for signs of bacterial superinfection, such as weeping of fluid and crusts (Fig. 33-6). Superinfection with Staphylococcus aureus may lead to worsening of atopic dermatitis as the bacteria functions as a super antigen. S. aureus superinfections are usually sensitive to methicillin, so oral cephalexin is frequently a good choice for treatment. Bleach baths are helpful to cut down on colonization. (Add 1⁄2 cup regular bleach per full tub of lukewarm water and soak for 5 to 10 minutes before washing off bleach water.)

Figure 33-6 Impetiginized atopic dermatitis.

(© Richard P. Usatine.)

Pityriasis Alba

Pityriasis alba is a common hypopigmented dermatitis that may affect nearly one third of school-age children in the United States. The condition is more common in patients with a history of atopic dermatitis. Patients present with numerous hypopigmented macules ranging from 1 to 4 cm in size on the face, neck, and shoulders (Fig. 33-7). The macules are poorly defined and may have fine scales. Occasionally, erythema and pruritus occur before the lesions. Generally, pityriasis alba is self-limited and asymptomatic, so therapy is typically unnecessary. Lesions usually fade by adulthood. Topical steroids, emollients, and phototherapy have limited efficacy. Hydrocortisone 1% cream or ointment may provide some benefit, and if used for no more than 2 weeks, the patients should be relatively safe from adverse effects.

Figure 33-7 Pityriasis alba.

(© Richard P. Usatine.)

Keratosis Pilaris

Keratosis pilaris is very common and presents as tiny (<1 mm) keratotic follicular papules found on extensor arms and thighs and occasionally the cheeks. The numerous papules give the skin a rough feeling. Often there is a ring of erythema around the follicle. Incidence of keratosis pilaris is increased in AD patients. Treatment consists of emollients combined with keratolytic agents; common preparations are 5% or 12% ammonium lactate (AmLactin, Laclotion, Lac-Hydrin) and urea-based creams or lotions. Patient education should stress that keratosis pilaris is genetic and cannot be cured. Any smoothing with topical agents is temporary and will return if the treatment is stopped.

Melanocytic Nevi

Nevi (moles) are benign lesions composed of collections of nevus cells of neuroectodermal origin. They appear in childhood, tend to increase in number throughout the adult years, and then resolve with age. Pigmented nevi can be flat, raised, or pedunculated and have impressive variations in size, color, and surface characteristics. Histologically, junctional nevi are located in the epidermis, intradermal nevi in the dermis, and compound nevi in the epidermis and dermis. Junctional nevi are flat and pigmented, intradermal nevi are raised and often not pigmented, and compound nevi may be raised and pigmented (Figs. 33-8 and 33-9).

Figure 33-8 Intradermal nevi.

(© Richard P. Usatine.)

Figure 33-9 Compound nevus.

(© Richard P. Usatine.)

Unless they become suspicious for melanoma, nevi need not be removed except for cosmetic reasons or because of chronic irritation based on their location. Nevi should be examined frequently, however, for changes in color, shape, or size. These changes may herald the onset of a melanoma in a previously benign nevus and warrant excision with pathologic evaluation of the tissue.

Nevi that are present at birth and are visible shortly thereafter are considered congenital nevi. Although these nevi may have a slightly higher risk of developing melanoma than acquired nevi, it is not cost-effective or sensible to recommend the removal of all congenital nevi. It is even controversial with regard to removal of large, “bathing suit” nevi, which have the highest risk of melanoma. Children born with these nevi are at risk for developing melanoma in the central nervous system (CNS) as well as subcutaneous melanoma, which is not visible and requires palpation in order to detect on routine skin examination.

Dysplastic nevi (atypical moles) are markers for increased risk of melanoma somewhere on the body. These nevi have more atypical features but are not at high risk of converting to melanoma (Fig. 33-10). Therefore, removing dysplastic nevi does not provide a survival benefit for patients. The presence of five or more dysplastic nevi should alert the patient and physician to this higher risk of melanoma, and therefore regular skin examinations should be performed, with sun avoidance and sun protection.

Figure 33-10 Dysplastic nevus.

(© Richard P. Usatine.)

