Chapter 250: Skin Disorders: Face and Scalp

Many generalized dermatologic conditions can affect the face and scalp. This chapter discusses the acneiform eruptions, seborrheic dermatitis, erysipelas and facial cellulitis, herpes zoster, herpes simplex, tinea capitis and barbae, head lice, allergic contact dermatitis, and photosensitivity/sunburn. Impetigo and bullous impetigo are discussed in chapter 141, "Rashes in Infants and Children."

The acneiform eruptions include acne vulgaris, rosacea fulminans, dissecting cellulitis of the scalp, and acne keloidalis nuchae. Pathophysiology of these disorders is similar. Sebum secretion is increased within the sebaceous follicle by androgen stimulation. Keratin accumulates in the hair follicle as well as sebum. Host inflammation occurs, and the bacteria Propionibacterium acnes (gram-positive rods) proliferate and accumulate, intensifying inflammation. At this stage, an inflammatory papule or pustule occurs with an influx of neutrophils and helper T cells. In addition, marked inflammation can cause a nodule or cyst, and scarring can occur.

Acne fulminans is the most severe form of nodulocystic acne and may prompt patients to seek emergency medical attention. It usually affects males between the ages of 13 and 16 years. Clinical features include acute onset of suppurative cysts and nodules with ulcerations and hemorrhagic crusting on the face, chest, and back (Figure 250-1). Ulcerating lesions can lead to severe scarring. Systemic symptoms also occur and include osteolytic bone lesions of the clavicle and sternum, fever, arthralgias, myalgias, and hepatosplenomegaly. Diagnosis is clinical. Acute treatment includes administration of 40 to 60 milligrams of prednisone once daily. If the patient is already taking isotretinoin, continue the medication in conjunction with corticosteroids. Isotretinoin should not be started in the acute care setting. Refer to a dermatologist.

Rosacea fulminans, or pyoderma faciale, is an inflammatory cystic acneiform eruption on the central face of young women. The eruption may occur with or without a history of rosacea. Inflamed papules and pustules are present on the centrofacial region and can coalesce into large plaques. Diagnosis is clinical. Severe scarring can occur without treatment. Treatment is similar to that of acne fulminans—oral prednisone, 40 to 60 milligrams once daily, and referral to a dermatologist for consideration of isotretinoin.

Dissecting cellulitis of the scalp, also called perifolliculitis capitis abscedens et suffodiens, is an inflammatory and scarring disease of the scalp and neck. It occurs most commonly in young men of African descent. It consists of boggy tender nodules in multiple areas of the scalp and the neck (Figure 250-2). It is not a true cellulitis but is an intense inflammatory condition of the scalp. The nodules suppurate and develop interconnecting sinus tracts. Hair loss develops over these nodules, and permanent scarring, alopecia, and keloids can occur. If associated with acne conglobata, hidradenitis suppurativa, and pilonidal cysts, the disease is referred to as the follicular occlusion tetrad. Osteomyelitis of the skull has developed under lesions of dissecting cellulitis.¹ ED therapy includes antibacterial washes, such as chlorhexidine, which is available without prescription, and oral antibiotics, such as doxycycline and minocycline. Refer to a dermatologist. Dapsone, intralesional corticosteroids, and prednisone can be initiated at follow-up but are often unsuccessful. Treatment with isotretinoin has been successful. Surgical excision, laser treatment, and tumor necrosis factor-α blockers have also been used successfully.²

Acne keloidalis nuchae is a perifollicular inflammation (Figure 250-3) consisting of follicular-based papules and pustules on the nuchal region. The individual keloidal papules enlarge and coalesce to form keloidal plaques with an associated scarring alopecia. At the edges of the plaque, hair that is tufted often resembles hair on a "doll's head." The area may also have a bad odor, which may be the patient's primary complaint. Treatment includes topical application of clindamycin solution, topical corticosteroids such as fluocinonide or clobetasol solution, and oral doxycycline or minocycline. Refer to a dermatologist for intralesional corticosteroids.

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 141 for further discussion in infants. Adults with acquired immunodeficiency syndrome and Parkinson's disease are predisposed to severe disease. Common dandruff is a mild form of seborrheic dermatitis. The cause is not known. The disorder occurs in areas of active sebaceous glands. Malassezia yeasts and underlying inflammation are implicated³ and may explain why seborrheic dermatitis responds to both antifungal and anti-inflammatory agents. In adults, the condition is chronic and without any systemic symptoms. Pruritus can be variable but is usually mild. Dandruff may be present. Lesions can extend onto the central upper chest and intertriginous regions. Erythema and scaling are present on the vertex and parietal regions diffusely. On the face, there is symmetric involvement of the eyebrows, nasolabial folds, and retroauricular areas (Figure 250-4). The skin is sensitive to sun and heat.

