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adolescent dermatology: Scaly scalp
ORIGINAL ARTICLE
Diagnostic Dilemmas in Pediatric/Adolescent Dermatology: Scaly Scalp ‘/
Lisa
L. McDonald,
Michael
MD,
L. Smith,
&
MD
S
kin diseases account for a large proportion of office visits in a general pediatric practice. A survey found that 24% of patient visits had a primary or secondary skin complication and that cutaneous lesions were observed at 31% of visits (Tunnessen, 1984). In many cases the diagnosis is very apparent, whereas in others a subtle point of history or physical examination is required to make the correct diagnosis. Confirmatory tests may also be necessary. This article will present one of the most common clinical complications, the patient with a scaly scalp. The differential diagnosis for scaly scalp includes common disorders such as tinea capitis, seborrheic dermatitis, atopic dermatitis, and psoriasis. Scaly scalp may also be seen in patients with histiocytic disorders and dermatomyositis. The immunocompromised patient may have a persistent scabetic infestation that presents as scaly scalp. TINEA CAPITIS
Tinea capitis has four distinct clinical presentations: (a) the classic presentation of patchy alopecia with scaling and raised borders (“ringworm”), (b) boggy, tender, inflammatory nodules known as kerions seen in children who have a brisk immune response to the fungus, (c) clusters of follicular pustules with mild alopecia, and (d) a pattern of diffuse seborrheic-like scaling with little or no alopecia. The latter two patterns are predominantly seen with infection with Trichophyton tonswans.
Letterer-Siwe dis&se. In’all cases a.thorough history and physical examination are important first steps to successful diagnosis and treatment. J Pediatr Health Care. (1998). 12, 80-84.
80
Lisa L. McDonald is a Resident at the Department University Hospital in Nashville, Tennessee.
of Medicine
Michael L. Smith is an Assistant Professor of Medicine Nashville, Tennessee. Reprint requests: Lisa L. McDonald, Nashville, TN 37232-5227. Copyright
MD, Vanderbilt
0 1998 by the National Association
0891-5245/98/$5.00
+0
in the Division
of Dermatology
and Pediatrics at Vanderbilt University
of Pediatric
Hospital,
University
at Vanderbilt Hospital
Suite 3900, The Vanderbilt
Nurse Associates
in Clinic,
& Practitioners.
25/l/81193
March/April
1998
McDonald
& Smith
Trichophyton tonsurans has largely replaced Microsporum species as the leading cause of tinea capitis in the United States and now accounts for 90% to 95% of cases (Frieden, 1994). Since the emergence of this relatively new etiologic agent, diagnosis and treatment have become more difficult.
Diagnosis More than 90% of patients with tinea capitis are black, although this infection may occur in persons of any race (Solomon, 1985). Although most patients are between 1 and 10 years old, infection in neonates is becoming more common (Smith, 1996). The scale in tinea capitis is usually fine but may become matted. The diffuse scaling pattern is often confused with seborrhea (dandruff). However, in tinea capitis the affected area often contains short broken hairs that are easily plucked (Figure 1). Because the sporulation pattern of ‘I’. tonsu~uns is endothrix (growing inside the hair shaft), it does not fluoresce with Wood’s light examination. Direct microscopic examination of affected hair is required for diagnosis. The broken hairs can be easily plucked or teased from the scalp with a no. 15 scalpel blade or sterile toothbrush. A nonthreatening approach is the use of a moistened 4 x 4 gauze. The moist gauze is rubbed over the affected areas, and broken hairs and scales are then removed from the gauze with forceps for culture or microscopic examination. The specimen is placed on a microscope slide with a solution of potassium hydroxide (KOH), which dissolves cellular debris. This procedure may be facilitated by gentle warming of the slide. Affected hairs will show rows and chains of spores within the hair shaft. It has been recommended that a culture be obtained from all patients in whom the KOH examination is negative and from patients with partially treated or recurrent infections. In patients with unequivocally positive microscopic evidence of fungal infection, obtaining a culture may not be necessary (Smith, 1996).
Treatment An oral antifungal agent is required for treatment of tinea capitis. Griseofulvin is
JOURNAL
OF PEDIATRIC
HEALTH
CARF
FIGURE 1
Diffuse
scalp
scaling
in tinea
the oral agent of choice. Doses of 15 to 25 mg/kg per day are required for eradication of T. tonsuruns. Microsized particle preparations are an option for patients who are able to swallow tablets. Ultramicrosized particle preparations are available only in tablet form but may be better absorbed. When this form is used, 20 mg/kg per day is the recommended dose. Absorption is also improved by taking the dose with fatty foods such as ice cream (Smith, 1996). Drugs that may interact with griseofulvin include aspirin, oral contraceptives, coumarin, cyclosporine, and phenobarbital. The most common side effects of griseofulvin are headaches, nausea, and photosensitivity. Laboratory abnormalities may include leukopenia, anemia, and elevated liver enzyme levels. It has been suggested that baseline hepatic profiles and complete blood counts should be obtained, and that these laboratory tests should be repeated in the future only if symptoms suggest or if there is a history of blood dyscrasia or hepatic dysfunction (Smith, 1996). Duration of treatment is 8 to 12 weeks. Patients should be reevaluated monthly, and a repeat fungal culture should be done approximately 2 weeks after therapy is completed to document a complete cure.
capitis.
