This is the last of Skin Facts series and as we come to a close in 2015 and usher in 2016, one Skin Fact to look at is how our skin renew itself. The dermatological terms are ‘epidermal cell proliferation‘ which takes into account the turnover of cells and there are differences between normal adult, baby and eczema skin. Here’s a look at Skin Renewal Facts!
Basics of Skin Renewal
The skin regenerate itself every 27 to 39 days, meaning that the cells from the lower layer of the epidermis (outer layer) move up to the surface and differentiate. The epithelial cells are called keratinocytes and they have different structures within the different layers of the epidermis (from the deeper basal layer, to spinous, granular to the corny layer at the surface). The top layer is also known as the stratum corneum, for which we have looked into the transepidermal water loss through stratum corneum.
This skin renewal is not related to wrinkles as wrinkles are primarily due to the loss of collagen, which is in the dermis (middle layer) of skin. Baby skin feels ‘softer’ and more elastic likely due to shorter collagen fibres.
Baby Skin – Cell Turnover Rate
Microscopic examination of baby skin showed that baby stratum corneum is 30% thinner than adult skin, and that baby epidermis is 20–30% thinner than adult skin. The cell size at the corny layer of the baby skin is smaller, which implies that the baby’s cell turnover rate is higher. This correlates with better wound healing in infant skincompared to adult skin. Epidermal cell proliferation rate decreases with age.
Eczema Skin – Defective Protein
As cells proliferate, there are proteins that are expressed by the skin cells. Studies have been made on various proteins and one of the most distinguishing (lack of) proteins is that of filaggrin (FLG), which serves to produce and protect the skin barrier. In people with eczema, there is lower level of FLG, resulting in flatter skin surface cells, disrupted protective fatty layer, reducing the moisturizing function of the skin and increasing water loss from the skin. Reduced FLG also increases the skin pH and leads to increased skin inflammation. It is possible that for eczema skin, the defective protein expression makes it unable to proliferate but instead ‘terminate’ at the basal layer. This has the effect of weakening the skin structure.
This is the 6th post exploring ‘Skin Facts’ and today’s focus is on the lipids/ fats in our skin. There is distinct difference between the skin lipids of normal adult skin, baby skin and eczema skin. Let’s explore skin lipids!
Types of Skin Lipids
There are lipids from both sebaceous and keratinocyte/ epidermis:
Sebaceous – from sebaceous glands and coats the skin surface, mainly triglycerides, wax esters and squalene, fatty acids and smaller amounts of cholesterol, cholesterol esters and diglycerides
Epidermal – found between the epidermal skin cells, mix of ceramides, free fatty acids and cholesterol
Lipids from Sebaceous Glands – Sebum
The concentration of sebum is higher at the forehead, face, scalp, upper chest and back and lower on the hands and feet and none on the palms and soles.
Function of Sebum
Deliver antioxidants to the surface of the skin in the form of vitamin E
Increased protection via increasing impermeability of skin
Maintenance of skin moisture content
Eczema and Lipids
Atopic dermatitis is associated with reduced epidermal lipids in all three categories – reduced ceramides, cholesterol and free fatty acids
The lack of lipids lead to a weak ‘brick and mortar’ structure where the lipids are akin to the mortar that keep the skin cells (bricks) together. This weakened skin barrier is associated with increased transepidermal water loss and increased skin permeability
The subcutaneous fat in baby skin is rich in the saturated oils – palmitic and esteric acid, with the following characteristics:
Higher melting point temperatures – freeze more easily (such as eating ice or popsicle for hours!), thus avoid extreme temperature for babies
Saturated vs Higher unsaturated oleic acid and linoleic acid in adults
Infant skin contains less total lipids compared to adults
Malnutrition is linked with changes in surface lipids, where an alteration in skin lipids has been observed due to essential fatty acid deficiency
With a lower lipid skin content, it is important not to excessively wash baby skin and further remove the skin lipids.
Other posts on EczemaBlues.com on skin lipids are:
Eczema News – ‘Lipid fingerprint’ Treatment Approach : Where the Oregon State University is developing a system to identify the missing lipids in an individual skin, thus the possibility of getting moisturizer to replenish the specific deficient lipid.
Many chemicals come into contact with our skin, some intentional and others inadvertently. How much chemicals penetrate our skin?What about that of a baby or those who have defective skin barrier like eczema sufferers? This 5th post of Skin Facts series explores the chemicals our skin comes into contact with.
Our Skin Structure – How do Chemicals Penetrate?
Chemicals definitely penetrate certain layers of our skin, otherwise, the skincare industry will collapse if all skincare products just stay on the skin surface and no product can claim to improve your skin! Chemicals penetrate different layers of skin barrier (that’s part of the ‘price’ we pay for a skincare product where technology is involved to enhance penetration).
Here are 3 Ways Chemicals Penetrate our Skin:
Penetration/ Transcellular absorption – via the stratum corneum through the corneocytes (flattened cells that made up the horny layer); Stratum corneum contains about 40% protein (primarily keratin), 15% to 20% lipids and 40% water.
Intercellular absorption (main route) – Chemical is transferred around the corneocytes in the lipid-richextracellular regions; Lipids present in the intercellular spaces of the stratum corneum are by weight: 45–50% ceramides, 25% cholesterol, 15% long-chain free fatty acids and 5% other lipids, the most important being cholesterol sulfate, cholesterol esters, and glucosylceramides.
Michaels et al. (1975) is the one who came up with the ‘brick and mortar‘ analogy describing corneocytes filled with lipids. Dermatologists explain eczema skin has the wall without strong mortar holding the bricks.
Appendageal absorption – Chemical bypasses the corneocytes, entering the shunts provided by the hair follicles, sweat glands, and sebaceous glands
Baby Skin – More Chemical Penetration?
The baby skin is not fully developed, where Infant stratum corneum was found to be 30% thinner and infant epidermis 20% thinner than in adults. More chemicals penetrate due to this and there’s higher risk associated with this penetration due to:
High surface-area to volume ratio
Higher metabolic rate, higher respiratory volume
Immature drug metabolism, drug carriage and detoxification systems
Decreased subcutaneous fat stores that (i) increase absorptive area and (ii) decrease the volume of distribution of the chemical
Higher chances of injured skin (for instance, from adhesive tapes) increase skin permeability
Vulnerable to endocrine disrupters
Eczema Skin – How Defective Skin Barrier Affect Chemical Penetration
Eczema skin is defective which allows more chemicals to penetrate and be absorbed with possible effects of:
Enhanced absorption of a specific chemical
Entrance of larger molecules such as proteins and nanoparticles
Facilitate entrance of chemicals into and through the skin
The Care in Chemicals
With increased chemical penetration, it follows then that we ought to be extra careful of what goes onto baby skin as well as eczema skin (and baby’s eczema skin!). It is impossible (and not necessary) to aim for zero chemical contact, instead know which types of products not to use and what skincare/ cosmetics ingredients to avoid:
Soap – Avoid as it is drying (due to alkalinity) and harsh for skin; alternative: use a gentle cleanser/ bath oil/ oatmeal bath
Anti-microbial wash – Avoid; read this post to learn more about effects of anti-microbial wash and its ingredients that irritate skin
Shampoo – Choose one without key irritants (see below)
Antiperspirant – Safe to use, can opt for an aluminium and paraben free one (see WebMD article)
Skincare moisturizer – Choose one without key irritants (see below)
Detergent and detergent residue on clothes – Use a hypoallergenic one and turn on a longer cycle (see this post)
Toothpaste – Safe to use, just don’t overuse
Baby wipe – Choose one without Methylisothiazolin (MI) and fragrance free (see this post)
Bubble bath – Avoid as the average bubble bath is irritating to skin
Cosmetics – Throw away expired cosmetics
Instead of trying to eliminate all chemicals, it’d be more practicable to avoid ingredients that are known irritants or suspected to cause harm:
AVOID #1 Perfume
Fragrance, phthalate esters, synthetic musk compound, Benzyl alcohol, scent, aroma, Abietic acid, alcohol, Abitol (see this post on various names of perfumes)
“The average fragrance product tested contained 14 secret chemicals not listed on the label,” reports EWG, which analyzed the Campaign’s data. “Among them are chemicals associated with hormone disruption and allergic reactions, and many substances that have not been assessed for safety in personal care products.” EWG adds that some of the undisclosed ingredients are chemicals “with troubling hazardous properties or with a propensity to accumulate in human tissues.” Examples include diethyl phthalate, a chemical found in 97 percent of Americans and linked to sperm damage in human epidemiological studies, and musk ketone, which concentrates in human fat tissue and breast milk. Fragrance secrecy is legal due to a giant loophole in the Federal Fair Packaging and Labeling Act of 1973, which requires companies to list cosmetics ingredients on the product labels but explicitly exempts fragrance.”
I find it interesting because if you look at your perfume, even the most expensive ones, you would find many of them are irritants and definitely hard to pronounce! There are also ingredients that are ‘hidden’ behind proprietary names given by the brand.
