Diaper rash (US) or nappy rash (UK), is a generic term applied to skin rashes in the diaper area that are caused by a various skin disorders.
Generic rash or irritant diaper dermatitis (IDD) is characterized by joined patches of erythema and scaling mainly seen on the convex surfaces, with the skin folds spared.
Diaper dermatitis with secondary bacterial or fungal involvement tends to spread to concave surfaces (i.e. skin folds), as well as convex surfaces, and often exhibits a central red, beefy erythema with satellite pustules around the border (Hockenberry, 2003).
Other rashes that often occur in the diaper area include Seborrheic dermatitis and Atopic dermatitis. Both Seborrheic and Atopic dermatitis require individualized treatment and are not the subject of this article.
Seborrheic dermatitis, typified by oily, thick yellowish scales, is most commonly seen on the scalp (cradle cap) but can also appear in the inguinal folds.
Atopic dermatitis, or eczema, is associated with allergic reaction, often hereditary. This class of rashes may appear anywhere on the body and is characterized by intense itchiness.
Irritant diaper dermatitis develops when skin is exposed to prolonged wetness, increased skin pH caused by urine and feces, and resulting breakdown of the stratum corneum, or outermost layer of the skin. In adults, the stratum corneum is composed of 25 to 30 layers of flattened dead keratinocytes, which are continuously shed and replaced from below. These dead cells are interlay with lipids secreted by the stratum granulosum just underneath, which help to make this layer of the skin a waterproof barrier. The stratum corneum’s function is to reduce water loss, repel water, protect deeper layers of the skin from injury and to repel microbial invasion of the skin (Tortora and Grabowski, 2003). In infants, this layer of the skin is much thinner and more easily disrupted.
Although wetness alone macerates the skin, softening the stratum corneum and greatly increasing susceptibility to friction injury, urine has an additional impact on skin integrity because of its effect on skin pH. While studies show that ammonia alone is only a mild skin irritant, when urea breaks down in the presence of fecal urease it increases skin pH, which in turn promotes the activity of fecal enzymes such as protease and lipase (Atherton, 2004; Wolf, Wolf, Tuzun and Tuzun, 2001). These fecal enzymes increase the skin’s permeability to bile salts and act as irritants in and of themselves.
The interaction between fecal enzyme activity and IDD explains the observation that infant diet and diaper rash are linked, since fecal enzymes are in turn affected by diet. Breast-fed babies, for example, have a lower incidence of diaper rash, possibly because their stools have lower pH and lower enzymatic activity (Hockenberry, 2003). Diaper rash is also most likely to be diagnosed in infants 8–12 months old, perhaps in response to an increase in eating solid foods and dietary changes around that age that affect fecal composition. Any time an infant’s diet undergoes a significant change (i.e. from breast milk to formula or from milk to solids) there appears to be an increased likelihood of diaper rash (Atherton and Mills, 2004).
The link between feces and IDD is also apparent in the observation that infants are more susceptible to developing diaper rash after treatment with antibiotics, which affect the intestinal microflora (Borkowski, 2004; Gupta & Skinner, 2004). Also, there is an increased incidence of diaper rash in infants who have suffered from diarrhea in the previous 48 hours, which may be due to the fact that fecal enzymes such as lipase and protease are more active in feces which have passed rapidly through the gastrointestinal tract (Atherton, 2004).
The significance of secondary infection in IDD remains controversial. Atherton contends that, “Candida albicans can only be isolated from a minority of IDD cases; in many cases this is a reflection of antibiotic therapy. It has also been established that bacterial infection does not play a substantial part in the development of IDD.” (Atherton, 2004, p. 646).
However, there is little argument that once the stratum corneum has been damaged by a combination of physical and chemical factors, the skin is necessarily more vulnerable to secondary infections by bacteria and fungi. In analyzing swab samples at the perianal, inguinal and oral areas of 76 infants, Ferrazzini et al. (2003) found that colonization with Candida albicans was significantly more likely in children with symptomatic diaper rash than without. Staphylococcus aureus was also present more frequently in symptomatic than in healthy infants, but the difference was not statistically significant. A wide variety of other infections has been reported on occasion, including Proteus mirabilis, enterococci and Pseudomonas aeruginosa, but it appears that Candida is the most common opportunistic invader in diaper areas (Ferrazzini et al., 2003; Ward et al., 2000).
Although apparently healthy infants sometimes culture positive for Candida and other organisms without exhibiting any symptoms, there does seem to be a positive correlation between the severity of the diaper rash noted and the likelihood of secondary involvement (Ferrazzini et al., 2003; Gupta & Skinner, 2004; Wolf et al., 2001).
The most effective treatment, although not always the most practical one, is to discontinue use of diapers, allowing the affected skin to air out. Other commonly recommended remedies include oil-based protectants, often using various over-the-counter “diaper creams”, but sometimes people use petroleum jelly and shark liver oil or cod liver oil; zinc oxide based ointments, and, in extreme cases, anti-fungal cremes. Low concentration hydrocortisone creams are also sometimes used to treat the symptoms of diaper rash, although they do little to clear up the rash itself.