Textbook of Chemical Peels: Superficial, Medium and Deep Peels in Cosmetic Practice

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Textbook of Chemical Peels

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SERIES IN COSMETIC AND LASER THERAPY Published in association with the Journal of Cosmetic and Laser Therapy Already available David Goldberg, Fillers in Cosmetic Dermatology ISBN 1841845094

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Textbook of Chemical Peels Superficial, Medium and Deep Peels in Cosmetic Practice Philippe Deprez MD Medical Director Policlinica Estetica & Anti-Aging Empuriabrava Spain

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© 2007 Informa UK Ltd First published in the United Kingdom in 2007 by Informa Healthcare, 4 Park Square, Milton Park, Abingdon, Oxon OX14 4RN. Informa Healthcare is a trading division of Informa UK Ltd. Registered Office: 37/41 Mortimer Street, London W1T 3JH. Registered in England and Wales number 1072954. Tel: +44 (0)20 7017 6000 Fax: +44 (0)20 7017 6699 Email: [email protected] Website: www.informahealthcare.com All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of the publisher or in accordance with the provisions of the Copyright, Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London W1P 0LP. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. The Author has asserted his right under the Copyright, Designs and Patents Act 1988 to be identified as the Author of this Work. Although every effort has been made to ensure that drug doses and other information are presented accurately in this publication, the ultimate responsibility rests with the prescribing physician. Neither the publishers nor the authors can be held responsible for errors or for any consequences arising from the use of information contained herein. For detailed prescribing information or instructions on the use of any product or procedure discussed herein, please consult the prescribing information or instructional material issued by the manufacturer. A CIP record for this book is available from the British Library. Library of Congress Cataloging-in-Publication Data Data available on application ISBN-10: 1 84184 495 0 ISBN-13: 978 1 84184 495 4 Distributed in North and South America by Taylor & Francis 6000 Broken Sound Parkway, NW, (Suite 300) Boca Raton, FL 33487, USA Within Continental USA Tel: 1 (800) 272 7737; Fax: 1 (800) 374 3401 Outside Continental USA Tel: (561) 994 0555; Fax: (561) 361 6018 Email: [email protected] Distributed in the rest of the world by Thomson Publishing Services Cheriton House North Way Andover, Hampshire SP10 5BE, UK Tel: +44 (0)1264 332424 Email: [email protected] Composition by Scribe Design Ltd, Ashford, Kent, UK Printed and bound in India by Replika Press Pvt Ltd

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Contents

Acknowledgment 1

vii

Chemical peels: definition and classification

1

2

Pre-peel care

5

3

Post-peel care

13

4

Factors influencing chemical peels

27

5

Choosing the right peel

31

6

Alpha-hydroxy acids: chemistry, pH and pKa, and mechanism of action

47

Alpha-hydroxy acids: histology and factors influencing penetration

53

7 8 9 10 11

12

13 14

109

Treating melasma, chloasma and post-inflammatory hyperpigmentation

121

17

Treating acne

125

18

Treating multiple keratoses on the scalp

131

Treating aging of the hands and forearms

135

20

Treating the neck and décolletage

141

21

Stretch marks and scars: dermabrasion and peeling

145

22

Actinic keratoses and lentigines

167

23

Trichloroacetic acid to the papillary dermis: Unideep®

177

Resorcinol: Unna’s paste/Jessner’s solution

183

Phenol: chemistry, formulations and adjuvants

193

26

Phenol: properties and histology

203

27

Phenol: skin penetration and detoxification

209

Toxicity of phenol: causes, prevention and treatment

213

Phenol: choice of peel and combination treatments

225

16

19

Alpha-hydroxy acids: indications and results

55

Alpha-hydroxy acids: application as cosmetics and as peels

59

Alpha-hydroxy acids: side-effects of AHAs

67

Alpha-hydroxy acids: a new slowrelease AHA complex with no neutralization required

Easy TCA®: basic protocol and skin aging

15

24 25

69

Trichloroacetic acid: general information, toxicity, formulations and histology

79

Trichloroacetic acid: indications and contraindications

95

28

Trichloroacetic acid: classic semiology 105

29

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Phenol: indications

31

Phenol: contraindications, precautions and safety

249

32

Phenol: pre-peel preparation

253

33

Full-face phenol: nerve block anesthesia and/or sedation

261

Full-face phenol: application

273

34

233

35

Phenol: post-peel care

283

36

Phenol: chemical blepharoplasty and cheiloplasty

295

37

Complications of chemical peels

313

38

Combination of techniques

371

Index

377

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Acknowledgment

The publication of this work has been assisted by an educational grant from Skin Tech (www.skintech.info; www.peeling.com). It should be noted that this textbook is comprehensive about all available peel products, but that there are many

ancillary products (such as sunscreens) manufactured in comparable formulations about which it cannot be expected to be comprehensive; the author is most familiar with and recommends those from Skin Tech, but does not imply by this that other products may not be comparable.

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1 Chemical peels: definition and classification

Definition of a chemical peel A chemical peel is a skin treatment intended to visibly improve the structure of treated tissue by the external application of a caustic solution. It can simply accelerate the natural processes of exfoliation, but can also completely destroy the epidermis and a more or less large proportion of the dermis, essentially by protein coagulation or lysis. The effect of any peel reaches the dermis, directly or indirectly and to varying depths, where the processes of regeneration are induced to a greater or lesser degree, depending on the molecule or molecules used and the application procedure. Chemical peels are among the oldest forms of skin rejuvenation and form a group of treatments in their own right. They are both flexible and effective, with a histological, chemical, toxicological and clinical basis. They have an ancient history, have evolved rapidly and can be adapted to almost any circumstances within the limits of their indications. Most peels, to varying degrees, cause the same types of histological changes, whose clinical results lead to a more or less rejuvenating effect on all or part of the skin. Classification is always restrictive, as it forces highly variable events into a rigid framework. We will see in this book that so many different factors come into play that it becomes difficult to fit all chemical peels into a simplified and rigid classification of ‘superficial’, ‘medium’ and ‘deep’. Let us take the well-known glycolic acid peel as an example: its depth of action depends on the patient’s skin type, the presence of associated disorders (e.g. seborrheic dermatitis), skin preparation in the long, medium and short term, the galenical form (gel, liquid, mask or self-neutralizing pseudogel), the concentration of the product, the m/m, m/v or m+v calculation, whether or not it is combined with other acid molecules (e.g. lactic or kojic), the pH of the solution (e.g. 0.5 or 3.5) and therefore the fraction of free glycolic acid, what it is applied with (brush, cotton pad, etc.), the number of coats, how forcefully it is applied, whether it is applied on the face or body, the exact location on the face (e.g. nostrils or eyelids1), the contact time, how or whether it is neutralized or diluted at the end of the peel, the immediate postpeel care, the quality of care between peels, the number and frequency of repeat sessions,... And the list goes on!

It is clear that it does not take much to turn a very light glycolic acid peel into a medium-depth peel that can even reach the deeper layers of the dermis and risk discoloration or even scarring. All it takes is for the peel not to be neutralized properly. The same goes for all of these caustic molecules, which is why, until recently, it was usually necessary to have a thorough knowledge of chemical peels and skin anatomy before undertaking this kind of treatment. Every practitioner, through personal experience and practice, should aim to standardize their treatments in order to eliminate the maximum number of variables. Fortunately, new chemical peel formulas are now available that are easier, safer and quicker to use, allowing young physicians to get on with the job of peeling without losing sleep and having post-peel nightmares. Sound knowledge and experience are still essential for peels to the papillary dermis.

Criteria for classification Molecular dependence It is very simple to understand that phenol is more aggressive than lactic acid.

Doctor dependence Classification may be personal; it may be related to the practice of one particular doctor who has standardized his methods of treatment with a view to limiting uncontrollable variables. But such a classification would not allow for any scientific exchange. What would produce a superficial peel with one practitioner could in fact result in a medium peel with another who uses the same product with a different application technique. This is why peels are often considered to be ‘doctor-dependent’. How can we give a valid classification for a treatment that is doctor-dependent? We should also compare products of the same type only, and yet the quality of the preparations and excipients is highly variable and impossible to control.

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Chemical dependence

Patient dependence

It is known that trichloroacetic acid (TCA) crystals, for example, are very hydrophilic, which means that they must be kept in perfect conditions so that the pharmacist can prepare the solutions we prescribe properly. How can we know how long the pharmacist’s bottle of TCA crystals has been open? If the crystals have not been hydrated inadvertently (if the pharmacist closes the bottle as soon as he has taken out the required amount), the final concentration will be correct. If, on the other hand, the crystals are mostly hydrated (if the pharmacist leaves the bottle of TCA open in order to serve another customer), the concentration of the solution provided by the pharmacy will be abnormally low and not very effective. Peels are therefore also considered to be ‘chemical-dependent’.

Each patient has a skin type that is genotypically and phenotypically unique. The skin has a history that the doctor must know about. Stable products that are properly prepared and applied with precise methodology, in the same way, by the same doctor, on the same day, can produce different results on different patients. Every morning, or maybe several times a day, patients go through their own particular skincare routine that the doctor doing the peel does not necessarily know about. Let us take for example the application of large quantities of topical benzoyl peroxide, which some teenagers use secretly for acne. It reduces the thickness of the stratum corneum and makes the skin more permeable. This of course makes it easier for the acids used for skin peeling to penetrate the skin, and can, in

Table 1.1 Summary of chemical peels Molecule

Depth

Application

Glycolic acid

Very superficial

25–50% partially buffered, for 1–2 min

Superficial

50–70% partially buffered, for 2–10 min

Medium (not recommended)

70% unbuffered, for 5–10 min

Mixture of AHAs

Dermal and epidermal stimulation

Easy Phytic®: pH 0.5, but slow-release effect + self-neutralizing

Jessner (Resorcinol)

Very superficial

1–3 layers

Superficial

4–8 layers

Medium (not recommended)

4–8 layers combined with 25% m/m TCA

Superficial

One application of 30% paste for 5 min

Intermediate

Two applications of 40% paste for 30 min

Medium

Three applications of 40% paste for 30 min, after skin preparation

Very superficial

• One application of 10% TCA • 10–20% TCA solution, depending on number of coats and skin preparation

Superficial

• Easy TCA® or 10–15% m/m solutions, depending on number of coats and preparation, or in combination (e.g. Abrasion, Dry Ice, Jessner)

Medium

• Unideep® • Solutions of >35% m/m

Deep

• Sandpaper abrasion + Easy TCA® • Unideep® • Only Touch® (AHA + TCA > 40% m/m – localized deep)

Localized deep

Lip & Eyelid® (wrinkles on lips and eyelids)

Full-face deep

Lip & Eyelid®, Baker, Litton, Exoderm, etc.

Unna (Resorcinol)

TCA

Phenol

AHA, alpha-hydroxy acid; TCA, trichloroacetic acid.

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some cases, cause unexpected burns. A similar situation arises with patients who want to present their doctors with perfectly clean skin and use abrasive creams – the intention is noble but the consequences are sometimes unpleasant. A peel is therefore also ‘patient-dependent’. If we leave aside these variables, we can fit the different types of peels into their appropriate slots. This is just for the beauty of the exercise however, as the variables still need to be taken into account. It is clearly possible to perform a superficial or medium peel using phenol. But, given the inherent toxicity of phenol, what would be the point? What is more, 70% unbuffered glycolic acid that is left for 10–15 minutes on a thin, sensitive skin that has been prepared with retinoic acid can result in a cosmetic disaster. It is possible to carry out good-quality, deep peels with TCA, but the risks can be greater than if phenol is used correctly.

Summary table Table 1.1 is intentionally incomplete. A peel is considered as ‘very superficial’ when its action is limited to the stratum corneum, ‘superficial’ if it does not go beyond the basal

3

layer of the epidermis, ‘medium’ if it reaches the papillary dermis and ‘deep’ if it reaches the reticular dermis. In reality, it is better to determine the depth of a peel by clinically observing what is happening to the skin during the course of the treatment than by blindly applying set recipes. When we say that the result of a glycolic acid peel is ‘time-dependent’, this does not mean having to watch the clock but rather continuously analyzing how the skin is reacting in order to determine the best moment to start neutralization. There is one basic principle to be respected: a peel should not be unnecessarily deep or unnecessarily superficial. There is no point completely destroying the papillary dermis when treating a purely epidermal problem, and it is pointless and ineffective to use an intraepidermal peel, even repeatedly, to treat a dermal problem.

Notes 1.

The nostrils can tolerate glycolic acid better than the skin around the eyelids, and many application procedures for glycolic acid peels recommend avoiding application to the eyelids.

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2 Pre-peel care

Is it necessary to prepare the skin? Depending on the type of peel, preparing the skin can be essential, completely pointless or even dangerous. The chapters devoted to the different types of peels give details of the preparation recommended in each particular case. This chapter deals with the generalities of pre-peel care.

Medium- and long-term preparation Alpha-hydroxy acid (AHA) peels produce the best results if they are preceded by careful preparation and followed by long-term daily cosmetic care. Easy Phytic® solution, on the other hand, does not allow any pre-peel preparation that is likely to accelerate penetration of the acids, as the stratum corneum must be intact for the peel to be safe. Classic trichloroacetic acid peels, in a simple aqueous solution in gel or mask form (TCA–SAS) always require around 1 month’s intensive pre-peel preparation. This preparation stimulates keratinocyte regeneration and reduces the risk of post-inflammatory pigmentary changes and/or scarring. It blocks the first stages of the biochemical conversion of tyrosine into indole groups and melanin and limits the reaction of melanocytes to ultraviolet light. Easy TCA® requires no preparation under its basic protocol (until scattered pinpoint or cloudy white frosting appears). The preparation required for its special deep-peel protocol or when combined with abrasion is discussed later in this book. Resorcinol produces far better results and fewer complications if the skin is well prepared. Phenol does not usually require any specific preparation, but needs careful post-peel care. As a general rule, it is worthwhile preparing the skin carefully with tyrosinase inhibitors if there is any risk of post-peel pigmentary changes or to optimize results when treating melasma. Retinoic acid and sometimes glycolic acid are used to make transepidermal penetration more even or to deepen the action of the acid solution.

Immediate pre-peel preparation Generally, patients must wash their skin with soap and water before going to the appointment. The doctor will disinfect the skin with alcohol and degrease it with acetone or ether. These degreasing products allow the peel solutions, which are usually hydrophilic and have difficulty penetrating the skin’s protective oils, to penetrate more deeply and evenly. They break down some of the proteins and phospholipids in the cell membranes, which enhances the action of the acids applied afterwards. AHA peels require very careful preparation before being applied. The skin should be cleaned with soapy water, rinsed thoroughly, degreased with acetone and disinfected with alcohol. Unlike the classic AHA peels, with Easy Phytic®, the skin must be cleaned with a gentle, nonaggressive cleansing foam that only contains surfactants, so that the acids do not penetrate the skin too quickly and saturate its natural buffer capacity, making it impossible for it to neutralize the sudden inflow of acids in time. Thorough cleansing and degreasing of the skin before Easy Phytic® would oblige the doctor to neutralize it in the classic manner – when there is no prior preparation, there is no need to neutralize it. With TCA–SAS, resorcinol, salicylic acid, azelaic acid or phenol peels, the skin needs to be thoroughly cleansed of make-up, degreased and disinfected. Easy TCA® solution, on the other hand, contains saponins that make pre-peel make-up removal and degreasing unnecessary; the skin’s natural defenses are only very slightly diminished by this peel, and therefore there is no need for any particular prepeel preparation against infections.

Products used to prepare the skin The products usually used to prepare the skin are sunscreens, tretinoin, AHAs and tyrosinase inhibitors. Jessner’s solution is sometimes used as a pre-peel preparation. It is often necessary to take measures to prevent infection, especially herpes.

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Prevention of infection Prevention of the herpes simplex virus is essential for patients who have a history of the infection (a single incidence of herpes is enough). Herpes prevention is necessary with a peel to the papillary dermis. It is also worthwhile when a more superficial peel is usually accompanied by a severe inflammatory reaction, as is the case with resorcinol, ‘classic’ AHAs and TCA–SAS. It is not necessary when using Easy TCA® under its basic protocol or Easy Phytic®. General infection prevention measures should be taken, depending on the depth of the peel. For more information, see the discussion of infections in Chapter 37.

Pre-peel sun protection It can be beneficial to protect the skin against the sun before certain peels. Effective sun protection should start 2 weeks before a medium or deep peel and even before a series of superficial peels to inhibit melanocyte activity and avoid excessive stimulation of melanin production before the peel.

Prevention of pigmentary changes Before any ‘classic’ peel, steps must be taken to limit the risk of pigmentary changes. Preparing the skin with tyrosinase inhibitors (hydroquinone, kojic acid, azelaic acid, arbutin, Morus Alba, licorice extracts, etc.) is especially recommended to curb the enthusiasm that certain melanocytes have for converting tyrosine into melanin. Preventive measures should begin 3–4 weeks before a medium or deep peel. Combinations of hydroquinone (2–4%) plus kojic acid (2–3%) or hydroquinone (2–4%) plus glycolic acid (8–10%) are effective, as are certain formulas containing several tyrosinase inhibitors, antioxidants and concentrated retinol (Blending Bleaching® cream). Some patients may develop hyperpigmentation, or even ochronosis, when treated with hydroquinone. Patients with dark skin types are most at risk. Long-term use of high-concentration hydroquinone can also cause confetti-like depigmentation (Figure 2.1). Hydroquinone is prohibited from sale as an ingredient in cosmetic or cosmeceutical products in many countries (although it is available on medical prescription) and has been successfully replaced by new formulas combining other tyrosinase inhibitors. Creams containing azelaic acid (usually at a concentration of 20%) are considered slightly bleaching when used for at least 4–6 months. Azelaic acid is an irritant, and is used mainly when other formulations cannot be used. For oily or thick skins, tyrosinase inhibitors can be prescribed in a gel form that penetrates the skin more easily and allows instant and easy application of make-up. For more information, see the discussion of pigmentary changes in Chapter 37.

Figure 2.1 Confetti-like depigmentation.

Even penetration of acids and stimulation of skin regeneration To perform a medium or deep TCA–SAS peel, the active molecule in the peel solution has to penetrate more deeply and the skin must regenerate more quickly. We have two large groups of molecules at our disposal: AHAs and retinoids. AHAs (e.g. 10–15% glycolic acid) break down corneodesmosomes that maintain intercorneocyte cohesion; they make it easier to shed this layer of dead cells (which are, however, essential to the skin’s defenses, as they are largely responsible for maintaining the permeability barrier function in the skin as a whole). The epidermis is thinned by the AHAs, making the stratum corneum more permeable, and the acids can penetrate more deeply and evenly. The risk with this preparation is that the epidermis may become too permeable and the effect of the peel can go too deep. A peel that is meant to reach the papillary dermis could penetrate as far as the reticular dermis as a result of too ‘strong’ a preparation of AHAs. A peel that is meant to remain intraepidermal could become intradermal and result in post-peel complications and more downtime: an intraepidermal peel removes several layers of ‘skin-color’ keratinocytes in light flakes for around 3 days, whereas an intradermal peel removes the entire epidermis in the form of strips of brownish skin. The darker the skin type, the more visible is the flaking. Retinoids form a growing range of products with everwidening indications. The retinoid most used in pre-peel preparation is tretinoin. Among other things, it stimulates keratinocyte growth in the basal layer and causes an overall thickening of the epidermis but also a relative thinning of the stratum corneum. The pre-peel use of tretinoin

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enhances penetration of the acids at the same time as stimulating the regeneration processes in the keratinocytes of the basal layer. The choice of one or another of these molecules depends on the condition of the patient’s skin. Tretinoin is not used if the patient has many telangiectasias; AHAs are avoided if the skin is very thin. Conversely, the two products can be mixed in the same prescription, in variable concentrations, depending on the skin type and the desired effect. The concentration of tretinoin would be increased to stimulate reepithelialization; the concentration of glycolic acid would be increased to improve and even out transcorneal penetration.

Tretinoin Tretinoin (all-trans-retinoic acid, ATRA) is the carboxylic acid form of vitamin A (retinol). It is one of the first-generation retinoids and has been used since the 1970s to treat acne complaints and dyskeratosis. It is important to know all about this molecule in order to obtain benefit from its actions.

Histological changes During long-term treatment with tretinoin, the results can first be seen through a microscope, long before they are clinically visible. These histological changes explain the indisputable clinical efficacy of continuous treatment. The epidermis increases in thickness by 10–40%, with a thickening of the stratum granulosum to the detriment of the superficial stratum corneum (which decreases by about 25%); the overall water content of the epidermis is thus increased and the skin appears more hydrated. This epidermal hyperplasia is observed both on the face and on the rest of the body, especially on the arms or forearms. Unfortunately, it is not certain whether the improvement is permanent, as some studies show a reversibility of the action of tretinoin (a habituation phenomenon?) after 6 months’ treatment on the forearms and the disappearance of histological improvement altogether 1 year after the start of the treatment, whereas clinically the improvement persists. Normal epidermal differentiation is restored and keratinocyte abnormalities gradually decrease. The atypical keratinocytes are eliminated and the tretinoin prevents or delays keratoses from reappearing. The melanocyte clusters in the basal layer gradually disperse as a result of the increased cell turnover. The marks on the skin thus tend to be more diffuse, or even to disappear. The overall pigmentation in the epidermis decreases in patients with black skin (32%1 and 23%2) and in patients with yellow skin (41%3). One year after the start of treatment, the melanin content of the epidermis continues to decrease and causes the skin to lighten in the long term. As with chemical peels, a newly formed collagen layer appears, in horizontal bands, just

7

beneath the basal membrane, in the Grenz zone. New active fibroblasts appear in the dermis, and new elastic and collagen fibers are secreted. An increase in glycosaminoglycans thickens the dermis, and elastotic tissue is pushed deeper down. After 26 months of daily treatment with 0.05% tretinoin, the events described above are extensive enough to push the elastotic tissue deep down and hide it under the new vascular, elastic, collagen and epidermal growth. It must be noted, however, that not all authors accept the existence of these histological changes in the dermis in the long term. In particular, a study by Gilchrest4 on 500 biopsies carried out during a 5-year observation of daily topical tretinoin treatments (in concentrations between 0.001% and 0.1%) could not find any evidence of histological changes in the dermal parameters. This is surprising, and contradicts the established fact that clinically visible angiogenesis exists.

Mechanism of action Tretinoin is a synthetic (all trans) retinoic acid. Retinol and retinaldehyde are also converted into retinoic acid in the target cell where it participates in metabolic activity. The retinoic acid penetrates the cell’s nucleus, where it binds with a retinoic acid receptor (RAR). The complex formed by the retinoic acid and the RAR (RA–RAR) interferes with certain areas of DNA by modulating the expression of some genes. It appears that retinoic acid alters the regulation of the cell cycle.4 For many years, tretinoin was considered capable of reducing sebum production in the sebaceous glands, but serious doubt has been cast on this theory. It is generally thought that the mode of action of tretinoin is essentially linked to the increase in epidermal turnover and enhanced exfoliation of the stratum corneum, which makes it easier for the pilosebaceous units to drain. A reduction in melanin production has also been observed. Used specifically as a pre-peel preparation, tretinoin evens out the thickness of the stratum corneum and reduces overall skin thickness. In these conditions, skin permeability increases significantly. Tretinoin also stimulates keratinocyte division and thus facilitates the regeneration phase, which can sometimes be too slow with certain peels. Topical tretinoin stimulates fibroblast production of collagen as well as other components of the dermal extracellular matrix, and sometimes creates a new layer of ‘repair’ collagen that is laid on top of the photodamaged collagen.

Indications Clinical results appear slowly and gradually, after histological improvement. The skin soon appears to be intensely hydrated, once the erythema has disappeared or subsided. Clinically, it takes a year for the rejuvenating action of tretinoin to show. Patients, who hope to see rapid

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improvement, are not best pleased with these slow clinical results on aging skin. Progress can sometimes be seen more quickly when treating dyschromia: some results may be seen after 1 month of daily application of 0.1% tretinoin cream. Comedonal acne and acne rosacea respond well to tretinoin. In fact, the anti-aging effect of tretinoin was first observed in patients being treated with tretinoin for comedonal acne: their skin texture and skin tone were gradually seen to improve. Oral isotretinoin (9-cis-retinoic acid) is often used in treating severe or stubborn acne rosacea. A 1994 study5 compared the treatment of rosacea with 10 mg/day lowdose oral isotretinoin, 0.025% low-dose topical tretinoin and a combination of the two. The results showed that before the 16th week of treatment, isotretinoin was more effective, but that afterwards there was no difference between tretinoin and isotretinoin. The combination of systemic and topical treatment does not give any further improvement in low doses. It is generally accepted that tretinoin with a concentration of 0.05% is as active as 5% benzoyl peroxide. Topical tretinoin makes the skin smoother: the same patients who benefited from the visible rejuvenating effect of tretinoin when being treated for acne noticed, among other things, that their skin had become smoother and softer after treatment. The improvement brought about by this topical treatment is therefore visual as well as tactile. The application of topical tretinoin improves senile atrophy of the skin: a decrease in cell abnormalities and dysplasias can be seen, as well as an antitumor effect that persists after the end of treatment if it has been administered correctly and for a sufficiently long period.6 Topical tretinoin reduces the size and number of lentigines and other age-related discolorations. In some cases, however, because of its photosensitizing potential, tretinoin can aggravate certain types of dyschromia. This can be problematic for Asian patients, for whom hyperpigmentation is more of a problem than wrinkles as they age. The study by Griffiths et al3 proved (clinically, histologically and by colorimetry) that 0.1% tretinoin significantly improved hyperpigmentation in these patients. There was a 41% improvement with tretinoin, compared with a 37% aggravation in patients receiving the vehicle alone. Post-inflammatory hyperpigmentation is also improved by tretinoin, as proved clinically, histologically and by colorimetry, in a study by Bulengo-Ransby et al2 on subjects with black skin. A 40% improvement can be expected after 40 weeks of treatment with 0.1% tretinoin. In the treatment of melasma, topical 0.1% tretinoin was studied in comparison with the vehicle alone in black patients.1 A 10-month treatment lightened the melasma by 32% (an improvement factor established both clinically and by colorimetry). Histological studies have shown a significant decrease in epidermal pigmentation in patients treated with tretinoin

compared with placebo. Of the patients treated with tretinoin, 67% developed only one side-effect, a mild ‘retinoid dermatitis’ (which is to be expected when using a concentration of 0.1%). This study also showed that the finest wrinkles disappeared and other wrinkles improved. Overall, skin tone improves because of the combination of histological events in the dermis and epidermis described above. The skin takes on a rosier complexion as a result of angiogenesis occurring deep down.

How to prescribe tretinoin One study7 showed that a tretinoin concentration of 0.01% is effective for the face, hands and forearms, whereas another8 showed that there is no difference between placebo, 0.01% tretinoin and 0.001% tretinoin. A concentration between 0.05% and 0.1% is, on the other hand, always considered active. The average concentration used is 0.05%, but different skin types or sensitivities may require different concentrations, and it is recommended to start any treatment with a trial dose of 0.02% or 0.03%. The following is one frequently used formulation (0.025%): tretinoin urea (carbamide) water Neribase® cream or Eucerin® O/W

15 mg 6g 4g ad 60 g ad 60 g

If this dose is well tolerated, it is possible to go immediately or gradually to a concentration of 0.05%. This concentration is common in proprietary medicines, but if prescription medicines are preferred, it is possible to prescribe 0.05% tretinoin in the following formulation: tretinoin urea (carbamide) water Neribase® cream or Eucerin® O/W

30 mg 6g 4g ad 60 g ad 60 g

Formulations in alcohol gels dry out the skin, increase the penetration of the tretinoin and make the treatment more uncomfortable. Gels should only be used on thick and oily skins. When the patient can tolerate a concentration of 0.05% without any notable side-effects, the concentration can gradually be increased to 0.07%, 0.09% and 0.1%. Concentrations higher than this are rarely used. If, on the other hand, the skin is very sensitive and becomes irritated in spite of a low concentration of 0.025%, the concentration must be decreased to 0.0125%9 or the patient should be asked to do one of the following. The skin can be sprayed with warm water immediately before applying a small

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quantity of cream. The cream will spread more easily and less of the active ingredient will be applied on the skin. Alternatively, the tretinoin cream can be mixed in the palm of the hand with an equal quantity of hydrating vitamin E cream10 in order to halve the final concentration. If the skin is still sensitive to the treatment, as a last resort, the treatment can be applied every other day or once every 3 days for the first month. Experience shows that daily application of low concentrations is a better way to prepare the skin for higher doses than applying higher concentrations two or three times a week. The ‘normal’ concentration for daily application (0.05%) is reached gradually over 2–3 months. It makes little sense to combine tretinoin with a topical corticosteroid to limit the inflammatory reaction. It may well be that this combination is supposed to stop inflammation, but inflammation is beneficial in that it stimulates the process of skin repair. Furthermore, the combined effect of corticosteroid and tretinoin could potentially cause telangiectasia. The tretinoin would stop skin atrophy as a result of the application of topical corticosteroid, whereas it should increase the thickness of the epidermis overall. A large part of the effect would therefore be lost. Finally, corticosteroids should not be applied to the skin for a prolonged period, whereas long-term application of tretinoin is necessary. If the skin is resistant from the start and does not respond at all to the above formulation at 0.05%, a concentration of 0.1% can be used. This high concentration has been shown to produce results rapidly, but can often have serious side-effects. Therefore, before such a sudden increase in concentration, there are a few ‘therapeutic tricks’ that can be tried: when the skin appears not to respond to a single daily application of 0.05%, a 0.05% cream can be applied twice a day – once in the morning followed by a sunscreen and again in the evening. To increase the effect, it is possible to prescribe an alcohol gel, starting with a concentration of 0.05%, and increasing to 0.1% if the patient can tolerate this. To increase the potency of the tretinoin, the impermeability of the skin barrier can be decreased, either by applying a 10% glycolic acid cream 20 minutes before applying the tretinoin or by using a mildly abrasive sponge (Buf-Puf®) on the skin before using the tretinoin. In some extreme cases, a light facial or body scrub twice a week increases skin permeability and makes it easier for the tretinoin to penetrate. Very superficial microdermabrasion with corundum crystals or sandpaper can also make the skin more permeable.

Age for starting treatment The lighter the phototype, the better it is to start treatment at a young age. For example, individuals with skin phototype II can start treatment in their 20s, whereas individuals with skin phototype IV should only start in their 30s.

9

Various recommendations Tretinoin cream should be kept out of direct sunlight and away from heat sources, to which it is sensitive. In spite of these precautions, it gradually loses its efficacy and it is recommended that the prescription be renewed every 3 months. Tretinoin is sensitive to oxidation, heat and ultraviolet light: the refrigerator (4°C) seems to be the best place to store this cream. The by-products of degradation turn the cream a yellowish color, in which case it should no longer be used. Tretinoin is photosensitizing, and it is therefore preferable to apply the cream in the evening and to use a hydrating antioxidant or a cream such as Blending Bleaching® combined with a sunscreen (UVB + UVA + HSP) of factor 20 or above in the morning. The tretinoin cream is applied after washing the skin with a mild soap (Avene® or Skin Tech’s Pre-Peel Cleanser®), and is rubbed gently onto the face and neck (very gently on the neck where the skin is more sensitive). It is striking to note that the earlobe is often missed out in skin rejuvenation or tretinoin cream treatments – and can be a telltale sign of a person’s real age. When tretinoin is applied to skin with seborrheic dermatitis (even when this is subclinical), it is common for erythema to develop, often in the middle of the face. One week’s preventive treatment with topical nystatin can often prevent erythema, and considerably improves treatment compliance. Men whose skin tends to become irritated or infected after shaving can use tretinoin as an aftershave cream. Shaving soon becomes more comfortable: within 48 hours, the irritation or potential acneform dermatitis has subsided or disappeared altogether. The tretinoin cream should be applied every day for at least 12–18 months and two or three times a week thereafter to maintain the results. When the treatment ends, the effect does not last indefinitely, and the skin slowly returns to a state close to its original condition. However, if the treatment is followed with one to three applications a week afterwards, the positive effects remain visible.11 When the treatment lasts 5–6 years, the elastotic material in the dermis is gradually replaced by new collagen and elastic structures.12 The results should last a long time if the skin is protected from factors that accelerate the aging process. Combining tretinoin and benzoyl peroxide could inactivate the tretinoin. If absolutely necessary, benzoyl peroxide can be applied in the morning and tretinoin in the evening.

Side-effects Patients should be warned of the high probability of adverse effects, which fortunately are only temporary. Tretinoin is more irritant than glycolic acid. The irritation is usually mild, but can take the form of ‘retinoid dermatitis’ if high concentrations are used or if the skin is delicate. This dermatitis is in fact a positive side-effect when tretinoin is used to prepare for a TCA–SAS peel, at least to

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the level of the papillary dermis, as it helps the TCA penetrate more deeply and evenly. A concentration of 0.05% tretinoin should be used once or twice a day (depending on the thickness and sensitivity of the skin) for 1 week; the following week, the concentration is increased to 0.07% and the third week to 0.1%. This relatively aggressive preparation improves the penetration, evenness and re-epithelialization of the TCA–SAS peel, but will not improve the cosmetic results (or will do so only very slightly). If the skin is not properly hydrated during treatment with tretinoin, it will usually flake visibly and fairly rapidly after a few days of treatment. Erythema is to be expected with effective tretinoin treatment. This is not an adverse effect, but rather is collateral and natural. The skin of a patient properly treated with tretinoin is pinker than normal, and this provides the doctor with an essential means of observation: a patient showing no erythema is undertreated or incorrectly treated. Erythema that appears very rapidly, 2–3 days after treatment begins, and that is localized in patches may be seborrheic dermatitis; it soon clears up with nystatin cream. Erythema that appears in the medium or long term, 1 or more weeks later, can spread over the whole face and sometimes to the neck in patients with very sensitive skin. If this should happen, treatment should be stopped for 1–2 weeks and started again at a lower dose, as explained above, to avoid excessive neoangiogenesis. More often than not, retinoid erythema does not last long in patients with a dark skin phototype, whereas patients with a lighter phototype can suffer from persistent, if not permanent, retinoid erythema. Sometimes, the redness is more of a passing flush than fully established erythema. The skin becomes more sensitive to the sun, perfumes and detergents. In fact, right from the start of treatment, the skin becomes more sensitive to any irritant: beware of chemical hair removal products, waxes, dyes, etc. People who use tretinoin often report that their skin is more sensitive to the sun and burns more easily. This photosensitization is better explained by the thinning of the stratum corneum rather than by a photochemical reaction between the tretinoin and the sun’s rays. It is therefore essential to recommend the use of a sunscreen (SPF 25–50 UVA + UVB + HSP induction) to patients being treated with tretinoin. It should also be borne in mind that there is a potential risk of skin cancers developing as a result of the stratum corneum thinning and the enhanced penetration of the sun’s rays. Nevertheless, it appears that patients on longterm tretinoin treatment do not have a higher incidence of skin cancers. Tretinoin has in fact proved to be effective in the treatment of photoaging and actinic keratoses.

Teratogenicity of tretinoin There is one important thing to note about the risk of teratogenicity: to date, and in spite of the fact that no terato-

genicity has been officially attributed to tretinoin,13 we do not have all the necessary facts at our disposal to allow its unreserved use during pregnancy or in women who wish to become pregnant. Despite the fact that application of tretinoin under occlusion on more than 30% of the body has not been found to lead to any abnormal increase in plasma levels, and despite there being no higher incidence of fetal deformities among the children of women who have used tretinoin during the first months of pregnancy, it is nonetheless possible for retinoic acid to penetrate the cell nucleus and alter the expression of certain genes.4 Caution dictates that one should not go ahead with treatment in a particular case until all the necessary facts are available to allow a risk-free choice to be made. Hypervitaminosis A is theoretically possible and could be insidious and chronic. 14 Practitioners should remain on their guard and make sure that patients are not taking extra vitamin A supplements.