Consequence: Irritate, allergenic, allergic rhinitis, chronic sinus, asthma, accumulate in the environment, the body and the breast milk, disrupt the endocrine system (Endocrine system is a network of glands that produce and release hormones).
1,2 Propanediol, 1,2-dihydroxypropane, methyl glycol, trimethyl glycol (Ethylene Glycol is more toxic than propylene glycol)
Found in: Skincare products, shampoo
Consequence: Known irritant for babies, infants and those with sensitive skin conditions such as eczema, or those with prolonged dermal contact e.g. during treatment of burns
Found in: Shampoos, conditioner, bath additives, toothpaste, baby wipes
Consequence: Irritant and drying to skin, corrodes hair follicle and impedes hair growth
Here’s what I learned from dermatologist Dr Cheryl Lee on surfactants used in our product (see post):
Surfactants are designed to remove dirt and oils from the skin, but the problem is that they can also remove the lipids from the skin as well. This leads to disruption in the skin barrier and exacerbates all the skin barrier problems in atopic dermatitis…Of note, a recent study by Belsito et. al., showed that the surfactant cocamidopropyl betaine (CAPB) is more likely to cause allergic contact dermatitis in people with atopic dermatitis than in those who do not have atopic dermatitis.
Some of the above chemicals are UV-filters such as oxybenzone that are excreted in the urine after application to the skin. Sun protection is a must, choose a physical blocker type and learn more in Skin Fact – Sun Protection in Adult, Infant and Eczema Skin
Consequence: Biochemical or cellular level changes, disrupts the endocrine system, accumulates in breast milk and in the environment, photo allergic reaction (PABA)
Others to Avoid
Triclosan – Present in shampoos, bath cleansers, toothpast and baby wipes, can cause allergies and bacterial resistance (see this eczema news on household products’ exposure)
It is studied that twice daily moisturization with a hypoallergenic (meaning no fragrances, no essential oils, no plant extracts, no formaldehyde-releasing preservatives, no lanolin, no neomycin, no bacitracin, no methylchloroisothiazolinone) moisturizer in high-risk newborn babies lead to an approximately 50% reduction in rates of new onset atopic dermatitis.
We have also looked at infants being more susceptible to sunburn. This, on surface, seems to suggest that putting on moisturizing and sunburn is good for the babies but there’s a major caveat that you should not be putting on harmful chemicals since so much more chemicals penetrates infant skin (and possibly even more for infants with defective skin). Use good quality moisturizer, tested safe for babies and without the key irritants AND avoid sun (rather than ‘suntan’ a baby with sunscreen as we’ve seen sunscreen contains quite a fair bit of irritants!).
We have been learning about skin facts and last week, we learnt about insensible perspiration – which is transepidermal water loss that we cannot control. This week we are learning about sweating, sweat glands and how sweat affects eczema skin. First, the basics:
Why, How Much, Where and What of Sweating
WHY – Sweating is a way to cool the body temperature whereby sweat glands in the skin are activated and release sweat. The evaporation of the sweat cools the body and those leftover sweat (on a humid day) leaves you soaked. See #SkinishMom post on sweaty occasions.
HOW MUCH – We sweat different amounts on different occasions; for an hour of exercise, one can sweat from 0.8 to 1.4 liters. Excessive sweating is ‘defined’ in terms of the sweating deteriorating the quality of life, a condition known as hyperhidrosis.
WHERE – This gets interesting as emotional sweating when you’re angry or anxious activate the sweat glands on the palms, soles and underarms! Sweating after eating spicy foods (gustatory sweating) are on the lips and forehead.
WHAT – Sweat is made up of water, ammonia, urea, minerals (like sodium and magnesium), trace metals, lactate and various salts and amino acids. The exact composition of sweat varies depending on diet, genetics and activity level.
Sweat Glands in Adults and Children
Sweat comes from two types of glands:
Eccrine glands – All over the body in the dermis (layer after the outer epidermis of skin), there are over 2 million eccrine glands. The sweat exit via a pore. The sweat from eccrine glands has no smell of its own but the smell comes from bacteria on our skin feeding on the oils in the sweat.
Apocrine sweat glands – At armpits and private parts, and the sweat exit via a hair follicle. Upon puberty, the glands make a thick, oily fluid which has a smell.
Women – More sweat glands then men, but less active
Babies – Babies are born with sweat glands but they are not activated, only the ones on the foreheads are! After the forehead, the sweat glands on the trunk, arms and legs are activated. In this Common Summer Skin Rash series – Heat Rash, dermatologist Dr Robin Schaffran explained heat rash, medically known as miliaria:
Miliaria occurs under conditions of high heat and humidity that lead to excessive sweating. Occlusion of the skin from too much clothing or blankets can aggravate the pooling of sweat on the skin surface leading to over-hydration of the skin. In susceptible persons such as infants who have immature sweat glands, this often leads to transient blockage of the sweat ducts. Therefore, as more sweat is produced, there becomes and inability to secrete the sweat because of the blockage.
Sweat and Eczema
Sweat is known to cause irritant reaction for those with eczema. However, what in the sweat irritates is not known. In the Skin pH series – Moisturizer and Skincare Products interview with dermatologist Dr Cheryl Lee:
As for sweat, the biggest problem is the irritancy of the sweat itself. The salts from sweat can crystalize and act as an irritant to the skin. If you can see that your baby’s sweat has dried and has a salty residue, then I would recommend rinsing it off with plain water (no soap) to prevent it from becoming an irritant.
It could be one of these compounds, the combination of them, the changing pH of the skin, or even the sweat’s water content that can cause the itching and stinging sensations to some people with eczema.
Eczema may also occur in those suffering from ichthyosis, a condition that has excessive skin scales, clogging sweat glands and preventing sweating normally. Pompholyx is another condition that some eczema sufferers also have, with a distinctive appearance of itchy small blisters on the palms of the hands. It is also more closely associated with excessive sweating and can be found on the soles and toes.
This is the third week of ‘Skin Facts’ and last week, we’ve looked into the sun protection function of children vs adult skin, and how the sun affects eczema skin. Today, we’re looking into another critical function of skin and one that is very relevant for eczema skin – our skin’s moisture retention property. One can also view it as how much moisture is lost from our skin, known as Transepidermal Water Loss (TEWL). TEWL is studied by dermatologists, as excessive TEWL points to a defective skin barrier, and in severe cases, affect the ability of the body to function. Let’s go “water deep” into this skin function!
Water and our Body
Water makes up a large point of our body weight, here are some interesting facts about the water in our body from water.USGS.gov (the US Geological Survey website):
Water content in our Body
Lungs 83%
Muscle 79%
Kidneys 79%
Brain 73%
Heart 73%
Liver 71%
Skin 64%
Bones 31%
Percentage of Body Weight that is Water
Fetus 94%
Infant at birth 78%
One-year old 65%
Female 55% (due to higher fat content)
Male 60%
Elderly 50%
Functions of Water in our Body
Forms the building material of cell
Regulates body temperature by sweating and respiration
Transport via the bloodstream
Flushes waste via urination
Absorbs shock for brain and spinal cord, also lubricates joints
Forms saliva
Water Loss from our Skin
Our skin allows water to be lost through it, as part of insensible perspiration (or transepidermal diffusion) and sweating. Insensible refers to us not being aware of it (another insensible loss of water is from respiration). Sweating helps regulate our body temperature, via cooling of the skin. However, sufficient intake of water is required in order for sweating to not dehydrate the body and continue to be effective in cooling our body temperature.
Much of the water is lost through the stratum corneum, the upper most layer of the epidermis made up of a dead cell layer. A defective stratum corneum layer will allow excessive epidermal water loss and potentially, increase risk of irritant and allergen sensitivity. Water loss from evaporation from our skin is about 400ml daily in an adult. For research news on how the skin can be a channel for allergy, see Food Sensitization from Eczema.
Transepidermal Water Loss (TEWL) from Children Skin TEWL from baby skin is higher than normal adult skin, due to their thinner stratum corneum. For premature infants less than 30 weeks, there are also fewer layers of stratum corneum resulting in increase fluid and heat loss. Interestingly, infant skin is found to have higher water content and able to absorb more water but lose excess water faster than adult skin.TEWL was also strongly predictive of AD at 12 months (study here). The natural moisturizing factor (protein breakdown products such as small amino acids, urea, pyrrolidone carboxylic acid, ornithine, citrulline, urocanic acid) in infant is also lower than an adult.
How this Impact Parents Caring for Baby Skin Protection of the stratum corneumis important, and this can be via:
Reduced bathing – Washing baby skin with a washcloth during the first 4 weeks of life is associated with increased TEWL and decreased stratum corneum hydration compared with simply soaking in water. The recommendation is to use a mild liquid cleanser with water (less drying than water alone), and that bathing should be brief (10 minutes or less) and no more than every other day with spot cleaning in between.
