Neonatal skin and cordcare - the way forward
The full reference for this draft article is: Trotter S (2008). Neonatal skin & cordcare – the way forward. Nursing in Practice (January/February) Number 40 – (Dermatology): 40-45
“It is no longer appropriate for hospitals and maternity units to openly supply free baby products when there is no evidence to support their use. Although predominantly involving skincare and cord care it is important to remember that anything placed on in or around the neonate has the capacity to harm” (Trotter 2004, 2006).
- Neonatal skin environment
- Vernix Caseosa
- Physiology of umbilical cord separation
- The evidence
- New guidelines
- Key points
Neonatal skincare has been an interest of mine since 1996 when I saw a short article in a midwifery journal questioning the use of manufactured baby products on newborn skin. Over the years, this has become a passion and I am proud to report that this passion has led to a change in practice for midwives in the UK and beyond.
I was fortunate to be given the opportunity to present my work at the recent NIP event in London. This enabled me to update primary care health professionals who like midwives and health visitors, look after babies during the first month of life, but may not be aware of the latest evidence-based skincare and cord care advice. I hope this article will demonstrate why it is so important to completely avoid the use of manufactured baby products for the first month of life (see key points for current advice) and why following this advice could play a significant part in reducing the worryingly high rates of dry skin conditions, asthma and related allergies. I will explain the anatomy and physiology of the skin and cord area, how this impacts on the skin’s natural barrier of protection and recommend the safest guidelines on care for newborn skin.
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Neonatal skin environment
The epidermis, or outer layer of the skin, is divided into four layers: the stratum corneum (inert) and three living layers: stratum granulosum, stratum spinosum and stratum basale.
The stratum corneum itself is made up of 10 to 20 microscopic layers in the term infant, similar to that seen in an adult. In premature infants, this number drops to between two to three layers. In extremely premature infants, of less than 23 gestational weeks, the stratum corneum may be virtually non-existent. (Holbrook 1982, Nonato 1998). Consequently, the risk of damaging these babies’ skin is even higher.
Babies are born with an alkaline skin surface, with an average pH of 6.34 (Peck & Botwinick 1964). However, within days, the pH falls to about 4.95 (acid) forming what is known as the ‘acid mantle’ - a very fine film that rests on the surface of the skin and acts as a protector. The development of this ‘acid mantle’ happens within days of birth, irrespective of gestational age, and probably occurs as a direct result of the skin’s exposure to air (Harpin & Rutter 1983, Evans & Rutter 1986).
The stratum basale is at the junction of the epidermis and dermis and is where the renewal of the basal cells is carried out. Basal cells, called keratinocytes, constantly divide. The granules in the keratinocytes of the stratum granulosum are bags full of newly synthesized and stored lipids. These will be released before the cell dies and are processed enzymatically to form the lipid barrier. These lipids surround the lifeless keratin disc made of a keratinocyte after its death and is now called a ‘corneocyte’. These can be thought of as the bricks in a wall, with the mortar between made up of lipids or fat molecules. This whole structure forms the skin barrier and is situated in the stratum corneum, the most superficial layer of skin. When intact, this imaginary wall regulates temperature, acts as a barrier to infection, balances water and electrolytes, stores fat and insulates against the cold. The skin is also a large tactile area used for the interpretation of stimuli.
The structure and function of this delicate layer is easily damaged, leading to a wide spectrum of inflammatory symptoms. The two main causes of such symptoms are the destruction of the skin’s barrier (delipidization) within the stratum corneum by the overuse of detergent based products (sulphates) and also the stimulation of an inflammatory immune response which in turn compromises the skin’s barrier (Kownatzki 2003).
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At birth a baby’s skin is covered with Vernix Caseosa (VC) which gives added protection over the first few days of life. The thickness of this layer varies according to the gestational age of the infant. VC is a highly sophisticated bio-film consisting of antimicrobial peptides/proteins and fatty acids. These combine to form a barrier that is not only antibacterial but also antifungal. A study by Tollin et al (2005) goes further by stating that:
‘Studies confirm that maintaining an intact epidermal barrier by minimizing exposure to soap and by not removing VC are simple measures to improve skin barrier function’.
Meanwhile the skin becomes colonized with micro-organisms and develops its own stable microbiota (Tierno 2006). This transitional environment, from alkaline to acid (known as the ‘acid mantle’ and described above) further adds to the protective barrier. Its delicate balance must be maintained if the skin is to achieve an optimum level of protection. There is no evidence to prove that the acid mantle exists beyond this point, so acidic pH detergents are not thought to provide any protection (Kownatzki 2003).
‘Epidermal lipids play a key role in maintaining the skin’s barrier, integrity and health’ (Ertel 2003). This is backed up by evidence of reduced levels of epidermal lipids seen in individuals suffering from atopic eczema (DiNardo et al 1996). As the epidermis continually sheds, it is vital for the lipid seal around each skin cell (keratinocyte) to be left undisturbed. This protective layer ensures that the skin does not dry out, but can only be achieved in the presence of certain enzymes and the right lipid precursors (Kownatzki 2003). This barrier cannot be reproduced by artificial means. Great care must therefore be employed to avoid its destruction by delipidization caused by chemicals used in manufactured personal care products.
Once damaged, the epidermis is more prone to Trans Epidermal Water Loss (TEWL) which leads to dry skin. This in turn increases the likelihood of sensitization by foreign materials such as micro-organisms & allergens and aggravates the damaging effects of chemical irritants.
Interaction with keratinocyte surface molecules or membrane lipids leads to cell activation. Once released, cytokines send signals requesting assistance to blood vessels and white blood cells. Activation of Langerhans cells initiates an immune response which is particularly effective when a foreign substance is encountered repeatedly. Once a certain level of response has been exceeded, inflammatory symptoms (for example skin irritation and eczema) become evident.
