1: Scalp dermatitis

Reid A. Waldman, Jane M. Grant-Kels

Abstract:

Scalp rashes are common and bothersome to patients. Scalp rashes have a broad differential diagnosis; accurate diagnosis is important because these conditions may lead to permanent hair loss. Additionally, several infections localize to the scalp and can flare if they are inappropriately treated with topical corticosteroids. This chapter will review scalp psoriasis, seborrheic dermatitis, lichen planopilaris, head lice, allergic contact dermatitis of the scalp, tinea capitis, and actinic keratosis, as well as their mimickers.

Key terms:

psoriasis

seborrheic dermatitis

lichen planopilaris

head lice

pediculosis capitis

allergic contact dermatitis

tinea capitis

actinic keratosis

Chapter outline

Scalp Psoriasis
Warning Signs/Common Pitfalls
- Counseling
Seborrheic Dermatitis—Scalp
Warning Signs/Common Pitfalls
- - In Adults
  - In Children
- Patient Information
  - For Adults
  - For Children With Cradle Cap
Lichen Planopilaris
Counseling
Head Lice
Allergic Contact Dermatitis of the Scalp
Counseling
Tinea Capitis
Actinic Keratosis
Counseling
Discoid Lupus Erythematosus

Scalp psoriasis

Clinical features

Scalp psoriasis is characterized by the presence of well-demarcated erythematous plaques with overlying white scale of variable thickness affecting the occipital scalp more commonly than the remainder of the scalp.

• The scalp may be the only area of the body affected by plaque psoriasis.
• More commonly, scalp psoriasis occurs concomitantly with psoriasis elsewhere.
• The main differential diagnosis for isolated scalp psoriasis is seborrheic dermatitis.

• In cases where scalp psoriasis and seborrheic dermatitis cannot be readily distinguished from one another, the rash is referred to as “sebopsoriasis.”
• Psoriasis can be differentiated from seborrheic dermatitis based on:

• The location of scalp involvement—Isolated occipital scalp involvement in subtler cases of scalp psoriasis versus encroachment onto the forehead and temples in seborrheic dermatitis;

• The presence of characteristic skin lesions elsewhere—The elbows, gluteal cleft, knees, nails, palms, soles, and trunk for psoriasis or the nasolabial folds, glabella, or chest for seborrheic dermatitis;

• Plaque and scale appearance—Psoriasis has more sharply circumscribed, redder-looking plaques and whiter-looking scale, whereas seborrheic dermatitis has thinner, pinker-looking plaques and greasier-looking scale;

• Degree of treatment responsiveness—Classically psoriasis is less treatment responsive than seborrheic dermatitis;

• Family history and past medical history of psoriasis.
• Differentiation of psoriasis from seborrheic dermatitis is important because:

• Antifungals are a mainstay of treatment in seborrheic dermatitis, but they are much less effective in psoriasis.

• Refractory cases of psoriasis benefit from the use of phototherapy or systemic therapy, whereas these are not recommended in seborrheic dermatitis.

• Psoriasis has comorbidities such as psoriatic arthritis and the metabolic syndrome that require prompt recognition and management, whereas seborrheic dermatitis does not.
• Uncontrolled, severe scalp psoriasis can present with a pityriasis amiantacea-like appearance where a patient’s hair is engulfed by scale; however, scalp psoriasis in and of itself does not result in alopecia. The presence of scaly alopecic plaques should prompt investigation for other causes of an itchy scalp rash, including tinea capitis.
• Scalp psoriasis often coexists with ear canal psoriasis, which is typically very pruritic and involves its own separate management. Nevertheless, ear involvement with pruritus can also be seen in seborrheic dermatitis and therefore is not always helpful to differentiate the two diseases.

Work-up

• A total-body skin examination should be performed to identify other areas of the body affected by psoriasis. Patients frequently do not realize that their scalp rash is related to their body rash.
• All patients with psoriasis require screening for psoriatic arthritis (PsA) at every single visit because a delay in diagnosis of PsA can result in irreparable joint damage.
• Patients with longstanding psoriasis that has suddenly worsened and patients with acute-onset psoriasis should have their medication list reviewed for possible exacerbating triggers (see Chapter 3).
• Routine evaluation for possible systemic triggers of psoriasis (e.g., HIV, streptococcal pharyngitis) is not indicated in the absence of clinical suspicion.
• Routine histologic confirmation is not indicated except in atypical-appearing cases or in cases that fail to respond to treatment as expected.
• Examination of hairs with potassium hydroxide (KOH) and/or submitted for culture should be considered to rule out tinea capitis if possible.

