CPD: Diagnosing Adverse Events in Darker Skin

Diagnosing Adverse Events in Skin of Colour

Dr Emmaline Ashley and Dr Amiee Vyas discuss the importance of recognition and management of aesthetic adverse events in patients with skin of colour

Within the field of aesthetic medicine, there has recently been a growing recognition of a gap in clinician knowledge around skin of colour (SOC). 1 This is partly due to a historical bias in Western medicine’s approach to dermatology, where white skin was considered the standard and default, and darker skin tones were relegated to being a curious footnote. This has led to a glaring lack of representation of SOC in the traditional medical curriculum and research journals.2 In fact, dermatology textbooks depict most skin diseases with images of light skin, with many textbooks containing no photographs of common concerns – like acne or dermatitis – in darker skin tones.3 Consequently many clinicians are not well-equipped to treat SOC, and our patients lack confidence that their skin concerns can be competently handled.2 To gain this trust, research suggests that patients with SOC disproportionately approach clinicians of the same race for treatment, if given a choice.4,5

A survey by the Black Aesthetics Advisory Board (BAAB) revealed the ongoing existence of knowledge gaps and myths concerning facial aesthetic treatments in SOC, and the need for clinicians to recognise nuances when approaching treatments in order to prevent and reduce the risk of adverse events in this patient population.5 Seven out of 10 black patients said they had difficulties finding a practitioner confident in treating their skin.5 Clinicians have a responsibility to be aware of these nuances, to avoid treating SOC homogenously, and recognise there is a wide spectrum of diversity within these groups.6 In this article, we summarise SOC nuances and how to recognise common and important complications when they present in patients with SOC.

Considerations in skin of colour

Anatomy and physiology Skin colour and its response to sun exposure, as well as other superficial phenotypic differences, have long been used to classify people into different races.7 While it is acknowledged that these classifications are largely arbitrary, they are still used as the basis of broad racial and ethnic categorisations for SOC – including African and Afro-Caribbean, Asian and Pacific Islander, Latinx or Hispanic, South Asian and Middle Eastern.7 Most clinicians will be very familiar with Fitzpatrick skin typing – a classification system based on skin’s reaction to UV exposure.8 However, as the field of aesthetic medicine has expanded, there is growing recognition that the Fitzpatrick Scale is an oversimplified and outdated system to categorise SOC, lacking both consistency and understanding of variation and photosensitivity in darker skin types.7,9 Broadly speaking, the unique colours and tones inherent in our skin are a consequence of the density and distribution of melanin pigment, haemoglobin, bilirubin, and carotenoids.8,10 All skin types have the same number of melanocytes: in darker skin melanocytes are highly active producing more melanin in a wider distribution.10 Melanosomes in SOC tend to be larger, more individually dispersed, and degrade more slowly than light skin.10 While the thickness of the stratum corneum is the same in all types of skin, the cells of the stratum corneum in SOC are more compact with more layers and greater intercellular cohesion.10 Additionally, the lipid content of darker skin tones has been described to be higher than lighter counterparts, while ceramide content is lower.10 The data on differences in transepidermal water loss and water content are inconclusive.10 In the dermis, evidence suggests that fibroblasts are larger and exist in greater number in SOC.10 This may explain why there is a greater propensity for hypertrophic and keloid scar formation.7 Additionally, collagen fibres are smaller and more compact in comparison to lighter skin tones, where they are larger with propensity for fibre fragmentation.10 There has not been a demonstrable difference in the elastin content between skin types.10 Additionally, there is huge diversity and variability between and within ethnic groups, and studies discussing the differences in anatomy and physiology thus far are small and methodologically flawed.7,10 It is therefore difficult to draw definitive conclusions, and is an area of expanding research and interest.

