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CHAPTER 250: Skin Disorders: Face and Scalp 1629 tissue areas with end circulation are affected. Large confluent ecchymoses can develop, often on the extremities, from distal to proximal, and on the perineum, buttocks, and abdomen. The extremities are often involved symmetrically. Treatment is directed at the underlying cause. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Skin Disorders: Face and Scalp Sam Wu Diana B. McShane Dean S. Morrell INTRODUCTION This chapter discusses common infections and inflammations affecting the face and scalp; allergic dermatitis involving the face (including poison ivy); and photosensitivity reactions. Erysipelas and facial cellulitis are discussed in Chapter 152, “Soft Tissue Infections, ” and impetigo and bullous impetigo are discussed in Chapter 142, “Rashes in Infants and Children. ”  FACE SEBORRHEIC DERMATITIS Seborrheic dermatitis has both infantile and adult forms. The infantile form is called “cradle cap” and peaks in the first 3 months of life (see Chapter 142, “Rashes in Infants and Children” for further discussion of infantile seborrheic dermatitis). Adult seborrheic dermatitis presents as white to yellow greasy scaling of the scalp (i.e., dandruff), eyebrows, nasolabial folds, ears, and postauricular skin associated with mild erythema and variable pruritus (Figure 250-1). Occasionally, the lesions may extend CHAPTER FIGURE 250-1. Adult seborrheic dermatosis. Erythema and scaling on face and facial skin folds. [Reproduced with permission from Wolff K, Johnson R, Suurmond R: Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology , 5th ed. New York, McGraw Hill, Inc.; 2005:51.] onto the upper central chest and intertriginous areas. Adults with acquired immunodeficiency syndrome and Parkinson’s disease are predisposed to severe disease. The typical distribution of seborrheic dermatitis is in areas with high concentrations of sebaceous glands. Malassezia yeasts residing on the skin may contribute to inflammation. 1 This factor may explain why seborrheic dermatitis responds to both antifungal and anti-inflammatory agents. In adults, the condition is chronic and recurrent but without any systemic symptoms. Treat adults with an antidandruff shampoo containing zinc pyrithi one, selenium sulfide 2.5%, salicylic acid, or tar. Ketoconazole can also be used and is available over the counter as 1% shampoo and by prescription at 2% for shampoo and cream. Lather the shampoo into the scalp and leave on briefly before rinsing. For severe cases, a topical corticosteroid such as fluocinonide solution may be applied to the scalp daily. For the face, low-potency topical corticosteroids applied twice per day may be used (Table 250-1). The use of higher potency topical corticosteroids on the face for more than a few days can lead to the development of perioral dermatitis or steroid rosacea and should be avoided. Treatment continues until the dermatitis is cleared. Re-treat recurrences as needed. TINEA BARBAE AND SYCOSIS BARBAE Tinea barbae is a dermatophyte infection involving the beard area of the face and neck and occurs in postpubertal males. The cause is usually the genus Trichophyton. Predisposing factors to tinea barbae include use of topical steroids, contact with infected pets, and diabetes mellitus. 2 Sycosis barbae is a deep folliculitis within the beard area with perifollicular inflammation. The causative agent is usually Staphylococcus aureus.