Benefits of skin preparation Major benefits Avoiding various side-effects Preparing the skin before a TCA–SAS peel helps prevent herpes and bacterial and mycotic infections. It also helps reduce the risk of inadequate results (thanks to combination with other treatments).

Improved penetration of the active product Preparation with AHAs or tretinoin reduces the thickness of the stratum corneum, the skin’s natural barrier. As the barrier is not as thick, it is easier for the products applied to the skin to penetrate to the basal layer of the epidermis and more deeply into the dermis. It should be noted that not all peels require this kind of preparation.15

Even penetration of the peel The skin does not have the same thickness all over, and this can produce differences in the level of penetration. Correct preparation with AHAs and/or tretinoin tends to even out the thickness of the skin and allow the active products of the peel to penetrate evenly. Areas of hyperkeratosis (senile keratoses, and flat and seborrheic warts) are a perfect example of this difference in the level of penetration. Keratoses, which are characterized by a localized thickening of the stratum corneum, are less permeable to the acids. Pre-peel preparation with tretinoin evens out the thickness of the stratum corneum and hence the overall permeability of the epidermis.

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11

Reduced risk of pigmentary change

Monitoring skin preparation

Patients with olive and dark skin, or of Hispanic or Asian origin, are more prone to pigmentary changes than patients of Caucasian origin. It should be remembered that genotype does not always correspond to phenotype and that there are light skins that react in the same way as dark skins.16 Tretinoin, even more than AHAs, disperses melanin granules and reduces the overall quantity of melanin in the epidermis. This reduces the risk of postinflammatory or post-peel pigmentary changes. Tyrosinase inhibitors should be used in post-peel treatment as well as in pre-peel preparation (1 month before the peel when there is a risk of pigmentary change, i.e. when TCA–SAS or AHA peels are used). Some commercial creams have interesting formulations with AHAs (to enhance penetration of the other active products), tretinoin precursors, lactic acid, extracts of Morus Alba and kojic acid, combined with Transcutol®, an adjuvant that concentrates the active products near the basal layer and the melanocytes.

Monitoring the preparation process can give an idea of how reactive and sensitive the skin is. Thus, a patient who cannot tolerate hydroquinone during pre-peel preparation will tolerate it even less in the days following the treatment as the skin becomes more sensitive to any irritant. Similarly, if the patient develops an allergy to one of the products used in the preparation, it can be isolated and avoided after the peel.

Combination treatments Other treatments can be combined with the pre-peel preparation: shave excision, electrocoagulation, ablations, botulinum toxin, dermal filling, mesotherapy, etc. Some peels can be used simultaneously with these techniques. For example, a phenol peel can be immediately preceded by shave excision of raised benign lesions. Easy TCA® can be immediately preceded by botulinum toxin, dermal filling, electrocoagulation of telangiectasias (Figure 2.2), mesolift, IPL, depilation, etc.

Accelerated healing of the skin After a peel, the skin needs to heal as quickly as possible in order to maintain homeostasis of the whole organism. Tretinoin accelerates re-epithelialization if used before the peeling. For this it must be used at a dose of 0.05%–0.1%, sometimes to the point of irritative dermatitis. Ideally, the treatment should start 3–4 weeks before a TCA–SAS peel. It is accepted scientifically that the preventive application of tretinoin promotes post-peel healing of the skin. In contrast, applying tretinoin during the post-peel period appears to slow down skin regeneration. Not all peels require this help with re-epitheliazation.

Minor benefits Testing patient compliance A patient who refuses to comply with instructions for preparing the skin before a peel will not be naturally inclined to heed advice for care during or after the peel sessions either. It is always preferable not to ‘peel’ a patient who is incapable of understanding or accepting these instructions. Testing patient compliance is all the more important since preparing the skin and keeping up cosmetic care afterwards affect the quality of the results.

Getting an idea of follow-up care For patients who accept it, preparation gives them a foretaste of between- and post-peel care.

Figure 2.2 Treatment of telangiectasias by (Ellman®) radiofrequency immediately before the application of Easy TCA®. Scattered pinpoint frosting signals the penetration of the acid at each point treated by radiofrequency. This combination significantly reduces scabbing and includes a ‘pixillized’ deeper peeling.

Notes 1. Kimbrough-Green CK, Griffiths CE, Finkel LJ, et al. Topical retinoic acid (tretinoin) for melasma in black patients. A vehicle-controlled clinical trial. Arch Dermatol 1994; 130: 727–33. 2. Bulengo-Ransby SM, Griffiths CE, Kimbrough-Green CK, et al. Retinoic acid treatment for hyperpigmented lesions caused by inflammation of the skin in black patients. N Engl J Med 1993; 328: 1486–7. 3. Griffiths CE, Goldfarb MT, Finkel LJ, et al. Retinoic acid treatment of hyperpigmented lesions associated with photoaging in Chinese and Japanese persons. J Am Acad Dermatol 1994; 30: 76–84

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4. Gilchrest BA. Retinoids and photodamage. Br J Dermatol 1992; 127(Suppl 41): 14–20. 5. Ertl GA, Levine N, Kligman AM. A comparison of the efficacy of topical tretinoin and low-dose oral isotretinoin in rosacea. Arch Dermatol 1994; 130: 319–24. 6. Published studies disagree on the efficacy of tretinoin. 7. Andreano JM, Bergfeld WF, Medandorp SV. Tretinoin emollient cream 0.01% for the treatment of photoaged skin. Cleve Clin J Med 1993; 60: 49–55. 8. Olsen EA, Katz HI, Levine N, et al. Tretinoin emollient cream: a new therapy for photodamaged skin. J Am Acad Dermatol 1992; 26: 215–29. 9. By altering the formulations given above: 7.5 mg tretinoin in 60 g of cream.

10. Vit E antioxidant® (Skin Tech) or a similar cream. 11. Thorne EG. Long-term clinical experience with a topical retinoid. Br J Dermatol 1992; 127 (Suppl 41): 31–6. 12. Not all studies endorse this long-term treatment. 13. Guzzo CA, Lazarus GS, Werth VP. Dermatological pharmacology. In: Hardman JG, Limbird LE, Molinoff PB, Ruddon RW, Gilman AG, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 9th edn. New York: McGrawHill, 1996: 1600. 14. Farnes SW, Setness PA. Retinoid therapy for aging skin and acne. Postgrad Med 1992; 92: 191–6, 199–200. 15. For example: Easy TCA® and Easy Phytic® need no pre-peel preparation. 16. Which is why it is important to question the patient.

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3 Post-peel care

Immediate post-peel care is described in detail in the chapters dealing with each type of peel. As a general rule, tretinoin and creams with an alpha-hydroxy acid (AHA) concentration of over 10% should be avoided before the exfoliation phase is completely finished.

Sun protection Any peel, even a very superficial one, reduces the thickness of the stratum corneum that protects the skin against the effects of radiation: the diffractive and reflective protection usually afforded in these outermost layers is no longer available, and the overall quantity of rays that penetrate the skin increases. This extra radiation can cause actinic damage in cells that are usually physically protected by the thickness of the skin. Melanocytes are more strongly stimulated, and there is an increased likelihood of pigmentary change. All peels thus allow the sun’s rays to penetrate more easily to at least the basal layer of the epidermis, where keratinocytes ensure re-epithelialization and melanocytes can induce hyperpigmentations. Greater irradiation increases the risk of these cells being genetically modified. All peels put the skin at risk of light stress, which makes the use of sun protection creams essential. A powerful, broad-spectrum sunscreen provides greater protection. The deeper the peel, the more important it is to use sun protection. After any medium or deep peel, it is necessary to use an effective sunscreen of factor 25–50 (Figure 3.1) (UVA + UVB + HSP inducers) for 6–12 weeks (depending on the depth of the peel). The sunscreen should be applied immediately after washing in the morning, preferably with a cleansing lotion. Post-peel sun protection should be re-applied every 3 hours on average under any make-up, even if the make-up itself is considered to be photoprotective. After a peel, sun protection is necessary even if the patient does not go outside and even in foggy or cloudy weather: windows block out most UVB but not UVA, and not all clouds filter UV. Halogen lamps and spotlights and cathode-ray screens also appear to produce a sufficient quantity of radiation to induce post-inflammatory hyperpigmentation (PIH) in sensitive individuals.

Effective sun protection factor The sun protection factor should be even more ‘aggressive’ when treating post-inflammatory hyperpigmentation, and should protect against UVA as well as UVB. Protection from the sun means not only avoiding lying on the beach but also avoiding daylight. The skin is subjected to many light shocks; it is constantly under attack from the sun and daylight. One pitfall to be avoided is applying sunscreens that contain tanning accelerators that could have a harmful effect.1 Between peels and during the first few weeks after a peel, a generous amount of Melablock HSP® 50+ sun cream, for example, should be applied every 3 hours.2 Thereafter, daily sun protection can be lighter: for example Melablock HSP® 25+ every 3 hours. Patients should be advised to keep their backs to the sun and to wear light protective clothing. UV is not the only cause of hyperpigmentary reactions: infrared can also cause them.

Heat-shock proteins (HSPs) The process of wound healing after thermal injury (e.g. from laser treatment) involves re-epithelialization that starts within the first few hours after injury and continues throughout the different proliferative phases of skin repair. Viable keratinocytes (Figure 3.2) that are at the edge of the wound and have not suffered lethal or sublethal heat shock

110 100 90 80 70 60 50 40 30 20 10 0

 90

% UVB blocked

ch03

 96

 98

 50

0 SPF0

SPF2

SPF10

SPF25

SPF50

Figure 3.1 An SPF of 50 protects the skin against 98% of UV. A higher protection factor is not necessary.

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Figure 3.2 Diagram of the peripheral thermal damage after ablative laser treatment. The number of lethal lesions is proportional to the degree of shading. The skin is repaired from peripheral keratinocytes: some have suffered sublethal damage. Heatshock protein (HSP) inducers help improve keratinocyte resistance to heat shock.

migrate horizontally and centripetally in order to form an initial single cell layer of keratinocytes, the ‘new basal layer’, before starting vertical growth that will regenerate a normal epidermal structure. Re-epithelialization uses up a lot of proteins, both during the synthesis of the temporary matrix that acts as a protein highway for the new keratinocytes and during the intense mitotic activity that creates new skin cells. Proteins are absolutely essential to cell life; each enzyme in the body is a protein whose unique three-dimensional structure is responsible for its highly specific action. They have vital functions that are specific and strictly linked to their threedimensional structure. The spatial structure of proteins is altered by even the slightest increase in temperature;3 any thermal stress can ‘unfold’ the cell proteins, making them ineffective and leading to apoptosis (programmed all death). In laser or flashlamp treatments, the temperature of the target must be raised in order to destroy it, but the normal cells around the target also undergo sufficient heat stress to induce apoptosis or severely disrupt cell function. The rise in temperature thus creates a central zone of lesions that are lethal to cells, surrounded by a peripheral zone of sublethal damage in which the heat-damaged cells must be repaired or replaced. As a result, skin regeneration may be slower than it should be as the cells on the edge of the treated area grow and migrate. Preventive protection of the proteins in the cells surrounding the target, increasing their resistance to heat, can help enhance the skin healing process and reduce the incidence of complications associated with slow re-epithelialization. Where there is sublethal damage, or very light damage, the cells must eliminate or repair the damaged and ineffective proteins, increase protection of the proteins that did

resist the heat and synthesize new replacement proteins. This is where heat-shock proteins (HSPs or stress proteins) are necessary. HSPs were discovered at the beginning of the 1960s in the fruit fly in response to an increase in cell temperature of just a few degrees. These proteins were subsequently found in all types of living cells; they are secreted in response to any kind of stress, not only in response to increased temperatures. HSP70 and other similar stress proteins appear rapidly in the cytoplasm and mitochondrial matrix of cells that are subjected to stress. Essentially, their role is to ensure protein viability. HSP70 binds to polypeptide chains as soon as the latter have been synthesized in ribosomes (which translate RNA information into the amino acid sequence of the polypeptide) and facilitate the folding of these chains into the three-dimensional structure essential for protein activity. The HSP70 then separates from the folded protein. HSP70 is a member of a group of diverse proteins (also including HSP60 and the chaperonins) that play an essential role in creating the appropriate three-dimensional structures of other proteins – but do not themselves form part of that final structure. This group of proteins are also known as ‘molecular chaperones’ and have a fivefold role: do well as providing the correct spatial structure for a new protein coming out of the ribosome, they also protect the structure of existing proteins, repair damaged proteins by refolding them correctly, and act as protein transporters, carrying proteins from one place to another within the cell and eliminating proteins that are irreparable. Some HSPs are constitutional and others are inducible. The latter are synthesized in greater numbers after stress and give the cell increased resistance to future stress, thus allowing the cell more time to repair itself without having to resort immediately to apoptosis. With age, HSP function deteriorates in human skin, and aging cells are increasingly more prone to protein destruction.

Sun protection and HSPs It is therefore beneficial to boost the synthesis of HSPs in the cytoplasm and mitochondrial matrix of cells subjected to heat and light stress, thus improving not only their resistance but also their defenses and better equipping them to repair proteins in case of stress. An interesting disaccharide, trehalose (Figure 3.3), was isolated from cells of organisms that can survive in extreme conditions such as dehydration; having this disaccharide in sufficient concentrations allows these organisms to increase their resistance to the lack of water. It has been shown4 that trehalose can stimulate HSP70 production. An interesting experiment showed that this disaccharide increases cell viability after exposure to UVB. The study involved subjecting a culture of keratinocytes to a slight increase in temperature of 3°C for 1 hour in order to induce slight heat stress. The ker-

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H

H

H

HO O H

OH

O O

HO

OH

H

OH

HO

H

H

H

H

H

OH HO

Figure 3.3 Chemical structure of trehalose.

atinocytes were then cultured for 6 hours either in a medium containing trehalose or in a medium without the disaccharide. After 6 hours, the culture medium was replaced by physiological saline solution and the keratinocytes were exposed to UVB radiation. Cell viability was studied after 48 hours. There was a huge difference in keratinocyte survival in the cells from the different culture media: only around 4% of viable keratinocytes remain when cultured without trehalose eter, whereas the survival rate was nearer 40% in the group of keratinocytes cultured in the medium rich in trehalose (Figure 3.4).

Keratinocytes percentage survival

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40 35 30 25 20 15 10 5 0

0%

0.5%

1%

Trehalose eter concentration

Figure 3.4 The viability of keratinocytes exposed to UV after a 3ºC increase in temperature is very low: just a few percent. When cultivated in an environment rich in trehalose eter, the viability is close to 40% under the same conditions.

Specific care for different peels AHAs If an AHA peel is done correctly, no particular medical care is necessary, no matter what concentration or pH is used. In general, after an AHA peel, all that is necessary is good hydration and effective sun protection for 2 weeks. AHA peels weaken the barrier function of the stratum corneum

15

and thus increase its permeability; they make it easier for the active molecules to penetrate the epidermis when creams are applied both immediately after and between peeling sessions. The type of cream depends on the problem being treated. The results for acne treatment can, for example, be improved by applying a layer of anti-acne cream immediately after a ‘classic’ AHA peel has been neutralized and leaving it to act under an occlusive dressing5 for around 30 minutes. The patient can apply the same cream twice daily thereafter. The same applies for melasma and aging or sagging skin, etc.6 After an AHA peel, the patient’s daily care routine plays an essential role in determining the quality of the results. Mesotherapy can be combined with AHA peels in a number of ways: the ‘mesolift’ mixture7 can be injected before the peel or immediately after the peel has been neutralized and before creams are applied under occlusion. There is no danger of the glycolic acid penetrating beneath the skin through the perforations made by the mesotherapy needle. Most often, however, the treatments are alternated every other week: in the first week, the peel and the cream under occlusion are applied, and in the following week, the mesolift is injected, followed by the cream under occlusion. If an AHA peel is done correctly, there is usually no downtime. Nevertheless, there can be complications, which are described in Chapter 10.

Resorcinol Resorcinol in paste form9 is used in a very specific manner: the paste is usually applied three times, once a day for 3 days in a row. Post-peel care is very important during the following week: the skin should not be hydrated at all, as it has to dry out completely for the peel to be effective and, above all, the patient must not pull off or pick at the flaking skin. Only the doctor can safely cut off any strips of flaking skin with sterile scissors. Cosmeceutical creams for age spots, acne, aging or sagging skin, etc. should only be applied after the skin has flaked. Effective sun protection (UVA + UVB + HSP inducers) is absolutely essential for approximately 6 weeks after the peel. Downtime may be around 4–5 days. After the first application of the paste, the patient can usually have a normal social life, but subsequent applications dry out the skin and leave it looking papery.

TCA–SAS Trichloroacetic acid in simple aqueous solution (TCA–SAS) involves pre-peel preparation, application of the TCA–SAS solution to the required depth (usually the papillary dermis), flaking, natural skin regeneration and post-peel care. The post-peel period for TCA–SAS requires special attention and, even if the peel is applied correctly, pigmentary changes are the most common and benign complication. It

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is clear from the many illustrations in books on TCA–SAS peels that there is an astonishing variety of post-TCA pigmentary changes, with varying degrees of severity. If pre-peel prevention does not prove effective, or in cases of localized overpeeling, post-inflammatory hyperpigmentation (PIH) usually appears within a week after the peel in the form of dark patches or persistent erythema that will become pigmented under the effect of the sun’s rays. For more information, see the section on hyperpigmentation in Chapter 37. These genuine pigmentary changes should not be confused with the darkening of epidermal melasma appearing the next day after the peeling, and caused by dehydration of the hydrophilic spaces between melanosomes, which makes the skin seem to have a greater concentration of melanin and hence appear darker. This darkening, which is temporary, is a positive sign and will fade at the end of the first week. Flaking should not be helped along under any circumstances. Peeling off any bits of skin can result in uneven skin tone, infection, hyperpigmentation, scars or localized achromia. It is also essential to take preventive measures against infection after a papillary TCA–SAS peel, as the latter destroys most of the skin’s defenses. An antibiotic cream is applied during the first week after the peel. The skin should be cleaned before each application of cream, and any occurrence of contact allergies, which can sometimes be confused with secondary infections, should be monitored. The results of a TCA–SAS peel also depend on the quality and consistent use of cosmeceuticals after the peel. It is clear that a melasma treatment will produce better results if the TCA–SAS peel is followed by the application of a retinol–anti-tyrosinase–anti-oxidant cream or a hydroquinone-based preparation. For acne or aging or sagging skin, the same comments apply as for AHAs above. These creams can be applied as soon as flaking is finished, usually on the 7th day. Effective sun protection is absolutely essential and should be used in the first few days after the peel, before the skin has stopped flaking. Even a total sunblock is not enough to avoid pigmentary changes altogether, and the patient should be told to completely avoid exposure to the sun. Sun creams containing tanning accelerators should, of course, not be used after the peel.9 Chemical tanning with sprays containing dihydroxyacetone should also be avoided, as these products, which are non-toxic when picked up by the corneocytes and eliminated within 1 week, are not intended for keratinocytes, which are the cells exposed to the external environment during the first days after a peel. Downtime is around 1 week following a TCA–SAS peel, after which make-up can be used from the 8th day to cover up any persistent erythema.

Easy TCA® Easy TCA® is an exception among TCA peels, and should be distinguished from TCA–SAS, as it does not require pre-

peel care in the medium term nor any immediate pre-peel preparation, and pigmentary changes are very rare if the ‘basic protocol’ is followed.10 Some brown discoloration is possible after the first or second application, but this should fade after the following peel. Flaking skin can be peeled off or a light cosmetic scrub can be used. With deeper protocols, which are not usually necessary with this peel, there is a greater likelihood of complications. Combining Easy TCA® with appropriate post-peel cosmeceuticals helps improve and maintain results. The cosmeceuticals should be applied the day after the first peel and continued between sessions and for at least 6 weeks after the last application. As with any peel, effective sun protection is necessary to make up for the temporary loss of the stratum corneum. Easy TCA® causes the skin to flake, but not so much as to disrupt the patient’s social life, although certain activities may be compromised: television presenting, customer contact in the food industry, etc. Easy Phytic® is recommended in these cases as there is almost no visible flaking of the skin (see Chapter 11).

Phenol Phenol entails the most complex post-peel care: occlusive masks, healing masks and cosmetic care during the months following the peel. Chapters 25–36 are devoted to this technique. The expected downtime is between 7 and 15 days, depending on the formula used. The patient will have to wear camouflage make-up to hide any redness, which can last for several weeks or months.

Post-peel cosmetics Chemical peels do not always treat the underlying cause of a skin problem. For example, there can be many causes of acne, and chemical peels do not alter the synthesis of testosterone or the potency of the 5α-reductase that converts testosterone into its active derivative, dihydrotestosterone. Acne may also be partly due to excessive cell cohesion that blocks the sebaceous glands or to an immunodeficiency of genetic origin. Chemical peels do not alter an individual’s genetic make-up. Follow-up care should come after the peel, which is only the first phase of the treatment. Topical anti-acne treatments or cosmetics should be used between and after the peels to improve and prolong results. The same goes for blemishes, melasma and aging. Peels can provide quick cosmetic results, but it is the care between and afterwards that improves and maintains them. This is why the same peel may be indicated for the treatment of acne, which typically affects young patients, as for aging, which affects older patients. In short, we can say that chemical peels regenerate, restructure and stimulate the skin, and that care between and after peels widens their

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indications to problems such as acne, dyschromia and aging.11 There are cosmetic products that have been specially created for application very soon after a peel. They can be used the morning after the first AHA peel, Easy Phytic® or Easy TCA®. With TCA–SAS, Only Touch® or phenol peels, cosmetics usually are not applied until the 8th day after the peel. With Unideep®, an anti-oxidant cream (Renutriv ACE Lipoic Complex®) can be applied two days after the peel.

Treatment for acne Tretinoin should be avoided between and after sequential peels, as it would irritate the skin and increase penetration of the acids during the next peel. Other topical products can be used. Glycolic acid can be applied in low concentrations (8%); it makes the skin softer to the touch. Like retinol, it prevents pores from clogging, helps the pilosebaceous units to drain and stimulates skin turnover. Tocopheryl acetate can be used as an antioxidant to combat the free radicals generated by inflammation. Triclosan12 is antiseptic, anti-inflammatory and antimycotic. Glycyrrhetinic acid is used for its hydrating, antipruritic and anti-allergic properties. It stops patients scratching. Tea tree oil (Melaleuca alternifomlia) is extracted from an Australian shrub and has a similar action to benzoyl peroxide but without its pro-oxidant effects. It is antiseptic (antibacterial: anti-gram-positive and -negative), anti-inflammatory (it can suppress the production of pro-inflammatory mediators), antimycotic (anti-candida and anti-dermatophyte) and even antiviral, acting before and after viral adsorption. Other topical treatments can also be applied: azelaic acid, antibiotic creams, disinfectants, etc.

Treatment for hyperpigmentation Chemical peels are one of the preferred indications for hyperpigmentation. A number of cosmetics can be used between and after peels. Hydroquinone was used for a long time, and still is in many countries. Its cosmetic use, however, is forbidden in Europe. There are many depigmenting derivatives that can be used in its place. Kojic acid can be used pure or as an extract of Aspergillus, and has an antityrosinase and antioxidant action. It even potentializes leukocyte phagocytosis. Glabridin (a licorice extract) inhibits the pigmentation and erythema caused by UV; it is anti-tyrosinase and anti-inflammatory. Liquiritin contains glycyrrhizin and glycyrrhetinic acid (which are antiinflammatory as they inhibit the degradation of endogenous cortisol) and antioxidant flavonoids. Extracts of Morus alba contain arbutin and mulberroside F, which are both tyrosinase inhibitors. Mulberroside F is also an antioxidant. Transcutol® helps build up a reserve of active products near the dermoepidermal junction and improves

Figure 3.5 Blending bleaching cream, contains antityrosinases and antioxidants.

the action of tyrosinase inhibitors (Figure 3.5). AHAs can be used to enhance penetration of active products through the skin. Lactic acid has also been described as having a tyrosinase-inhibiting action. Finally, various vitamins (A, C and E) can be used in the treatment of hyperpigmentation: they are antioxidant and anti-inflammatory, protect against UV damage and stimulate epidermal turnover. The well-known Kligman’s formulas combine the action of tretinoin, a corticosteroid and hydroquinone, but are more irritating than medical cosmetics. The cosmetics used for hyperpigmentation should be applied very soon after the peels (if possible the very next day). If possible they should be applied two or three times a day, before effective sun protection. For more information on topical depigmenting agents, see the section on hyperpigmentation in Chapter 37.

Treatment for aging The author’s cosmetic post-peel treatment for aging skin is simple.

Patients under 40–45 years old The main thrust of the treatment is daily oxidation. In the morning, an antioxidant cream with vitamin E should be applied, and in the evening another anti-oxidant cream: Renutriv ACE Lipoic Complex®. Vit E Antioxidant® is a cream with a relatively complex but complete formulation. It does not contain AHAs, so

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can be applied daily without the risk of interference with the protective function of the corneocytes. It has been specially formulated for use very soon after a chemical peel. Its qualitative formulation is as follows: ■ Biosaccharides: these are polymers of the sugar, fucose. – They have filmogenic properties that induce immediate hydration. – They are slowly metabolized on the surface of the skin, giving a long-term hydrating effect. – They have an anti-inflammatory effect. ■ Ceramides: these are natural components of the skin. – They have an anti-aging action. – They have hydrating and protecting actions. – They encourage skin repair after different types of injury. ■ Vitamin E: this protects against anti-free radicals. The tocopheryl acetate used in this cream is one of the most stable derivatives of vitamin E, and forms a reservoir in the skin after penetration ■ Glycyrrhetinic acid: this is hydrating and anti-allergic; it reduces itching. ■ Natural moisturizing factor (NMF): this comprises amino acids + hexoses + urea + aspartic acid + hexylnicotinate ■ PFPE (perfluoro polymethyl isopropyl ether): this is a filmogenic polymer that protects the skin without any occlusive effect. Renutriv ACE Lipoic Complex® is ideal for dry skin, and can also be applied in the morning. With normal or oily skin, it is better applied in the evening. It does not contain any AHAs, for the reasons explained above. Its qualitative formulation includes the following ingredients: ■ ■ ■ ■

vitamin A: pure encapsulated retinol vitamin C: pure encapsulated ascorbic acid vitamin E: tocopheryl acetate lipoic acid

Lipoic acid exists in different racemic forms. Only the R form is active (Figure 3.6). Lipoic acid is absorbed rapidly both orally and topically. Enzymes in cell cytoplasm convert it into dihydrolipoate (DHLA). DHLA penetrates the cell and mitochondrial membranes easily. It is a mitochondrial cofactor that boosts mitochondrial activity at the

O HO

Figure 3.6 Chemical structure of (R)-lipoic acid.

SH

S

Fe2+

O O

O

S

S

O–

Fe2+

Figure 3.7 Iron chelation by lipoic acid.

same time as protecting against excess production of free radicals. Lipoic acid has the major advantage of being both fat-soluble and water-soluble, which means that it is active at all levels in the cell. It recycles vitamin C, when it is converted into the ascorbyl radical after acquiring a free electron, thus restoring its antioxidant activity. It also recycles vitamin E indirectly. Lipoic acid protects the natural enzymatic antioxidant defenses, such as catalase, coenzyme Q10, glutathione and cysteine. It is an iron, copper, mercury and aluminum chelator (Figure 3.7). It combats excessive secondary cell apoptosis resulting from various stresses.

Patients over 40–45 years old The fight against aging should take into account not only the damage caused by the various sources of cell oxidation but also the fall in hormone levels. For menopausal or postmenopausal women, a standard formula is testosterone propionate 100 mg, estrone 5 mg, estradiol benzoate 5 mg, and water in oil excipient ad 100 g. Extracts of Mexican wild yam (Dioscorea) can also be used, or other estrogen precursors or dehydroepiandrosterone (DHEA).

S H

S

Sagging skin – DMAE One of the common signs of aging is loss of skin elasticity. The skin appears devitalized and slack. One substance that

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A

19

B

Figure 3.8 A tightening effect can be seen after the first application of N,N-dimethylaminoethanol (DMAE) in the form of Skin Tech’s Actilift®: (a) before; (b) after. Photograph by John Jairo Hoyos, Colombia.

is of special interest in the treatment of sagging skin is N,N-dimethylaminoethanol (DMAE) (Figure 3.8). DMAE has been used for several years as a topical application to produce a ‘face-lift’ effect. Even if there is no doubt that it produces a tightening effect on the face, there is no definitive evidence regarding its mode of action. We will see below what type of skin structures respond to DMAE and why it would be difficult to explain this action by an improvement in tension of the striated muscle mass of the face.

Chemistry of DMAE DMAE (also called deanol, dimethylethanolamine and norcholine) is a small hydrophilic molecule. Its low molecular weight (89.1) allows it to penetrate the skin easily. DMAE is a precursor of acetylcholine (ACh), via choline (Figure 3.9). It is a viscous liquid, as transparent as water, that is often said to smell like ammonia but is in fact more reminiscent of fish long past its sell-by-date. Anchovies, sardines and salmon are important natural sources of DMAE. It is naturally present in the body, and there are traces of it in the brain. DMAE is a very basic molecule (pH 11) that cannot be used in its pure state without the risk of causing chemical skin burns. It must be partially neutralized for use at pH 7. Many derivatives have been used in its place (e.g. DMAE bitartrate or acetamidobenzoate), but these are more suitable for oral rather than topical use. DMAE formulations tend to give only the total dosage of the DMAE derivative used, of which pure DMAE is only

(CH3)2NCH2CH2OH DMAE (CH3)3N+CH2CH2OH Choline O > (CH3)3N+CH2CH2OCCH3 Acetylcholine

Figure 3.9 Chemical structures of N,N-dimethylaminoethanol (DMAE), choline and acetylcholine.

part of the weight. For example, 100 mg of DMAE cyclohexylcarboxylate contains only 33 mg of pure DMAE, while 350 mg of DMAE bitartrate contains 130 mg of pure DMAE. The author prefers to use a formulation with DMAE lactate (Skin Tech’s Actilift®) in order to benefit from the properties of an AHA (lactic acid) combined with the DMAE.

Side-effects and precautions The high pH of DMAE means that the pure compound should not be brought into contact with strong acids, mucous membranes or the eyes. Pure DMAE is also incompatible with copper and zinc. DMAE is volatile and should be contained in sealed tubes rather than bottles, to prevent its evaporation. Some cases of allergic dermatitis have been reported after prolonged contact with very high

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concentrations of DMAE, and it should be applied with extreme caution around the eyelids of atopic subjects. DMAE is not considered to be carcinogenic, cocarcinogenic or immunosuppressive. Chronic exposure to concentrated fumes of DMAE in the workplace can cause visual problems.

Toxicity DMAE has mostly been used orally. It is most widely available in 100 mg tablets for the treatment of cognitive disorders associated with senile dementia, at a dose of 600 mg/day. The LD50 for oral administration in rats is 2 g/kg. The LD50 in rabbits after application to the skin is 1.370 mg/kg. For subcutaneous injection in mice, the LD50 is 961 mg/kg. In a human clinical study,13 oral administration of 1600 mg/day showed no side-effects. The doses used in topical applications are nowhere near the theoretical toxicity limit. It takes a twice-daily application of around 30–50 mg of DMAE on the skin to improve skin tension and achieve the ‘lifting’ effect. It is important to remember that a topical application, even if it is very effective, cannot as yet compete with a surgical procedure. DMAE and N,N-dimethylisopropanolamine (DMIPA) solutions are used in high concentrations (45–50%) in industry, especially in the printing industry. They are used in sprays, and a study was conducted on their role in the appearance of intermittent corneal opacity in workers in certain types of printing works.14 The corneal opacities caused blurry vision on the way home from work. These problems were only evident from Mondays to Thursdays, but never at the end of the week. Eye tests revealed the appearance of intermittent and reversible corneal opacity, limited to the part of the cornea in contact with the droplets of vaporized solution and lasting just a few hours. A complete study was undertaken that put the blame on DMIPA but cleared DMAE of involvement. Lowering the concentrations of DMIPA without changing the concentrations of DMAE solved the problem once and for all and produced no visual sequelae. DMAE has also been claimed to be teratogenic. Studies on this subject remain controversial: some have shown that DMAE can be teratogenic in mouse embryos at high doses;15,16 other studies have shown no evidence of toxicity in rodents.17 In my knowledge nothing has been published on teratogenic effects in humans, and no research has shown teratogenicity in humans, despite the wide use of DMAE in industry.

Historical and ‘usual’ use of DMAE Procaine, which is used widely in mesotherapy, is one of the active principles of the well-known (and at times much

O  CO.CH2CH2N(C2H5)2

NH2

Figure 3.10 Chemical structure of procaine.

criticized) Gerovital H3 developed by Dr Ana Aslan of Rumania. Procaine or 2-diethylaminoethyl 4-aminobenzoate hydrochloride (Figure 3.10) was synthesized in 1905 by the German chemist Alfred Einhorn, who called it ‘novocaine’ (from the Latin novus = new, with the added suffix of cocaine, a gold-standard product up until then). Another German, Dr Heinrich Braun, introduced the use of novocaine in medicine. In the body, the ester link of procaine is hydrolyzed, yielding p-aminobenzoic acid (PABA) and N,N-diethylaminoethanol (DEAE), an analog of DMAE. It is PABA (Figure 3.11) that is responsible for the large majority of allergic reactions to ‘procaine’; it is excreted rapidly by the kidneys. PABA is most often used as a sunscreen, but is sometimes called ‘vitamin B-x’, although it is not essential for humans and the body cannot synthesize folate from PABA. According to some authors, the ‘Aslan’ method relies solely on the combined action of PABA and DEAE/DMAE. It is assumed that the action of PABA is due to its anti-free-radical properties. O NH2

C OH

Figure 3.11 Chemical structure of p-aminobenzoic acid (PABA)

Another local anesthetic used in mesotherapy, lidocaine, goes through a different metabolic pathway from procaine, being converted into monoethylglycine, xylididide (MEGX) and acetaldehyde. Its action in this context must therefore have a different basis from that of procaine. As well as having an anti-oxidant19 and anti-inflammatory effect, DMAE taken orally has been claimed to have many properties: an anti-aging effect, improvement of memory and intelligence, increased synthesis of acetylcholine, amelioration of depressive states, improvement in motor coordination, improvement in compulsive, impulsive, hyperactive or antisocial behavior, reduction of chronic fatigue and improvement in the quality of sleep, aid in giving up alcohol and tobacco, reduction of headaches, improved ability to concentrate, improvement in schizophrenia, improved muscle tone, and overall higher energy levels. DMAE can be incorporated into the membrane structure of cells, where its anti-oxidant properties improve

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membrane resistance to the oxidative stress resulting from the release of free radicals from the phospholipid bilayer and the production of eicosanoids associated with skin inflammation. The degradation of cell membranes and subsequent inactivation of the transmembrane proteins and receptors are considered to be the main factors responsible for cell aging. Carbachol (Figure 3.12), and the closely related bethanechol, is a powerful cholinergic agent (used to induce miosis). Its structure is similar to that of choline and its precursor, DMAE. Other muscarinic agents (e.g. pilocarpine), have a completely different chemical structure to choline. O 

(CH3)3N+CH2CH2CNH2

Figure 3.12 Chemical structure of carbachol. Note the similarity between part of the molecule and DMAE and choline.