Good bathing regimen – Includes not using hot water, not scrubbing the skin dry (but pat dry), keeping it short to 10 minutes, not using soap and moisturizing right after (see video)
Good skincare regimen – Moisturizing protects the skin barrier (see video). It is important to note that given the thinner stratum corneum of infants, their higher surface area to body ratio, infants are more vulnerable to toxicity of products. Therefore, be sure you understand the product label (there’s a comprehensive Sensitive Skin Products blog series to help you with that).
Transepidermal Water Loss (TEWL) from Eczema Skin
TEWL is studied to be higher in eczema skin and also dry skin (without eczema). The water content of stratum corneum is also lower in adults with eczema than normal skin. It is also studied at the natural moisturizing factor of eczema skin is defective, lacking in proteins that are able to play a role in the skin’s humectant property – the ability to pull moisture from the environment and retain this water (which is why 2nd generation moisturizers incorporated humectant property, learn more here).
Drinking Water and Skin
A myth. Dehydration will affect skin but drinking excess water will not lead to ‘glowing’ skin. Drinking enough water will also not prevent skin aging or wrinkles as these are related to genetics, sun and oxidative stress brought on by pollutants. Read this #SkinishMom Investigation! – Drinking water for dry skin
To round-up, we learnt that water is integral to our body and to our skin. We have insensible water loss and a thinner stratum corneum in baby skin and a defective stratum corneum in eczema skin both results in increased transepidermal water loss (TEWL). This knowledge should encourage (not discourage!) us to be more committed to a good bath and skincare routine.
We have started learning skin facts last week, specifically on the skin (surprise) isn’t the largest organ and that well, we don’t really know what’s in our dust. This week, we’re taking up a notch on going ‘intensive’ into the difference in the sun protection function of adult, child and eczema skin.
Normal Adult Skin
Adult skin has a fully developed sun protection function, in the form of pigment melanin which gives the skin its color. Therefore, the darker one’s complexion, the higher the sun protection. Melanocytes are the melanin-producing skin cells and it is the activity of the melanocytes, i.e. the amount of melanin produced, and not the number of melanocytes that determine the skin color.
When one is exposed to sun, more melanin is produced to help protect the skin against UV rays, thus giving a ‘tan’. Melanin can reduce the oxidative damage caused by UV rays but isn’t able to fully protect from the damaging effects of UV rays (see this news on potential harm of ‘sun-activated’ melanin to our skin).
Children Skin
An infant’s skin has not fully developed in many ways that make a baby more vulnerable to the damaging effects of UV rays – it has less pigment/ melanin, thinner skin/ stratum corneum and a higher surface area to body ratio.
Studies have also pointed to infants with exposure to UV rays will show skin pigmentation on exposed skin from as young as one year old (first summer). This was true even for infants who used sun protection when outdoors but not when in the car, in the shade or on a cloudy day. There are also studies showing that exposure to UV during childhood and adolescence can lead to skin cancer later in life.
Eczema Skin
There is no study that points to differences in melanocytes/ melanin due to eczema. However, the sun is known to both improve and aggravate eczema, for instance:
Some eczema sufferers report improved eczema during holiday when outdoors more often (no study confirmed why holiday seems to improve eczema).
Phototherapy is used as an eczema therapy for adults.
Active eczema flare-up should stay away from the sun as it can worsen eczema, and increase vulnerability to sun burn.
Certain skincare products increase sensitivity to sun, such as those containing ingredients alpha-hydroxy acids (AHAs), beta-hydroxy acids (BHAs), salicyclic acid, glycolic acids, Retin-A and hydrocortisone. Moisturized skin may get sun burn more easily, thus put on moisturizer and wait for 30 minutes before applying sunscreen.
Sun – We need it, but not too much of it.
Our skin play an important role in the synthesis of vitamin D, where vitamin D can increase the production of skin proteins (cathelicidin) and antimicrobial peptide (AMP) which protects against skin infection. However, just 15 minutes a day is enough and it’s referring to getting sun on the face and arms (i.e. no need to be in a bathing suit!). During summer, 2-3 direct sun exposures of 20 minutes per week is sufficient. Short frequent sun exposure is better than long exposure.
Rays from the Sun
There are 3 different rays from the sun:
UVA – 320 to 400 nm : passed through the atmosphere
UVB – 290 to 320 nm : passed through the atmosphere
UVC – 100 to 290 nm : most dangerous, but filtered and do not pass through the atmosphere
UVA – UVA activates melanin already present in the upper skin cells but the tan is lost quickly. Penetrates deeper into the skin, damages the dermis (middle skin layer), accelerates aging, causes wrinkles, increases oxidation and suppresses cutaneous immune function.
UVB – UVB stimulates the production of new melanin, and a longer lasting tan. Also stimulates a thicker epidermis. Absorbs by the epidermis (top skin layer).
It’s not just the sun, it’s also the ozone.
We all know that the ozone layer is thinning and the thinner ozone has allowed more UVB rays to come through the atmosphere.
Sun protection
Sun protection has been covered in various interviews with dermatologists on this blog but the point to emphasize is that for babies, it is very important to avoid the sun and practice sun protection because:
Thinner skin
Less melanin-producing skin cells
Larger surface area to body ratio
Increased absorption of chemicals and vulnerability to irritants in sunscreen products make sun avoidance a wiser choice
Lips and eyes are also affected by UV rays, thus wearing a wide-brimmed hat and sunglasses are also part of sun protection.
It is recommended to use physical blockers/ inorganic filters such as zinc oxide (more UVA protection) and titanium dioxide (more UVB protection). As opposed to chemical absorbers, physical blockers do not penetrate more than two layers of stratum corneum and therefore less likely to induce skin irritation and sensitization. Moreover, infants tend to rub their eyes and may inadvertently rub the sunscreen into their eyes and won’t be able to ‘get rid’ of it as (i) their tear secretions and (ii) their blinking mechanism are not fully developed.
A note on SPF
SPF is the measure of ratio of UV rays before sunburn and SPF 30 means that the skin is able to take 30 times higher dose of UV rays before sunburn. The amount of sunscreen to apply is 2mg/cm2. Broad spectrum refers to additional UVA absorbers (avobenzone and octocrylene) being added to the physical blockers.
This is the final post of the 5-part series and today, I will try to apply all that we have learnt in the past 4 posts to eczema skin consultations. I have presented it in survey format for each step of teledermatology and look forward to hearing your experience!
Before the Teledermatology Process
Q1 Were you given a leaflet to explain teledermatology and what form of teledermatology is available to you?
Q2 Were you aware that you do not have to consent to teledermatology?
Q3 Were you told that if an in-person consultation is deemed required during the process, you will have access to the dermatologist?
Q5 Were you told that your eczema is suitable or not suitable for teledermatology? For instance, full body eczema, or rashes in scalp, private parts or pigmented rash are difficult to capture fully in images. Or that your eczema is localised and can be clearly identified in image.
Q6 Were you told that teledermatology may not be as accurately diagnosed than face-to-face consultation?
Starting the Teledermatology Process
Q7 Were you told who is the dermatologist and his/her licensure and board certification?
Q8 Were you told what images of your eczema will be taken and how these will be stored and protected?
Q9 Were you given the instructions on how you can access your own patient record?
Q10 Did you feel that the referring physician is comprehensive in recording your medical history?
Q11 Were you asked these questions on your eczema?
Previous treatment for eczema and response to medication
Personal and family history of skin disease and atopy
Body map is recommended to show the site of lesions and the extent of inflammation at each site
Q12 Did you feel you were treated with dignity during the photography session?
Q13 Were you told that you can have a companion during the consultation with the referring physician?
Skin Management Plan
Q14 Were you provided with a skin management plan? e.g. what medication, for how long/ which part of skin/ frequency/ how much to use
Q15 Was it made clear to you who is responsible for your care? e.g. to communicate with you and ensure that treatment is clearly communicated
Q16 Was there nursing staff to help you with skin care? e.g. guidance on how to moisture and wet wrap
Q17 Could your referring physician explain clearly which type of eczema you have, and the steps to reduce flare-ups e.g. allergy avoidance, active steps to reduce staph bacteria
Follow-up with Face-to-Face Skin Specialist Consultation
Q18 Did you have to wait longer than traditional referral to see the dermatologist who has provided the skin management plan?
Q19 Did you have to provide the same information again at the skin specialist clinic?
If you were referred for videoconferencing with the dermatologist,
Q20 Did the dermatologist have your information and referral form?
Q21 Was the videoconferencing set up in advance and smooth?
Q22 Were you told beforehand where you would need to uncover for the skin to be imaged?
Q23 Were all the persons in the room identified?
In instances where the set up or preparation for teledermatology is inadequate, the dermatologist may only confirm a diagnosis/ provide a treatment plan in-person. As such, it may end up being more time consuming to engage in teledermatolgy. What’s your experience? How many of the 23 questions were ‘checked’ for you?