les. The cause is usually the genus Trichophyton. Predisposing factors to tinea barbae include use of topical steroids, contact with infected pets, and diabetes mellitus. 2 Sycosis barbae is a deep folliculitis within the beard area with perifollicular inflammation. The causative agent is usually Staphylococcus aureus. In tinea barbae, severe inflammatory plaques and follicular pustules occur in the beard area ( Figure 250-2). Kerion-like lesions can develop as well as abscesses and sinus tracts. Hairs are usually loosened or bro ken off. In sycosis barbae, discrete pustules, usually involving S. aureus, with perifollicular inflammation are evident ( Figure 250-3). Unlike tinea barbae, the hairs are usually not loosened or broken off. The diagnosis is clinical, but tinea barbae sometimes can resemble acne vulgaris or bacterial folliculitis. A potassium hydroxide prepara tion or fungal culture can be done to confirm the diagnosis. Permanent alopecia and scarring can result if left untreated. Treatment of tinea barbae requires oral antifungals. Microsize griseofulvin, 500 milligrams PO daily, or ultramicrosize griseofulvin, 375 milligrams PO daily, for 6 weeks can be used. Terbinafine 250 milligrams PO daily for 2 to 4 weeks can also be used; both griseofulvin and terbinafine should be avoided in patients with known hepatic dysfunction (Table 250-1). Supportive care includes shaving or depilating the hair and warm compresses to remove the crust. For sycosis barbae, initial treatment with warm compresses and mupirocin ointment may be sufficient. If lesions are chronic, treatment usually requires systemic antibiotics with adequate S. aureus coverage (Table 250-1). HERPES ZOSTER INFECTION Herpes zoster or “shingles” is a cutaneous manifestation of reactivation of varicella-zoster virus from its latent state in neural ganglia following primary infection. For discussion of other manifestations of varicellazoster virus infection, see Chapter 154, “Serious Viral Infections. ” Pain or dysesthesia typically precedes cutaneous findings of herpes zoster by 3 to 5 days. Erythematous papules progress to clusters of vesicles and pustules on an erythematous base in a dermatomal dis tribution ( Figure 250-4). Vesicles crust over in about 1 week. While zoster typically involves the thoracic and lumbar dermatomes, presence of lesions within the ophthalmic branch (V1) of the trigeminal nerve and especially on the tip of the nose is concerning for herpes zoster ophthalmicus, which requires emergent ophthalmology evaluation. Ramsay Hunt syndrome results from reactivation of varicella-zoster virus in the geniculate ganglion and presents with ear pain, vesicles in Tintinalli_Sec20_p1607-1668.indd 1629 8/2/19 7:24 PM

pecially on the tip of the nose is concerning for herpes zoster ophthalmicus, which requires emergent ophthalmology evaluation. Ramsay Hunt syndrome results from reactivation of varicella-zoster virus in the geniculate ganglion and presents with ear pain, vesicles in Tintinalli_Sec20_p1607-1668.indd 1629 8/2/19 7:24 PM 1630 SECTION 20: Dermatology FIGURE 250-2. Tinea barbae. [Photo contributed by University of North Carolina Department of Dermatology.] FIGURE 250-3. Sycosis barbae. [Photo contributed by University of North Carolina Department of Dermatology.] TABLE 250-1 Clinical Features and Treatment of Seborrheic Dermatitis of the Face, Tinea Barbae, Sycosis Barbae Condition Clinical Features Treatment Comments Seborrheic dermatitis White to yellow scale involving scalp, eyebrows, nasolabial folds, and chest with variable erythema and pruritus OTC antidandruff shampoo Ketoconazole 2% shampoo Ketoconazole 2% cream Desonide 0.05% or hydrocortisone 2.5% Leave shampoos on for 3–5 minutes before rinsing Tinea barbae Scaly erythematous plaques, follicular pustules, or erythematous boggy plaques in beard distribution; associated with loosened/broken hairs Griseofulvin, microsize 500 milligrams PO daily for 6 weeks Griseofulvin, ultramicrosize 375 milligrams PO daily for 6 weeks Terbinafine 250 milligrams daily for 2–4 weeks Avoid griseofulvin and terbinafine in patients with known hepatic disease; reasonable to obtain baseline liver function tests when prescribing Sycosis barbae Follicular pustules and perifollicular erythema in beard distribution Warm compresses Mupirocin 2% ointment Oral antistaphylococcal antibiotics Abbreviation: OTC = over the counter. the external auditory canal, facial nerve paralysis, and vestibulocochlear dysfunction. The key to diagnosis is the unilateral distribution and pronounced pain in the area of involvement. Diagnosis can be confirmed by poly merase chain reaction analysis of swabs taken from the base of an intact vesicle. Tzanck smear can also demonstrate multinucleated giant cells, but unlike polymerase chain reaction, it cannot differentiate between varicella-zoster virus, herpes simplex virus 1, or herpes simplex virus 2 infection. Treatment is most effective if it is initiated within the first 72 hours of symptoms and decreases healing time, new lesion formation, and the risk of postherpetic neuralgia. Treatment options in an immuno competent patient include oral acyclovir or valacyclovir ( Table 250-2). In immunocompromised patients, intravenous acyclovir is necessary. Local care can be provided with aluminum acetate compresses three times daily followed by antibiotic ointment to prevent secondary bacterial infection. Assess and treat associated pain, which may be severe. Vaccination against zoster reduces the incidence and severity of illness as well as risk of postherpetic neuralgia and is indicated for adults over the age of 50. Patients with herpes zoster are contagious to nonvaccinated indi viduals without natural immunity, and isolation is needed for patients suspected of the disease at triage. Patients should be instructed to cover all open areas when visiting the physician at follow-up. HERPES SIMPLEX VIRUS INFECTIONS Herpes simplex virus type 1 most commonly occurs on the face. Pri mary infection occurs during childhood or adolescence and is typically asymptomatic but occasionally presents with painful orofacial vesicular lesions associated with systemic symptoms. Recurrences tend to be milder and occur primarily on the lips, nose, and oral cavity. The typical lesions of herpes simplex virus are painful, grouped vesicles on an erythematous base (Figure 250-5).