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Physiology of umbilical cord separation
The umbilical cord is a unique tissue consisting of two arteries and one vein covered by a mucoid connective tissue known as Wharton’s jelly, which is covered by a thin layer of mucous membrane (a continuation of the amnion). During pregnancy, the placenta provides all the nutrients for fetal growth and removes waste products simultaneously through the umbilical cord.
Following delivery, the cord quickly starts to dry out, harden and turn black (a process called dry gangrene). This is helped by exposure to the air. The umbilical vessels remain patent for several days, so the risk of infection remains high until separation.
Colonisation of the area begins within hours of birth as a result of non-pathogenic organisms passing from mother to baby via skin-to-skin contact. Harmful bacteria can be spread by bad hygiene’ poor hand washing techniques and especially cross infection by health care workers.
Separation of the umbilical cord continues at the junction of the cord and the skin of the abdomen, with leucocyte infiltration and subsequent digestion of the cord. During this normal process, small amounts of cloudy mucoid material may collect at the junction. This may unwittingly be interpreted as pus. A moist and/or sticky cord may present, but this too is part of the normal physiological process. Separation should be complete within five to 15 days, although it can take longer. The main reasons for prolonged separation include the use of antiseptics and infection.
Antiseptics appear to reduce the number of normal non-pathogenic flora around the umbilicus. This reduction in leucocytes prolongs the healing process and hinders cord separation.
After the cord has separated, a small amount of mucoid material is still present until complete healing takes place a few days later. This means that there is still a risk of infection, although not as great as in the first few days.
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Many studies have been carried out to compare differing treatments and their effect on infection rates, colonization and length of cord separation. (Bain 1994, Barr 1984, Dore 1998, Medves 1997 Mugford et al 1986, Pezzati 2002, Salariya 1988, Verber 1992). The overall results conclude that the more the cord is treated, the longer it will take to separate. Prolonged cord separation rates are also associated with reduced colonization levels.
This would suggest that a certain level of colonization is actually a healthy sign and not necessarily a pre-curser to infection. This is why 24hr rooming-in is such an important factor in the care of the newborn. It not only avoids cross infection by healthcare workers, but also encourages early colonization of non-pathogenic organisms, which in turn promotes faster healing (Rush 1987).
Maybe J Barr (1984) was right when she postulated that: ‘Wharton’s Jelly may possess an, as yet, unknown factor, that is essential to the natural healing process’. It certainly seems to be true that the use of treatments on the umbilical cord appears to interrupt and prolong the natural process of cord separation.
As there is no evidence to recommend the widespread use of topical treatments for cord care, further studies would be helpful, especially in developing countries where neonates are at higher risk of contracting infections. However, for the healthy term infant ‘open cord care’ using no topical treatments continues to be the safest and most cost-effective advice. These guidelines are based on the WHO (1998) review of the evidence and the recent Cochrane Database Systematic Review (Zupan & Garner 2004) on topical umbilical cord care at birth.
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As a stakeholder with NICE, the author’s comments were considered during the consultation process before the July 2006 update of the postnatal care guidelines (NICE 2006).
The guidelines now state that: ‘Bathing (cleansing agents, lotions and medicated wipes) are not recommended’ and ‘Parents should be advised how to keep the umbilical cord clean and dry and that antiseptics should not be used routinely’.
‘Babycare: back to basics™’ (version 4, Trotter 2007a) presents the latest evidence based advice regarding safe skincare for babies. This is now available to health professionals and maternity units in the UK. Free samples can be ordered from TIPS Ltd.
Following requests from parents looking for advice on safe baby skincare products, the author has recently set up an independent testing programme. Having signed up online, all the parent testers taking part in the TIPS testing programme do so on a strictly voluntary basis. Products are only tested on babies over six months of age and all the products tested are free from sulphates, parabens, phthalates and propylene glycol. TIPS have just published the results of the tests carried out on 50 baby skincare products (across seven categories). These can be viewed on www.tipslimited.com
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The author’s latest article (Trotter 2007) on baby skincare concentrated on the way baby products are labelled and how legislation is prompting companies to become more responsible in the way they market such products. This is encouraging and we can hope that these new guidelines will effect a marked improvement in the quality of information provided with products and online. By raising the profile of neonatal skin care and cord care, the author hopes to encourage health care professionals to start reviewing and updating existing policies in line with the latest NICE guidelines (NICE 2006). This would lead to standardised best practice throughout the United Kingdom, and prompt manufacturers to rethink their marketing strategies by ceasing to promote their baby skincare products for neonatal use.
If you are caring for babies in their first month of life, find out if there are skincare and cord care guidelines in place together with a robust local policy to back them up. If this is not the case, take this article to your clinical risk manager and suggest this omission in clinical practice poses a potential risk.
As there is no evidence to support the use of such products on the neonate, common sense dictates that we should ere on the side of caution.
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Maintenance of the skin’s natural protective barrier is paramount.
Wash your hands before and after carrying out any baby care.
Use water only for baby skincare for at least the first month of life.
Once introduced, read the labels of all products and avoid the chemicals mentioned in this article.
Demand new products that have been reformulated to be as safe as possible.
Breastfeeding your baby will strengthen their immune system.
Do not overload your washing machine. This will help to avoid a build up of chemical residues on clothing from washing powders.
Cloth nappies are as efficient as disposables and do not present a higher risk of napkin rash. They are also kinder to the environment.
Use a thin layer of barrier cream on the napkin area to help protect against the development of napkin rash.
Massage oils should be vegetable (not nut) based and free from mineral oils, perfume and colours, if there is any history of allergies in the family.
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