Teledermatology takes away the need to travel and meet in person with the skin specialist. This brings about numerous advantages such as:
Shorter wait time – Compared to traditional referrals, a referring physician that a patient sees (nearer and more accessible) can help to capture, store and transmit the patient information and skin images to a dermatologist. The access to a dermatologist is therefore faster.
Accessibility for patients who live in areas without dermatology care – Singapore is small but in many other countries, specialist dermatology department may only be available in certain areas and teledermatology is a way for patients living in more remote areas to have access to specialist care.
Familiarity – For skin issues that both the referring clinician and the dermatologist feel that it is appropriate for the dermatologist to prescribe a skin management plan and the referring clinician to administer and be responsible for the patient interaction and care, the patient will then be seeing the same doctor (referring clinician) who he/she has already established a relationship with.
Convenience – Potentially faster, cheaper and less stressful than to travel and visit another doctor.
More detailed record – As the process of teledermatology is reliant on the transmission of patient information, images and then the relay of the diagnosis and treatment plan, followed with the outcome of previous treatment, there is a well documented record of the patient information and the skin condition. This record may be more detailed in in-person consultation.
Reduction of waiting lists at dermatology clinics – As certain skin conditions do not warrant establishing a relationship with dermatologist but rather straightforward in the diagnosis and treatment, the waiting lists at dermatology clinics can be shortened.
However, it is NOT ALWAYS that these advantages can materialize and both the referring physician and dermatologist can take actions and have systems in place to ensure success in teledermatology:
At the Referring Physician
Proper record of patient information, medical history and the history of the skin lesions
Staff to take skin images that meet the guidelines of images in teledermatology – dermatology nurse trained to take high quality skin images
Integrated system at the referring physician to incorporate teledermatology
Proper planning of the consultation process at the referring physician to take the images required after the consultation
Selection of patient – Patients who are resistance to teledermatology, for instance, elderly, shy or young patients, or with rash at private parts should not be pressured to consent to teledermatology
Educational materials on the diagnosed skin condition to be available for the patient and the care team
At the Dermatologist
Dermatologists who signed up for teledermatology should have the resources to promptly feedback on the information provided by the referring clinician
Dermatologists should have resources for the referring clinician and his/her clinic on various skin conditions
Close communication and record of patient care with a system to obtain feedback and address weakness in the process
Patients should not have to furnish information all over again if referred for an in-person consultation at the skin specialist clinic, i.e. teledermatology should be integrated with the specialist clinic system
Patients should have a shorter waiting time for in-person specialist skin consultation compared to traditional referral
Patients should have easy access to dermatologist for face-to-face session
Patients should be given clear skin management plan
If traveling to the dermatologist is not an issue to begin with and the mode of teledermatology is video conferencing, there may not be much cost/time-savings involved. On the other hand, it benefits certain situations such as elderly living in a home who may not have access to specialist care if not for teledermatology.
If you want to understand more of the quality standards in teledermatology, do read British Association of Dermatologists’ standards. Share in the comments if you have benefited from teledermatology and what advice you have for patients to get the most out of it, your sharing will help another!
Last week we covered a critical part of the teledermatology process – getting quality patient information and skin images (for Store and Forward). This week we break down the various steps in teledermatology and explore why each step may not work as well as in-person consultation.
Face to face consultation remain the gold standard as there are many areas where teledermatology may fall short. The referring provider and the dermatologist must be familiar and trained to conduct teleconsultation to mitigate these shortfalls.
Step 1 – Understanding the Patient
In face to face consultation, non-verbal cues can be noted including signs of stress that may be important in measuring the quality of life and severity of skin condition e.g. eczema. In triage teledermatology, it is often limited to paper documentation or standard referral letter.
Mitigating factors – There should be a system in place at the referring physician clinic to understand the patient. For instance, comprehensive questionnaires, trained doctors and nurses to capture patient information and images and sufficient time to do so.
Step 2 – Skin Evaluation
In face to face consultation, the physician can use sense of touch and able to see ALL the skin areas. In teledermatology, it is limited to the skin area where the photograph has taken. There are certain skin areas where it is recommended to have an in-person consultation, such as:
The whole body has skin problems, for instance, generalized eczema rather than localized. Physicians have to note to treat the patient as a whole, even when the information is centered on the lesions (a potential pitfall of teledermatolgoy is focusing only on the skin lesion).
The skin conditions are on areas of skin with hair that cover up the skin rash, for instance, the scalp.
The skin lesions if pigmented are harder to view as an image.
Mucosal lesions and orifices, e.g. genital, present difficulty to take accurate image.
Mitigating factors – Skin images have to be taken from various angles, with mid close-up and macro close-up distance and skin lesions clearly marked. Therefore, the referring physician who takes the image or review the suitability of the image has to be trained. Special lighting or dermatoscopes may be required.
Step 3 – Administering the Treatment
It is more likely for the treatment to be carried out as prescribed if there is in-person interaction. Patients have an opportunity to ask their questions directly to the dermatologist and such interaction provide opportunity to optimize patient care.
Mitigating factors – If the treatment is to be handled by the referring physician, educational materials may need to be provided for both the referring physician and the patient. There ought to be close communication between the referring physician and the dermatologist so that the treatment and skin management plan for the patient is agreed and both physicians feel confident with the plan.
Step 4 – Responsibility for the Patient Care
It should be clear within the care team and clearly communicated who is responsible for the patient. In particular, in the quality standards by BAD, it is stated under ‘Patients with long-term skin conditions (eg eczema or psoriasis)’ that
Patients with chronic inflammatory skin disease should be managed through teledermatology only if the referring clinician has the facilities and clinical experience to provide on-going patient support and review based on the skin care management plan provided by the reporting skin specialist.
The rationale is that these skin conditions fluctuate significantly in severity and may require complex treatment plans for safe and effective long-term management. Patients (and parents/carer) should have access to suitable nursing expertise for treatment, counseling, education and advice. Another rationale is that these skin conditions may come with significant physical, social and psychological impairment and therefore the ability to provide on-going patient support is critical to patient care.
There is a reported loss of rapport with the patient through the teledermatology. As such for certain skin conditions that are chronic, fluctuating and require long-term care, teledermatology may not be suitable.
Next week, we will explore what are the advantages of teledermatology. Have you tried teledermatology? Did you feel at any time that your health and skin conditions are not fully understood? Was your referring physician convinced with the skin management plan and were you confident in following through with it?
Share in the comments, especially important as teledermatology is gaining in popularity and we want to do our little part to steer it in the right direction for skin/eczema patients!
Last week, the basics of teledermatology was introduced – What Teledermatology is, its different forms and patient points when getting started on it. Today, we continue with the 2nd part of this 5-part series, focusing on a central part of the teledermatology process – Skin Images and Patient Information. Much of the guidelines are obtained from the British Association of Dermatologists’ Quality Standards for Teledermatology.
Information for Skin Patients
Before getting started on (and providing consent to) teledermatology, there are good practices on what Information You (as the skin patient) Ought To Be Provided With:
What the tele dermatology process involves and why it is helpful in your case
Why there may be a difference in diagnostic accuracy from in-person consultation
Process in place to have an in-person consultation should the need arise
Who takes the images and what images are needed
What information will be sent with the images
How the images are transferred
Information about the specialist to whom the images are sent to and what the specialist will do with the information
What happens in response to the teledermtaology consultation
How you can access your own information
Where your skin images are stored, for how long and who have access
The fact that you do not have to consent for teledermatology
Information from Skin Patients
Once you have consented to teledermatology, a critical part of the process is compiling complete and accurate Information on You and Your Skin Condition. Information that are expected to be collected, stored and transmitted (Store-and-Forward) are:
Personal Information on Patient
Date of birth
Gender
Ethnic group
Address, contact number
Information on Patient’s Skin Condition
Date of onset and duration of skin lesions
Whether single or multiple skin lesions
Locations of the skin lesions
Changes in size, shape and colour
Any bleeding and/or ulceration
Symptoms that accompany the skin lesions
Information on Patient’s Medical History
Any personal and/or family history of skin cancers
Other risk factors, e.g. excessive sun exposure, fair skin, large number of birth marks, currently on immunosuppressant medication
Other medical conditions
Repeat and recent medications
In particular, for those with inflammatory skin condition, e.g eczema, information from you that is required are:
Previous treatment for eczema and response to medication
Personal and family history of skin disease and atopy
Body map is recommended to show the site of lesions and the extent of inflammation at each site
A note on Skin Images
If the skin images are to be taken at the clinic of your referring physician, a few points that they ought to bear in mind are:
Protecting your modesty – You have the right to have a chaperone or bring a companion
Images should be a minimum of 2000×1500 pixels or 3 megapixels
Images should be taken at least at two different angles, to compensate for loss of details from reflection
Images should be mid-close up to identify where the lesion is and macro (close-up)
The focusing distance should be at least 20cm for macro close-up.
