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Cutaneous Drug Eruptions
Skin Cancer Prevention
Skin Disease in HIV
Seborrheic dermatitis is a chronic, recurring skin disorder that has no cure.Current clinical research has implicated Malassezia yeast in the etiology. Using a clear, concise clinical picture and a thorough patient history, even the novice NP can formulate an effective treatment plan.
Seborrheic dermatitis is an acute and chronic inflammatory disorder of the sebaceous glands. It is primarily confined to the areas of the body that contain the most sebaceous glands such as the head and trunk, but it occasionally involves intertriginous areas of the body.1 The disorder is estimated to affect between 1% and 3% of the immunocompetent population.2,3 Seborrheic dermatitis causes social embarrassment and may lead to a reduction in quality of life for those afflicted by this disorder.2,4 It occurs throughout one's lifetime, and certain populations are at increased risk.
Seborrheic dermatitis follows a specific pattern throughout the life span. It is more prevalent in male than in female patients, and its incidence peaks in infants, adolescents, and adults over the age of 50.5
Infantile seborrheic dermatitis can affect as many as 70% of newborns up to 3 months of age, and usually disappears by age 1.4 It generally skips school-aged children, and reappears in adolescents due to the increased amount of skin lipids because of rising hormonal levels.6
A cross-sectional study of 300 children with scalp scaling found a 7.3% prevalence rate for seborrheic dermatitis between the ages of 2 and 10.7 It is most notably seen in the fourth through seventh decades of life. Rates as high as 31% are seen in the older adults.8
Among high-risk patients for seborrheic dermatitis are those with neurologic disorders such as parkinsonism, poststroke, epilepsy, spinal injuries, depression, nervous system trauma, and facial nerve palsy.2,3,6 The occurrence in this population appears to be related to immobility, which leads to excessive pooling of sebum that increases the growth of yeasts.9
Seborrheic dermatitis is also one of the most common dermatoses found in patients with HIV, affecting up to 85% of them.2,10 Typically, the onset of its clinical features occurs before the development of AIDS symptoms. The severity of skin manifestations correlates with the degree of clinical deterioration such as the appearance of AIDS-defining illnesses.1
Prescribing patterns and practices differ depending on the NP's area of specialty. A study analyzing outpatient visits over a several-year period in different specialties including family practice and dermatology found that family practice providers were under or incorrectly treating seborrheic dermatitis.11 Furthermore, it was noted that the evidenced-based medicine found in specialty journals had not made its way into the mainstream literature.11 Therefore, it is important for all NPs to gain an understanding of the etiology and treatment modalities of seborrheic dermatitis based on location and severity.
Malassezia yeasts were first described in the 19th century, and were named after Louis-Charles Malassez. Malassez first identified these yeasts in the dermis of patients with seborrheic dermatitis.12Malassezia yeasts are lipophilic and are of normal cutaneous flora. This genus was formally named Pityrosporum; however, as the field of molecular science advanced, it was found that the genus of Malassezia and Pityrosporum were identical. Malassezia can assume fungi and yeast presentations and different cell morphology depending on environment.12 There are seven identified species of Malassezia including M. globosa, M. restricta, M. furfur, M. sympodialis, M. slooffiae, M. obtusa, and M. pachydermatis.6,13 Recently, two new Malassezia species have been isolated: M. dermatis, found in patients with atopic dermatitis; and M. equi (tentatively named, and not yet formally described), found in the skin of healthy horses.6
It is clear that lipid-dependent Malassezia yeasts are causal factors in the development of seborrheic dermatitis, most commonly M. globosa, with its high lipase activity, and M. restricta.9 Because this disorder responds to antifungal medications and the yeast counts diminish as the condition improves, it has been strongly suggested that these yeasts play a causative role in the pathogenesis of seborrheic dermatitis.3,9
Controversy still remains on whether a definite relationship exists between the Malassezia yeast and seborrheic dermatitis. Some experts believe that Malassezia is undoubtedly involved in disease progression of seborrheic dermatitis and its response to antifungal therapy, but the specific role of the yeast in the pathology has yet to be clarified.5 Others state that an inflammatory response may be mediated by fungal metabolites (free fatty acids) that are released from sebaceous triglycerides.4 This inflammatory response gives rise to erythema, inflammation, and scaling. Other researchers suggest that an abnormal host response may be suggested by the increased incidence in the immunocompromised population.6 A study of skin biopsies from patients with seborrheic dermatitis revealed an increased number of natural killer cells and CD16 cells along with complement activation. This leads to an irritant response rather than an underlying immune deficiency.2 The etiology of seborrheic dermatitis continues to be studied, but research does show that patients with seborrheic dermatitis are thought to have higher Malasezzia counts than healthy controls.9