Topical skin application of DMAE Topical application of DMAE has a visible tightening, firming effect, often called the ‘lifting effect’. This tightening effect can already be felt 20–30 minutes after the product has been applied to the skin, and, when only one side of the face is treated with DMAE, the difference in tension between the two sides is clear. Skin tension continues to improve during the first 6 months of twice-daily application, with individual variations, and remains stable for 4–8 weeks after topical treatment is finished. This would seem to indicate that the product accumulates in the skin and forms a reservoir.

Potential mode(s) of action of DMAE DMAE is a precursor of choline; it also inhibits the metabolism of choline in the tissues. As there is more choline available, the biochemical reactions may tip the balance towards an increase in ACh synthesis. DMAE may stimulate macrophage activity and improve the skin’s defenses. The mode of action of DMAE is not yet fully understood, and its action as a local application even less so. We must therefore put forward several hypotheses in an attempt to understand this tightening effect.

Action on the striated facial muscles Botulinum toxin (BTX), which is used to ‘smooth the skin’, like DMAE, acts on ACh, although its action is the reverse

21

of that of DMAE. BTX relaxes the muscles, whereas DMAE increases muscle tone. Are these two compounds therefore incompatible? It appears not, as they have different targets, and the muscle cells that are deactivated by BTX are not the same as those activated by DMAE. BTX is a large molecule with a high molecular weight, which means that it cannot pass through the skin when applied topically. To achieve a cosmetic result, BTX must be injected directly into the muscle to be paralyzed. BTX has no effect on the epidermis or dermis, as it blocks cholinergic transmission in the neuromuscular junction of the striated muscles and in this way limits the facial expressions that cause expression lines. BTX is picked up immediately, and there is no chance of it diffusing up through the hypodermal fat layer. DMAE, on the other hand, is a very small hydrophilic molecule with a molecular weight of 89.1 that can easily penetrate the epidermis and the dermis but cannot penetrate the hypodermal fatty layer. DMAE cannot act on the striated muscle groups that produce voluntary facial movements, and so cannot counter the effects of BTX. This physiological hypothesis is confirmed clinically when the two treatments are used together. The physicochemical properties of DMAE give this molecule a great affinity for the dermis and epidermis. As the action kinetics of DMAE lead to the hypothesis of a cutaneous ‘reservoir’, this could only be located in the deep epidermal layers, as, if it was in the dermis, this small molecule would soon be eliminated by venous or lymphatic resorption because of its concentration gradient. The way in which they are administered, their targets, their characteristics and their different modes of action do not make BTX and DMAE incompatible: administering one will not alter the effectiveness of the other. There is no established link between age-related sagging skin and muscles and a deficiency in ACh in the muscles. Any action of DMAE on striated facial muscles is thus not only unlikely but also pointless. We must therefore look for other more likely modes of action than muscle stimulation, especially as there have been reports of improvements in tone and younger-looking skin around the eyes and lips after only a few days of treatment. Given that it is accepted that paralysis (or hypotonia) of the muscles by BTX ‘smoothes’ the skin, it would be illogical to claim that stimulating the same muscle groups (with DMAE) can give similar results. We must therefore look elsewhere: in the skin structures that have cholinergic receptors.

Epidermal action Human keratinocytes express cholinergic receptors in the cells of the stratum basale, the stratum spinosum and the stratum granulosum. They use ACh, among other things, to stick together. They also synthesize, store, degrade and release ACh. ACh synthesis has been shown to occur in the perinuclear regions of human keratinocytes due to the presence of

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a choline acetyltransferase (this enzyme converts acetyl coenzyme A into ACh). On the other side of the cell, inside or near the cell membranes, an acetylcholinesterase has been identified. This enzyme degrades ACh in order to prevent a toxic build-up. Keratinocytes can move, which is essential during the second phase of healing, thanks to cytoplasmic myosin and actin: the actin moves in relation to the myosin when the two interact,19 in the same way that an oar stroke moves a kayak or an athlete runs on a treadmill (the athlete representing the myosin and the treadmill the actin). It has recently been shown, by immunohistochemistry, that there are free nerve endings in all of the layers of the epidermis, and it is now suspected that keratinocytes have a neurotropic function. The ACh acts locally, in the epidermis, like a hormone that can also be a ‘messenger’ stimulating the dermis. We can then suppose that an epidermal reservoir of DMAE can interact with the dermis via ACh, of which it is a precursor. DMAE is also assumed to inhibit formation and enhance elimination of lipofuchsin, a waste product of the aging cell metabolism of fatty acids. Experiments have shown that lipofuchsin is eliminated from the liver by DMAE. This build-up, which occurs in all organs, has not been associated with any disorder apart from lentigines. Some authors have reported a gradual reduction in lentigines on the hands with oral DMAE treatment. To date, there have been no studies published on the topical use of DMAE in the treatment of lentigines.

Dermal action DMAE is used for its antioxidant properties, membrane stabilization and inhibition or repair of protein cross-links that clearly play a role in the aging process. It could thus help maintain good-quality collagen and elastin and slow down dermal aging.

that contribute to the overall rejuvenating effect observed when DMAE is applied topically.

Effect on myofilaments and smooth muscle cells Myofilaments make up the endoskeleton of a cell (Figure 3.13). They can be found in the smooth muscle cells (SMCs) and in the cytoplasm of ‘non-muscle’ cells, where they are capable of moving and contracting. SMCs can regulate contraction far more subtly than striated muscle cells. SMCs can shorten to a greater extent than striated muscle cells. Shortening of striated muscle cells is limited to movement within the sarcomere, whereas with SMCs, the myosin filaments can move over a far greater distance, along the network of actin filaments in the cytosol. The force generated by SMCs is less than that generated by striated muscle cells, but can be sustained for much longer. The arrector pili muscle is under adrenergic control and does not respond to a local increase in ACh concentration. The fibroblasts and myofibroblasts are very interesting cells as far as the possibilities of the action of DMAE is concerned. Fibroblasts have cytoplasmic myofilaments that help them move in the dermis when necessary.20 There are different types of fibroblast subpopulations. Some authors maintain that these different subpopulations expand when they are needed through different phenotype expressions, whereas others believe that these subpopulations coexist permanently in the dermis. These two hypotheses are not incompatible. Myofibroblasts (MFBs) are phenotypically modified fibroblasts that have the secretory capacity of fibroblasts, which helps them synthesize strong fibronectin fibers. They express the phenotypic characteristics of ‘nonmuscle’ cells, but with the contractile capacities (of SMCs) that make them responsible for most of the phenomena of fibrotic contraction in the body. The fibronectin fibers syn-

Vasomotor effect The dermal blood vessels are innervated by adrenergic fibers, which cause vasoconstriction, and cholinergic fibers, which cause vasodilation. DMAE, as a precursor of ACh, could cause vasodilation that is clinically undetectable but sufficient to produce temporary edema, a build-up of water in the hydrophilic structures of the dermis, and, as a result, a tightening of the skin. This hypothesis only partly explains the particular kinetics of topical DMAE. The fact that treating one side of the face only shows improvement on one side only suggests that the DMAE has a purely local action and is not converted into ACh throughout the organism. Local blood flow, which decreases with age, is vital for the nutrition and defense of the dermis and epidermis. Constant slight vasodilation would thus improve skin perfusion – especially in smokers – and by diffusion would bring in more of the elements

Network tightened with actin microfibrils

Direction of displacement ‘Stress’ contractile fibers + Microtubule

+ Cellular center Nucleus

Radial network with actin microfibrils

+ +

+

+ + Dense bodies

+

+

+

Loose network with actin microfibrils in all cytosol

Figure 3.13 Different types of organization of actin microfibrils (MF) and microtubules (MT) in a moving cell – organized polarization of the MF and the MT.

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thesized by the MFBs serve as a support for them to ‘pull’ on during contraction, which helps the wound to close by as much as 40%. MFBs synthesize far more actin fibers than ‘standard’ fibroblasts, and also have myosin fibers that, when interacting with actin, constitute the contractile motor activity of MFBs. MFBs are found in healing tissue, of which they form 40% of the total number of fibroblasts present. A large number of MFBs are also found in the periprosthetic capsule of encapsulated breast implants, while there is no evidence of MFBs if no capsule has formed around the prosthesis. In pathology, abnormal quantities of MFBs are found in diseases such as pulmonary fibrosis and Crohn’s disease. Many SMCs respond to a kind of paracrine stimulation, where the mediator is released into the environment of the target cells and diffuses towards the cell, where it interacts with a membrane receptor. MFBs are not linked to any synapse, which would make it impossible for them to move, but the exposure of MFBs to certain mediators causes significant contraction, comparable to that in SMCs. We can imagine the contractile potential of these SMCs when we recall that the nipples, as well as the scrotum, have many contractile cells of this type that are sensitive to different stimuli. The difference is that the contraction of MFBs during wound healing is irreversible. Fibroblasts and MFBs, like many SMCs, have numerous receptors on their surface for different mediators: ACh, adrenaline (epinephrine), noradrenaline (norepinephrine), oxytocin, vasopressin, histamine, angiotensin II and prostaglandins. As ACh is a small water-soluble molecule, its membrane receptor can be a ligand-gated ion channel receptor or can be coupled with the heterotrimeric G proteins (RCPGs) that control the activity of a target protein, which can be an enzyme or an ion channel. Opening and closing of the ion channels causes polarization or depolarization of the myofilaments, and the SMCs (e.g. endothelial cells) contract or dilate. The G protein acts as a transducer. As ACh is a small ligand, the N-terminus of the G protein in the extracellular environment will be small. The presence of a larger quantity of ACh in the pericellular environment of the MFBs could then stimulate certain membrane receptors more strongly and increase their contractile potential. DMAE, a precursor of ACh, might then stimulate the contraction of MFBs. However there must be a reactivity threshold for MFBs to ACh, to guard against unnecessary contraction of these cells and the formation of pathological fibroses. The hypothesis put forward here is that a slight increase in the extracellular concentration of ACh (by conversion from DMAE) could slightly stimulate the contraction of the fibroblasts and do so reversibly, without fibrosis setting in, as, clinically, the effect of a topical application of DMAE is reversible 4–8 weeks after treatment has stopped. This improved tone, the reversible contraction of the fibroblasts, could explain the clinical kinetics of DMAE in a topical application.

23

Exocrine glands The sweat glands have cholinergic innervation.21 The eccrine sweat glands, which open directly onto the skin, have denser autonomous innervation than the apocrine sweat glands associated with pilosebaceous units. ACh is the active neurotransmitter at this level, and the response of the sweat gland will depend on the dose of ACh that stimulates it. The myoepithelial cells contract in response to the ACh. In strong doses,22 the muscarinic receptors are stimulated, and the gland reacts by producing large drops of sweat. At lower concentrations,23 the nicotinic receptor is stimulated, and the gland will react by producing tiny droplets of sweat. The possible increase in ACh caused by the application of DMAE cannot, of course, stimulate the muscarinic receptors, and no profuse sweating has been noted after application of DMAE. On the other hand, a slight increase in the concentration of dermal ACh could stimulate the sweat glands’ nicotinic receptors – in a paracrine manner – and increase hydration of the stratum corneum, making the skin more ‘supple’ and resistant. The sweat glands themselves are controlled by circulating hormones and are not under cholinergic control. DMAE will not alter their function.

Conclusions DMAE is a precursor of ACh, a neuromediator that is important to the skin. Keratinocytes, as well as fibroblasts, myofibroblasts, sweat glands and endothelial cells, have receptors that respond to ACh. They are not stimulated pre- or post-synaptically but by paracrine diffusion, which can activate specific membrane receptors. The hypothesis is that DMAE in a topical application cannot stimulate the striated muscle fibers, to which it has no access. Furthermore, muscle sagging associated with aging is not caused by a deficiency in ACh. The tightening effect of DMAE may result from cholinergic stimulation of the membrane receptors of (myo)fibroblasts and stimulate the gradual contraction of the myofilaments in their cytosol. DMAE also has anti-free-radical and anti-lipofuchsin activities and repairs protein (collagen and elastin) cross-linking. The mode of action of topical DMAE could therefore stem from a combination of effects working together at different levels: tension of the ‘non-muscle’ dermal cells, keratinocyte cohesion and movement, hydration and suppleness of the stratum corneum, improved skin nourishment and defense, antioxidant, and skin tone evener. As a result, it is very effective at improving skin tone and firmness.

Summary of the main cosmeceuticals used post peel See Table 3.1 for a list of post-peel cosmeceuticals according to skin type, together with their times of application.

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Table 3.1 Main cosmeceuticals used post peel Skin type

Daily care product

When and how often to apply

Sagging skin

Dimethylaminoethanol (DMEA): Actilift® face cream or Actilift® body lotion (Figure 3.14)

Morning and evening

Patients under 40–45: skin aging

Vit E Antioxidant®

Morning

Lentigines

Re-Nutriv ACE Lipoic Complex®

Evening

Patients over 40–45: skin aging

DHEA–PHYTO®

Morning

Lentigines

Re-Nutriv ACE Lipoic Complex®

Evening

Acne

Purifying cream or gel Purifying cream or gel

Morning (all over) Evening (only on the lesions)

Hyperpigmentation (melasma–lentigines) (Avoid exposure to sun: Melablock® HSP 50+ at 9 AM, 11 AM, 2 PM; serious cases: 3–4 times a day)

Blending Bleaching® cream

Morning (all over)

Blending Bleaching® cream

Evening (only on the lesions)

Dry skin

Vit E Antioxidant®

Morning, midday, evening

Post-peel sun protection

Melablock HSP® 50+

Every 3 hours

Everyday sun protection

Melablock HSP® 25+

Every 3 hours

Trolamine Trolamine (triethanolamine salicylate, TEAS) is a salicylate derivative, which is also known as ‘topical aspirin’. It is an amino alcohol that is used for its topical analgesic and antiinflammatory properties. Like the better-known salicylate derivative, methyl salicylate – which has a rubefacient action used to good effect in sports injuries and rheumatism – TEAS is rapidly absorbed through normal skin after topical application. It is used widely for treating sunburn.

of mild erythema, while a superficial second-degree burn consists of painful blisters but does not reach the dermis. Medical advice is essential before applying the product to a second-degree burn.

Mode of action and absorption Various studies show that salicylate derivatives act as much through direct local diffusion as through absorption by the dermal blood vessels and redistribution of salicylates in the whole body. The blood level of salicylates increases in direct proportion to the quantity applied, the resorption surface and the number of topical applications. A large amount of salicylates can be absorbed through the skin. When TEAS is applied unilaterally on one limb, the concentration of salicylates has been found to be identical in the corresponding tissues of the contralateral limb. This supports the theory of action by redistribution through the blood. The use of radiolabeled TEAS also shows renal and fecal elimination. Phonophoresis helps salicylates penetrate further into the skin.

How to apply trolamine Salicylate derivatives, especially trolamine, are applied to first- and second-degree burns. A first-degree burn consists

Figure 3.14 Actilift® cream with pure DMAE. There is a face cream and body lotion.

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Post-peel care

Precautions Trolamine must not be applied in cases of infection: salicylates can accelerate the penetration of microbes into the skin and aggravate any pre-existing infection. It has been shown to cause local skin irritation and scabs to form on the areas to which it has been applied. Skin irritation increases the more it is applied. In smaller quantities, repeated application only induces epidermal hyperplasia. Some authors consider TEAS to be a potential cytotoxic agent. It is a potential skin irritant that makes the skin sensitive and can cause contact allergies. Trolamine is a salicylate derivative, and salicylic acid is a keratolytic agent that dissolves the intercorneocyte amorphous matrix and impairs the barrier function of the stratum corneum. Symptoms of salicylism can appear with chemical peels when large amounts of salicylate derivatives are applied on the skin, on large surface areas or repeatedly, causing a high blood level of salicylates. In cases of toxic levels of salicylate in the blood, an increase in oxygen consumption causes hyperthermia by the uncoupling of oxidative phosphorylation. Trolamine should therefore not be used during the immediate post peel period.

Tips for the care of sensitive skin ■ Prolonged use of creams containing more than 8–10% of AHAs can make some skins more sensitive by reducing the thickness of the stratum corneum for long periods. ■ Use cleansing milks, lotions or mineral water sprays to wash. ■ Do not let water dry on the skin; when it evaporates, it soon dries the skin out. Damp skin should be dried with a soft cloth or paper tissues. ■ Avoid exfoliating scrubs, repeated micropeels and creams containing microcrystals on sensitive skins. Do not use any masks that might dry out the skin. ■ Do not use aggressive soaps. ■ Tretinoin (vitamin A acid) makes the skin more sensitive. One Easy TCA® peel per week for 4 weeks can restructure the skin and eliminate any abnormal sensitivity. In this indication, the cosmeceuticals that can be combined with it are restricted to Vit E Antioxidant® cream in the morning and the more nourishing Renutriv ACE Lipoic Complex® cream in the evening.

Characteristics of ‘normal skin’ Normal skin should be:

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■ Firm: contain a sufficient quantity of elastin and collagen ■ Soft: compact stratum corneum protected by skin lipids ■ Hydrated and unwrinkled: hydrated keratinocytes and dermis ■ High in color: active microcirculation; pink color visible through the skin ■ Resistant to external aggression: active protective function •■ Unscarred: no stellate or secondary scars

Notes 1. Even though this type of sunscreen can protect the skin against free radicals some could also cause post-inflammatory hyperpigmentation. 2. SPF 50+ protects the skin against 98% of UV, while SPF 25+ protects against about 96% of UV. 3. A typical example of this is seen when cooking an egg white as it goes from transparent to white as a result of structural modification of the proteins under the effect of heat. 4. By polymerase chain reaction (PCR). 5. Occlusion consists in applyng an impermeable plastic film. 6. In the case of sagging skin, Actilift® face or body can be applied as appropriate. 7. Example of mesolift mixture: 2.5 cm3 non-cross-linked 2% hyaluronic acid + 2.5 cm3 organic silicium + 2 cm3 vitamin C + 2 cc of NA-nocleinate + 1 cm3 lidocaine. 8. Unna’s paste (see Chapter 24). 9. Molecules similar to tyrosine are used: e.g. Tyrosilane C®. 10. Summary of Easy TCA® ‘basic protocol’: no pre-peel treatment, application of the solution until scattered pinpoint or cloudy white frosting appears, application of the post-peel cream (tyrosinase inhibiting, anti-oxidant, stimulating). Repeat this process four times at weekly intervals. 11. This paragraph particularly concerns superficial peels or peels to the ‘Grenz zone’. Papillary dermal peels are not really indicated in cases of active acne. 12. Triclosan can be used as it is or encapsulated in cyclodextrins. 13. Casey DE, Denney D, Dimethylaminoethanol in tardive dyskinesia. N Engl J Med 1974; 291: 797. 14. NIOSH Publications Office. Health Hazard Evaluation Report 2002-03 79-2901 Superior Label Systems. May 2003; Cincinnati; Ohio. 15. Fisher MC, Zeisel SH, Mar MH, Sadler TW. Inhibitors of choline uptake and metabolism cause developmental abnormalities in neurulating mouse embryos. Teratology 2001; 64: 114–24. 16. Fisher MC, Zeisel SH, Mar MH, Sadler TW. Perturbations in choline metabolism cause neural tube defects in mouse embryos in vitro. FASEB J 2002; 12: 619–21. 17. Leung HW, Tyl RW, Ballantyne B, Klonne DR. Developmental toxicity study in Fischer 344 rats by whole-body exposure to N,N-dimethylethanolamine vapor. J Appl Toxicol 1996; 16: 533–8. 18. The antioxidant effect of DMAE has been shown by electron spin resonance (ESR) for the hydroxyl radical. It does not seem to have any anti-superoxide action.

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19. There are different types of myosin for different types of movement; cell movements (myosin II) are not facilitated by the same myosin that permits endocytosis (myosin VI) or the movement of vesicles between cells (Myosin V). 20. For example, movement along the fibrin/fibronectin fibers during the healing process.

21. Catecholamines, vasoactive intestinal peptide and natriuretic peptide have also been detected near the sweat glands. 22. Intradermal injection of 0.1 mg of ACh: postganglionic cholinergic stimulation (Biology of the Skin: 58). 23. Hurley HJ. The eccrine sweat glands: structure and function. In: The Biology of the Skin, Parthenon Publishing, Lancaster 2001; 47–76.

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4 Factors influencing chemical peels

Allergies These are common when using antibiotic creams or ointments in the post-peel period: between 5% and 10% of allergies should be expected when using antibiotic creams containing neomycin after a peel. The temporary thinning of the stratum corneum allows products applied on the skin after peels to penetrate more easily, which promotes the development of contact allergies.

Infections These are more common when patients have to undertake complex post-peel care themselves. The basic principles of sterility are not widely known by the public and require special training in order to be effective. The more patients have to take part in the post-peel care, the higher the risk of infection.

Pulling off small scabs This often leads to infection, prolonged erythema and even scarring. The less patients touch their skin, the better!

The sun It should be remembered that direct exposure to the sun for 10 minutes is enough to trigger pigmentary changes in sensitive individuals during the post-peel period. See the section on effective sun protection in Chapter 3.

line® immediately improves the pruritus and the feeling of tightness in the skin after a medium or deep peel. Sterile white Vaseline® is an excellent topical ointment that can be applied to the treated areas in the first few days after a medium peel or after removing the healing mask (after the 8th day) following a phenol peel. Only a thin layer need be applied to avoid itching caused by the drying out of surface keratinocytes that have not yet differentiated into corneocytes. The Vaseline® creates an impermeable layer on the surface of the skin and prevents the water in the epidermis from evaporating. The water accumulates under the layer of Vaseline® and provides instant natural hydration that soon relieves the itching caused by the keratinocytes drying out.

Influence of age post peel Older patients Intraepidermal and dermal peels are performed as usual even on patients aged 80 or over. With elderly people, there seem to be fewer pigmentary changes, but the theoretical risk of infection is higher. In theory, the weakened capacities of the keratinocytes to regenerate, the presence of numerous cell abnormalities, dormant fibroblasts and underlying vascular sclerosis should slow down healing after a peel in older people. In practice, the only real problem is increased susceptibility to infection resulting from a weakened immune system. A more important factor seems to be the degree of skin photoaging rather than age itself. Many phenol peels have been performed on patients who are well into their 80s, without any particular problems.

Young patients Dehydration of the skin after a peel Drying and flaking skin causes an irresistible urge to scratch and therefore a risk of complications (including secondary infections, inflammation and scars). Applying white Vase-

At the other end of the scale, what is the minimum age for having a chemical peel? The answer is simple: in the majority of cases, a peel is only necessary for young patients if they have acne. Acne responds extremely well to intraepidermal peels or peels to the basal layer of the epidermis. Deeper peels are not recommended when the skin is infected. Very young patients benefit from relatively superficial techniques

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with a high safety level (Easy Phytic®). The presence of acne means that the young patient’s developing hormone system has created an adult skin – thick and oily and resistant to acids.

Use of corticosteroids Topical corticosteroids These are only indicated in cases of serious edema or pruritus during the first few days after an aggressive peel. It is always best to start with a short-acting corticosteroid (hydrocortisone or betamethasone). A cortisone-based cream can be used during the first few days after a peel to reduce excessive edema or pruritus. The deeper the peel, the greater is the need for emollients. Hydration after a peel is vital (except after a peel with Unna’s paste); the hydrating cream should contain no alcohol or perfumes.

Oral corticosteroids These are very rarely indicated in combination with peels, and then only in the case of very specific problems (see Chapter 37).

Intravenous corticosteroids These can be used before a deep peel to limit edema immediately after the peel and avoid any allergic or laryngeal reactions.1 They reduce post-peel inflammation, which is in fact necessary to initiate the skin repair processes. If the degree of inflammation is reduced, there is a risk of slowing down the first stages of skin regeneration.

Understanding the healing process Understanding the skin healing process after a peel allows evaluation of the risks of scarring, infection and dyschromia. For more information on how the skin heals in relation to the depth of the peel and on risk evaluation, see the section on scars in Chapter 37. Histologically, the skin healing process follows a precise sequence of different stages. The process starts almost immediately: neutrophils enter the treated area as soon as the peel has been applied, and stay there for 3–5 days. Macrophages are present from the 3rd to the 10th day and lymphocytes from the 6th or 7th day. Re-epithelialization starts just 24 hours after the peel and first manifests as a centripetal migration of keratinocytes, followed by rapid cell proliferation. After the re-epithelialization phase, dermal collagen is regenerated over a 2- to 3-month period. Assessing the final results of a peel calls for patience.

How quickly the skin regenerates after a medium peel depends on the concentration of pilosebaceous units (PSUs) in the treated area: the face has many PSUs, and the nose and forehead have more than the cheeks and temples. Statistically, the cheeks and temples prove more sensitive to scarring. The dermis of the eyelids is thinner but denser than the rest of the face, and the dermoepidermal junction is flatter. The skin on the back of the hand has few PSUs and little subcutaneous fat. Atrophy develops there fairly rapidly. The skin on the back is very thick, and its dermis is dense in collagen. Nevertheless, it has fewer PSUs than the face, and the risk of developing post-peel scars there is higher. The dermis of badly sun-damaged skin has a depleted cell population, and is thin and slower at detoxifying acids. The effect of the acids is therefore increased, and peels on sun-aged skin are more dangerous than on young, well-hydrated skin. Moreover, skin with actinic damage has fewer appendages (PSUs), and tends to regenerate more slowly. Healing is slower when a wound is left to heal in the open air than when the wound is covered. This does not matter much for intraepidermal peels, but is more important when dealing with medium or deep peels. One advantage that peels have over laser treatments is that they leave a layer of dead, but protective, skin in place, and this enhances re-epithelialization. The strips of skin that remain after a peel should be left alone, as they protect the regenerating skin. Lasers, on the other hand, gradually vaporize the layers of skin to be removed, and the skin is left to heal uncovered. The colloid dressings available on the market (e.g. Convatec, Omniderm, Vigilon) allow better-quality healing, in a moist environment, after laser treatment. The problem with occlusive dressings is that there is an increased risk of infection, and they need to be monitored carefully, as bacteria are known to proliferate much more quickly under an occlusive dressing than in the open air. As bacterial proliferation increases under occlusive dressings and as the skin’s immune defenses are reduced after a deep peel, it is often preferable for the skin to heal ‘under a scab’. To do this, a mask of bismuth subgallate should be used (Figure 4.1, and see Chapter 35).

Preparing the skin This is worthwhile when the patient is willing and when it is carried out under medical supervision. Unsupervised or secret use of aggressive products by the patient can sometimes cause problems for the doctor who has not been informed of the patient’s self-administered treatment. The doctor should watch out for unacknowledged use of tretinoin or other retinoids, concentrated glycolic acid, benzoyl peroxide, or any other product that increases penetration of the acids, making them penetrate more quickly and deeply than originally intended. Some patients can

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The fact that in most cases they cannot use camouflage make-up makes it difficult to carry out a local or full phenol peel. Moreover, phenol peels produce less spectacular results on thick skins than on thin skins. Shaving does not pose a problem, as a peel to the basal layer of the epidermis does not rule out shaving, even with a blade. For a peel to the papillary or reticular dermis, it is best not to shave while the skin is flaking. It is usually possible to shave after the 8th day. Alcohol-based aftershaves should be avoided, and a hydrating, anti-oxidant or firming cream should be used instead, followed by effective sun protection.

Make-up Figure 4.1 After a phenol peel the crust of bismuth subgallate appears dry but actually helps healing in a moist environment.

turn up with their skin thoroughly scrubbed (with an abrasive sponge or creams), wanting to impress the doctor with skin that is nice and clean, but also hyperpermeable and dangerous.

Skin color This must be taken into account when choosing a peel: Fitzpatrick skin phototypes I–III can tolerate any kind of peel. Patients of type IV with light-colored eyes have fewer problems with dyschromia after a peel than dark-eyed patients of the same type. Type V and VI patients are at most risk with peels, and it is recommended not to go beyond the papillary dermis with these patients to avoid hypochromia. Type V patients are also quick to develop hyperpigmentation. Special care should be taken with patients who have prolonged hyperpigmentation with mosquito bites or small wounds. Localized phenol peels should only be carried out on patients with a skin phototype lower than IV, so that the area treated with phenol is not left lighter than the surrounding skin, even if it has been treated with a medium peel to even out the color. The same applies to patients with many freckles, which mostly disappear after a peel to the papillary dermis.

Patients often ask about make-up. The general principle is that it is possible to wear make-up, even when the skin is flaking, after an epidermal peel or a peel to the basal layer, but it is unlikely to look good. After a peel to the papillary or reticular dermis, make-up is usually allowed, and even recommended, on the 8th day. Patients who do not like wearing make-up should be warned of the likelihood of post-peel erythema, depending on the depth of the treatment. Some patients are thus ruled out, as their professional lives do not allow any visible erythema or they cannot stand the idea of wearing make-up. In these cases, it is recommended to repeat an Easy TCA® peel four times rather than use Unideep®.2

Smoking and peels It is generally accepted that the free radicals produced each time smoke is inhaled contributes to the overall aging of the body and of the skin in particular. Publications that show the difference in skin quality between two twins, one of whom is a smoker and the other not, speak for themselves, so marked is the deterioration of the smoker’s skin. Smoking causes repeated vasoconstriction and chronic microvascular damage, which contribute to the overall impoverishment and aging of the skin. There are no major problems, however, with heavy smokers who have peels to the papillary dermis. Full-face phenol peels should be carried out with caution because of the increased risk of laryngeal edema. A localized phenol peel does not pose this kind of problem, and phenol can, for example, be applied around the edges of the mouth (which is usually very damaged in smokers), while the rest of the face is treated with a trichloroacetic acid peel to the papillary dermis.

Chemical peels for men There is an increasing demand from men for basic treatments. Their skin is thicker, and results are not as good as for women. On the other hand, as men have more PSUs, they heal more quickly and pose fewer risks of scarring.

Mental retardation and peels The more severe the retardation, the more superficial the peel should be. The same applies to hypersensitive patients.

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Nutrition and peels The patient’s nutritional condition at the time of a peel is an important factor in the treatment. For all the phases of healing to take place correctly, a perfect balance of nutrition and micronutrition is necessary. It is clear that poor nutritional balance will have more impact on healing after a deep peel than after a light peel – all the more so as deep peels, rather than light peels, are usually intended for older people. Many proteins are synthesized during healing after an intraepidermal peel: many amino acids are needed to form the provisional matrix as well as to synthesize new collagen. Catabolic patients, or patients who have recently had significant, involuntary weight loss, do not have sufficient protein reserves for the skin to regenerate properly. A dermal peel also induces stress, which causes a hypercatabolic state that is more or less acute depending on the depth of the peel. Patients with insulin-dependent diabetes or patients who have recently undergone significant trauma or surgery, who have liver or kidney deficiencies, or who suffer from chronic inflammation are not the best candidates for dermal peels, as the need for protein increases sharply. The average daily protein requirement is 1.5 g/kg per day. The amino acids considered most essential include arginine and glutamine. However, to date, it has not been proved that supplements improve the quality of wound healing. Arginine is a precursor of proline and collagen, and the recommended dose is between 15–25 g/day. It acts as a local stimulant of lymphocytes and a general stimulant of human growth hormone (HGH) and insulin-like growth factor I (IGF-I) production. Glutamine also stimulates the production of HGH, and is an anti-oxidant and an energy source for fibroblasts, keratinocytes, lymphocytes and macrophages. A daily intake of 10–30 g/day is recommended.

Carbohydrates and fatty acids are also necessary for rapid and good-quality skin regeneration. The extracellular matrix is made up of glycosaminoglycans and proteoglycans, which are polysaccharides linked to proteins. Omega6 fatty acids are essential for cell membrane formation. Supplements of linoleic and linolenic acid can be recommended when the patient’s blood is not properly balanced.3 Numerous trace elements are necessary for many enzymes to function properly: copper is needed for the formation of the collagen network and the anti-oxidant action of superoxide dismutase; iron is needed for collagen synthesis; zinc is a cofactor for DNA and RNA polymerases, plays a part in protein synthesis and stimulates cell division. Vitamins also play a role in the healing process. Vitamin A is involved in angiogenesis and keratinocyte differentiation, stimulates collagen synthesis, and enhances intercellular adhesion and skin immunity. Vitamin E can be used as a lipophilic antioxidant. Vitamin C is necessary for collagen synthesis, and for stabilizing the collagen triple helix. Between 500 and 1000 mg/day can be given before and after an intradermal peel.

Notes 1. 2.

3.

Preventing laryngeal edema in smokers undergoing a phenol peel. Unideep® (Skin Tech) TCA peel: to the papillary dermis, with a qualitative formulation based on Easy TCA®, but with a more concentrated solution and post-peel cream. The Roman Pais laboratory in Nivelles, Belgium, provides – among other nutritional and micronutritional tests – a very precise and scientifically annotated blood count of circulating fatty acids.

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5 Choosing the right peel

The possibilities for treatment with chemical peels are many and varied and depend on the agent chosen as much as on the way in which it is used. We can, of course, take the narrow view of peels as the destruction of damaged tissue with acid.1 From this perspective, a result can only be achieved by ‘destroying beneath the lesion’. This is, of course, often the case, but we must not forget that chemical peels help to stimulate as much as destroy. Many of their positive effects are largely due to this stimulation. Let us take glycolic acid, for example, whose action is mainly intraepidermal2 but which is associated with activation of the papillary dermal fibroblasts. The destructive effect, which removes the stratum corneum and even part of the epidermis (depending on the concentration used), improves the appearance of rough skin, while the effects of remote stimulation improve the extracellular matrix constituents secreted by the fibroblasts. Choosing the right peel is often a source of stress for a doctor who is starting his career in peeling: opting for a technique that is too superficial will satisfy neither patient nor doctor, while using a medium-strength product could cause unexpected side-effects that can be hard to cope with, especially if the results are mediocre. Deep peels have their own particular indications and their own particular risks. Sometimes, only a deep peel can solve a cosmetic problem, but the level of complexity and danger of such peels means that they are often rejected by beginners, who will instead attempt to push the limits of a peel and do a medium peel with an agent that is intended to be superficial. They will often pay for the consequences in cash. When choosing a peel, a simple equation should be taken into account: the results expected from the peel must be greater than the sum of the fear of the treatment’s complexity, the risk of complications, and the downtime and financial cost for the patient. The ratio [Results/(complexity + complications + downtime + cost)] must always be positive. During the preliminary consultation, the doctor should first discuss downtime and treatment cost with the patient, who always expects breathtaking results. It is easier to deal with these two factors first before embarking on the complexity of the technique and the potential risks and

complications. In this way, the treatment can quickly be oriented to what the patient is prepared to go through. If patients say straight off that they cannot accept any downtime or have limited funds, it is pointless wasting their time, which is as precious as yours, explaining unnecessary technical details about deep peels.