Initial steps in management

General management comments

• Noncompliance with topical therapies is common among patients with scalp dermatoses because of the poor cosmesis of these products.
• There is no cure for psoriasis. Patients will have flare-ups if they discontinue therapy. The goal of therapy is symptom management. It is important to convey this to patients. The course is usually chronic, with a history of waxing and waning.
• Class I, II, and III topical corticosteroids are the mainstay of treatment for scalp psoriasis and are clinically superior and better tolerated than topical vitamin D analogue monotherapy.
• In cases refractory to Class I topical corticosteroids, combination topical corticosteroid vitamin D analogue products can be considered because they have demonstrated superiority over topical corticosteroid monotherapy.

• Combination products are frequently prohibitively expensive and often require prior authorization by insurance companies.
• Topical vitamin D analogue monotherapy can be used in mild cases where patients prefer to avoid topical steroid use.
• Nowhere is topical medication vehicle more important than on the scalp. Compliance is highly affected by vehicle type. Suitable vehicles for the scalp (in order of suitability) include solution, spray, foam, oil, lotion, and shampoo. Often, insurance formularies dictate which vehicle type is available to the patient. In cases where multiple vehicle types are available, deference to patient preference is reasonable.
• If shampoos are going to be prescribed, then patients must be counseled that these must be left in contact with the scalp for around 15 minutes before rinsing. In the authors’ experience, compliance with scalp shampoos is variable.
• If scalp oils are going to be prescribed, then occluding the oil under a shower cap can be considered because scalp oils are frequently very messy. Importantly, children should never be encouraged to use oils under shower cap occlusion because of the risk of shower cap-induced asphyxiation. Additionally, scalp oils should not be used in patients with peanut allergies because the oil vehicle is peanut oil.

Recommended initial regimen

• Clobetasol propionate 0.05% scalp solution, spray, or foam (depending on patient preference and insurance formulary) daily until clear followed by PRN use. Care should be taken to avoid exposure of facial skin to this medication. Patients should be counseled about signs of steroid-related atrophy; however, realistically, this almost never occurs on the scalp.
• A nonexhaustive list of alternatives to clobetasol propionate include in decreasing order of potency: halobetasol propionate 0.05% lotion or foam, betamethasone dipropionate 0.05% lotion or spray, fluocinonide 0.05% topical solution, betamethasone valerate 0.12% foam, fluocinolone 0.025% oil or solution.

What to do if there is a partial but inadequate response after a 4-week trial of potent topical corticosteroid monotherapy:

• Either switch to a combination topical corticosteroid vitamin D analogue product (e.g., betamethasone dipropionate-calcipotriene 0.005%-0.064% scalp solution daily) or add a topical vitamin D analogue product (e.g., calcipotriene 0.005% scalp solution) to the existing corticosteroid regimen.
• Almost all patients who are compliant with therapy should become clear or almost clear with combination therapy.
• In the experience of the authors, compliance is superior for combination products; however, they are often not covered by insurance without prior authorization.

What to do if the response continues to be inadequate:

• Reconsider the diagnosis. If you are not confident in the diagnosis of psoriasis, it is reasonable to consider a punch biopsy of an affected area at this time. Punch biopsies on the scalp are technically more difficult than punch biopsies elsewhere and should only be performed by experienced practitioners. Additionally, the pathology requisition form for a punch biopsy from the scalp must specify that the biopsy is from the scalp because horizontal sectioning is often performed.
• Because scarring alopecia can result from some inflammatory scalp dermatoses, referral to a dermatologist is indicated at this point in time unless one is not available.
• If you are confident that the patient has psoriasis and it is refractory to a combination topical corticosteroid–vitamin D analogue product, then next steps in therapy include intralesional corticosteroid injections, phototherapy (including narrowband ultraviolet B [UVB] and even localized psoralen and ultraviolet A [PUVA] and xenon chloride laser), oral immunosuppressive medications (e.g., methotrexate), acitretin, and biologic medications (reserved for severe scalp psoriasis or for patients with psoriasis elsewhere).

