Справочник врача 21

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Vernix caseosa




Кожа недоношенного ребёнка прозрачная, истончённая, ладони и стопы слабо исчерчены. В области спины повышено пушковое оволосение. Барьерные функции кожи слабо развиты, в особенности из-за недоразвитости рогового слоя. С этим же связаны повышенные трансэпидермальные потери воды, а также активное всасывание любых веществ, нанесённых на поверхность кожи. Величина потерь воды через кожу зависит от гестационного и постнатального возраста. У новорождённых, выхаживаемых под источником лучистого тепла, трансэпидермальные потери — главная причина потерь жидкости. У глубоконедоношенных новорождённых величина потерь воды через кожу может составлять 2,5 мл/кг/ч) и более. Кожа переношенного ребёнка сухая, бледная, шелушащаяся. Казеозная смазка практически отсутствует. Одна из важнейших функций кожи — защита от проникновения инфекционных агентов, что прямо зависит от уровня кислотности (pH) кожи. У доношенных новорождённых после четырёх дней жизни реакция кожи кислая (рН <5), тогда как у недоношенных кожа приобретает кислую реакцию не ранее восьмого дня жизни. Эти особенности создают благоприятные условия для роста микробов. Кожа новорождённого покрыта естественным кремом — первородной смазкой (vernix caseosa), защищающей кожу в период внутриутробного развития. Известно, что компоненты белка vernix содержат несколько антибактериальных олигопептидов, активных против бактериальных и грибковых подобных антибактериальным пептидам грудного молока, поэтому первородную смазку с кожи новорождённого удалять не следует. Если кожа и волосы новорождённого загрязнены кровью, после перевода из родильного зала в отделение лучше выкупать ребёнка в ванночке с тёплой водой, а не обтирать влажной пелёнкой (A. Henningsson, B. Nystrom, R. Tunell. Bathing or washing Babies after birth. — 1981. — Lancet. — 19/26). Примечание редакторов: в приказе N 345 от 26.11.97 «О совершенствовании мероприятий по профилактике внутрибольничных инфекций в акушерских стационарах» сказано, что первичная обработка кожных покровов новорождённого следует осуществлять... [стр. 40 ⇒]

Околоплодные воды, или амниотическая жидкость (АЖ), в начале беременности желтоватые, а затем более светлые и прозрачные; pH 7,0, удельный вес – 1007; содержание белка – 500 мг%, глюкозы – 22 мг%, мочевины – 23 мг%. АЖ образуется в основном за счет секреции жидкости клетками амниона и в определенной степени за счет мочевыделения плода. В центрифугате АЖ находят волосы (lanugo), клетки эпидермиса, клетки сальных желез (vernix caseosa). Считается, что АЖ обеспечивает защиту плода от механических повреждений, а также осуществляет транспортную функцию и участвует в обмене веществ. [стр. 133 ⇒]

Околоплодные воды, или амниотическая жидкость (АЖ) — среда обитания плода, выполняющая одновременно несколько функций: создание пространства для свободных движений растущего плода, защита от механической травмы, поддержание температурного баланса, предотвращение компрессии пуповины в родах, осуществление транспортной функции и участие в обмене веществ. АЖ в начале беременности желтоватая, затем более светлая и прозрачная, в конце беременности — мутная, опалесцирующая; pH — 6,98–7,23, удельный вес — 1007–1080 г/л, содержание белка — 0,18–0,2%, глюкозы — 22 мг%, мочевины — 23 мг%. При исследовании центрифугата АЖ выявляют волосы (lanugo), клетки эпидермиса, клетки сальных желёз (vernix caseosa). [стр. 417 ⇒]

Во всяком случае это состояние измеряется не минутами, а часами, при особых обстоятельствах даже днями. Следует помнить, что врачи понимают под родами физиологический акт рождения, а юристы — всю совокупность обстоятельств, сопутствующих родам (Фрич). Признаки новорожденности на ребенке определяются н а р у ж н ы м осмотром и вскрытием трупа. Из внешних признаков следует отметить : а) загрязнение трупа кровью матери или из пуповины ; б) присутствие на теле (особенно в подмышечных и паховых складках к о ж и ) сыровидной смазки (vernix caseosa). Последняя представляет собой выделение к о ж н ы х сальных желез ( ж и р , холестерин) с примесью сл у щ и вающегося эпителия к о ж и (эпидермоидальные клетки) и п у ш к а . Количество смазки различно, она может быть незаметной. Сыровидная смазка может, впрочем, оставаться долгое время на теле, если ребенок не помыт, а потому лишена значения достоверного признака новорожденности ; загрязнение тела меконием (см. ниже) также не служит доказательством новорожденности ; в) важнейший признак — состояние пуповины. Если на ребенке находится целая пуповина с последом, то это верный признак новорожденности. Теоретически рассуждая, может представиться случай, когда ребенка находят с п у л ь с и р у ю щ е й пуповиной- и требуется точно определить момент родов. Спрашивается, сколько времени может пульсировать пуповина после рождения ребенка, отрезанная или находящаяся в связи с последом? Как известно, пупочные артерии пульсируют еще некототорое время после рождения младенца, причем пульсация постепенно прекращается. О б ы ч н о со стороны последа пульсация продолжается до 5 минут, но наблюдались случаи, когда она продолжалась 30 минут и дольше. Я лично наблюдал рождение доношенного младенца одновременно с последом, причем пупочные артерии продолжали биться 12 минут, закончивши биение у самого пупочного кольца. У новорожденного младенца остаток пуповины (культя) свеж и сочен. Если ребенок продолжает жить, то культя начинает сохнуть, мумифицируется и превращается в жесткий 19. Судебная гинекология... [стр. 291 ⇒]

AMNIOTIC FLUID Amniotic fluid is a dialysate of maternal serum, essential for the maintenance of an even fetal temperature and biochemical homeostasis. Its presence allows fetal movement and growth, and it is thought to be essential for the development of the tracheobronchial tree.6 Typically anechoic, occasionally sonographers find echogenic material moving within the fluid. In one study of 19 fetuses with very echogenic amniotic fluid that soon after had a third-trimester amniocentesis, the echogenicity was caused by vernix caseosa in all but one case of fetal distress and intrauterine meconium passage.72 At 12 weeks’ gestation, amniotic fluid volume averages 60 mL, increasing 20 to 25 mL per week until 16 weeks and then increasing 50 to 100 mL per week until 20 weeks. The mean fluid volume at 20 weeks is 500 mL. The fetus may contribute to amniotic fluid volume by fluid transfer across the fetal skin surfaces, including skin, cord, chorion, and amnion. Fetal urine production begins at 12 weeks, but the amount is insignificant until the 18th to 20th weeks of gestation. By the late third trimester, the fetus is producing approximately 450 mL of urine per day. Beyond 20 weeks, transudation of fluid across fetal surfaces is inadequate to maintain normal amniotic volume, and the fetus essentially modifies fluid volume and composition only by swallowing and urination.1,2,6 Normal amniotic fluid volume may be maintained by one functioning kidney and a nonobstructed GU tract. Oligohydramnios of fetal origin results from... [стр. 580 ⇒]

В неонатальном периоде (28 дней после рождения) и далее в первые месяцы жизни могут возникать разнообразные изменения кожи, среди которых принято различать болезни кожи и особые состояния кожи новорожденных, являющиеся пограничными, близкими к физиологическим особенностям. Сюда относят первородную смазку (vernix caseosa), умеренную эритему с небольшой отечностью в течение 2-3 дней, шелушение кожи в первой -- второй недели жизни, физиологический катар кожи новорожденных, телеангиэктатические пятна на затылке и лбу у значительной части детей, физиологическую желтуху у новорожденных. У недоношенных детей наблюдаются более обильные пушковые волосы на первой неделе жизни, гипопластические ногтевые пластинки, которые не доходят до кончиков пальцев, которые иногда даже отсутствуют. Своеобразную особенность представляет вертикальная темная линия живота (linea fuscha). наблюдающаяся у некоторых младенцев в первые недели жизни и сохраняющуюся до 2-3 месяцев, а также монгольские пятна. На 3-4 месяце жизни ребенка нередко очень заметно физиологическое выпадение волос, могут образоваться облысевшие участки на затылке и в лобно-теменной области, что вызывает часто необоснованный страх у родителей. К переходным состояниям относят поражения кожи во время формирования организма новорожденных преходящие отеки, сосудистые изменения цвета кожи «типа арлекина». Токсическую эритему и крапивницу новорожденных одни авторы включают в число переходных состояний, другие - в число болезней с иммунологическим нарушением. Клиническая характеристика состояний и болезней. М О НГОЛЬСКИЕ ПЯТНА... [стр. 29 ⇒]

На большей части поверхности кожи у здоровых людей pH варьирует от 3 до 5, по некоторым данным, от 4,2 до 5,6. Кислотность кожи зависит от функционального состояния секреции потовых желез. У новорожденных pH кожи варьирует от 6,12 до 6,04, либо ближе к нейтральному - 6,7 [62]. Кислотность кожи более постоянная в местах локализации эккриновых потовых и более изменчивая в местах расположения апокриновых желез. В подмышечных впадинах с возрастом pH становится более щелочной. По-видимому, это является одним из предрасполагающих факторов в развитии гидраденита. В период новорожденности имеются специфические состояния, которые характерны только для этого периода и исчезающие позже. Vernix caseosa. В период новорожденности кожа ребенка покрыта серовато-белого или желтоватого цвета вязкой массой, называемой vernix caseosa. Наиболее она выражена в области ушей, лица, в подмышечных и паховых складках, на пояснице. Данная смазка состоит из измененных эпителиальных клеток, холестерина, гликогена, элеидина. По мнению исследователей, Vernix caseosa является защитным барьером от пиококковых инфекций. В связи с этим во многих родильных домах оставляют данную смазку до первого купания. Волосяной покров. Кожа новорожденного покрыта нежным пушком (Lanugo), который в большей части выпадает до рождения, заменяясь другим. Окончательное состояние волосяного покрова определяется к началу второго года жизни ребенка. Ногти. У новорожденных ногти доходят до конца пальцев. Однако у некоторых детей они могут быть недоразвиты, и не достигать кончиков пальцев кистей рук. Данное состояние не обязательно указывает на степень их незрелости. У некоторых детей изредка наблюдается симптом «белых ногтей» как семейная аномалия, развивающаяся в результате подногтевого гиперкератоза. ЖЕЛТУХА НОВОРОЖДЕННЫХ Код МКБ-10:Р58.4 Встречается примерно у 50-70 % новорожденных и является вариантом нормы состояния детей при рождении. Желтуха проявляется на 2-4-е сутки жизни и полностью регрессирует через две недели после рождения. Клинически желтуха новорожденных характеризуется желтушной окраской кожных покровов различной степени интенсивности, склер и слизистых оболочек. Желтуха новорожденных появляется в результате гипербилирубинемии, которая возникает после установления легочного дыхания и сопровождается распадом избыточного гемоглобина в периферической крови детей. [стр. 349 ⇒]

Keratinocytes in the skin have toll-like receptors, which allow recognition of molecular patterns on a wide variety of pathogens. They are also capable of producing antimicrobial peptides and cytokines. Even in preterm neonates, the skin is capable of well-developed inflammatory responses, limiting damage from pathogens, toxins and trauma and promoting wound healing. However, the skin of the preterm infant is slow to mature both as a barrier and organ of innate immunity. Enhancing the local immunity and barrier function of the skin (e.g. application of vernix caseosa) may be a potential strategy to decrease the risk of infection in the preterm population. In the third edition of this textbook (previously edited by Solomon and Esterly) the editors, Eichenfield, Frieden, Mathes and Zaenglein, have expanded its scope to include skin disorders arising in the neonatal period and infancy. The wonderful aspects of the prior editions have been preserved or improved upon. The text is clearly written and enhanced by the many color photographs of dermatologic disorders. Whenever possible there is a renewed effort to include evidence-based recommendations. The genetic basis for many of the skin disorders is now known, and up-to-date information on the developmental differences in term and preterm infant skin has been expanded. Neonatal and Infant Dermatology is far more than an atlas. It is a state-of-the-art presentation of the diagnosis and management of skin disorders, and a road map for future interventions to enhance the well-being of the newborn infant. Richard A. Polin MD 2014... [стр. 8 ⇒]

Cells in this inner root sheath arise from self-renewing progenitor cells at the base of the follicle, which differentiate as they move upward toward the skin surface surrounding the hair shaft. Likewise, the three internal concentric layers of the hair shaft – cuticle, cortex, and medulla (from outer to inner) – arise from the matrix cells at the base of the follicle. These deep matrix cells sit on the basement membrane ‘mat,’ along the concavity of the hair follicle invagination in close proximity to the dermal papillae mesenchymal cells. By 19–21 weeks’ EGA, the hair canal has fully formed and the scalp hairs are visible just above the surface of the fetal epidermis.137,145,146 They continue to lengthen until 24–28 weeks, when they shift from the active growing phase (anagen) to the short-lived degenerative phase (catagen) and then to the resting phase (telogen).26,147 They then re-enter the active growing stage (second anagen), and the first wave of hairs is shed into the amniotic fluid as the new hairs grow out. Cycling through active and inactive phases continues for all hairs throughout the life of an individual,148 although cycles for individual hairs become asynchronous postnatally. The maintenance of a tight anatomic relationship between dermal papilla cells and the cycling ectodermal portion of the hair follicle is critical for follicular selfrenewal, and the inability to maintain this relationship results in a form of inherited alopecia, in which hair neogenesis is normal but, after the first resting phase, cycling is aberrant.132 Perinatally the second wave of fine lanugo hairs is shed. With subsequent cycles, hairs increase in diameter and coarseness, forming first vellus and then adult-type terminal hair shafts on the scalp and brow.147 During adolescence, vellus hairs of androgen-sensitive areas undergo a similar transition to terminal-type hair follicles. Sebaceous gland maturation occurs in parallel with that of the follicle proper and begins between 13 and 16 weeks’ EGA.149 Lipogenic cells produced by the outer proliferative layer of the sebaceous gland progressively accumulate lipid/sebum until they terminally differentiate, which results in their disintegration and the release of their products into the upper portion of the newly formed hair canal.150,151 The synthesis and secretion of sebum is accelerated in the second and third trimesters under the influence of maternal steroids and/or fetal adrenal dihydroepidandrosterone.152–154 Of note, the first evidence of the human epidermal permeability barrier in utero is in the vicinity of the pilosebaceous unit.15 Sebaceous lipids are also a prominent component of vernix caseosa.155 Fetal corneocytes associated with vernix may also derive from the pilosebaceous unit. Sebaceous gland hyperplasia and activity generally becomes quiescent during the first few postnatal months of life but may persist in cases of infantile acne (see Chapter 7). NAIL DEVELOPMENT The first evidence of nail formation is delineation of the flat surface of the future nail bed on the dorsal digit tip at 8–10 weeks,112,156 slightly earlier than the initiation of hair follicle development (Fig. 1.7). Along the proximal boundary of the early nail field a wedge of ectoderm buds inward at an oblique angle to the surface, forming the proximal nail fold. The presumptive nail matrix cells, which will give rise to the differentiated nail plate, reside on the ventral (deeper) side of the proximal invagination. At around 11 weeks, the dorsal surface of the nail... [стр. 26 ⇒]