When compared with griseofulvin, ketoconazole has shown slower clearing and a poorer overall cure rate (Tanz, Herbert, & Esterly, 1988). Itraconazole has been shown to be an effective agent with minimal side effects in preliminary studies (Legendre & Esola-Maci, 1990). Topical medications, although not curative, may be useful adjunctive therapy. Shampoo containing 2.5% selenium sulfide has been shown to reduce shedding of spores when used three times weekly (Solomon, 1985).
SEBORRHEIC DERMATITIS Seborrheic dermatitis is a mild inflammatory dermatitis that often causes a thick greasy scaling of the vertex scalp known as “cradle cap” (Figure 2). Other areas that may be affected are the face and diaper area. Although these areas may also be involved in atopic dermatitis, axillary involvement and lack of pruritus help differentiate seborrheic dermatitis from atopic dermatitis (Janniger & Schwartz, 1993). This disorder is seen predominantly during the first few months of life. The borders of individual patches are often distinct, in contrast to psoriasis. Lack of broken or easily plucked hairs, fungal culture, and KOH examination distinguish seborrheic dermatitis from tinea capitis.
March/April
1998
81
ORIGINAL ARTICLE
McDonald & Smith
matitis. Impaired functioning of delta6-desaturase, the enzyme that desaturates linoleic acid to gammalinoleic acid, was the possible etiologic agent addressed in that study.
ATOPIC DERMATITIS
FIGURE
2 Thick greasy scaling of vertex scalp in seborrheic
dermatitis
(“cradle
cap”).
Diagnosis Seborrheic dermatitis is diagnosed on clinical grounds. Factors that differentiate it from other common disorders were outlined previously in this article. In the diagnosis of seborrheic dermatitis investigating the overall health of the infant is especially important. Leiner’s disease consists of a seborrheic eruption associated with failure to thrive, diarrhea, and a functional defect in the fifth component of complement. These infants are vulnerable to recurrent infections with gram-negative organisms (Glover, Atherton, & Levinsky, 1988). Letterer-Siwe disease is a subset of the histiocytic disorders. The symptoms of this rare disease include crusted lesions of the scalp, groin, trunk, and face. The presence of petechiae, fever, lymphadenopathy and hepatosplenomegaly are features of Letterer-Siwe disease not seen in uncomplicated seborrheic dermatitis (Arnold, 1990). Severe generalized seborrheic dermatitis has been reported to occur in up to 83% of patients infected with HIV. Seborrheic dermatitis in these patients is often inflammatory and markedly hyperkeratotic. Lesions may progress to nonscarring alopecia and
82
Volume I2 Number 2
postinflammatory hyperpigmentation or hypopigmentation (Janniger, 1995). In patients with severe symptoms failing to respond to conventional therapy, HIV testing may be considered.
Treatment A gentle approach to infantile seborrheic dermatitis is recommended. Because of the possibility of significant absorption and systemic effects, the use of topical corticosteroids and salicylic acid is not recommended. In mild cases of cradle cap the application of white petrolatum or mineral oil for several hours followed by a nonmedicated baby shampoo is often all that is required. If this approach is not effective, a shampoo containing tar may be used. Because seborrheic dermatitis has been associated with proliferation of Pifyrosporum ovale, a common superficial fungal inhabitant of the skin, shampoos and creams containing ketoconazole have also been used in the treatment of seborrheic dermatitis (Janniger, 1993). The treatment of seborrheic dermatitis with borage oil, an organic oil rich in gammalinoleic acid, has also been reported by Tollesson and Frithz (1993) to be an effective treatment of seborrheic der-
Atopic dermatitis is a chronic pruritic disease associated with a high incidence of allergic respiratory disease and an elevated level of serum immunoglobulin E. Presentation is usually between 2 and 6 months of age (Charlesworth, 1994). The distribution of skin lesions varies according to different age populations. In infants the face is usually the first area involved. The scalp is involved in approximately half of the cases of atopic dermatitis in the first 6 months of life (Bonifa, 1992). In older children the extensor limb surfaces are frequent sites of involvement. Pruritus with weeping or oozing of lesions is consistent with atopic dermatitis. Axillary involvement is more suggestive of seborrheic dermatitis than atopic dermatitis. The scalp lesions of psoriasis tend to be more sharply circumscribed with thick silvery scale.
Diagnosis The diagnosis of atopic dermatitis is a clinical one. As in other causes of scaly scalp, a thorough history and physical examination are important steps to the correct diagnosis. A family history of asthma, hay fever, or seasonal allergies is often seen in patients with atopic dermatitis. In infants with scalp lesions associated with atopic dermatitis, careful skin examination will often reveal patches of dry skin elsewhere or the typical extensor surface involvement. A diagnostic system proposed by Hanifin and Rajka (1980) uses a system of major and minor criteria to help define the clinical features of atopic dermatitis. The major features include pruritus, typical morphology and distribution of dermatitis, chronic or chronically relapsing dermatitis, and personal or family history of atopy. Three or more of these features plus three or more of the 23 minor criteria such as xerosis, recurrent conjunctivitis, or Dennie-Morgan lines (infraorbital folds) are required for diagnosis with this criteria.