Other treatment options

• Topical coal tar preparations, salicylic acid, glycolic acid, and anthralin are all reported treatments for scalp psoriasis. Data supporting the use of these agents are much weaker than data supporting the use of topical corticosteroids and vitamin D analogues. These agents should only be considered as adjuncts to combination topical corticosteroid vitamin D analogue therapy in patients who fail combination therapy and who are uninterested in phototherapy or systemic therapy for treatment of their psoriasis. The authors’ preferential use of these treatments is listed in order of decreasing preference as follows: glycolic acid > salicylic acid > coal tar > anthralin.

Warning signs/common pitfalls

• Patients with psoriasis should be screened at regular intervals for psoriatic arthritis. If any clinical suspicion for psoriatic arthritis exists, then the patient should be referred urgently to a rheumatologist. There are validated screening tools that can easily be implemented in the clinical setting.
• Occasionally, discoid lupus erythematosus can mimic scalp psoriasis. Discoid lupus erythematosus can be differentiated from psoriasis based on its focal, annular nature; the more violaceous hue of its plaques; and its different scale quality; however, this is not always obvious. Promptly recognizing and treating discoid lupus is essential because it is a form of scarring alopecia that causes irreversible hair loss. It is also occasionally associated with systemic lupus erythematosus (around 5% of the time for scalp-only disease).
• Tinea capitis must be excluded if suspected with KOH examination or cultures.
• Never treat scalp psoriasis with systemic corticosteroids. This will almost always trigger a flare once corticosteroids are tapered. This is a chronic disease that requires chronic management.

Counseling

Psoriasis is a rash that results from your genetics (family history) and immune system causing inflammation in your skin. Psoriasis is a chronic disease that tends to wax and wane. It is incurable, meaning that it lasts for years. Treatments for psoriasis are directed at decreasing inflammation in the skin. The goal of treating psoriasis is to manage symptoms.

Importantly, some people with psoriasis also develop a condition called psoriatic arthritis where they experience painful swelling of the joints and stiffness in the joints when they wake up in the morning that lasts for hours. If you think you may have psoriatic arthritis, it is important that you let us know because psoriatic arthritis can irreversibly damage your joints if it is not treated.

Some patients with psoriasis are at risk for metabolic syndrome (diabetes, obesity, cardiovascular disease, etc.). Therefore weight control and exercise are important to include in your daily routine.

I have prescribed you a topical corticosteroid. You should apply this to your scalp every day while you have the rash. When no rash is present, you do not need to use this medication. It is okay to resume use of the medication when the rash comes back. The major side effect of this medication is that it can thin the skin and cause the blood vessels in the skin to dilate and become visible. This typically does not occur on the scalp but may occur if you use the medication more frequently than instructed or if you apply this medicine to other places on your body, such as your face.

Seborrheic dermatitis—scalp

Clinical features

Seborrheic dermatitis is characterized by the presence of poorly circumscribed, thin, pink plaques with an overlying greasy-looking scale that appear on the seborrheic areas of the body. Seborrheic dermatitis is on a continuum with dandruff because both impact seborrheic areas of the body. Dandruff, however, is limited to the scalp and presents with pruritus and scaling but not erythema. Seborrheic dermatitis can impact other seborrheic areas in addition to the scalp and demonstrates itching, scaling, and evidence of inflammation.

• In adults, seborrheic dermatitis most commonly involves the scalp and is the most common cause of scalp itch.

• Seborrheic dermatitis may also affect other so-called seborrheic areas, such as the eyebrows, glabella, nasolabial folds, retroauricular area, and chest.
• When seborrheic dermatitis affects the scalp of an infant, it is called “cradle cap.”

• Infantile seborrheic dermatitis also commonly affects the diaper area, axillae, and retroauricular area.
• Uncontrolled, severe seborrheic dermatitis can present with a pityriasis amiantacea-like appearance where a patient’s hair is engulfed by scale; however, seborrheic dermatitis in and of itself does not result in alopecia.
• Seborrheic dermatitis commonly develops in immunosuppressed individuals and in individuals with Parkinson disease. In rare cases, severe seborrheic dermatitis can be the presenting sign of HIV.

The etiology of seborrheic dermatitis is multifactorial and is likely because of a normal body yeast called Malassezia. If the immune system has a somewhat irregular response to Malassezia, it may result in this inflammatory condition. The disease is very common, impacting 1% to 5% of the population and including all races and sexes.