Seborrheic dermatitis has a widely variable clinical presentation. There are different manifestations of severity of seborrheic dermatitis. Dandruff, the mildest form, is characterized by dry, white, scaling flakes from the scalp with minimal pruritus. A moderate presentation is characterized by excessive oiliness of the skin, especially the face and scalp with distinct erythema, visible scales, and pruritus that interferes with daily activities (see Seborrheic dermatitis with scales and erythema evident along the frontal hairline). More severe seborrheic dermatitis is characterized with inflammation, intense, fiery-red erythema, coarse thick scales, and pruritus that disrupts daily activities and/or sleep.2,14
In infancy, seborrheic dermatitis presents as thick, greasy scales on the vertex of the scalp also known as cradle cap. The scales may vary in color and may appear white, off-white, or yellow, and pruritus is absent.4 Infants with generalized seborrheic dermatitis must be examined and evaluated for Leiner disease, which has coinciding concomitant diarrhea and failure to thrive.3
Clinically, in the adolescent and adult population, seborrheic dermatitis usually presents as greasy scales on irregular erythematous patches that are confined to areas of prominent sebaceous gland activity.5 These areas include the scalp, auricles, nasolabial folds, eyebrows, glabella, and the beard, moustache, and sideburn areas in males (see Retroauricular seborrheic dermatitis with erythema and scales).
Less commonly, it is found on the presternal area, male external genitalia, and the females' inframammary folds.1
The diagnosis of seborrheic dermatitis is based on clinical history. The appearance of the patient's skin can be confused with a number of other skin disorders. A negative potassium hydroxide (KOH) test will help rule out tinea and candidiasis infections.1-3,15
Many skin disorders resembling seborrheic dermatitis can be distinguishable (see Differential diagnosis of seborrheic dermatitis).
For instance, psoriasis of the scalp presents with sharply demarcated plaques and may also present with nail pitting.1,3 Tinea capitis, tinea faciei, and tinea corporis present with erythematous annular patches with active edges slightly raised, scale around the edges, and a positive KOH cytologic exam.3 Atopic dermatitis can be differentiated by the location of an erythematous papular rash. It typically appears in the antecubital and popliteal fossae.3 Rosacea can also be mistaken for seborrheic dermatitis. Rosacea appears on the face with persistent erythema, papules, tiny pustules, telangiectasia, and is nonscaling.1
Management of seborrheic dermatitis traditionally involves topical anti-inflammatory (immunomodulatory), antifungal, and keratolytic agents. NPs may prescribe a regimen based on the severity of the disorder, sites of the body affected, and previous efficacy of treatments.5
Traditionally, the treatment of seborrheic dermatitis includes topical corticosteroids. They come in different vehicles for the areas of the body affected by seborrheic dermatitis. High-potency topical corticosteroid applications have limited long-term use due to increased risk of skin atrophy, hypothalamic-pituitary-adrenal axis suppression, telangiectasia, and steroid dermatitis.2,5,16 Clobetasol 0.05% and betamethasone 0.05% are high-potency corticosteroids used in the acute phase of scalp involvement. However, they should be used only for a short duration (2 weeks) because of the adverse reaction profile. Additionally, rebound dermatitis has been noted in patients attempting to stop topical steroid therapy after long-term continued use.5 A pilot study using clobetasol 0.05% shampoo twice weekly for 5 minutes (short contact) over a 4-week period showed the same clinical efficacy as a comparative antifungal foam without the typical adverse reactions of a corticosteroid.16 Low to medium potency class corticosteroids, such as desonide 0.05% lotion and hydrocortisone 1% cream, should be used on areas other than the scalp for mild-to-moderate seborrheic dermatitis.4
One alternative to corticosteroids is a class of topical immunomodulators called calcineurin inhibitors. Pimecrolimus and tacrolimus are drugs that affect T cell activation, which is a critical step in the inflammatory process.5 In addition, these drugs have been found to have activity against Malassezia.5 These drugs may provide an important alternative to corticosteroid treatment. The most common adverse reaction is transient local burning/irritation at the site of application, often subsiding after 24 to 72 hours.
