DEFINITION
Napkin dermatitis (also known as nappy rash or diaper rash) is a non‐specific term used to describe inflammatory eruptions in the napkin area. Nappy rash is most commonly characterised by confluent erythema (i.e. joined patches of redness) of the convex surfaces of the buttocks, the areas of skin in closest contact with the nappy (Atherton 1998).

IMPACT
Most infants develop such an eruption at least once during their infancy, and napkin dermatitis is the most common cause for dermatological consultation in infancy (Concannon 2001). Napkin dermatitis is most commonly seen between 6 and 12 months of age (Lane 1990).

CAUSES
The exact cause of napkin dermatitis remains unclear (Atherton 1998). Friction and maceration (i.e. the softening of skin by soaking) are recognised as key causative factors in the pathogenesis of napkin dermatitis (Atherton 1998). Increased hydration increases the risk of frictional damage and impairs the skin's barrier function, increasing its susceptibility to irritants. Increased skin wetness allows growth of microorganisms on the surface of the skin (Lane 1990). Friction may produce the initial breech in the protective coating of the skin. The preterm infant is more vulnerable to mechanical injury because of its thin stratum corneum, lack of dermal papillary projections and a thinner, less collagenized dermis (Williams 2001). Contact with components of urine and faeces and the contribution of microorganisms in the napkin area have also been considered as possible causative agents in napkin dermatitis (Atherton 1998). Faeces contain a variety of bacteria, some of which contain urease, which releases ammonia from the urine and raises the pH (Lane 1990). Ammonia is considered a contributory cause in the aetiology of napkin dermatitis as it is only irritant when applied to a damaged stratum corneum (Lane 1990). Faeces contain other enzymes such as proteases and lipases which also irritate the skin of infants (Lane 1990). Faecal enzymes also increase the permeability of the skin to bile salts, which act as irritants to the skin (Wong 1992). Occlusion of the skin, by means such as napkins, elevates the surface pH (Lane 1990). Increased urinary pH is a contributory factor in napkin dermatitis through its action in increasing the activity of irritant faecal enzymes (Fischer 2002).

TREATMENT
Numerous treatments have been tried for napkin dermatitis, with varying success. Current treatment regimens emphasise the type of nappies used and the skin care of the napkin region (Atherton 1998). It is suggested that good quality disposable napkins and frequent nappy changes may decrease the incidence of maceration and thus the incidence of nappy rash (Atherton 1998). Specific therapies aimed at reducing the inflammation of the napkin area may also be employed. Traditional topical napkin rash treatments included topical corticosteroids used in isolation and combination preparations of anticandidal and antibacterial agents with corticosteroids. Topical vitamin A has been suggested as a possible treatment for napkin dermatitis and is contained in many preparations available for the treatment of napkin dermatitis (Bosch‐Banyeras 1988). The value of vitamin A in preventing napkin dermatitis has been studied (Bosch‐Banyeras 1988). Vitamin A deficiency can cause skin changes and subclinical deficiency of vitamin A has been associated with increased infections (including skin) (Soni 1999).

ADVERSE EFFECTS
Consideration must be given to potential side effects as a result of systemic absorption of topical preparations in infants and neonates. The keratinised stratum corneum is the skin's major protection against absorption (Evans 1986). Keratinization begins at 22 weeks gestation (Haake 1999) and infant skin demonstrates barrier function similar to that of an adult by 32 weeks gestation (Rutter 1988). Barrier function of the stratum corneum develops rapidly after birth (regardless of gestation), achieving the epidermal development of the term infant at two weeks of age (Rutter 1988). The penetration of the skin is altered by site, reflecting the varying thickness of the stratum corneum (Shupack 1999).

The absorption of tretinoin through the skin is limited (approximately 2%), and is not increased despite long term administration (Latriano 1997; Shapiro 1998). Differing formulations of tretinoin did not alter percutaneous absorption (Latriano 1997). No rise in tretinoin levels has been demonstrated regardless of the surface area of application (Latriano 1997). Minimal percutaneous absorption of tretinoin suggests that the adverse effects of oral retinoid therapy (e.g. teratogenicity, mucocutaneous and gastrointestinal disturbances) are unlikely with topical applications.

Topical application of retinoic acid has been associated with some local adverse effects (predominantly in adult subjects for the treatment of acne). Common adverse effects of topical tretinoin include increased solar sensitivity and local irritation, causing erythema and peeling (Skov 1997).