JOURNAL OF PEDIATRIC HEALTH CARE
McDonald
& Smith
Treatment The successful treatment of atopic dermatitis requires a fourfold approach: intensive skin moisturization, relief of pruritus, diminution of inflammation, and identification and elimination of exacerbating factors. Patients with mild atopic dermatitis should be treated with frequent applications (four to six times per day) of an emollient to dampened skin. Thick nonscented creams or petrolatum are preferable to lotions. Oral antipruritic agents such as diphenhydramine or hydroxyzine are often required for control of pruritus. As with treatment of seborrheic dermatitis, topical steroids should be of low or medium strength, and their use should be minimized because of the risk of skin atrophy and systemic absorption. Identification and avoidance of environmental triggers can significantly improve symptoms. Soaps, detergents, and lotions should be unscented. The sheet forms of fabric softeners that are added to the clothes dryer should be avoided. Patients with severe atopic disease may require special testing to identify exacerbating factors. Significant airway disease requires careful management.
PSORIASIS The scalp has been identified in many studies as the most common site of involvement in childhood psoriasis (Farber, 1992). A family history of psoriasis often exists. Alongitudinal study of nine infants with psoriasis showed that most did not have a severe disease course (Farber, Mullen, Jacobs, & Nall, 1996).
Diagnosis In patients with psoriasis, thick silvery scale adheres to sharply demarcated plaques. When the scale is removed, small bleeding points can be seen (Auspitz’s sign). The scalp lesions may extend beyond the hairline onto the skin of the neck or forehead, an unusual finding in seborrheic dermatitis (Figure 3). Periumbilical, postauricular, and gluteal fold skin areas are often involved in psoriasis. Nail abnormalities such as pitting or onycholysis also suggest psoriasis. Fungal culture and KOH examination of skin scales are
JOURNAL OF PEDIATRIC HEALTH CARE
FIGURE
3 Psoriasis with extension
negative. Pruritus minent symptom.
is usually
not a pro-
of thick silvery scale beyond scalp margin.
Mild scalp involvement may be controlled by the simple measures outlined for the initial treatment of seborrheic dermatitis. The same concerns regarding systemic effects of strong topical steroids and preparations that contain salicylic acid also apply to the treatment of psoriasis. The efficacy and safety of lo- to 15minute (short contact) application of anthralin was investigated in a series of 58 patients ranging from 3 months to 10 years of age. This therapy was believed to be an effective and well-tolerated treatment for scalp psoriasis (Zvulunov, Ansfeld, & Metzken, 1994). A pilot study was performed to study the use of the topical vitamin D analog, Calcitriol, in pediatric patients. Four patients from 13 to 17 years of age were treated with marked clinical improvement and hypercalciuria or hypercalcemia (Perez, Chen, Turner, & Holick, 1995). This medication has not been studied in younger patients.
ules. In infants, lesions may be seen in a generalized distribution, whereas in older children and adolescents the eruption tends to be concentrated in the finger webs, volar wrists, axillae, and groin. Pruritus is a prominent symptom. An unusual presentation of this common infestation is that of scaly scalp. Duran, Tamayo, Orozco, and RuizMcDonald (1993) described two patients, 5 and 7 years of age, who were immunocompromised as a result of chemotherapy when they were noted to have scaling of their scalps. The physical examination was consistent with seborrheic dermatitis, and pruritus was a variable symptom. Microscopic examination of the scale revealed scabies mites and ova. These patients were treated with gammabenzene hexachloride (Lindane) with resolution of their symptoms. Scaly scalp in the setting of scabies was also reported in an adult who was using a topical corticosteroid for seborrheic dermatitis (Elmros & Homquist, 1981). It was postulated that this medication contributed to the atypical location in this patient.
SCABIES
Diagnosis
The eruption seen most commonly in scabies infestation consists of pruritic papules, burrows, and sometimes nod-
A high index of suspicion is required to diagnose atypical scabies infestations. Skin scrapings from the scalp exam-
Treatment
March/April 1998
83
I I ‘ti
ORIGINAL
ARTICLE
ined in a drop of saline solution or mineral oil should reveal the scabies mites, eggs, or feces. Pruritus in other family members or close contacts is often reported.
Treatment The treatment of choice for scabies in pediatric patients is 5% permethrin cream (Elimite). The Food and Drug Administration has approved the use of Elimite in infants as young as 2 months of age (Pruksachatkunakorn, Duarte, & Schachner, 1992). A thin layer of the cream should be applied from head to toe with careful application under the fingernails. The medication is left on for at least 8 hours. Bed linens should be changed daily during the course of treatment, because the female mite can live for up to 2 to 3 days without human contact. All laundry should be done with hot water and high dryer settings (Belkengren, 1995). Simultaneous treatment of family members and contacts is appropriate. Although one treatment is usually curative, it may be repeated in 1 week in cases of severe infestation.