A few logical rules make it easier to choose ■ Sagging skin only responds to a phenol peel and only if the skin is relatively thin. Peels are not indicated for sagging in thick skins or for nasolabial folds. Chemical peels cannot compete with surgical face-lifts; they cannot stretch the skin as well as the latter do. ■ The neck does not respond well to chemical peels. Results are often disappointing. ■ Expression wrinkles benefit from treatment with botulinum toxin prior to any peel; it allows the skin to regenerate on a non-moving base. ■ Photoaging and free-radical aging from smoking and pollution can be treated with a peel; the speed and quality of the results depend on the depth of the treatment. ■ Active acne should only be treated by a medium peel after it has been treated medically and the infection has cleared up;3 it can, however, be treated by lighter peels even during the active infectious phase. ■ Facial acne scars are difficult to treat, sometimes even with phenol. Acne scars on the back, décolletage or face can fade or improve with a combined technique of chemical peeling and dermabrasion. It is still difficult, however, to get rid of them completely. ■ Results of the treatment of hyperpigmentation disorders depend entirely on the depth of the problem and the depth of the treatment. They are frequently treated with peels that reach or go beyond the Grenz zone, in conjunction with appropriate daily care. The only way to treat melasma permanently is by completely destroying the cells that produce melanin, by peeling ‘beneath the

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lesion’ with an agent that is toxic to melanocytes, which is a fairly aggressive treatment. Another option is to treat the skin more superficially in order to reduce the risk of complications. Only a certain proportion of melanocytes are destroyed in order to lighten the melasma at the same time as stimulating keratinocyte turnover. The relative increase in the number of keratinocytes compared with the number of melanocytes dilutes the melanin produced in the epidermal cells (the blending effect). Melanogenesis is reduced with tyrosinase inhibitors and antioxidants, which are applied in the long term and combined with effective sun protection (bleaching effect). Solar or senile lentigines respond partially to peels to the Grenz zone and the papillary dermis. They sometimes require a peel to the reticular dermis to get rid of them completely. This deep peeling can be local. Stretch marks can only be treated definitively by applying aggressive treatments that can improve the epidermal and dermal atrophy that accompanies them. Peels are not indicated for hypertrophic scars. Some fine facial scars (from a face-lift, for example) improve vastly after local application of some phenol peels; others are improved by a combination of abrasion and peeling. Body peels produce fewer results and more problems that facial peels. Peels on the backs of the hands are very easy and cause few complications with trichloroacetic acid in the form of Easy TCA®.

Nothing speaks louder than pictures when it comes to chemical peels: we will look at different clinical cases to discuss the choice of an appropriate peel.

Start of photoaging The patient shown in Figure 5.1, who is approaching 40, has a few lentigines and a thick and oily skin with dilated pores. There are no wrinkles, but a slight sagging of the skin that is only noticeable in a standing position. A deep peel would not be the best way to treat this patient, as the ratio of results to complexity + complications + downtime + cost would not be favorable. The possibility of a medium peel to the papillary dermis could be discussed, if the patient wanted fairly quick results or if she did not have enough time for a series of lighter peels. She could also be advised to have a series of peels, either intraepidermal (to remove the epidermis) or down to the basal layer, combined with appropriate daily care. Another possibility would be one alpha-hydroxy acid (AHA) peel per week for 6–10 weeks or one Easy TCA® (pinpoint frosting) per week for 4 weeks. The daily care routine should include DMAE4 to firm the skin, tyrosinase inhibitors and antioxidants to limit melanin production,5

Figure 5.1 Stimulating superficial peels and appropriate daily care are indicated for this patient.

and, of course, effective sun protection. If the lentigines do not clear quickly, they should be treated locally with a single careful application of Only Touch®, immediately before the last of the four Easy TCA® peels.

Under-eye bags Many patients want to get rid of or improve under-eye bags (Figure 5.2) that leave them looking permanently tired. This is a purely surgical problem, although it has been suggested that local injections of phosphatidycholine would dissolve the fat, but this treatment can be very risky.6 Peels and cosmetic products cannot improve them. In some circumstances, a phenol peel can improve bluish circles under the eyes if it succeeds in making the thin skin in this area thicker. The best treatment is to remove the weak veins of the inner and outer canthus with a Müller hook, followed by treatment with blue laser light.7

Figure 5.2 A peel is not an indication for under-eye bags.

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Sagging skin Apart from an improvement in overall skin quality and tone, the patient shown in Figure 5.3 will not benefit from any peeling technique – either repeated superficial peels or a deep phenol peel. Actinic damage is light and there are not many lines or wrinkles. On the other hand, the folds of sagging skin are very marked in this patient, who is a heavy smoker. Examination and palpation show that the dermis has emptied of its ground substance and atrophied. The daily care routine should combine powerful antioxidants,8 DMAE and possibly DHEA. This patient refused to have any surgical treatment, and was treated with a phenol peel in an attempt to get the skin to retract. Unfortunately, on a dermal base totally emptied of ground substance, this treatment resulted in an ‘accordion effect’.9 This patient would only benefit cosmetically from a surgical face-lift, possibly followed by peels to the Grenz zone to improve the quality of the skin. The patient in Figure 5.4, on the other hand, received much benefit from the stimulating and evening effect of Easy Phytic® on the epidermis and dermis.

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The skin tension is better and the yellow discoloration caused by actinic damage has been reduced. The daily care routine also consists here in Actilift® (DMAE cream) and DHEA-Phyto®: see Chapters 2 and 3 for more information on these two products. When retightening is indicated, Easy Phytic® can be applied in a single layer every morning for several days, depending on how the skin reacts. The results are surprisingly quick, and the skin soon tightens visibly (see Chapter 11).

Comedonal acne Comedonal acne (Figure 5.5) can be treated with an intraepidermal peel or a peel to the basal layer. A trichloroacetic acid (TCA) peel to the papillary or reticular dermis could be considered, but such a deep treatment would be pointless for this type of disorder, which can be treated with a lighter peel and, in any case, requires longterm maintenance treatment. It is essential to ‘clean’ the skin beforehand with a comedone extractor to limit damage to the skin; the skin should be cleaned in this way a week before an alpha-hydroxy acid (AHA) peel10 or immediately before each of four Easy TCA® peels. Removing the comedones helps produce quicker results and prevents post-peel infections.

Macrocomedones (1–2 mm in diameter) These can be treated locally with Only Touch®, a solution with a high concentration of saponified and stabilized TCA.

Figure 5.3 General sagging of the skin with little actinic damage: this is not a good indication for a peel.

Figure 5.4 (a, b) A moderate improvement in sagging skin can sometimes be achieved by applying superficial peels: here, after three Easy Phytic® peels.

Figure 5.5 Comedonal acne.

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Either the applicator provided with the product or the point of a 30G1/2 needle should be used to limit the action precisely to the head of the comedone. In 95% of cases, comedolysis is achieved. Very large macrocomedones (>2 mm in diameter) can benefit from careful infiltration of Easy TCA® or Easy Phytic® solution into the center of the comedone. Post-peel care, which is very important, consists in avoiding comedogenic cosmetics, having the skin cleansed professionally once a month, and applying an antiacne cream containing AHAs, tretinoin or precursors, disinfectants, anti-inflammatories, tea-tree oil, etc.11 once or twice a day. For details of this treatment, see Chapter 15.

Photoaging

The patient shown in Figure 5.6(a) has numerous treatments to choose from. She does, however, have an important restriction to take into account: downtime must be minimal and the overall cost low. Resorcinol, TCA to the papillary dermis and phenol are all automatically ruled out. However, a relatively strong acid is needed to treat the lentigines that can be seen at the top of Figure 5.6(a). For this, Only Touch® can be used, applied locally and precisely on the lentigines, with Easy TCA® being applied on the rest of the face to treat the dyschromia, superficial lentigines, photoaging and acne and to even out the result. See Chapter 15 for details on applying this product. Daily post-peel care should consist of an anti-acne cream and a blending and bleaching cream to even skin tone. Figure 5.6(b) shows the lentigines clearing up, an improvement in the overall appearance of the skin and the dyschromia evening out. This improvement can still be seen 1 year after treatment.

The more severe the photoaging, the more important it is to consider the depth of the peel. The patient shown in Figure 5.7 has a light skin type that is sensitive to the sun’s rays. She has developed a number of solar lentigines and fine wrinkles caused by UV rays. The eyelids are very wrinkled and the nasolabial folds and marionette lines are slack. In the long term, this patient’s nasolabial folds and marionette lines will only improve slightly, even with a deep peel. Other techniques12 should be used to treat them. There are many peels to choose from. The wrinkles on the lower eyelids can be softened with a TCA peel to the Grenz zone (Easy TCA®) or to the papillary dermis (Unideep®), but only phenol can be guaranteed to get rid of them. Many lentigines respond to a TCA peel to the basal layer of the epidermis, the majority to a TCA to the papillary dermis, while the deepest should be treated to the reticular dermis. Fine wrinkles on the cheeks can improve with TCA,13 but only phenol can really get rid of them and tighten the skin. There are two choices of treatment open to this patient. The first option would be an aggressive treatment, to be done in a single session: a full-face phenol peel that will treat all the symptoms of photoaging at once and tighten the skin. If the patient opts for this treatment, she must accept at least 8 days’ downtime and a high treatment cost. The second option is a less aggressive, more gradual and stimulating treatment that can be combined with a local phenol peel on the lower eyelids. Only Touch® is applied locally on the deeper lentigines and Easy TCA® on the rest of the face to even out the result and improve the fine wrinkles. A localized phenol peel on the lower eyelids14 is recommended if the patient wants to get rid of her eyelid wrinkles. If this course of action is chosen, the possibility of combining a localized phenol peel with Unideep®, a TCA

A

B

Lentigines, acne and dyschromia

Figure 5.6 (a) Combination of lentigines, acne and dyschromia. (b) Results 1 year after combining Easy TCA® and Only Touch®.

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hyperpigmentation that the patient hid for years under camouflage make-up. Given the extent of the problems to be treated, a full-face phenol peel was suggested straightaway, but was then ruled out because of the high cost of the treatment. The glabellar scar could not be improved by anything but a phenol peel, which was then applied locally, as can be seen in Figure 5.8(b): this photograph shows the pure white frosting resulting from the local application of

A

Figure 5.7 More severe photoaging.

peel to the papillary dermis, should be discussed. With phenol, the downtime is 8 days and it might be more appropriate to combine the local phenol peel with a single session of Unideep® that has a downtime of 5–6 days, instead of having four weekly sessions of Easy TCA®. As the results are comparable,15 the decision is often based on cost or the risk of complications, which is higher with a dermal peel. Depending on requirements, daily post-peel care should include a vitamin E antioxidant cream, a blending and bleaching cream, and/or a DMAE cream.16 Some solar and senile lentigines may only respond to peels to the reticular dermis as, histologically, the lentigines may be characterized by deep dermal papillae and elongated rete ridges with golf club-shaped extensions.

Post-inflammatory hyperpigmentation and scarring The patient shown in Figure 5.8(a) had had a serious road accident 6 years before the treatment. The surgeon did a perfect job given that the face had been completely lacerated by the car’s windscreen. Severe post-traumatic inflammation quickly turned into post-inflammatory

B

C

Figure 5.8 (a) Post-traumatic scars and hyperpigmentation. (b) Following treatment with a local phenol peel. (c) Four Easy TCA® peels and Blending Bleaching® cream were applied to even out the skin color.

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phenol. The skin color was evened out by applying four Easy TCA® peels until a cloudy white frosting was achieved, combined with Blending Bleaching® cream that was applied twice a day from the day after the first peel and continued for at least 6 months (Figure 5.8(c)). An effective sunscreen (see Chapters 3 and 35) must be applied every day between the four weekly peels and until the end of the maintenance treatment.

Severe aging of the skin The patient shown in Figure 5.9 has thin skin marked by expression wrinkles, sagging skin and photoaging. Using a peel that does not reach the dermis is always disappointing in cases like this. Some light peels might tighten the skin temporarily as a result of the edema that occurs afterwards. It would be impossible to attempt to correct all of these wrinkles, even by frequent repetitions of an intraepidermal peel or even a peel to the Grenz zone. A peel to the papillary dermis might improve the finer wrinkles and the quality of the skin, but only a full-face phenol peel could tighten the skin definitively through a ‘three-dimensional facelift’.17 The expression wrinkles should be treated first – 1 week before the phenol – with botulinum toxin, which will allow the skin to regenerate without the movements that would soon reimprint the wrinkles on a healing dermis.

Perioral wrinkles Perioral wrinkles (around the upper lip and chin) only respond to very deep peels (Figure 5.10). Many different agents have been tried: e.g. pyruvic acid, that has a high potential for scarring, and this particular agent, which is difficult to control in concentrated solutions, is very rarely used. Chemical cheiloplasty can only be considered under three conditions: ■ The natural skin color allows treatment without the risk of pigmentary changes. ■ The skin around the area to be treated is in good enough condition that the demarcation line will not be too obvious. ■ Other treatments (i.e. hyaluronic acid, collagen, etc.) would have no effect. Patients with skin phototype above IV are therefore ruled out from this treatment, as are patients with a light skin phototype but a lot of freckles,18 and patients whose skin is severely photoaged. Phototype IV patients should make a choice between deep wrinkles and a possible depigmentation. Lip & Eyelid® formula was originally developed to treat only the lips and eyelids before its indications were extended to the full face. It can be applied locally without nerve blocks or any kind of anesthetic (see Chapter 36). A TCA Unideep® peel (to the papillary dermis) is applied to the rest of the face immediately after the phenol peel has been applied locally (Figure 5.11). The Unideep® must not come into contact with the skin that has been treated with phenol. Botulinum toxin often has to be used at the same time as a deep peel on patients with thick skins in order to limit the contractions of the orbicular muscle of the lips and to improve/maintain results. The horizontal fold between the lower lip and the prominence of the chin does not usually respond well to peels, even deep ones. It can easily be filled in, however, together with the nasolabial folds 1–2 months after the phenol peel.

Dermal atrophy

Figure 5.9 A clear indication for a phenol peel.

The wrinkles on the cheeks of the patient shown in Figure 5.12(a) have been caused by dermal and hypodermal atrophy. Only a deep peel could improve the cosmetic appearance of this patient. Dermal fillers are, however, another possibility for treatment. Figure 5.12(b) shows the rejuvenating effect of injecting 2.5 cm3 of Bioalcamid® 19 in each cheek. The deep wrinkles have completely disappeared and the shape of the face has been restored to look like it did in a photograph of the patient when younger. Note the persistent bruising in the injected areas. This bruising can largely be avoided by using a trocar or blunt-tipped needle instead

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A A

B

Figure 5.11 B

(a, b) Wrinkles on the upper lip treated with a single application of Lip & Eyelid®, with the rest of the face being treated with a Unideep® peel in the same session. Note the excellent results for facial skin tension with TCA.

of a conventional needle. This treatment can of course be combined with a peel: Bioalcamid® can be used perfectly safely with Easy TCA® in the same session. The peel is performed after the liquid implant has been injected. A deeper peel, on the other hand, should only be applied a few weeks after the filling to avoid interference with the necessary process of encapsulation that fixes the filler material in place.

C

Deep wrinkles

Figure 5.10

If the patients in Figures 5.13(a) and 5.14(a) want quick rejuvenation that will last around 15 years, a phenol peel is the only indication (Figures 5.13(b) and 5.14(b)). The extent of the problems would be beyond dermal fillers, and if these were used, the results would be temporary.

(a) Deep wrinkles on the upper lip and chin. (b) Bismuth subgallate powder mask during the first few days after a phenol peel. (c) Results after treatment of these wrinkles with Lip & Eyelid® formula (phenol peel – chemical cheiloplasty).

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A

B

Figure 5.12 (a) This patient’s wrinkles are caused by severe skin atrophy. A peel is not the best indication. (b) Results of treatment with a dermal filler: 2.5 cm3 of Bioalcamid® in each cheek.

Botulinum toxin, used alone, would only partially improve the areas around the eyes, lips and cheeks. A surgical facelift would tighten the neck and the cheeks, but it would not treat the crow’s feet satisfactorily and would have no effect at all on the wrinkles on the lips and the overall skin quality. A light peel would only improve skin quality and even out skin tone, but would not get rid of the wrinkles. A peel to the papillary dermis would have a similar and more noticeable effect, but would not get rid of these deep and long-standing wrinkles. An experienced

doctor could use full-face dermabrasion. Full-face carbon dioxide laser treatment used to be very popular, but is gradually being abandoned because of the serious complications faced by both patients and doctors. A phenol peel will treat the sun-damaged skin and tighten these patients’ faces. An inexperienced doctor should not, of course, use this type of peel. Treating the deep wrinkles on the upper lip often calls for a combination of techniques: phenol plus dermabrasion, phenol plus botulinum toxin, second phenol treatment, etc.

B

Figure 5.13 A

(a) Deep wrinkles. (b) Results after a session of full-face Exoderm®.

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B

Figure 5.14 (a) Deep wrinkles. (b) Results after a full-face phenol peel; second treatment of the upper lip.

Melasma Many techniques are now available for treating melasma. Some are more aggressive, some more effective and others more costly or complex. Only one technique can provide a definitive and effective treatment in one single session: a phenol peel. After a phenol peel, melanocytes can no longer produce melanin. If we rule out this treatment, which would be extreme for melasma alone, then the basic principle is relatively clear, if not always 100% effective. The existing melanin reserves must be eliminated by carrying out one or more peels, and melanin must be prevented from building up again by long-term topical post-peel treatment and effective sun protection. How quickly the melanin reserves can be eliminated depends on the strength of the peel: an intraepidermal peel will be extremely slow, a peel to the basal layer will be slow, a peel to the Grenz zone will be quicker, and a peel that destroys most of the papillary dermis will be quicker still. This progression raises the following problems: if the peel acts too slowly, either the patient will tire of the treatment, or the skin, once exposed to the sun’s rays, will resynthesize the melanin as it is being eliminated; if the peel is deeper, to the papillary dermis, and the inflammation is not controlled, the skin might react and develop post-inflammatory

hyperpigmentation. In any event, success depends on sun protection/avoidance and long-term topical treatment. Patients who refuse to go through with post-peel care should not be accepted for melasma treatment. The choice of treatment for the patient shown in Figure 5.15(a) was four sessions of Easy TCA® (Figure 5.15(b)). The solution was first applied to the melasma spots until cloudy white frosting appeared; it was then applied to the whole face to even out skin tone.20 One session was done per week. Antityrosinase and antioxidant Blending Bleaching® cream was used twice a day. The cream was first applied the morning after the first peel, on the whole face in the morning and on the melasma spots in the evening. Any melasma treatment (apart from phenol) must be accompanied by long-term care with antioxidants, tyrosinase inhibitors and effective sun protection for a minimum of 6 months (although 1 year would be more effective).

Complexity of choosing a TCA peel TCA peels are doctor-, chemical- and patient-dependent. Penetration depends on how the skin is prepared, and the

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A

B

Figure 5.15 (a) Melasma before treatment. (b) After four Easy TCA® peels and Blending Bleaching® cream.

doctor’s choice of preparation depends on the patient and the method of application (when pre-peel preparation is indicated). It also depends on how rigorously the actual patients, who will only really benefit from TCA in simple aqueous solution (TCA–SAS) when the skin has reached the stage of ‘retinoid dermatitis’, prepare their skin. The results of a TCA peel vary – from ‘inadequate’ to ‘excellent’. As there is no general toxicity, the peel can be applied to all areas of the skin. Pigmentary changes are always a risk with TCA–SAS, and should be prevented as much as treated. There is also a risk of scarring when the concentration of TCA is higher than 35% m/m. Treating the neck and décolletage is dangerous, as effective treatment depends on relatively high concentrations of TCA–SAS being applied to an area that is quick to scar because it has few appendages, because of its histological structure and because of the twisting and stretching movements it is constantly undergoing. For an inexperienced doctor, the choice may seem daunting! What is the best way to deal with general skin aging of ‘average severity’? Phenol would be too aggressive and glycolic acid not strong enough. A TCA peel would be more appropriate, but how much preparation would the patient accept? What concentration of TCA should be

used? 25%, 35% or 50%? m/m, m/v or m + v? How much acid solution should be applied and how many coats? What depth should be reached? How much pressure should be applied on the gauze pad? And is it better to use gauze or a cotton swab? Or a brush? What kind of postpeel care should be used? What are the usual developments? What will the results be? What complications could arise? Should the peel be repeated? If so, how many times and how often? The questions posed to an inexperienced doctor are endless. Fortunately, a new concept in TCA peels came into being in the second half of the 1990s: Easy TCA®. This peel can be performed in a doctor’s surgery, without preparation, without anesthetics, without close follow-up, on all skin types, on all areas of the skin and in all seasons.

Differences between Easy TCA® (ETCA) and TCA in simple aqueous solution (TCA–SAS) There are many differences between ETCA and TCA–SAS applied in the classic manner.

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ETCA logic versus TCA–SAS logic The logic behind a TCA–SAS peel is different to that for ETCA. TCA–SAS is used to destroy damaged tissue (removing the papillary dermis) with the skin being left to heal naturally. It is a destructive rather than a stimulating process. The indications for ‘destructive’ peels are different to those for ‘stimulating’ peels. An ETCA peel is stimulating rather than destructive: it does not destroy much skin (the Grenz zone or basal epidermis is removed: see Chapter 12), but strongly stimulates the regeneration process. All peels induce inflammation (tumor – dolor – rubor – calor), which is responsible for the redness, swelling and most of the pain21 and heat felt in the treated skin. The swelling and edema come from rapid permeation of the dermal blood vessels, which pour out a large quantity of neutralizing serum, oxygen and pro-inflammatory components into the dermis and maintain vasodilation. Free radicals are also soon released and damage all the surrounding structures, especially those needed for re-epithelialization. Every peel has to take the advantages and disadvantages of inflammation into account:

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Box 5.1 Surfactants Emulsifiers are necessary to allow water and lipids to combine. A surfactant is an amphiphilic molecule that has affinities for fats as well as water and that can be incorporated into lamellar lipid structures (e.g. cell walls). Surfactants increase the fluidity of the lipid structures by partitioning into the lipid membranes, as their lateral interactions with the membrane-forming lipids reduce the force of their attractive interaction. The mobility of the membrane lipids increases considerably in a similar manner to when a liquid crystal is converted into a gel. Finally, lipids can be seen to micellize or simply dissolve. Membranes lose their relative impermeability. See Figure 5.16.

Normal membrane structure: active transmembrane protein

■ The upside is the stimulation without which regeneration could not take place. ■ The downside is the self-maintained production of free radicals that damage the skin and slow down re-epithelialization. An ETCA peel attempts to make the most of the positive effects of inflammation at the same time as limiting, as far as possible, the negative effects of oxidation with the help of the post-peel cream. TCA–SAS, on the other hand, has to contend with the good and bad sides of inflammation.

ETCA solution versus TCA–SAS solution TCA–SAS TCA–SAS is a simple dilution of TCA in water. Its characteristics are described at length in Chapter 12, together with the various approaches used to counter the difficulties arising in its use. TCA–SAS is usually considered to be effective from 25% m/m.

ETCA ETCA consists of a base solution to which the doctor must add a specific quantity of TCA to make up a peel solution that contains 15% m/m TCA. This solution is saponified, stabilized and adjuvanted. Saponins are natural extracts, glycosides, which have lathering and binding properties for water-soluble prod-

Lipid breakdown: inactive transmembrane protein

Figure 5.16 Effect of surfactants on cell membranes.

ucts in the skin’s lipids. They help the acids spread and penetrate evenly, on and through the skin. Some studies have shown that saponins have antimicrobial properties that enhance skin regeneration after a peel. ETCA solution also contains the surfactant (Box 5.1) sodium laureth sulfate (SLES).22 SLES degreases the skin, emulsifies fats and holds skin impurities in suspension. Coconut fatty acid monoethanolamide (cocamide) improves the effectiveness of saponins. Citric acid is a tricarboxylic AHA, an antioxidant, chelator and buffer that helps break down corneodesmosomes and makes it easier for the TCA to penetrate the epidermis. Ascorbic acid has a

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dual role, acting as a buffer and protecting against free radicals. It protects the solution as well as the skin from oxidation.

epidermal pinpoint frosting appears, contains tretinoin precursors that boost the LCs and improve their antigenpresenting function.

Pre-peel ETCA versus pre-peel TCA–SAS

Immediate pre-peel ETCA versus TCA–SAS

TCA–SAS should be preceded by several weeks of skin preparation to even out and reduce the thickness of the stratum corneum, reduce melanocyte activity and enhance re-epithelialization. ETCA, on the other hand, is applied on unprepared skin, as the acid and the post-peel cream penetrate evenly; the risk of pigmentary changes (basic protocol) is extremely low and re-epithelialization takes place without prestimulation.

With a TCA–SAS peel to the papillary or reticular dermis the patient’s skin needs to be properly cleansed, cleaned of make-up, disinfected (with alcohol) and degreased (with acetone). The doctor must disinfect his hands properly and the patient must be kept away from any potentially infectious staff. The TCA–SAS cannot penetrate the skin properly through grease and make-up, and the skin must be disinfected to limit the risk of post-peel secondary infection. ETCA is usually applied without any prior cleansing, make-up removal, degreasing or disinfection. The peel solution can even be applied on top of make-up, as the emulsifiers in the base solution hold these molecules in suspension and allow the TCA to come into contact with the skin. The endpoint of ETCA treatment is scattered pinpoint frosting or cloudy white frosting, and there is therefore no need to increase penetration of the peel solution artificially. Make-up removal, disinfection and degreasing are not forbidden before an ETCA peel, but could increase skin permeability and cause the solution to penetrate too deeply and destroy the dermis. A TCA to the dermis is not the same as an ETCA peel.

Calculating the solution mix: ETCA versus TCA–SAS We saw that preparing a TCA–SAS solution appears easy at first sight but that numerous factors come into play that can change the behavior of a solution, gel or paste considerably. ETCA provides a standardized solution that always produces the same results when the same protocol used.

Herpes prevention: ETCA versus TCA–SAS Herpes prevention is essential before a TCA–SAS peel, as the dermis of the skin has to be destroyed for the peel to be effective, and the skin’s immune defenses suffer from this destruction. ETCA is more stimulating than destructive; it will not destroy the skin’s immune defenses. On the contrary, repeated peels appear instead to stimulate it. No herpes prevention is necessary before using ETCA in the ‘basic protocol’ (scattered pinpoint or cloudy white frosting).

Bacteria prevention: ETCA versus TCA–SAS For the same reasons outlined above, the risk of secondary bacterial infection is considerably lower with ETCA than with TCA–SAS. Systematic prevention of infection is not necessary with ETCA: no antibiotics, no disinfectants. The Langerhans cells (LCs) in the epidermis and papillary dermis are not destroyed, nor are the other antigen-presenting cells, and they continue to prepare the body’s defenses against microscopic predators. The lymphocytes, macrophages and other defense cells remain present in the dermis. The ‘post-peel cream’, applied as soon as the first

Depth of peel: ETCA versus TCA–SAS TCA–SAS is applied with a view to destroying damaged (usually sun-damaged) skin structures and benefiting from the skin regeneration that naturally follows a peel. It is really effective when it destroys the papillary dermis. With ETCA, the aim is not to destroy the dermis in the hope of its rebuilding later, but rather to stimulate all the phenomena of skin repair repeatedly, in all the different layers of the skin. With frequently repeated ETCA sessions (every 8 days), the sum of the results is comparable to that of a papillary peel without any of the drawbacks. The ‘basic protocol’ for ETCA is intended to reach the basal layer of the epidermis or the Grenz zone. There are (many) other deeper protocols but they are not as straightforward as ETCA and the risk of complications is relatively much higher. ETCA is not necessarily a light peel; it can be used to reach all depths, from the basal layer of the epidermis to the reticular dermis, depending on the protocol used. The relatively superficial action of the ETCA solution (basic protocol) strongly stimulates the skin regeneration

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process and increases the permeability of the epidermis. The ETCA post-peel cream penetrates the skin more easily, as it is permeabilized by the peel solution.

Anesthesia, pain, monitoring: ETCA versus TCA–SAS A TCA–SAS peel to the dermis is painful and requires the use of analgesics. Some resistant patients can tolerate a peel reaching the superficial dermis, but are left with such unpleasant memories that they might well refuse further treatment. A peel to the papillary dermis should not be done without facial nerve blocks (FNB) and/or sedation. Performing FNB requires a whole series of measures, including pulse oximetry at the very least. Any painful intervention can trigger vagal reactions for which the doctor must be prepared. Pain after a peel can be dealt with easily by prescribing oral analgesics (e.g. acetaminophen (paracetamol) or codeine/ acetaminophen). ETCA does not require any type of anesthetic, sedation or analgesics. Any mild pain caused by the application of the ETCA solution can be dealt with immediately, as soon as frosting occurs, by applying the post-peel cream.23 No pulse oximetry monitoring is necessary and no vagal reaction has been described, perhaps because it is a short procedure.

Length of peel: ETCA versus TCA–SAS It takes 10 minutes to apply ETCA to the basal layer or the Grenz zone, from the time patients lie down to when they get up. Applying a TCA–SAS peel, usually to the papillary dermis, takes a lot longer: at least an hour should be allowed for settling the patient in, disinfection, make-up removal, setting up the monitoring equipment, FNB or sedation, a series of applications and letting the patient rest after the peel.

Post-peel care day 1 to day 8: ETCA versus TCA–SAS Post-ETCA care consists simply of asking patients to protect their skin from the sun (Melablock®-HSP) and to apply the most suitable cosmeceutical for their particular problem (see Chapter 3). They should start the very day after the first of the four peels and continue until the end of the 6th week after the last peel. The post-treatment care after a TCA–SAS peel is more complex and needs much closer monitoring, as the risk of complications is much higher. Follow-up monitoring after a TCA peel to the papillary dermis is described in Chapter 23.

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Repeating peels: ETCA versus TCA–SAS A TCA–SAS peel can only be repeated after a rest period of usually 6 weeks to allow the skin to regenerate completely. It provides a single strong stimulation that decreases with time. ETCA is repeated four times at weekly intervals to provide ideal stimulation of the skin regeneration processes. The post-peel cream and ETCA application technique allows for this repetition. If the ETCA were repeated less often (once every 2–3 weeks), the effects of stimulation would not be cumulative. Weekly repetition, in contrast, ‘stimulates the stimulation’ resulting from the previous peel.

Combination treatments: ETCA versus TCA–SAS TCA–SAS allows hardly any concomitant combinations, and most of the treatments that one might wish to combine it with must be carried out 8–15 days before the peel. For example, nothing can be injected immediately before a TCA–SAS peel. It is, of course, possible to inject botulinum toxin in the upper part of the face just before or after applying a TCA–SAS peel to the area around the lips, but the toxin should not be injected before applying a TCA–SAS peel in the same area. The immediate inflammation induced by the peel could cause the toxin to migrate. ETCA, on the other hand, allows all concomitant combinations.

Botulinum toxin This can be injected immediately before applying ETCA in the same area. The technique is simple: inject the toxin, wait 5 minutes, apply the ETCA until pinpoint frosting appears and then apply the post-peel cream. The cream has an immediate and pronounced anti-inflammatory effect, which prevents edema and toxin migration. The restructuring of the skin by the peel improves the results of the toxin, and resting the muscles improves an even collagen deposition.

Filling wrinkles Filling techniques can also be used immediately before ETCA, as the ETCA post-peel cream soon stops inflammation and oxidation. The cream can also absorb the free radicals that are released by the peel and that could damage the three-dimensional structure of dermal fillers, such as hyaluronic acid. In fact, the instructions for most dermal filler products specify not to apply a peel after the filler, but

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this does not apply to ETCA.

Flashlamps ETCA can be used after flashlamp treatment24 when treating pigmentation or photoaging on the face, décolletage or hands. It is preferable to start with the lamp and to follow up with the peel, for the following reasons: ■ Epidermal permeability does not seem to change significantly after the lamp and there is no marked change in the penetration of the ETCA. Caution is, however, advised when applying ETCA solution to make sure that it does not penetrate the skin further than anticipated: the cotton-tipped applicators should be squeezed out properly after the first application and the treatment should not go beyond scattered pinpoint frosting. ■ Applying ETCA and the post-peel cream before the flashlamp would change the refractive and diffractive properties of the epidermis, as well as its water content and color.

Risk of complications: ETCA versus TCA–SAS ETCA carries far fewer risks for the patient than TCA–SAS.

Infections As described above, no herpes or bacteria prevention is necessary with ETCA, unlike TCA–SAS.

Risk of exhausting the skin’s resources At the level of the dermis, the fibroblast is a cell of major interest in understanding how peels work. Like Langerhans cells, they have dendritic morphology; they are fusiform or stellate but have no antigen-presenting activity. Fibroblasts synthesize all the constituents of the extracellular matrix and play an essential role in the formation and contraction of granulation tissue during wound repair. Peels to the dermis destroy a large number of fibroblasts, and the survivors must multiply in order to reconstitute the fibroblast population. Each time they do this, their telomeres shorten, which gradually exhausts their capacity for future multiplication. Peels to the dermis should therefore not be repeated too often. ETCA, on the other hand, does not destroy dermal fibroblasts (and there is no shortening of telomeres), but stimulates their metabolism and obliges them to produce more and more rapidly. Logically, repeating ETCA (basic protocol) cannot accelerate skin aging, which is not the case with repeated peels to the dermis.

Scarring During the healing process, hybrid cells, known as myofibroblasts, appear in the dermis. They have the morphological characteristics of both fibroblasts and smooth muscle cells. They are responsible for tissue contraction–retraction during healing. Their cytoplasm contains networks of myofilaments that are in contact with specialized zones of the plasma membrane and can interact with the adjacent cells or connective tissue. These myofibroblasts appear to be differentiated fibroblasts that have acquired the properties of smooth muscle cells. Controlled stimulation with DMAE, for example, is a good way to achieve a tightening effect on the skin. Correlating this theoretical data with the clinical data on peels is not without interest, as it allows us to anticipate which peels might potentially cause scarring and which ones will not. Deep peels, which go beyond the upper reticular dermis and practically lay the hypodermis ‘bare’, are more dangerous as far as retractile scarring is concerned, as they stimulate the conversion of fibroblasts into retractile myofibroblasts that can cause scarring. Not all agents are equally potent; there are more descriptions in the literature of problems with scarring with deep TCA peels than with phenol-based peels. There is no reason why peels that do not go beyond the Grenz zone should stimulate the conversion of fibroblasts into myofibroblasts, as there is no ‘laying bare’ of the internal tissue and hence no need for retraction. Retractile scar reactions are therefore extremely rare with the basic ETCA protocol; they can only occur when the peel has not been applied correctly. Peels that reach the Grenz zone or the papillary dermis stimulate small fibroblasts that are parallel to the epidermis and have dendritic processes that connect with several collagen and elastin bundles. The synthesized collagen is aligned horizontally in the border zone (Grenz zone), and the resulting tension from the activity of any potential myofibroblasts produces a positive cosmetic effect: improved tension in the papillary dermis, which can be called the ‘lifting effect’. The ‘lifting effect’ achieved with medium-depth peels in no way compares with the lift achieved when sagging skin and muscle mass are treated surgically. In some cases, doctor and patient can be sent off on the wrong track and delay taking the often dreaded and sometimes formidable decision to go ahead with surgery.

Post-inflammatory hyperpigmentation (PIH) It is clear from the medical literature on chemical peels that TCA–SAS is the agent responsible for the majority of postpeel pigmentary problems. Photographs abound in specialist books. A TCA–SAS peel does in fact cause severe inflammation after the peel, and it is therefore not surpris-

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ing to come across many cases of post-inflammatory hyperpigmentation (PIH).25 ETCA, in the basic protocol, causes almost no PIH. Generally, IV, V and ‘light VI’ skin phototypes are at greater risk of PIH.

Downtime During the post-peel period after a TCA peel to the papillary dermis, the patient has to put up with a week of edema, scabbing, erythema, pain and other inconveniences. Any form of social life is out of the question, and the patient can only return to normal social activities, with the help of make-up, after the 8th day. It is several weeks before the skin returns to normal. With ETCA (basic protocol), on the other hand, the patient can lead an almost perfectly normal social life, as the flaking is no more serious than with sunburn and only lasts for 48–72 hours.