cally asymptomatic but occasionally presents with painful orofacial vesicular lesions associated with systemic symptoms. Recurrences tend to be milder and occur primarily on the lips, nose, and oral cavity. The typical lesions of herpes simplex virus are painful, grouped vesicles on an erythematous base (Figure 250-5). The characteristic primary eruption is a gingivostomatitis with herpetic lesions on the lips and in the oral cavity that may persist for weeks accompanied by fever and malaise. Recurrences may be induced by ultraviolet light, fever, stress, or local trauma and typically present as herpes labialis (“fever blisters” or “cold sores”). Individuals often experience a prodrome of localized tingling or burning several hours before the onset of the eruption. The herpetic lesion usually occurs along the lip margin and completely heals within 10 days. In patients with underlying atopic dermatitis, a severe form of her pesvirus infection can occur called eczema herpeticum in which herpes simplex virus or varicella-zoster virus can infect active atopic dermatitis lesions (see Chapter 142, “Rashes in Infants and Children”). Treatment for primary herpes simplex virus gingivostomatitis works best when given within the first 24 hours (Table 250-2). 5 Treat ment can continue for up to 10 days if lesions have not crusted. Tintinalli_Sec20_p1607-1668.indd 1630 8/2/19 7:24 PM

ermatitis lesions (see Chapter 142, “Rashes in Infants and Children”). Treatment for primary herpes simplex virus gingivostomatitis works best when given within the first 24 hours (Table 250-2). 5 Treat ment can continue for up to 10 days if lesions have not crusted. Tintinalli_Sec20_p1607-1668.indd 1630 8/2/19 7:24 PM CHAPTER 250: Skin Disorders: Face and Scalp 1631 Ophthalmic Maxillary Mandibular Auricular Rami of the trigeminal N. Ramus of vagus *Overlapping of greater auricular and facial nerves * Post cev. Gr. occipital Sm. occipital Cervical cutaneous FIGURE 250-4. A. Herpes zoster in trigeminal nerve distribution. Note the lesion on the tip of the nose, which suggests nasociliary branch involvement. B. Dermatomes of the head and neck. Cev = cervical; gr = greater; N = nerve, Sm = smaller [A. Reproduced with permission from Fleischer A Jr, Feldman S, McConnell C, et al: Emergency Dermatology: A Rapid Treatment Guide. New York: McGraw-Hill, Inc.; 2002, p. 157. B. Reproduced with permission from Wolff K, Johnson R, Suurmond R: Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology , 5th ed. New York: McGraw-Hill, Inc.; 2005.] TABLE 250-2 Clinical Features and Treatment of Herpes Zoster and Herpes Simplex Condition Clinical Features Treatment Options Comments Herpes zoster Vesicles and pustules on erythematous base in dermatomal distribution; associated pain, pruritus, dysesthesia Acyclovir: 800 milligrams PO 5 times a day for 7 d Valacyclovir: 1000 milligrams PO 3 times a day for 7 d Treatment should be initiated within the first 72 h after symptom onset, if possible Herpes simplex, initial episode Asymptomatic infection or painful vesicles and ulcers with surrounding erythema on mucosa associated with fevers, malaise, lymphadenopathy Acyclovir: 400 milligrams PO 3 times a day for 7–10 d or 200 milligrams PO 5 times a day for 7–10 d Valacyclovir: 1000 milligrams PO twice a day for 7–10 d Can extend treatment of acyclovir or valacyclovir if not healed after 10 d Herpes simplex, recurrence Recurrent painful vesicles at or near site of primary infection preceded by prodrome of pruritus or dysesthesia Acyclovir: 400 milligrams PO 5 times a day for 5 d or 800 milligrams PO twice a day for 5 d Valacyclovir: 2000 milligrams PO twice a day for 1 d Avoid triggers: ultraviolet exposure, trauma, stress, illness; may require referral to dermatology for suppression of frequent flares Immunocompromised patients with severe involvement require hos pitalization for IV acyclovir. Suppressive treatment with acyclovir or valacyclovir can decrease outbreaks of herpes labialis. 