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Children With Wounds

New Year, Old Problem: Diaper Dermatitis

January 2020
Wound Manag Prev. 2020;66(1):8–10

Diaper dermatitis (DD), one of the most common problems among both hospitalized and at-home neonates, has led to a billion dollar industry, products galore, parental confusion, frequent doctor visits, and discomfort or pain for the children.

Why is diaper rash so common? A review of the physiology is revealing. The epidermis, including the lower 4 viable layers (stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale) and an outer acellular layer (stratum corneum [SC]) are essential for normal skin development. The SC provides the main barrier, regulates temperature and moisture, controls transepidermal water loss (TEWL), filters transcutaneous substances, and helps ensure an effective acid mantle. Birth is an important event, leading to many changes in SC. In a preterm baby, SC is very underdeveloped, and 23- to 24-week neonates have only 1 to 2 layers of SC, along with a small amount of intercellular lipids and weak connections between the cells. Their TEWL can be up to 10 times higher than their full-term counterparts,1 they lack vernix caseosa (VC), and their skin’s pH is very basic, leading to increased bacterial colonization risk, decreased free fatty acids and antioxidants, and increased risk of irritation. Preterm skin hydration is low, and the process of physiologic skin maturation is enhanced.1 Cells from the stratum basale continuously migrate up to the SC via a preprogrammed process. 

In a full-term neonate, the SC is comprised of 16 to 20 layers of a “brick and mortar” combination. Flat acellular corneocytes will be joined by desmosomes and enveloped by lamellar bodies made up of fatty acids, ceramides, triglycerides, and cholesterol (the mortar layer). The lipids, water, and cells make a strong barrier, penetrable by water vapor but not by larger molecules and microbes. In preterm babies, this layer is much thinner and easily injured and becomes a nidus for microbial penetration, irritation, homeostasis imbalance, and pain. Normally, 1 SC layer is lost daily via desquamation.1 This maintains the integrity of SC. 

In preterm neonates, temperature and humidity are maintained by warmed, humidified isolettes. If humidity is too high (>80%) or too low (<40% to 50%) during the first 1 to 2 weeks, there is risk for abnormal physiologic maturation and potentially hyperdesquamation (see Figure 1) or delay in skin development. The moisture level is regulated by fillagrin, a protein present in corneocytes and converted to small water-binding amino acids, which provides natural moisturizing factor (NMF) that is responsible for maintaining an appropriate level of SC hydration.2 Disruption or loss of NMF (by abnormal humidity, an epidermal tear, or an occlusive topical dressing) will result in low SC moisture and excessive desquamation. On the other hand, a thick occlusive product (such as pure petrolatum) might be too much for preterm skin. The moisture or water vapor will accumulate under the occlusive, unable to escape, leading to microscopic breaks in the skin, barrier damage, and either microbe or irritant penetration. 

Nature has provided one of the best natural “dressings” — VC. Delivery and nursery personnel often have the knee-jerk reaction to remove this white, cheesy substance. The best recommendation is to leave VC on the babies because it contains some of the most important elements for the body, especially for preterm babies. VC consists of 80% water, 10% lipids, and 10% proteins, sebum, lanugo, and desquamated cells.3 Its production begins in the second trimester and most is present by 36 weeks. VC detaches from the body when adequate pulmonary surfactant is produced, signifying adequate lung development and upcoming birth. Its multiple functions in utero include ensuring SC development in a caustic, aqueous environment; serving as a physical barrier, providing anti-oxidant and anti-infective properties; and inducing an acid mantle; it also is an extremely important moisturizer. 

The antimicrobial properties of VC components are remarkable; lysozyme, lactoferrin, cytokeratin, immunoglobulin, and surfactant protein D are naturally found in human milk and lung surfactant; they are all paramount to the human anti-infection armamentarium. The lipids include cholesterol, triglycerides, ceramides, squalene, sterol esters, and free fatty acids (FA) such as linoleic, oleic, and very long chain fatty acids3 (VLCFA, an essential anti-inflammatory FA for a preterm baby). Preterm babies have a relative FA deficiency; therefore, leaving VC on gives the newborn a natural boost. Amino acids combined with essential proteins such as calprotectin, cystatin A, cytokines, antimicrobial peptides (ά-defensins), asparagine, and glutamine provide superior antimicrobial, acid-building, and anti-inflammatory protection for the newborn. 