Notes 1. Although some peels with an alkaline formulation do exist. 2. Apart from Easy Phytic® Solution, whose acids can penetrate to the papillary dermis. 3. With Easy TCA® and Easy Phytic®, papulopustular acne can be treated during its active phase. 4. Dimethylaminoethanol, a precursor of acetylcholine. See the section on DMAE in Chapter 3. 5. Blending Bleaching® cream (see www.skintech.info) 6. By injecting phophatidylcholine/deoxycholate into undereye bags, there is a risk – among other complications – of disrupting the adipocyte cell walls as well as the muscle cells that come into contact with this product. Moreover, it triggers severe and painful edematous erythema that lasts several days and is only really effective after several sessions. For the moment, fatty bags under the eyes can only be treated surgically. 7. Source: Dr Robert Vergereau, Spain. 8. For example Renutriv ACE Lipoic Complex®: vitamins A + C + E and lipoic acid. 9. See the section on the area around the mouth in Chapter 37. 10. The same applies for Easy Phytic® solution. 11. For example, Purifying cream® by Skin Tech. 12. Depending on preliminary examination of the patient and the doctor’s experience: dermal filling, botulinum toxin,

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cannulation, threading, etc. 13. Either four Easy TCA® peels to the basal layer or a Unideep® peel to the papillary dermis. 14. See Chapter 34 for application of the Lip & Eyelid® formula. 15. Although it must be taken into account that four peels to the Grenz zone are not necessarily as efficient as one peel to the papillary dermis. The latter can destroy a large number of lesions that peels to the Grenz zone do not always reach. 16. Some studies suggest that DMAE can eliminate the lipofuchsin in lentigines. 17. As the much missed Dr Yoram Fintsi called it. 18. To avoid leaving an obvious demarcation line. 19. This is a permanent polyalkylimide filler in the form of a removable endoprothesis. Fat transfer is used more often, as there is no risk of rejection and the implant is autologous. 20. See the details of melasma treatment in Chapter 15. 21. The ‘burning’ sensation soon improves on application of a cold pack. 22. SLES is not the same as sodium lauryl sulfate (SLS, also known as sodium dodecyl sulfate (SDS)), a powerful surfactant and very irritating to the skin, with which it is often confused. 23. It is not neutralizing, however, as we shall see further on. 24. Provided that this is classic flashlamp treatment and not a device combining pulsed light and radiofrequency, for example. These machines significantly change skin permeability and can cause the acids to penetrate too far, with the risk of scarring. 25. See Chapter 37 for more details.

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6 Alpha-hydroxy acids: chemistry, pH and pKa, and mechanism of action

Glycolic acid

—

Glycolic acid (hydroxyethanoic acid, hydroxyacetic acid) is the shortest AHA, with just two carbon atoms (Figure 6.2). It was originally extracted from sugar cane, but the acid used in treatment today is synthesized chemically. AHAs have become popularized as ‘fruit acids’, and this benignsounding name has had a great influence on the interest shown by patients. The situation is similar to that when patients talk of lasers, gold threads or caviar rejuvenating creams. These words evoke dreams of miracle cures in the imaginations of some: odorless, colorless and painless, permanently effective and, of course, without side-effects. Glycolic acid is extremely hydrophilic, and a pure aqueous solution of glycolic acid, saturated at a concentration of about 80%, has a pH of 0.5. This pH, considerably lower than its pKa of 3.83, shows that the solution consists mostly of pure acid and is effective for performing a peel. The pH of a glycolic acid solution determines its acidifying power on the skin: a 3% glycolic acid solution at pH 3 can acidify the first five layers of corneocytes, whereas at 10% and pH 3, it causes a deeper and more rapid acidification of the

Carboxylic acid group

—

H

O



Hydroxy group  OH O  R — Cα — C  OH H

cannot or do not want their skin to flake, often because of their professional activities, which are incompatible with visible peeling. A number of AHAs have been proposed for medical use: glycolic acid, lactic acid, malic acid (with two COOH groups), tartaric acid (with two OH and two COOH groups), citric acid (with three COOH groups) and mandelic acid (which has an aromatic (phenyl) group attached to the alpha carbon atom) – see Table 6.1 below.

—

H—C—C

Figure 6.1

General chemical structure of an alpha-hydroxy acid. α indicates the alpha carbon atom; R represents a general organic group.

—

Alpha hydroxy acids (AHAs) occur naturally in a number of fruits (from where they get their ‘eco-friendly’ name of fruit acids) and dairy products. This class of acids contains a number of molecules that have in common the presence of a carboxylic acid group (COOH) and a hydroxy group (OH) in the alpha position relative to the acid group (Figure 6.1). As early as 1946, the application of a 3% lactic acid solution at pH 3.8 was already considered a treatment for ichthyosis, although cosmetic dermatologists only really started using AHAs when in 1974 Van Scott and Yu described how effective they were in the treatment of dry or ichthyotic skin. From then on, the scope of AHAs broadened, and some authors reported their beneficial effects on acne, photoaging and benign hyperplastic epidermal lesions. It was often suggested that AHAs should be used to treat age-related wrinkles and sagging skin. Although the direct target of AHAs seems to be corneodesmosomes, the indirect action of topically applied AHAs affects not only the whole of the epidermis but also the papillary dermis and the pilosebaceous units. However, while all peels produce similar1 histological effects on the different layers of the skin, clinical results clearly show that AHAs, used as light peels, do not improve the skin’s appearance to the same extent as TCA or phenol. Moreover, indications for glycolic acid peels tend to be restricted to the treatment of sun-damaged or acneic skin, especially in patients who



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Figure 6.2 Chemical structure of glycolic acid.

OH

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epidermis.2 Note that ‘acidification of the epidermis’ does not mean ‘peeling effect’. Acidifying several layers of the skin does not necessarily mean destroying the cells. Up to a certain point, cells resist acidification.

—

HO

O



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H3C — C — C H

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OH

Figure 6.3 Chemical structure of lactic acid.

Lactic acid Lactic acid (2-hydroxypropanoic acid, α-hydroxypropionic acid) is the next shortest AHA after glycolic acid. A methyl group (CH3) replaces the terminal hydrogen atom on the alpha carbon (Figure 6.3). It has a pKa of 3.86, which is close to that of glycolic acid. Lactic acid occurs naturally in sour milk. After penetrating the skin, lactic acid is converted automatically and reversibly into pyruvic acid, the alpha-keto acid derivative of lactic acid: a keto (=O) function replaces the hydroxy (–OH) function on the alpha carbon. At identical concentrations, lactic acid destroys the epidermis more slowly than glycolic acid. Concentrations of lactic acid of 10–20% or stronger begin to destroy the stratum corneum and stimulate skin regeneration, the renewal of epidermal cells. However, some studies have shown that cell renewal is not maintained uniformly during long-term treatments with 3% lactic acid

at pH 3. In fact, cell renewal gradually falls off during the first 10 weeks of treatment with 3% glycolic or lactic acid at pH 3, decreasing to 29.3% and 28.3%, respectively.3 When applied regularly, lactic and glycolic acids (at 3%, pH 3) lose a significant percentage of their capacity to destroy corneocytes and renew the epidermis around the 12th week. Salicylic acid (a beta-hydroxy acid), on the other hand, retains its ability to destroy corneocytes much longer. At a concentration of 50–70%, lactic acid produces the same amount of exfoliation as glycolic acid. As early as 1974, it had been shown that lactic acid improved skin hydration and suppleness and that a pH of 3 was more effective than a pH of 5. Lactic acid is also a better hydrator than urea or glycerol. Some studies tend to show that 3 weeks of daily application of 12% lactic acid would allow as much collagen to be deposited in the papillary dermis as

Table 6.1 Hydroxy and keto acids used in cosmetic treatments Acida

pKa

Chemical structure and alternative names

Tartaric acid

pKa1 = 3.02 pKa2 = 4.54

HOOC.CH(OH).CH(OH).COOH (+)-2,3-dihydroxybutanedioic acid; d-2,3-dihydroxysuccinic acid (only the dextrorotatory (+, or d) form is active) [dicarboxy dialpha-hydroxy acid]

Citric acid MW 192.13

pKa1 = 3.06 pKa2 = 4.74 pKa3 = 5.40

HOOC.CH2.C(OH)(COOH).CH2COOH 2-Hydroxy-1,2,3-propanetricarboxylic acid [Tricarboxy alpha-hydroxy acid]

Mandelic acid MW = 122.14

pKa = 3.36

C6H5.CH(OH).COOH (+)-phenylhydroxyethanoic acid; d-α-hydroxyphenylacetic acid; d-phenylglycolic acid; amygdalic acid [alpha-hydroxy acid]

Pyruvic acid MW = 88.06

pKa = 2.50

CH3.CO.COOH 2-Oxopropanoic acid; acetylformic acid; α-ketopropionic acid; pyroracemic acid [alpha-keto acid]

Malic acid MW = 134.09

pKa1 = 3.40 pKa2 = 5.5

HOOC.CH2.CH(OH).COOH hydroxybutanedioic acid; hydroxysuccinic acid, [dicarboxy alpha-hydroxy acid] HOCH2.(CHOH)4.COOH 2,3,4,5,6-pentahydroxyhexacetic acid

D-Gluconic acid MW = 196.16

pKa = 3.86

α,β,γ,δ,ε-pentahydroxycaproic acid; dextronic acid; glycogenic acid; glyconic acid; maltonic acid [alpha-hydroxy acid]

Salicylic acid MW = 138.12

pKa = 2.98

HO.C6H4.COOH o-Hydroxybenzoic acid, [beta-hydroxy acid]

a

MW, molecular weight.

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applying 25% trichloroacetic acid (TCA) or phenol. We must remember, however, that histological findings, as important as they are, do not always translate into cosmetically visible clinical results and that laying down new collagen is only one of the changes associated with peels.

Buffers In low concentrations, the pH of a glycolic acid solution varies with the concentration of acid: an unbuffered glycolic acid solution, at less than 1%, has a pH of approximately 2.5.4 At 2%, the pH is 2.1. When the concentration reaches 5%, the pH goes down to 1.9. It is 1.7 for a 10% unbuffered glycolic acid solution. Higher concentrations, 50–80%, have a pH close to 0.5. At identical pH about 0.5, a solution with a concentration of 80% is more aggressive than a 50% solution. A concentrated glycolic acid solution at pH 0.5 consists of free and active acid, and is aggressive to the skin. It is a thousand times more acidic than a solution at pH 3.5.5 A solution this strong needs to be properly neutralized by the doctor applying it. Applying a 70% non-neutralized glycolic acid solution to the skin can destroy the epidermis in 2–7 minutes, depending on the skin type, the thickness of the stratum corneum, the degree of photoaging and the pre-peel preparation of the skin. The pH values on the surface of normal skin vary between 4.5 and 6, and up to a certain point the skin has the ability to defend itself against pH variations and can maintain a stable pH in the face of moderate acid or alkali attacks. This is the skin’s ‘buffer’ capacity (Box 6.1). Applying large quantities of pure acid to the skin (during a glycolic acid peel with a non-neutralized solution) saturates its natural buffer capacity, and the excess acid must be neutralized to avoid burning the skin. The contact time for a glycolic acid peel, as well as for other AHAs, is the time between applying the peel6 and

Other hydroxy and keto acids Many other hydroxy acids (and the related keto acids) are used in cosmetic treatments (Table 6.1). Ascorbic acid (vitamin C) is an alpha-hydroxy acid derivative. It has been shown to stimulate collagen production and reduce melanin production. Under identical conditions, classification of the acids described above in order of strength would give the top three as: 1. pyruvic acid 2. glycolic acid 3. lactic acid In the rest of this chapter, it is mainly the use of glycolic acid that will be discussed – and by default this is what the information given applies to. It is clear, however, that, as a general rule, and even if some acids have specific properties, most of the hydroxy acids (alpha or beta), carboxylic acids (containing the COOH group), dicarboxylic acids and alpha-keto acids produce the same positive effects on the skin, depending on the concentration, the pH of the solution (Figure 6.4) and how they are applied.

0

1.5

Easy TCA® Unideep®

3 Lemon juice

5.5 Red wine

7 Milk Saliva

9.5

11

12.5

14

Egg white Seawater

ACIDIC

BASIC

70% unbuffered glycolic acid 1 M HCl

Gastric juices

Beer Phenol peel

Coca Cola® Vinegar

EMLA Sodium bicarbonate Human blood Tears

pH 3 is 10 times more acidic than pH 4 pH 3 is 100 times more acidic than pH 5 pH 0.5 is 1000 times more acidic than pH 3.5

Figure 6.4 pH of various substances.

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Ammonia

1 M NaOH

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Box 6.1 Importance of buffers in the body The body’s – and the skin’s – enzyme reactions are pHsensitive. It is vital for the body to keep the pH of an organ stable in order to stabilize enzyme reactions. Protection against pH variations – the buffer capacity – must be extremely active and strong, as natural metabolic processes permanently synthesize acids and alkalis that are liable to modify the pH. The blood, for example, is protected by two important buffer systems: the hemoglobin system and the bicarbonate system, which stabilize its pH between 7.37 and 7.43. The bicarbonate system is the most important buffer for plasma and interstitial fluids. Neutralizing the skin with sodium bicarbonate is the most ‘natural’ method.

neutralizing it. The contact times for partially buffered AHAs, at pH>2.5, are far longer than for pure unbuffered AHA solutions at pH 0.5,7 which are a hundred times more acidic.

Box 6.2 Effect of dilution on the pH of a solution 5 ml of the base solution has pH 2.7–3. Adding 20 cm3 of water does not change the pH. The total volume must be brought up to 85 ml for the pH to rise from 3 to 4. See Figure 12.9.

Neutralizing an AHA peel consists in applying a base solution (usually pH 9–10) to the treated area. Rinsing with water only dilutes the acid without neutralizing it (Table 6.2) – an acid is neutralized by a base. However, dilution does have the merit of reducing the proton concentration8 and so eventually increases the pH (without changing the pKa, of course) when enough water is added. The high acidity of concentrated and unbuffered AHA solutions, as well as the complications that stem from such treatments, has brought the pH of many glycolic acid solutions to around pH 4–5.5.9 Ammonium salts, sodium bicarbonate or sodium hydroxide (NaOH) are often used for this. The resulting chemical reaction produces a salt10 and water – the pH increases and the potency of the acid solution decreases: glycolic acid + NaOH ← sodium glycolate + H2O

pKa The natural pH of an aqueous solution of 60% glycolic acid is 0.5. The gradual addition of a base slowly raises the pH of

this solution. When the pH reaches a value of 3.83 as a result of the gradual addition of the base, we know that this solution contains exactly 50% of active free acid and 50% of salt produced by the reaction of the glycolic acid with the base (e.g. sodium glycolate or ammonium glycolate). A pH of 3.83 corresponds to the pKa value of a glycolic acid solution. If we keep on adding a base solution to the glycolic acid solution, the pH will gradually increase, while the proportion of free and active acid and the strength of the solution decrease. A glycolic acid solution whose pH had been brought up to 7 would be completely neutralized or buffered and inactive. A glycolic acid solution at pH 5 is partially neutralized or buffered and partially inactive, as it does not contain much free acid. It is far less aggressive to the skin, of course, but it is also less active. The pKa is therefore an important notion that allows us to understand and anticipate how aggressive an AHA peel solution will be, on condition that we also know the pH of the solution. Knowing the pKa alone, which is a definitive and set parameter for each acid, does not help determine how aggressive a peel solution is. The pKa of glycolic acid is and will always be 3.83, whereas the pH of the solution could vary between 0.5 and 7 or above. The greater the pH than the pKa of an acid solution is, the less aggressive it will be. The lower the pH than the pKa of an acid solution is, the more aggressive it will be. It is therefore not possible to choose the pKa of the solution that we want to use, as this parameter has been determined chemically, once and for all, for each acid, and it gives the exact pH at which 50% of the active molecules remain. We can, on the other hand, change the pH of the solution and make it lower than the pKa to make the solution more aggressive. We can also raise the pH above the pKa to soften the effect. A partially neutralized solution at pH 4 still contains enough free acid to achieve a clinical effect, but is far less effective than a solution at a lower pH. Partial neutralization of a glycolic acid solution is therefore a compromise between effect and risk. It is, in fact, surprising that glycolic acid is still partially active at pH levels of around 5. It seems that the alpha position of the hydroxy group in a small molecule like glycolic acid is the reason for this partially maintained effectiveness, even if the pH is relatively high. Other AHAs do not appear to remain active at high pH levels. Using a partially neutralized solution at pH 4.5 achieves the same results in a few months that could be obtained in a few weeks with the same unbuffered concentration. It is therefore true to say that it is possible to achieve the same results using neutralized or non-neutralized peel solutions. But patients would then have to be convinced to have many more peels, which, on top of the inconvenience of repeated visits to the surgery, means more expense – and that is never appreciated. The doctor may think it necessary to sacrifice effectiveness to safety,

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but the patient usually thinks that the doctor should find a quicker and more effective solution without sacrificing safety. An application of dansyl chloride accumulates in the epidermis and stains the skin. It is possible to measure the rate of disappearance of this coloration after the application of different hydroxy acid solutions at a constant pH. The rate at which the color disappears is correlated with the rate of cell replacement, and therefore provides information on the stimulation of epidermal turnover and on the capacity of the acid to stimulate skin regeneration. TCA (which is not a hydroxy acid), at 0.5%, stimulates skin renewal up to 50%, lactic acid (at 4%, pH 3) stimulates up to 34%, acetic acid (3%, pH 3) up to 30%, and pyruvic acid (4%, pH 3) up to 23%. Partial neutralization of these solutions, to pH 5, quite clearly reduces the rate of renewal, and neutralizing these same solutions to pH 7 takes away all of their clinical effectiveness. The ultimate goal of treatment with AHAs is to stimulate skin regeneration at the same time as avoiding as far as possible the side-effects that stem from their irritant potential. It is not easy to achieve this goal, as a very acid pH is required to ensure optimum clinical effectiveness. The aggressiveness of these acid solutions usually entails a higher risk of complications. We shall see further on that it is possible, however, to use a solution made up of different AHAs at a concentration higher than 60% and pH 0.5, at the same time as limiting the risk of complications: Easy Phytic® is an unbuffered solution of three AHAs, at pH 0.5. This solution uses a slow-release technology that does not need neutralizing in spite of its very acid pH, which is much lower than its pKa.

Mechanism of action AHAs do not coagulate proteins. Applying them in a peel should not therefore produce a ‘whitening effect’. According to Forestier, the mechanism of action of AHAs is as follows. Even at low concentrations, AHAs can insert themselves between two protein chains. Here, they build a sort of bridge that reduces corneocyte cohesion. As a result of the lytic action of AHAs on corneodesmosomes, corneocytes are shed more easily from the skin, and the thickness of the stratum corneum is reduced. The skin appears more hydrated as the stratum corneum is thinned or disappears temporarily. AHAs, even at low concentrations, acidify the upper layers of the skin. Experimentally, at pH <5, this acidification causes an increase in the epidermal activity of lipases, phosphatases and transforming growth factor beta (TGF-β). At higher concentrations, the protein chains are separated from each other, and this causes epidermolysis – more or less visible exfoliation. Because of this corneocyte-shedding activity, AHAs have been used primarily to treat certain

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hyperkeratinization disorders. Not all corneocytes react in the same way to AHAs: the more superficial, less hydrated corneocytes seem to be less sensitive to the action of AHAs than the corneocytes at the base of the stratum corneum. AHAs may also limit or prevent the cross-linking of proteins in the extracellular matrix. Unlike TCA or phenol, AHAs do not bind with proteins and so are not neutralized by them. The type of action they produce depends on their concentration, the pH of the solution, the pKa of the acids and the contact time with the skin before neutralization with a base solution. For example, a 70% glycolic acid solution (pH 0.5 for pKa 3.83) in contact with the skin for 5 minutes will be more aggressive than a partially buffered (pH 3.5) 50% solution left in contact with the skin for 2 minutes before neutralization with a base solution (a saturated solution of sodium bicarbonate, for example). The type of AHA molecule used is also of prime importance. Glycolic acid is the most aggressive AHA because it is the smallest. The type of vehicle used, the skin type and the disorder being treated are also factors to be taken into account when anticipating the action of a peel. The accelerated shedding of corneocytes disrupts the protective barrier function of the epidermis. From there, a cascade of secondary events stimulates growth in the basal layer of the epidermis and accelerates the conversion of keratinocytes into corneocytes11 to restore optimum barrier function as soon as possible. Stimulation of the mother cells by the keratinocytes of the basal layer can unfortunately go hand in hand with reactional and inflammatory melanocyte stimulation, the cause of potential pigmentary changes.12 The stimulation of keratinocyte growth is also accompanied by positive stimulation of fibroblast proliferation and synthesis of proteins in the dermis (collagen, elastin and glycosaminoglycans).13 Another indirect effect of AHAs, which also comes from the disruption of the barrier function of the epidermis, is that they enhance the penetration of other topical agents with which they are mixed. AHAs are often used as agents to enhance the penetration of other molecules, in the treatment of acne or melasma, for example. Histological studies show that the injury to the skin and the principles of repair are similar during a peel and during dermabrasion. The extent of repair is directly related to the depth of injury. In the case of glycolic acid peels, scabbing occurs only when the peel has penetrated too deeply. The scab consists of keratin, necrotic keratinocytes and a protein precipitate. Glycolic acid may be an antioxidant and protect against UV radiation through the same mechanism of action as ascorbic acid, but, given that it reduces the thickness of the stratum corneum, it can also enhance penetration of UV radiation through the epidermis. Even if the thinning of the stratum corneum is only temporary, AHAs are therefore not used to protect the skin against the sun, but can be applied after exposure for their anti-free-radical effects.

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Notes 1. In quality but not quantity. 2. Pons Gimier L, Parra Juez JL. Ciencia Cosmetica. Consejo General de Colegios Oficiales de Farmaceuticos, 1995: 285–6. 3. Pons Gimier L, Parra Juez JL. Ciencia Cosmetica. Consejo General de Colegios Oficiales de Farmaceuticos, 1995: 284–5. 4. A pH similar to that of vinegar or lemon juice. 5. The pH scale is logarithmic rather than linear. 6. Which must be done as quickly as possible so that all areas of the face are at practically the same level of acid attack at the time of neutralizing.

7. Except for Easy Phytic®, which is not neutralized. 8. An acid is, by definition, a molecule that can donate a proton. 9. Lidocaine with epinephrine (adrenaline) has a similar acid pH, but it is impossible to do a peel with lidocaine. Acidity is therefore not the only important parameter. 10. A salt is formed by the interaction of an acid and a base; an ester (R–COO–R' if R' is not –H) is formed by the interaction of an acid and an alcohol. 11. Via tumor necrosis factor alpha (TNF-α), among other mediators. 12. Known as post-inflammatory hyperpigmentation (PIH). 13. Ammonium lactate has been shown to prevent dermal atrophy resulting from the use of topical corticosteroids.

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7 Alpha-hydroxy acids: histology and factors influencing penetration Histological changes Epidermis Epidermal regeneration is histologically visible after 2–7 days, and the epidermis is completely replaced 2 weeks after a single light alpha-hydroxy acid (AHA) peel. A single application of a glycolic acid peel (20–30%) reduces corneocyte cohesion, which accelerates the elimination of cells in the stratum corneum and hence reduces the thickness of the epidermis for around 2 weeks (the time it normally takes for the superficial layers of the epidermis to heal). Using 50% concentrations of glycolic acid ‘unglues’ the cells in the stratum granulosum. Higher concentrations (70%) or a more aggressive mode of application cause epidermolysis, or skin necrosis, beneath the stratum corneum. Unlike single applications, daily use of AHAs seems to thicken the epidermis over time because of the constant stimulation it provides.1 However, other authors suggest instead a possible thinning of the epidermis in the long term.

essential elements of cosmetic improvement and skin rejuvenation. Some studies have presented biopsies showing the presence of new collagen arranged horizontally, with a predominance of fibroblasts 2–3 weeks after a peel.3 This new collagen remains for around 1 year.2 The concentration of glycosaminoglycans increases and gradually stabilizes. This effect could be one of the mechanisms responsible for the positive effect of glycolic acid on fine wrinkles (a filling effect after several peeling sessions). ‘Chronic’ use of AHAs seems to allow the dermis and epidermis to thicken gradually and regenerate after an initial period of flaking that, in contrast, thins the epidermis and requires the daily use of effective sun protection.

Factors influencing AHA penetration Other factors also influence the aggressiveness of a glycolic acid solution (Box 7.1).

Dermis

Other components of the solution

The histological effects of AHAs also reach the dermis. Moy showed that fibroblast cultures in a glycolic environment produced up to 10 times as much hydroxyproline (a precursor of collagen) than when cultivated in a normal saline environment.1 A practical problem is that AHAs do not normally reach the dermis (because, apart from Easy Phytic® solution, they are neutralized before they can penetrate that far) and therefore cannot directly stimulate fibroblasts as well as they did in this in vitro study. In the papillary dermis and sometimes even in the upper reticular dermis, mild edema, an inflammatory reaction and production of new collagen and elastin are observed. Production of these dermal components does not appear to be directly proportional to the extent of the inflammatory reaction. Glycolic acid stimulates fibroblasts to produce collagen, but not in the same way as trichloroacetic acid (TCA) or phenol, which produce a thick horizontal layer of papillary dermal collagen proportional to the dermal injury and hence the repair caused by the acid.2 However, the laying down of a new layer of collagen in the dermis is one of the

Some components can slow down or accelerate the penetration of AHAs. Let us bear in mind the esterification reaction: an organic acid (R.COOH) reacts with an alcohol (R'.OH) to form an ester (R.COO.R') and water: acid + alcohol a ester + water R–COOH + R'–OH a R–COO–R' + H2O

Box 7.1 Parameters determining the extent of skin necrosis pH The lower the pH is in relation to the pKa, the more aggressive the solution is Concentration The closer the glycolic acid concentration is to 80% (a saturated solution), the more aggressive the solution is

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This reaction is slow and reversible. The ester does not produce a peel. An alcoholic solution of AHAs would partially consist of ineffective esters that could be converted back into acid by shifting the balance of the reaction, after the acids in the solution have been medically or naturally neutralized. Applying alcohol to the skin, as a pre-peel disinfectant, does not interfere with the peel if the alcohol is given time to evaporate.

Preparing the skin in the weeks before the first peel Any treatment that thins the stratum corneum increases the permeability of the epidermis4 and the speed of penetration of AHA. Tretinoin, AHA creams and benzoyl peroxide are all examples of products that allow AHAs to penetrate more deeply.

Preparing the skin just before the peel Before an AHA peel, the skin must be cleansed and degreased – but not aggressively. AHAs are actually hydrophilic, and fats in the skin reduce their clinical effectiveness. Degreasing the skin vigorously, by using an ether swab firmly pressed on the skin for example, would make it difficult to predict how far the AHAs would penetrate. Immediately before an AHA peel, the skin should be cleansed and degreased with alcohol and acetone (although not aggressively), in contrast to what can be done before a TCA peel to the papillary dermis.

Contact time Neutralizing the peel too soon stops its effect. Neutralizing too late can potentially cause serious side-effects.

Neutralization versus simple rinsing Rinsing with water only dilutes the acid without neutralizing it. Only the application of a base solution can neutralize the acid.

Force of application of a peel The more forceful the application, the deeper is the penetration.

Type of applicator A brush simply spreads the acid solution on the stratum corneum, whereas using gauze causes some abrasion at the moment of applying the acid solution and makes it penetrate more deeply.

Skin condition before a peel A young, healthy and hydrated skin is less permeable than skin treated with tretinoin or skin with seborrheic dermatitis, severe photoaging or acne.

Volume of acid applied on the skin At the same pH and concentration, applying a greater volume of acid on the skin of course induces greater necrosis; applying just a few drops of 70% unbuffered glycolic acid solution on the face will be far less aggressive than applying 5 ml of the same solution.

Other factors The penetration of AHAs through the skin is also increased by prior use of: ■ wax and other hair-removal products (watch out for the upper lip area) ■ exfoliants or scrubs ■ preparatory masks and vinyl masks ■ tretinoin and other retinoids ■ benzoyl peroxide creams ■ hair perms (increased penetration on the hairline)

Notes 1. 2.

Frequency of repeated peel sessions Repeating peels too often gradually deepens their action and can cause chemical burns. Repeating peels after too long a delay does not allow gradual stimulation of the dermis – the peel will not be able to achieve its full effects.

3.

4.

Rubin MG. Manual of Chemical Peels, Superficial and Medium Depth. Philadelphia: JB Lippincott, 1995. Moy LS, Mene R. Glycolic acid chemical peel. In: Roenigk & Roenigk’s Dermatoligic Surgery, Principles and Practice, 2nd edn. 1103–12. For this reason, it pays to inject botulinum toxin before starting the peel: immobilizing the muscle mass will allow the smooth synthesis of new collagen. Epidermal permeability in descending order: genital organs > facial skin > skin on torso > skin on upper and lower limbs.

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8 Alpha-hydroxy acids: indications and results

The results following daily topical application of low concentrations of glycolic acid in a simple aqueous solution start to show after 2–3 months of continuous treatment, if the concentration is higher than 8%. Alpha-hydroxy acids (AHAs) produce almost no results after a single application;1 they have to be repeated several times to produce clinical results. Whatever the number of AHA peels, the results for wrinkles, dyschromia or photoaging will never compare with the results of a medium or deep peel (cf. the indications for phenol), except in rare cases where the dermatological problem being treated is very superficial in origin. The results are not permanent, and biological analysis shows a return to the original condition 1–2 years after AHA peels. We must accept these limitations of superficial peels. AHAs are not toxic to melanocytes, and can therefore be applied on dark skins and in all seasons, on condition that effective sun protection is used.2 Contact time (Table 8.1) depends on skin type, peel concentration and formulation, its pH, the method of application, preliminary skin preparation, etc. At an identical pH, a 50% concentration of glycolic acid will penetrate half as deep as a 70% concentration, and will take twice as long to do so.

Table 8.1 Suggested contact times for glycolic acid Condition

Glycolic acid concentration (%)

Contact time (min)

Acne Keratoses Fine wrinkles Back

50–70 70 50–70 70

1–3 4–8 4–8 4–10

in the follicles is also reduced, and this stops the follicle canals closing. AHAs are excellent comedolytics: glycolic acid eliminates the hyperkeratosis responsible for the clogged pores. After a glycolic acid peel, the top of the lesion will sometimes whiten to a certain degree as a result of the increase in epidermal permeability around the edge of the inflamed lesion. The whitened areas will disappear in a few days, allowing the sebaceous glands to open and drain. When treating facial acne, concentrations of 50% or more seem to be the most effective, with contact times of 1–3 minutes. Higher concentrations or prolonged contact times cause unexpected frosting (areas of epidermolysis) and slow down post-peel healing. When treating the back, a concentration of 50% is not enough, and concentrations of 70% should be used for 4–10 minutes. If frosting occurs on the back, it is a sign of greater effectiveness, in contrast to facial treatment. Maximum effectiveness is achieved when treating active inflammatory acne. Superficial scars are only rarely and very slightly improved by repeated AHA peels. Ice-pick acne scars are not an indication for superficial peels, and deep scars only respond to a combination of other treatments: dermabrasion, punch elevation, deep peels, filling, dermal stimulation or laser. Treatment of active acne (comedonal, papular or papulopustular) involves a combination of skin preparation, weekly sessions of glycolic acid peels and appropriate and effective daily cosmetic care (see Chapter 3). AHAs produce only a cosmetic result and do not alter the particular genetic traits that lead to acne in some patients: a peel does not change the blood testosterone level, the activity of 5α-reductase, receptor sensitivity or the tendency of the corneocytes to stick together and block the pilosebaceous units. AHA peels must be accompanied by appropriate long-term anti acne daily cosmetic care (Skin Tech’s Purifying® cream or gel).

Acne The use of AHAs (especially glycolic or lactic acid) in treating acne has often given good or even excellent results. Easy Phytic® solution (see Chapter 11) is especially safe, effective and comfortable for this indication. Keratinocyte cohesion

Aging of the skin AHAs were first used to treat dry skin (hyperkeratinization and xerosis) before the positive effects on photoaging skin

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gradually came to light. Photoaging causes the stratum corneum to thicken (the skin becomes dry and rough), local proliferation of melanocytes (lentigines and pigmented hyperkeratosis) and dermal elastosis (wrinkles, fine lines and sagging skin). AHAs can partially help to fight these three types of involution that progressively and inexorably make the quality of the skin deteriorate. AHAs can only provide superficial treatments, whose direct action is limited to the epidermis. However, for the careful observer equipped with good photographs, longterm repetition of AHA peels shows a gradual improvement in the quality and tone of the skin, which becomes softer and more even in tone, as well as partial correction of the appearance of fine lines.3 Contact times can be relatively short when AHAs are being used to prevent aging, but when the photodamage is more severe, the length of contact time between the glycolic acid peel and the skin before neutralization should be increased to help improve penetration, as sun-damaged skin is more resistant.4 When using glycolic acid creams, the photodamaged skin soon becomes less dry and rough: results start to show after 3–4 weeks of daily treatment, but obvious clinical results can be seen more clearly after several months of treatment. Patients should never be led to expect too much too soon. Even though patients soon feel an improvement in the ‘feel’ and quality of their skin, it is pointless to exaggerate and promise that wrinkles, folds or fine lines will disappear altogether: a long series of 50–70% unbuffered glycolic acid peels (for 6–12 months) only moderately improves fine lines. Wrinkles and skin folds are not indications for AHAs. A histological study did not show any significant change after four monthly AHA peels.5 The long rest period between peels could be to blame for the lack of histological results, as the peels must be repeated in relatively close succession to be effective and benefit from the gradual cumulative effect of the stimulation produced by the different peels. Once a month is too infrequent and, clinically, weekly repetition is far more effective. Weekly sessions should be kept up for the first 4–6 weeks of treatment, if the patient’s skin can tolerate it. Thereafter, peels should be repeated twice monthly, and eventually once a month as maintenance treatment. Treatment for aging skin should, of course, be accompanied by active daily cosmetic care: DHEA-Phyto®, Actilift® or Renutriv ACE Lipoic Complex®.6 Treatment of photoaging is the second preferred indication for Easy Phytic® solution, and results (tightening effect) appear rapidly, after the first few sessions.

There is relatively little risk of post-peel pigmentary changes if the peel is applied correctly, but this risk cannot be ruled out, even when the glycolic acid peel has been kept in technically perfect conditions (see Figure 37.28, p 331). When treating hyperpigmentation, the skin must be cleansed and degreased with the utmost care before the peel, since if the skin is handled too roughly, too much glycolic acid could penetrate too quickly locally and cause post-inflammatory hyperpigmentation.

Dyschromia – melasma

Xerosis, ichthyosis and warts

Combining glycolic acid in a 50% peel and daily creams of 8–12% helps moderately improve dyschromia of a purely epidermal origin.

AHAs have been prescribed for a long time in the treatment of xerosis, ichthyosis and sometimes warts. Dry and rough skins are an excellent indication for AHA creams and peels.

Use of an AHA cream alone More often than not, it takes 3–4 months of daily applications of AHA creams alone to get a clinical result. AHAs are not renowned for their anti-tyrosinase action; they limit melanin synthesis mainly through their antioxidant power and increase the turnover and renewal of cells laden with pigment. Using just AHA creams as the only form of treatment for melasma is disappointing.