Differential diagnosis

• In adults, the main differential diagnosis for seborrheic dermatitis is scalp psoriasis (Fig. 2.8). Rarely, tinea capitis can be mistaken for seborrheic dermatitis (Fig. 2.9).
• Seborrheic dermatitis can be differentiated from scalp psoriasis based on the following characteristics:

• The location of scalp involvement—Plaques of seborrheic dermatitis are ill defined and can affect anywhere in the scalp. Psoriasis plaques often develop near the hairline in the frontotemporal scalp and may extend onto the forehead and temples. In contradistinction, milder cases of scalp psoriasis are localized to the occipital scalp.

• Presence of characteristic skin lesions elsewhere—As previously mentioned, seborrheic dermatitis often also affects other seborrheic areas, whereas psoriatic plaques most frequently develop on extensor surfaces.

• Plaque and scale appearance—Plaques of seborrheic dermatitis are thin, ill defined, and pink and have a greasy-looking scale, whereas psoriatic plaques are thicker, well circumscribed, and covered in white, micaceous scales.

• Response to antifungals—Seborrheic dermatitis responds to azole antifungals within 4 weeks of treatment; psoriasis, meanwhile, will not typically respond as rapidly to antifungals and even when it does, it tends to recur and to be more resistant.

Tinea capitis can be distinguished from seborrheic dermatitis because tinea capitis usually presents as a solitary, discrete plaque, has overlying alopecia, and predominantly has peripheral scaling rather than diffuse scaling. If there is concern that the patient may have tinea capitis, a KOH examination and fungal culture can distinguish tinea capitis from seborrheic dermatitis.

Testing and work-up

• In both adults and infants, a total-body skin examination, with a focused examination of seborrheic areas (such as the eyebrows, beard, nasolabial folds, retroauricular area, and central chest) should be performed to identify all areas of the body that may be affected by seborrheic dermatitis.
• Adults who present with subacute onset severe seborrheic dermatitis affecting the face and chest should be screened for HIV unless another obvious trigger for development of seborrheic dermatitis has been identified (e.g., organ transplant immunosuppression, Parkinson disease; Fig. 2.10).
• Seborrheic dermatitis is generally a clinical diagnosis; rarely is a biopsy required to make a diagnosis of seborrheic dermatitis.

How to manage seborrheic dermatitis

Management of seborrheic dermatitis is divided into two phases: (1) an intensive initial treatment phase, which is followed by a (2) less intensive maintenance phase. There is no cure for seborrheic dermatitis. The course is chronic with waxing and waning. Failure to emphasize the importance of using a maintenance therapy virtually guarantees disease recurrence and patient dissatisfaction.

• After an initial period of treatment responsiveness, some patients can become treatment resistant and require a change in therapy. This most frequently is seen in patients receiving antifungals.
• In elderly patients, especially institutionalized elderly patients who require assistance when bathing, a common cause of treatment failure is that these patients are only showered once or twice weekly. Daily bathing is both a treatment for seborrheic dermatitis and is required for medicated shampoos to be effective. Tailoring therapy based on patient bathing habits is essential to success.
• In all infants with cradle cap and in adults with substantial scaling, emollients (e.g., plain petroleum jelly or mineral oil) are necessary for loosening scale. Gentle debridement with a hairbrush is also helpful.
• Treatment options are divided into antifungal and antiinflammatory approaches:

• Antifungals

• Azoles (e.g., ketoconazole, clotrimazole, etc.) – The initial treatment of all adults with seborrheic dermatitis should include a topical azole. For scalp disease, shampoos are most commonly prescribed. Ketoconazole is the only prescription azole shampoo available in the United States. It is generally used 2 to 3 times a week. On alternate days, other medicated shampoos are recommended that contain selenium, zinc, salicylic acid, etc. Other azole shampoos (miconazole and climbazole) are available over the counter but do not have the same degree of clinical efficacy as ketoconazole.

• Ciclopirox—Ciclopirox is a reasonable second-line antifungal. Although it is equally as effective as topical azoles, it is more likely to cause scalp irritation and is typically more expensive. In patients who are bathed infrequently, ciclopirox shampoo is preferential to ketoconazole because it requires less frequent applications (1–2 times a week has been demonstrated to be effective).