DERMATOMYOSITIS Dermatomyositis is a connective tissue disease characterized by proximal muscle weakness and tenderness, periocular “heliotrope” (dusky purple-colored) cutaneous eruption, and widespread eczematous skin changes. In a retrospective survey of 17 patients, scaling of the scalp was found to be the presenting symptom in 50% of the subjects. The scaling was characterized as diffuse and was often associated with erythema, atrophy, and nonscarring alopecia. Two of the reported
84
Volume
12 Number
2
McDonald
patients were children (Kasteler & Collen, 1994). Although dermatomyositis is an uncommon disease, this possibility should be entertained in the patient with scaling of the scalp accompanied by other cutaneous findings or symptoms consistent with dermatomyositis.
CONCLUSION Scaly scalp is a common problem in the pediatric and adolescent population. The possible causes range from the commonly seen tinea capitis and seborrheic dermatitis to rare systemic diseases such as dermatomyositis and Letterer-Siwe disease. In immunocompromised patients unusual or severe presentations of seborrheic dermatitis or scabies should also be included in the differential diagnosis. In all cases a thorough history and physical examination are important first steps to successful diagnosis.
REFERENCES Arnold, H. L. (1990). Macrophage/monocyte and lymphocytic infiltrates. In H. L. Arnold, R. 8. D. Odom, & W. D. James, eds., Andrew’s Diseases ofthe Skin (pp. 831-853). Philadelphia: WB Saunders Company. Belkengren, R., & Sapala, S. (1995). Pediatric management problems. Pediatric Nursing, 21, lf& 165. Bonifazi, E. (1992). Factors influencing the localization of atopic dermatitis. Acta DermatoVenereologica (Stockholm), 176(Suppl), 24-25. Charlesworth, E. N. (1994). Practical approaches to the treatment of atopic dermatitis. A2lerg-y Proceedings, 15,269-274. Duran, C. D., Tamayo, L., Orozco, M., & RuizMaldonado, R. (1993). Scabies of the scalp mimicking seborrheic dermatitis in immunocompromised patients. Pediatric Dermatology, 20,136138. Elmros, T., & Homquist, R (1981) Infestation of scabies in the scalp area. Acta Dermuto-Venereologica (Stockholm), 61,360-362.
& Smith
Farber, E. M., Mullen, R. H., Jacobs, A. H., & Nall, L. (1996). Infantile psoriasis: a followup study. Pediatric Dermatology, 3,237-243. Farber, E. M., & Nail, L. (1992). Natural history and treatment of scalp psoriasis. Cutis, 49,396400. Frieden, I. J., & Howard, R. (1994) Tinea capitis: epidemiology, diagnosis, treatment and control. Journal of the American Academy of Dermatology, 31, %X46. Glover, M. T., Atherton D. J., & Levinsky, R. J. (1988). Syndrome of erythroderma, failure to thrive and diarrhea in infancy: A manifestation of immunodeficiency. Pediatrics, 82,66-72. Hanifin, J. M., & Rajka, G. (1980) Diagnostic features of atopic dermatitis. Acta Dermafo-Vetweologica (StockhoZm~, 92(Suppl), 44-47. Janniger, C. K. (1993). Infantile seborrheic dermatitis: An approach to cradle cap. Cutis, 51,233~2.35. Janniger, C. K., &Schwartz, R. A. (1995) Seborrheic dermatitis. American Family Physician, 52, 149. 155. Kasteler, J. S., & Callen, J. P. (1994). Scalp involvement in dermatomyositis: Often overlooked or misdiagnosed. Journal of the American Medical Associafion 272,192-194. Legendre, R., & Esola-Macre, J. (1990). Itraconazole in the treatment of tinea capitis. Journal of the American Academy of Dermatology, 23,559-560. Perez, A., Chen, T. C., Turner, A., & Holick, M. F. (1995). Pilot study of topical calcitriol (1,25dihydroxyvitamin D3) for treating psoriasis in children. Archives ofDermatology, 131,961-962. Pruksacchatkuakom, C., Duarte, A. M., & Schachner L. (1992). Scabies: How to find and stop the itch. Postgraduate Medicine, 91,263.269. Smith, M. L. (1996). Tinea capitis. Pediatric Ann&, 25,101-105. Solomon, L. M. (1985). Tinea capitis: Current concepts. Pediatric Dermatology, 2,224-237. Tanz, R. R., Hebert, A. A., & Esterly, N. B. (1988) Treating tinea cap&: Should ketwonazole replace griseofulvin? Journal of Pediatrics, 112, 987-991. Tollesson A., & Frithz, A. (1993). Borage oil, an effective new treatment for infantile seborrheic dermatitis. British Journal of Dermatology, 129,95. Tunnessen, W. (1984). A survey of skin disorders seen in pediatric general and dermatology clinics. Pediatric Dermatology, 1,219~222. Zvulunov, A., Ansfeld, A., & Metzker, A. (1994). Efficacy of short-contact therapy with dithrano1 in childhood psoriasis. Inntemafional Journal of Dermatology, 33,80&810.