AHA cream and peel Combining regularly applied glycolic acid peels with AHA daily care creams increases the effectiveness of both. One of the mechanisms of action of AHAs is to facilitate penetration of the components of cosmeceutical creams used between the different peel sessions. AHA peels help rid the superficial layers of the epidermis of an excess of melanin, and AHA creams applied daily increase keratinocyte turnover, with the melanin produced being diluted in the increased number of keratinocytes. Combined used of effective sun protection reduces melanocyte production and improves the results.

AHA peels and non-AHA cosmetics Combining regular peels with Blending Bleaching® cream and effective sun protection (see Chapters 2 and 3) is the most effective option for treating melasma. Tretinoin can be combined with other cosmetics, as can hydroquinone, tyrosinase inhibitors and antioxidants. It has been proved that applying a depigmenting cream between peeling sessions is more effective than applying a glycolic acid cream. It has also been proved that a treatment combining peels and a depigmenting cream is more effective than treatment with depigmenting cream alone. AHA peels are not, of course, the first choice of treatment for melasma.

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Easy Phytic® (see Chapter 11) solution is particularly well tolerated by patients with ichthyosis, who soon feel an improvement in the elasticity of the superficial layers of the skin, which ‘pulls less’ after the first applications.

Hyperkeratotic eczema Glycolic or lactic acid 15–20% has been used in the treatment of hyperkeratotic eczema and hyperkeratosis of the palms and soles.

Glycolic acid as a pre-peel treatment Glycolic acid helps to increase penetration and enhances the action of the active molecules in the cosmeceuticals or medication applied between peeling sessions. It may act as an antioxidant and chelate iron ions (reducing the production of free radicals). Applying a 12% glycolic acid cream after exposure to the sun helps reduce the duration of the erythema. Glycolic acid has also been used as a preparation for a medium-depth peel, to enhance the penetration of trichloroacetic acid (TCA) to the papillary dermis (i.e. before a 35% m/v TCA), for example. However, in my opinion, the uneven penetration of the glycolic acid peel is not ideal for enhancing TCA penetration. The TCA will penetrate more deeply where the glycolic acid penetrated most, and the overall result could be uneven. AHA peels have been used unsuccessfully in the treatment of stretch marks, both as monotherapy and in combination with corundum crystal microdermabrasion before the peel. Treating the stretch marks with microdermabrasion beforehand enhances AHA penetration, but does so linearly, in the form of claw marks (Figure 8.1). The results are poor, even on fine, white, superficial stretch marks.

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Effectiveness of AHA peels The effectiveness, in cosmetic terms, of a glycolic acid peel can sometimes be miraculous, sometimes non-existent. Some patients are delighted and others are deeply disappointed, but more often than not the result of a series of peels with glycolic acid in an aqueous solution is considered ‘average’. However, long repetition of the peels can maintain the appearance of the skin or even visibly improve it. One clear advantage of glycolic acid lies in the fact that patients can carry on with their professional and social lives immediately after the peel, without any visible signs of flaking7 in the days following the treatment. Cosmetic improvement is very gradual, and often, if there is no good-quality pre-treatment photographic record, the patient as well as the practitioner may wonder if the treatment has really been effective. Although the patient’s immediate entourage might not really notice any difference, the people the patient meets less often will notice some change and might comment on how rested or youthful they look. Repeating peels over a long period of time ensures the progressive effectiveness of peels with glycolic acid in an aqueous solution.

Effectiveness is doctor-dependent The application technique used by the doctor, how carefully he applies the peel and his experience are all factors that influence the outcome of treatment.

Effectiveness depends on the galenical form Not all glycolic acid peels are the same as far as the skin is concerned. The peels that are the most difficult to use are glycolic acid in simple aqueous solution and glycolic acid masks (because it is difficult to monitor how the skin is reacting). The most effective peel would be one that does not need neutralizing, in spite of having a pH of 0.5 for a solution with a pKa between 3 and 4.

Effectiveness is doubly timedependent

Figure 8.1 Alpha hydroxy acids peel after microdermabrasion.

The effectiveness of a peel with glycolic acid in aqueous solution depends on the amount of time for which the acid is contact with the skin and therefore on how soon it is neutralized.8 Neutralizing too soon only allows a small proportion of the acid to act. Effectiveness also depends on the number of sessions. The greater the number of sessions, the more visible are the results. The effectiveness of glycolic acid is therefore entirely dependent on time in both the short and long

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term. In the short term, the same concentration will reach the deeper layers if it is left on longer before being neutralized. In the long term, for the results to be visible, a number of repeated peels are necessary, even with 70% unbuffered glycolic acid on a well-prepared skin. A single application of partially buffered 50% glycolic acid only allows exfoliation ‘just beneath the surface’ – plainly subclinical.

Effectiveness is patient-dependent Preparing the skin properly during the weeks before the peel helps the glycolic acid penetrate more evenly and deeply. The quality of the results will be better if the patient follows the doctor’s recommendations to the letter. Some patients underestimate the importance of preparation and do not put on the creams they have been prescribed. The upshot is inadequate and uneven penetration, which leads to inadequate results and an increased risk of complications. Some overenthusiastic patients, on the other hand, think they can get into the doctor’s good books by applying the pre-peel treatment more often or more liberally than prescribed. This results in an unexpected increase in skin permeability that deepens the effect of the glycolic acid and increases the risk of complications, without the advantage of a better outcome. With Easy Phytic®, there should be no pre-peel preparation, as the stratum corneum must be intact to allow it to act progressively. Creams likely to facilitate AHA penetration should be stopped 2 weeks before the first Easy Phytic® treatment.

should be a specially detailed file recording the various events of the peel and the treatments accompanying it.

Effectiveness on wrinkles, fine lines and folds A glycolic acid peel is not an effective treatment for folds and wrinkles. Fine lines can improve gradually over the course of repeated glycolic acid peels. New collagen synthesis has been noted in the papillary dermis, but what seems to be responsible for a large part of the results of a glycolic acid peel on fine lines is the edema that is caused and maintained by the repeated application of the acid. The tautening and filling effect on the skin is sadly only temporary. Whatever the case may be, it is interesting to note that it is possible to improve fine lines, if only slightly, without causing skin necrosis. The treatment plan must be rigorous, and care between and after peels is of vital importance.

Notes 1. 2. 3.

4.

A glycolic acid peel is not an ‘end in itself’ A glycolic acid peel should never be considered as an end in itself, but as part of an overall care plan for the past and future of a patient’s skin. Pre- and post-peel care plays a large part in the final outcome. For the follow-up, there

5.

6. 7. 8.

Except that the skin’s texture may feel smoother. Peyronnet B. Acide trichloracétique ou acide glycolique? J Med Esth Chir Derm 1994; XXI (84): 257–60. Wrinkles can only be improved by using deep peels; folds usually only respond to surgery, support threads or fillers. An improvement in the appearance of fine lines can be seen after 4–6 months of daily application of 10–12% glycolic acid cream. The stratum corneum is thicker and so more impermeable in photoaged skin. Piacquadio D, Grove MJ, Dobry M. Efficacy of glycolic acid peels questioned for photodamaged skin: a pilot study. Dermatol Times 1992; May: 52. Skin Tech (www.skintech.info). If the glycotic acid is neutralized as soon as erythema appears and before any frosting appears. In other words, it depends on the ‘contact time’.

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9 Alpha-hydroxy acids: application as cosmetics and as peels

Cosmetic application of glycolic acid Since the application of glycolic acid at first reduces the thickness of the epidermis, the skin can no longer provide the same protection against light, and it is essential to use effective sun protection to avoid the risk of accelerated photoaging. A glycolic acid cream or gel can easily be prepared in a pharmacy dispensary, at concentrations of 8–15%. There are many commercial preparations of glycolic acid that have the combined advantage of spreading evenly and a galenical form that allows better penetration of the acid. These low-concentration, daily topical treatments are mainly indicated for preparing the skin for other techniques, for follow-up treatment between peels or for maintenance treatment afterwards. In general, patients who use glycolic acid as a cosmetic do not expect or will not accept any flaking. If the skin does flake, treatment should be stopped and started again a few days later at a lower concentration (or warm water can be sprayed on the face before applying the glycotic acid cream to dilute it). As monotherapy, 8–15% gels (which can be buffered to the physiological pH to 4.55)1 are applied twice a day, after washing the face with a mild soap (e.g. Avene®) if the skin is ‘normal’. If the skin is dry, care should be taken not to degrease the skin, so that the gel does not penetrate too deeply. If the skin is oily and/or acneic, it should be degreased with a glycolic acid-based cleanser before applying the gel. It is essential to use effective sun protection. As a precaution, the initial concentration of glycolic acid should not be more than 8% and the gel should be applied every other day at first. The concentration and frequency of application can be increased, depending on the skin’s response and tolerance. When treating severe photoaging, the concentration of the glycolic acid should be gradually increased from 8% to 12%, 15% or possibly 20%. Alpha-hydroxy acids (AHAs) can be applied on the face as well as the neck, décolletage, hands, forearms and other parts of the body. It must be remembered that the skin on the face is far more permeable than the skin on the limbs or torso.

Combination of AHAs and tretinoin Shared effects Tretinoin and AHAs act on the epidermis and the dermis. When used over a long period of time, they both have the following effects: ■ an increase in the overall thickness of the epidermis at the same time as a decrease in the thickness of the stratum corneum: the skin appears smoother and more hydrated ■ increased dermal thickness and new synthesis of collagen and elastin fibers

Specific effects Retinoids induce neoangiogenesis, whereas AHAs act on the dermis without necessarily going through a phase of inflammatory reaction. We can therefore assume that their combined effects can produce better results at the same time as reducing the incidence of side-effects thanks to the use of lower doses of each of these two potential irritants. For example, if there is resistance to (daily or twice daily) monotherapy with tretinoin2 at 0.1%, applying an 8–10% glycolic acid gel beforehand helps the retinoid to penetrate more efficiently. Tretinoin and AHAs can be applied separately, but they can also be mixed in the same gel. If, on the other hand, a patient cannot tolerate a concentration of tretinoin at 0.05%, applying an 8–10% glycolic acid cream in the morning will make a tretinoin cream at 0.015% applied in the evening more effective, at the same time as reducing the irritation caused by the retinoid. These combinations must always be used under close medical supervision, however, as in dual therapy, skin reactions can be highly unpredictable and severe in some patients. More sensitive skins can be treated as follows: ■ days 1–15: 8–10% glycolic acid cream in the morning

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■ days 15–30: 10–12% glycolic acid in the morning ■ days 30–60: 8–10% glycolic acid in the morning plus 0.015% tretinoin in the evening The doses of each product should be increased gradually thereafter. If the patient has a tendency to erythema, photosensitivity or telangiectasias, the glycolic acid should be increased and the concentration of the tretinoin decreased. If the patient has thin skin, the tretinoin should be increased more quickly than the glycolic acid.

Combination of AHAs and hydroquinone There is no point combining hydroquinone and AHAs in a peel solution, as hydroquinone has a tyrosinase-inhibiting action that can only establish itself gradually and act on the first biochemical stages of melanin synthesis. On the other hand, it is worthwhile combining the two in the daily treatment of melasma between or after peels. The pharmacist should be asked to add 3–8% hydroquinone to a water-in-oil cream with an 8–10% glycolic acid concentration. Gels are more active and better tolerated by oily skins, while the most suitable galenical form for dry skins is cream. Kojic acid (2–5%) can also be added gradually to the combined glycolic acid plus hydroquinone formulation to enhance its action.

Combination of AHAs and other topical pharmaceuticals The reduction in corneocyte cohesion caused by AHAs allows topical preparations containing cortisone, antifungal and antimitotic agents, etc. to penetrate more easily. 5-Fluorouracil (5-FU) has been widely combined with glycolic acid in the treatment of severe photoaging. Application should be ‘pulsed’ to limit the inflammatory reaction caused by daily application of 5-FU. Glycolic acid 10% should be applied once or twice a day while the 5-FU (as a cream with a concentration of 1–5%) should only be applied on two consecutive days per week, every other week. Actinic keratoses on the scalp can tolerate a weekly application of 5-FU combined with glycolic acid. David R. Harris3 reports treating actinic cheilitis by applying a Vaseline® or silicone ointment containing 5% glycolic acid and paraffin. This treatment can be deepened by periodic applications of 5-FU and/or light trichloroacetic acid (TCA) peels. AHA peels can be used to treat patients of all skin phototypes who cannot accept any downtime. Results are, however, difficult to predict: some patients show a rapid

improvement in the quality and color of the skin, while others do not notice any cosmetically visible change. The unexpected, though rare, occurrence of complications always poses a major problem when a treatment has been guaranteed ‘not be noticed by a third party’.

Application of glycolic acid peels Pre-peel preparation Long-term preparation Long-term preparation starts 4–6 weeks before a waterbased AHA peel. It can be non-specific or specific. It is not essential, but noticeably improves results by ensuring deeper and more even penetration of the glycolic acid peel. Greater vigilance is required when applying the peel, however, as it must be neutralized more quickly. Non-specific preparation to make a water-based AHA peel deeper and more even In the evening, a 0.05% tretinoin cream should be applied (see Chapter 2). This cream reduces the thickness of the stratum corneum and provides a deeper peel with the same concentration. A 10% (non-photosensitizing) glycolic acid gel could be applied on younger women in the morning. Specific preparation: to give patients a focused care plan Preparing a patient who has acne is not the same as preparing a patient with photoaging or melasma. Hyperpigmentation of all sorts responds extremely well to pre-peel treatments. Menopausal or post-menopausal women can benefit from a hormone cream as part of anti-aging treatment. The following formulation can be prescribed: testosterone propionate 100 mg estrone 5 mg estradiol benzoate 5 mg eucerin® O/W 45 g or Neribase® 45 g See Chapter 2 for more details.

Medium-term preparation This concerns combined treatments used before the peels as well as the cosmeceuticals or pharmaceutical products used by the patient (see above). Medium-term preparation starts 2–4 weeks before a peel.

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Folds, wrinkles and fine lines should be treated beforehand with dermal fillers, thread lifts, mesotherapy, stimulation or any other treatment chosen by the doctor. Benign tumors can be excised or treated by shave biopsy or lasers. Rosacea should be treated before the peel during this same period. Botulinum toxin, ideally should be injected 8 days before the first water-based glycolic acid peel.

Short-term preparation It is preferable not to put on any cream that could permeabilize the skin or use any technique likely to damage the stratum corneum during the few days before an AHA peel. Small retention cysts can be removed with a needle or number 11 scalpel blade 1 week before applying the waterbased glycolic acid.

Desquamation Buffered solutions of glycolic acid, when applied correctly, only produce virtual desquamation. Water-based glycolic acid does not penetrate evenly, and the risk of localized overpeeling, scabbing or post-inflammatory hyperpigmentation is not insignificant. The destruction of the epidermis that causes visible flaking depends on how the peel is applied, as well as on the type of peel used. A short contact time with a 50% glycolic acid peel at pH 3.5 produces almost no visible flaking, while a longer contact time with 70% glycolic acid at pH 0.5 induces epidermolysis and the appearance of small scabs and visible flaking. The correct contact time with a water-based 70% glycolic acid at pH 0.54 causes little or no flaking, but repeating it too soon could trigger visible flaking. Applying a water-based 70% glycolic acid peel at pH 0.5 with a flat brush will cause less flaking than if it is applied with a gauze pad (which is slightly abrasive) after the skin has been disinfected with alcohol or degreased with acetone or ether, or after the skin has been prepared for several weeks with tretinoin cream. All other conditions being equal, applying a greater quantity of AHA causes more of the epidermis to be destroyed and more visible flaking. Easy Phytic® solution, in spite of its pH of 0.5, causes almost no flaking and penetrates more evenly than other AHAs, because of its formulation and application procedure.

Treating the face or body AHA peels have mostly been used to treat the face, but can also be used to treat other areas of the body. Facial skin is more permeable to AHA peels than the skin on the rest of the body. The neck, décolletage, hands and forearms can be treated with a combination of AHA peels and effective post-peel care (see Chapter 3).

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With these body treatments, we can expect an improvement in the quality of the structure of the skin, improved hydration and some temporary lightening of the complexion. Lentigines and keratoses should be treated by another method in parallel with AHA peels. There are other, more efficient, techniques to treat these problems: liquid nitrogen, dry ice, Only Touch® peel, ‘intense pulsed light’ (IPL), laser, etc. Dr Robert Vergereau (France) compared the use of dry ice, Erbium laser, Q-switched laser, coagulation and Only Touch® peel. He concluded that: ‘If all these methods are satisfactory, in my opinion, the technique using trichloroacetic acid5 is the most beneficial’. Treatment of other areas of the body with AHAs is not often described, because of the poor penetration of these acids through the skin of the body. A technique combining abrasion and an application of Easy Phytic® solution (see Chapter 11) is more successful on the legs, arms and torso.

Buffered or unbuffered AHAs? The results produced by buffered AHA peels can, in a way, be compared to those produced by unbuffered peels, but only when applied over a longer period of time and more frequently. From a histological point of view, all peels produce comparable results depending on the strength of the peel. The action of an AHA peel with a pH higher than its pKa and close to the skin’s physiological pH (4.5–6) is very slow. A buffered solution will often only be applied for the first ‘reconnaissance’ peels or on sensitive skins. Thereafter, the peels will be performed with 70% unbuffered glycolic acid solution in a gel or Easy Phytic® solution.

How many sessions should be anticipated? AHA peels should be considered a long-term treatment. No noticeably visible improvement, except for a softer skin, should be expected until after many sessions. Sometimes, the results do not become obvious until after 8–10 sessions of water-based unbuffered 70% glycolic acid peels. How frequently the sessions should be repeated depends on how the skin reacts or how sensitive it is. Some thin and sensitive skins will not tolerate more than one session every 2 weeks, whereas thicker or oilier skins will easily tolerate a weekly session or even more. It is clearly difficult for people who can only tolerate one session a month to achieve visible results. Even the most willing patients can be worn down by the boredom of repeated sessions that can sometimes be unpleasant and have a limited effect. Patients who cannot be treated more than once a month often give up treatment long before it has finished.

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Classic application technique for glycolic acid A glycolic acid peel can be applied in an aqueous solution or in a gel, with a gauze pad, a brush, presoaked cotton swabs or pads, gloved fingers, etc. Compact and opaque AHA masks have been used, but monitoring the skin while the mask is on is neither easy nor certain. The glycolic acid solution is applied quickly (in 15–20 seconds maximum), so that the contact time is the same for the whole face. The solution should be applied to the most resistant areas first (the forehead) and to the more sensitive areas last (the eyelids). It is important to develop application habits and always use the same system, both for applying and neutralizing the peel. Partially squeezing out the applicator before using it guards against the product forming ‘pools’ on the skin. Massaging the skin with a gloved finger allows more even penetration or deeper local penetration if the doctor considers it necessary. By closely monitoring changes in skin color, the AHA solution can be neutralized before any frosting occurs. To a certain degree, the contact time is more important than the total quantity of AHAs applied to the skin: a low overall quantity of glycolic acid left to act for a longer time can penetrate the skin more deeply than a larger quantity that is neutralized immediately. As well as the choice of peel, monitoring the contact time is an essential part of any glycolic acid peel. This is why the glycolic acid peel has been called ‘time-dependent’, prompting the purchase of many completely redundant timers. Glycolic acid can be applied up to a few millimeters from the eyelashes, no matter what its concentration. If any glycolic acid comes into contact with the eyes, they should be rinsed immediately with plenty of water, and drops of artificial tears or physiological solution should be applied. Glycolic acid is not a protein coagulant like TCA or phenol, and the risk of damage to the eye after contact is not high. In fact, dilution from teardrops appears to be enough to avert most of the danger. The author has never come across any objective ocular damage, even in the extremely rare case of contact between glycolic acid and the eyes. Sometimes, a very small quantity of glycolic acid can be drawn up into the eye by capillarity if the peel is applied too close to the conjunctivae. This immediately causes the formation of tears, which dilute the acid and reduce its aggressiveness. Patients should be asked to keep their eyes shut while waiting to have eye drops put in that will bring immediate relief.

Contact time The contact time is the time during which the AHA is left to act before being neutralized and stopping its effect. It depends more on the appearance of erythema than on the

Table 9.1 Correlation between skin appearance and depth of AHA peel No erythema Spots of erythema Patches of erythema Widespread erythema Frosting

Virtual peeling effect Very, very superficial Very superficial Superficial peel, suitable depth for AHAs Too deep for an AHA peel

concentration, the pH, the total volume applied, the number of applications, etc. AHAs in aqueous solution do not penetrate the epidermis evenly, and the erythema, which is the first sign of the skin reacting to a peel (Table 9.1), does not appear evenly either, but rather in spots or patches. It is therefore essential for the doctor to stay beside the patient during this phase of the peel and not to take his eyes off the treated area. The safety limits are not very flexible when using AHA in aqueous solution, and a peel can go from ‘too superficial’ to ‘too deep’6 very quickly. Contact time should end as soon as erythema begins. The problem is that it is not long before erythema turns to frosting, and the doctor is often faced with the following dilemma: neutralize too soon and have limited results, or try to neutralize a bit later and risk complications. It was to avoid this dilemma that the author developed Easy Phytic® solution.

Contact time for a glycolic acid peel Each patient’s skin reactivity should be tested by an initial application of a less concentrated and/or a partially neutralized peel (e.g. 50% at pH 3.5). As a precaution, the initial contact times should be short, in order to test the skin’s reactivity. When we say that an AHA peel is ‘time-dependent’, we mean that the contact time depends on examining the skin directly and not on the clock. We do not really need to know exactly how long the product should be left to act: the right contact time is enough time for erythema to occur, but no frosting at all. Table 9.2 shows, as an approximate guide, the depths reached by unbuffered 70% glycolic acid (pH 0.5) with different contact times on the face. It should always be remembered, however, that AHAs should never be used to do anything other an epidermal peel. Each patient has their own particular level of sensitivity and contact time. It is therefore important to take precise notes on the treatment given: the type of solution, the concentration used, the contact time (except in the case of Easy Phytic® solution, which does not need neutralizing), the places where erythema first appears,7 the number of coats,

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Table 9.2 Depths reached by unbuffered 70% glycotic acid (pH 0.5) as a function of contact time Contact time (min)

Depth of effect

1–5

Gradually deepening epidermolysis, depending on contact time and skin sensitivity

5

The acid reaches the dermoepidermal junction

10

The acid reaches the dermis – which is not desirable, as its effect, locally, will be similar to that of 30–35% TCA m/v

15

The depth of skin necrosis, locally, is histologically comparable to or greater than that reached with 35–40% TCA m/v

The problem with AHA peels clearly lies in the neutralization. Easy Phytic® provides a solution to this difficult problem, as, in spite of its pH of 0.5, this peel does not need to be neutralized and therefore benefits from the effectiveness of 100% of the molecules applied to the skin. It should be remembered that rinsing with pure water dilutes an acid (lowers its concentration), whereas a base solution neutralizes it (raises its pH). The neutralizing solution should be prepared before the peel so that it is instantly available when neutralization is necessary (Box 9.1). Skin burns as a result of neutralizing too late because of lack of preliminary preparation of the neutralizer would always be considered as professional misconduct by an expert.

Box 9.1 Preparing the neutralizing solution The simplest neutralizing solution consists of a solution saturated with sodium bicarbonate: fill a bowl with warm water and gradually add the sodium bicarbonate powder (Figure 9.1a), stirring all the time. When the sodium bicarbonate no longer dissolves and forms a sediment in the bottom of the bowl, the solution is saturated (Figure 9.1b). There is no point trying to get a more concentrated solution.

the type of neutralizing solution applied, etc. These notes will come in very useful for working out any potential change in contact time for subsequent peels. A cautious contact time of 2 minutes for a first peel with 70% glycolic acid, pH 0.5, on a patient with healthy skin of normal thickness can gradually be prolonged by 30–60 seconds in subsequent peels, if the skin can tolerate it – that is to say as long as there is no frosting.

Neutralization An AHA peel should be neutralized as soon as erythema appears and before (or, at the very latest, just as) the first pinpoints of protein coagulation (frosting) appear. The peel can be neutralized with a solution saturated with sodium bicarbonate, for example. We saw above that the ‘bicarbonate system’ is a natural and powerful system for neutralizing organic acids. Neutralizing an AHA peel with a bicarbonate solution immediately stops its action. The reaction of an acid with a base produces a salt that has no peeling activity. The question is then what proportion of acid was effective during the AHA peel. If unbuffered 70% glycolic acid is applied and neutralized after a few minutes’ contact time, what is the proportion of free acid that will have been effective: 30% or 50%? If a solution is applied with a concentration of 70% but buffered at exactly pH 3.83 (which is the pKa of any glycolic acid solution), it contains only 50% free and active glycolic acid; the other 50% consists of an inactive salt. In reality, this solution corresponds to only 50% of the 70%, that is 35% of pure glycolic acid. Rapid neutralization of this solution reduces its effectiveness even further.

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A

B

Figure 9.1 (a) Sodium bicarbonate powder. (b) Saturated solution of sodium bicarbonate.

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The doctor and assistant should carefully monitor all the areas treated with acid. Surfaces that develop any local erythema should be neutralized there and then with the tip of a sponge soaked in saturated bicarbonate solution (sodium bicarbonate is readily available at pharmacies). It is possible to apply corticosteroid cream to the localized erythema. When several areas have become erythematous and been neutralized, the whole face should be neutralized by applying strips of paper, for example,8 soaked in the neutralizing bicarbonate solution (Figure 9.2). If the glycolic acid is not completely neutralized, applying a solution of sodium bicarbonate triggers a chemical reaction that produces a warm tingling sensation and may contribute to the development of temporary postneutralization erythema together with bubbles. The skin is

completely neutralized when no more ‘bubbles’ are felt. Neutralizing with a bicarbonate solution, or any other commercial neutralizing solution, is only obligatory when using unbuffered solutions. When the pH is close to the physiological limits (pH >4), thoroughly rinsing with running water is enough,9 since the relatively high pH of these partially buffered solutions is not too aggressive for the skin, and diluting the acid is all that is needed to increase its pH sufficiently. AHAs are the only peels where neutralization is important – TCA, resorcinol, salicylic acid and phenol do not need neutralizing. Glycolic acid is not a protein coagulant. It does not combine with proteins and is not neutralized, like TCA. It remains aggressive until it is neutralized, diluted or picked up by the skin’s buffer systems. After neutralization, the patient may continue to feel the acid burning in places. The patient can be given a cotton pad soaked in bicarbonate solution and asked to neutralize the more sensitive areas more thoroughly until the burning sensation has completely gone. The patient will often go back to the nostrils and eyebrows several times. More sensitive areas can actually be protected before the peel with Vaseline® applied on a cotton bud.

Neutralizing partially buffered solutions A

A (partially) buffered solution has an artificially high pH that makes it less aggressive. In fact, to allow doctors to do their job properly, the pH of glycolic acid or other AHA solutions should be given on the bottle. When using a prescription solution from a pharmacy dispensary, it is vital for the doctor to take the trouble to check the pH of each solution himself (with a pH test strip, pH meter, etc.). Checking the pH personally can sometimes bring surprises – and confirms the need to do so. In case of doubt or if the pH is not known, it is, in any event, better to opt for neutralization: there is no danger in neutralizing a peel, whereas it can be disastrous not to (Table 9.3). In the interests of caution, it is best to neutralize the peel in the face of any doubt. After neutralization, spraying the skin with warm water gets rid of any excess bicarbonate, and the face can then be dried.

Table 9.3 Neutralization of glycotic acid peels: appropriate guide B

pH of peel

Procedure

Figure 9.2

>3.5 0.5–3.5

Rinse with water Neutralize, then rinse with warm water

(a) Soaking paper strips in the bicarbonate saturated solution. (b) Application of paper strips.

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Post-peel care

Maintaining the results after peels

Further information is available in Chapter 3.

When it comes to the patient’s overall treatment plan, he or she will often ask how best to maintain or improve the results achieved. A monthly maintenance peel can be recommended, as well as continued use of the treatment started between peels. Sun protection is indicated in all cases to limit UV penetration through a temporarily thinned and hyperpermeable skin. See Chapter 3.

Immediate post-peel care The appearance of uniform erythema indicates that the glycolic acid has penetrated properly, and is the signal for neutralization. After neutralization, spraying with warm water cleans the skin of any residual chemicals. Immediately after the glycolic acid peel, the skin is very permeable, and products applied to it during this period will penetrate more deeply and thoroughly. This is an ideal time to apply the classic post-peel care treatments: see Table 3.1 in Chapter 3.

Care between peels Glycolic acid peels help cosmetic or medical treatments applied between peeling sessions to penetrate more easily. Tretinoin should be used carefully during the days immediately following a peel, especially when the skin is thin and dry. The choice of vehicle should be discussed with patients: a patient with oily skin will not always like using creams and might prefer a gel; the same gel would be unpleasant for a patient with thin, dry skin.

Notes 1. 2.

3.

4. 5. 6. 7. 8. 9.

See comments on buffering AHAs later in this chapter. Resistance to tretinoin: no visible signs and no discomfort, even with relatively high doses; there is no erythema and no unpleasant sensation in the skin. Harris DR. Treatment of aging skin with glycolic acid. In: Elson ML, ed. Evaluation and Treatment of the Aging Face; Springer-Verlag, NY. 1995: 31. Effective neutralization as soon as erythema appears. Author’s note: The comparison was made using Only Touch® peel combined with Easy TCA®. That is, too deep in relation to the peel used: a glycolic acid peel should be superficial. During the next peel, the AHA should be applied last on the areas where erythema appeared soonest. Cotton pads or any other means of application can also be used. It is often when rinsing with a lot of water that a drop of acid can come into contact with the eye.

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10 Alpha-hydroxy acids: side-effects of AHAs Complications with alpha-hydroxy acid (AHA) peels are rare, easily avoided, and often spontaneously reversible or treatable by simple topical applications. More details on complications, their origins, prevention and treatment can be found in Chapter 37.

Allergies The author is not aware of any documented case of allergy to glycolic acid or other AHAs. In the case of an allergic reaction, the doctor should test for allergies to the solvents or additives in the AHA solution. Some allergic-type reactions are, in fact, caused by the AHA penetrating the dermis, which triggers a limited and localized inflammatory reaction whose symptoms are redness and swelling. This reaction disappears without treatment within 48 hours.

Pain There may be some irritation and a burning sensation, especially at the beginning of treatment. Even AHA creams (or especially gels) can cause irritation at the start of treatment. The more the skin has been ‘prepared’ or the thinner it is, the more painful it will feel when the peel is applied. The pain is proportional to the concentration of the acid and inversely proportional to the pH. A 70% peel is more painful than a 50% peel. A 50% peel at pH 3.5 is not as painful as a peel at pH 1.5. A 70% unbuffered solution applied to a thin skin prepared with tretinoin will be more painful than a 50% solution at pH 4 applied to an oily, unprepared skin. Whatever the case, this pain – a kind of tingling or burning sensation – is quite bearable. There is no need for anesthesia, analgesia or nerve blocks. More nervous patients might appreciate having their faces fanned (with an electric or hand-held fan) or the calming effect of a voice during the peel. Neutralizing the peel with sodium bicarbonate solution stops the pain.

pale pink; this coloring lasts between 15 and 60 minutes. Solutions that are too highly concentrated or are left on too long and allowed to penetrate too deeply locally can cause the formation of scabs, which, if pulled off, leave persistent erythema for several weeks or months. This eventually resolves naturally and leaves the skin a little softer. It is best to increase concentrations and contact times gradually with patients whose professional lives will not allow them to spend time locked away recovering.

Telangiectasias Although there is evidence of a certain degree of angiogenesis with AHAs, telangiectasias are rare.

Dryness, desquamation, sensitization Long-term topical use of 8–15% glycolic acid creams gradually reduces corneocyte cohesion and can cause the skin to flake. This effect is not as pronounced as with tretinoin. Dampening the skin before applying the cream dilutes the product and reduces the risk of skin sensitization. Daily use of progressively higher concentrations of AHAs can, however, cause continuous lysis of the corneodesmosomes and permeabilization – a long-term thinning of the epidermis. Patients may then complain that their skin is getting more and more sensitive. However, some histological studies show that the skin thickens with long-term treatment with AHAs.

Hyperpigmentation Post-inflammatory hyperpigmentation (PIH) is rare after an AHA peel. It may result from an error in assessment, indication or monitoring, but sometimes it can occur suddenly when a peel has been performed and neutralized correctly. PIH can be treated: for more details, see Chapter 37.

Erythema

Bacterial or viral infections

The skin must be neutralized as soon as erythema appears. At the end of the peel, after neutralizing, the skin is usually

Bacterial infections result from scratch lesions or epidermolysis from overpeeling. Bacterial infections do not occur

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when using topical treatments with 8–15% AHA cream. The incidence of herpes outbreaks after a glycolic peel has been performed correctly is no higher than in the untreated population at large. In instances of overpeeling and epidermolysis, the probability of a secondary herpes infection increases with the depth of injury. There is no need for systematic herpes prevention before an AHA peel, but if a patient is very prone to herpes, it would be wise to prescribe valaciclovir to be taken before the peel.

ate, could seriously damage the skin and produce unsightly scars. Any danger of scarring can be avoided by neutralizing areas of local erythema with sodium bicarbonate solution and not allowing any frosting to occur. If the texture of the skin should become uneven as a result of particularly uneven penetration, it can be evened out in the course of later peels.

Shiny skin Scarring A correctly applied glycolic acid peel does not reach the reticular dermis, and there is therefore no reason for it to cause scarring. I have never come across any cases of scarring after a glycolic peel, no matter what skin preparation or concentration of acid has been used. It is obvious, though, that a combination of technical errors can result in a cosmetic disaster. Applying 70% unbuffered glycolic acid in multiple coats with a gauze pad pressed firmly onto a thin and dry skin that has been irritated by a strong dose of tretinoin, without constant monitoring and diluting simply in water instead of neutralizing with sodium bicarbon-

The effect of AHAs on corneodesmosomes can cause all the pores of the skin to unblock and allow all the sebaceous glands to empty at the same time. The skin will remain shiny until it is next washed.

Achromia If the peel penetrates too deeply in a particular place, causing scabbing and delayed healing, it could lead to total and irreversible depigmentation that, fortunately, is limited to the surface area of the scab. It is a rare complication of AHA peels.