Although a causal relationship has not been established, the FDA has put a black box warning label on these medications that recommend limiting continued use not to exceed 1 year. The warning also recommends not using these products on children under the age of 2 as they can cause malignancy, especially skin and lymphoma.9 The black box warning, in part, was related to a 39 consecutive week toxicology study of monkeys given oral pimecrolimus that resulted in a dose-dependent increase in expression of an immunosuppressive-related lymphoproliferative disorder.5 The dosing and treatment regimen used in the study far exceeded current recommended guidelines. Furthermore, since the FDA warning, the safety of pimecrolimus and tacrolimus has been reviewed, and no definitive causal link has been established between the topical use and malignancy. The research into the pharmacokinetics, toxicity, and systemic immune effects supports this finding.5
Topical antifungal agents attack Malassezia and are the mainstay of therapeutic drugs in combating seborrheic dermatitis. Several antifungal treatments are available. Of these medications, the most common is ketoconazole due to its anti-inflammatory and antibacterial properties.9,17,18 The topical formulation of ketoconazole 2% is approved for seborrheic dermatitis and is available in shampoo, foam, gel, or lotion. It is used twice a week on the scalp and twice daily on the face/body for clearance, then once weekly for maintenance.1,4
Other commonly used topical antifungal agents used are ciclopirox (Loprox) 1% and 1.5%, and terbinafine solution.1 The adverse reaction profile includes irritant contact dermatitis, pruritus, and burning sensation. Minor symptoms of seborrheic dermatitis of the face may not respond as well and may require the addition of low-potency topical corticosteroids for control.1
Systemic agents that are used in severe cases are ketoconazole, terbinafine, itraconazole, and fluconazole.18,19 These agents provide relief when the disorder is refractory to topical treatment or when compliance is an issue. Itraconazole has been shown to have a lasting effect on symptoms due to its high affinity for keratinized tissues, which persists in the skin for 2 to 4 weeks following cessation of drug treatment.18 Because of this, itraconazole is dosed daily for 7 days. On the other hand, ketoconazole and terbinafine must be taken daily for 4 weeks.18
Selenium sulfide and zinc pyrithione are antifungal over-the-counter shampoo agents sold as Selsun Blue and Head & Shoulders. These are generally used to control mild symptoms.4,6 A study comparing ketoconazole 2% shampoo and prescription-strength selenium sulfide 2.5% shampoo in the treatment of moderate-to-severe dandruff showed that reductions in the score for dandruff at week 4 were 67% with selenium sulfide, 73% with ketoconazole, and 44% with placebo.4 Itching and burning sensations were more common with selenium sulfide shampoo than with ketoconazole.
Keratolytics act by causing the cornified epithelium to swell, soften, macerate, and desquamate.9 The most commonly used agents are coal tar, sulfur, and salicylic acid. To remove thick scales on the scalp, the effective combination prescription medication Derma-Smoothe/FS Scalp Oil, which contains peanut oil, mineral oil, and the corticosteroid fluocinolone acetonide 0.01%, can be applied under occlusion such as a shower cap. The patient should then gently shampoo to remove scales.1
Caution and observation must be exercised when prescribing Derma-Smoothe/FS Scalp Oil to patients with peanut allergies. These patients should tolerate the medication because it contains refined peanut oil.2,4
Special consideration must be made in treatment options with infants.20 Coal tar-based shampoos must be avoided based on the carcinogenicity of coal tar. Salicylic acid shampoos are also contraindicated in infants due to the risk of metabolic acidosis and salicylism.20
Several complementary and alternative therapies for seborrheic dermatitis show promise. Tea tree oil has been shown to have antibacterial and antifungal properties, and has been reported to decrease mild-to-moderate scalp flaking.21 A study evaluating patients with scalp seborrheic dermatitis using 5% tea tree oil demonstrated a 41% improvement, whereas patients receiving a placebo showed an 11% improvement.21 Other therapies include honey and cinnamic acid.18 A study investigating the use of crude honey on 20 patients with scalp/face/chest seborrheic dermatitis showed that gentle rubbing of honey into lesions for 2 to 3 minutes, then leaving it on for 3 hours every other day responded markedly with relief of itching and disappearance of scaling within 1 week. Skin lesions healed and disappeared completely within 2 weeks.22
Patient education is crucial because seborrheic dermatitis is a controllable condition. It is imperative to inform patients that seborrheic dermatitis is a chronic and often relapsing disorder that requires special attention for skin care. NPs should provide written instructions with easy-to-follow steps outlining care, and thoroughly discuss them with the patient.