5 Patients with recurrent disease should be instructed to avoid triggers, especially the sun, by using sunscreen and a lip balm with ultraviolet light protection.  SCALP DISSECTING CELLULITIS OF THE SCALP Dissecting cellulitis of the scalp is an intense inflammatory and scarring disease of the scalp and neck, driven by follicular occlusion and often complicated by secondary bacterial infection. It occurs most commonly in young men of African descent and consists of boggy tender nodules in multiple areas of the scalp and the neck (Figure 250-6). Osteomyelitis of the skull has been reported as a sequela. 6 The nodules suppurate and develop interconnecting, draining sinus tracts. Hair loss develops over these nodules, and permanent scarring, alopecia, and keloids can occur. ED therapy includes antibacterial washes, such as chlorhexidine, which FIGURE 250-5. Herpetic gingivostomatitis. [Photo contributed by University of North Carolina Department of Dermatology.] Tintinalli_Sec20_p1607-1668.indd 1631 8/2/19 7:24 PM

ver these nodules, and permanent scarring, alopecia, and keloids can occur. ED therapy includes antibacterial washes, such as chlorhexidine, which FIGURE 250-5. Herpetic gingivostomatitis. [Photo contributed by University of North Carolina Department of Dermatology.] Tintinalli_Sec20_p1607-1668.indd 1631 8/2/19 7:24 PM 1632 SECTION 20: Dermatology FIGURE 250-6. Dissecting cellulitis of the scalp. [Photo contributed by University of North Carolina Department of Dermatology.] TABLE 250-3 Clinical Features and Treatment of Pediculosis Capitis, Tinea Capitis, and Dissecting Cellulitis of Scalp Condition Clinical Features Treatment Comments Dissecting cellulitis of scalp Tender, suppurative nodules and sinus tracts associated with scarring and alopecia Over-the-counter antibacterial wash, doxycycline or minocycline 100 milligrams PO twice a day; incision and drainage for painful, fluctuant nodules Due to chronic condition, referral to dermatology recommended Tinea capitis Scalp pruritus, broken hairs, alopecia, and lymphadenopathy Griseofulvin, microsized 20–25 milligrams/kg/d PO (<1 gram/d) for 8 wk or Griseofulvin, ultramicrosized 15–20 milligrams/kg/d PO (<750 milligrams/d) for 8 wk or Terbinafine 125–250 milligrams/d PO for 6 wk May be associated with id reaction or kerion formation; treatment duration may be extended based on response Pediculosis capitis (head lice) Scalp pruritus (especially behind ears), presence of adult lice and/or nits along hair shaft Permethrin cream, pyrethrin lotion, ivermectin lotion, or malathion cream; repeat treatment in 7–10 d Machine wash and dry recently used clothing and bed linens is available without prescription, and oral antibiotics such as doxycycline and minocycline ( Table 250-3). Incision and drainage of individual suppurative nodules does not treat the underlying condition but may provide symptomatic relief. Refer to a dermatologist for continued management. Dapsone, intralesional corticosteroids, and prednisone have variable efficacy in treating this challenging condition. Isotretinoin, surgical excision, laser treatment, and tumor necrosis factor-α blockers have also been used successfully. TINEA CAPITIS Tinea capitis is a dermatophyte infection of the scalp. Causative agents are usually from the genus Trichophyton. The fungi invade the hair shaft and stratum corneum of the skin. Clinically, there are nonscarring patches of alopecia with broken hairs and scale at the periphery. Occasionally, there is intense inflam mation, with a boggy, tender, indurated plaque with superficial pustules and overlying alopecia (Figure 250-7). This reaction, referred to as a kerion, may result in permanent scarring and alopecia. Cervical and/or FIGURE 250-7. A. Tinea capitis with Wood’s light fluorescence. B. Kerion. [Photo contributed by University of North Carolina Department of Dermatology.] occipital lymphadenopathy may be present. In some cases of tinea capitis, especially after initiation of oral antifungal therapy, patients will mount an immune response to the dermatophyte, called an id reaction, at distant sites. This id reaction appears as widespread, symmetric, pruritic, monomorphic, eczematous papules and responds to topical Tintinalli_Sec20_p1607-1668.indd 1632 8/2/19 7:24 PM

