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How Does Infant Skin Differ from Adult Skin?

Authors: Peter Lio, MDFaculty and Disclosures


"Smooth as a baby's bottom" summarizes the popular notion of infant skin: the soft, supple, and practically flawless integument that is the unattainable objective of all cosmetic treatments. Indeed, it can be difficult to imagine what problems a pediatric dermatologist could possibly address given how perfect newborn skin appears to be. And while there are undoubtedly plenty of skin maladies that affect those at the beginning of life, even for the smoothest of bottoms, there are critical differences worth thinking about, both in health and disease. In this article, we review some of the important structural and physiologic differences between infant (defined here as the first few years of life) and adult skin. We also consider some of the clinical and practical ramifications of these distinctions using evidence whenever possible.

The functions of the skin remain essentially the same at all phases of life, including: barrier, photoprotection, thermoregulation, immune surveillance, hormonal synthesis, insensible fluid loss prevention, and sensory perception.[1] However, there are several important structural differences between the skin of babies and adults, differences immediately accentuated as the newborn transitions from the intrauterine environment to the outside world.

Barrier function of the skin is vital for survival for all human beings. With increasing prematurity, there is increasing barrier dysfunction with higher transepidermal water loss (TEWL) and increased percutaneous absorption of chemicals.[2] As a result, there is greatly increased mortality in premature infants with impaired barrier function, generally due to microbial invasion.[3] Remarkably, this can be demonstrated experimentally by application of emollients that enhance barrier function. In a randomized, controlled trial, massaging premature infants with sunflower seed oil 3 times daily resulted in a 41% reduction in sepsis and a 26% reduction in mortality.[4]

Although the TEWL in full-term infants is generally agreed to be close to that of healthy adults,[1] there is recent evidence that the barrier development continues during the first year of life.[5] Infant skin is found to have higher water content and is able to absorb more water and lose excess water faster than adult skin.[6] Other microstructural differences include thinner stratum corneum and papillary dermis in infant skin.[6]

Beyond these structural points, however, several factors converge to make infants more susceptible to percutaneous toxicity. Their high surface area-to-volume ratio, immature drug metabolism systems, and decreased subcutaneous fat stores effectively increase the absorptive area while decreasing the volume of distribution of a drug or toxin.[3,7] This is compounded by the fact that once absorbed, the infants lack fully developed drug carriage and detoxification systems. Furthermore, direct barrier injury can occur because of the increased fragility of infant skin, particularly from the removal of adhesive tapes and monitors, thus increasing local permeability.[3] Finally, given the estimated 20% incidence of atopic dermatitis among children,[8] there are yet other reasons for barrier function to be impaired at baseline. Because of these factors, it seems prudent to advise that only essential products be applied to the skin, particularly in the first several months of life.

Below the skin, in the subcutaneous fat, there are also discrepancies between mature and immature. In newborns, the subcutaneous fat is rich in the saturated oils palmitic and esteric acid. These fats have higher melting point temperatures than the increasingly unsaturated fats of adulthood; as more oleic acid becomes present, the melting point diminishes.[9] The higher melting point means that the fat in infants can freeze more easily: approximately 64°C vs the much lower adult melting point of 14°C.[10] This principle is typified by "popsicle panniculitis," a fairly common form of fat necrosis in the cheeks of infants several hours after eating popsicles or ice, and the closely related equestrian panniculitis, seen after the cold exposure from riding horses, bicycling, or riding motorcycles.[9] Subcutaneous fat necrosis of the newborn, a condition frequently associated with hypothermia, trauma, or other perinatal stressors, is a panniculitis that may also be related to the higher melting point of infant fat.[11] Because of this limitation in infant skin, extra care must be made to avoid temperature extremes.

Bathing an infant provides important psychological benefits between parent and child.[12] However, oddly enough, it can also provide an opportunity to damage the skin. There is evidence to suggest that washing the skin with a washcloth during the first 4 weeks of life is associated with increased TEWL and decreased stratum corneum hydration compared with simply soaking in water.[13] Another study found that tub bathing an infant was actually associated with an increased risk of cord infection vs no washing at all.[14] Several papers have examined the use of mild liquid cleansers vs using water alone for bathing. The consensus appears to be that a mild liquid cleanser may actually be less drying and less irritating than water alone, and that bathing should be brief (10 minutes or less) and no more than every other day[15] with spot cleaning in between.