Cultural considerations Clinicians should be aware of cultural practices relevant to the skin health of our SOC patients. This includes cultural stigmas, including concepts like ‘colourism’. Colourism is still prevalent in many communities – the misconception within people of the same ethnicity that lighter skin tones are preferable to darker ones.11,12 This may lead to the use of commercial and non-prescribed skin lightening or bleaching treatments, often found under-the-counter in beauty supply stores. The practice of skin bleaching is a public health concern affecting many SOC communities throughout the world and is harmful beyond the skin potentially causing systemic complications.7,11,12 Clinicians should also have familiarity with traditional beauty products and practices. For example, hair pomades popular in some African and Afro-Caribbean communities may contain mixtures of petrolatum or different oils, which can lead to seborrheic dermatitis of the scalp

or acne formation.7 Many Asian communities still use traditional beauty practices like coining, cupping, or gua sha, an alternative therapy which involves scraping the skin with a massage tool to improve circulation.7 These practices can lead to characteristic, temporary skin changes, petechiae, and ecchymoses that clinicians should learn to recognise.13

Dyschromias

Multiple epidemiological studies have revealed that dyschromias occur more commonly in SOC.14,15-17 Dyschromias are acquired conditions where cutaneous inflammation from a variety of different aetiologies can lead to hyperpigmentation, hypopigmentation, or a combination of the two – depending on the number and activity of the affected melanocytes.14 Post-inflammatory hyperpigmentation (PIH) is a very common skin concern in SOC, where there is an increased production of melanin in response to skin insult. It can be classified as either epidermal, dermal, or mixed depending on the location of the pigment. It is theorised that the degree of hyperpigmentation correlates to the severity and duration of the inflammation the skin has endured.18 The lesions typically present as small, darkened macules at the site of the original injury.14 Post-inflammatory hypopigmentation is not well-described in the literature, and the pathogenesis is not well understood. These lesions present as acquired areas of reduced pigmentation at the site of original injury to the skin. It is proposed that postinflammatory hypopigmentation occurs after inflammation or insult to the skin and leads to decreased melanin production, blocked transfer of melanosomes to keratinocytes, and melanocyte loss.19 The theory is that each patient has an individual chromatic tendency, with a predisposition towards either over- or underproduction of melanin in response to inflammation due to the inheritance of either ‘weak’ or ‘strong’ melanocytes. Weak melanocytes exposed to inflammation will produce less pigment, and strong melanocytes will produce more.20 There have not been alternative hypotheses proposed to this date to explain why some patients suffer hypopigmentation versus hyperpigmentation. The cornerstone of good management for all dyschromias is the prevention of further inflammation and excellent sun protection.21 Prompt initiation of treatments when managing dyschromias also aids faster resolution and prevents worsening of the condition.18 In addition, for aesthetic injectable therapies proper injection technique and using fewer injection sites will help decrease the trauma that could lead to risk of dyschromia.6