Clinical paradigms INNATE IMMUNE FUNCTION A critical intrauterine function of the skin is the provision of innate immune protection from exogenous infection. Preterm delivery is highly associated with ascending infection from the vaginal vault and subsequent chorioamnionitis. When the infection cannot be confined to the amniotic sac, the fetus responds with a well-coordinated systemic inflammatory response linked to long-term neurological sequelae.10,21,22 During the last trimester, increasing levels of pulmonary surfactant are present in the amniotic fluid as measured by lung lamellar body counts.177 Significantly, analysis of these lamellar bodies show a paucity of contamination with lamellar bodies derived from the epidermis. Vernix caseosa, produced in part by the pilosebaceous apparatus, is present on the skin surface in the last trimester, interacts with pulmonary surfactant with subsequent detachment,178 and is swallowed by the fetus with potential effects on the developing gut (Fig. 1.9).179 Pulmonary surfactant and vernix caseosa both contain significant innate immune modulators and provide a first line of defense against microbial invasion of the amniotic fluid.10,180... [стр. 29 ⇒]

REFERENCES 1. Hoath SB. Physiological development of the skin. In: Polin RA, Fox WW, Abman SH, editors. Fetal and neonatal physiology. Philadelphia: Elsevier Saunders; 2011. p. 679– 95. 2. Hooker D. Development reaction to environment. Yale J Biol Med 1960;32:431–40. 3. Humphrey T. The development of human fetal activity and its relation to postnatal behavior. Adv Child Dev Behav 1970;5:1–57. 4. Martin DS, Khosravi M, Grocott MP, et al. Concepts in hypoxia reborn. Crit Care 2010; 14(4):315. 5. Leung A, Crombleholme TM, Keswani SG. Fetal wound healing: implications for minimal scar formation. Curr Opin Pediatr 2012;24(3): 371–8. 6. Montagu A. Touching: the human significance of the skin. 3rd ed. New York: Perennial Library; 1986. 7. Bradley RM, Mistretta CM. Fetal sensory receptors. Physiol Rev 1975;55(3):352–82. 8. Wakai RT, Lengle JM, Leuthold AC. Transmission of electric and magnetic foetal cardiac signals in a case of ectopia cordis: the dominant role of the vernix. caseosa. Phys Med Biol 2000;45(7):1989–95. 9. Niederkorn JY, Wang S. Immune privilege of the eye and fetus: parallel universes? Transplantation 2005;80(9):1139–44. 10. Hoath SB, Narendran V, Visscher MO. Vernix caseosa and innate immunity. In: Dayan N, Wertz P, editors. Innate immune system of skin and oral mucosa: properties and impact in pharmaceutics, cosmetics, and personal care products. New Jersey: John Wiley; 2011. 11. Brazelton T. Behavioral competence. In: Avery G, Fletcher M, MacDonald M, editors. Neonatology: pathophysiology and management of the newborn. Philadelphia: JB Lippincott; 1994. 12. van der Loos H, Dorfl J. Does the skin tell the somatosensory cortex how to construct a map of the periphery? Neurosci Lett 1978;7(1): 23–30. 13. Morris D. The naked ape: a zoologist’s study of the human animal. New York: Random House; 1999 (paperback edition). 14. Ambalavanan N, Carlo WA, Tyson JE, et al. Outcome trajectories in extremely preterm infants. Pediatrics 2012;130(1):e115–25. 15. Hardman MJ, Moore L, Ferguson MW, et al. Barrier formation in the human fetus is patterned. J Invest Dermatol 1999;113(6): 1106–13. 16. Madison KC. Barrier function of the skin: ‘la raison d’etre’ of the epidermis. J Invest Dermatol 2003;121(2):231–41. 17. Schaal B. Mammary odor cues and pheromones: mammalian infant-directed communication about maternal state, mammae, and milk. Vitam Horm 2010;83:83–136. 18. Schaal B, Marlier L, Soussignan R. Olfactory function in the human fetus: evidence from selective neonatal responsiveness to the odor of amniotic fluid. Behav Neurosci 1998; 112(6):1438–49. 19. Oftedal OT. The evolution of milk secretion and its ancient origins. Animal 2012;6(3): 355–68. 20. Hermansen MC, Hermansen MG. Perinatal infections and cerebral palsy. Clin Perinatol 2006;33(2):315–33. [стр. 33 ⇒]

Proc Natl Acad Sci U S A 1997;94(24):13069–74. Kere J, Srivastava AK, Montonen O, et al. X-linked anhidrotic (hypohidrotic) ectodermal dysplasia is caused by mutation in a novel transmembrane protein. Nat Genet 1996; 13(4):409–16. Holbrook KA, Odland GF. Structure of the human fetal hair canal and initial hair eruption. J Invest Dermatol 1978;71(6):385–90. Pinkus H. Embryology of hair. In: Montagna W, Ellis RA, editors. The biology of hair growth. New York: Academic Press; 1958. p. 1–32. Carlsen RA. Human fetal hair follicles: the mesenchymal component. J Invest Dermatol 1974;63(2):206–11. Hashimoto K. The ultrastructure of the skin of human embryos. V. The hair germ and perifollicular mesenchymal cells. Hair germmesenchyme interaction. Br J Dermatol 1970; 83(1):167–76. Breathnach AS, Smith J. Fine structure of the early hair germ and dermal papilla in the human foetus. J Anat 1968;102(Pt 3):511–26. Robins EJ, Breathnach AS. Fine structure of the human foetal hair follicle at hair-peg and early bulbous-peg stages of development. J Anat 1969;104(Pt 3):553–69. Lavker RM, Sun TT, Oshima H, et al. Hair follicle stem cells. J Invest Dermatol 2003; 8(1):28–38. Montagna W, Van Scott E. The anatomy of the hair follicle. In: Montagna W, Ellis RA, editors. The biology of hair growth. New York: Academic Press; 1958. p. 39–64. Serri F, Montagna W, Mescon H. Studies of the skin of the fetus and the child. II. Glycogen and amylophos-phorylase in the skin of the fetus. J Invest Dermatol 1962;39:199–217. Smith DW, Gong BT. Scalp-hair patterning: its origin and significance relative to early brain and upper facial development. Teratology 1974;9(1):17–34. Barth JH. Normal hair growth in children. Pediatr Dermatol 1987;4(3):173–84. Paus R. Principles of hair cycle control. J Dermatol 1998;25(12):793–802. Serri F, Huber MW. The development of sebaceous glands in man. In: Montagna W, Ellis RA, Silver AF, editors. Advances in biology of skin. The sebaceous glands. Oxford: Pergamon; 1963. p. 1–18. Fujita H, Asagami C, Murota S, et al. Ultrastructural study of embryonic sebaceous cells, especially of their sebum droplet formation. Acta Derm Venereol 1972;52(2):99–115. Williams ML, Hincenbergs M, Holbrook KA. Skin lipid content during early fetal development. J Invest Dermatol 1988;91(3):263–8. Pochi PE, Strauss JS, Downing DT. Age-related changes in sebaceous gland activity. J Invest Dermatol 1979;73(1):108–11. Zouboulis CC, Baron JM, Bohm M, et al. Frontiers in sebaceous gland biology and pathology. Exp Dermatol 2008;17(6):542–51. Zouboulis CC, Fimmel S, Ortmann J, et al. Sebaceous glands. In: Hoath SB, Maibach HI, editors. Neonatal skin: structure and function. 2nd ed. New York: Marcel Dekker; 2003. p. 59–88. Rissmann R, Groenink HW, Weerheim AM, et al. New insights into ultrastructure, lipid composition and organization of vernix caseosa. J Invest Dermatol 2006;126(8):1823–33. [стр. 35 ⇒]

Science 1996; 272(5268):1668–71. Xie J, Murone M, Luoh SM, et al. Activating Smoothened mutations in sporadic basal-cell carcinoma. Nature 1998;391(6662):90–2. Ridsdale R, Lewis DF, Weaver TE, et al. Proteomic analysis of lamellar bodies isolated from amniotic fluid: implications for function. Am J Perinatol 2012;29(6):419–28. Narendran V, Wickett RR, Pickens WL, et al. Interaction between pulmonary surfactant and vernix: a potential mechanism for induction of amniotic fluid turbidity. Pediatr Res 2000; 48(1):120–4. Ran-Ressler RR, Devapatla S, Lawrence P, et al. Branched chain fatty acids are constituents of the normal healthy newborn gastrointestinal tract. Pediatr Res 2008;64(6):605–9. Akinbi HT, Narendran V, Pass AK, et al. Host defense proteins in vernix caseosa and amniotic fluid. Am J Obstet Gynecol 2004;191(6): 2090–6. [стр. 36 ⇒]

Stratum corneum and epidermis The most obvious clinical difference between the skin of the term newborn and that of an adult is the presence of the moist, greasy, yellow-white substance called vernix caseosa, which is a coating comprised of a combination of sebaceous gland secretions, desquamated skin cells, and shed lanugo hairs.2,3 The vernix caseosa has an important role in maintaining hydration and pH balance, and preventing infection during the first few days of life.4,5 Certain components of the innate immune system, termed antimicrobial polypeptides (see ‘Cutaneous immunosurveillance, Langerhans’ cells, and cytokines’, below), have been isolated in the vernix and probably play an important role in surface defense in the newborn.4,6,7 This coating persists for the first several days of postnatal life, eventually disappearing completely to reveal the more typical, moderately dry newborn skin. Vernix provides water-binding free amino acids, which may help to facilitate the neonate’s adaptation from the amniotic fluid intrauterine milieu to the ambient dryness of the extrauterine environment.8 Vernix-based topical creams have been investigated for treatment of epidermal wounds and augmentation of barrier repair in infants.9 14... [стр. 37 ⇒]

Various models and terms have been used to describe the immunologic capacities of the skin, including skin-associated lymphoid tissues (SALT), skin immune system (SIS), dermal microvascular unit (DMU), and dermal immune system (DIS).161,162 SALT are composed of epidermal Langerhans’ cells and keratinocytes, as well as dermal endothelial cells and the skin-draining lymph nodes, and are an important system in the induction of immunity and tolerance.162 The broader terminology of the SIS refers to the entire complex interplay of immune response-related systems in the skin, including cellular components and humoral factors,162,163 and both dermal and epidermal components. These immunologic systems in the skin provide cutaneous immunosurveillance, which functions in the prevention of the development of cutaneous neoplasms and mediates against persistent infections with intracellular pathogens.164 Cellular components include keratinocytes, antigen-presenting cells (APCs), monocytes and macrophages, granulocytes, mast cells, lymphocytes, and endothelial cells, whereas humoral constituents include antimicrobial peptides, complement proteins, immunoglobulins, cytokines, and prostaglandins.162 Antimicrobial peptides and proteins are an important innate cutaneous defense mechanism against microbial intruders. They have a broad-spectrum killing activity, and their presence in both amniotic fluid and vernix caseosa has been well documented, suggesting that effective innate immune protection begins during fetal and early neonatal life.4,6,165,166 Human antimicrobial peptides include the cathelicidin, dermacidin and β-defensin families. Regulation of these peptides may involve Ca2+, 1, 25(OH)2VD3, retinoic acids, and kallikreins.167,168 Characterization of lymphocyte populations within normal human skin has revealed that they are predominantly T cells, with 90% of cells clustered around postcapillary venules or adjacent to cutaneous appendages.163,169 Intraepidermal localization of T lymphocytes accounts for less than 2% of skin lymphocytes normally present. B lymphocytes are not present in normal human skin, but may be found in mucosal locations. LANGERHANS’ CELLS The cell that sets the SIS apart from others is the Langerhans’ cell (LC). This APC resides in the epidermis and is involved in skin allograft rejection, delayed hypersensitivity reactions, and specific T-cell responses.170 LCs are derived from the bone marrow and migrate via a hematogenous route to the skin. They are present in the fetus as early as 16 weeks’ gestation, with early restriction to the basal layer and eventual distribution among suprabasal cells.171 The function of the LC was unclear until the 1970s, when surface Fc receptors, major histocompatibility complex (MHC) class II molecules, and C3 receptors were described on its surface,164 suggesting an immunologic role. It is now well accepted that the epidermal LC is involved in antigen processing and presentation in a variety of skin-induced immune responses against a variety of antigens, including contact allergens, alloantigens, tumor antigens, and microorganisms.172 These cells have been found to have positive staining for other characteristic surface markers, including CD1a and S100 proteins and membrane-bound adenosine triphosphatase (ATPase).172 Although the exact function of the CD1a glycoprotein remains... [стр. 45 ⇒]