Infantile Hemangioma

A hemangioma is an extremely common type of benign tumor that occurs most frequently in infants and children. It is composed of newly formed blood vessels that result from malformation of angioblastic tissue during fetal life. The two main types are capillary (superficial) and cavernous (deep) hemangiomas (Figs. 33-11 and 33-12).

Figure 33-11 Strawberry hemangioma.

(© Richard P. Usatine.)

Figure 33-12 Cavernous hemangioma.

(© Richard P. Usatine.)

Hemangiomas undergo a growth phase before resolving spontaneously. Although some regression begins by the end of the first year of life, many hemangiomas do not completely resolve until the child is 10 to 12 years old. Although typically benign, rapidly proliferating hemangiomas can ulcerate. Those on the face may obscure vision and can cause blindness. Hemangiomas of the genital region are also problematic and may indicate other internal malformations. Persistent or obstructive hemangiomas have been successfully treated with propranolol, lasers, excision, systemic corticosteroids, interferon, imiquimod, and cryosurgery.

Acne Vulgaris

Acne is a disorder of the pilosebaceous follicles on the face, chest, and back. Follicular obstruction leads to comedones, and inflammation results in papules, pustules, and nodules. The four most important steps in acne pathogenesis are (1) sebum overproduction related to androgenic hormones and genetics, (2) abnormal desquamation of follicular epithelium (keratin plugging), (3) Propionibacterium acnes proliferation, and (4) follicular obstruction, which leads to inflammation and follicular disruption. These steps are stimulated by androgens, and strong genetic factors determine a person’s likelihood of developing acne. Although common, acne can cause physical pain, psychosocial suffering, and scarring. Acne may be associated with fever, arthritis, and other systemic symptoms in acne fulminans (Fig. 33-13).

Figure 33-13 Acne fulminans.

(© Richard P. Usatine.)

Topical treatments include retinoids, antibiotics, benzoyl peroxide (BP), azelaic acid, and alpha or beta hydroxyl acid products. Topical retinoids are comedolytic and anti-inflammatory, normalize follicular hyperproliferation and hyperkeratinization, and reduce the numbers of microcomedones, comedones, and inflammatory lesions. The most frequently prescribed topical retinoids include tretinoin (Retin-A), adapalene (Differin), and tazarotene (Tazorac, Avage). Patients are frequently sensitive to topical retinoids and may have skin irritation, peeling, and redness. Mild cleansers and noncomedogenic moisturizers can reduce the inflammation, as does less frequent dosing of the retinoids. Glycolic acid (α-hydroxy acid) or salicylic acid (β-hydroxy acid) come in various products, are used in chemical peels, and are also effective for hyperkeratinization.

Topical antibiotics are effective against P. acnes and also act as anti-inflammatories. Erythromycin and clindamycin are frequently used once or twice daily. Topical dapsone (Aczone) was approved in 2008 for acne treatment. Benzoyl peroxide is also effective against P. acnes and is available over the counter (OTC) in various preparations. Combination products with antibiotics and BP are a convenient method of delivering synergistic medications in one preparation.

Oral medications used in acne treatment include antibiotics, hormone therapies, and isotretinoin. Isotretinoin is a known teratogen and should not be used in women of childbearing age unless avoidance of pregnancy is ensured. Contraception counseling is mandatory, and two negative pregnancy test results are required before initiation of therapy. The baseline laboratory examination should also include determination of cholesterol, fasting triglycerides, transaminase levels, blood urea nitrogen (BUN)/creatinine, and complete blood count (CBC). Pregnancy tests and laboratory examinations should be repeated monthly during treatment.

KEY TREATMENT

Topical benzoyl peroxide (gel, cream, lotion, wash) has an antimicrobial effect in acne treatment. Higher-percentage products (10%) cause more irritation and are not more effective (Agency for Healthcare Research and Quality, 2001) (SOR: A).

Topical antibiotics such as clindamycin and erythromycin are beneficial treatments (AHRQ, 2001) (SOR: A).

Combination products with antibiotics and BP deliver synergistic medications in one preparation (AHRQ, 2001) (SOR: B).

Topical retinoids (tretinoin, adapalene, tazarotene) are excellent to treat all types of acne and the primary treatment in comedonal acne (AHRQ, 2001) (SOR: A).

Azelaic acid is useful to treat spotty hyperpigmentation and acne (AHRQ, 2001) (SOR: B).