Image filenames should be clearly identified
Skin lesions can be identified using sticky labels, surgical tape or washable markers.
In Store and Forward Teledermatology, capturing quality images, recording accurate and complete information is a critical success factor. If the dermatologist is comfortable with the quality of imaging and information, it is less likely that you will be called in for an in-person consultation.
What is your experience? Were you provided with adequate information BEFORE you consent to teledermatology and did you feel that your referring physician recorded all the requisite information? Share in the comments so we can benefit from your experience!
With many people having access to cameras and internet, teledermatology is gaining popularity with the potential of getting a dermatologist’s consultation in a shorter time (compared to a long referral wait). This 5-part series explore the numerous aspects of teledermatology, much of the information is from dermatology associations like the American Telemedicine Association, American Academy of Dermatology, British Association of Dermatologists (BAD) and numerous published research/review papers.
What is Teledermatology?
Teledermatology is a skin consultation carried out remotely using telecommunications, it can take different forms such as:
Store and Forward – This refers to images being stored, sent to the dermatologist with patient information who will then revert with the consultation. Thus, it is not ‘real time’.
Real-time Interactive – This uses videoconferencing.
Direct-to-patient – Images are sent to the dermatologist and there is a live interaction.
Triage consultation – This involves two physicians, where one physician (referring physician) will send the patient information and images to the dermatologist and interact with the dermatologist. The patient interacts with the referring physician.
Store and Forward – When is it Used?
Store and forward is increasingly used, in various forms of skin consultations.
In direct-to-patient teldermatology, store and forward is between:
Patient and Dermatologist
Patient sends his medical history and images directly to dermatologist
Dermatologist provides care directly to patient
Store and forward can also be used in teletriage, whereby:
Referring physician interacts with patients, to obtain medical history and skin images
Referring provider sends the patient information to dermatologist
Dermatologist decides on next step – in-person consultation, tele consultation or no specialist consultation required
If it is to be via tele consultation, the dermatologist provides a consultative report back to the referring provider with a skin management plan
Referring physician is responsible to carry out the treatment recommendations
Some ‘Get Started’ Pointers for Patients:
#1 Be clear about what you sign up for
As there are various forms teledermatology can take, make sure you find out which one your referring provider has in mind – will he remain as your primary care doctor or it is expected to eventually lead to a referral to see a dermatologist directly
#2 Licensure and board certification of dermatologists
In certain countries/states, there are regulations that mandate patients have a choice of dermatologist, access to where the dermatologist is licensed and what are his/her board certifications. Sometimes dermatologists can provide teledermatology only in states where he/she is licensed. Other states regulate that prescription can only be provided when there is a live interaction. Being licensed in a particular state may also mean being familiar with the health care infrastructure and the resources you (as the patient) have access to.
#3 Access to in-person followup
It would be ideal for you to have the option to access to the dermatologist in-person even if the teledermatology is currently not direct-to-patient form. Where the teledermatology is direct-to-patient, dermatologists are expected to have met you in person or to do so via a live video conferencing before prescribing medication.
#4 Expect your medical history to be stored and transmitted
As opposed to in-person consultation where images of your skin may not be taken, teledermatology relies on the storage of such images to be transmitted to a dermatologist. There are guidelines on collection of patient data and on privacy. Some data that are required to be collected are:
Medical history – for instance, history of eczema or atopic conditions in family
Medical records – past treatment given and current treatment will be documented electronically for all physicians in your care team to have access to. The patient’s existing primary care physician and dermatologist (if any) should be identified.
#5 Right doctor at right time and place
No matter what form ofteledermatology, it should be no less effective and efficient than a in-person referred consultation. The main advantage of teledermatology is the potential to receive a specialist consultation sooner and to have access to the right doctor. The teledermatology process should not end up being convoluted and time-consuming.
Have you tried teledermatology? Has it benefited you? Share in the comments so that the rest of us can benefit!
Toxic shock syndrome is rare but life threatening, caused by bacterial toxins from staphylococcus aureus. Toxic Shock Syndrome commonly affects teens and young adults, from age 15 to 35 and majority, female.
What Causes Toxic Shock Syndrome?
Toxic Shock Syndrome is due the bacterial infection via the skin, vagina or pharynx into the bloodstream. While it is not uncommon for Staph bacteria to colonize the skin, a cut, surgery or wound in some individuals may lead to the bacteria entering the blood without immunity to fight it. The conducive environment for the toxin is protein-rich and oxygen, which is what the use of tampons during menstruation provides. Tampons with higher absorbency (polyester, carboxymethylcellulose and polyacrylate) increases the risk of TSS. The toxins can cross the vaginal wall to the blood stream, possibly through tear when inserting the tampon.
Symptoms of Toxic Shock Syndrome
Flu-like symptoms
Confusion, dizziness due to low blood pressure
Skin rash
Swelling and redness in mucous membrane
Shock
Multi-organ failure
Diagnosis is made based on physical examination, blood or urine test or swaps from the cervix, vagina and throat.
Skin rash – generalized, flat and red (characterized by turning white when pressed)
Shock occurs when the blood pressure cannot be maintained
Skin rash disappears on recovery.
Skin on palms of hands and soles of feet flake and peel off.
Fingernails, toenails and hair may fall out.
Types of Toxic Shock Syndrome
Toxic Shock Syndrome due to bacteria Staphylococcus aureus
Streptococcal Toxic Shock Syndrome due to bacteria Streptococcus pyogenes
Treatment of Toxic Shock Syndrome
TSS is considered a medical emergency that required hospitalisation. An intravenous antibiotic will be prescribed to fight the bacteria infection, or medication to stabilize blood pressure and to prevent dehydration. Injections may also be given to suppress inflammation and increase body’s immunity. Also the cause of the bacterial infection will be removed, for instance, removal of the tampon or draining pus from the skin wound.
Complications of Toxic Shock Syndrome
If the internal organs are affected, it can lead to liver, kidney, heart failure, seizure and shock. Early detection of toxic shock syndrome has a much higher chance of recovery. The mortality rate is about 5-15% and rate of recurrence at 30-40%.
Toxic Shock Syndrome and Eczema
It is observed that patients recovering from TSS tend to develop chronic eczema. I couldn’t find literature on the likelihood of having TSS if one has eczema. I wonder if there’s increased risk since the skin of eczema patients tend to have staph bacteria colonization.
Prevention of Toxic Shock Syndrome
Certain precautions for menstruating female who uses tampon are to change the tampon every 4 to 8 hours and to use a low-absorbency tampon. Wash hands and keep skin cuts and wounds clean with frequent dressing change. TSS may recur, thus tampon should not be worn by those who had TSS before.
Anyone have experience with toxic shock syndrome? Do share, it will be useful to the rest of us and to be more aware of the risks.
Stevens-Johnson Syndrome (SJS) is a rare, severe disorder that causes pain, red/purplish skin, blisters and shedding of skin. It can be drug-induced or due to infection. It is a medical emergency and takes from weeks to months to recover. It is more common in adults or older people and men who use more of the possible drugs that trigger the SJS.
What Causes Stevens-Johnson Syndrome?
Its cause is largely drug-induced (more than 70%) or due to infection. However, genetics, family history and weakened immune system are also risk factors.
In children, Epstein-Barr virus, enteroviruses and upper respiratory tract infection.
Bacterial diseases:
Group A beta-hemolytic streptococci
Diphtheria
Brucellosis
Lymphogranuloma venereum
Mycobacteria
Mycoplasma pneumoniae
Rickettsial infections
Tularemia
Typhoid
Symptoms of Stevens-Johnson Syndrome
Flu-like symptoms
Rash – Pain, Red, Purplish Skin
Blisters
Shedding Skin (Nikolsky’s sign)
Eye-related – Painful red eye, purulent conjunctivitis, photophobia, blepharitis
Diagnosis is usually made via physical examination or skin biopsy.
Stages of Stevens-Johnson Syndrome
Fever, sore throat or mouth sores
Fatigue, cough, headache
Swelling (face, tongue), Hives
Rash – Pain, Red, Purplish Skin, Symmetric on face and torso
Formation of blisters on skin and mucous membranes of mouth, nose, eyes, genitals
Shedding of skin
Types of Stevens-Johnson Syndrome
The types are categorized by the extent of the body surface area (BSA) affected:
Stevens-Johnson syndrome: Less than 10% BSA detached
Toxic epidermal necrolysis: More than 30% of the BSA detached
Treatment of Stevens-Johnson Syndrome
Finding out the cause, in particular for drug-induced cases, is critical. Discontinue the drug. Treatment is to reduce pain, control itch, prevent dehydration, infection and inflammation. Oral corticosteroids and antibiotics may be prescribed. The patient is usually hospitalized.
Care of the skin includes application of lotions and wet dressings (wound care, wet compress). Particular to Stevens-Johnson Syndrome, eye care is also important to clean and prevent dry eyes.