JOURNAL
OF PEDIATRIC
HEALTH
CARE
Diagnostic Dilemmas in Pediatric/Adolescent Dermatology: Scaly Scalp ‘/
Lisa
L. McDonald,
Michael
MD,
L. Smith,
&
MD
S
kin diseases account for a large proportion of office visits in a general pediatric practice. A survey found that 24% of patient visits had a primary or secondary skin complication and that cutaneous lesions were observed at 31% of visits (Tunnessen, 1984). In many cases the diagnosis is very apparent, whereas in others a subtle point of history or physical examination is required to make the correct diagnosis. Confirmatory tests may also be necessary. This article will present one of the most common clinical complications, the patient with a scaly scalp. The differential diagnosis for scaly scalp includes common disorders such as tinea capitis, seborrheic dermatitis, atopic dermatitis, and psoriasis. Scaly scalp may also be seen in patients with histiocytic disorders and dermatomyositis. The immunocompromised patient may have a persistent scabetic infestation that presents as scaly scalp. TINEA CAPITIS
Tinea capitis has four distinct clinical presentations: (a) the classic presentation of patchy alopecia with scaling and raised borders (“ringworm”), (b) boggy, tender, inflammatory nodules known as kerions seen in children who have a brisk immune response to the fungus, (c) clusters of follicular pustules with mild alopecia, and (d) a pattern of diffuse seborrheic-like scaling with little or no alopecia. The latter two patterns are predominantly seen with infection with Trichophyton tonswans.
Letterer-Siwe dis&se. In’all cases a.thorough history and physical examination are important first steps to successful diagnosis and treatment. J Pediatr Health Care. (1998). 12, 80-84.
80
Lisa L. McDonald is a Resident at the Department University Hospital in Nashville, Tennessee.
of Medicine
Michael L. Smith is an Assistant Professor of Medicine Nashville, Tennessee. Reprint requests: Lisa L. McDonald, Nashville, TN 37232-5227. Copyright
MD, Vanderbilt
0 1998 by the National Association
0891-5245/98/$5.00
+0
in the Division
of Dermatology
and Pediatrics at Vanderbilt University
of Pediatric
Hospital,
University
at Vanderbilt Hospital
Suite 3900, The Vanderbilt
Nurse Associates
in Clinic,
& Practitioners.
25/l/81193
March/April
1998
McDonald
& Smith
Trichophyton tonsurans has largely replaced Microsporum species as the leading cause of tinea capitis in the United States and now accounts for 90% to 95% of cases (Frieden, 1994). Since the emergence of this relatively new etiologic agent, diagnosis and treatment have become more difficult.
Diagnosis More than 90% of patients with tinea capitis are black, although this infection may occur in persons of any race (Solomon, 1985). Although most patients are between 1 and 10 years old, infection in neonates is becoming more common (Smith, 1996). The scale in tinea capitis is usually fine but may become matted. The diffuse scaling pattern is often confused with seborrhea (dandruff). However, in tinea capitis the affected area often contains short broken hairs that are easily plucked (Figure 1). Because the sporulation pattern of ‘I’. tonsu~uns is endothrix (growing inside the hair shaft), it does not fluoresce with Wood’s light examination. Direct microscopic examination of affected hair is required for diagnosis. The broken hairs can be easily plucked or teased from the scalp with a no. 15 scalpel blade or sterile toothbrush. A nonthreatening approach is the use of a moistened 4 x 4 gauze. The moist gauze is rubbed over the affected areas, and broken hairs and scales are then removed from the gauze with forceps for culture or microscopic examination. The specimen is placed on a microscope slide with a solution of potassium hydroxide (KOH), which dissolves cellular debris. This procedure may be facilitated by gentle warming of the slide. Affected hairs will show rows and chains of spores within the hair shaft. It has been recommended that a culture be obtained from all patients in whom the KOH examination is negative and from patients with partially treated or recurrent infections. In patients with unequivocally positive microscopic evidence of fungal infection, obtaining a culture may not be necessary (Smith, 1996).
Treatment An oral antifungal agent is required for treatment of tinea capitis. Griseofulvin is
JOURNAL
OF PEDIATRIC
HEALTH
CARF
FIGURE 1
Diffuse
scalp
scaling
in tinea
the oral agent of choice. Doses of 15 to 25 mg/kg per day are required for eradication of T. tonsuruns. Microsized particle preparations are an option for patients who are able to swallow tablets. Ultramicrosized particle preparations are available only in tablet form but may be better absorbed. When this form is used, 20 mg/kg per day is the recommended dose. Absorption is also improved by taking the dose with fatty foods such as ice cream (Smith, 1996). Drugs that may interact with griseofulvin include aspirin, oral contraceptives, coumarin, cyclosporine, and phenobarbital. The most common side effects of griseofulvin are headaches, nausea, and photosensitivity. Laboratory abnormalities may include leukopenia, anemia, and elevated liver enzyme levels. It has been suggested that baseline hepatic profiles and complete blood counts should be obtained, and that these laboratory tests should be repeated in the future only if symptoms suggest or if there is a history of blood dyscrasia or hepatic dysfunction (Smith, 1996). Duration of treatment is 8 to 12 weeks. Patients should be reevaluated monthly, and a repeat fungal culture should be done approximately 2 weeks after therapy is completed to document a complete cure.
capitis.