ally after initiation of oral antifungal therapy, patients will mount an immune response to the dermatophyte, called an id reaction, at distant sites. This id reaction appears as widespread, symmetric, pruritic, monomorphic, eczematous papules and responds to topical Tintinalli_Sec20_p1607-1668.indd 1632 8/2/19 7:24 PM CHAPTER 250: Skin Disorders: Face and Scalp 1633 TABLE 250-4 Fluorescence From Wood’s Lamp •  Nits •  Lice •  Microsporum •  Malassezia FIGURE 250-8. Head lice. [Photo contributed by the Department of Dermatology, University of North Carolina.]  POISON IVY/OAK, OTHER ALLERGIC CONTACT DERMATITIS, AND PHOTOSENSITIVITY Two types of contact allergies are likely to result on the face. The first is the result of an aerosolized allergen. The second is due to direct physical contact that is most prominent on the sensitive parts of the face. POISON IVY AND POISON OAK/SUMAC About 70% of individuals are sensitized to poison ivy, oak, or sumac. Involvement of the face can be through aerosolization or direct contact with the plant. Exposure to aerosolized poison ivy or oak presents as erythema and scale with or without vesiculation (Figure 250-9). The involvement is diffuse, with upper and lower eyelids affected. Aerosolization can occur if plants are burned or from activities that can cause the toxic urushiols to become airborne, such as using a weed wacker or lawnmower in a poison ivy patch. Direct contact from plants or contaminated clothing results in the typical linear lesions with vesicle and bullae formation. Treatment is prednisone, 0.5 milligram/kg/d for 2 to 3 weeks. Wash ing with water, alcohol, or Tecnu  can help remove the urushiol. OTHER ALLERGIC CONTACT DERMATITIS Examples of common direct contactants affecting the face include nickel, nail polishes, toothpaste, preservatives in makeup, contact lens solutions, eyeglasses, and hair care products. Chemical-splash injuries are a com mon cause of facial irritant contact dermatitis. A thorough history is steroids. Development of an id reaction does not require discontinuation of antifungal therapy. Diagnosis is mainly clinical. Wood’s lamp examination (Table 250-4) is not helpful because more than 90% of cases of tinea capitis are due to Trichophyton species, which do not fluoresce . If necessary, diagnosis can be confirmed by a positive potassium hydroxide preparation or positive fungal culture. Scraping only the scalp rarely gives a positive potassium hydroxide examination because Trichophyton species invade the hair shaft. If fungal culture is necessary to establish or confirm the diagnosis, it usually takes 3 to 4 weeks for the culture to grow. A positive culture will help to exclude other conditions such as atopic dermatitis or seborrheic dermatitis. Topical treatment alone is not effective for tinea capitis. The cur rent first-line therapy is oral griseofulvin or terbinafine. Higher doses of griseofulvin are needed to treat Trichophyton species, which represent the most common cause of tinea capitis. Ultramicrosize griseofulvin or liquid microsize griseofulvin for those who cannot swallow pills is an effective treatment (Table 250-3). Treat for a minimum of 8 weeks, and then reevaluate to determine whether therapy should be continued. Alternatively, treatment with weight-based terbinafine dosing can be used. To decrease contagiousness and scale, patients should also wash hair with antifungal shampoo (ketoconazole 2% or selenium sulfide 2.5%) three times per week for the first 2 weeks of therapy. Other family members, especially children, and other close contacts, such as classmates at school or day care, should be evaluated. Other affected members should be treated simultaneously to prevent reinfec tion.

