Diaper rash pathophysiology

Jump to navigation Jump to search

Diaper rash Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Diaper rash from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Diaper rash pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Diaper rash pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Diaper rash pathophysiology

CDC on Diaper rash pathophysiology

Diaper rash pathophysiology in the news

Blogs on Diaper rash pathophysiology

Directions to Hospitals Treating Diaper rash

Risk calculators and risk factors for Diaper rash pathophysiology

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).

References

Template:WH Template:WS