Photoprotection is an important function of the skin, though in the process of preventing ultraviolet (UV) sun damage to certain structures, the skin can itself accrue damage, increasing the chances of skin cancer. As for adults, sun protection is important in childhood. This topic takes special importance because the damage from UV radiation is cumulative: children spend more time doing outdoor activities, younger skin is more susceptible to damage, and UV damage in childhood may have particularly profound consequences later.[16,17] It is also important to remember that infants are entirely dependent upon their caregivers to practice sun protection and are generally not able to communicate the symptoms of early sunburn.

In recent years, concerns have emerged over possible hormone-disrupting chemicals in sunscreens, such as oxybenzone. In children, the doubly worrisome scenario of increased percutaneous absorption of chemicals and the enhanced developmental sensitivity to hormone disruption makes this topic extremely contentious. Evidence for such absorption is fairly abundant with 1 study concluding: "...whilst limited absorption across the skin was observed for the majority of the sunscreens tested, [oxybenzone] demonstrated sufficiently high penetration to warrant further investigation of its continued application."[18]

Evidence for hormone disruption is another issue that is well established for benzophenone-3, homosalate, 4-methyl-benzylidene camphor (4-MBC), octyl-methoxycinnamate (OMC), and octyl-dimethyl-para-aminobenzoic acid (PABA). All show estrogenicity,[19] and studies document environmental persistence and widespread presence in the population.[20] Unfortunately, even the mineral sunscreens such as titanium dioxide and zinc oxide are not without risk. There is evidence that the nanoparticles present in many of these mineral sunscreens can cause cellular damage.[21] Although most studies have shown that there is minimal penetration into the skin,[22] no studies have yet tested these particles in fragile or damaged skin. Infant skin is more fragile, and with the incidence of atopic dermatitis approaching 20% in some populations, there is a reasonably high chance that there will be areas of skin damage in some infants.[23] My conclusion strongly reinforces the message conveyed by the American Academy of Pediatrics: minimize the reliance on topical products in infancy by avoiding sun exposure and using sun-protective clothing whenever possible.[24]

Skin diseases in infants and adults can vary as much as the difference in fundamentals of the skin. Even disorders that may sound familiar from experience in older patients may be distinct in infants: acne, skin infections, and nutritional dermatoses, to highlight a few.

Classical teenage acne (acne vulgaris) is well known to all of us; however, there are 2 distinct forms of acne that can affect patients in the first few years of life: neonatal acne and infantile acne. Neonatal acne is perhaps more accurately referred to as neonatal cephalic pustulosis (NCP) and can affect up to 20% of newborns.[25] This papulopustular disorder lacks the comedones of true acne and may actually be related to colonization with Malassezia yeast species on the skin. Generally benign and self-limited, treatment with topical ketoconazole may shorten the duration of the disease.[26]

Infantile acne, on the other hand, is far more rare than neonatal acne, and generally occurs between 3 months and 1 year.[26] Both comedones and inflammatory papules are seen in this disease, and like its teenage counterpart, scarring may be an issue. Sometimes infantile acne will resolve by school age without specific treatment, but it may also be a harbinger for severe forms of acne in adolescence and appears to be more common in families with a strong family history of acne.[25] Here the differences end: treatment can be very similar to that for teenage acne, including a topical retinoid and topical benzoyl peroxide.[25]

Staphylococcal scalded-skin syndrome in infants and children is caused by staphylococcal bacteria that release exfoliative toxin and can also be seen in adults with renal failure. This suggests that it is the inability to clear the toxin that causes the characteristic superficial bullae and widespread sloughing, with crusting and impetiginization at the orifices.[2] Prompt diagnosis and treatment with systemic antibiotics and skin barrier support are necessary to minimize morbidity from this disease.

Infants are also particularly susceptible to nutritional deficiencies, and zinc deficiency may be acquired or inherited. Acrodermatitis enteropathica (AE) is the rare, autosomal-recessive disease of impaired zinc absorption that usually presents upon weaning from breast milk.[27] Acrodermatitis enteropathica-like eruption can be seen in the setting of insufficient dietary zinc, including breast milk deficiency.[28] Symptoms of periorificial dermatitis, diarrhea, and hair loss frequently are mild and incomplete, making this disease a challenge to diagnose at times. Once the diagnosis is made, zinc supplementation is required, which generally results in dramatic reversal of skin lesions within several days.

Infant skin is often thought of as ideal skin, and its characteristics are frequently sought by adults. However, beyond the smooth and supple beauty, there are significant structural and functional differences that make infant skin more susceptible to certain problems. During the first years of life, there are considerable developments of the skin and subcutaneous fat that warrant handling infants differently—and much more gingerly—than adults.

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