For parents of infants, treatment teaching is conservative. Mineral oil may be used to soften scales in mild cases, before gentle removal with a soft bush. For thicker scales, it is suggested to soak the scalp overnight with a warmed mineral oil, and wash in the morning with a mild shampoo.20
Basic hair and body care should be reviewed. Patients must keep their body and hair clean by washing and shampooing daily and applying a basic body and facial moisturizer.2
Blacks have kinky hair that requires sebum to add shine, decrease combing friction, and increase manageability.23 Kinky hair naturally stands away from the scalp; therefore, excess sebum can increase styling ease.23 Black patients with seborrheic dermatitis should at minimum wash their hair twice weekly.23
If medicated shampoos are prescribed, corticosteroid applications are generally applied to affected areas once to twice daily for 5 to 10 minutes depending on severity for 2 weeks, then two times a week as needed for control. Antifungals are typically applied twice a week for clearance, then every other week for maintenance.4
Patients are encouraged to engage in outdoor recreation as UV-A and UV-B light have shown to inhibit Malassezia yeast growth during summer months, provided sun safety precautions are taken against sun damage that can lead to skin cancer, such as avoiding the midday sun.9 They should also be encouraged to get plenty of rest, control emotional stress, and avoid fatigue, as these may exacerbate flare-ups.5
Seborrheic dermatitis is a chronic and relapsing skin disorder that has several treatment modalities. The increasing amount of research has implicated Malassezia yeast as the main causative agent of seborrheic dermatitis. Ketoconazole, with its antifungal and anti-inflammatory properties, remains at the forefront of treatment.
The frequent prescribing of betamethasone by family practice providers, as opposed to the use of a low-potency corticosteroid with an antifungal such as ketoconazole, increases the need for education in primary care.11 Under-treatment and/or inappropriate treatment of seborrheic dermatitis results in frequent flares and increased office visits.
Current clinical knowledge of using evidence-based research not only assists the NP in effectively treating seborrheic dermatitis, but also improves the patient's outcome when adherence to the therapeutic regimen is followed. Often, several skin dermatoses may closely mimic seborrheic dermatitis, but by having a clear, concise clinical picture and a thorough patient history and physical, even the novice NP is better equipped to formulate an effective treatment plan.
Recalcitrant seborrheic dermatitis may arise after several treatment modalities have failed. In these cases, the NP should feel comfortable in making a prompt referral to a dermatologist.
The author acknowledges the Capstone Project for the Family Nurse Practitioner program at Southern Illinois University Edwardsville.