REFERENCES 1. White CR, Bigby M, Sangueza OP. What is normal skin? In: Arndt KA, LeBoit PE, Robinson JK, et al, editors. Cutaneous medicine and surgery. An integrated program in dermatology. Philadelphia: WB Saunders; 1996. p. 3–45. 2. Holbrook KA. A histological comparison of infant and adult skin. In: Maibach HI, Boisits EK, editors. Neonatal skin, structure and function. New York: Marcel Dekker; 1982. p. 3–31. 3. Solomon LM, Esterly NB. Neonatal dermatology. I. The newborn skin. J Pediatr 1970;77: 888–94. 4. Marchini G, Lindow S, Brismar H, et al. The newborn infant is protected by an innate antimicrobial barrier: peptide antibiotics are present in the skin and vernix caseosa. Br J Dermatol 2002;147:1127–34. 5. Visscher MO, Narendran V, Pickens WL, et al. Vernix caseosa in neonatal adaptation. J Perinatol 2005;25:440–6. 6. Yoshio H, Tollin M, Gudmundsson GH, et al. Antimicrobial polypeptides of human vernix caseosa and amniotic fluid: implications for newborn innate defense. Pediatr Res 2003;53: 211–6. 7. Yoshio H, Lagercrantz H, Gudmundsson GH, et al. First line of defense in early human life. Semin Perinatol 2004;28:304–11. 8. Visscher MO, Utturkar R, Pickens WL, et al. Neonatal skin maturation – Vernix caseosa and free amino acids. Pediatr Dermatol 2011; 28(2):122–32). 9. Visscher MO, Barai N, LaRuffa AA, et al. Epidermal barrier treatments based on vernix caseosa. Skin Pharmacol Physiol 2011;24(6): 322–9. 10. Serri F, Montagna W. The structure and function of the epidermis. Pediatr Clin North Am 1961;8:917–41. 11. Holbrook KA, Sybert VP. Basic science. In: Schachner LA, Hansen RC, editors. Pediatric dermatology. 2nd ed. New York: Churchill Livingstone; 1995. p. 1–70. 12. Evans NJ, Rutter N. Development of the epidermis in the newborn. Biol Neonate 1986;49:74–80. 13. Wickett RR, Mutschelknaus JL, Hoath SB. Ontogeny of water sorption–desorption in the perinatal rat. J Invest Dermatol 1993;100: 407–11. 14. Fuchs E. Keratins: mechanical integrators in the epidermis and hair and their role in disease. Prog Dermatol 1996;30:1–12. 15. Fuchs E, Weber K. Intermediate filaments: structure, dynamics, function, and disease. Annu Rev Biochem 1994;63:345–82. 16. Byrne C, Tainsky M, Fuchs E. Programming gene expression in developing epidermis. Development 1994;120:2369–83. 17. Coolen NA, Schouten KC, Middelkoop E, et al. Comparison between human fetal and adult skin. Arch Dermatol Res 2010;302:47–55. 18. Bressler RS, Bressler CH. Functional anatomy of the skin. Clin Podiatr Med Surg 1989;6: 229–46. 19. Haake AR, Holbrook KA. The structure and development of skin. In: Freedberg IM, Eisen AZ, Wolff K, et al., editors. Dermatology in general medicine. 5th ed. New York: McGrawHill; 1999. p. 70–114. 20. Dale BA, Holbrook KA, Steinert PM. Assembly of stratum corneum basic protein and keratin... [стр. 47 ⇒]

Introduction The premature infant assumes the challenge of postnatal life, despite the immaturity of essential functions. Skin functions are primarily protective, and immaturity of the skin contributes to the vulnerability of the preterm infant. The main function of the skin is to provide a permeability barrier that both protects the aqueous interior of the infant from desiccation in the xeric atmosphere and prevents massive influx of water when immersed in hypotonic solutions.1 Other important functions of skin include barriers to percutaneous absorption of exogenous xenobiotics, to injury from mechanical trauma, to colonization and penetration by microorganisms, and to injury from ultraviolet light. In addition to its barrier functions, skin also participates in the thermoregulatory, neurosensory, and immunologic systems. The consequences of skin immaturity for the premature infant depend on the infant’s position on the maturational timetable for each cutaneous function, which is in turn dependent on the infant’s gestational and postnatal ages. All skin layers (i.e. epidermis, dermis, and subcutaneous fat) are thinner in the preterm infant than at term (Table 4.1).2 Because the outermost layers of the epidermis (i.e. the stratum corneum) are the primary effectors of most of the barrier properties of skin, the timetable for maturation of the stratum corneum predicts the competence of many skin functions. Stratum corneum begins to form around hair follicles at about 14 weeks’ gestational age and spreads to include the epidermis between hair follicles by 22–24 weeks’ gestational age (see Table 1.2). During the ensuing weeks, the thickness of the stratum corneum increases from only a few to several cell layers,2 such that by term, it is actually thicker than adult stratum corneum. The ‘excess’ outermost layers of stratum corneum are then shed during the first days of life; this process of physiologic desquamation is accentuated in postmature babies. Another component of fetal skin, the vernix caseosa (a complex proteolipid material) is formed in part by sebaceous gland secretions beginning at about 28 weeks’ gestational age. The percentage surface area covered with vernix peaks at 33–37 weeks’ gestational age, then decreases in full-term and post-term infants. Its functions may include roles in temperature regulation, permeability barrier, and innate immunity.3 The histologic features described above underlie the clinical characteristics of skin maturation embodied in the Ballard scale (see Table 1.5) widely used for assessing gestational age.4 In the extremely premature infant (<24 weeks), the skin is sticky, friable, and transparent (Fig. 4.1); lanugo hairs are absent. As gestation progresses, the skin becomes less transparent, and peeling and surface cracking are increasingly seen, indicative of a thickening stratum corneum, and lanugo hair density peaks and then regresses. Despite definition of these milestones of gross and microscopic skin development, with the exception of 36... [стр. 64 ⇒]

102 Skin fragility is a major problem in the care of the preterm infant. They are vulnerable to abrasions and deeper wounds from the use of adhesive tapes to secure monitors, airways, and intravenous lines (see Fig. 4.3B; see also Chapter 8). Similarly, the threshold for irritant contact dermatitis from fecal contact (diaper dermatitis), for chemical burns from prolonged contact with antiseptics,90 or for thermal burns is much reduced.103 Gentle handling, minimal use of adhesives coupled with substitution of hydrophilic gel104 or pectin barrier105 adhesives only when required, and the use of adhesive removers,106 can minimize these injuries. A regimen of emollient lubrication or use of nonadherent, semipermeable dressings may also help protect against mechanical injuries (see above). CUTANEOUS BARRIER TO INFECTION Although mature skin is colonized by a variety of bacteria and other microorganisms, these organisms are effectively excluded from the interior. The basis for the barrier to transcutaneous infection includes both provision of a mechanical shield against invading microorganisms and specific components, such as certain lipids107,108 and antimicrobial peptides (defensins and cathelicidins) in the stratum corneum, that inhibit the growth of microorganisms and modulate immune responses.109 The thinner, easily abraded stratum corneum of the preterm infant constitutes an impaired mechanical shield against the ingress of microorganisms. In addition, specific biochemical components of the cutaneous barrier to infection may also be immature in preterm infants. Extremely preterm infants also lack the initial protection of antimicrobial peptides in vernix caseosa.3,110 The contribution of the vernix to the antimicrobial barrier is unknown. Preterm infants’ skin is colonized soon after birth with coagulase-negative staphylococci, predominantly S. epidermidis. Colonization with Malassezia and Propionibacterium occurs later, after 3 weeks,111 coincident with the maturation of the permeability barrier. S. epidermidis has become the most frequent cause of postnatally acquired systemic infections in these infants.112–115 Malassezia, as well as the opportunistic fungi Aspergillus, Candida, and Rhizopus, are also systemic pathogens in this group.116–119 Direct invasion across the immature epidermis by fungi of low pathogenicity in very preterm infants has been documented,120 although exploitation of a portal of entry, such as site of skin injury or along transcutaneous catheter lines, is probably a more common means of entry. Regardless of the route of transcutaneous entry, the immaturity of the immune system, particularly opsonic mechanisms, then permits organisms of low pathogenic potential to mature hosts to establish disease in the preterm infant.121 The use of intravenous lipid supplements also favors the establishment of a nidus of infection once entry into the circulation has been obtained.113 CUTANEOUS BARRIER TO LIGHT INJURY Energy absorbed from ultraviolet (UV) light passing through the skin may damage critical cellular functions through the generation of free radicals, principally singlet oxygen, as well as through inflammatory responses initiated by cytokine release and the generation of eicosanoids. [стр. 69 ⇒]

REFERENCES 1. Elias PM, Menon GK. Structural and lipid biochemical correlates of the epidermal permeability barrier. Adv Lipid Res 1991;24:1–26. 2. Evans NJ, Rutter N. Development of the epidermis in the newborn. Biol Neonate 1986; 49(2):74–80. 3. Visscher MO, Narendran V, Pickens WL, et al. Vernix caseosa in neonatal adaptation. J Perinatol 2005;25(7):440–6. 4. Ballard JL, Khoury JC, Wedig K, et al. New Ballard Score, expanded to include extremely premature infants. J Pediatr 1991;119(3): 417–23. 5. Hammarlund K, Sedin G. Transepidermal water loss in newborn infants. III. Relation to gestational age. Acta Paediatr Scand 1979;6 8(6):795–801. 6. Harpin VA, Rutter N. Barrier properties of the newborn infant’s skin. J Pediatr 1983;102(3): 419–25. 7. Nachman RL, Esterly NB. Increased skin permeability in preterm infants. J Pediatr 1971; 79(4):628–32. 8. Okah FA, Wickett RR, Pickens WL, et al. Surface electrical capacitance as a noninvasive bedside measure of epidermal barrier maturation in the newborn infant. Pediatrics 1995; 96(4 Pt 1):688–92. 9. Emery MM, Hebert AA, Aguirre Vila-Coro A, et al. The relationship between skin maturation and electrical skin impedance. J Dermatol Sci 1991;2(5):336–40. 10. Aszterbaum M, Menon GK, Feingold KR, et al. Ontogeny of the epidermal barrier to water loss in the rat: correlation of function with stratum corneum structure and lipid content. Pediatr Res 1992;31(4 Pt 1):308–17. 11. Williams ML, Hanley K, Elias PM, et al. Ontogeny of the epidermal permeability barrier. J Investig Dermatol Symp Proc 1998;3(2):75–9. 12. Kalia YN, Nonato LB, Lund CH, et al. Development of skin barrier function in premature infants. J Invest Dermatol 1998;111(2):320–6. 13. Agren J, Sjors G, Sedin G. Transepidermal water loss in infants born at 24 and 25 weeks of gestation. Acta Paediatr 1998;87(11): 1185–90. 14. Hanley K, Jiang Y, Elias PM, et al. Acceleration of barrier ontogenesis in vitro through air exposure. Pediatr Res 1997;41(2):293–9. 15. Williams ML, Feingold KR. Barrier function of neonatal skin. J Pediatr 1998;133(3):467–8. 16. Agren J, Sjors G, Sedin G. Ambient humidity influences the rate of skin barrier maturation in extremely preterm infants. J Pediatr 2006; 148(5):613–17. 17. Hammarlund K, Sedin G. Transepidermal water loss in newborn infants. IV. Small for gestational age infants. Acta Paediatr Scand 1980;69(3):377–83. 18. Aszterbaum M, Feingold KR, Menon GK, et al. Glucocorticoids accelerate fetal maturation of the epidermal permeability barrier in the rat. J Clin Invest 1993;91(6):2703–8. 19. Effect of corticosteroids for fetal maturation on perinatal outcomes. NIH Consensus Development Panel on the Effect of corticosteroids for fetal maturation on perinatal outcomes. JAMA 1995;273(5):413–18. 20. Omar SA, DeCristofaro JD, Agarwal BI, et al. Effects of prenatal steroids on water and sodium homeostasis in extremely low birth weight neonates. Pediatrics 1999;104(3 Pt 1): 482–8. [стр. 74 ⇒]

Egypt: a randomized, controlled clinical trial. Pediatr Infect Dis J 2004;23(8):719–25. 57. Darmstadt GL, Saha SK, Ahmed AS, et al. Effect of skin barrier therapy on neonatal mortality rates in preterm infants in Bangladesh: a randomized, controlled, clinical trial. Pediatrics 2008;121(3):522–9. 58. Darmstadt GL, Saha SK, Ahmed AS, et al. Effect of topical treatment with skin barrierenhancing emollients on nosocomial infections in preterm infants in Bangladesh: a randomised controlled trial. Lancet 2005; 365(9464):1039–45. 59. Man MQ, Feingold KR, Elias PM. Exogenous lipids influence permeability barrier recovery in acetone-treated murine skin. Arch Dermatol 1993;129(6):728–38. 60. Zettersten EM, Ghadially R, Feingold KR, et al. Optimal ratios of topical stratum corneum lipids improve barrier recovery in chronologically aged skin. J Am Acad Dermatol 1997;37(3 Pt 1):403–8. 61. Sugarman JL, Parish LC. Efficacy of a lipidbased barrier repair formulation in moderateto-severe pediatric atopic dermatitis. J Drugs Dermatol 2009;8(12):1106–11. 62. Visscher MO, Barai N, LaRuffa AA, et al. Epidermal barrier treatments based on vernix caseosa. Skin Pharmacol Physiol 2011;24(6): 322–9. 63. West DP, Halket JM, Harvey DR, et al. Percutaneous absorption in preterm infants. Pediatr Dermatol 1987;4(3):234–7. 64. Rutter N. Percutaneous drug absorption in the newborn: hazards and uses. Clin Perinatol 1987;14(4):911–30. 65. Scheuplein RJ, Blank IH. Permeability of the skin. Physiol Rev 1971;51(4):702–47. 66. West DP, Worobec S, Solomon LM. Pharmacology and toxicology of infant skin. J Invest Dermatol 1981;76(3):147–50. 67. Menon GK, Elias PM. Morphologic basis for a pore-pathway in mammalian stratum corneum. Skin Pharmacol 1997;10(5–6): 235–46. 68. Froman RD, Owen SV, Murphy C. Isopropyl pad use in neonatal intensive care units. J Perinatol 1998;18(3):216–20. 69. Linder N, Davidovitch N, Reichman B, et al. Topical iodine-containing antiseptics and subclinical hypothyroidism in preterm infants. J Pediatr 1997;131(3):434–9. 70. Lashkari HP, Chow P, Godambe S. Aqueous 2% chlorhexidine-induced chemical burns in an extremely premature infant. Arch Dis Child Fetal Neonatal Ed 2012;97(1):F64. 71. Bringue Espuny X, Soria X, Sole E, et al. Chlorhexidine-methanol burns in two extreme preterm newborns. Pediatr Dermatol 2010; 27(6):676–8. 72. Mannan K, Chow P, Lissauer T, et al. Mistaken identity of skin cleansing solution leading to extensive chemical burns in an extremely preterm infant. Acta Paediatr 2007;96(10): 1536–7. 73. Harpin V, Rutter N. Percutaneous alcohol absorption and skin necrosis in a preterm infant. Arch Dis Child 1982;57(6):477–9. 74. Reynolds PR, Banerjee S, Meek JH. Alcohol burns in extremely low birthweight infants: still occurring. Arch Dis Child Fetal Neonatal Ed 2005;90(1):F10. 75. Rogers SC, Burrows D, Neill D. Percutaneous absorption of phenol and methyl alcohol in Magenta Paint B.P.C. Br J Dermatol 1978; 98(5):559–60. [стр. 75 ⇒]