When compared with griseofulvin, ketoconazole has shown slower clearing and a poorer overall cure rate (Tanz, Herbert, & Esterly, 1988). Itraconazole has been shown to be an effective agent with minimal side effects in preliminary studies (Legendre & Esola-Maci, 1990). Topical medications, although not curative, may be useful adjunctive therapy. Shampoo containing 2.5% selenium sulfide has been shown to reduce shedding of spores when used three times weekly (Solomon, 1985).
SEBORRHEIC DERMATITIS Seborrheic dermatitis is a mild inflammatory dermatitis that often causes a thick greasy scaling of the vertex scalp known as “cradle cap” (Figure 2). Other areas that may be affected are the face and diaper area. Although these areas may also be involved in atopic dermatitis, axillary involvement and lack of pruritus help differentiate seborrheic dermatitis from atopic dermatitis (Janniger & Schwartz, 1993). This disorder is seen predominantly during the first few months of life. The borders of individual patches are often distinct, in contrast to psoriasis. Lack of broken or easily plucked hairs, fungal culture, and KOH examination distinguish seborrheic dermatitis from tinea capitis.
March/April
1998
81
ORIGINAL ARTICLE
McDonald & Smith
matitis. Impaired functioning of delta6-desaturase, the enzyme that desaturates linoleic acid to gammalinoleic acid, was the possible etiologic agent addressed in that study.
ATOPIC DERMATITIS
FIGURE
2 Thick greasy scaling of vertex scalp in seborrheic
dermatitis
(“cradle
cap”).
Diagnosis Seborrheic dermatitis is diagnosed on clinical grounds. Factors that differentiate it from other common disorders were outlined previously in this article. In the diagnosis of seborrheic dermatitis investigating the overall health of the infant is especially important. Leiner’s disease consists of a seborrheic eruption associated with failure to thrive, diarrhea, and a functional defect in the fifth component of complement. These infants are vulnerable to recurrent infections with gram-negative organisms (Glover, Atherton, & Levinsky, 1988). Letterer-Siwe disease is a subset of the histiocytic disorders. The symptoms of this rare disease include crusted lesions of the scalp, groin, trunk, and face. The presence of petechiae, fever, lymphadenopathy and hepatosplenomegaly are features of Letterer-Siwe disease not seen in uncomplicated seborrheic dermatitis (Arnold, 1990). Severe generalized seborrheic dermatitis has been reported to occur in up to 83% of patients infected with HIV. Seborrheic dermatitis in these patients is often inflammatory and markedly hyperkeratotic. Lesions may progress to nonscarring alopecia and
82
Volume I2 Number 2
postinflammatory hyperpigmentation or hypopigmentation (Janniger, 1995). In patients with severe symptoms failing to respond to conventional therapy, HIV testing may be considered.
Treatment A gentle approach to infantile seborrheic dermatitis is recommended. Because of the possibility of significant absorption and systemic effects, the use of topical corticosteroids and salicylic acid is not recommended. In mild cases of cradle cap the application of white petrolatum or mineral oil for several hours followed by a nonmedicated baby shampoo is often all that is required. If this approach is not effective, a shampoo containing tar may be used. Because seborrheic dermatitis has been associated with proliferation of Pifyrosporum ovale, a common superficial fungal inhabitant of the skin, shampoos and creams containing ketoconazole have also been used in the treatment of seborrheic dermatitis (Janniger, 1993). The treatment of seborrheic dermatitis with borage oil, an organic oil rich in gammalinoleic acid, has also been reported by Tollesson and Frithz (1993) to be an effective treatment of seborrheic der-
Atopic dermatitis is a chronic pruritic disease associated with a high incidence of allergic respiratory disease and an elevated level of serum immunoglobulin E. Presentation is usually between 2 and 6 months of age (Charlesworth, 1994). The distribution of skin lesions varies according to different age populations. In infants the face is usually the first area involved. The scalp is involved in approximately half of the cases of atopic dermatitis in the first 6 months of life (Bonifa, 1992). In older children the extensor limb surfaces are frequent sites of involvement. Pruritus with weeping or oozing of lesions is consistent with atopic dermatitis. Axillary involvement is more suggestive of seborrheic dermatitis than atopic dermatitis. The scalp lesions of psoriasis tend to be more sharply circumscribed with thick silvery scale.