Prevention and management of dyschromias Evidence supports topical skincare treatments as first-line, with chemical peels and laser therapies as second-line treatments for refractory or dermal pigmentation.18,21 It is important to bear in mind that pigmentation disorders can be exacerbated by irritation caused by over-aggressive treatment,18,19 a slow and stepwise approach is therefore essential. There are a multitude of skincare ingredients that play a role in the treatment of PIH. Treatment often focuses on the use of tyrosinase inhibitors which halt the melanin synthesis pathway. The strongest evidence supports the use of triple combination therapies of hydroquinone (HQ), retinoids, and steroids, or monotherapy with retinoids or HQ.14 Topical retinoid use has also been supported by many studies in the treatment of acne-associated PIH in SOC.22 Topical hydroquinone is particularly effective when combined with a retinoid.22 Overuse or incorrect application of HQ can lead to side effects or complications (discussed below). For this reason, over-the-counter HQ is even banned for use in cosmetic products in Europe, Japan, and Australia,23 and it is vitally important that clinicians are well educated and its appropriate use. Azelaic acid has also shown promising results in early investigations into the treatment of acne-related PIH.22 Other tyrosinase inhibitors used to treat PIH include kojic acid, liquorice extract, arbutin, ascorbic acid and N-acetyl glucosamine.18 Niacinamide is another effective agent which inhibits melanin transfer.23 Chemical peels work by creating a controlled chemical injury, stimulating new skin growth, regulating the thickness of the epidermis, improving the uniformity of melanin in the basal layer, and inducing neocollagenesis.18,24 Safe and effective peel treatments for hyperpigmentation include glycolic and mandelic acid peels. It is a common misconception that these hydroxy acids cannot be used in SOC, due to the fear of triggering PIH. Proper counselling, patient education and informed consent are crucial.21 Skin should be appropriately prepared over a period of two to four weeks with a homecare regimen to protect and strengthen the skin barrier prior to their use. This priming can be done with topical depigmenting agents as described above.25,26 This reduces healing time, improves the uniform penetration of the peel, and reduces the risk inducing or worsening PIH.24 Salicylic acid peels (20-30%) have been shown to be a well-tolerated and safe option for treating SOC patients.24,27 While monotherapy has not been shown to be effective at PIH, combination treatments with hydroquinone and tretinoin may be beneficial.22 Glycolic acid peels are composed of the smallest molecular size of alpha hydroxy acid, so are able to penetrate more deeply into the skin.26 These peels can be both superficial and medium depth, depending on the concentration and length of time the peel is applied. When the skin is properly prepared, there are very minor side effects.26 A recent review of its efficacy showed complete resolution of PIH after six to eight peel treatments in SOC patients.26 It is particularly effective in combination treatment with tretinoin and hydroquinone.22,28,29 Using lasers to treat PIH carries significant risk of exacerbating the dyschromia, as some studies show either no improvement, or worsening of pigment after laser treatment.30 There is a lack of large randomised clinical trials in this area, and most studies reviewed were methodologically flawed.22,30 This is still an area that requires further research to determine the true benefits. However, current recommendations are that lasers may have a role to play in treating dermal pigment.14 A recent systematic review of lasers in treating post-inflammatory found that the best evidence supported the use of the Q-switched Nd:YAG laser.30 There is a lack of evidence on the treatment of hypopigmentation, hence treatment focuses on managing patient expectations, managing the underlying cause of the inflammation and advice on camouflaging methods.19 Some cases of hypopigmentation will self-resolve weeks to months after the inciting cause is treated.19 Topical therapies that have been trialled with varying success in case reports or small case series include calcineurin inhibitors, prostaglandin analogues, and psoralen plus UVA (PUVA) photochemotherapy.19 The use of laser therapy has shown some success in treating hypopigmentation with both non-ablative and ablative lasers in small studies.19,31-34

Complication

Post-inflammatory hyperpigmentation Epidermal

Dermal

Post-inflammatory hypopigmentation

Skin bleaching

Hypertrophic and keloid scars Presentation

A darkened, red-brown papule in the area of the original insult to the skin

Acquired area of reduced pigmentation at a site of original insult to the skin - UV protection broad spectrum SPF 30+ daily - Avoidance/ treatment of drivers of skin inflammation - Good injection technique First line - Conservative management and reassurance - Camouflage advice

Skin – exogenous ochronosis, patchy depigmentation, dermatitis, black colloid milia and skin atrophy, reduced wound healing, infection

Systemic – nephropathy, neurotoxicity, endocrine complications of long-term steroid use

Hypertrophic – raised, red areas confined to the edges of the original wound

Keloid – progressive scar tissue that extends beyond the edges of the original injury First line - UV protection - Tension-free skin closure40 - Taping or silicone sheeting 12hr/day (2-3 months)18, 19

Table 1: How to recognise, treat and prevent common skin of colour issues

Skin bleaching and management

Skin bleaching is the process of depigmentation of the skin through the use of topical and oral products.12 Long-term and incorrect use of products, which include prescription-strength hydroquinone, banned ingredients like mercury, and potent corticosteroids, are known to have serious health implications.35 This includes ochronosis (a blue-black hyperpigmentation consisting of macules), patchy depigmentation, dermatitis, black colloid milia and skin atrophy.12,35 Skin bleaching can also cause a deterioration in overall skin health, with impaired wound healing and wound dehiscence, as well as a predisposition to skin infections.35 Skin bleaching can cause systemic complications. Mercury use can lead to nephropathy, neurotoxicity, and memory loss.12,35 Widespread and prolonged corticosteroid use leads to steroid addiction syndrome, where withdrawal of a topical steroid causes severe burning only relieved by further steroid use.37 Long-term steroid application also leads to endocrine complications such as suppression of the hypothalamic-pituitaryadrenal axis, glucose intolerance, hypertension, and features of Cushing’s syndrome.12,35 The management of skin bleaching begins with open communication, establishing a relationship of trust where SOC patients are comfortable disclosing and discussing skin bleaching practices. A blanket recommendation to avoid skin bleaching is often completely ineffective if a clinician has no understanding of the cultural and historical context in which these practices take place.12 Rejecting or criticising the use of skin bleaching products will only further stigmatise patients.12 It is important to be aware that skin colour is often linked to concepts like socioeconomic status or marital prospects.12 There are also individual psychosocial drivers for skin lightening, including feelings of being unattractive and pressure from relatives or friends.12 Clinicians should also be aware of the prevalence of these products on social media platforms, where health information tends to neglect to mention any harmful side effects.12 Current recommendations ask that clinicians adopt a multifaceted approach. Neutral, non-judgmental advice that is patient-centred and tailored to each individual is vitally important in discussing the health risks of skin bleaching.12,36-38