Oral antibiotics with proven benefit in acne include tetracycline, doxycycline, minocycline, and erythromycin and are particularly useful for inflammatory acne and trunk acne (AHRQ, 2001; Strauss et al., 2007) (SOR: A).

Isotretinoin is the most powerful treatment for cystic and scarring acne that has not responded to other therapies (Fig. 33-14) (Strauss et al., 2007) (SOR: A).

Figure 33-14 Acne conglobata.

(© Richard P. Usatine.)

Viral Exanthems

Viral causes of rashes include varicella, rubeola, rubella, roseola, and erythema infectiosum (fifth disease). Treatment is aimed at symptoms using acetaminophen or ibuprofen for fever and diphenhydramine for pruritus.

Varicella

Varicella is now much less common with universal varicella vaccination of children. Occasionally the family physician sees a case of breakthrough chickenpox in a vaccinated child. Unvaccinated adults may also present with varicella. Patients with varicella have fever and general malaise as a mild prodrome lasting 1 to 2 days before the rash appears. The rash typically begins on the face, scalp, or trunk and then spreads to the extremities. The lesions appear as erythematous macules and progress to papules with an edematous base. The papules quickly evolve into vesicles, appearing as “dewdrop on a rose petal” (Fig. 33-15). The vesicles evolve into pustules, which become umbilicated and subsequently crust over in the ensuing 8 to 12 hours. A defining characteristic of varicella is that lesions may be present in all stages simultaneously.

Figure 33-15 Chickenpox.

(© Richard P. Usatine.)

In children the most common varicella complication is secondary bacterial infection of excoriated lesions. Other complications include cerebellar ataxia, encephalitis, meningitis, transverse myelitis, and rarely Reye’s syndrome. Varicella pneumonia and encephalitis can be serious complications in adults. Because of the risk of Reye’s syndrome, aspirin use should be avoided in patients with varicella. Acyclovir is recommended for adolescents, adults, and children with varicella who are taking steroids or otherwise immunocompromised.

Seborrhea

Seborrheic dermatitis is a chronic inflammatory disorder affecting areas of the head (scalp, face) and body where sebaceous glands are prominent. The inflammation is thought to be caused by Malassezia (Pityrosporum) species. All age groups may be affected, and seborrhea can be chronic or intermittent. On the scalp, seborrhea can range from mild dandruff to thick, adherent plaques. Seborrhea on the face and body appears as greasy scales in skin folds and along hair margins, with a symmetric distribution bilaterally. On the face, two common locations are around the eyebrows and around the beard and mustache in men (Fig. 33-16 and 33-17)

Figure 33-16 Seborrheic dermatitis.

(© Richard P. Usatine.)

Figure 33-17 Seborrheic dermatitis around beard and mustache.

(© Richard P. Usatine.)

Treatments are aimed at the inflammation and the Malassezia overgrowth and include shampoos containing selenium sulfide, ketoconazole, or pyrithione zinc that target the fungus. Topical antifungal lotions and corticosteroid preparations are also effective. Low-potency corticosteroids used intermittently are safe and effective. In infants, seborrheic dermatitis might only involve the scalp (cradle cap) or can be seen in other areas of skin folds such as the diaper area. If not treated prophylactically, seborrheic dermatitis has a tendency to recur.

Psoriasis

Psoriasis is a common skin disorder that most often appears as inflamed plaques covered with a thickened, silvery-white scale. Psoriasis is divided into the following nine categories, although a patient can have more than one type at the same time:

Figure 33-18 Psoriatic plaques.

(© Richard P. Usatine.)

Figure 33-19 Scalp psoriasis.

(© Richard P. Usatine.)

Figure 33-20 Guttate psoriasis after streptococcal throat infection in child.

(© Richard P. Usatine.)

Figure 33-21 Inverse psoriasis under breasts.

(© Richard P. Usatine.)

Figure 33-22 Palmoplantar psoriasis as a form of localized pustular psoriasis.

(© Richard P. Usatine.)

Figure 33-23 Generalized pustular psoriasis presenting as erythroderma.

(© Richard P. Usatine.)