Diagnosis The diagnosis of atopic dermatitis is a clinical one. As in other causes of scaly scalp, a thorough history and physical examination are important steps to the correct diagnosis. A family history of asthma, hay fever, or seasonal allergies is often seen in patients with atopic dermatitis. In infants with scalp lesions associated with atopic dermatitis, careful skin examination will often reveal patches of dry skin elsewhere or the typical extensor surface involvement. A diagnostic system proposed by Hanifin and Rajka (1980) uses a system of major and minor criteria to help define the clinical features of atopic dermatitis. The major features include pruritus, typical morphology and distribution of dermatitis, chronic or chronically relapsing dermatitis, and personal or family history of atopy. Three or more of these features plus three or more of the 23 minor criteria such as xerosis, recurrent conjunctivitis, or Dennie-Morgan lines (infraorbital folds) are required for diagnosis with this criteria.
JOURNAL OF PEDIATRIC HEALTH CARE
McDonald
& Smith
Treatment The successful treatment of atopic dermatitis requires a fourfold approach: intensive skin moisturization, relief of pruritus, diminution of inflammation, and identification and elimination of exacerbating factors. Patients with mild atopic dermatitis should be treated with frequent applications (four to six times per day) of an emollient to dampened skin. Thick nonscented creams or petrolatum are preferable to lotions. Oral antipruritic agents such as diphenhydramine or hydroxyzine are often required for control of pruritus. As with treatment of seborrheic dermatitis, topical steroids should be of low or medium strength, and their use should be minimized because of the risk of skin atrophy and systemic absorption. Identification and avoidance of environmental triggers can significantly improve symptoms. Soaps, detergents, and lotions should be unscented. The sheet forms of fabric softeners that are added to the clothes dryer should be avoided. Patients with severe atopic disease may require special testing to identify exacerbating factors. Significant airway disease requires careful management.
PSORIASIS The scalp has been identified in many studies as the most common site of involvement in childhood psoriasis (Farber, 1992). A family history of psoriasis often exists. Alongitudinal study of nine infants with psoriasis showed that most did not have a severe disease course (Farber, Mullen, Jacobs, & Nall, 1996).
Diagnosis In patients with psoriasis, thick silvery scale adheres to sharply demarcated plaques. When the scale is removed, small bleeding points can be seen (Auspitz’s sign). The scalp lesions may extend beyond the hairline onto the skin of the neck or forehead, an unusual finding in seborrheic dermatitis (Figure 3). Periumbilical, postauricular, and gluteal fold skin areas are often involved in psoriasis. Nail abnormalities such as pitting or onycholysis also suggest psoriasis. Fungal culture and KOH examination of skin scales are
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FIGURE
3 Psoriasis with extension
negative. Pruritus minent symptom.
is usually
not a pro-
of thick silvery scale beyond scalp margin.
Mild scalp involvement may be controlled by the simple measures outlined for the initial treatment of seborrheic dermatitis. The same concerns regarding systemic effects of strong topical steroids and preparations that contain salicylic acid also apply to the treatment of psoriasis. The efficacy and safety of lo- to 15minute (short contact) application of anthralin was investigated in a series of 58 patients ranging from 3 months to 10 years of age. This therapy was believed to be an effective and well-tolerated treatment for scalp psoriasis (Zvulunov, Ansfeld, & Metzken, 1994). A pilot study was performed to study the use of the topical vitamin D analog, Calcitriol, in pediatric patients. Four patients from 13 to 17 years of age were treated with marked clinical improvement and hypercalciuria or hypercalcemia (Perez, Chen, Turner, & Holick, 1995). This medication has not been studied in younger patients.
ules. In infants, lesions may be seen in a generalized distribution, whereas in older children and adolescents the eruption tends to be concentrated in the finger webs, volar wrists, axillae, and groin. Pruritus is a prominent symptom. An unusual presentation of this common infestation is that of scaly scalp. Duran, Tamayo, Orozco, and RuizMcDonald (1993) described two patients, 5 and 7 years of age, who were immunocompromised as a result of chemotherapy when they were noted to have scaling of their scalps. The physical examination was consistent with seborrheic dermatitis, and pruritus was a variable symptom. Microscopic examination of the scale revealed scabies mites and ova. These patients were treated with gammabenzene hexachloride (Lindane) with resolution of their symptoms. Scaly scalp in the setting of scabies was also reported in an adult who was using a topical corticosteroid for seborrheic dermatitis (Elmros & Homquist, 1981). It was postulated that this medication contributed to the atypical location in this patient.
SCABIES
Diagnosis
The eruption seen most commonly in scabies infestation consists of pruritic papules, burrows, and sometimes nod-
A high index of suspicion is required to diagnose atypical scabies infestations. Skin scrapings from the scalp exam-
Treatment
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ined in a drop of saline solution or mineral oil should reveal the scabies mites, eggs, or feces. Pruritus in other family members or close contacts is often reported.
Treatment The treatment of choice for scabies in pediatric patients is 5% permethrin cream (Elimite). The Food and Drug Administration has approved the use of Elimite in infants as young as 2 months of age (Pruksachatkunakorn, Duarte, & Schachner, 1992). A thin layer of the cream should be applied from head to toe with careful application under the fingernails. The medication is left on for at least 8 hours. Bed linens should be changed daily during the course of treatment, because the female mite can live for up to 2 to 3 days without human contact. All laundry should be done with hot water and high dryer settings (Belkengren, 1995). Simultaneous treatment of family members and contacts is appropriate. Although one treatment is usually curative, it may be repeated in 1 week in cases of severe infestation.