Treat adults with an antidandruff shampoo containing zinc pyrithione, selenium sulfide 2.5%, salicylic acid, or tar. Ketoconazole shampoo can also be used and is available over the counter at 1% and by prescription at 2%. The shampoo should be lathered into the scalp and left on briefly before rinsing. Ketoconazole 2% cream can also be used. A topical corticosteroid such as fluocinonide solution may be applied to the scalp in severe cases. For the face, hydrocortisone 2.5% or desonide 0.05% cream or lotion applied twice per day should be the initial management. The use of higher potency topical corticosteroids on the face can lead to the development of perioral dermatitis or steroid rosacea and should be avoided. Treatment continues until the dermatitis is cleared. Re-treatment is needed for recurrences.

Erysipelas and cellulitis are infections of the dermis and subcutis, respectively. Erysipelas is most often caused by group A Streptococcus, specifically Streptococcus pyogenes. It usually affects the very young or elderly. Episodes increase in the summer. Bacterial inoculation into the skin may be caused by trauma. Cellulitis extends deeper than erysipelas, although treatment is the same. The two main causes of cellulitis in immunocompetent patients are S. pyogenes and Staphylococcus aureus.

Erysipelas and cellulitis of the face present as hot, bright red, tender, edematous, indurated plaques that can be unilateral or bilateral (Figure 250-5). The area of involvement is sharply demarcated and expands peripherally. There is no central clearing. Vesicles or bullae may be present. Systemic symptoms include fever, chills, regional lymphadenopathy, and malaise. The infection resolves with desquamation and possibly pigmentary change. In children, Haemophilus influenzae is a rare cause of erysipelas due to widespread use of the H. influenzae type b vaccine.

If unilateral, erysipelas and cellulitis must be distinguished from early herpes zoster infection. When bilateral, these diseases may be mistaken for the malar eruption of systemic lupus erythematosus. If there is eye involvement, consider periorbital cellulitis and obtain a CT scan to exclude orbital cellulitis. Bacterial cultures from the portal of entry should be done when possible for directed therapy. Anti-DNase and anti-streptolysin O titers can be done to confirm group A streptococcal infections. Skin biopsies are not usually helpful.

Unless history is suggestive of an unusual organism, direct treatment toward Staphylococcus and Streptococcus species in adults. Typically, if there is no clinical toxicity, cephalexin is initially prescribed with follow-up in 24 hours. In children, coverage should include these organisms and H. influenzae. If the patient does not respond to conventional therapy, other causes should be considered such as Moraxella species.⁴ If bullous lesions are present, suspect methicillin-resistant S. aureus infection and add appropriate antibiotics.⁵

Patients who are toxic, immunocompromised, very young or elderly, or unable to complete the outpatient antibiotic regimen require admission for IV antibiotics.

Herpes zoster, or "shingles," usually involves the thoracic dermatomes. Eruptions on the face are due to trigeminal nerve involvement, which can have serious sequelae. Herpes zoster results from reactivation of latent varicella-zoster virus. The initial eruption of varicella-zoster virus is chickenpox.

Pain or dysesthesia precedes herpes zoster by 3 to 5 days. Erythematous papules progress to clusters of vesicles with an erythematous base in a dermatomal distribution (Figure 250-6). The vesicles evolve to pustules and then crust in about 1 week. Generalized eruptions may occur in immunocompromised patients. Any of three branches of the trigeminal nerve may be involved on the face. Involvement of the ophthalmic branch (V1), especially with vesicles on the tip of the nose indicating involvement of the nasociliary branch, raises concern for keratitis and other ocular complications. Emergency ophthalmologic consultation is needed. The virus may spread to motor root ganglia, resulting in motor weakness or paralysis. Ramsay Hunt syndrome results from reactivation of varicella-zoster virus in the geniculate ganglion and may present with ear pain, vesicles in the external auditory canal, facial nerve paralysis, and vestibulocochlear dysfunction.⁶

Differential diagnosis includes other blistering disorders, such as herpes simplex infection, bullous impetigo, and contact dermatitis. The key to diagnosis is the unilateral distribution and pronounced pain in the area of involvement. Diagnosis can be confirmed by a Tzanck preparation showing multinucleated giant cells. However, Tzanck preparations have largely been replaced by polymerase chain reaction analysis of swabs taken from the base of a vesicle. Polymerase chain reaction results are generally available within 24 hours and can differentiate between varicella-zoster virus, herpes simplex 1, and herpes simplex 2.

