Diaper rash pathophysiology: Difference between revisions
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{{CMG}} {{AE}} {{VVS}} | {{CMG}} {{AE}} {{VVS}} | ||
==Pathophysiology== | ==Pathophysiology== | ||
=== Primary | === Primary Infections === | ||
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 interlaid 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 [[Microbe|microbial]] invasion of the skin (Tortora and Grabowski, 2003). In infants, this layer of the skin is much thinner and more easily disrupted. | 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 interlaid 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 [[Microbe|microbial]] invasion of the skin (Tortora and Grabowski, 2003). In infants, this layer of the skin is much thinner and more easily disrupted. | ||
=== Secondary | === Secondary Infections === | ||
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). | 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). | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]
Pathophysiology
Primary Infections
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 interlaid 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.
Secondary Infections
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).