From 1% to 2% of the U.S. population has plaque psoriasis. Genetic factors are involved; when both parents are affected by psoriasis, the rate of psoriasis may be as high as 50%; with one parent affected, the rate is approximately 16%. Psoriasis can appear at any age, but the two peak age ranges are 16 to 22 and 57 to 60. Guttate psoriasis often occurs after streptococcal pharyngitis or another upper respiratory infection. Pustular psoriasis may be provoked by the withdrawal of systemic steroids in a patient already diagnosed with psoriasis.

The most common areas involved include the elbows, knees, extremities, trunk, scalp, face, ears, hands, feet, genitalia, intertriginous areas, and the nails. In most cases, diagnosis of psoriasis is based on the clinical appearance. The differential diagnosis list is long, however, and a KOH preparation or skin biopsy may be needed. A biopsy may also be helpful to establish the diagnosis in less common types of psoriasis (pustular, palmar-plantar, inverse). Do not treat psoriasis with oral or systemic steroids; this can precipitate a life-threatening case of generalized pustular psoriasis.

A meta-analysis showed that 68% to 89% of patients treated with clobetasol (ultrahigh-potency steroid) had clear improvement or complete healing (Nast et al., 2007). Comparable efficacy was shown for topical calcipotriene (vitamin D analogue) and tazarotene (retinoid), with a slight increase in adverse effects for tazarotene (Afifi et al., 2005). Combination topical steroids and calcipotriene or tazarotene is the most promising current topical treatment and seems to have increased efficacy and fewer side effects (Afifi et al., 2005; Nast et al., 2007). Clinical trials suggest that tacrolimus (0.1 %) ointment twice daily produces a good response in a majority of patients with facial and intertriginous (inverse) psoriasis (Brune et al., 2007; Lebwohl et al., 2004; Martin et al., 2006). Methotrexate as a weekly oral dose of 5 to 15 mg can be very effective for widespread psoriasis not responding to topical treatments (Saporito and Menter, 2004). Acitretin (Soriatane) is a potent systemic retinoid used for psoriasis that is widespread or palmar-plantar and not responding to topical treatments (Pearce et al., 2006)

Etanercept (Enbrel) is a subcutaneous biologic agent that is especially valuable in patients with psoriatic arthritis, as well as those with moderate to severe cutaneous psoriasis (Nast et al., 2007). Adalimumab (Humira), a subcutaneous biologic agent, and infliximab (Remicade), an intravenous biologic agent, are effective for patients with psoriatic arthritis as well as those with moderate to severe cutaneous psoriasis (Bansback et al., 2009). Ustekinumab (Stelara), the most recently approved subcutaneous biologic agent, significantly reduced signs and symptoms of psoriatic arthritis and diminished skin lesions compared with placebo (Gottlieb et al., 2009).

Pityriasis Rosea

Pityriasis rosea is a common acute eruption usually affecting children and young adults; the cause is unknown. It is characterized by the formation of an initial herald patch (Fig. 33-24), followed by the development of a diffuse papulosquamous rash. Pityriasis rosea is difficult to identify until the appearance of characteristic, smaller, secondary lesions that follow Langer’s lines in a “Christmas tree” pattern (Fig. 33-25). The rash of pityriasis rosea typically lasts 5 to 8 weeks, with complete resolution in most patients. An important goal of treatment is to control pruritus, which may be severe; zinc oxide, calamine lotion, topical steroids, and oral antihistamines are usually helpful. Systemic steroids are generally not recommended.

Figure 33-24 Pityriasis rosea with herald patch on neck.

(© Richard P. Usatine.)

Figure 33-25 Pityriasis rosea with “Christmas tree” pattern on back.

(© Richard P. Usatine and E.J. Mayeaux, Jr. The Color Atlas of Family Medicine.)

Ultraviolet (UV) radiation and erythromycin have been used with varying results. Because no bacterial cause has been associated with the disease, the likely effect of erythromycin is a result of its anti-inflammatory properties. Postinflammatory hyperpigmentation may occur with UVB radiation therapy, so some experts recommend against its use. High-dose acyclovir (800 mg qid) may help shorten disease, especially if instituted early in the disease course, but studies are limited.

Patients should be reassured about the self-limited nature of pityriasis rosea. Persistence of the rash or pruritus beyond 12 weeks should prompt reconsideration of the original diagnosis, consideration of biopsy to confirm the diagnosis, and questioning the patient again about use of medications that may cause a rash similar to that of pityriasis rosea.