Acta Paediatr Scand Suppl 1989;360: 37–42. 95. Oh W, Poindexter BB, Perritt R, et al. Association between fluid intake and weight loss during the first ten days of life and risk of bronchopulmonary dysplasia in extremely low birth weight infants. J Pediatr 2005;147(6): 786–90. 96. Musemeche CA, Kosloske AM, Bartow SA, et al. Comparative effects of ischemia, bacteria, and substrate on the pathogenesis of intestinal necrosis. J Pediatr Surg 1986;21(6):536–8. 97. Willoughby RE Jr, Pickering LK. Necrotizing enterocolitis and infection. Clin Perinatol 1994;21(2):307–15. 98. Bell EF, Warburton D, Stonestreet BS, et al. High-volume fluid intake predisposes premature infants to necrotising enterocolitis. Lancet 1979;2(8133):90. 99. Nowicki PT, Nankervis CA. The role of the circulation in the pathogenesis of necrotizing enterocolitis. Clin Perinatol 1994;21(2): 219–34. 100. Crissinger KD, Granger DN. Mucosal injury induced by ischemia and reperfusion in the piglet intestine: influences of age and feeding. Gastroenterology 1989;97(4):920–6. 101. Williams ML, Le K. The permeability barrier in the preterm infant: Review of the clinical consequences of barrier immaturity and of insights derived from an animal model of barrier ontogenesis, with a call for future studies. Eur J Pediatr Dermatol 1998;8(8): 101–6. 102. Morasso MI, Chu DH, Schwartz T. Structure and function of the skin. In: Schachner LA, Hansen RC, editors. Pediatric dermatology. 4th ed. Philadelphia: Elsevier; 2011. p. 1. 103. Rimdeika R, Bagdonas R. Major full thickness skin burn injuries in premature neonate twins. Burns 2005;31(1):76–84. 104. Lund CH, Nonato LB, Kuller JM, et al. Disruption of barrier function in neonatal skin associated with adhesive removal. J Pediatr 1997; 131(3):367–72. 105. Dollison EJ, Beckstrand J. Adhesive tape vs pectin-based barrier use in preterm infants. Neonatal Netw 1995;14(4):35–9. 106. Denyer J. Reducing pain during the removal of adhesive and adherent products. Br J Nurs 2011;20(15):S28, S30–5. 107. Miller SJ, Aly R, Shinefeld HR, et al. In vitro and in vivo antistaphylococcal activity of human stratum corneum lipids. Arch Dermatol 1988;124(2):209–15. 108. Bibel DJ, Aly R, Shinefield HR. Topical sphingolipids in antisepsis and antifungal therapy. Clin Exp Dermatol 1995;20(5):395–400. 109. Braff MH, Bardan A, Nizet V, et al. Cutaneous defense mechanisms by antimicrobial peptides. J Invest Dermatol 2005;125(1):9–13. 110. Marchini G, Lindow S, Brismar H, et al. The newborn infant is protected by an innate antimicrobial barrier: peptide antibiotics are present in the skin and vernix caseosa. Br J Dermatol 2002;147(6):1127–34. 111. Eastick K, Leeming JP, Bennett D, et al. Reservoirs of coagulase negative staphylococci in preterm infants. Arch Dis Child Fetal Neonatal Ed 1996;74(2):F99–104. 112. Freeman J, Epstein MF, Smith NE, et al. Extra hospital stay and antibiotic usage with nosocomial coagulase-negative staphylococcal bacteremia in two neonatal intensive care unit populations. Am J Dis Child 1990;144(3): 324–9. [стр. 75 ⇒]

Skin care practices SKIN CLEANSING For both children and adults, bathing is a hygienic necessity. The goal of hygiene is the preservation of skin health. However, there is a balance between cleansing the skin and preservation of its homeostatic properties such as skin barrier integrity.49 Cleansing is essential to remove pathogenic bacteria such as those from feces. Feces, saliva and other body secretions contain enzymes such as lipases and proteases that breakdown the skin barrier. However, frequent bathing of infants is more of a cultural and aesthetic practice that allows for tactile interaction with the caregiver. Benefits must be carefully considered along with the detrimental effects that can occur with bathing, especially in premature infants.49,50 A balance needs to be reached between the frequency of bathing to achieve optimal cleansing and maintaining an intact skin barrier. For neonates, bathing can lead to hypothermia, increased oxygen consumption, respiratory distress, and destabilized vital signs.51 Therefore, the first bath should be delayed until after vital signs and temperature have remained stable for at least 2–4 h.52,53 Immersion bathing, when feasible, may be beneficial from a developmental perspective. It is more soothing, and can promote enhanced sleep,54,55 and in studies, was not associated with significant differences in oxygen saturation, respiratory rate, or heart rate in premature infants of less than 32 weeks’ gestation.56 The water level should be high enough to cover the infant’s entire body to aid temperature control and decrease evaporative heat loss. The optimal temperature of bath water is 100.4°F, which should always be accurately measured. Second-degree burns have been reported after immersion into overly hot bath water tested only by touch.57 Sponge bathing with a moistened cotton ball or cloth is an acceptable alternative. Immediately after bathing, the infant’s skin should be gently towel dried and a head covering applied.52 Vernix caseosa, composed of sebaceous gland secretions, desquamated skin cells, and shed lanugo hairs,58 is negligible in preterm infants. Vernix need not be removed,49 as this layer may aid in thermoregulation, hydration, bacterial protection, and wound healing.58–61 The first bath should be given respecting universal precautions to limit contact with transmissible pathogens. The optimal frequency of bathing is open to debate.62–64 Research suggests that bathing twice a week will not affect TEWL or skin surface pH, assuming that mild products are used,65 and as such, Blume-Peytavi and colleagues recommend that bathing take place no more frequently than every other day.13 The use of water alone or water with added skin cleaning products for bathing has led to considerable debate.66 Soaps and... [стр. 80 ⇒]

Pediatrics 1996;98: 963–5. 58. Joglekar VM. Barrier properties of vernix caseosa. Arch Dis Child 1980;55:817–19. 59. Hoath SB. The stickiness of newborn skin: bioadhesion and the epidermal barrier. J Pediatr 1997;131:338–40. 60. Tollin M, Bergsson G, Kai-Larsen Y, et al. Vernix caseosa as a multi-component defence system based on polypeptides, lipids and their interactions. Cell Mol Life Sci 2005;62: 2390–9. 61. Yoshio H, Tollin M, Gudmundsson GH, et al. Antimicrobial polypeptides of human vernix caseosa and amniotic fluid: implications for newborn innate defense. Pediatr Res 2003;53: 211–16. 62. Camm J. Skincare for newborns: guidelines and advice. RCM Midwives 2006;9:126. 63. Drennan VG, Goodman C. Oxford handbook of primary care and community nursing. Oxford: Oxford University Press; 2007. 64. Hughes K. Advocating good practice in skin protection. Br J Midwifery 2011;19:773–5. 65. Garcia Bartels N, Mieczko A, Schink, T, et al. Influence of bathing or washing on skin barrier function in newborns during the first four weeks of life. Skin Pharmacol Physiol 2009; 22(5):248–57. 66. Lavender T, Bedwell C, Tsekiri-O’Brien E, et al. A qualitative study exploring women’s and health professional’s views of newborn bathing practices. Evid base Midwifery 2009;7:112– 21. 67. Gfatter R, Hackl P, Braun F. Effects of soap and detergents on skin surface pH, stratum corneum hydration and fat content in infants. Dermatology 1997;195:258–62. 68. Tsai TF, Maibach HI. How irritant is water? An overview. Contact Dermatitis 1999;41:311–14. 69. Ananthapadmanabhan KP, Moore DJ, Subramanyan K, et al. Cleansing without compromise: the impact of cleansers on the skin barrier and the technology of mild cleansing. Dermatol Therapy 2004;17(Suppl. 1): 16–25. 70. Crozier K, Macdonald S. Effective skin-care regimes for term newborn infants: a structured literature review. Evid base Midwifery 2010;8: 128–35. 71. Garcia Bartels N, Scheufele R, Prosch F, et al. Effect of standardized skin care regimens on neonatal skin barrier function in different body areas. Pediatr Dermatol 2010;27:1–8. 72. Dizon MV, Galzote C, Estanislao R, et al. Tolerance of baby cleansers in infants: a randomized controlled trial. Indian Pediatr 2010; 47:959–63. 73. Lavender T, Bedwell C, Roberts SA, et al. Randomized, controlled trial evaluating a baby wash product on skin barrier function in healthy, term neonates. J Obstet Gynecol Neonatal Nurs 2013;42:203–14. 74. Simon NP, Simon MW. Changes in newborn bathing practices may increase the risk for omphalitis. Clin Pediatr (Phila) 2004;43: 763–7. 75. Archer GL. Alteration of cutaneous staphylococcal flora as a consequence of antimicrobial prophylaxis. Rev Infect Dis 1991;13(Suppl. 10):S805–9. 76. Chen YE, Tsao H. The skin microbiome: Current perspectives and future challenges. J Am Acad Dermatol 2013;69:143–55. 77. Janniger CK, Bryngil JM. Hair in infancy and childhood. Cutis 1993;51:336–8. [стр. 89 ⇒]

’ It occurs primarily in fullterm African-descent infants in both sexes. In the 1976 report, 4.4% of African-American and 0.6% of Caucasian infants were affected.61 Lesions were always present at birth. TNPM has three phases and hence three types of lesion. First, very superficial vesicopustules, ranging in size from 2 mm to as large as 10 mm, may be present in utero and are virtually always evident at birth (Fig. 7.11A). Because they are intracorneal and subcorneal, and thus very fragile, the pustules may be easily wiped away during the initial cleaning of the infant to remove vernix caseosa, so that the pustular phase may not be evident (Fig. 7.11B). The second phase is represented by a fine collarette of scale around the resolving pustule (Fig. 7.11C). The third phase consists of hyperpigmented brown macules at the site of previous pustulation (Fig. 7.11D). Although these macules have been called ‘lentigines’ (because of their resemblance to lentils), they are not true lentigines but appear to represent transient postinflammatory hyperpigmentation. They may last for up to several months before they fade. Some infants are born with these macules, the pustular phase having presumably occurred in utero. The most common location for TNPM has been under the chin, on the forehead, at the nape, and on... [стр. 108 ⇒]

TRANSIENT PIGMENTARY CHANGES NOT CAUSED BY MELANIN Physiologic jaundice results from transient elevation of serum bilirubin, resulting in a generalized yellow discoloration of the skin in the first few days of life (Figs 7.25, 7.26). With jaundice, in contrast to carotenemia, which occurs later in infancy at age 1–2 years, there is yellow discoloration of the sclerae as well as the skin. Physiologic jaundice fades after the bilirubin returns to normal. Meconium staining often will darken the vernix caseosa but can also leave patchy, yellow-brown pigmentation, especially on desquamating epidermis. COLOR CHANGES RESULTING FROM VASCULAR ABNORMALITIES Cutaneous vasomotor instability The ability of neonates to adjust to extrauterine surroundings is at first immature, and they can exhibit distinct cutaneous blood flow abnormalities. When neonates are cold, their constricted capillaries and venules may produce a reticulated, mottled, blanchable, violaceous pattern termed cutis marmorata (Figs 7.27, 7.28). Exposure to cold temperatures may also induce more vasoconstriction in acral than central areas of the body, resulting in deep violaceous to blue coloration of the hands, feet and lips, termed acrocyanosis (Fig. 7.29). Both of these conditions occur more often in premature infants. These transient conditions rapidly improve upon rewarming of the infant, and the tendency to occur diminishes with age. Cutis marmorata should not be confused with cutis marmorata telangiectatica congenita, a vascular malformation that persists for several years and occurs in large, well-defined patches. The so-called ‘harlequin’ color change is a rare physiologic phenomenon, whereby the amount of blood flow differs markedly on the right and left sides of the body, with a sharp cutoff at the midline.82,83 This is most often seen when a child is lying on one side, the dependent side exhibiting vasodilation and being strikingly redder than the upper half of the body (Fig. 7.30). The face and genitalia may be spared. Episodes last from seconds to minutes and are rapidly reversible with a change in... [стр. 116 ⇒]

