Alopecia in childhood is a source of high concern, frustration, and anxiety. Delineating types of alopecia and those that are chronic or potentially related to underlying medical problems is important. There are 5 common types of hair loss in children: alopecia related to tinea capitis, alopecia areata spectrum/autoimmune alopecia, traction alopecia, telogen effluvium, and trichotillomania/trichotillosis. Hair-cycle anomalies including loose anagen syndrome can lead to sparse-appearing hair. Rarer reasons for alopecia in children include pressure-induced alopecia, alopecia related to nutritional deficiency or toxic ingestion, and androgenetic alopecia. Congenital lesions should be considered for areas of localized alopecia occurring at birth.
Key points
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Alopecia in childhood is not uncommon.
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Tinea capitis is the most common cause of loss of hair in childhood and should be excluded in an evaluation.
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Clues to the type of hair loss include evidence of scale, hair breakage, and location of the hair loss.
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The age of the child and whether there are other comorbidities are additional clues to diagnosis.
Introduction
Overview
The ideal evaluation of a child with scalp hair loss should include a full history and physical examination with a detailed evaluation of the hair and scalp. In the pediatric office, it is usually possible to send dermatophyte screens or fungal cultures to rule out tinea as a source of alopecia, perform a hair pull test to see if hair is actively shedding, and assess overall pattern of hair loss and scalp health. A thorough history must include whether hair was never present/sparse after birth or whether hair was later lost in a localized manner or shed more diffusely. The history should also include diet and nutrition and underlying medical problems, with special attention to autoimmune disease. If medical providers suspect that alopecia is congenital, a detailed evaluation/history of teeth and tooth eruption, nails, skin, and the ability to sweat is needed. Congenital alopecia can be associated with general abnormalities of the ectoderm referred to as the broad category of diseases known as ectodermal dysplasias . Patients with ectodermal dysplasias will have long-term problems with dentition, hair, nails, sometimes heat regulation, and occasionally bones. In most cases, alopecia occurs after the development of full scalp hair and is related to infection, an autoimmune process, or trauma/traction.
Pathophysiology
All human hairs regularly cycle through anagen, the growth phase; telogen, the resting phase; and catagen, the transition phase. The first anagen phase starts at about 18 to 20 weeks of gestation, with the first normal shedding period occurring sometime between 4 and 8 months of age. This period can occur as late as 1 year of age. This hair loss is the typical pattern hair loss seen in infants at their well visits. The occiput of the scalp differs in that it has expected telogen shedding that occurs earlier at about 2 to 3 months of age and accounts for the bald spot seen in the occiput of most infants around that time. Pressure and rubbing from sleeping on the back accentuate this hair loss. The number of hair follicles during the first 2 years does not change, but there is a transition from vellus hairs to terminal hairs. Because terminal hairs are larger in caliber, the density of hair seems to increase. Hair darkens with age in most cases.
Introduction
Overview
The ideal evaluation of a child with scalp hair loss should include a full history and physical examination with a detailed evaluation of the hair and scalp. In the pediatric office, it is usually possible to send dermatophyte screens or fungal cultures to rule out tinea as a source of alopecia, perform a hair pull test to see if hair is actively shedding, and assess overall pattern of hair loss and scalp health. A thorough history must include whether hair was never present/sparse after birth or whether hair was later lost in a localized manner or shed more diffusely. The history should also include diet and nutrition and underlying medical problems, with special attention to autoimmune disease. If medical providers suspect that alopecia is congenital, a detailed evaluation/history of teeth and tooth eruption, nails, skin, and the ability to sweat is needed. Congenital alopecia can be associated with general abnormalities of the ectoderm referred to as the broad category of diseases known as ectodermal dysplasias . Patients with ectodermal dysplasias will have long-term problems with dentition, hair, nails, sometimes heat regulation, and occasionally bones. In most cases, alopecia occurs after the development of full scalp hair and is related to infection, an autoimmune process, or trauma/traction.
Pathophysiology
All human hairs regularly cycle through anagen, the growth phase; telogen, the resting phase; and catagen, the transition phase. The first anagen phase starts at about 18 to 20 weeks of gestation, with the first normal shedding period occurring sometime between 4 and 8 months of age. This period can occur as late as 1 year of age. This hair loss is the typical pattern hair loss seen in infants at their well visits. The occiput of the scalp differs in that it has expected telogen shedding that occurs earlier at about 2 to 3 months of age and accounts for the bald spot seen in the occiput of most infants around that time. Pressure and rubbing from sleeping on the back accentuate this hair loss. The number of hair follicles during the first 2 years does not change, but there is a transition from vellus hairs to terminal hairs. Because terminal hairs are larger in caliber, the density of hair seems to increase. Hair darkens with age in most cases.
The history and physical examination
The most important question in the history is whether the hair loss is acute or gradual. Did the hair loss occur over months or within days? Alopecia areata (AA) will often occur with very rapid localized loss over days, whereas traction alopecia will occur slowly overtime with gradual thinning at the hairline or wherever there is tension on the hair. Telogen effluvium will start rapidly, but then the shedding stabilizes; there is increased but steady shedding over weeks to months. This type of shedding decreases with time until it shifts back to the patient’s normal hair-shedding pattern.
