Open Access
Feature Article

Scalp pruritus – scratching for answers

Open Access
Feature Article

Scalp pruritus – scratching for answers

SARAH ROSE ADAMSON, RACHAEL DAVENPORT, ALVIN H. CHONG, Peter Foley

Figures

© nobeastsofierce/ shutterstock.com
© nobeastsofierce/ shutterstock.com
Dr Adamson is a Dermatology Research and Education Fellow at the Skin Health Institute, Melbourne; and a Dermatology Fellow at The Royal Women’s Hospital, Melbourne. Dr Davenport is a Dermatology Registrar at St Vincent’s Hospital, Melbourne. Adjunct Associate Professor Chong is a Specialist Dermatologist at St Vincent’s Hospital, Melbourne; Head of the Transplant Dermatology Clinic and Producer of Spot Diagnosis Podcast at Skin Health Institute, Melbourne. Associate Professor Foley is the Director of Research at the Skin Health Institute, Melbourne; Head of Dermatology Research at St Vincent’s Hospital, Melbourne; and Associate Professor of Dermatology at The University of Melbourne, Melbourne, Vic.

Less common causes of scalp pruritus

Tinea capitis

Tinea capitis is a dermatophyte infection of the scalp that occurs primarily in children. The causative organism varies with geographic location. In Australia, Microsporum canis and Trichophyton tonsurans predominate. There have been increasing reports of tinea capitis caused by Trichophyton soudanense (Figure 5), Trichophyton violaceum and Microsporum audouinii in immigrant children from East Africa, and confirmation of transmission to local populations.9

The two main patterns of tinea capitis invasion are: ectothrix and endothrix. In ectothrix infection (e.g. M. canis infection), arthroconidia (fungal spores) surround and destroy the cuticle, resulting in annular patches of partial alopecia. In endothrix infection (e.g. T. tonsurans infection), the arthroconidia are found within the hair shaft. This weakens the cuticle, and the hair breaks off level with the follicular orifice giving rise to ‘black dot’ tinea capitis in patients with dark hair. Inflammation varies from a fine scale to kerion formation, characterised by a boggy, purulent mass.

Clinical diagnosis of tinea capitis can be difficult owing to its varied presentation. An approach is to consider and exclude a fungal infection in patients (especially children) with hair loss and scale. To confirm the diagnosis, six to eight hairs should be plucked for fungal culture and microscopy.9 A Wood’s lamp is helpful in identifying tinea capitis only when the causative organism fluoresces (e.g. M. canis), as not all dermatophytes exhibit this phenomenon.

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Treatment of tinea capitis requires oral antifungals, as topical therapy alone is rarely successful. Current evidence supports terbinafine for empiric treatment of tinea capitis caused by Trichophyton or griseofulvin for tinea capitis caused by Microsporum spp.10 Oral griseofulvin is given at a recommended dose of  20 mg/kg/day up to 500 mg orally for a minimum of six to eight weeks, or until a clinical and mycological cure is achieved. Terbinafine is given to adults at a dose of 250 mg once daily, and to children at a recommended dose of 62.5 mg (body weight under 20 kg) or 125 mg (body weight 20 to 40 kg) once daily for four weeks.11-13 Terbinafine is available on the PBS for children with tinea capitis only when initial treatment with griseofulvin has failed. Side effects are comparable between griseofulvin and terbinafine; nasopharyngitis, headache and pyrexia are most common.14 Concurrent use of ketoconazole or selenium sulfide shampoo can help prevent spread.10 Alternative oral agents include itraconazole and fluconazole, but these are suboptimal choices for Trichophyton infections.11 Culture should be repeated at the end of treatment to confirm microbiological cure. 

Contact dermatitis

Scalp pruritus can be caused by contact dermatitis, due to either an irritant or an allergen. The scalp is relatively resistant to contact dermatitis because of rapid epidermal turnover and a thick epidermis and stratum corneum. It is also well protected by hair. Often the ears, forehead, neck or face are affected first.

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Major allergens are found in hair dyes (e.g. paraphenylenediamine), bleaches, permanent wave solutions and hair creams. Potential irritants include bleaching agents (the most common irritant), agents containing thioglycolates for permanently waving hair and blow drying the hair.

Clinically, the scalp may be erythematous, vesicular and weeping (Figure 6). The timing of onset can help differentiate irritant and allergic contact dermatitis; irritant contact dermatitis appears after the first exposure, whereas allergic contact dermatitis requires sensitisation and develops after repeated exposure.

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