Treatment is most effective if it is initiated within the first 72 hours of symptoms—this shortens healing time, decreases new lesion formation, and decreases the risk of postherpetic neuralgia. Treatment in an immunocompetent patient is acyclovir, 800 milligrams PO five times a day for 7 days, or valacyclovir, 1 gram PO three times a day for 7 days. In immunocompromised patients, treatment with acyclovir, 10 milligrams/kg IV every 8 hours for 7 to 10 days, is indicated. Valacyclovir should not be prescribed in patients with human immunodeficiency virus/acquired immunodeficiency syndrome due to risk of hemolytic-uremic syndrome. Local care can be provided with aluminum acetate compresses three times daily followed by antibiotic ointment. Narcotic analgesics may be needed. The zoster vaccine markedly reduces morbidity from herpes zoster and postherpetic neuralgia among older adults, reducing the burden of illness by 61.1%, the incidence of postherpetic neuralgia by 66.5%, and the incidence of herpes zoster by 51.3%.⁷

Patients with herpes zoster are contagious to individuals who have not had chickenpox. In the ED, isolation is needed for patients suspected of the disease at triage. In follow-up instructions, patients should be told to cover all open areas when visiting the physician.

Herpes simplex virus (HSV) type 1 most commonly occurs on the face. Initial infection occurs during childhood or adolescence and varies in its presentation. Many individuals experience mild symptoms, whereas a few experience a debilitating eruption. Recurrences tend to be mild and occur primarily on the lips, nose, and oral cavity.

The typical lesions of HSV are painful, grouped vesicles on an erythematous base (Figure 250-7). The primary eruption may be preceded by constitutional symptoms. The characteristic primary eruption is a gingivostomatitis with herpetic lesions on the lips and in the oral cavity. It may persist for weeks. Recurrent herpes simplex virus is typically seen 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. Ultraviolet light, fever, or local trauma can induce these eruptions.

In patients with underlying atopic dermatitis, a severe form of herpes infection can occur called eczema herpeticum in which herpes simplex virus or varicella-zoster virus can infect active atopic dermatitis lesions (see chapter 141).

Treatment for primary HSV gingivostomatitis works best when given within the first 24 hours (Table 250-1).⁸ Treatment can continue for up to 10 days if lesions have not crusted. Immunocompromised patients with severe involvement require hospitalization for IV acyclovir. Suppressive treatment with acyclovir or valacyclovir has been shown to decrease outbreaks of herpes labialis.⁸ Patients with recurrent disease should be instructed to avoid triggers, especially the sun, by using sunscreen and a lip balm with ultraviolet light protection.

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 areas of alopecia with broken-off hairs and scale at the periphery (see Figure 141-13). Occasionally, there is intense inflammation, with a boggy, tender, indurated plaque with superficial pustules and overlying alopecia. This reaction, referred to as a kerion, may result in permanent scarring and alopecia. Cervical and/or 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, and monomorphic eczematous papules and responds to topical steroids.

Diagnosis is based on 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. Wood's lamp examination (Table 250-2) is becoming less helpful, because the most common types of dermatophyte infections fail to fluoresce. More than 90% of dermatophyte cultures are due to Trichophyton, which do not fluoresce. 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 current first-line therapy is oral griseofulvin. Higher doses of griseofulvin are needed to treat Trichophyton species, which represent the most common cause of tinea capitis. Liquid microsize griseofulvin, 20 to 25 milligrams/kg/d (maximum, 1 gram/d), is an effective treatment. Ultramicrosize griseofulvin (tablets only), 10 to 15 milligrams/kg/d (maximum, 750 milligrams/d), can also be used if patients are able to swallow pills. Individuals should be treated for a minimum of 8 weeks. At that point, patients should be reevaluated to determine whether therapy should be continued. Alternative treatment is with terbinafine granules, which are given at 125 milligrams/d for patients weighing <25 kg, 187.5 milligrams/d for patients weighing 25 to 35 kg, and 250 milligrams/d for patients weighing >35 kg for 6 weeks. 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 reinfection. 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 only be manifest as scale and go unrecognized by caregivers.

Tinea barbae is a dermatophyte infection involving the beard area of the face and neck and occurs in postpubertal males. Etiology usually involves the genus Trichophyton. Predisposing factors to tinea barbae include use of topical steroids, contact with infected pets, and diabetes mellitus.⁹ Sycosis barbae is a deep folliculitis within the beard area. Perifollicular inflammation also occurs. The causative agent is usually S. aureus.

In tinea barbae, severe inflammatory plaques and follicular pustules occur in the beard area (Figure 250-8). A kerion-like lesion can develop as well as abscess and sinus tracts. Hairs are usually loosened or broken off.

In sycosis barbae, discrete pustules, usually involving S. aureus, with perifollicular inflammation are evident (Figure 250-9). 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 preparation 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 4 to 6 weeks can be used. Terbinafine can also be used, but baseline liver function studies should be drawn in adults prior to starting the medication. Supportive care is done with shaving or depilating the hair along with 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.