Januário G, Salgado M. The Harlequin phenomenon. J Eur Acad Dermatol Venereol 2011; 25(12):1381–4. 84. Cordoro KM, Speetzen LS, Koerper MA, et al. Physiologic changes in vascular birthmarks during early infancy: Mechanisms and clinical implications. J Am Acad Dermatol 2009;60(4): 669–75. 85. Juern AM, Glick ZR, Drolet BA, et al. Nevus simplex: a reconsideration of nomenclature, sites of involvement, and disease associations. J Am Acad Dermatol 2010;63:805–14. 86. Bergsson TM, Kai-Larsen G, Lengqvist J, et al. Vernix caseosa as a multi-component defence system based on polypeptides, lipids and their interactions. Cell Mol Life Sci 2005;62:2390–9. 87. Narendran V, Visscher MO, Abril I, et al. Biomarkers of epidermal innate immunity in premature and full-term infants. Pediatr Res 2010; 67(4):382–6. 88. Visscher MO, Utturkar R, Pickens WL, et al. Neonatal skin maturation – vernix caseosa and free aminoacids. Pediatr Dermatol 2011;28(2): 122–32. [стр. 123 ⇒]

V Vaccination, cutaneous reactions to, 91–92 Vacuum extraction, untoward effects of, 80, 80f Vancomycin, 308 Varicella embryopathy. see Varicella infection Varicella infection, 124–125, 182–186 fetal varicella syndrome, 182–184, 182f infantile herpes zoster, 181t, 185–186, 185f, 185. e1f infantile varicella (chickenpox), 181t, 186, 186. e1f neonatal, 146, 181t, 184–185, 184f neonatal nursery and intensive care unit, special concerns for, 185 Varicella zoster immunoglobulin (VZIG), 184 Varicella zoster virus (VZV), 182 DFA for, 57 diagnosis of, 179t Vascular anomalies, ulcerations in, 136–137 Vascular malformations, 352–368 combined, 359 syndromes associated with, 359–367, 360t Vascular networks, in newborn skin, 20–21, 21f Vascular tumor, tufted angioma, 524 Vasculogenesis, 6 Vasomotor instability, cutaneous, 74, 74.e1f–74.e2f Vasomotor tone, in newborn skin, 20–21 Vasospasm, in umbilical artery catheterization, 85 Vegetant bromoderma, 308 Venous malformations (VM), 355–357, 498t, 501–502 course of, 356 cutaneous findings in, 355–356, 355f diagnosis of, 356 differential diagnosis in, 356 extracutaneous findings in, 356 management of, 356–357 pathogenesis of, 355 syndromes associated with, 361–363 Vernix caseosa, 9, 11, 14, 36, 49, 75–76, 75f Vernix detachment in utero, and multiple fetal organ interactions, 11f Verrucae, 34f, 258 Verrucous hemangioma (VH), 363 Vesicles, 25t–27t, 26f, 111–139 conditions presenting with, 114b in hand, foot, and mouth disease, 259f in impetigo, 156... [стр. 750 ⇒]

DESQUAMATION So far, the above discussion has centered on natural ways in which the human skin has evolved to retain water. In addition to hydrating the skin, water also plays a crucial role in the exfoliation or desquamation of corneocytes. Corneocytes are linked in the lower stratum corneum by corneodesmosomes, which are macromolecular glycoprotein complexes. As the corneocytes move from the lower to the outer region of the stratum corneum, the corneodesmosomes are progressively degraded by hydrolytic enzymes. This leads to desquamation in the outer stratum corneum. These enzymes include serine proteases such as stratum corneum chymotryptic enzyme (SCCE) and stratum corneum tryptic-like enzyme (SCTE), which are more effective at neutral pHs and are most active on the outermost layers of the stratum corneum (19,47,93–95). The cathepsin family of proteases is more active under lower pH conditions and are present throughout the stratum corneum. Other proteases include cysteine proteases, sulfatases, and glycosidases. Many of these enzymes are localized in the intercellular space, and their activity is affected by both the lipid organization and water content (20,96). Clearly, low water content within the stratum corneum affects the activities of stratum corneum proteases, which leads to dry, flaky skin. Recently, these changes have been studied as a function of season, anatomical site, and skin depth (97). To maintain these processes, in vitro results suggest that optimally hydrated skin requires water content between 10% and 20% (13). ENVIRONMENTAL IMPACT ON SKIN HYDRATION Changes in lipid biosynthesis (71,98), epidermal DNA synthesis (9), barrier function (99), and skin thickness (100) are all influenced by the skin’s water content. There are many studies showing that biochemical processes are also altered as a function of changes in the environmental relative humidity (101,102). Rawlings et al. demonstrated that dry conditions inhibit corneodesmosomal degradation, while increasing humidity increases corneodesmosomal degradation (103). Moreover, when the human skin was exposed to low humidity conditions (10%) even for short exposure periods (3 and 6 hours), a significant decrease in water content of the stratum corneum and increase in skin roughness was observed (3). Even in humid conditions, the skin is still subject to a number of environmental insults that can negatively affect skin hydration. Excess UV radiation, for example, causes UVinduced erythema leading to a compromised barrier (104). Several animal studies have demonstrated that abrupt changes in the environment, such as going from humid (80% relative humidity) to dry (less than 10% relative humidity) conditions, increases the time required for barrier function to return to normal (99). In this situation, the skin does not have enough time to adapt to the new climatic conditions. Declercq et al. have further demonstrated that skin can adapt to dry climatic conditions (5). They found that the panelists living in a hot, dry climate such as Arizona had a better barrier function and less dry skin compared with the panelists living in New York, which had a more humid climate (5). While prolonged exposure to conditions of low relative humidity (<20%) enhance barrier function, sustained exposure to high-humidity conditions leads to a gradual deterioration in the barrier (1). A relative humidity greater than 80% is associated with a decrease in NMF and corneocyte hydration in the epidermis of hairless mice (1). It has also been shown that when normal skin is exposed to a moist environment, the kinetics of barrier recovery is delayed because of a reduction in the number of epidermal lamellar bodies and lipid content, in direct contrast with what is observed at low humidities (102). Therefore, when the skin adapts to a high-humidity environment, its capacity to respond to external changes is decreased, partially because of a reduction in the reservoir of stratum corneum lipids. It is remarkable that a human fetus has a mechanism to protect the outermost skin barrier to the damaging effects of amniotic fluid, an environment that would result in a loss of barrier function in adults (105). During the third trimester of gestation, a biofilm known as vernix caseosa forms and coats the prenatal skin. This film acts as a barrier and facilitates the formation of the acid mantle, which provides an optimal environment for inhibiting bacterial colonization (106,107). Vernix caseosa consists of *80% water, 10% protein (corneocytes with no desmosomal attachments), and 10% lipids by weight (consisting of barrier and sebaceous... [стр. 114 ⇒]

This material has been shown to have multiple functions, besides being an efficient moisturizer and osmoregulator (108). On the basis of transmission electron microscope images, the limited structure of vernix caseosa is very similar to that of the topmost layers of the stratum corneum. The body appears to have retained this structural feature of vernix caseosa during the course of stratum corneum maturation. PERSONAL CARE PRODUCTS AND SKIN HYDRATION The Effect of Cleansing Systems Cleansers are designed to remove unwanted materials from the skin such as dirt, oils, and sebum. However, the use of harsh surfactants damages the skin barrier; increases the skin’s susceptibility to environmental sources of irritation and sensitization; and reduces skin moisture and smoothness (109). Charged surfactants, such as anionic and cationic, are the most aggressive. Sodium lauryl sulfate (SLS) is a harsh surfactant that, given its small hydrodynamic radius, is the only surfactant that can extract the intercellular lipids and disrupt the lipid bilayer (110). It, along with most of the charged surfactants, adsorb skin proteins, causing them to denature and swell. Rhein et al. reported that the extent of protein denaturation is dependent on the surfactant monomer concentration and exposure time (111). As surfactants denature skin proteins, enzymatic reactions that control desquamation, inflammation, and oxidation processes are negatively impacted (112,113). The resulting enhanced barrier permeability leads to skin dryness, roughness, cracking, and inflammation (10,47,114). Fortunately, there are a number of surfactants used commercially that are mild to the skin. These include mostly nonionic and amphoteric variants and the anionic variants: highly ethoxylated (at least 5-EO) alkyl sulfates, sulfosuccinates, isethionates, sarcosinates, taurates, alkyl phosphates, and alkyl glutamates. The aggressiveness of charged surfactants can be mitigated by reducing the concentration of the surfactant’s monomer species, reducing the charge by incorporating various counterions and/or cosurfactants to form mixed micelles, and introducing ethoxylation (10). The improved mildness reduces the incidence of barrier damage, which aids in the maintenance of hydrated skin (i.e., nondrying cleansers). Surfactants also negatively impact the skin hydration properties by removing NMF. Blank and Shappirio (14) showed that when isolated human stratum corneum was exposed to 1% solutions of soap, alkyl sulfate or alkyl benzylsulfonate, all surfactants reduced the ability of the tissue to absorb water from the atmosphere, relative to water. This water-holding capacity is correlated with the loss of NMF. A similar correlation has been found between natural saponified soaps and mild synthetic surfactants using confocal Raman spectroscopy (115) (Fig. 3). There has been a great deal of research focused on delivering enhanced skin moisturization using cleansers (109). Emollient-containing cleansers have been found to alleviate the dry skin condition of people having rosecea, sensitive skin, and/or atopic dermatitis (116,117). Emulsion-based liquid body washes are commonly employed to mildly... [стр. 115 ⇒]

DIETARY IMPACT ON SKIN CONDITION It is generally stated that topically applied cosmetic products can be helpful in restoring normal hydration to dry skin. However, less recognized is the positive influence that drinking plenty of water can have on the skin’s appearance. Approximately 45% to 70% of human body weight consists of water. One-third of the total body water is extracellular, and two-thirds are within the intracellular compartment (133). Water is free to move between the cell membranes with any net movement controlled by the effective osmotic and hydrostatic pressures. This balance of body fluid is dependent on the intake of water through drinking, food, and metabolism and the loss of water through natural processes. The three components of the skin, the epidermis, dermis, and subcutaneous fat tissue, play a major role in water regulation, with the SC water content helping to maintain many of the skin’s biophysical properties (134). Soft, smooth skin has an optimally hydrated SC with a water content of approximately 20% to 30%, and a water content of less than 10% to 20%, resulting in abnormally dry skin (133,134). While the environment can play a role in TEWL, a good balance between water intake and loss is vastly important in helping to maintain healthy water content in the SC, which has a positive influence on skin hydration. An increased intake of pure, healthy water helps to enhance nutrient absorption, skin hydration, detoxification, and virtually every aspect of better health. However, studies have also shown that drinking dietary natural mineral water or taking a food supplement containing pro-hydrating actives maintains adequate skin hydration as well. Mac-Mary et al. (135) showed that the magnitude of change in a Corneometer1 measurement on the forearm of healthy subjects increased by 14% when 1 L of mineral water was consumed per day for 42 days, which was clinically significant and similar to the observed modifications with moisturizing cosmetic products (10–30%). Primavera and Berardesca (133) investigated how a capsule containing an active product based on vegetable ceramides, amino acids, sea fish cartilage, antioxidants, and essential fatty acids improved skin hydration after oral use. Significant improvement in Corneometer readings were seen in the active-treated groups (þ30%), in addition to a decrease in skin roughness and improved skin smoothness after 40 days, as measured using a VisioScan1. Self- and clinical-assessment data confirmed the results of the biophysical measurements. These studies demonstrate that a proper diet with adequate water and mineral intake is just as important in the management of skin hydration as a complementary cosmetic approach. Puch et al. further showed that ingesting a probioticcontaining dairy product enriched in g-linolenic acid (an o-6-polyunsaturated fatty acid that has been shown to enhance the rate of barrier recovery when applied topically and when taken orally), vitamin E, and catechins improved barrier function after six weeks of taking twice a day dosage. The average improvement was 13% (136). The reduction in TEWL was observed throughout the six-month study, despite the changes in season. SUMMARY Maintaining hydration of the stratum corneum can be accomplished using a number of different mechanisms. From using mild surfactants that minimally compromise the skin barrier to delivering moisturizers (humectants, occlusive oils, and lipid modulating agents), these materials offer a means of adding moisture back to the skin or, alternatively, reducing water loss (137,138). The skin itself, in fact, has a natural process to minimize excess water loss. Through the water-dependent production of intercellular skin lipids and NMF, an intricate mechanism is in place to function optimally in an often arid, external environment. The skin is a remarkable organ, producing vernix caseosa to protect (as a barrier, anti-infective and antioxidant) the fetus while it is immersed in amniotic fluid, a potential damaging environment, and following birth enhancing the acid mantle development, which facilitates skin maturation during the postnatal period. The production of urocanic acid and free fatty acids in the stratum corneum further contributes to the regulation of stratum corneum pH (139,140). As for those living in dry climates, the skin is adaptable and can generate an improved barrier function and increased water content. The development of the confocal Raman spectrometer has allowed researchers to noninvasively monitor the skin’s water content and composition changes as a function of the environment and product use... [стр. 117 ⇒]