l shampoo (ketoconazole 2% or selenium sulfide 2.5%) three times per week for the first 2 weeks of therapy. Other family members, especially children, and other close contacts, such as classmates at school or day care, should be evaluated. Other affected members should be treated simultaneously to prevent reinfec tion. If Microsporum is diagnosed by culture, pets (cats and dogs) should be examined by a veterinarian. Follow-up with a primary care provider or dermatologist is crucial, because persistent infection may manifest only as scale and go unrecognized by caregivers. HEAD LICE (PEDICULOSIS CAPITIS) Head lice, or pediculosis capitis, is a common worldwide infestation that usually occurs in children age 3 to 11 years, but can occur at any age. It is caused by the head louse, Pediculus capitis, which is approxi mately 2 to 3 mm in size. Lice need a blood meal every 4 to 6 hours and live for 30 days while laying numerous eggs. Adult lice cannot survive more than 24 hours without a blood meal. The eggs are cemented to the hair by a proteinaceous matrix ( Figure 250-8). Transmission occurs by head-to-head contact and by brushes and combs. Head lice are limited to the scalp, behind the ears, and on the back of the neck. Intense pruritus is a feature. Diagnosis is made by identifica tion of nits and/or adult lice in the scalp hair. Nits are oval, gray-white egg capsules. If all nits are located >7 mm from the scalp surface, active infestation is unlikely. Nits and lice fluoresce with a Wood’s lamp (Table 250-4). Topical application of permethrin cream (1% or 5%) is the first-line treatment. Apply to the hair, leave on overnight, and rinse off in the morning (Table 250-3). Alternatively, pyrethrin cream or ivermectin lotion can be applied for 10 minutes and then rinsed off. Malathion 0.5% cream is another alternative and is applied to the scalp overnight, but malathion is flammable and should not be used in children less than 6 years old. Application of thick moisturizing creams to hair followed by drying with a blow dryer has also been used for resistant cases. Repeat treat ment in 7 to 10 days is recommended for the above therapeutic options. Children with head lice do not need to be removed from school, because “no-nit” policies have been shown to be excessive. Tintinalli_Sec20_p1607-1668.indd 1633 8/2/19 7:24 PM

ing with a blow dryer has also been used for resistant cases. Repeat treat ment in 7 to 10 days is recommended for the above therapeutic options. Children with head lice do not need to be removed from school, because “no-nit” policies have been shown to be excessive. Tintinalli_Sec20_p1607-1668.indd 1633 8/2/19 7:24 PM 1634 SECTION 20: Dermatology FIGURE 250-9. Poison ivy. [Photo contributed by University of North Carolina Depart ment of Dermatology.] FIGURE 250-10. Photosensitivity reaction. [Photo contributed by University of North Carolina Department of Dermatology.] TABLE 250-5 Clinical Features and Treatment of Poison Ivy or Oak, Allergic Contact Dermatitis, and Photosensitivity Condition Clinical Features Treatment Comments Poison ivy/oak Pruritic, linear, erythematous, edematous plaques with vesicles and excoriations Oral antihistamines Clobetasol 0.05%, fluocinonide 0.05%, or other high-potency topical steroids Prednisone 0.5 milligram/kg/d for 2 to 3 wk Severe cases may require oral prednisone Direct contact allergens Pruritic, scaly, erythematous papules and plaques with or without vesicles in distribu tion suggestive of exposure Identification and avoidance of allergen Mid- to high-potency topical steroids such as triamcinolone 0.1% or fluocinonide 0.05% Severe cases may require oral prednisone Photosensitivity Sunburn-like erythema (phototoxic) or pruritic erythematous papules and plaques with or without vesicles (photoallergic) in sun-exposed distribution Photoprotection Identification and avoidance of photosensitizer See Table 250-6 for list of common photosensitizing medications necessary to uncover the offending agent. Referral to a dermatologist may be necessary if the history is unrevealing. This distribution is in contrast with photosensitive eruptions in which non–sun-exposed areas, such as the upper eyelids and the upper lip, are spared (see Figure 250-10). Direct allergic contact dermatitis tends to be most prominent on the most sensitive skin, such as the eyelids. Medical treatment is of little value if the offending agent is not removed from the patient’s environment. Depending on the severity, topical or oral corticosteroids and oral antihistamines are used. Alumi num acetate (Burow’s solution, available commercially as Domeboro ) compresses can be beneficial as well. Short duration (3 to 5 days) of medium- to high-potency topical corticosteroids can be used on the face (Table 250-5). Often, extensive and severe periocular involvement requires oral prednisone. See Chapter 253, “Skin Disorders: Extremities” for further discussion of treatment of poison ivy, oak, or sumac. PHOTOSENSITIVITY Photosensitivity is suspected when exposure to ultraviolet light either exacerbates or directly causes certain conditions. Examples of the for mer include lupus erythematosus, dermatomyositis, porphyria cutanea tarda, dermatitis of niacin deficiency (pellagra), and recurrences of herpes simplex virus. Examples of the latter include exogenous photosensitivity disorders and the sunburn reaction (see Chapter 217, “Thermal Burns”). Exogenous photosensitivity disorders result from topical application or ingestion of agents that increase the sensitivity of skin to ultraviolet light. Photosensitivity disorders may be phototoxic or photoallergic. Phototoxic reactions occur quickly and appear similar to a sunburn and are thought to be due to direct damage to keratinocytes by UV radiation. Photoallergic reactions occur later and exhibit eczema-like changes in the skin with vesiculation (Figure 250-10). Photoallergic reactions are a form of delayed-type hypersensitivity reaction to an allergen formed in the skin after exposure to ultraviolet radiation. Tintinalli_Sec20_p1607-1668.indd 1634 8/2/19 7:24 PM