Complications of Stevens-Johnson Syndrome
Complications include sepsis (blood infection), secondary skin infection (cellulitis), eye inflammation (tearing and scaring of cornea and even blindness) and permanent skin discoloration and damage (including nails).
Anyone have had SJS? Do share in the comments, thanks loads for spreading encouragement and experience.
Pemphigus Vulgaris (PV) is a rare, auto-immune disease that mistakes skin cells and mucous membranes as foreign matters and attacks them. This results in blisters and sores of the skin and the mucous membranes. It is more common in middle-aged and older people. PV is not infectious.
What Causes Pemphigus Vulgaris?
Pemphigus vulgaris is caused by an increase in the desmoglein antibodies where these antibodies incorrectly binds to protein desmoglein 3, which is found in desmosomes in the keratinocytes near the bottom of the epidermis. It then results in a separation of the skin layer and formation of blisters. The triggers of this faulty immune systems are not fully known though genetics play a part.
Types of Pemphigus Vulgaris
Mucosal PV: Only the mucous membranes are affected, but not the skin. This may include the mucous membranes lining the mouth, nose, throat and genitals.
Mucocutaneous PV: Both the mucous membranes and skin are affected.
Symptoms of Pemphigus Vulgaris
Fever, Chills
Muscle aches
Rash, first appearing in mouth and then to rest of the skin
Blisters
Raw, moist, tender skin
Peeling Skin
Fluid loss
Pain
Diagnosis is usually made by a skin specialist because it is uncommon, thus not often seen by general practitioners. Physical examination and lesion biopsy (including immunofluorescence to assess level of antibodies) are used to diagnose PV. Early treatment helps to prevent PV from being widespread.
Stages of Pemphigus Vulgaris
Formation of blisters and sores around the mouth
Bursting of mouth blisters, similar to ulcers
More widespread blisters at other parts of skin with oozing, crusting and peeling of skin.
Separation of outer layer skin with gentle touch (“Nikolsky’s sign”)
Recovery of raw skin (6 to 8 weeks)
Treatment of Pemphigus Vulgaris
There is no treatment that specifically cures PV but instead treatment is to reduce blistering and limit flare-up. This is often via immunosuppressant therapy. Oral corticosteroids and immunosuppressive drugs may be prescribed. In more severe cases, it can be via intravenous methylprednisolone and cyclophosphamide (Pulsed therapy) which can last from 6 months to a year. Dosages are typically higher at the start of treatment and gradually reduces when the condition is stable (without flare-up).
For severe cases, the patient will be hospitalized in the burn unit as the skin requires similar care to burns. Apart from immunosuppressant therapy, treatment also encompasses (i) pain relief, (ii) anesthetic lozenges to reduce mouth ulcer pain, (IiI) prevention of dehydration through intravenous drip, (Iv) medication to prevent bacterial or fungal infection
Care of the Skin
Care of the skin includes application of lotions and wet dressings (wound care, wet compress). Also minimize contact sports to avoid skin trauma.
Mouth Blisters and Care
If blisters occur in the voice box (larynx), the voice will be hoarse. If the blisters occur in the gullet, swallowing is painful. Where mouth blisters make it difficult to eat, supplements may be prescribed. Steroid, antiseptic or anesthetic mouth wash may also be prescribed for the mouth blisters. Avoid foods that may irritate the inside of mouth such as spicy, acidic or hard foods.
Pemphigus Vulgaris and Eczema
PV is sometimes diagnosed late as mistaken for dyshidrotic eczema or pompholyx which also has blisters. However, dyshidrotic eczema is not life threatening and believed to be due to stress or allergies.
Complications of Pemphigus Vulgaris
It is a difficult condition to treat as it is an autoimmune disease that has no cure. The mortality rate is 10%. There can also be complications associated with long-term use of oral corticosteroids and immunosuppressants. Other complications are secondary skin infection, dehydration and sepsis (bloodstream infection).
Anyone have had PV? Do share in the comments, thanks loads for spreading encouragement and experience!
Staphylococcal scalded skin syndrome (SSSS) is one skin rash that affects children (newborn to 5 years old), caused by infection from certain strains of Staphylococcus aureus bacteria. The bacteria produces toxins (epidermolytic toxins A and B) that bind to a molecule within the part of skin cell (demosomes) that adhere skin cells together. The damaged desmosome cannot continue to adhere skin cells and the skin break up, leading to fluid filling in the spaces (blisters) and peeling skin.
What Causes Staphylococcal Scalded Skin Syndrome?
Staphylococcal scalded skin syndrome is caused by certain toxic strains (exotoxin of group II, phage type 71) of the staphylococcus bacteria found on skin. However, when there is broken skin from scratching, cut, a minor infection that can escalate to SSSS in children and in people with weakened immune system or renal insufficiency.
Symptoms of Staphylococcal Scalded Skin Syndrome
Fever
Chills
Lethargy
Skin redness (Erythema)
Blisters
Raw, moist, tender skin
Peeling Skin
Fluid loss
Physical examination is often sufficient to diagnose SSSS. Where unsure, other tests like skin biopsy, blood tests may be ordered.
Stages of Staphylococcal Scalded Skin Syndrome
Begins with signs of infection like fever, chills and irritability
Followed by skin redness and formation of lesions – for infants, lesions often start at diaper area or at umbilical cord (triggered by other conditions such as purulent conjunctivitis, nasopharyngeal infection or an infected umbilicus). For older children, usually the flexural areas and skin folds like the face, mouth/nose, neck, groin and armpit (triggered by impetigo or infected eczema or wound infection).
Skin wrinkles and Formation of blisters – Irregular, large and loose blisters
Rupturing of blisters
Formation of yellow crust, followed by drying and cracking
Peeling of outer layer skin (Exfoliation) – Revealing red, raw and wet skin. The outer skin falls off with gentle pressure, known as the Nikolsky’s sign.
Recovery of raw skin (takes from 5 to 10 days)
Treatment of Staphylococcal Scalded Skin Syndrome
Hospitalization is often required, at the burn unit of the hospital as the risk of complication is similar to burns. Treatment options include
antibiotics to treat the staph bacteria infection,
drip to prevent dehydration and
care of the skin.
With SSSS, the child will feel pain at the skin and experience fluid and heat loss via exposed skin. Therefore, treatment will include caring for the child in a warm environment with minimal clothing. Pain control such as analgesia and paracetamol may be given to the child. The child should drink extra fluids to replenish the excess moisture loss from skin and prevent dehydration (check weight and urine for signs of dehydration).
Care of the Skin
Given the fragile skin, care must be taken when handling the skin to reduce trauma, such as when administering intravenous drips, creams and using non-adherent dressing to prevent further tearing of the skin. Moisturizer is applied to reduce fluid loss and soothe the skin until full recovering with smooth skin.
Staphylococcal Scalded Skin Syndrome and Eczema
Severe eczema presents higher risk due to broken skin (with scratching) and higher chance of staph bacteria colonization.
Complications of Staphylococcal Scalded Skin Syndrome
For children who are treated promptly, there is a high chance of recovery without scarring (mortality rate below 5%). In adults, it can be life threatening.
Other possible complications are cellulitis (deeper skin infection), sepsis (bloodstream infection) and pneumonia, though not common.
Prevention of Staphylococcal Scalded Skin Syndrome
Prevention of outbreaks in neonatal and nursery day cares are critical – adults who carry the bacteria (5% of adults) can spread to infants who may develop SSSS due to weaker immunity. Isolating the infected healthcare worker, hand washing and alcohol hand rubs should be practiced in the ward. Towels should not be shared.
If you have experienced SSSS, do share in the comments, thanks!
This is another 4-part series, focusing on elderly. For those of you who have been following this blog, you know I’ve been passionately persevering in bringing you information for eczema children. This month, however, I’m inspired to focus on elderly because (i) I see a desire among elderly ladies in the eczema support group meeting to care for their skin and (ii) I am ashamed that I can’t convince my own elderly parents of the right skincare. Hopefully, with this series, elderly who surf the internet and found this blog will find the series useful and adult kids (yes, you and me included!) will be empowered to help their aged parents with the correct skincare. So here we go!
So far we have covered stasis dermatitis (at the lower extremity), incontinence associated dermatitis (at the genital area up to upper thigh) and for the last part of this series, we will explore asteatotic eczema, another common elderly skin condition affecting the lower leg.
What is Asteatotic Eczema?
Also known as xerosis (abnormal dryness), cracked skin eczema or eczema craquele, it is a scaly, flaky, cracked skin condition due to dry skin. The symptoms are scales, cracks, fissures, redness, dryness and itch. If the skin is cracked deeply to injure the capillaries, bleeding fissures may be seen. These symptoms usually present at the lower leg but may also affect the arms, thighs, hands and lower back.
Asteatotic eczema is most prevalent in elderly, above age 65.
What Causes Asteatotic Eczema?