Norlen L. Skin barrier formation: the membrane folding model. J Invest Dermatol 2001; 117(4): 823–829. 83. Sparr E, Wennerstrom H. Responding phospholipid membranes—interplay between hydration and permeability. Biophys J 2001; 81(2):1014–1028. 84. Warner RR, Myers MC, Taylor DA. Electron probe analysis of human skin: determination of the water concentration profile. J Invest Dermatol 1988; 90(2):218–224. 85. Forslind B, Engstrom S, Engblom J, et al. A novel approach to the understanding of human skin barrier function. J Dermatol Sci 1997; 14(2):115–125. 86. Ma T, Fukuda N, Song Y, et al. Lung fluid transport in aquaporin-5 knockout mice. J Clin Invest 2000; 105(1):93–100. 87. Ma T, Hara M, Sougrat R, et al. Impaired stratum corneum hydration in mice lacking epidermal water channel aquaporin-3. J Biol Chem 2002; 277(19):17147–17153. 88. Hara M, Ma T, Verkman AS. Selectively reduced glycerol in skin of aquaporin-3-deficient mice may account for impaired skin hydration, elasticity, and barrier recovery. J Biol Chem 2002; 277(48): 46616–46621. 89. Hara M, Verkman AS. Glycerol replacement corrects defective skin hydration, elasticity, and barrier function in aquaporin-3-deficient mice. Proc Natl Acad Sci U S A 2003; 100(12):7360–7365. 90. Boury-Jamot M, Sougrat R, Tailhardat M, et al. Expression and function of aquaporins in human skin: is aquaporin-3 just a glycerol transporter? Biochim Biophys Acta 2006; 1758(8):1034–1042. 91. Brandner JM, Kief S, Wladykowski E, et al. Tight junction proteins in the skin. Skin Pharmacol Physiol 2006; 19(2):71–77. 92. Furuse M, Hata M, Furuse K, et al. Claudin-based tight junctions are crucial for the mammalian epidermal barrier: a lesson from claudin-1-deficient mice. J Cell Biol 2002; 156(6):1099–1111. 93. Egelrud T. Desquamation in the stratum corneum. Acta Derm Venereol (Suppl) (Stockh) 2000; 208:44–45. 94. Lundstrom A, Egelrud T. A chymotrypsin-like proteinase that may be involved in desquamation in plantar stratum corneum. Arch Dermatol Res 1991; 283:108–112. 95. Caubet C, Jonca N, Brattsand M, et al. Degradation of corneodesmosome proteins by two serine proteases of the kallikrein family, SCTE/KLK5/hK5 and SCCE/KLK7/hK7. J Invest Dermatol 2004; 122(5):1235–1244. 96. Van Overloop L, Declercq L, Maes D. Visual scaling of human skin correlates to decreased ceramide levels and decreased stratum corneum protease activity (abstr) J Invest Dermatol 2001; 117:811. 97. Voegeli R, Heiland J, Doppler S, et al. Efficient and simple quantification of stratum corneum proteins on tape strippings by infrared densitometry. Skin Res Technol 2007; 13(3):242–251. 98. Rogers J, Harding C, Mayo A, et al. Stratum corneum lipids: the effect of ageing and the seasons. Arch Dermatol Res 1996; 288(12):765–770. 99. Denda M, Sato J, Masuda Y, et al. Exposure to a dry environment enhances epidermal permeability barrier function. J Invest Dermatol 1998; 111(5):858–863. 100. Sato J, Denda M, Nakanishi J, et al. Dry condition affects desquamation of stratum corneum in vivo. J Dermatol Sci 1998; 18(3):163–169. 101. Katagiri C, Sato J, Nomura J, et al. Changes in environmental humidity affect the water-holding property of the stratum corneum and its free amino acid content, and the expression of filaggrin in the epidermis of hairless mice. J Dermatol Sci 2003; 31(1):29–35. 102. Sato J, Denda M, Chang S, et al. Abrupt decreases in environmental humidity induce abnormalities in permeability barrier homeostasis. J Invest Dermatol 2002; 119(4):900–904. 103. Rawlings A, Harding C, Watkinson A, et al. The effect of glycerol and humidity on desmosome degradation in stratum corneum. Arch Dermatol Res 1995; 287(5):457–464. 104. Corcuff P, Leveque JL. Corneocyte changes after acute UV irradiation and chronic solar exposure. Photodermatol 1988; 5(3):110–115. 105. Willis I. The effects of prolonged water exposure on human skin. J Invest Dermatol 1973; 60(3): 166–171. 106. Rissman R, Groenink H, Gooris G, et al. Temperature-induced changes in structural and physiochemical properties of vernix caseosa. J Invest Dermatol 2007; 128:292–299. 107. Hoath SB, Pickens WL, Visscher MO. The biology of vernix caseosa. Int J Cosmet Sci 2006; 28: 319–333. 108. Haubrich KA. Role of vernix caseosa in the neonate: potential application in the adult population. AACN Clin Issues 2003; 14(4):457–464. 109. Ertel K. Personal cleansing products: properties and use. In: Draelos ZLT., eds. Cosmetic Formulation in Skin Care Products. New York: Taylor and Francis, 2006:35–65. 110. Moore PN, Puvvada S, Blankschtein D. Challenging the surfactant monomer skin penetration model: penetration of sodium dodecyl sulfate micelles into the epidermis. J Cosmet Sci 2003; 54(1):29–46. 111. Rhein LD, Robbins CR, Fernee K, et al. Surfactant structure effects on swelling of isolated human stratum corneum. J Soc Cosmet Chem 1986; 37:125–139. [стр. 121 ⇒]

The immature hypodermis of baby skin consists of small lobules of roundly shaped adipoblasts that are richly vascularized. The fatty acid composition of the triglycerides is more saturated, which results in a higher fusion point of the lipids than measured for adult skin (1,5). The hairs of a newborn are well developed. Sometimes some lanugo hairs are still observed. After birth, the hairs pass from the anagenic into the telogenic phase. As a consequence, baby’s hairs fall out after about eight weeks. Afterward, the hair cycle becomes similar to the one observed for adults, and hairs will be present in different phases. The hairs, however, are very thin and only faintly pigmented, but these phenomena normalize as a function of time (7). Sebaceous glands, when stimulated by the androgens originating from the mother, are well developed. Their secretions constitute the largest part of the vernix caseosa. That is why at birth, the skin is covered with a white fatty substance. The vernix caseosa is a naturally occurring fetal barrier film produced in late pregnancy (8). Besides the secretion of sebaceous and epidermal lipids, desquamation of maturing fetal corneocytes also takes part in the development of the fetal barrier. The vernix is thought to have multiple overlapping biological functions like moisturization, antiinfective, antioxidant, wound healing, and waterproofing (9,10). Because it lacks desmosomal interconnections between corneocytes, it is also referred to as the “mobile phase” stratum corneum. Removal of vernix lipids can modify the water sorptiondesorption profile (11,12). The vernix caseosa is taken away during the first washing of the baby. After loss of this protective layer and the onset of a desquamative stratum corneum, the skin is exposed to a much dryer environment than the one present during fetal development (13). Erythema occurs that changes in appearance and gets a more marbered aspect that progressively disappears. This is an adaptation of the microvascular system (6). Because of the different biological effects of the vernix caseosa, the question is often raised whether it would not be better to leave this natural film on the baby instead of washing it away. Several publications investigating the effect of immediate bathing of newborns, however, are contradictory (14–17). Vernix distribution is dependent on gestational age, delivery mode, gender, race, and meconium exposure and positively affects skin hydration, skin pH, and erythema. These multiple effects would support its retention on the skin surface after birth (8). Vernix films also retain endogenous chymotrypsin, thus preventing loss of this epidermal enzyme and protecting the epidermal barrier from noxious substances (18). In this respect, the World Health Organization (WHO) developed general guidelines recommending that neonatal bathing should not be undertaken within the first six hours of birth (19). In certain cases, large sebaceous glands are observed together with the occurrence of the typical symptoms of so-called acne neonatorum. This particularly happens in male newborns and can persist for a few months. It is seen as a temporary effect of the androgens that are present in the mother’s blood. Reactivation of the sebaceous glands only occurs later on, around puberty (17). The hydrolipidic layer, mainly composed of sebum from the sebaceous glands and water originating from eccrine glands and the transepidermal water loss (TEWL), is not fully developed in babies. This protective water-in-oil (w/o) mixture is sometimes even nearly absent, which also has an effect on the skin pH of the newborn (20). Consequently, the observed skin pH imbalance might be responsible for a lower capability to neutralize the alkalinization, especially seen in the diaper area due to urine and defecation. [стр. 631 ⇒]

As a consequence, fecal enzymes such as lipases and proteases become activated and damage the fragile skin in the diaper area. Despite modern diaper technology, irritant diaper dermatitis can not completely be avoided, favoring dermal absorption of xenobiotics. A number of molecules, which historically have been used in the diaper area, are known to induce systemic toxicity and must be used very carefully and only when indicated, e.g., hexachlorophene, dichlorophene, corticosteroids, boric acid, and ethanol (24). In risk assessment of cosmetics, the margin of safety (MoS) approach is used when defining acceptable human exposure levels. When extrapolating from experimental studies to human, the magnitude of the uncertainty factor must take into account a variety of considerations, such as species differences, sensitive subpopulations, duration and route of exposure, and vehicle or matrix effects. In addition, when the diaper area is irritated, 100% dermal absorption should be used (19,33). Innovative hygiene absorbent and baby care products, however, provide an increasingly good skin compatibility profile, making the frequency and severity of diaper dermatitis declining (34,35). Transepidermal Water Loss The barrier function of the skin not only prevents absorption of toxic substances, but also controls TEWL. In particular when skin is damaged, excessive TEWL occurs (36–38). In a healthy, fully developed newborn, TEWL values of 6 to 8 g/m2h water are being measured, depending on the measuring technology (39). TEWL increases proportionally with immaturity, which means that premature children have an increased evaporative heat loss and subsequently a poor temperature control (38,40). Although skin maturation occurs rapidly, fluid and electrolyte shift as well as body temperature have to be controlled frequently (41). Also increased risk of local and systemic toxicity from topically applied substances rises with increasing TEWL or barrier damage (42). In the diaper area TEWL is often defined as skin surface water loss (SSWL) and is used to measure the capability of a diaper to keep the skin dry (43,44). Defense Against Infection: Skin Thickness, Skin pH, Stratum Corneum Hydration The water content of the stratum corneum influences the barrier function, dermal absorption, reactivity to irritants, and the skin’s mechanical properties. Although healthy infants and adults tend to have similar TEWL values, newborns (until 8–24 months) still present somewhat higher water contents in the horny layer and a greater variation than adults up to one year (38,39,45). In newborns, skin tends to have a higher pH at birth than a few days later. Among other factors, this higher pH might reflect the influence of the vernix caseosa and the amniotic fluid (both pH values above 7) during the first days of life (38). The pH stabilizes at a slightly acidic range (pH ¼ 5–6), although values of less than 5 also have been reported (31,38,46). Acidic skin protects against pathogenic microorganisms to which the baby is exposed after birth and serves in the defense against infections. Indeed, microbial colonization of the skin starts immediately after birth by so-called saprophytes that are not pathogenic and are credited with protective properties against some harmful microorganisms (5). They require an acidic surrounding for optimal living conditions (39). Whereas the pH value of baby skin is, after a few days, comparable to the pH value of adult skin, the buffering capacity of baby skin is much lower. Therefore, baby skin is more susceptible to pH changes induced by metabolic pathways such as the enzymatic generation of free fatty acids from phospholipids or urocanic acid from histidine, the desquamation process of the stratum corneum with formation of filaggrin and keratohyalin breakdown products, and the formation of pyrrolidone carboxylic acid and Nþ/Hþ antiporter (31,47). BABY CARE PRODUCTS FOR SKIN AND HAIR From the anatomical and physiological differences between baby skin and adult skin, it appears that frequent contact with xenobiotics, which could damage or disrupt the barrier function of the stratum corneum and change the skin pH, may be at the basis of an increased... [стр. 633 ⇒]

Systemic side effects are not to be expected with mild rinse-off products (shampoos, bath additives, toilet bars) but should be carefully looked for when leave-on products for babies are being developed (body milks, hydrating creams, ointments, powders, sunscreens). REFERENCES 1. Hardman MJ, Byrne C. Skin structural development. In: Hoath SB, Maibach HI, eds. Neonatal Skin: Structure and Function. 2nd ed. New York: Informa Health Care, 2003:1–20. 2. Holbrook KA. A histological comparison of infant and adult skin. In: Maibach HI, Boisits EK, eds. Neonatal Skin. New York: Marcel Dekker Inc., 1982:3–31. 3. Holbrook KA, Sybert VP. Basic science. In: Schachner LA, Hansson RC, eds. Pediatric Dermatology. 2nd ed. New York: Churchill Livingstone Inc., 1995:1–70. 4. Holbrook KA. Structure and function of the developing skin. In: Goldsmith LA, ed. Physiology, Biochemistry and Molecular Biology of the Skin. 2nd ed. Oxford: Oxford University Press, 1991: 63–110. 5. Lund CH. Newborn skin care. In: Baran R, Maibach HI, eds. Cosmetic Dermatology. London: Martin Dunitz, 1994:349–357. 6. Rutter N. The dermis. Semin Neonatol 2000; 5:297–302. 7. Trüeb RM. Shampoos: composition and clinical applications [German]. Hautarzt 1998; 49:895–901. 8. Visscher MO, Narendran V, Pickens WL, et al. Vernix caseosa in neonatal adaptation. J Perinatol 2005; 25:440–446. 9. Haubrich KA. Role of vernix caseosa in the neonate: potential application in the adult population. AACN Clin Issues 2003; 14:457–464. 10. Hoeger PH, Schreiner V, Klaassen IA, et al. Epidermal barrier lipids in human vernix caseosa: corresponding ceramide pattern in vernix and fetal skin. Br J Dermatol 2002; 146:194–201. 11. Rissmann R, Groenink HWW, Weerheim AM, et al. New insights into ultrastructure, lipid composition and organization of vernix caseosa. J Invest Dermatol 2006; 126:1823–1833. 12. Tansirikongkol A, Hoath S, Pickens WL, et al. Equilibrium water content in native vernix and its cellular component. J Pharm Sci 2008; 97:972–981. 13. Walker L, Downe S, Gomez L. Skin care in the well term newborn: two systematic reviews. Birth 2005; 32:224–228. 14. Franck LS, Quinn D, Zahr L. Effect of less frequent bathing of preterm infants on skin flora and pathogen colonization. J Obstet Gynecol Neonatal Nurs 2000; 29:584–589. 15. Gelmetti C. Skin cleansing in children. J Eur Acad Dermatol Venereol 2001; 15(suppl 1):12–15. 16. Nako Y, Harigaya A, Tomomasa T, et al. Effects of bathing immediately after birth on early neonatal adaptation and morbidity: a prospective randomized comparative study. Pediatr Int 2000; 42:517–522. 17. Quinn D, Newton N, Piecuch R. Effect of less frequent bathing on premature infant skin. J Obstet Gynecol Neonatal Nurs 2005; 34:741–746. 18. Tansirikongkol A, Wickett RR, Visscher MO, et al. Effect of vernix caseosa on the penetration of chymotryptic enzyme: potential role in epidermal barrier development. Pediatr Res 2007; 62:49–53. 19. World Health Organization. Pregnancy, childbirth, postpartum and newborn care: a guide for essential practice. Available at: http://www.who.int/reproductive-health/publications/pcpnc/ index.html. Accessed December 2007. 20. Rogiers V, Derde MP, Verleye G, et al. Standardized conditions needed for skin surface hydration measurements. Cosmet Toilet 1990; 105:73–82. 21. Moisson YF, Wallach D. Pustular dermatoses in the neonatal period [French]. Ann Pediatr 1992; 39:397–406. 22. Chiou YB, Blume-Peytavi U. Stratum corneum maturation. A review of neonatal skin function. Skin Pharmacol Physiol 2004; 17:57–66. 23. Kravchenko I, Maibach HI. Percutaneous penetration. In: Hoath SB, Maibach HI, eds. Neonatal Skin— Structure and Function. 2nd ed. New York: Marcel Dekker, 2003:285–298. 24. West DP, Worobec S, Solomon LM. Pharmacology and toxicology of infant skin. J Invest Dermatol 1981; 76:147–150. 25. Wester RD, Maibach HI. Understanding percutaneous absorption for occupational health and safety. Int J Occup Environ Health 2000; 6:86–92. 26. Renwick AG. Toxicokinetics in infants and children in relation to the ADI and TDI. Food Addit Contam 1998; 15:17–35. 27. Ginsberg G, Hattis D, Sonawane B, et al. Evaluation of child/adult pharmacokinetic differences from a database derived from the therapeutic drug literature. Toxicol Sci 2002;66:185–200. 28. Renwick AG, Dorne JL, Walton K. An analysis of the need for an additional uncertainty factor for infants and children. Regul Toxicol Pharmacol 2000; 31:286–296. [стр. 638 ⇒]