Prevention

- UV protection broad spectrum SPF 30+ daily - Avoidance/ treatment of drivers of skin inflammation - Good injection technique

Skin priming - Skin preparation 2-4 weeks prior to cosmetic treatments Management

First line - Triple therapy (8 weeks)14 or - Retinoid daily (12-18wks)14 or - HQ 4% BD (12 wks)14 or - 15% azelaic acid BD (16wks)14

Second line - Glycolic acid peel every six weeks14 - 4% HQ and salicylic acid peel14

Q-switched Nd:YAG laser (3-12 treatments)22,30

Second line (limited evidence) - Pimecrolimus 1% BD (16 wks)19

- Understanding of the culture and historical context of these practices - Patient-centred approach taking into account individual psychological and social factors - Non-judgmental communication - Patient education into harmful side effects of skin bleaching

Second line (Limited evidence) - Flavonoids BD (4-6 months)18 - Pressure therapy 23hr/day (6 months)18 First line - Intralesional corticosteroid (TAC) injections 1-2x/ mo (2-3 sessions)40 Second line/Adjunct therapies - Scar revision (1 yr post primary closure)18 - Adjuvant radiotherapy (1-2 day after scar revision)18 - 585 nm pulsed dye laser (2-6 sessions) every 3-4wks18 - Cryotherapy (10-20s freeze-thaw cycles) in combination18 - 5-FU injections 50mg/mL once weekly (12 wks) in combination18

Hypertrophic and keloid scarring

Hypertrophic and keloid scarring are the consequence of abnormal, pathological wound healing where there is disordered regulation of collagen production.39 This is a fibroproliferative disorder, causing both cosmetic and functional problems.40 In hypertrophic scars, this fibroproliferation is limited to the borders of the original scar, whereas in keloid scarring the scar tissue can extend far beyond these borders. Particularly in keloids, fibroblasts in these abnormal scars are more resistant to apoptosis.41 Keloid scarring occurs up to five to 15 times more frequently in SOC.7,42 However, in the case of aesthetic injectable therapies, it is important to note that the development of keloids following filler or botulinum toxin is rare in SOC, and dermal injury from needles is not associated with a significant keloid risk.6

Prevention and management of abnormal scarring For aesthetic treatments, it is advisable to avoid injectables and microneedling in patients if they have a known history of abnormal scarring to prevent its occurrence. Intralesional corticosteroid injections have an anti-inflammatory effect and reduce collagen synthesis and fibroblast proliferation.40 This is

one of the first-line treatment options, but can be excessively painful leading to patient non-compliance.43 The most studied treatment is triamcinolone acetonide (TAC), injected from 10-40mg/mL one to two times a month.40 Between 50-100% of patients respond to this treatment, with approximately 9-50% suffering recurrence.43 There is also a growing amount of evidence supporting the use of more novel agents in scar treatment, including bleomycin, 5-fluorouracil, onion extract, imiquimod, and mitomycin C.43,44 Laser therapy can be used to improve the appearance of erythema, telangiectasia, or hyperpigmentation in abnormal scarring. The greatest evidence supports the use of pulsed dye laser 585 nm, particularly in combination with compression or steroid therapies.43,45,46 This is another area that requires further research to elucidate the exact devices and regimens that would be most beneficial for abnormal scarring. Additionally, radiotherapy and cryotherapy have been used as adjuvant or combination treatment modalities.40 Surgical revision of abnormal scarring used to be a common method of management. However, surgical intervention alone usually leads to disappointing results and high recurrence rates of keloid scars.40 Because these scars arise as a result of abnormal wound healing, recreating the original injury often leads to more pathological scarring. It does still have a role to play in some cases in combination with other therapies.