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 approximately 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. Adults cannot survive more than 24 hours without a blood meal. The eggs are cemented to the hair by a proteinaceous matrix (Figure 250-10). 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 identification 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.

Topical application of permethrin cream is the first-line treatment and should be repeated 1 week later to kill any surviving active nits. Apply 1% or 5% permethrin cream to the hair and leave it on overnight. The next morning, follow with a shampoo. Or, apply pyrethrin cream or ivermectin lotion for 10 minutes and then rinse out. Malathion 0.5% cream is another alternative and is applied to the scalp overnight, but malathion is flammable, so be careful in application. Do not use malathion in children <6 years old. Application of thick moisturizing creams to hair followed by drying with a blow dryer has also been used for resistant cases. Children with head lice do not need to be removed from school, because "no-nit" policies have been shown to be excessive.¹⁰

Two types of contact allergies are likely to result on the face. The first is the result of an aerosolized allergen. The second is direct physical contact that is most prominent on the sensitive parts of the face. Examples of aerosolized contactants include poison ivy and poison oak when the plant has been burned. 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 common cause of facial irritant contact dermatitis. A thorough history is necessary to uncover the offending agent. Referral to a dermatologist or allergist may be necessary if the history is unrevealing.

Clinically, allergic contact dermatitis from an aerosolized allergen presents as erythema and scale with or without vesiculation (Figure 250-11). The involvement is diffuse, with upper and lower eyelids affected. 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. 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 in medical management. Aluminum acetate (Burow 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. Often, extensive and severe periocular involvement requires oral prednisone. See chapter 253, "Skin Disorders: Extremities" for further discussion of treatment of rhus, or poison ivy or oak.

Reactions to ultraviolet light are varied. In many disorders, ultraviolet light aggravates but does not cause disease. Examples of this type of reaction include lupus erythematosus, dermatomyositis, porphyria cutanea tarda, dermatitis of niacin deficiency (pellagra), and recurrences of herpes simplex virus. Other disorders are caused by the sun, the most common of which is a sunburn reaction. A sunburn reaction is the inflammatory response to skin injury as a result of ultraviolet radiation. Individuals with fair skin, light eyes, and naturally light hair color are more susceptible to sunburns; however, darker pigmented skin can develop skin injury with sufficient ultraviolet light exposure.

Exogenous photosensitivity disorders result from topical application or ingestion of an agent that causes the skin to be more sensitive to ultraviolet light. Photosensitivity disorders may be phototoxic or photoallergic. Phototoxic drug reactions occur quickly and appear as a sunburn. Photoallergic reactions occur later and exhibit eczema-like changes in the skin with vesiculation (Figure 250-12).

Topical photosensitizers usually result in a cutaneous eruption at the sites of application. Ultraviolet exposure is necessary for the eruption to occur. Furocoumarins are the most common group of agents causing topical photoeruptions. Lime juice, fragrances, figs, celery, and parsnips contain furocoumarins. Table 250-3 lists some ingested substances that can result in a photosensitivity eruption.

The sunburn reaction begins 2 to 6 hours after exposure and peaks in 1 to 3 days. It may be minimal with little discomfort to the patient, or it may be severe with extensive blistering. Erythema and warmth in sun-exposed areas occurs. Vesiculation is equivalent to a second-degree burn.

The diagnosis of sunburn is clinical and typically self-reported by the patient. For phototoxic and photoallergic reactions, history and distribution of the eruption can assist in differentiation. Often a linear or spray pattern suggests that an externally applied substance is the culprit. Because photosensitizing medications are ingested and distributed throughout the body, the eruption can involve all sun-exposed areas. The characteristic distribution of a photosensitivity eruption is the face, posterior neck, dorsal hands, and extensor arms. Certain areas, including the creases of the eyelids, upper lip, submental anterior neck, and posterior auricular neck, are spared.

The diagnosis is based on identifying the offending agent. Photopatch testing performed by a dermatologist or allergist may be helpful in identifying the photosensitizing agent. If the diagnosis is unclear, other photosensitivity disorders, such as lupus erythematosus, dermatomyositis, and polymorphous light eruption, should be excluded.

The most important part of treatment of sunburn and photosensitivity is prevention. Avoid the midday sun, apply sunscreen liberally and frequently (ultraviolet A and B protection with sun protection factor of at least 30), wear protective clothing, and seek shade. Manufactured clothing with a sun protection factor of 50+ is available and helpful. Sunburns can be treated symptomatically with nonsteroidal anti-inflammatory drugs and tepid baths and by application of topical antibiotics to areas of vesiculation. Emollients may be soothing but will not prevent eventual exfoliation. Individuals should also be advised to avoid the sun until the eruption resolves.

In cases of photosensitivity, discontinue the causative agent. Initial management includes topical corticosteroids and management similar to a sunburn reaction. The patient should avoid the sun until the eruption has cleared completely.