1. Habif T. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 5th ed. St. Louis: Mosby; 2010. [Context Link]
2. Bikowski J. Facial seborrheic dermatitis: a report on current status and therapeutic horizons. J Drugs Dermatol. 2009;8(2):125-133. http://jddonline.com/articles/dermatology/986. [Context Link]
3. Schwartz RA, Janusz CA, Janniger CK. Seborrheic dermatitis: an overview. Am Fam Physician. 2006;74(1):125-130. http://www.aafp.org/afp/2006/0701/p125.html. [Context Link]
4. Naldi L, Rebora A. Clinical practice. Seborrheic dermatitis. N Eng J Med. 2009;360(4):387-396. [Context Link]
5. Cook BA, Warshaw EM. Role of topical calcineurin inhibitors in the treatment of seborrheic dermatitis: a review of pathophysiology, safety, and efficacy. Am J Clin Dermatol 2009;10(2):103-118. [Context Link]
6. Gupta AK, Nicol KA. Seborrheic dermatitis of the scalp: etiology and treatment. J Drugs Dermatol. 2004;3(2):155-158. http://jddonline.com/articles/dermatology/286. [Context Link]
7. Williams JV, Eichenfield LF, Burke BL, Barnes-Eley M, Friedlander SF.Prevalence of scalp scaling in prepubertal children. Pediatrics. 2005;115(1):e1-e6. [Context Link]
8. Farage MA, Miller KW, Berardesca E, Maibach HI. Clinical implications of aging skin: cutaneous disorders in the elderly. Am J Clin Dermatol. 2009;10(2):73-86. doi: 10.2165/00128071-200910020-00001. [Context Link]
9. Elewski BE. Safe and effective treatment of seborrheic dermatitis. Cutis. 2009;83(6):333-338. http://cms.qhc.com/viewpdf.asp?PubCode=CT&ArticleID=2545. [Context Link]
10. Khambaty MM, Hsu SS. Dermatology of the patient with HIV. Emerg Med Clin North Am. 2010;28(2):355-368. doi:10.1016/j.emc.2010.01.001. [Context Link]
11. Gupta AK, Bluhm R, Barlow JO, Fleischer AB Jr, Feldman SR. Prescribing practices for seborrheic dermatitis vary with the physician's specialty: implications for clinical practice. J Dermatolog Treat. 2004;15(4):208-213. [Context Link]
12. Levin NA. Beyond spaghetti and meatballs: skin diseases associated with the Malassezia yeasts. Dermatol Nurs. 2009;21(1):7-13, 51. [Context Link]
13. Borgers M, Degreef H. The role of ketoconazole in seborrheic dermatitis. Cutis. 2007;80(4):359-363. http://cms.qhc.com/viewpdf.asp?PubCode=CT&ArticleID=2016. [Context Link]
14. American Academy of Dermatology. 2008. Types of eczema: seborrheic dermatitis. http://www.aad.org/public/publications/pamphlets/common_seb_dermatitis.html. [Context Link]
15. Hill M, ed. Dermatologic Nursing Essentials: A Core Curriculum. 2nd ed. New Jersey: Anthony J. Jannetti, Inc; 2003. [Context Link]
16. Reygagne P, Poncet M, Sidou F, Soto P. Clobetasol propionate shampoo 0.05% in the treatment of seborrheic dermatitis of the scalp: results of a pilot study. Cutis. 2007;79(5):397-403. http://cms.qhc.com/viewpdf.asp?PubCode=CT&ArticleID=1869. [Context Link]
17. Elewski B, Ling MR, Phillips TJ. Efficacy and safety of a new once-daily topical ketoconazole 2% gel in the treatment of seborrheic dermatitis: a phase III trial. J Drugs Dermatol. 2006;5(7):646-650. http://jddonline.com/articles/dermatology/395. [Context Link]
18. Gupta AK, Nicol K, Batra R. Role of antifungal agents in the treatment of seborrheic dermatitis. Am J Clin Dermatol. 2004;5(6):417-422. [Context Link]
19. Comert A, Bekiroglu N, Gurbuz O, Ergun T. Efficacy of oral fluconazole in the treatment of seborrheic dermatitis: a placebo-controlled study. Am J Clin Dermatol. 2007;8(4):235-238. [Context Link]
20. Elish D, Silverberg NB. Infantile seborrheic dermatitis. Cutis. 2006;77(5):297-300. [Context Link]
21. Morelli V, Calmet E, Jhingade V. Alternative therapies for common dermatologic disorders, part 1. Prim Care. 2010;37(2):269-283. [Context Link]
22. Al-Waili NS. Therapeutic and prophylactic effects of crude honey on chronic seborrheic dermatitis and dandruff [abstract]. Eur J Med Res. 2001;6(7):306-308. http://www.ncbi.nlm.nih.gov/pubmed/11485891. [Context Link]
23. Draelos ZD. Understanding African-American hair. Dermatol Nurs. 1997;9(4):227-231. [Context Link]
24. Hill Dermaceuticals, Inc. Prescribing information for Derma-Smoothe/FS. http://hillderm.com/prescribing-information/derma-smoothe-so.shtml.
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