In my hospital, I take every opportunity to emphasize to newborn caregivers the importance of  vernix retention, appropriate humidity for very preterm neonates, and delayed baths for older children to allow skin acidification and maturation. Despite these measures, virtually all newborns develop DD at some point. Several factors are important to mention. DD can present as erythema, edema, erosions, weepy exudate, or bleeding areas that involve the buttocks, perineum, groin, and/or anal areas. Skin folds may be involved or spared. The most common cause is the fact that newborns may urinate more than 10 times/day and produce stool more than 6 to 9 times daily, especially if breastfed. Urine contains ammonia that alkalinizes surrounding skin. Wearing occlusive diapers protects the outside but changes the inside microclimate, increasing moisture, humidity, and even temperature at times. This leads to more basic skin pH, a propensity for maceration, and prolonged exposure to elements. Certain illnesses and conditions can predispose the skin to DD: viral gastroenteritis produces liquid, frequent stool; bacterial sepsis may contain inflammatory mediators and bacteria; malabsorption syndromes come with increased bacterial and carbohydrate load; and higher stool pH contributes to increased irritation. Short gut syndromes hasten transit time, producing undigested food and caustic enzyme exposure. Fecal enzymes, bile acids, and irritants are known to degrade SC proteins, causing breaks in skin that lead to irritant entry, inflammation, erythema, edema, and a potentially denuded, bleeding surface (see Figure 3). In preterm babies this cascade often is exacerbated, which can cause poor SC repair, hyperproliferation, and desquamation (see Figure 4). Neonates born with neonatal abstinence syndrome (ie, exposure to illegal or prescription drugs in utero) often have diarrhea and severe diaper rash (see Figure 2), and babies with congenital metabolic syndromes often require caustic supplements.

Reduction of exposure to all these elements, minimizing moisture, and improving occlusiveness and breathability are essential in diaper care. The diaper industry has evolved a great deal over the last 10 to 20 years. We went from cloth diapers to disposable diapers with a plastic outer layer and significant occlusion to disposable diapers with superabsorbent polymers to absorbent gel material with a breathable outer layer.4 Advanced design has diminished moisture and increased wicking and evaporation, contributing to lower skin pH and reduced DD. Visscher et al4 reported that with cloth diapers, DD was 60% compared to 39% with cellulose, 29% with superabsorbent, and 13% with superabsorbent with a breathable outer cover. Moderate rash actually increased from mid-30% to mid-50% with technology advances, reflecting a decrease in severe cases; with the advent of the breathable outer cover, even moderate dermatitis decreased from 50% to 30%.4 In addition, a decrease in Candida-associated dermatitis was noted, which was directly related to improved breathability.3

Diaper design and understanding of skin care have made great strides. We now know certain ingredients in diaper wipes are highly allergenic and cause significant dermatitis. We know fragrance, natural oils, and various preservatives are irritating if not toxic (once absorbed) to neonatal skin. We know water, mild neutral pH cleansers, and wipes with minimal ingredients and infused with a small amount of emollient provide optimal management. We understand the dangers of antiseptics, such as alcohol and chlorhexidine and minimize their use. We are studying the frequency, types, and protocol of newborn bathing, minimizing the frequency, delaying the first bath, and teaching caregivers to both swaddle and immerse babies to improve temperature and physiologic tolerance. These changes have improved skin integrity and DD rates. The number of diaper area topical products and emollients in general has exploded. It is important to understand what is inside these products and what we are putting on baby skin.

Next month I will review the topical treatments for DD. 

Affiliation

Dr. Boyar is Director of Neonatal Wound Services,  Cohen Children’s Medical Center of New York, New Hyde Park; and an Assistant Professor of Pediatrics, Zucker School of Medicine, Hofstra/Northwell, Hempstead, NY. This column was not subject to the Wound Management & Prevention peer-review process.

References

1. Kalia YN, Nonato LB, Lund CH, Guy RH. Development of skin barrier function in preterm infants. J Investig Dermatol. 1998;111(2):320–326.

2. Sandilands A, Sutherland C, Irvine AD, McLean WH. Filaggrin in the frontline: role in skin barrier function and disease. J Cell Sci. 2009;122(Pt. 9)1285–1294.

3. Visscher MO, Narendran V, Picken WL, et al. Vernix caseosa in neonatal adaptation. J Perinatol. 2005;25(7):440–446.

4. Visscher M, Adam R, Brink S, Odio M. Newborn infant skin: physiology, development and care. Clin Dermatol. 2015;33(3):271–280.

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