As discussed in the very first post of this series, elderly skin has weaker ability to retain moisture, thus more likely to have dry skin. Less oil and sweat glands also contribute to skin dryness. Their skin is also thinner. The dryness is worsened during winter or cold air-conditioning where the humidity is low (below 50). Other possible factors that contribute to dry skin are long, hot showers, rubbing to towel dry (instead of dab dry), harsh soaps and lack of moisturizing. Dehydration and malnutrition may also play a role, for instance not drinking enough fluids and lacking essential fatty acids and zinc.
Other causes include underactive thyroid, severe weight loss and lymphoma. Medications such as retinoids, diuretics and protein kinase inhibitors may also cause asteatotic eczema.
Complications of Asteatotic Eczema
As with all dry, itchy skin conditions that lead to chronic scratching, infection can occur. Lesions may form and overtime rubbing causes skin discoloration. Also possible are thickened skin (lichenification) or red patches of skin. With damaged skin barrier, the potential for allergic and irritant contact dermatitis increase.
Prevention of Asteatotic Eczema
Good Skincare Routine – Refer to these videos on skincare (shower, moisturizing), with the few basics below:
Avoid harsh soap and products with top irritants, like fragrance
Lukewarm shower, keep it short and for elderly who do not sweat much/head outdoors, daily shower is sufficient (or wet wipe the body on few days/week)
Moisturize after shower
Have humidifier if bedroom’s humidity is below 50.
Dab dry and not rub dry after shower
Do not use products that increase friction to skin, e.g. exfoliating bits found in facial wash or wool/scratching material
Frequent change of towel, and use softer material towels
Treatment of asteatotic eczema may include a combination of keratolytics (able to soften, loosen and facilitate exfoliation of upper skin cells), moisturizers and topical steroids (again, use with care given the already thin skin of elderly and higher potential for irritant dermatitis from chemicals in creams).
While looking up asteatotic eczema, I realized that there isn’t much written on it including research in Pubmed. I wonder if it’s because it seems not as serious as other skin conditions, or that research is often more focused on children and adults (or difficulty to conduct studies). In any case, we should not forget the skin health of our elderly family members and that’s what this entire past 4 weeks have been about! Share and support each other in our elderly skincare!
This is another 4-part series, focusing on elderly. For those of you who have been following this blog, you know I’ve been passionately persevering in bringing you information for eczema children. This month, however, I’m inspired to focus on elderly because (i) I see a desire among elderly ladies in the eczema support group meeting to care for their skin and (ii) I am ashamed that I can’t convince my own elderly parents of the right skincare. Hopefully, with this series, elderly who surf the internet and found this blog will find the series useful and adult kids (yes, you and me included!) will be empowered to help their aged parents with the correct skincare. So here we go!
Last week, we covered a very common skin condition affecting elderly, Stasis Dermatitis. For those of you with aged parents with hyper-pigmented, itchy, swollen/ulcerated skin on the legs, coupled with varicose vein condition, read more in last week’s post. This week, we’re covering another common skin condition affecting elderly with incontinence issue who have to wear adult ‘diapers’. They may be too embarrassed to share with you their skin problem at the genital area, so it’s good to know so that you can ask gently about it.
What is Incontinence Associated Dermatitis (IAD)?
It is an inflammatory skin condition that affects elderly who wear absorptive products to manage their urinary or fecal incontinence issues. Incontinence associated dermatitis is also known as perineal dermatitis. Its prevalence range from 5% to as high as over 20% in various studies. It is characterized by skin damage, inflammation and erythema (skin redness).
Is it Eczema? If not, what causes IAD?
Eczema is atopic dermatitis, meaning there is atopy/allergic reaction involved that triggered the skin reaction. In the case of incontinence associated dermatitis, it is the constant contact to the urine/stool in the adult diaper that damages the skin. This skin damage weakens the skin barrier and leads to deteriorating skin functions, mainly protective and moisture retention functions.
The skin barrier becomes less protective and more susceptible to penetration of irritants (urine/stool), thus more likely to suffer from irritant dermatitis (vs atopic dermatitis).
The skin barrier’s ability to retain moisture already weakens with age and further exposure to urine/liquid stool/sweat increases the rate of this water loss (known as trans-epidermal water loss TEWL).
Skin damage via friction with absorptive products is higher in elderly with IAD and it is possible that the constant exposure to urine raises the skin pH level which makes it more susceptible to damage from friction/pressure.
For elderly with both urine and fecal incontinence (known as double incontinence), there is higher likelihood of skin damage as the liquid stools/stools mixed with urine, leads to higher volume of digestive enzymes that breakdown the fats and proteins of the skin layer.
Just the genital area?
No, incontinence associated dermatitis can extend beyond the genital area to the buttocks and upper thighs.
Complications of Incontinence Associated Dermatitis
A frequent complication of skin inflammation is skin infection. The other complication is candidiasis (fungal infection from yeast called Candida albicans) that appears like a red/brownish red rash with ‘satellite’ lesions. Incontinence associated dermatitis should be differentiated from skin ulcers, which is pressure ulcer/deep tissue damage from pressure (sometimes at area of bone prominence).
Prevention of IAD
Minimize time wearing absorptive products, for instance use of hand-held urinal or catheter
Frequent change of the adult diapers to minimize the amount of time the skin comes into contact with urine
If there is diarrhea or liquid stools, be sure to change adult diaper frequently
Daily proper cleaning (without using harsh soap) of genital area at each change of absorptive products and protection with moisturizer (non-fragrance and without common irritants). An ointment containing zinc oxide, similar to baby diaper cream/ointment can also be used to protect against irritant/urine/stool.
Similar to baby skin care, frequent washing, use of hot water, rubbing dry with towel should be avoided to minimize drying and wear and tear of skin.
Other methods to manage the incontinence issue can be explored, such as diet/fluid management, pelvic muscle and bladder training and toileting technique. Surgical procedure is often presented as an option, but the pros and cons have to be weighed properly given that no surgical procedure is 100% risk-free. Particularly for an elderly, being subject to a surgical procedure so as not to have to wear ‘diaper’ may end up with more complications (This is outside the scope of this skin post, but more can be read here and here).
For those of us with elderly family members with continence issue, maybe tactfully drop reminder of extra skincare when they are wearing the absorptive products. Share your experience in the comments too, we all need support!
This is another 4-part series, focusing on elderly. For those of you who have been following this blog, you know I’ve been passionately persevering in bringing you information for eczema children. This month, however, I’m inspired to focus on elderly because (i) I see a desire among elderly ladies in the eczema support group meeting to care for their skin and (ii) I am ashamed that I can’t convince my own elderly parents of the right skincare. Hopefully, with this series, elderly who surf the internet and found this blog will find the series useful and adult kids (yes, you and me included!) will be empowered to help their aged parents with the correct skincare. So here we go!
Stasis dermatitis is a common inflammatory skin condition that occurs on the lower extremities (our body from the hip to the toes, including also the knee, ankle joints, the thigh, leg and foot). Stasis dermatitis is also known by various names, such as varicose eczema, venous eczema, venous dermatitis and gravitational dermatitis.
Its prevalence is about 7% in elderly persons above the age of 50 and can be up to 20% for those above age 70. The main cause of stasis dermatitis is venous insufficiency, which has been reported to affect more than 50% of elderly above age 50 internationally (thus, making stasis dermatitis a common skin condition for elderly).
What Causes Stasis Dermatitis?
Venous insufficiency is the main cause – a term that you’d see being commonly mentioned.
Venous insufficiency refers to the poor blood circulation, commonly due to weakening of the valvular function with age. The malfunction allowed a backflow of the blood from deep venous system into the superficial venous system, creating venous hypertension.
It is hypothesized that this increased pressure leads to the dermal capillaries being more permeable. This results in the leaking out of macromolecules (fibrinogen) that eventually polymerized and form a cuff (fibrin cuff) that reduces oxygen to the skin cells. White blood cells that help the body to fight inflammation becomes activated and trapped in the fibrin cuff resulting in a hyper state of inflammation.
Who gets Stasis Dermatitis?
Typically middle-aged and elderly patients, from age 50s onward
Patients with venous insufficiency due to surgery, trauma or thrombosis (blood clot)
Women, due to increased stress on the lower extremity venous system from pregnancy
Patients with health conditions such as high blood pressure (hypertension with diastolic dysfunction) and congestive heart failure
Patients taking medications such as antihypertensive medication, e.g. amlodipine
Sedentary lifestyle and Obesity
Symptoms of Stasis Dermatitis
Symptoms may show at area at the lower leg and around the ankle, such as
Itch
Hyperpigmentation/discoloration, usually reddish-brown skin
Atrophic skin patches (small/white scarred skin that is decreasing/thinning)
Edema (swelling from excess fluids, e.g. blood pooling from faulty varicose veins)
Dilated superficial veins
Infection with honey-colored crust over infected area
Pain
Slow healing of open sores
Lichenification (thickening of skin from repeated scratching)
Complications of Stasis Dermatitis
Chronic stasis dermatitis where the skin is inflamed severely for prolonged period can lead to weeping patches, plaques (solid, raised lesion), on-healing venous ulcers and higher likelihood of contact dermatitis. It can also aggravate into other conditions such as:
Cellulitis – Streptococcus or staphylococcus bacteria entering through a break in the skin, causing infection that can spread quickly from a reddened skin to lymph nodes/blood stream
Lipodermatosclerosis – Underlying fat necrosis (degeneration of fat cells), with appearance of “inverted champagne bottle” on the inner leg
Prevention of Stasis Dermatitis
To prevent stasis dermatitis, measures can be taken to reduce venous insufficiency. This can be prompt treatment of varicose veins, treatment of health conditions, management of venous insufficiency and preventing deep vein thrombosis.