Physical examination should evaluate all areas of the scalp in a systematic fashion. The scalp should be evaluated for localized or diffuse hair loss. The location of loss should be noted. Locations include periphery, occiput, vertex, temples, and parietal scalp. An evaluation should be performed for scale and redness of the scalp, which are signs of inflammation. In all cases, if redness or scale is present, tinea capitis should be ruled out. Scale can also be a sign of other inflammatory disorders like psoriasis, cutaneous lupus, eczema, or seborrheic dermatitis, which can lead to hair loss because of associated scale and inflammation. Clues to these other inflammatory disorders include cutaneous signs of inflammation in other parts of the body; previous atopic disease; or, in the case of cutaneous lupus, scarring on the scalp and a negative dermatophyte screen.
A hair pull test is a simple tool all pediatricians can use because it requires no special instruments. The hair pull test involves gently pulling 20 to 60 hairs between the thumb and forefinger in multiple locations of the scalp. Anagen or growing hairs should remain rooted in place, whereas hairs in the telogen phase should come out easily. One can roughly estimate the number of hairs in telogen. If 2 hairs come out on a hair pull of approximately 20 hairs, telogen is about 10%. Normal telogen is between 10% and 20%. It is important to ask patients about when they last washed their hair. Ideally, it is the day before the examination. If it was the same day, you should expect fewer hairs to be shed. If it was 1 week before, you should expect more telogen hairs to be shed. Hairs from the pull test can be mounted and reviewed under microscope for hair shaft abnormalities as well as the phase of the cycle of the hair when practical. This practice is rare outside of specialist offices. A full skin examination including an evaluation of eyelashes, eyebrows, and nails should be completed. Evaluation of cervical chain lymphadenopathy should be performed and is often present in tinea capitis but can also be seen in other inflammatory disorders of the scalp, notably atopic dermatitis.
The history should include questions about general health; illness in the last 4 to 6 months, including illness with high fevers; and other stressors, including surgeries, new medications, and changes in school or home life. A good review of systems should be performed to look for concerns for hypothyroidism, anemia, diabetes, and other autoimmune disease. In children, this would include but is not limited to new constipation, fatigue, and increased nighttime urination. A family history of alopecia and autoimmune disease should also reviewed. Potential contacts at home or at school with alopecia should also be reviewed if there is concern for tinea capitis. Diet and nutrition should be reviewed, and risks for toxic exposures like lead should also be elicited.
Review of common alopecias
Tinea Capitis
Overview
Tinea capitis is a dermatophyte infection that primarily affects children ( Fig. 1 , Table 1 ). Adult cases may be seen in the setting of immunosuppression.
| Types of Alopecia | Definition | History | Physical Examination | Diagnosis | Treatment |
|---|---|---|---|---|---|
| Tinea capitis | Dermatophyte infection | Acute | Scaly red alopecia patches | Dermatophyte screen | Oral antifungal medications |
| Can be scarring | Can be recurrent | Diffuse scale | KOH microscopic examination | Antifungal shampoos | |
| Some chronic carriers | Broken hairs/black dots | ||||
| Cervical lymphadenopathy | |||||
| AA | Autoimmune hair loss | Acute then chronic | Areata: round patches of smooth bald scalp | Smooth scalp | Topical/oral or intralesional corticosteroids |
| Nonscarring | Episodes of activity and remission | Areata ophiasis: smooth hair loss on the periphery scalp | Exclamation point hairs | Topical retinoids | |
| Totalis: complete hair loss of scalp | Fine regrowing hairs | Contact irritants | |||
| Universalis: complete hair loss on scalp, body | No lymphadenopathy | Systemic antiinflammatories | |||
| Nail pitting, ridges | No redness or scale | Hair pieces/other cosmetic | |||
| Exclamation point hairs, lighter/thinner regrowing hairs | |||||
| Traction alopecia | Hair loss related to tension | Slow process, months to years | Decreased density of hair at areas of maximal tension | History of tension | Changing hair styles |
| Can be scarring | Folliculitis (redness and pustules) around hair follicle | Decreasing friction | |||
| White hair casts/pseudonits on hairs with increased tension | |||||
| Telogen effluvium | Shedding of hair | Rapid shedding, weeks to months | Decreased density of hair throughout scalp | Positive hair pull test | Treat underlying cause |
| Nonscarring | Occurs 3–4 mo after inciting event | Positive hair pull test | Shed hairs in telogen phase | Reassurance |
Epidemiology
Children aged 3 to 7 years are the most commonly affected with slightly more cases in male patients. The epidemiology of tinea capitis varies within different geographic areas throughout the world. In inner-city schools in the United States, the prevalence of tinea capitis among African American children have been reported to be from 12% to as high as 30%, with higher numbers for younger grammar school children. Infection rates for Hispanic and white children tend to be markedly lower, with an average prevalence of about 1% to 2%. Tinea may occur sporadically or epidemically and an increase in its incidence has been noted over the last few decades. Two species of dermatophyte are predominant in the United States. Trichophyton tonsurans is the most common cause of tinea capitis in children in the United States and is passed from human to human. Microsporum canis is the second most common and can be acquired from domestic pets. By some estimates, Microsporum accounts for less than 10% of all tinea capitis cases in the United States.