...van der Waals, 693 Vellus hair follicles, in ethnic races, 50 Vernix caseosa, 97–98, 614 Vertical suction method, 821 Very sensitive skin, 60 Vesicles, for topical applications, 791–792 Virgin hair surfaces, 689 Viscoelastic properties of skin, 821 using Cutometer1, 294 VisioScan camera, 283, 284 Vitamin C, 303–304 Vitamin derivatives, 130 Vitamin E, 301–303 oral supplementation, 591 Vitamins, 679–680 Volatile siloxanes, 372... [стр. 885 ⇒]

А. Переношенность. Б. Преэклампсия–эклампсия. В. Материнская гипертония. Г. Сахарный диабет матери. Д. Аномальная частота сердцебиений плода, подтвержденная диагностическими методами. Е. Внутриутробная задержка развития. Ж. Аномальный биофизический профиль. З. Олигогидроамнион. И. Курение, хронические респираторные и сердечно-сосудистые заболевания матери. К. Низкие баллы по шкале Апгар в течение первых 5 минут жизни. Л. Наличие дистресса плода. М. Этническая принадлежность. У чернокожих американцев и африканцев наблюдается повышенный риск развития САМ по сравнению с другими этническими группами. Также повышенныму риску развития САМ подвержены жители Тихоокеанских островов и коренные австралийцы. Н. Роды в домашних условиях. Повышенный риск САМ отмечен при запланированном родоразрешении в домашних условиях. V. Клинические проявления. При заглатывании плодом амниотической жидкости, окрашенной меконием, наблюдаются различные симптомы. В основном клинические проявления зависят от тяжести гипоксии и количества и вязкости аспирированного мекония. А. Общие черты 1. Новорожденные. У новорожденных с САМ часто наблюдаются признаки переношенности: они малы для своего гестационного возраста, имеют длинные ногти и шелушащуюся желто-зеленую кожу. При этом при рождении имеет место транзиторная или постоянная дыхательная недостаточность. Если выражена перинатальная асфиксия, у новорожденных может развиться угнетение дыхания с плохими дыхательными усилиями и ослаблением мышечного тонуса. Наличие мекониальных пятен на коже пропорционально продолжительности воздействия мекония и его концентрации. При тяжелом САМ прокрашивание пуповины возникает через 15 минут экспозиции мекония. Желтая окраска ногтей новорожденного наблюдается через 4–6 ч; окрашивание vernix caseosa (сыровидной смазки) наблюдается примерно через 12 ч. 2. Амниотическая жидкость. Меконий, присутствующий в амниотической жидкости, изменяется по своему внешнему... [стр. 325 ⇒]

Следует иметь в виду, что запах может появиться не с первых дней жизни ребенка. Кроме того, собственный запах ребенка надо дифференцировать с запахами, обусловленными вводимыми ему медикаментозными средствами (антибиотиками, витаминами). Кожа здорового доношенного ребенка нежная, эластичная, бархатистая на ощупь. Если собрать ее в складку, она тут же расправляется. Некоторая ее суховатость обусловлена низкой функциональной активностью потовых желез. Кожа только что родившегося ребенка покрыта творожистой смазкой (vernix caseosa), которую в настоящее время не принято удалять, так как она служит защитой от инфицирования. При осмотре кожи новорожденного можно выявить ряд особенностей, не относящихся к патологии: • МШа — беловато-желтые точки, выступающие над поверхностью кожи. Наиболее характерная их локализация — кончик и крылья носа, реже — носогубный треугольник. Это ретенционные кисты сальных желез; к середине — концу периода новорожденное™ они, как правило, исчезают; лечения не требуют. • Необильные петехиальные кровоизлияния в кожу предлежащей части и кровоизлияния в склеры. Их возникновение связано с повышенной проницаемостью сосудистых стенок у новорожденных. Появляются в процессе родов. Кровоизлияния в склеры тем не менее могут свидетельствовать о травматичное™ родового акта. • Телеангиэктазии — красновато-синюшные сосудистые пятна. Локализуются на спинке носа, верхних веках, на границе волосистой части головы и задней поверхности шеи. Не выступают над поверхностью кожи. Исчезают при надавливании, что является дифференциально-диагностическим признаком, позволяющим отграничить их от гемангиомы. Представляют собой локальное расширение мелких сосудов кожи (подробнее см. гл. XIII). • Lanugo — пушковые волосы; наиболее частая их локализация — лицо, плечи, кожа спины. Обильный рост встречается у недоношенных детей. Рост волос на гребне ушных раковин относят к дизонтогенетическим стигмам (диабетическая фетопатия). • Монгольские пятна расположены в области крестца и ягодиц, реже на бедрах; имеют синюшный цвет, что обусловлено наличием пигментообразующих клеток (подробнее см. гл. XIII). • Родимые пятна. Возможна любая локализация; чаще коричневого или синюшно-красного цвета. В последнем случае необходима дифференциация с гемангиомами и телеангиоэктазиями. Иногда это возможно только при наблюдении в динамике. Остаются на всю жизнь. Существует наследственная предрасположенность. • Miliaria crystalline — точечные пузырьки, выступающие над поверхностью кожи, наполненные прозрачной жидкостью; напоминают «капли росы»; локализуются на коже лица. Представляют собой ретенционные кисты потовых желез. Встречаются у новорожденных редко. Лечения не требуют. Непатологические изменения кожи, связанные с особенностями адаптации (пограничными состояниями) и дефектами ухода, описаны в гл. IV, XIII. [стр. 162 ⇒]

Эталон ответа к задаче № 8. 1. Поставьте диагноз. Телеангиоэктазии затылочной области, переносицы, верхней губы. 2. Определите прогноз. Благоприятный. Через 1-1,5 года пятна исчезают. 3. Какие анатомо-физиологические особенности кожи характеризуют новорождѐнного ребенка? Кожа состоит из трѐх слоев: эпидермиса, дермы и гиподермы (подкожной клетчатки). Толщина эпидермиса у новорожденных детей, особенно на ладонях и подошвах меньше, чему взрослых. Образование меланина в коже недостаточное. Базальная мембрана между эпидермисом и дермой слабо развита, что обусловливает лѐгкое отделение верхнего слоя кожи и образование пузырей (эпидермолиз) в местах давления и при пиодермиях. Поверхностный секрет кожи у новорождѐнных имеет рН близкую к нейтральной (6,7-6,3), что отражает еѐ низкую бактерицидность. Резорбционная способность кожи из-за тонкости рогового слоя и обилия сосудов повышена, что необходимо учитывать при назначении различных мазей. Защитная функция кожи от механических повреждений также снижена. У новорождѐнных детей несовершенна терморегулирующая функция кожи. Поэтому новорождѐнные дети легко перегреваются или переохлаждаются. Число сальных желез у новорождѐнных в 4-8 раз больше, чем у взрослых. Эти железы расположены поверхностно. Они морфологически зрелые и начинают функционировать еще внутриутробно с 28 нед гестации, поэтому при рождении ребѐнок покрыт толстым слоем сыровидной смазки (vernix caseosa). Сальные железы у новорождѐнных могут перерождаться в кисты, особенно на носу и других участках лица с образованием бело-жѐлтого цвета milia. Волосы при рождении мягкие и слабо пигментированы. В течение первых двух дней жизни бледность кожи сменяется реактивной краснотой с незначительным цианотичным оттенком (физиологический катар кожи у недоношенных особенно выражен). Затем появляется мелкое шелушение эпидермиса и нерезкая желтуха (icterus neonatorum), максимум которой приходится на 2-3 сутки жизни и исчезает к 7-10 дню. У новорождѐнных детей имеются все виды чувствительности. Подкожная жировая клетчатка при рождении имеет относительную массу в 4-5 раз больше, чем у взрослых. Во время 100... [стр. 100 ⇒]

Кроме того, эффект действия местного вещества может зависеть от обмена веществ новорожденного ребенка. Значение первородной смазки (Vernix caseosa) для формирования здоровья кожи новорожденного ребенка Первородная смазка - это пленка, защищающая кожу плода и присущая только людям. Она служит химическим и механическим барьером в утробе матери и облегчает послеродовую адаптацию кожи к внеутробной среде. Выработка первородной смазки начинается в конце второго триместра, её распределение на коже плода происходит цефалокаудальным путем (С). Отделение первородной смазки от кожи начинается при повышении уровня 12... [стр. 12 ⇒]

СПИСОК ИСПОЛЬЗОВАННОЙ ЛИТЕРАТУРЫ: 1. Agren J., Sjors G., Sedin G. Transepidermal water loss in infants born at 24 and 25 weeks of gestation. Acta Paediatrica 1998; 87, 1185–1190. 2. Aitken J, Williams F. A systematic review of thyroid dysfunction in preterm neonates exposed to topical iodine. Arch Dis Child Fetal Neontal Ed. 2014; 99: F21-F28. 3. Akinbi HT, Narendran V, Pass AK, Markart P, Hoath SB. Host defense proteins in vernix caseosa and amniotic fluid. Am. J. Obstet. Gynecol. 2004; 191, 2090–2096. 4. Andersen C, Hart J, Vemgal P, Harrison C. Prospective evaluation of a multi-factorial prevention strategy on the impact of nosocomial infection in very-low-birthweight infants. Journal of Hospital Infection 2005; 61: 162–167. 58... [стр. 58 ⇒]

Hoath SB, Pickens WL, Visscher MO. The biology of vernix caseosa. International Journal of Cosmetic Science 2006; 28: 319–333. 37. Hoeger P, Enzmann C. Skin physiology of the neonate and young infant: a prospective study of functional skin parameters during early infancy. Pediatr Dermatol. 2002; 19: 256-262. 38. Hon KL, Leung AK, Barankin B. Barrier repair therapy in atopic dermatitis: an overview. Am J Clin Dermatol 2013;14:389–399. 39. Iarkowski LE, Tierney NK, Horowitz P. Tolerance of skin care regimen in healthy, fullterm neonates. Clin Cosmet Investig Dermatol 2013;6:137–144. 40. Jackson PD. Diaper dermatitis. Protecting the bottom line. Adv Nurse Pract 2010;18:38– 41. 41. Kalia Y, Nonato L, Lund C, Guy R Development of skin barrier function in preterm infants. J Invest Dermatol. 1998: 111; 320-326. 42. Kanda K, Tochihara Y, Ohnaka T. Bathing before sleep in the young and in the elderly. Eur J Appl Physiol Occup Physiol 1999;80:71–75. 43. Kiechl-Kohlendorfer U, Berger C, Inzinger R. The effect of daily treatment with an olive oil/lanolin emollient on skin integrity in preterm infants: a randomized controlled trial. Pediatr Dermatol. 2008; 25(2): 174-178. 44. Kikuchi K, Kobayashi H, O’Goshi K, Tagami H. Impairment of skin barrier function is not inherent in atopic dermatitis patients: a prospective study conducted in newborns. Pediatr Dermatol 2006: 23: 109–113. 45. Kulkarni A, Kaushik JS, Gupta P. Massage and touch therapy in neonates: the current evidence. Indian Pediatr 2010;47:771–776 46. Lavender T, Bedwell C, Roberts SA. Randomized, controlled trial evaluating a baby wash product on skin barrier function in healthy, term neonates. J Obstet Gynecol Neonatal Nurs 2013;42:203–214. 47. Lavender T, Furber C, Campbell M. Effect on skin hydration of using baby wipes to clean the napkin area of newborn babies: assessor-blinded randomized controlled equivalence trial. BMC Pediatr 2012;12:59. 48. Little K, Cutcliffe S. The safe use of children’s toys within the healthcare setting. Nurs Times 2006;102:34–37. 49. Lund C. Bathing and Beyond. Current Bathing Controversies for Newborn Infants. Advances in Neonatal Care. 2016; 16: 5S: S13-S20. 50. Lund C. Medical adhesives in the NICU . Newborn Infant Nurs Rev. 2014; 14: 160-165. 51. Maffeis L, Pugni L, Pietrasanta C. Iatrogenic anetoderma of prematurity: a case report and review of the literature. Case Rep Dermatol Med. 2014; 2014: 781493. 61... [стр. 61 ⇒]