Rosacea

Rosacea, sometimes called “acne rosacea,” is an inflammatory disease with unknown etiology. Various facial manifestations occur, and symptoms differ from patient to patient. The four types of rosacea are erythematotelangiectatic, papulopustular, phymatous, and ocular. Patients may have overlapping features of more than one type. The predominant manifesting complaints of erythematotelangiectatic rosacea are intermittent central facial flushing and erythema. Itching is often absent; however, many patients complain of a stinging pain associated with flushing episodes. Common triggers include exposure to the sun, cold weather, sudden emotion including laughter or embarrassment, hot beverages, spicy foods, and alcohol consumption.

Papulopustular rosacea presents with acnelike papules and sterile pustules and can occur alone or in combination with the erythema and telangiectasias (Fig. 33-26). Intermittent or chronic facial edema may also occur in all forms. Some patients develop rhinophyma, a coarse hypertrophy of the connective tissue and sebaceous glands of the nose. This can be extremely disfiguring and even cause nasal airway obstruction. Approximately one third of patients with rosacea develop ocular symptoms, including eyes that are itchy, burning, or dry; a gritty or foreign body sensation; and erythema and swelling of the eyelid. The ocular changes can become chronic. Corneal neovascularization and keratitis can occur, leading to corneal scarring and perforation. Episcleritis and iritis have also been reported to occur in patients with rosacea.

Figure 33-26 Rosacea.

(© Richard P. Usatine.)

First-line treatment is avoidance of triggering or exacerbating factors. Although patients have different trigger(s), almost all patients benefit from strict sun avoidance and protection. Acnelike lesions respond well to long-term topical treatment using metronidazole, azelaic acid, erythromycin, and clindamycin. Oral tetracyclines used in antimicrobial (high) doses or anti-inflammatory (low) doses are helpful for moderate to severe rosacea. Oral or topical retinoid therapy may also be effective. Laser treatment is an option for progressive telangiectasia, erythema, or rhinophyma. Ocular symptoms generally require oral tetracyclines. Consultation may be required for the management of rhinophyma, ocular complications, or severe disease.

Lichen Planus

Lichen planus is a papular pruritic skin eruption characterized by its violaceous color and polygonal shape. Most frequently, flat-topped papules and plaques are found on the flexor surfaces of the upper extremities, on the genitalia, around the ankles, and on the mucous membranes (Figs. 33-27 and 33-28). Lesions can be intensely pruritic. Because lichen planus is thought to be immune-mediated, it may be found in conjunction with ulcerative colitis, vitiligo, myasthenia gravis, dermatomyositis, and alopecia areata. Lichen planus is also associated with primary biliary cirrhosis, chronic active hepatitis, and hepatitis C infection.

Figure 33-27 Lichen planus with linear papules.

(© Richard P. Usatine.)

Figure 33-28 Lichen planus on lateral ankle.

(© Richard P. Usatine.)

Patients with lichen planus are usually between 30 and 60 years old, although the disorder may occur at any age. Men and women are equally affected, and there is no racial predisposition. The cutaneous form spontaneously resolves within 6 months in about half of patients, and most forms resolve within 18 months. Mucous membrane lesions may become chronic and persist for years. Mild cases can be treated symptomatically with antihistamines and topical steroids. More severe cases or those involving the mucous membranes can be treated with systemic steroids, oral acitretin, or UV light. Other immunosuppressants, such as mycophenolate mofetil and cyclosporine, have also been used with some success.

Lichen Simplex Chronicus

Lichen simplex chronicus (LSC) is a secondary condition that results from repeated mechanical trauma to the skin, usually through rubbing and scratching, which causes lichenification (thickening of epidermis). Skin appears leathery, violaceous to hyperpigmented, and scaly (Fig. 33-29). Involved areas are within the patient’s easy reach, such as arms, legs, posterior neck, upper back, buttocks, and scrotum. The cycle of pruritus, which is alleviated by scratching, perpetuates the condition. Pruritus is usually worse during periods of inactivity, usually at bedtime and during the night. Stress also may provoke pruritus, which is relieved by rubbing and scratching and often becomes an unconscious behavior.

Figure 33-29 Lichen simplex chronicus.

(© Richard P. Usatine.)