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11 Alpha-hydroxy acids: a new slow-release AHA complex with no neutralization required

General remarks Since the 1980s, alpha-hydroxy acids (AHAs) have been used alone or in combination with other acids with a view to achieving good cosmetic results, locally or generally, temporarily or permanently, and without running the risks of deeper peels. The natural origins of the first AHAs – fruit or dairy extracts – account for much of their resounding success. How could anyone resist such a benign-sounding name as ‘fruit acids’? The AHA most often used is without doubt glycolic acid, a small molecule with a low molecular weight that has no difficulty penetrating the stratum corneum, where it acts as a ‘corneodesmosome chainsaw’. It was for this property that it was first indicated in the treatment of ichthyosis and other disorders involving hyperkeratinization. An AHA applied to a clean and degreased skin breaks down the protein structures that form corneodesmosomes. The superficial cell layers are then shed from the epidermis. The skin immediately feels more hydrated, as the fingers no longer touch the dead and dehydrated corneocytes that have been shed but rather living and well-hydrated keratinocytes. AHAs are not toxic to melanocytes, and can therefore be applied on all skin types. They can also be used at any time of the year, on condition that they are combined with a strong sunscreen. AHA peels have other advantages as well: they are non-toxic and hypoallergenic, do not cause protein coagulation, have an excellent safety record, are easy to use and produce satisfactory results in a variety of indications. There is one sizeable cloud on this bright horizon, however: AHAs have to be neutralized at the right moment to limit their penetration. If they are not neutralized, AHAs will continue working until they go beyond their desired effect. Neutralizing too late may cause serious side-effects, while neutralizing too soon makes the peel completely ineffective. Nor is neutralizing the peel the easiest part of the procedure either: the action of the acids has to be stopped when erythema occurs and before the first pinpoint frosting appears. The moment the AHAs have to be neutralized comes between two events that are open to subjective judgment, which increases the degree of risk. Many doctors will

run through the following interior monologue: ‘I should have left the product to act longer for it to be effective’, or worse, ‘I should have neutralized the AHAs much earlier, because now there are going to be complications and unwanted reactions after the peel.’ With the second scenario comes a long period of uncertainty for the doctor, sleepless nights and early mornings filled with anxiety, because complications resulting from neutralizing AHAs too late can only be treated slowly and gradually, sometimes taking several months. The problems raised by neutralization are well known, and various solutions have been put forward to minimize the danger and risk involved with neutralizing conventional AHAs too late. Partially neutralized, less aggressive AHAs with a pH of between 3.5 and 5 can be found on the market. These acid solutions do not need neutralizing, but they do need diluting with water before any frosting occurs. Less risk, however welcome, goes hand in hand with a less effective peel. Another drawback to having to neutralize conventional AHAs with a very acid pH is that the effectiveness of an AHA largely depends on how long the acid is left in contact with the skin. The longer the contact time, the more active the peel will be. Hence, there is a temptation to leave an AHA peel to act as long as possible, in spite of the risk of facing complications. The aim of neutralizing is to stop the effect of the acid. A contact time of just a few minutes before neutralizing the peel gives it just a few minutes to be effective. I therefore aimed to develop a low-pH formulation – between 0 and 1 for maximum effectiveness – that does not need neutralizing. Easy Phytic® solution (EPS: Figure 11.1) was the first of this new class of low-pH AHAs that are active with no need for neutralization. Its pH of 0.5–1 (Figure 11.2) is much lower than the pKa of the different components in the solution,1 which consists mostly of free acid with no ineffective salts.2 Not having to neutralize the solution also means that there is only a minor risk of side-effects, even when each molecule is left to achieve its full effect, undisturbed by external neutralization. It is the skin itself that neutralizes the acids in the EPS. EPS can therefore be defined as a slow-release AHA solution for patients who do not want any visible flaking (it is a

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Figure 11.1 Bottle of Easy Phytic®.

Figure 11.2 Easy Phytic® solution has a pH of 0.5.

non-flaking peel) or for doctors who want to minimize the risk of the sometimes serious complications of conventional AHAs. The solution is saponified3 and adjuvanted, and consists of glycolic, lactic, mandelic (phenylglycolic) and phytic acids. The peel solution – which does not need neutralizing – allows the acids to work gradually and to full effect. This particular property allows a ‘bipolar’ action: the solution starts working on the superficial layers of the epidermis, shedding corneocytes in the same way as conventional AHAs. It then continues working its way through the skin to reach the deeper layers, slowly and not too aggressively. The acid molecules gradually lose their effectiveness as they are neutralized by the natural buffer capacity of the epidermis. The skin can in fact defend itself perfectly well against acid or base attacks thanks to its buffer capacity, which is its ability to maintain the homeostasis of its pH as long as the attack is not disproportionate to its defenses.

When its defenses are overwhelmed by a massive acid or base attack,4 the skin cannot defend itself, and its proteins are destroyed, denatured or coagulated; the skin is ‘chemically burned’. With EPS, the acid molecules in the peel solution are stabilized on the surface of the skin and concentrate in the stratum corneum.5 They are released slowly and therefore reach the epidermis gradually. This ‘slow release’ allows the epidermis to use its full buffer capacity to neutralize the acid molecules that are slowly attacking it. Unfortunately, there is another significant problem with water-based AHAs: they do not penetrate evenly.6 They penetrate more quickly in areas where the stratum corneum is thinner – and therefore more permeable – and more slowly where the stratum corneum is thicker. They penetrate more slowly on the oilier6 parts of the face and more quickly where the skin is dry, infected or irritated. It is therefore essential to prepare the skin for 2–3 weeks before the first water-based AHA peel to even out the thickness of the stratum corneum. The melanocytes also need to be ‘stabilized’ to avoid any potential pigmentary changes. With EPS, the AHAs penetrate far more evenly because of the type of vehicle used and the slow-release mechanism, which eliminates the need for pre-peel preparation. The different types of AHAs used in EPS are important: the three AHAs in the solution actually penetrate at different speeds. Small molecules penetrate the skin more rapidly than larger molecules: the glycolic acid is therefore the first to penetrate, followed by the lactic acid and finally the mandelic acid, the largest molecule, which relies on the lytic action of the other acids on the corneodesmosomes to help it penetrate the skin more easily. Phytic acid, the other active component in the solution, is not an AHA. It is a large molecule: inositol hexaphosphoric acid or cyclohexanehexyl hexaphosphate (Figure 11.3). Because of its high molecular weight, 660.08, it does not pass easily through the epidermis. The action of the three AHAs combined with the phytic acid in the solution, however, makes the stratum corneum more permeable and O O

HO HO

OH

O O

O

O

O

HO

P

O

HO OH

Figure 11.3

OH P

O

P O

Phytic acid.

OH

O

P

HO

P

P

HO

OH

O

OH

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therefore easier for the phytic acid to penetrate. Phytic acid is well known for its anti-tyrosinase and antioxidant action. It is also an iron chelator. This molecule is therefore a good indication for skin-lightening and anti-aging treatments. Finally, phytic acid scavenges the free radicals produced by the inflammation that follows any peel and breaks the usual vicious cycle of post-peel inflammation: peel → inflammation7 → vasodilation → O2 intake + pro-inflammatory components → free-radical production → cell damage → self-perpetuating inflammation → more free radicals ⇒ vicious cycle established There are two sides to inflammation. The first is positive, as it is an essential trigger for post-peel regeneration and the synthesis of new dermal components – no inflammation, no repair. The other side is negative, as the combination of vasodilation (which, among other things, helps improve tissue oxygenation) and pro-inflammatory components increases the generation of free radicals that damage the cell structures upon which the body relies to repair the skin. The presence of phytic acid, an excellent antioxidant thanks to its 12 hydroxy groups, could reduce the incidence of post-peel inflammatory reactions.

Indications AHAs thicken the epidermis and papillary dermis, increase the production of mucopolysaccharides, improve the quality of the elastin produced and increase collagen density.8 Patients treated with EPS also describe an appreciable tightening effect. Although EPS can be used for the same indications as other AHAs, its two areas of choice are aging and acne. EPS can be used as a combined treatment or as a maintenance peel with other deeper treatments; it can also be used alongside other techniques such as mesotherapy and pulsed light.9 EPS is more of a stimulating and regenerating treatment than an actual peel, as there is almost no visible flaking. The epidermis flakes almost cell by cell and not in ‘cell plates’. Patients who are put off having a ‘peel’ for fear of downtime seem to prefer EPS being presented as a ‘stimulating solution’. The term ‘superficial peel’ conjures up images of something relatively ineffective that causes unsightly flaking. EPS can be combined with ‘mesolift’ mesotherapy to particularly good effect: alternating a mesolift and EPS every other week would seem to be the best way to proceed.

Aging skin Aging skin is an excellent indication for EPS. Note, however, that it is still a relatively superficial peel and cannot claim to eliminate folds or wrinkles, which have to be

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treated by surgery and deep peels or laser treatments. EPS could be called a ‘lunchtime peel’, as it can be performed during the lunch hour and the patient can go back to work immediately.

EPS as a classic anti-aging treatment The classic treatment consists of weekly applications of EPS together with use of a suitable cosmeceutical cream (see Chapters 2 and 3,10 and also the section later in this chapter application protocol). The total number of peels will vary between 6 to 10, depending on the skin and how it reacts. At the end of the active phase of the treatment, a maintenance peel can be applied once every 2 weeks and eventually once every month.

EPS combined with mesotherapy A mesolift is a mesotherapy technique that involves injecting stimulating, relaxing or tensing or filling agents such as hyaluronic acid, polymerized DNA, vitamins, trace elements, dimethylaminoethanol (DMAE), eligopeptides, etc. into the dermis. Facial mesotherapy can be rather painful, however, and may require the use of topical anesthetics such as EMLA. The side-effects are not always invisible either: redness, swelling and minor bruising may occur. EPS is therefore ideal for use with a mesolift: mesolift one week, EPS the week after. It is wiser not to apply EPS immediately after a mesolift, because the multiple needle perforations in the dermis and epidermis would enhance local penetration of the peel solution. Similarly, a mesolift performed immediately after an EPS peel would be extremely painful for the patient and the acids in the EPS solution would penetrate through to the deep dermis. Nevertheless, many European, American and Asian doctors have reported using a combination of ‘EPS + mesolift’ or ‘mesolift + EPS’ at the same time, and have achieved excellent results.

EPS combined with botulinum toxin Ideally, the botulinum toxin should be injected a few days before the first EPS session. In this way, the two products can work together to good effect (Figure 11.4). If preferred, the botulinum toxin can of course be used after the EPS. If the botulinum toxin is injected immediately after the EPS, the needle will have to go through the non-neutralized acid solution on the skin and will take a few acid molecules into the dermis, which will make the injection more painful. It is not known how botulinum toxin and the AHAs in EPS interact in the body. The injection could be given, say, a

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A

B

Figure 11.4 (a) Before treatment with botulinum toxin and EPS. (b) After botulinum toxin and two sessions of EPS.

quarter of an hour before the EPS. Another potential problem is that the post-peel inflammatory reaction – even if minor – could move the toxin. Leaving a few days between EPS and the botulinum toxin would seem to be a wise choice. Handling the skin during the peels and post-peel vasodilation11 does not seem to have much effect on the outcome of the botulinum toxin injection. In 10 years of experience injecting botulinum toxin immediately before applying the trichloroacetic acid peel Easy TCA®, I have seen no evidence of any direct interaction between these two procedures.

Combining EPS and ‘flashlamp’ in anti-aging treatments The use of ‘intense pulsed light’ (IPL) for treating aging skin (Figure 11.5) is a widely used technique nowadays. However, many doctors are disappointed with the results obtained with pulsed light as a monotherapy and are look-

Figure 11.5 Sun aging, thinning skin, yellowish color.

ing for a combination of treatments that will benefit their patients. Phototherapy should not be used immediately after EPS, as the light rays will have a much greater depth of action, and may cause photochemical reactions. The presence of EPS on the skin could also refract the pulsed light. EPS can be used after flashlamp treatment, but it is best to be cautious, as the energy from the lamp might breach the stratum corneum and the acids in the EPS might penetrate more quickly. The doctor should be ready to neutralize the peel at the least sign of protein coagulation (frosting). It is a good idea to alternate flashlamp treatment and EPS, as with the mesolift: EPS one week and flashlamp the following week.

Anti-aging treatment for the body EPS does not penetrate body skin as easily as it does facial skin. Several coats are needed to trigger erythema and large amounts of solution have to be used. Treating the body with EPS takes a long time and large quantities of the product. A combination of sandpaper abrasion and EPS (Figure 11.6) can be used to treat photoaging on the back, upper or lower limbs. Light abrasion12 can thin the stratum corneum enough to allow the EPS solution to penetrate the skin

Figure 11.6 Day 4 after EPS preceded by superficial abrasion with 3M Wetordry® sandpaper P220.

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more easily and more quickly. The sandpaper should be used gently and evenly, without causing any unpleasant sensation, pain or bleeding. Only the most superficial layer of the stratum corneum should be removed. Any deeper abrasion that destroys the stratum corneum completely is to be avoided, as the active components of the EPS would penetrate the skin too quickly and soon saturate its defenses, its buffer capacity. When using this abrasive technique, it is essential to have the necessary equipment at hand to neutralize the peel (see the section on neutralizing glycolic acid in Chapter 9) in case it penetrates more deeply than desired. This technique can be repeated at a minimum of 2-weekly intervals only. A

More frequent application Another application technique for EPS can be considered, especially for patients with resistant skin who would benefit from a more intense tightening effect. EPS is applied following the usual protocol as described later on in this chapter, but it is repeated more frequently. Applying the solution more frequently requires great care and experience. Daily applications of EPS allow the peel to gradually penetrate more deeply. After a few days, small scabs will start to appear, signaling that the maximum depth has been reached and must not be passed. Within about 2 weeks, the scabs will have healed, and daily applications can be started again. Appropriate cosmeceuticals should be used between the two series of daily peels. For quicker results, the EPS can also be applied two or three times a week (e.g. on Saturday, Monday and Wednesday), especially on thick and oily male skin or in cases of acne.

B

Used as an anti-aging maintenance treatment EPS can be used to maintain the results of other peels when the patient wants a maintenance treatment without visible flaking. It should then be applied once a month.

Acne EPS is an excellent treatment for mild comedonal, papular or papulopustular acne. Peels are obviously not indicated in more severe cases of acne, for which only dermatological treatments will do. Comedones, microcysts and ‘whiteheads’ should be removed13 during the week before the first EPS to avoid handling the skin immediately before the peel at the risk of the EPS penetrating too deeply. Some doctors report removal of comedones or microcysts immediately before EPS, with good results. EPS can improve the appearance of acneic skin in just a few sessions when it is combined with Skin Tech’s Purifying® cream, which consists of glycolic acid, retinol, vitamin E, tri-

C

Figure 11.7 (a) Active papulopustular acne and post-acne pigmentation. (b) After four EPS and Purifying® cream. The acne has almost disappeared. (c) Substitution of Purifying® cream with Blending Bleach® cream for PIH treatment.

closan, glycyrrhetinic acid and tea-tree oil. As can be seen in Figure 11.7(a, b) (see also Figure 11.8), four EPS peels used in conjunction with Purifying® cream can vastly improve a patient’s pustular acne. After four sessions, the acne is almost

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inactive. The oldest post-acne pigmentation persisted, however, and in this case we continued to apply EPS once a week (four extra sessions), combining it with Blending Bleaching® cream (containing tyrosinase inhibitors and antioxidants) to treat the persistent pigmentation. After eight sessions of EPS, of which the first four were combined with Purifying® cream and the last four with Blending Bleaching® cream, the patient’s skin started to look healthier (Figure 11.7c).

Pigmentation disorders and other indications EPS acts similarly to other AHAs. A

Unwanted effects – precautions

B

EPS is a very particular peel and has its own particular sideeffect. The day after application, an average of 2% of patients develop an allergic-type reaction consisting of small, slightly pruritic pinkish nodules (Figure 11.9). This reaction is only seen with this peel. It can often result from using products before a peel that enhance penetration of the acids or from post-peel treatments that are unnecessarily aggressive or incompatible. Questioning patients closely about their cosmetic routine may provide an answer. In most cases, however, it seems to be for the following reason: in classic AHA peels,14 the AHAs have to be neutralized, but with EPS they are not; as they are not neutralized, the acids may penetrate as far as the dermis and cause a local inflammatory reaction (a source of fibroblast stimulation and new collagen production as well) in the ‘highest’ dermal papillae. This inflammatory reaction subsides by

C

Figure 11.8 (a,b) Papulopustular acne before treatment. (c) After four sessions of EPS and Purifying® cream, the acne is no longer active. After cleaning active acne, the Purifying® cream should be replaced by Blending Bleaching® cream to get rid of the pigmentation.

Figure 11.9 A complication that is specific to EPS: an acne-like reaction that lasts 24–48 hours and subsides by itself, occurring in average 2% of patients.

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patient was showing areas of local erythema that were treated with topical cortisone. On the 10th day, there were no visible sequelae. Other complications caused by AHAs are extremely rare with EPS. Infection or pigmentation problems are often caused by errors made when neutralizing AHA peels. EPS is automatically neutralized by the skin’s buffer capacity, and post-peel complications are far rarer than with conventional AHA peels.

Application protocol Pre-peel preparation This is likely to increase the penetration of the acids unnecessarily. EPS was designed to avoid any pre-peel treatment. Application of EPS should be delayed for 2 weeks if there has been any pre-peel preparation: EPS uses the stratum corneum as a reservoir for the slow release of the acids, and if it has been damaged, it can no longer fulfil this role and the acids will penetrate too rapidly through the thinned layer of skin. Body skin is much less permeable than face skin. This is why an abrasive technique has been described earlier in this chapter.

Figure 11.10 Abnormally deep penetration in a young patient who had been applying benzoyl peroxide locally for acne.

itself within 1–2 days at most. An allergic reaction is also theoretically possible, and should be treated accordingly. That will also disappear within a few days. This type of reaction should be seen as purely inflammatory – a positive reaction if the inflammation is controlled by antioxidants and does not last more than 2 days. If it does go on any longer, it could be considered an allergy. Contact of EPS with the eyes should be avoided: in the case of contact, the eyes should be rinsed with artificial tears or physiological saline solution. EPS may also, in some cases, penetrate too deeply or too quickly if the patient has been using skincare products that thin or remove the stratum corneum. Patients using topical retinoids, AHA creams or benzoyl peroxide should stop using them 2 weeks before EPS to ensure that the stratum corneum regains its normal thickness and function. Figure 11.10 shows the results of overpeeling in a young patient who had been using a benzoyl peroxide cream. Benzoyl peroxide is a powerful pro-oxidant used in the antibacterial treatment of acne, and it reduces the stratum corneum’s impermeability properties. The EPS can then penetrate more deeply into the skin. In this case, a fluorocortisone cream was applied immediately. Between the second and sixth day, the

Figure 11.11 Pre-peel cleanser with a physiological pH (6.5).

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Cleaning the skin Any make-up should be removed and the skin cleansed twice with Skin Tech’s cleanser (foam without glycolic acid (Figure 11.11–11.13)); the skin should then be rinsed with

warm water and dried with a swab. Alcohol or acetone should not be used before EPS: these products remove surface lipids and increase skin permeability (which is not necessary with EPS).

Application

Figure 11.12 Skin Tech cleanser has a neutral pH.

Small cotton wool balls seem to be the best method of application. A syringe is used to draw out 2–2.5 cm3 of the EPS. The cotton wool ball is soaked (not too much), and the solution is applied evenly and quickly over the whole face. Two coats are usually enough to produce a tingling sensation on the skin. When the patient can feel some tingling, one last coat is applied with the same applicator. There should be no frosting. In the case of inadvertent frosting,15 a neutralizing solution of sodium bicarbonate should be applied immediately. If there is no frosting, a neutralizing solution should not be applied – the skin neutralizes EPS automatically. Patients with very permeable skin may feel some tingling as soon as the first coat is applied. They should be given a total of two coats only: the first triggers the tingling and the second finishes off the peel. Patients with thick skin may not feel anything before the third coat. They should be given a total of four coats (Box 11.1). The treated area should be massaged with a gloved hand to ensure even penetration until the tingling sensation

Box 11.1 Average number of EPS Coats Thin skin: Normal skin: Thick skins:

Figure 11.13 Pre peel skin cleansing using the pre peel cleanser foam.

2 2–3 3–4

Figure 11.14 Post-peel occlusion with a suitable cosmeceutical for a duration of 15–30 minutes.

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8 days

8 days

8 days

8 days

15 days

4–6 weeks

7

7

7

7

7

7

77

Time line

1st EPS

2nd

3rd

4th

5th

6th

7th

Figure 11.15 Diagram of repeated EPS peels.

subsides. Slight tingling is normal and can last between 30 to 60 minutes after the application of this slow-release solution.

Immediate post-peel period As soon as the patient says that the tingling has subsided, the skincare cream best suited to the patient’s skin should be rubbed in: Purifying® cream in the case of acne, Blending Bleaching® cream in the case of pigmented marks, DHEA cream for anti-aging in the over-40s and Renutriv ACE® with lipoic acid to prevent aging in the under-40s. Actilift® cream with DMAE can be used to increase skin firmness. These creams penetrate much more easily immediately after the AHAs have been applied, but using a plastic occlusive film (Figure 11.14) for 20–30 minutes further enhances penetration of the skincare creams. In vivo, the natural water content of the stratum corneum is relatively low. When the surface of the skin is occluded with an impermeable plastic film, the water that normally evaporates through the epidermis (TEWL16) can no longer do so, and water of endogenous origin gradually soaks the stratum corneum, which can absorb up to 5–6 times its dry weight. The thickness of the stratum corneum increases in proportion to the amount of endogenous water absorbed and can become up to four times thicker.17 It is then far more permeable to the water-soluble ingredients, and this improved permeability lasts for several hours after the occlusive film has been removed. Occlusion raises the temperature of the hyperhydrated epidermis and makes the various hydrophilic ingredients in the creams more soluble. Finally, occlusion prevents the active components in the creams from evaporating too quickly. The plastic film is then removed and any excess cream is rubbed in to enhance penetration one last time. All of the products – EPS and cream – are left on the skin until the following morning, when the patient can wash his or her face.

vitamin E but without fruit acids (Vit E Antioxidant®), and the cream most appropriate for the problem under treatment should continue to be used – this will often be the same cream applied to the skin immediately after the peel (see Table 3.1 in Chapter 3).

Period between peels (between two EPS sessions) The appropriate cream should continue to be used between peels. Exposure to the sun’s rays must be avoided: this means keeping out of the sun and using an effective sun protection cream for 2 weeks after the last peel.

Repeating the peel When EPS is the main treatment, it can be repeated once or several times a week (see above). When EPS is used as a maintenance treatment with other peels, it can be repeated once or twice a month. In standard treatment, EPS can be applied once a week for 6–8 weeks. Thereafter, it is applied as a maintenance treatment: four extra EPS peels, once every 2 weeks. Finally, in the long term, EPS can be applied once every 4–6 weeks (Figure 11.15).

Contraindications ■ Women who are pregnant or breast-feeding (as a precaution) ■ Presence of herpes or other active lesions ■ Lesions of unknown origin ■ Allergy to one of the components ■ Unrealistic hopes

Post-peel period (3–4 days)

Conclusions

The skin flakes only very slightly, usually unseen by the naked eye, because it practically flakes ‘cell by cell’. The skin should be kept fully hydrated with a cream containing

EPS is the first slow-release AHA peel not to need neutralizing, in spite of its pH of 0.5–1. This makes it extremely safe to use. It combines the known superficial peeling

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effects of three AHAs with the antioxidant, chelating and tyrosinase-inhibiting action of phytic acid. It is a new type of peel that overcomes all the problems associated with neutralizing conventional AHAs. It allows each of the molecules in the solution to act to full effect, without being neutralized. The best indications for EPS are the treatment of adolescent acne and aging skin, on which it has a tightening effect.

Notes 1. Glycolic acid has a pKa of 3.83, lactic acid a pKa of 3.86 and mandelic acid a pKa of 3.36. 2. See Chapter 6 for a reminder of pKa. 3. Saponification allows the acids to act more evenly. 4. As is the case when unbuffered peel solutions are applied to the skin. 5. It is therefore essential for the stratum corneum to be complete when using EPS. If any preliminary treatments reduce its thickness, the solution may penetrate too quickly and saturate the skin’s buffer capacity. 6. AHAs are water-soluble. 7. Dolor – Rubor – Tumor – Calor.

8. Ditre CM, Griffin TD, Murphy GF, Sucki H et al. Effects of alpha-hydroxy acids on photoaged skin: a pilot clinical, histologic, and ultrastructural study. J Am Acad Dermatol 1996; 34(2 pt 1): 187–95. 9. EPS can be applied after pulsed light treatment, unless the skin has been made excessively permeable. See later in this chapter. 10. Although EPS does not require any specific pre-peel care. 11. It should be noted that EPS and Easy TCA® are both used in conjunction with anti-free radicals that control the post-peel inflammatory reaction. This is not the case with the majority of other peels. My experience is only based on the combination of botulinum toxin and EPS or Easy TCA®. Combinations with other peels have not been tested. 12. For example with 3M Wetordry® sandpaper P220. 13. Comedone remover, No.11 scalpel blade, point of a needle. 14. For example, a 70% unbuffered glycolic acid peel. 15. Frosting has rarely been described – I have never personally come across it. 16. Transepidermal water loss: 5–20 g of water/m2 of skin under normal physiological conditions. 17. The increase in permeability is also due to a reduction in corneocyte cohesion related to the unusual hyperhydration of the stratum corneum.

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12 Trichloroacetic acid: general information, toxicity, formulations and histology

Haloacetic acids Haloacetic acids are derivatives of acetic acid in which one or more hydrogen atoms on the alpha carbon1 are replaced by halogens (fluorine, chlorine, bromine or iodine) (Figure 12.1). The haloacetic acid most commonly used in peels is trichloroacetic acid, and we will therefore look at the chlorine derivatives of acetic acid.



X O  Y — Cα — C  OH Z

General chemical structure of a haloacetic acid. α indicates the alpha carbon atom. X, Y and Z represent hydrogen (H) or a halogen (F, Cl, Br or I) – at least one of these must be a halogen.

Acetic acid Acetic acid (Figure 12.2), also known as echanoic acid, has a low molecular weight of 60.05 and a pKa of 4.76.2 It is obtained by distilling vinegar (the acetic acid which comes from the action of certain aerobic bacteria on dilute alcohol) or through the Monsanto process by the reaction of carbon monoxide with methanol at high temperature and pressure. It is a strong irritant to the eyes, mucous mem-

Monochloroacetic acid (Figure 12.3), also known as chloroacetic acid and chloroethanoic acid, which has a molecular weight of 94.5, can be obtained from the reaction between acetic acid and chlorine under high pressure. The pH of an 80% MCA solution is lower than 1 and its pKa is 2.82. In both its acid form and its salt forms (e.g. sodium monochloroacetate), MCA is highly toxic to the skeletal muscles, the renal system and cardiovascular system and is rapidly absorbed through the skin and mucous membranes. MCA poisoning by ingestion, inhalation or exposure of more than 5% of the body surface area is frequently lethal. The symptoms of poisoning are not immediate: they can appear between 1 and 4 hours after exposure. The non-corrosive sodium salt does not penetrate the skin and is not toxic by skin contact (unlike MCA, which passes through the skin very easily). It is, on the other hand, highly toxic by the oral route. There are no data available on the parenteral administration of MCA in humans. In laboratory animals, H

— H—C—C —



H—C—C H

OH

—

—

—

OH O

CI



—

Figure 12.1

H

branes and skin. Prolonged contact between the skin and ‘glacial’ acetic acid3 can cause skin necrosis. Applying 6–8% acetic acid to the skin of patients with seborrheic dermatitis can trigger temporary frosting through protein coagulation. This disorder is in fact often improved by daily application of white vinegar (which contains 4–8% acetic acid), used as an aftershave before the morning shower (to avoid smelling of vinegar!). Acetic acid has disinfectant and fungicidal properties. It is not carcinogenic, mutagenic or teratogenic to animals or humans. The oral LD50 in rats is 3.310 mg/kg.

Monochloroacetic acid (MCA)

Carboxylic acid group

—

ch12

O

Figure 12.2

Figure 12.3

Chemical structure of acetic acid.

Chemical structure of monochloroacetic acid (MCA).

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Dichloroacetic acid (DCA)

H

OH

—

however, an injection is rapidly lethal. MCA accumulates in the liver and kidneys before it accumulates in the brain. Elimination of MCA is renal in humans: most of it is eliminated in its free form, with a small part being eliminated in conjugated form with glutathione. The mechanism of MCA toxicity seems to be via inhibition of the enzyme pyruvate dehydrogenase; this inhibition blocks the Krebs (tricarboxylic acid) cycle and disrupts the cell’s energy supply. Almost immediately, the cell finds itself without energy. Ketoglutarate dehydrogenase activity is also reduced, which causes lactic acidosis. The MCA also damages the blood–brain barrier, probably through the formation of vascular endothelial microlesions. Symptoms of poisoning begin with nausea and vomiting, diarrhea, and central nervous system (CNS) excitation with disorientation. The effects observed later on or with higher doses include CNS depression, cerebral edema, severe myocardial depression, coma and cardiogenic shock resulting from non-specific myocardial lesions and significant arrhythmias. Within the first few hours, severe metabolic acidosis4 with hypokalemia occurs. The severity of the rhabdomolysis causes myoglobinuria severe enough to cause kidney failure5 in those who survive it. One treatment involves administering dichloroacetate by slow (in 10 minutes) intravenous injection (50 mg/kg), if possible before metabolic acidosis begins. The dichloroacetate is only active as long as all the pyruvate and ketoglutarate dehydrogenase molecules have not been deactivated by the MCA. The severity of poisoning due to skin contact depends on the surface area of skin exposed: applying an 80% MCA solution on less than 5% of the body surface area can cause severe poisoning, while exposing 6–10% of the body surface to MCA is often lethal. MCA has nevertheless been suggested as a dermatological treatment for mosaic warts or periungual warts at a concentration of 80% or 60 g of MCA + 10 ml of water. Treating warts involves MCA coming into contact with a very limited area of skin, which explains the absence of poisoning when the treatment is carried out carefully. MCA has also been combined with salicylic acid and is considered more effective than dichloro- or trichloroacetic acid in the treatment of warts. Because of this product’s very high and potentially fatal toxicity, its use and indications should be strictly limited. Monofluoroacetic acid is even more toxic than MCA, being fatal after ingested doses of 2 mg/kg whereas MCA is fatal after doses of 50 mg/kg.6

CI — C — C CI



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—

ch12

O

Figure 12.4 Chemical structure of dichloroacetic acid (DCA).

DCA has been used in the treatment of severe lactic acidosis. No clinical side-effects have been observed after parenteral administration. On the contrary, intravenous administration of DCA during experimental poisoning of rodents with MCA increased the survival rate, bringing it from 8% to 83% after an injection of 50 mg/kg and from 8% to 100% after an injection of 100 mg/kg. There are strict protocols for the injection of DCA in the case of MCA poisoning. When ingested, DCA is rapidly absorbed by the digestive tract. In animals, only 1–2% of the quantity ingested is found in the feces, which means that the acid is almost completely absorbed. Only 1% is found, in free form, in the urine. In humans, up to 5% of DCA can be found in the urine, very soon after DCA has been absorbed. Peak plasma levels are reached within 15–20 minutes in humans. Intoxication by inhalation is rare, as DCA is not a very volatile substance. DCA causes the liver to increase in volume as a result of a build-up of glycogen. Increases in aminotransferase (transaminase) levels have been observed during treatment with high doses of DCA, in both rodents and humans. DCA can cause focal, or even widespread, hepatocellular necrosis in mice, but no cases have been described in rats, dogs or humans, even when administered in high doses. Neurological toxicity in humans is limited to sedation and potential peripheral neuropathy that is reversible. DCA undergoes oxidative dechlorination that converts it into glyoxylate,7 which is in turn oxidized into oxalate,8 reduced into glycolate9 and eventually transaminated into glycine.10 However, in certain individuals, the DCA can be partially converted into MCA. This has been described in a child suffering from congenital lactic acidosis. It appears that the DCA may enhance the development of hepatocellular carcinoma in animals, although not in humans.11 DCA is genotoxic in vitro and in vivo and induces DNA hypomethylation in vivo. The oral LD50 in rats is 2.820 mg/kg. The human toxicity of DCA is mainly local, through chemical burns, but DCA could be considered to be potentially carcinogenic in humans. To date, there is no convincing data on this subject.

Chemistry and toxicity of DCA

Application protocol for DCA

Dichloroacetic acid (Figure 12.4), also known as bichloroacetic acid and dichloroethanoic acid, has a molecular weight of 128.94 and a pKa of 1.3. It is soluble in water, alcohol and ether.

DCA has been shown to stimulate keratinocyte growth and differentiation in vitro.12 It has been used in the treatment of human papillomas, without much success,13 as well as in the treatment of epistaxis.

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DCA is used as a cauterizing agent in the treatment of all types of warts, calluses, corns, xanthelasma, seborrheic keratoses, ingrown toenails, etc. It is just as effective as other methods such as electrodessication or dry ice. DCA is a powerful keratolytic and it is important to apply it only to the lesion being treated. Before any treatment, Vaseline® should be applied around the lesion to prevent any contact with healthy skin. The doctor should also have some water at hand to wash the skin in case of inadvertent contact. A neutralizing solution of sodium bicarbonate can also be used immediately in case of accidental contact with the skin. The quantity of DCA required largely depends on the type of lesion being treated. Very thick and horny lesions are treated using a cotton bud. A wooden toothpick soaked in DCA solution can also be used; it should be pushed inside the callus or wart. Three to five applications are necessary to get results on very thick lesions, whereas only one or sometimes two applications are enough on relatively flat lesions. The depth of application is monitored by watching out for the appearance of protein coagulation, which turns the skin a whitish-grey color. A combination of shave excision and chemical coagulation can also be used. The top of the wart is first removed with an electrosurgical or radiofrequency knife. The DCA is applied after the edges of the wart have been protected with a thin layer of Vaseline®. Foot calluses should be pared surgically before the acid is applied. Post-treatment care consists of covering the skin with Vaseline® to help it flake more quickly. Large calluses often have to be treated several times. Treating xanthelasma with DCA is fairly common.14 The skin around the xanthelasma must be protected with Vaseline® and the DCA applied carefully and not to excess. The scars are mostly invisible. Treating xanthelasma with phenol, however, leaves no scarring (see Chapter 36). The potential toxicity of DCA means that it cannot be used on a large absorbent surface area. The author has found no significant references to the use of DCA in full-face or body peels.

Trichloroacetic acid (TCA) Chemistry and toxicity of TCA Trichloroacetic acid (Figure 12.5), also known as trichloroethanoic acid and trichloromethane carboxylic acid, comes in the form of colorless or white crystals and has a distinctive sharp, pungent odor. As far as its toxicity is CI

—

—

OH

CI



CI — C — C —

ch12

O

Figure 12.5 Chemical structure of trichloroacetic acid.

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concerned, industrial accidents have been reported in which individuals were subjected to high doses of TCA, either by being splashed with the solution over large areas of the body or by accidental ingestion or inhalation of concentrated vapors. However, such toxicity has never been described when TCA has been used as a chemical peel. It is nevertheless worthwhile becoming acquainted with the potential symptoms of industrial poisoning. TCA is readily absorbed through the respiratory and digestive tracts. Acute accidental exposure to TCA has caused skin necrosis. Contact with the eyes causes burns or irritation, depending on the concentration of the acid. Exposure of the eye to small amounts of solution with a concentration equal to or lower than 15% m/m does not appear to cause any irreversible damage to the cornea. Immediate dilution with physiological saline solution instantly stops the burning and any risk of damage to the eye. However, the proteins in the cornea could coagulate with larger amounts of low-concentration TCA or smaller amounts of high-concentration TCA. Inhaling concentrated vapors of TCA can irritate the respiratory tract. Poisoning through inhaling high doses of TCA can cause headache accompanied by nausea, vomiting and coughing. Higher concentrations cause weakness, dizziness, bronchitis and/or pneumonia. Acute poisoning with TCA vapor can lead to chest pains, breathing difficulties, low blood pressure, edema of the respiratory tract, suffocation and death. Accidental ingestion of TCA causes irritation and burns in the digestive tract, vomiting, diarrhea, and low blood pressure. Accidental ingestion of high concentrations can erode the teeth and cause necrosis of the jaw. Controlled ingestion of 3 mg/kg of TCA in three male volunteers showed a half-life of 50 hours. Liver toxicity has been studied in mice: hepatomegaly (30% enlargement) was observed in male mice given water containing 1 g/l of TCA for 52 weeks. In a group given water with a concentration of 2 g/l of TCA, the liver enlarged by 63%. The incidence of liver carcinoma did not increase, irrespective of the administered dose. In another study, it was proved that TCA does not cause adenomas or liver cell carcinoma, even in rodents pretreated with ethylnitrosourea, conventionally used to induce carcinomas. No in vitro studies using human cells have shown any chromosomal abnormalities after contact with TCA. To the best of my knowledge, no studies have shown any link between even chronic exposure to TCA15 and cancer in humans. When TCA is applied to the skin, it is not absorbed, and is therefore not toxic in this application.