Medves J, O’Brien B. Does bathing newborns remove potentially harmful pathogens from the skin? Birth. 2001; 28: 161-165. 53. Medves JM, O’Brien B. The effect of bather and location of first bath on maintaining thermal stability in newborns. J Obstet Gynecol Neonatal Nurs 2004;33:175–182. 54. Moraille R, Pickens W, Visscher M, Hoath S. A novel role for vernix caseosa as a skin cleanser . Biol Neonate. 2005; 87: 8-14. 55. Nako Y, Harigaya A, Tomomasa T. Effects of bathing immediately after birth on early neonatal adaptation and morbidity: a prospective randomized comparative study. Pediatr Int. 2000; 42: 517-522. 56. Neonatal skin care evidence-based clinical practice guideline, 3rd ed. Washington, DC: Association of Women’s Health, Obstetric and Neonatal Nurses, 2013. 57. O’Grady NP, Alexander M, Burns LA. Guidelines for the prevention of intravascular catheter-related infections . Healthcare Infection Control Practices Advisory Committee. http://www.cdc.gov/hicpac/pdf/guidelines/bsi-guidelines-2011.pdf. Published 2011. Accessed July 7, 2016. 58. Ponnusamy V, Venkatesh V, Clarke P. Skin antisepsis in the neonate: what should we use? Curr Opin Infect Dis. 2014; 27: 244-250. 59. Preer G, Pisegna JM, Cook JT. Delaying the bath and in-hospital breastfeeding rates. Breastfeed Med. 2013; 8: 485-490. 60. Quach C, Milstone AM, Perpete C. Chlorhexidine bathing in a tertiary care neonatal intensive care unit: impact on central line-associated bloodstream infections. Infect Control Hosp Epidemiol. 2014; 35: 158-163. 61. Ramos-e-Silva M, Boza JC, Cestari TF. Effects of age (neonates and elderly) on skin barrier function Clinics in Dermatology 2012; 30: 274-276. 62. Rawlings AV, Lombard KJ. A review on the extensive skin benefits of mineral oil. Int J Cosmet Sci 2012; 34:511–518. 63. Sankar M, Paul V. Efficacy and safety of whole body skin cleansing with chlorhexidine in neonates—a systematic review . Pediatr Infect Dis J. 2013; 32: e227-e234. 64. Schmid-Wendtner MH, Korting HC. The pH of the skin surface and its impact on the barrier function. Skin Pharmacol Physiol 2006: 19: 296–302. 65. Shin HT. Diaper dermatitis that does not quit. Dermatol Ther 2005;18:124–135. 66. Simpson EL, Berry TM, Brown PA. A pilot study of emollient therapy for the primary prevention of atopic dermatitis. J Am Acad Dermatol 2010;63:587–593. 67. Sobel H, Silvestri M, Mantaring J. Immediate newborn care practices delay thermoregulation and breastfeeding initiation . Acta Paediatr. 2011; 100: 1127-1133. 62... [стр. 62 ⇒]

Деятельность сальных желез зависит от андрогенной стимуляции (у плода стимуляция материнскими андрогенами). Сальные железы активно функционируют уже в периоде внутриутробного развития, в избытке выделяя секрет - первородную смазку (vernix caseosa), которая имеет выраженные бактерицидные свойства. Сальные железы могут образовывать кисты, которые часто расположены на коже носа и выглядят как мелкие бело-желтые образования, «millia». [стр. 72 ⇒]

Перевязка пуповины. Для предупреждения инфекции первичную обработку новорожденного производят с соблюдением асептики рук (см. приложение 2), перевязочного материала, инструментов. Перевязку пуповины осуществляют в 2 этапа. Первый этап, или отделение ребенка от матери. Ребенок к этому времени обсушен и помещен на живот матери — обычно через 1 мин, к моменту окончания пульсации пуповины (при отсутствии показаний к более раннему отделению ребенка — резус-конфликт, асфиксия и др.). На пуповину на расстоянии 10—15 см от пупочного кольца накладывают 2 зажима Кохера с расстоянием между ними 2—3 см. Поверхность между зажимами обрабатывают марлевым шариком, смоченным 95% спиртом или 5% спиртовым раствором йода. Пересекают пуповину стерильными ножницами. Второй этап, или окончательная обработка остатка пуповины у новорожденного. Проводится на специальном пеленальном столике с обогревом. На расстоянии 0,5—1 см от пупочного кольца на пуповину накладывают пластмассовую скобу Роговина, которая плотно фиксирует остаток пуповины. Скобу накладывают с помощью специального зажима, вследствие чего прекращается поступление крови в пуповинный остаток и обеспечиваются его высыхание и мумификация (сухая гангрена). Вместо скобы Роговина иногда применяют резиновое кольцо, шелковую или кетгутовую лигатуру, которую накладывают на остаток пуповины в 2 -3 см, чтобы можно было его использовать для инъекций и проведения заменного переливания крови (ЗПК). Пуповинный остаток отрезают на расстоянии 1—2 см от скобы или лигатуры, вытирают кровь, место среза обрабатывают йодом, а весь остаток пуповины — спиртом. Пуповинный остаток отпадает в течение 1-й недели жизни. В отечественной практике до момента заживления пупочной ранки 1 раз в день применяют местные антисептики, хотя за рубежом не рекомендуют никаких вмешательств на пупочной ранке (считается, что местное использование антибактериальных средств не только не уменьшает частоту инфекций, но и задерживает спонтанное отпадение пуповинного остатка). Уход за кожей. Кожа новорожденного покрыта естественным кремом — первородной смазкой (vernix caseosa), обеспечивающей дополнительную защиту от проникновения инфекционных агентов. Удалять первородную смазку с кожи новорожденного не следует. Для удаления с кожи ребенка крови и мекония используют стерильную марлевую салфетку, смоченную теплой водой. Обмывать ребенка под краном в родильном зале не рекомендуется. [стр. 108 ⇒]

Глава 7. Клиническая анатомия кожных покровов по областям. Кожная пластика. Ожоги. Особенности лечения Клиническая анатомия кожных покровов по областям Изучение клинической анатомии кожных покровов в различных областях тела человека имеет важное практическое значение, т.к. позволяет правильно выполнять разрез, производить выбор его направления и протяженности, глубины и силы нажима на кончик скальпеля и мн.др. Любая операция начинается с обоснования рационального хирургического доступа к органу, сосудистонервным образованиям или гнойному очагу, патологическому образованию и др. Очень часто используется в качестве аутопластики материала для лечения ожогов, а также восстановления кожных дефектов при многочисленных пластических и реконструктивных операциях. Широко применяется кожная пластика в челюстно-лицевой и эстетической хирургии. С этих позиций хотелось бы обратить внимание молодых специалистов на возрастные и индивидуальные особенности строения кожных покровов. Возрастные особенности кожи В детском возрасте кожа значительно отличается от строения взрослого человека. Она более тонкая, эластичная и легкоподвижная, образующая поперечные складки, особенно в области конечностей. В момент рождения кожа покрыта слоем розовой смазки (vernix caseosa), имеет бледно-голубоватый цвет. В течении первых суток она приобретает красновато-бурую окраску с цианотичным оттенком, которая затем сменяется желтушностью. Последняя исчезает к 7-10 дню жизни ребенка. В этот период эпидермис хорошо развит, определяются ростковый и ороговевающий слои. Блестящий слой выражен только на ладонях и подошвах, а зернистый – состоит только из одного ряда клеток. У маленьких детей кожные покровы в 1,5-3 раза тоньше по сравнению со взрослыми людьми. У детей рано формируются пото182... [стр. 182 ⇒]

Некоторые антропологи, например, Бернард Вуд, Кевин Хант и Филипп Тобиас, считают теорию саванны устаревшей. Альтернативная гипотеза допускает, что человек эволюционировал под влиянием приспособления к земноводному существованию, то есть к собиранию моллюсков и прочей пищи на мелководье, что требовало, в частности, способности плавать и нырять, отличающей человека от прочих обезьян. Эта гипотеза объясняет многие анатомические особенности современного человека, такие как прямохождение [10] , отсутствие шерсти [11] , развитый слой подкожного жира [12] , низкое положение гортани относительно носоглотки, характерное для морских млекопитающих,[13] , vernix caseosa или первородная смазка новорождённых детей, также характерная для морских млекопитающих, а не обезьян[13] , крупный мозг[14] , высокий нос с направленными вниз ноздрями (не вперёд, как у обезьян), предотвращающий попадание воды в носоглотку и жирная кожа с обилием сальных желёз, которая может служить для защиты от воды [15] . Обсуждается несколько вариантов приспособления протолюдей к жизни в водной стихии, в том числе собирательство на мелководье и развитие новых способов передвижения в воде и доставки собранной пищи на берег[10] , плавание[16] и ныряние [12][17][18] . Получить палеоантропологические доказательства земноводного обитания протолюдей крайне сложно, по крайней мере, из-за повышения уровня моря по окончании ледникового периода, из-за чего бывшее мелководье оказалось теперь на глубине 100—120 м[19] . Однако археология и палеонтология позволяют исследовать рацион питания различных видов Homo и его влияние на эволюцию анатомии и поведения[20][21][22][23][24] . [стр. 7 ⇒]

Заселение им Европы происходило из северной Африки несколькими волнами. Под влиянием изоляции и генного дрейфа в Европе сформировались классические неандертальцы. Более поздние мигранты Homo sapiens, попадая в Европу, смешивались с неандертальским населением и в результате возникла современная форма человека. Таким образом, согласно этой точки зрения предками современного человека являются только африканские Homo erectus. Сторонники полицентризма считают, что существовало несколоко центров формирования человека современного типа и его рас. Например, основатель гипотезы полицентризма Франц Вейденрейх в конце 30-х – начале 40-х годов выделял такие 4 центра: Юго-Восточная Азия (австралоиды), Южная Африка (негроиды), Восточная Азия (монголоиды), Передняя Азия (европеоиды). Альтернативная саванной гипотеза происхождения человека Некоторые антропологи считают теорию саванны устаревшей. Альтернативная гипотеза допускает, что человек эволюционировал под влиянием приспособления к земноводному существованию, то есть к собиранию моллюсков и прочей пищи на мелководье, что требовало, в частности, способности плавать и нырять, отличающей человека от прочих обезьян. Эта гипотеза объясняет многие анатомические особенности современного человека, такие как прямохождение, отсутствие шерсти, развитый слой подкожного жира, низкое положение гортани относительно носоглотки, характерное для морских млекопитающих, , vernix caseosa или первородная смазка новорождённых детей, также характерная для морских млекопитающих, а не обезьян, крупный мозг, высокий нос, предотвращающий попадание воды в носоглотку и жирная кожа с обилием сальных желёз, которая может служить для защиты от воды. Обсуждается несколько вариантов приспособления протолюдей к жизни в водной стихии, в том числе собирательство на мелководье и развитие новых способов передвижения в воде и доставки собранной пищи на берег, плавание и ныряние. Получить палеоантропологические доказательства земноводного обитания протолюдей крайне сложно, по крайней мере, из-за повышения уровня моря по окончании ледникового периода, из-за чего бывшее мелководье оказалось теперь на глубине 100—120 м. Модель эволюции гоминид Оуэна Лавджоя (C. Owen Lovejoy) на основе данных по ардипитеку (Science October 2009) Ключом к пониманию нашего происхождения являются не увеличенный мозг и не каменные орудия (эти признаки появились в эволюции гоминид очень поздно), а черты «человеческой» эволюционной линии, связанные с половым поведением, семейными отношениями и социальной организацией. Стратегии размножения – К-стратегия – самка долго выращивает детеныша и не способна к рождению нового –дефицит «кондиционных» самок – «спермовые войны» у полигамных приматов - у ардипитека маленькие клыки и у самок и у самцов – значит он не агрессивный и не занимался «спермовыми войнами»-значит другая стратегия обеспечения себя потомством- моногамия – «секс в обмен на пищу» - свободные руки чтобы ее приностить. Если самцы гоминид начали систематически носить самкам еду, это должно было сильно изменить направленность отбора. Самка была заинтересована прежде всего 16... [стр. 16 ⇒]

Застой мочи может вызвать пиелонефрит беременных, который представляет угрозу дальнейшему развитию плода. На 19-й неделе рост ребѐнка — 15 см, вес — 240 г. Кроха вырос до размера небольшого баклажана. Его тело покрыто белой вязкой субстанцией, называемой vernix caseosa (сыровидной смазкой). Она защищает тонкую нежную кожу от повреждений. Недоношенные детки могут быть покрыты такой смазкой и при рождении. Яичники девочки уже содержат фолликулы с формующимися яйцеклетками. УЗИ на этом сроке беременности показывает, как ребѐнок трогает стенку плодного пузыря, прикасается к своему лицу, дотягивается ручками до пуповины, берет ногами, сосет палец. Ребѐнок уже может использовать преимущественно правую руку или, наоборот, левую. В его мозгу сформированы нервные клетки, которые отвечают за осязание, вкус, свет, обоняние и слух — теперь все эти системы совершенствуются. Громкие звуки извне могут передаваться ребѐнку. Он отвечает на стресс повышением своей активности. Начинается процесс миелинизации нервов, функционирует кровобращение плода. В кишечнике накапливается меконий — продукты клеточной гибели, деятельности пищеварительных желез с примесью амниотической жидкости. К концу 20-й недели рост ребѐнка — 16 см, вес — не более 300 г. За двадцать недель он ощутимо подрос по сравнению с той единственной клеткой, с которой все начиналось. Образуется плодовая смазка, покрывающая все тело. Под защитным слоем кожа ребѐнка утолщается и делится на слои. Ребѐнок уже разделяет ночь и утро, день и вечер — и становится более активным в определѐнное время дня. Формируются ресницы. Глаза ещѐ закрыты, но плод хорошо ориентируется в полости матки. Например, близнецы и двойни способны находить лицо друг друга и держаться за руки. Ребѐнок активно движется в утробе матери, начинает глотать амниотическую жидкость. 21-22 недели... [стр. 104 ⇒]

Смотреть страницы где упоминается термин "vernix caseosa": [20] [17] [51] [110] [6] [280] [86] [86] [334] [401] [437] [682] [919] [16] [16] [14] [76] [84] [193] [115]