Treatment of LSC is aimed at treating existing lesions, reducing pruritus, providing insight into the itch-scratch cycle, and eliciting behavioral changes, Topical steroids decrease inflammation and pruritus and help “thin down” the hyperkeratosis. Because lesions are by nature chronic, long-term treatment should be stressed. Occlusion can be used to increase potency and enhance delivery of the topical steroid and also provides a barrier to scratching. Flurandrenolide tape (Cordran) is very effective and can be cut to fit each lesion of LSC. Anxiolytics and antihistamines such as diphenhydramine and hydroxyzine may be considered as adjunct treatments. In severe, debilitating cases, oral doxepin and clonazepam may be considered. For secondary infections, a topical or oral antibiotic is appropriate.

Contact Dermatitis

Key Points

Contact dermatitis may be classified by cause into two subgroups: irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD). ICD occurs when the skin is exposed to an environment or substance in a sufficient frequency, quantity, or duration that it overcomes the barrier function of the skin. Therefore, given adequate exposure, anyone may experience ICD. ACD is a delayed-type hypersensitivity (type 4) reaction to a topical agent and requires initial contact with a substance causing a T helper cell type 2 (Th2)–mediated immune response in a predisposed individual. Only with repeated exposure do the primed T cells cause the clinical response of dermatitis.

Findings of contact dermatitis can include erythema, vesicles, bullae, exudation, and crusting from breaking of blisters, swelling, and scaling. Common areas affected are the hands, neck, eyelids, face, genitalia, and legs. ICD and ACD can look identical and can present on similar body areas. Both may be intensely pruritic, further complicating the diagnosis. In addition, ACD and ICD can be present simultaneously, as with the health care worker allergic to latex who washes the hands repeatedly throughout the day. A careful history and patch testing are often the key to diagnosis.

Each year, millions of patients develop an allergic rash after contact with poison ivy, poison sumac, or poison oak, and contrary to popular belief, the fluid within these vesicles does not cause poison ivy “to spread.” Nickel is the most common nonplant cause of ACD and historically more common in women because of costume jewelry and ear piercing (Fig. 33-30). With the increased popularity of jewelry and body piercing, the prevalence is rising in men. The 10 top causes of ACD in North America are nickel, neomycin, balsam of Peru (common fragrance), fragrance mix, thimerosal (preservative no longer used in vaccines but still found in eye preparations), sodium gold thiosulfate, quaternium-15 (preservative), formaldehyde (preservative), bacitracin, and cobalt (metal often in conjunction with nickel in silver-colored jewelry).

Figure 33-30 Contact dermatitis to nickel jewelry in umbilicus.

(© Richard P. Usatine.)

In the workplace, ACD is very common. For skin conditions, 90% of workers’ compensation claims result from contact dermatitis. Common offenders in specific occupations are rubber or latex in health care workers, hair and clothing dyes in hairdressers, chromates in cement workers, and the Rhus family (poison ivy, oak, and sumac) in agricultural workers. ICD most often develops in response to excessive exposure to soaps, cleansers, hand sanitizers, and water. Therefore the primary treatment is avoidance of these irritating substances, application of a barrier ointment such as petrolatum, and protective equipment such as gloves.

For ACD caused by plants, the skin and clothes with soap and water should be thoroughly washed as soon as possible to minimize exposure to the antigen. Cool, wet soaks for 10 to 15 minutes may be soothing. Superpotent topical steroids, such as clobetasol propionate or betamethasone dipropionate applied twice daily for 1 to 2 weeks, are effective for treating small areas of moderate ACD. Systemic steroids are reserved for severe episodes of and should be continued for at least 2 weeks to prevent rebound dermatitis. In otherwise healthy persons, a tapering dose of prednisone is not required for short courses of systemic therapy. Severe pruritus may respond to antihistamines such as hydroxyzine, diphenhydramine, or a nonsedating H₂ blocker such as loratadine, cetirizine, or fexofenadine.

If ACD is suspected based on history, consultation for patch testing with a dermatologist can be customized to the patient’s occupation or hobbies. Once the offending agent is identified, avoidance is crucial. When the offending agent is occupational, a change in jobs may be required. Alternative protective equipment can be sufficient in other cases, such as substituting nitrile gloves for latex. Generalized dry-skin care, topical steroids, or immunomodulators (pimecrolimus, tacrolimus) can help prevent recurrence and treat flares.