Final thoughts

Initiatives like the BAAB, together with resources like the Centre for Evidence-Based Dermatology’s Skin of Colour Resource47 and Mind the Gap: A Handbook of Clinical Signs in Black and Brown Skin48 are trying to address shortcomings in medical education. Moving forward as clinicians, we must ensure we are both competent and confident in managing complications in skin of colour. Aesthetic brands must also ensure their devices and treatments have been safety tested on a diverse population and ensure this evidence is readily available to clinicians. This means that ultimately the responsibility is ours to seek out the knowledge and training needed to provide the best care for all our patients, no matter what their background or skin type.

Dr Emmaline J Ashley holds a first-class honour’s degree in biology from Carleton College in the US and completed her honour’s degree in medicine from University College Dublin, a Master’s in Surgery with the Royal College of Surgeons Ireland, and a Professional Certificate in Clinical Dermatological at University College Dublin. She is completing her Level 7 Diploma in Aesthetic Injectable Therapies with Acquisition Aesthetics. She divides her time between working for the NHS and developing her own private aesthetics practice, Ashley Aesthetics. Qual: BA, MCh, MBBChBAO, PGCert Dermatology

Dr Amiee Vyas is the founder of Doctor Amiee Facial Aesthetics and Skin, Mayfair. She is a KOL and trainer in cosmetic dermatology, an expert trainer in injectables, the founder of the Ultimate Aesthetics Mentorship Programme and a founding member of the Black Aesthetics Advisory Board. She serves an international patient base in her clinics. Her passion is empowering skin confidence regardless of skin colour or concern, and she champions understanding skin of colour in her training courses, mentoring programmes and patient consultations. Qual: MBBS, BSc. Test your knowledge! Complete the multiple-choice questions below and go online to receive your CPD certificate!

Questions

1. Which of the following structures has shown no demonstrable difference between skin types and colours?

2. Which of the following treatments is not recommended in the management of post-inflammatory hyperpigmentation? 3. Which of the following is not a known complication of skin bleaching agents?

4. What percentage of patients suffer from abnormal scarring recurrence after treatment with triamcinolone acetonide?

5. Which of the following statements is false? a. Patients with SOC disproportionately approach clinicians of the same race for treatment. b. A blanket recommendation to avoid skin bleaching is the best approach. c. Colourism is still prevalent in many communities. d. Dermatology textbooks depict most skin disease with images of light skin.

Possible answers

a. Fibroblasts b. Elastin c. Collagen d. Melanosomes

a. Glycolic acid b. Steroids c. Azelaic acid 15% d. CO2 lasers

a. Ochronosis b. Nephropathy c. Hepatitis d. Cushing’s syndrome

a. 25-30% b. 11-15% c. 66-70% d. 9-50%

Answers: 1-B, 2-D, 3-C, 4-D, 5-B

TO VIEW THE REFERENCES GO ONLINE AT WWW.AESTHETICSJOURNAL.COM

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REFERENCES:

1. www.accessdata.fda.gov/cdrh_docs/pdf13/k134032.pdf Accessed September 2019 2. Ulthera release: Ultherapy® décolletage treatment now FDA-cleared. BioSpace website. https://www.biospace.com/ article/releases/ulthera-release-ultherapy-and-0174-d%C3%A9colletage-treatment-now-fda-cleared-/. Accessed January 21, 2020. 3. Fabi SG, Joseph J, Sevi J, Green JB, Peterson JD. Optimizing patient outcomes by customizing treatment with microfocused ultrasound with visualization: gold standard consensus guidelines from an expert panel. J Drugs Dermatol. 2019;18(5):426-432 Adverse events should be reported. Reporting forms and information for United Kingdom can be found at www.mhra.gov.uk/yellowcard. Reporting forms and information for Republic of Ireland can be found at https://www.hpra.ie/homepage/about-us/report-anissue/mdiur. Adverse events should also be reported to Merz Pharma UK Ltd at the address above or by email to UKdrugsafety@merz.com or on +44 (0) 333 200 4143.

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