Pathophysiology
Tinea capitis is caused by fungi of species of the genera Trichophyton and Microsporum. Through direct inoculation, the fungal hyphae grow centrifugally in the stratum corneum and into the hair follicle. The zone of involvement extends upward at the rate at which hair grows, and it is visible above the skin surface by days 12 to 14. Endothrix infections are characterized by arthroconidia (spores) within the hair shaft. The cuticle is not destroyed. Ectothrix infections are characterized by hyphal fragments and arthroconidia outside the hair shaft, which lead to eventual cuticle destruction.
Clinical appearance
It invariably includes scale and some degree of redness and alopecia. It can be divided in diffuse scale, patch, black dot, diffuse pustular, and kerion varieties (see Fig. 1 ) Inflammation is more intense with zoophilic fungi. Kerions, which are swollen and sometimes purulent and boggy-appearing plaques, can occur with both zoophilic (fungi like Microsporum that prefer other animals to humans) and anthropophilic fungi (fungi like Trichophyton that prefer humans to other animals). Kerions are the body’s unsuccessful attempt to clear tinea at the site of infection with increased inflammatory cells and soft tissue swelling. The actual kerion is often dermatophyte negative, but the increased inflammation can lead to scarring and alopecia.
Differential diagnosis
Seborrheic and atopic dermatitis and psoriasis should be considered in the differential diagnosis of tinea capitis with diffuse scale and the patch variant. AA and trichotillomania are in the differential diagnosis of black dot tinea capitis. Bacterial folliculitis and dissecting folliculitis of the scalp should be considered in the differential diagnosis of diffuse pustular tinea capitis. Dissecting cellulitis is an inflammatory process considered part of the acne family whereby patients develop inflammatory papules and pustules in the scalp with accentuation in the occiput, which can lead to scarring. A cutaneous abscess and, less commonly, a neoplastic process like lymphoma are in the differential diagnosis for a kerion.
Prognosis
Most cases of tinea capitis can be successfully treated with the use of appropriate oral antifungal therapy and antifungal shampoos to prevent persistent shedding of spores. Extensive inflammation can lead to scarring, which leads to permanent localized alopecia. Recurrence can occur if hair grooming devices and other fomites are not cleaned properly.
Diagnostic studies
A dermatophyte culture will readily confirm the diagnosis of tinea capitis. Dermatophyte cultures in contrast to fungal cultures are plated to look for specific causes of tinea and exclude other molds and yeasts that can be contaminants from the environment. There will be a better yield and higher detection if a specific dermatophyte screen is performed. In order to properly obtain a specimen, an alcohol pad should be used to clean off any ointments or topical therapies previously applied to the scalp. A toothbrush or conventional bacterial swab can be used to plate material on Sabouraud agar containing antibiotics (penicillin/streptomycin or chloramphenicol) and cyclohexamide. Many centers will send swabs or toothbrushes to the laboratories to be plated later. Most dermatophytes can be identified within 2 weeks of plating. Standard potassium hydroxide (KOH) preparations for immediate microscope review can determine if tinea infection exists in many cases but are infrequently available in the pediatrician office. Conventional sampling of kerions often yield negative results because it mostly represents the inflammatory response to tinea; however, a moistened bacterial swab obtained from a pustular area and inoculated on a dermatophyte culture plate may yield a positive result, as may pressing the agar plate onto the kerion directly. Wood’s lamp can be used to look for green fluorescence; however Trichophyton species, which are the most commonly isolated species in the United States, do not fluoresce. Microsporum species do fluoresce but are much less commonly seen.
Therapy
For infections involving Trichophyton species, terbinafine for 4 weeks and griseofulvin for 8 weeks show similar efficacy ( Table 2 ). Itraconazole and fluconazole have also been used with high cure rates. Griseofulvin seems to be superior to terbinafine for cases caused by Microsporum . The addition of selenium sulfide or other antifungal shampoo used at minimum of 2 times a week for 4 weeks decreases the carriage of visible spores and is assumed to help prevent reinfection. Terbinafine is approved for tinea capitis infection in children older than 4 years. Griseofulvin is approved for the treatment of dermatophyte infections in children older than 2 years. In children aged 1 month to less than 2 years, there is limited data for the use of griseofulvin; however, in practice, it is used frequently with few side effects and high efficacy. The most-cited data for this age group suggest that 10 mg/kg/d is safe and effective. Many children under 1 year of age respond to topical therapy with azoles alone and do not need systemic medications. For the treatment of a kerion, the use of gentle soaks and/or keratolytic emollients can aid to remove crust. Some individuals advocate topical or oral steroids to decrease inflammation.