• Selenium sulfide (active ingredient in Selsun Blue)

• Zinc pyrithione (active ingredient in Head and Shoulders)

• Antiinflammatory drugs
• Topical corticosteroids—These are equally as effective and possibly more effective than antifungals, but they are more likely to cause cutaneous adverse effects and more likely to cause early disease rebound after discontinuation. Topical corticosteroids should be added in cases that do not respond appropriately to topical antifungals and should be used preferentially in patients with scalp disease who are bathed infrequently. These drugs should be used with caution in cases of cradle cap. Topical steroid scalp preparations can be prescribed as solutions, foams, and even shampoos.
• Topical calcineurin inhibitors—These are equally effective to antifungals and topical corticosteroids. Topical calcineurin inhibitors are only commercially available as ointments and creams, making them less cosmetically acceptable for scalp dermatitis. There is no topical calcineurin inhibitor formulation that is designed for scalp disease.
• Crisaborole—There is limited experience with crisaborole at this point. It is only available as an ointment and therefore is not ideal for scalp disease; it is also often not cosmetically desirable for facial diseases.
• Promiseb—There is not one specific active ingredient in Promiseb. It is a combination of antiinflammatory agents. It is often very expensive but can be considered in refractory cases.

Recommended initial treatment regimen in adults

• Initial treatment phase (first 4 weeks of treatment)—Ketoconazole 2% shampoo 2 to 3 times weekly for 4 weeks. The shampoo should be kept in contact with the scalp for 5 to 15 minutes before rinsing. On all other days of the week, over-the-counter (OTC) antifungal shampoos containing either zinc pyrithione or selenium sulfide should be used. Salicylic acid shampoos (such as T-Sal) are also helpful for debridement.
• Maintenance phase (after initial treatment phase)—Ketoconazole 2% shampoo once weekly indefinitely. The shampoo should be kept in contact with the scalp for 5 to 15 minutes before rinsing. On all other days of the week, OTC antifungal shampoos containing either zinc pyrithione or selenium sulfide should be used.
• Patients with severe scaling should also be encouraged to apply mineral oil or another emollient to their scalp nightly. In adults, a shower cap can be used to keep the oil from creating a mess on the patient’s bedding. In the morning, a comb can be used to gently debride the now-loosened scale before shampooing.
• Derma-Smooth/FS (fluocinolone acetonide in a peanut oil base) can be prescribed for overnight application. Most patients with a known peanut allergy tolerate this topical therapeutic. Skin testing has shown no immediate (15-min) or delayed (72-h) skin test reactivity, suggesting that refined peanut oil–containing oils are safe to use, even in patients with a history of sensitivity to peanuts. Even the use of this product in atopic children with a history of peanut allergy was found to be safe.

What to do if there is a partial but inadequate response after a 4-week trial of topical azole monotherapy:

• Steroid solutions and foams can be applied to the scalp to reduce inflammation. This should only be done as needed in the acute phase to avoid secondary side effects from the topical steroids because the scalp skin is highly vascularized and not particularly thick, making it susceptible both to absorption of medications systemically and local atrophy.
• Add or switch to a topical corticosteroid (e.g., clobetasol dipropionate 0.05% solution nightly or fluocinonide acetate 0.05% solution nightly). In cases with severe scaling, fluocinolone acetonide 0.01% scalp oil with or without shower cap occlusion nightly is preferred because the fluocinolone scalp oil serves both as an antiinflammatory and emollient. A much milder topical steroid, topical 1% hydrocortisone scalp solution, is also available over the counter; patients should be warned to use even this mild topical steroid only intermittently.

What to do if response to azole monotherapy wanes over time:

• Initial treatment phase (first 4 weeks of treatment)—Switch to ciclopirox 1% shampoo twice weekly for 4 weeks. The shampoo should be kept in contact with the scalp for 5 to 15 minutes before rinsing. On all other days of the week, OTC antifungal shampoos containing either zinc pyrithione or selenium sulfide should be used.
• Maintenance phase (after initial treatment phase)—Ciclopirox 1% shampoo once weekly indefinitely. The shampoo should be kept in contact with the scalp for 5 to 15 minutes before rinsing. On all other days of the week, OTC antifungal shampoos containing either zinc pyrithione or selenium sulfide should be used.