Leg elevation – above the heart when lying down to improve blood circulation and reduce swelling
Compression socks – also improve circulation
Not standing for long periods
Taking regular walks
Moisturizing (avoiding harsh soaps and perfumed products)
Protecting from further injury (e.g. knocks or falls)
Treatment of Stasis Dermatitis
Treating the cause of the venous insufficiency is one part of treating the skin condition. Avoid scratching and follow the nurse’s instruction for wound care. Antibiotics may be prescribed, either topically or orally, if there is infection. Topical steroid may be prescribed but since the skin is already thin, talk to the doctor about alternative non-steroid options or be careful to apply only the low potency for limited time.
As I look through the pictures of stasis dermatitis, I really feel very sad. It’s an age-related problem and the thought that our parents who bore the hard work to raise us have to bear this pain is very heart-breaking. The irony is that they don’t quite believe in skincare or compression stocking – encourage one another to stay positive in helping our parents!
This is another 4-part series, focusing on elderly. For those of you who have been following this blog, you know I’ve been passionately persevering in bringing you information for eczema children. This month, however, I’m inspired to focus on elderly because (i) I see a desire among elderly ladies in the eczema support group meeting to care for their skin and (ii) I am ashamed that I can’t convince my own elderly parents of the right skincare. Hopefully, with this series, elderly who surf the internet and found this blog will find the series useful and adult kids (yes, you and me included!) will be empowered to help their aged parents with the correct skincare. So here we go!
How does Skin Age?
It is obvious that our skin ages as we age – even if we don’t look into the mirror or care to look at our own skin, the number of anti-ageing, whitening and anti-wrinkle products remind us that our skin grow old. Aging can be intrinsic (i.e. genetics) and extrinsic, with the main factor being sun exposure, although lifestyle (smoking, alcohol, obesity, diet, exercise) and pollution also play a role.
We have covered skin functions in this blog, so below explains how our skin age and loses its ability to perform its functions.
Differences in Elderly Skin
Thinner skin that appears more transparent, due to loss of epidermis (surface layer of skin)
Decreasing and increasingly fragmented collagen, thus less supple skin
Wrinkles, from sagging of elastic fibres and more reasons here
More fragile skin due to flattening of skin cells, prone to blisters, burns and tears
Loss of elasticity (from less fibroblasts), thus ‘loose’ skin
Fewer Langerhans cells, which are immune cells of skin
Reduced lipids within skin
Reduced sebum (oil) production, leading to dry/itchy skin
Reduced cutaneous blood flow
Reduced sweat glands, from shrinkage of eccrine glands
Reduced pigment cells
Photaging, due to sun exposure
Lower cell replacement
Less acidic pH of epidermis
Thinner blood vessel walls at the dermis, thus easier to bruise
Skin Function Loss for Elderly
With the above skin changes, there is associated loss of skin function:
Weakening of the skin barrier function, more permeable to irritants
Less able to regulate temperature, due to loss in fats and sweat glands
Less able to protect against sun
Less able to retain water in skin (stratum corneum)
Less able to repair the skin and heal wound, aggravated by health conditions that reduce healing such as diabetes
More susceptible to infection (from fewer AND less responsive Langerhans cells)
More susceptible to injury due to reduced ability to sense pressure and temperature, and thinner blood vessel walls
With the skin changes in elderly, there are numerous skin conditions that affect them. Most of the skin disorders have signs of skin inflammation and itch (pruritus). General itch without an underlying skin disorder is very common and mainly due to the breakdown of skin barrier, thus normally tolerated soaps and detergents start to trigger rash and itch (i.e. increasing risk of contact dermatitis). Atopic dermatitis is also common because of increased penetration of allergens via the defective skin barrier. As eczema, contact dermatitis and itch has been discussed in this blog (type into search box for all related posts), this series won’t cover these skin conditions despite being very common in elderly (as well as kids!).
For this series, I’m covering 3 skin disorders which are common and that I see in elderly around me (aka Singapore). These are Statis Dermatitis (affecting varicose vein area), Incontinence Associated Dermatitis (from exposure to urine or stools) and Asteatotic eczema (cracked skin). Older people may also have health conditions where either the condition itself predisposes them to skin disorders (atherosclerosis, diabetes, HIV, congestive heart failure) or the medication might. For instance, non-enzymatic metabolites, diuretics and calcium blockers affect the skin. So take time to Google, research and ask the doctor for elderly in your family about potential side effects of the medication they are taking. Elderly who are immobile (i.e. always on the chair or bed) or live in homes are also at higher risk of skin disorders.
Catch up next week on Statis Dermatitis and meanwhile, drop me a comment if you have a condition for elderly skin that you’d like me to look into!
This is a 4-topic series focused on complications from eczema and mainly inspired because my daughter recently had impetigo. Moreover, the potential complications from bacterial, viral and fungal infection are not very often emphasized yet a child with eczema is often vulnerable to infections. So let’s explore!
Erythroderma and its Causes
Erythroderma refers to generalized redness of skin due to skin inflammation. It is a complication associated with severe eczema, psoriasis and other skin inflammatory diseases. It can also be caused by drug reaction or even without a known cause(idiopathic erythroderma). Other possible causes are:
Other forms of dermatitis, apart from eczema, such as contact dermatitis, stasis dermatitis (skin inflammation from blood pooling in leg veins, common for women above 50) and seborrheic dermatitis
Staphylococcal scalded skin syndrome, with fever, skin tenderness and irritability (staph bacteria infection causing blisters, aka scalded skin appearance, affecting kids below age 5)
Pityriasis rubra pilaris, appears as reddish-orange scaling patches, more common in adults
Pemphigus vulgaris and bullous pemphigiod, which refers to autoimmune blistering skin disease
Lymphoma of the cutaneous T-cells, also known as Sezary syndrome
Leukemia
Malignant rectum, lung, colon and fallopian tubes
Graft vs Host disease
HIV infection and other immune-deficiency conditions
The common drugs causing erythroderma in children are sulfonamides, antimalarials, penicillins, isoniazid, thioacetazone, streptomycin, nonsteroidal anti-inflammatory drugs (NSAIDS), topical tar, homeopathic and ayurvedic medicines. For general population, drugs such as allopurinol, arsenicals, aspirin, carbamazepine, captopril, gold, hydantoins, mercurials, penicillin, phenothiazines, phenylbutazone, quinacrine, sulfonamides, homeopathic and ayurvedic medication as well.
Symptoms of Erythroderma
The onset of erythroderma can be sudden and spread quickly. Apart from skin redness, it is often seen with:
Skin exfoliation, also known as exfoliative dermatitis where about 90% of skin peel off in scales or layers
Swelling (oedema)
Oozing skin
Itch
Thickening of palms or soles or nails (even shedding nails)
Erythroderma of the scalp may result in hair loss
Erythoroderma of the eyelid may result in ectropian, which is rolling outwards of the inner eyelid (may also have conjunctivitis)
Measle-like eruptions if due to drug reaction
Treatment of Erythroderma
The underlying cause has to be treated, with the following general treatment steps:
Wet wrap for skin moisture retention, with moisturizer and mild steroids
Maintain hydration, fluid and electrolyte balance
Antihistamines for itch
Stop unnecessary medication, in case erythroderma is drug-induced
Bacterial skin infection commonly accompanies erythroderma, and therefore antibiotics may be prescribed. Where fluids have to be given intravenously, hospitalization is required.
Complications of Erythroderma
Most important to watch out in erythroderma is compensating for the loss of skin’s ability to temperature control and maintain fluids. Complications include:
Pigment changes in skin to brown and white patch
Secondary infection with the oozing and crust
Swollen lymph nodes
Dehydration, from fluid loss through skin from higher metabolism
Heart failure from increased heart rate (usually in elderly)
Hypothermia, from abnormal temperature regulation, thus hydration and temperature control are important
Malnutrition, from protein loss and higher metabolism (to compensate for heat loss)
As I researched on erythroderma, I felt really sad for those suffering with it. As to why some people with inflammatory skin condition have an onset of erythroderma, it is not clear. I do hope though that keeping the underlying skin condition under control will forever keep erythroderma at bay. Anyone has experience with this?