DERMATOMYOSITIS Dermatomyositis is a connective tissue disease characterized by proximal muscle weakness and tenderness, periocular “heliotrope” (dusky purple-colored) cutaneous eruption, and widespread eczematous skin changes. In a retrospective survey of 17 patients, scaling of the scalp was found to be the presenting symptom in 50% of the subjects. The scaling was characterized as diffuse and was often associated with erythema, atrophy, and nonscarring alopecia. Two of the reported
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patients were children (Kasteler & Collen, 1994). Although dermatomyositis is an uncommon disease, this possibility should be entertained in the patient with scaling of the scalp accompanied by other cutaneous findings or symptoms consistent with dermatomyositis.
CONCLUSION Scaly scalp is a common problem in the pediatric and adolescent population. The possible causes range from the commonly seen tinea capitis and seborrheic dermatitis to rare systemic diseases such as dermatomyositis and Letterer-Siwe disease. In immunocompromised patients unusual or severe presentations of seborrheic dermatitis or scabies should also be included in the differential diagnosis. In all cases a thorough history and physical examination are important first steps to successful diagnosis.
REFERENCES Arnold, H. L. (1990). Macrophage/monocyte and lymphocytic infiltrates. In H. L. Arnold, R. 8. D. Odom, & W. D. James, eds., Andrew’s Diseases ofthe Skin (pp. 831-853). Philadelphia: WB Saunders Company. Belkengren, R., & Sapala, S. (1995). Pediatric management problems. Pediatric Nursing, 21, lf& 165. Bonifazi, E. (1992). Factors influencing the localization of atopic dermatitis. Acta DermatoVenereologica (Stockholm), 176(Suppl), 24-25. Charlesworth, E. N. (1994). Practical approaches to the treatment of atopic dermatitis. A2lerg-y Proceedings, 15,269-274. Duran, C. D., Tamayo, L., Orozco, M., & RuizMaldonado, R. (1993). Scabies of the scalp mimicking seborrheic dermatitis in immunocompromised patients. Pediatric Dermatology, 20,136138. Elmros, T., & Homquist, R (1981) Infestation of scabies in the scalp area. Acta Dermuto-Venereologica (Stockholm), 61,360-362.
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Farber, E. M., Mullen, R. H., Jacobs, A. H., & Nall, L. (1996). Infantile psoriasis: a followup study. Pediatric Dermatology, 3,237-243. Farber, E. M., & Nail, L. (1992). Natural history and treatment of scalp psoriasis. Cutis, 49,396400. Frieden, I. J., & Howard, R. (1994) Tinea capitis: epidemiology, diagnosis, treatment and control. Journal of the American Academy of Dermatology, 31, %X46. Glover, M. T., Atherton D. J., & Levinsky, R. J. (1988). Syndrome of erythroderma, failure to thrive and diarrhea in infancy: A manifestation of immunodeficiency. Pediatrics, 82,66-72. Hanifin, J. M., & Rajka, G. (1980) Diagnostic features of atopic dermatitis. Acta Dermafo-Vetweologica (StockhoZm~, 92(Suppl), 44-47. Janniger, C. K. (1993). Infantile seborrheic dermatitis: An approach to cradle cap. Cutis, 51,233~2.35. Janniger, C. K., &Schwartz, R. A. (1995) Seborrheic dermatitis. American Family Physician, 52, 149. 155. Kasteler, J. S., & Callen, J. P. (1994). Scalp involvement in dermatomyositis: Often overlooked or misdiagnosed. Journal of the American Medical Associafion 272,192-194. Legendre, R., & Esola-Macre, J. (1990). Itraconazole in the treatment of tinea capitis. Journal of the American Academy of Dermatology, 23,559-560. Perez, A., Chen, T. C., Turner, A., & Holick, M. F. (1995). Pilot study of topical calcitriol (1,25dihydroxyvitamin D3) for treating psoriasis in children. Archives ofDermatology, 131,961-962. Pruksacchatkuakom, C., Duarte, A. M., & Schachner L. (1992). Scabies: How to find and stop the itch. Postgraduate Medicine, 91,263.269. Smith, M. L. (1996). Tinea capitis. Pediatric Ann&, 25,101-105. Solomon, L. M. (1985). Tinea capitis: Current concepts. Pediatric Dermatology, 2,224-237. Tanz, R. R., Hebert, A. A., & Esterly, N. B. (1988) Treating tinea cap&: Should ketwonazole replace griseofulvin? Journal of Pediatrics, 112, 987-991. Tollesson A., & Frithz, A. (1993). Borage oil, an effective new treatment for infantile seborrheic dermatitis. British Journal of Dermatology, 129,95. Tunnessen, W. (1984). A survey of skin disorders seen in pediatric general and dermatology clinics. Pediatric Dermatology, 1,219~222. Zvulunov, A., Ansfeld, A., & Metzker, A. (1994). Efficacy of short-contact therapy with dithrano1 in childhood psoriasis. Inntemafional Journal of Dermatology, 33,80&810.
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