Aqueous solutions of TCA Hydrophilicity of TCA crystals TCA crystals are very hydrophilic and therefore unstable in the presence of water: they readily dissolve on exposure to

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atmospheric humidity. This extreme hydrophilicity can cause problems when TCA solutions are made up in a pharmacy. In fact, the packaging of pure TCA crystals usually allows for the preparation of far more peel solution than the doctor actually needs. The pharmacist does not usually dissolve all the crystals at one time, as this would produce a large quantity of solution that is difficult to store. He will usually measure out the quantity of crystals needed for each order of peel solution. Every time the bottle is opened and every time the pure TCA crystals are taken out, they come into contact with atmospheric water, which gradually hydrates them. The larger the bottle, the more likely it is that the remaining crystals will be hydrated every time the bottle is opened. The longer it takes to weigh the crystals, the more hydrated they will become. Peel solutions are therefore prepared by diluting crystals that are gradually becoming more and more hydrated: at the same weight, the pharmacist is in fact weighing TCA crystals that are slowly swelling with water. The solutions that he prepares are more and more diluted and therefore less and less effective. The doctor, for his part, gets into the habit of applying increasingly weaker TCA peels with increasing firmness, in spite of the fact that the same labels show the same concentration. The doctor therefore gets used to applying ever increasing volumes of peel solution to achieve the same results – until the day when the pharmacist starts using a new bottle of pure TCA crystals and makes up a peel solution with fresh, anhydrous crystals that are more aggressive than the ‘old’ hydrated crystals. Applying this new and more concentrated solution of course results in a peel that is deeper than the doctor expected, and the risk of complications is increased, even though there is no apparent difference in the application procedure. Unlike pure crystals, TCA solutions do not hydrate by themselves. It is therefore safer not to keep TCA in crystal form and instead to use reconstituted solutions whose concentration is more stable than crystals.

Inhomogeneity of TCA solutions A solution is said to be homogeneous when the different elements of which it is made up are evenly distributed in the container that holds it. The homogeneity of peel solutions is one of the essential elements of their safety.

Simple aqueous solutions of TCA (TCA–SAS) Unfortunately, TCA–SAS16 solutions are neither homogeneous nor stable. The TCA molecule is very mobile in the solution and its motion has both a random element and a component determined by its chemical structure. When an aqueous solution of TCA is left in an unmoving container, the concentration of the solution does not remain uniform. The TCA temporarily becomes more

concentrated in some parts of the container and more dilute in others. For example, if a TCA solution of 33% m/m is prepared and left at room temperature, some regions of the solution will have a concentration of 35% for a certain length of time while neighboring regions will have concentrations of 30% or 40% (Figure 12.6). As this process continues, the region that just had a concentration of 35% will now have a concentration of 37%, while other areas of the solution will have different concentrations again, for example 25% and 29%, and so on and so forth.17 Depending on the position of the tip of the needle used for taking the acid out of the bottle, the solution will be more concentrated or more dilute. A solution that is too dilute or too concentrated could be applied to different parts of the face. Simple aqueous solutions of TCA have to be mixed continuously, both when they are being taken out of the bottle and while they are being used. Certain complications that arise unexpectedly after a TCA–SAS peel can be explained – at least partially – by this phenomenon of inhomogeneity. Awareness of this problem led to the rapid development of new TCA peel formulas between 1990 and 2000. One of the first solutions put forward was the New Peel® combination of TCA and Mikuda® complex. The soft Peel® formulation used asiaticosides and ginsenoids, glycerol, urea (carbamide), sorbitan monolaurate and methyldibromoglutaronitrile, among other ingredients. Easy TCA®, Unideep® and Only Touch Peel® (OTP) provided another answer to the problem: these stabilized solutions consist of a base solution to which a determined quantity of 50% m/m TCA is added. There are no complicated calculations to be performed, the directions for use state precisely what volume of 50% m/m TCA solution should be added to the base solution to make up the Easy TCA®, Unideep® and OTP solutions, which provide peels to the basal layer, the papillary dermis and the reticular dermis, respectively.

Calculating the concentration of TCA Since TCA peels first came into use, practitioners have suffered from a lack of standardization regarding how a solution’s concentration is to be calculated. The calculation can be done in different ways: by mass per mass (m/m), mass per volume (m/v) or mass plus volume (m + v, e.g. m + 100 ml). There are also different formulas for diluting these solutions using approximate curves. Therefore, ‘50%’ TCA does not really mean very much if we do not know whether the calculation is m/m, m/v or m + 100 ml. In 1995 and 1996, Trauchessec and Pissot18,19 suggested standardizing the calculation of the concentration of a TCA solution by expressing it in mass per mass (m/m), which is the only logical way of calculating a percentage. It should be possible to make a strict comparison of the terms of a percent-

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Figure 12.6 Inhomogeneity of simple aqueous solutions of TCA. (a) A solution with a presumed concentration of 33% contains mobile regions of different concentrations. (b) At a later time, same TCA solution with a presumed concentration of 33% contains mobile areas of concentrations that are different.

30%

29% 25%

37%

15%

40%

age. For example, the carbohydrate content of a meal is given in %: a content of 20% carbohydrate means that 100 g contains 20 g of carbohydrate and 80 g of something else. Unless it is clearly indicated on the packaging, there is no way of knowing that a volume of 100 ml of this meal would contain 20 g of carbohydrate. It would be impossible to understand exactly how much carbohydrate is in the food. Unfortunately, it is this very type of calculation (weight by volume, w/v) that is widely used in some countries: a volume of 100 ml of TCA solution contains x grams of TCA. If we know the concentration in w + v only, it is difficult to calculate the exact amount of TCA in the solution. To get the correct answer, one has to calculate mass with mass, volume with volume, and not volume with mass.20 Examples of calculations of concentration using the w/w, m/v and w + v methods are given in Boxes 12.1–12.3. Methods of calculation based on volume lead to values of concentrations that can be as high as 140%. Since a ‘0% solution’ is pure water and a ‘100% solution’ pure TCA, values greater than 100% are essentially meaningless. Ideally, therefore, these methods should not be employed for the calculation of concentrations – only the m/m method should be used. Nevertheless, for the sake of simplicity, pharmacists often prefer to use dilutions in volume whenever possible, as they can buy ‘standardized’ TCA solutions at 20%, 50%, etc. – then, in theory, all the pharmacist has to do is add 100 ml of water to 100 ml of TCA solution at ‘50%’ to get a ‘25%’ solution. It is not easy for a doctor to calculate how

Box 12.1 TCA solution at 50% mass per mass (m/m)a 100 g of TCA solution at 50% m/m contains 50 g of pure, unhydrated TCA crystals and 50 g of water. 100 g of this solution is not, however, 100 ml, but only 79 ml. In fact, 1 g of TCA displaces 0.6 ml and not 1 ml of water.b Scientifically, this is the most rigorous method of calculation, as 100 ml of a solution at 50% m/m would contain (50/79) × 100 = 63.3 g of TCA. %

Mass of TCA (g)

Volume of water (ml)

Final mass (g)

Final volume (ml)

10 20 30 40 50 60 70

10 20 30 40 50 60 70

90 80 70 60 50 40 30

100 100 100 100 100 100 100

96 92 88 83 79 75 71

a Taken from Trauchessec JM, Pissot F. Solutions d’acide trichloroacétique masse pour masse pour peelings dermatologiques. Nouv Dermatol 1996; 15: 252–5, with the authors’ permission. b According to Trauchessec, the exact value is 0.59 ± 0.01. The value of the constant 0.60 used here is an acceptable approximation. It means that 1 g of TCA displaces 0.6 ml of pure water, whatver the concentration of the solution.

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Box 12.2 TCA solution at 50% mass per volume (m/v)a This solution is prepared in the following manner: 50 g of TCA is diluted in a small amount of distilled water to get a small amount of solution, then the volume is made up by adding distilled water until the final volume reaches 100 ml. To get 100 ml of solution and an end mass of 121 g, 50 g of TCA will be dissolved in 71 ml of water. This method of calculation is easy for the pharmacist, as 100 ml of solution contains 50 g of TCA (100 g of this solution would contain 41.32 g of TCA). %

Mass of TCA (g)

Volume of water (ml)

Final mass (g)

Final volume (ml)

10 20 30 40 50 60 70

10 20 30 40 50 60 70

94 88 82 77 71 65 59

104 108 112 117 121 125 129

100 100 100 100 100 100 100

a Taken from Trauchessec JM, Pissot F. Solutions d’acide trichloroacétique masse pour masee pour peelings dermatologiques. Nouv Dermatol 1996; 15: 252–5, with the authors’ permission.

much TCA these solutions contain! Examples of calculations of dilutions using the m/m, m/v and m + v methods are given in Boxes 12.4–12.6 and Tables 12.1 and 12.2.

Publications can be misleading A major problem arises when reading publications from different sources. Suppose that an American doctor wants to use a peeling technique described by a European author who gives concentrations in m/m but does not mention this in the publication, as is too often the case. The American

Box 12.4 Dilution of a base solution at 50% mass per mass (m/m) 100 g of a solution of TCA at 50% m/m contains 50 g of TCA and 50 g of water (50 g of water is in fact equivalent to 50 ml of water) and has a volume of 79 ml. If 79 ml of solution contains 50 g of TCA, then 1 ml contains 0.633 g of TCA and so 100 ml of TCA solution at 50% m/m contains 63.3 g of TCA. If this solution is diluted with the same volume of water (i.e. 100 ml), it produces 200 ml (but not 200 g) of TCA solution, in which there is still 63.3 g of TCA. Therefore, 100 ml of the new diluted solution contains 31.65 g of pure TCA.

Box 12.3 TCA solution at 50% mass + volume (m + 100 ml)a

Box 12.5 Dilution of a base solution at 50% mass per volume (m/v)

This method of preparation involves adding 100 ml of water to 50 g of pure TCA crystals. The final volume of this solution is 129 ml for a mass of 150 g. 100 ml of this solution contains 38.75 g of TCA, while 100 g of this solution m + 100 ml contains 33.33 g of TCA. This is the easiest but also the worst method of calculation, as it is extremely difficult to work out the exact amount of TCA.

100 ml of TCA solution at 50% m/v contains 50 g of TCA diluted in 71 ml of water, to give a solution with a volume of 100 ml for a mass of 121 g. If 100 ml of pure water is added to 100 ml of solution at 50% m/v, it produces 200 ml of solution, which weighs 221 g and contains 50 g of TCA. 100 g of this solution contains 22.6 g of TCA, while 100 ml of the same solution contains 25 g.

%

Mass of TCA (g)

Volume of water (ml)

Final mass (g)

Final volume (ml)

10 20 30 40 50 60 70

10 20 30 40 50 60 70

100 100 100 100 100 100 100

110 120 130 140 150 160 170

106 112 117 123 129 135 141

a Taken from Trauchessec JM, Pissot F. Solutions d’acide trichloroacétique masse pour masse pour peelings dermatologiques. Nouv Dermatol 1996; 15: 252–5, with the authors’ permission.

Box 12.6 Dilution of a base solution at 50% mass + volume (m + 100 ml) 100 ml of TCA solution at 50% m+100 ml contains 38.75 g of pure TCA for a mass of 116.27 g. Adding 100 ml of water with the aim of converting the theoretical concentration into 25% therefore gives a solution of volume 200 ml, whose mass is 226.27 g and which still contains the same 38.75 g of TCA. 100 g of the new solution therefore contains 17.12 g of TCA. 100 ml of the new solution contains half of the 38.75 g, which is 19.38 g of TCA.

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Table 12.1 Calculation of a TCA solution at 50% in mass or in volume Method of calculation

Grams of TCA in 100 ml Grams of TCA in 100 g

m/m

m/v

m + 100 ml

63.3 50

50 41.32

38.75 33.33

Table 12.2 Obtaining a solution at ‘25%’ by adding 100 ml of water to a solution at ‘50%’ Method of calculation

Grams of TCA in 100 ml Grams of TCA in 100 g

m/m

m/v

m + 100 ml

31.65 25

25 22.6

19.38 17.12

doctor gets his pharmacist to make up the solution as described by the European doctor. The American pharmacist, however, prepares a solution in m/v or m+v, or even dilutes it as described above. The European technique may well be based on an aggressive TCA, with a concentration of 45% m/m. The American doctor orders a solution at 45% from his pharmacy, but is in fact using a concentration of 38.1% m/m when the calculation has been made at 45% in m + 100 ml. A solution with a concentration of 31% m/m will clearly not produce the same results as a concentration of 45% m/m. The American doctor cannot achieve the same results as the European author, whose results might therefore easily be considered exaggerated or even rigged. The situation is more serious when a European doctor wants to use an American application technique with a TCA solution at 50% m + 100 ml. This solution contains 50 g of pure TCA to which 100 g of water is added. The final volume of the solution will be 129 ml for a mass of 150 g, and 100 g of this solution is actually equivalent to 33% m/m. The American author who applies a TCA solution at 50% m/v – which is in fact a European 33% m/m solution – to a patient’s face can achieve excellent results. The European doctor, who wants to achieve the same results by applying a solution at 50% m/m provided by the pharmacist, is running a huge risk of burning the patient’s skin and causing hypo- or hyperpigmentation, scarring,21 etc. It is therefore essential to stipulate the type of concentration to use, and this is one of the first pitfalls awaiting any doctor who is new to peeling. The technique for applying TCA, which is actually very easy, has for a long time been made difficult because of the different methods for calculating concentrations (see above) and the approximate explanations given in many

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publications.22 There are many inconsistencies: some publications consider a TCA peel at 50% to be a ‘superficial peel’. Yet we know that a peel at 50% reaches the reticular dermis easily and quickly, and can sometimes even go beyond it: this is a deep peel – in most cases too deep. This solution penetrates the whole of the papillary dermis immediately, achieving a ‘medium’ or ‘deep’ peel, but certainly not a superficial one. The same solution at 50%, but calculated in m + 100 ml, would be equivalent to a 33.3% m/m solution, and the first coat of TCA at 33% m/m would soon reach the papillary dermis. It is then difficult to understand how anyone can say that a ‘TCA peel at 50% produces a superficial peel’: in whatever way the calculation is made, it is wrong and a TCA solution at 50% will produce, at the very least, a medium-depth peel even if it is calibrated in m + 100 ml. The type of applicator used, the number of coats and the total quantity of TCA applied to the skin, as well as any pre-peel preparation, etc. must also be taken into account. There have been histological studies comparing the depths reached by different concentrations of TCA used in conjunction with different techniques such as dry ice or prior application of Jessner’s solution. A histological study by Brody and Stegman, at 3, 30 and 90 days,23 showed that the deeper the injury, the more necrosis and regeneration are histologically visible. It has thus been shown that three successive applications of TCA cause deeper necrosis than one application.24 The technique used in this study involved the application of TCA at a concentration of 35% – presumably calculated in mass per volume, although it was not stated whether this was a w/v calculation, m + 100 ml calculation or a dilution of TCA solution. The Jessner’s solution in the study was supposed to be prepared from lactic acid crystals rather than from an 80% (w/w, w/v?) lactic acid solution. This solution was applied with a cotton bud: the volume, form and texture of the cotton bud has an influence on the quantity of solution that comes into contact with the skin. The dry ice was applied firmly (how firmly was not stated) in acetone (exactly how much and at exactly what temperature were also not stated) for 15 seconds. The importance of studies such as this should not be underestimated, but it is necessary to draw attention to the number and importance of the variables that have to be taken into account when evaluating results.

A good method of calculation A consistent method of calculating concentrations must be adopted. It would of course be preferable to use pharmacological concepts such as molar mass, but practitioners are not used to handling such data. From a practical point of view, there are two units of measurement that are easily accessible: mass and volume. As we have just seen, the only acceptable values are calculations in m/m (if we are referring to mass) or in m/v (if we are referring to volume).

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Measurements in m + 100 ml are too approximate, as is using dilutions of pre-existing solutions. Anyone is capable of measuring an approximate volume, although not an exact one, and this introduces another margin of error. With the help of precision scales, it is possible to measure a mass precisely – more precisely, in any case, than by judging gradients on a measuring glass with the naked eye. This confusion over concentrations is extremely dangerous, and a standardized concentration should be used to avoid disappointment as well as complications. McCullough25 has drawn attention to the discrepancies between calculations of TCA concentrations, but prefers to use the m/v method. We have chosen to calculate the concentration in m/m for the following reasons, as expressed by Trauchessec:19 1. Measuring mass is more precise than measuring volume. 2. A real percentage can only be calculated m/m or v/v. 3. The use of approximate dilution curves is avoided with m/m calculations. 4. With m/m calculations, there can be no potential errors caused by the existence of three types of mass per volume concentrations: m/v in QS, adding 100 ml of water to a mass of TCA or diluting pre-existing TCA solutions. 5. The m/m calculation does not produce values of TCA ‘concentrations’ reaching 140% – which make no sense. 6. Finally, the size of TCA crystals, how compact the mass of crystals is and the temperature of the solution are all elements that have to be taken into account when making m/v or m + v calculations. The m/m calculation does not depend on these parameters.

Easy TCA®, Unideep® and Only Touch® solutions Easy TCA® is a stabilized,26 homogeneous and adjuvanted solution with a final TCA concentration of 15% m/m, combined with alpha hydroxy acids (AHAs), antioxidants, vitamins and saponins. Unideep® is a TCA peel based on the same principles as Easy TCA® and reaches the papillary dermis readily and evenly; it has a TCA concentration of 23% m/m. The application protocols for these two peels allow all depths to be reached. There is no point using higher concentrations that could cause complications (see Chapter 37).

TCA in simple aqueous solution (TCA–SAS) Simply diluting TCA crystals in water produces an unstable solution whose characteristics have been discussed

above. TCA-SAS solutions are the cheapest a doctor can buy. They are also the most dangerous.27,28 It is clear from the literature on chemical peels how dangerous these solutions are – most photographs of serious complications show patients treated with TCA–SAS. It is clear that an experienced doctor can avoid most of the serious complications, but an inexperienced one can easily fall into each and every trap that these cheap solutions set. To paraphrase: it is definitely cheaper to spend the night on a park bench in a big city than to rent a room in a decent hotel, but it is nonetheless true that you would get a much better and safer night’s sleep in a hotel room than you would in the park or subway! Even though some of the world’s best peelers can use TCA–SAS with complete safety, it is still true that the vast majority of all complications occur after the application of these cheap solutions. Some ill-informed doctors have ended up claiming that TCA simply cannot be used to treat melasma, for example. Reading the textbooks on chemical peels is very instructive, and the pictures of complications often reflect the complexity of using TCA–SAS correctly. Today’s new TCA peel solutions have been developed with a view to convenience and safety. I can already hear reproaches from those who claim the contrary and are perfectly able to use TCA–SAS safely, but I can also hear the sobs and regrets of those who listened to them and whose patients have suffered for it. The simple aqueous solution of TCA was born in the 19th century: it has had its day – let us move on!

‘Adjuvanted’ TCA Applying TCA–SAS to the skin causes frosting that is rarely even,28 especially when using intermediate concentrations. Applying TCA–SAS at 10% m/m does not usually cause any frosting at all and is almost risk-free; applying TCA–SAS at 50% m/m causes very rapid frosting whose depth is difficult to evaluate and control.29 Intermediate aqueous concentrations (e.g. at 25% or 30% m/m) do not penetrate evenly and produce intraepidermal peel zones next to peel zones to the papillary or reticular dermis. It is difficult to get even frosting, and the results of the peel are not homogeneous: undertreated areas are next to overtreated areas that could easily create problems with post-inflammatory hyperpigmentation (PIH), hypopigmentation, or even scarring (Figure 12.7). Various adjuvants have been added to TCA to even out its effect. The term ‘adjuvanted’ is used to describe a TCA solution to which something has been added to enhance or even out its action. Many different products have been added to TCA.

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H | H — C — OH | H — C — OH | H — C — OH | H

Figure 12.8 Chemical structure of glycerol.

tein stabilizer (which seems a little paradoxical, considering that the effect sought by applying TCA is the destruction of proteins). Soft Peel® was presented as a solution for improving the tolerance and effectiveness of TCA. Nevertheless, adding glycerol did not remove the need to prepare the skin beforehand, 3 weeks before the peel:30

Figure 12.7 Technical error during the treatment of stretch marks using an abrasive procedure (see Chapter 21). Typically, a halo of hyperpigmentation surrounds the depigmented area, which in turn surround a scar response. Hyperpigmentation develops where the peel solution goes slightly deeper than it should, and scars form where the peel is much too deep.

Glycerol Glycerol (Figure 12.8), also known as glycerine, glycerin, 1,2,3-propanetriol or 1,2,3-trihydroxypropane, has a molecular weight of 92.09. It is often used as an antimicrobial preservative (in concentrations >20%), a humectant (≤ 30%), an emollient (≤ 30%) or a solvent. It is used in cosmetic products, as well as in parenteral or oral preparations. Adding glycerol to a solution increases its viscosity. Glycerol does not oxidize easily on contact with air. It is not toxic: after absorption by the digestive tract, it is metabolized into carbon dioxide and glycogen or is used for lipid synthesis. High doses of glycerol taken orally have a laxative effect and can cause headaches, hyperglycemia, thirst and nausea. Glycerol is also used in the laboratory as a pro-

■ with a depigmenting formula to prevent pigmentary changes in patients with a high skin phototype (over Fitzpatrick IV); it was also necessary to wear a total sunblock before this peel – this suggests that pigmentary changes are common after this type of peel ■ with retinoids or benzoyl peroxide in cases of acne: treatment with isotretinoin was not given as a strict contraindication to Soft Peel® on condition that the daily prescribed dose 2 or 3 weeks earlier did not exceed 0.3 mg/kg per day ■ with tretinoin at 0.05% once a day in the evening combined or not with glycolic acid to increase and even out penetration of the TCA and accelerate regeneration of the epidermis after the peel, which suggests that the solution did not penetrate evenly and readily and that healing was slow The total number of ‘soft peels’ required was 5–10, with an interval of 8–21 days in between, depending on the depth reached by each peel. The peel solution had to be ‘neutralized’ with water as soon as frosting occurred.31 It should be remembered, however, that adding water to an acid solution does not neutralize it but simply dilutes it. The pH increases very slowly when the solution is diluted, and large quantities of water are needed (Figure 12.9). Rinsing with water was necessary, however, to remove the excess solution that was no longer needed after the appearance of frosting on the skin. It would be more correct to say ‘remove any surplus solution with water as soon as frosting appears’ instead of ‘neutralize the acid’. Without rinsing, the TCA in the TCA–glycerol solution would continue to destroy the skin proteins and deepen the effect of the peel. Choosing the right moment to rinse is therefore essential and has to be timed very carefully, which is not easy for an inexperienced doctor. Some formulations

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H | H —C — H | H — C — OH | H — C — OH | H

Figure 12.11 Chemical structure of propylene glycol.

Figure 12.9 Effect of dilution on the pH of 5 ml of an organic acid solution at pH 2.7: 80 ml of water must be added before the pH rises a little more than 1 point.

(called ‘composite’ or ‘compositum’) still use solutions with glycerol and the post-peel rinsing technique, which is both restrictive and the source of errors. It is also important to make sure that the water does not carry the TCA into the eyes or onto the neck and décolletage, where it will cause an accidental peel.

Glyceryl monooleate Some glycerol derivatives can be used as adjuvants. Glyceryl monooleate (Figure 12.10), for example, is a nonionic surfactant and polar lipid with a molecular weight of 356.55. It is a monoester of glycerol in which one of the hydroxy groups is replaced by a long side-chain derived from oleic acid (CH3(CH2)7CH=CH(CH2)7COOH).32 H O | || H — C — O — C —C17H33 | H — C — OH | H — C — OH | H

Figure 12.10 Chemical structure of glyceryl monooleate.

Propylene glycol Propylene glycol (Figure 12.11), also known as 1,2propanediol and 1,2-dihydroxypropane, has a molecular weight of 76.1. It is used as an antimicrobial preservative (at 15–30%), a disinfectant, a humectant (at 15%), a solvent or co-solvent, and a stabilizer for vitamins, both in

cosmetics and in parenteral pharmaceuticals (10–60%). Although propylene glycol is considered to be non-toxic, parenteral administration of high doses can cause problems, especially in patients with renal insufficiency. Its disinfecting power is slightly lower than that of ethanol. Propylene glycol is stable at low temperatures. At high temperatures, it tends to oxidize and form lactic acid, acetic acid, pyruvic acid and propionaldehyde. Locally, propylene glycol is more of an irritant than glycerol, especially if it comes into contact with the mucous membranes or is used under occlusion. It is neither mutagenic nor teratogenic.

Stability of TCA solutions with glycerol or propylene glycol Attempts to stabilize TCA solutions by adding glycerol (‘soft peeling’31) or propylene glycol improved the safety of TCA peels, although they did not necessarily make them completely stable. Moreover, the addition of glycerol or its derivatives was still empirical and varied from one doctor to another – more of a do-it-yourself approach than a professional one. It is difficult to compare the different solutions, since the exact concentrations of these adjuvants were neither uniform nor even known for certain. Soft Peel® involved the ad hoc combination of TCA at variable concentrations with the same quantity (volume) of glycerol.

Other adjuvants Other attempts to stabilize and even out TCA were made in the 1990s.

‘Enzymatic’ TCA An enzyme is, by definition, a protein. TCA coagulates proteins. It is therefore difficult to include active proteins and TCA in the same solution, since, even if some enzymes are acid resistant (e.g. in the stomach), the conditions for acid resistance are strict and not reproducible in a TCA solution. To my knowledge, there is no preparative approach that would allow proteins to be encapsulated in nanosomes, liposomes, cyclodextrins, etc. to protect them from the coagulating action of concentrated TCA.

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Sorbitan monoesters are partial esters of sorbitol with fatty acids (monolaurate in this case). They have a molecular weight of between 346 and 964. Sorbitan monolaurate is widely used in cosmetics, the food industry and pharmaceutical preparations. Sorbitan monoesters are non-ionic surfactants, dissolving and dispersing agents. One of the problems of using sorbitan monoesters is that in the presence of strong acids (like TCA) they tend to form soaps that have no power to attack the skin. This is partly why TCA ‘adjuvanted’ with sorbitan monolaurate is less aggressive for the skin.

therefore presented as the ultimate solution to all the problems posed by TCA. The most scientific-sounding explanation seems to be of a specific technique where, and I quote, ‘the TCA binds to metallic ions in bentonite clay’. It is not therefore strictly chelation, which would imply the binding of metallic poisons and their elimination through urine. But it is partly true insofar as an organic substance (the TCA) binds with silicon and metal ions (aluminum and magnesium). Even if the process is the exact opposite of chelation – since in this case it is the TCA itself that is the chelating agent – this explanation merits closer examination to understand the possible interactions between the TCA and the structure of the clay.

Phenoxyethanol

TCA in clay masks

Phenoxyethanol, C6H5OCH2CH2OH, also known as ethylene glycol monophenyl ether, 2-hydroxyethyl phenyl ether, 1-hydroxy-2-phenoxyethane, β-phenoxy-ethyl alcohol and 2-phenoxyethanol, has a molecular weight of 138.16. It is a simple disinfectant in the adjuvant solution, an antimicrobial agent that seems not to have a real adjuvant effect on the peel.

TCA sometimes comes in the form of a clay paste. Generally, clays consist of two types of compounds: aluminum silicates (bentonites) and magnesium silicates (hectorites). Clays36 are made up of stacked three-layer platelets (Figure 12.12): a middle layer of magnesium oxide (in the case of hectorites) or aluminum oxide (in the case of bentonites), surrounded by two layers of silicon dioxide (silica). The lateral surfaces of each platelet are positively charged37 and the lower and upper surfaces are negatively charged.38 The clay platelet therefore reacts like a dipole, and the different particles rearrange themselves depending on the electrical charges that encourage contact between the lateral surface and the upper surface. Clay has a ‘house of cards’ structure, and macroscopically forms a coarse gel with a grainy texture in the aqueous phase. The TCA molecule is itself electrically neutral. When it is in an unbuffered solution, it more or less completely breaks up, releasing its proton (H+) into the solution, which then becomes acidic. The TCA, without its proton (i.e. trichloroacetate anion), has an overall negative charge that can therefore combine electrically with the positively charged lateral surfaces of the clay, while the positively charged protons will combine more readily with the lower and upper surfaces of the negatively charged clay particles (Figure 12.13). The protons therefore combine with the

Sorbitan monolaurate

Chelation of TCA Some TCA masks33 have been presented as ‘chelated’ TCA. Chelation34 is a medical therapy that aims to detoxify the body of harmful minerals and metals. Chemically, chelation is the process by which an organic substance (the chelator) binds metal ions (iron, copper, lead, calcium, etc.) into inactive, non-toxic and water-soluble complexes that are easily eliminated in the urine. Intravenous chelation therapy (e.g. with ethylenediamine tetra acetic acid, EDTA) is often used to treat poisoning with heavy metals, including lead. The use of the term ‘chelation’ therefore seems inappropriate as far as TCA is concerned, and has no chemical basis since TCA is not a metal. The little information available states that chelation reduces the speed of penetration of TCA and therefore its depth of action.35 Might what we call chelation be partial inactivation of the TCA? The directions of use for Accu Peel® state that a ‘process called chelation allows the TCA to reach an even depth at the same time as using lower concentrations of TCA’. Might chelation, on the contrary, be a process that activates the TCA? But how can TCA be activated? The directions for use of TCA Cream Peel® tell us that, thanks to chelation, not only is this peel as deep and smooth (sic) as regular TCA but also that it uses much milder concentrations (the stakes are being raised) and so there is less pain and stinging and healing is faster. Is chelation the ultimate answer for TCA? The Holy Grail of the peeler? The Plastic Surgery Group states that ‘chelation’ of Accu Peel®, on the contrary, provides a superficial peel that heals more quickly – which at least seems logical. Chelation is

Figure 12.12 Clays consist of a stack of platelets that are electrically linked. This diagram shows the typical structure of a clay platelet and its electrical charge.

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Figure 12.14 TCA green clay mask (TCArcil® mask). The hands and forearms are covered in a clay paste layer that spreads easily.

Figure 12.13 A possible arrangement of TCA in a solution with clay in the gel phase, on the basis of electrical charges.

oxygen atoms of the silica molecules on the lower and upper surfaces, whereas the negatively charged trichloroacetate anion will combine with the metallic cations on the other surfaces of the clay particles. This then explains how the TCA binds with metallic ions. It is easy to understand how this might stabilize the TCA, as once it has broken up, it binds electrically with the different parts of the clay particles. It is, however, difficult to understand the real clinical advantage of this combination, as the protons that produce the peeling effect are still attached to the part of the TCA that has not broken up or else they have to break away from the clay in order to be effective. It could then be argued that the protons (and the trichloroacetate) and the clay are relatively united and that the TCA in a clay mask will act more slowly and be less aggressive. It is difficult to reconcile this with the statement that a low-concentration TCA clay mask produces the same effect as a more concentrated water-based TCA in which all the molecules exert their peeling effect at the same time. It cannot seriously be claimed that a clay paste of ‘chelated’ TCA at 20% is equivalent to any other TCA liquid at 45–50%. Even then, it would be necessary to know whether the concentration is m/m, m/v or m + v. It cannot possibly be m/m, as a TCA at 50% m/m is extremely aggressive and causes more complications than effective results. Besides, 20% TCA masks are marketed as superficial peels, which is incompatible with the gratuitous claim that ‘20% in mask form is equivalent to 50% in liquid form’, but completely compatible with the scientific explanation given above. Another major problem comes from the fact that the clay mask forms a coarse and opaque layer: it is impossible to observe the effect of the TCA directly and continuously through the clay mask (Figure 12.14). One common method of monitoring the peel consists in using a tongue depressor to remove the clay from a small area to

see if, or how much, frosting has occurred. If there is no frosting, the acidified clay is replaced. This examination is repeated after a few minutes or if the patient makes any comment. It should be noted that removing the clay with a spatula creates an abrasion on the skin where the acid can penetrate more deeply. The next time, therefore, the same area must be checked again as well as a different area. When a TCA paste is called ‘homogeneous’, it should not automatically be assumed that the TCA is distributed evenly, although it may well be. It should be assumed that the paste itself has a homogeneous consistency and is not grainy. It is possible – though not easy – to spread TCA homogeneously in a clay paste. However, the even distribution of TCA in a paste does not in itself guarantee that the acid will penetrate the skin evenly. Another argument that counters the claim that lower concentrations are more effective is that the application technique for a TCA mask involves degreasing the skin and applying glycolic acid or tretinoin beforehand.35 This makes the skin far more permeable and enhances the penetration of the TCA,39 which means being very careful about how long the paste remains in contact with the skin. Some TCA clay pastes are presented as causing simple erythema with no protein coagulation, but they nevertheless have a downtime of 6–8 days.35 The absence of frosting is compatible with a superficial peel – but not with an improvement in the appearance of deep wrinkles, which can only be treated with a deep peel. Then again, a downtime of 6–8 days is not compatible with a superficial peel, as it is the same as the downtime following a ‘medium’ TCA peel to the papillary dermis. The TCA mask is not the easiest40 or safest of peels, as it is not possible to check in real time whether the TCA is penetrating too deeply under the mask. It does, however, make application a little easier for doctors who doubt their ability to apply a superficial TCA peel evenly. We can therefore conclude by saying that TCA masks are easy to apply but difficult to monitor. Even if ‘chelation’ makes the clay mask less aggressive, it is on the whole not as safe as an ‘open’ TCA peel, which can be monitored at all times. My experience with a TCA mask preceded by a glycolic acid mask is in the context of a regular medium-depth TCA peel to the papillary dermis.

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effects of four different types of peels against a control group:

Histology Even though histological sections taken 30 minutes after the application of a medium-depth TCA peel on the skin have not revealed any skin necrosis, and even though histologically everything appears normal, it is certain that necrosis is taking place both clinically and chemically. The epidermis is functionally dead, although it appears to be histologically normal. Maybe this can be explained by the protein-coagulating action of the TCA: with conventional histology, it is not possible to see membrane proteins (essential to cell life) coagulating. It is only later on that necrosis can be detected histologically when the normal cell structure has radically changed as a result of its protein membranes becoming devitalized. The overall histological effect of a TCA peel consists in the destruction of the living cells of the epidermis and possibly the dermis (the depth of destruction depends on the concentration used). Abnormal keratinocytes are replaced by healthy cells from deep surviving islets of keratinocytes, the pilosebaceous units and the sweat glands.41 As the skin re-epithelializes, new collagen is formed. The depth of skin necrosis is directly proportional to the concentration of the TCA. Necrosis should not be the only endpoint of a TCA peel – stimulation also plays an important role. Repeated application of less concentrated TCA helps rebuild the papillary dermis directly and/or indirectly as a result of the repeated dermal irritation of the peelinduced inflammation. It is possible to reach the dermis using a low-concentration solution applied to an epidermis that has been made temporarily more permeable by a prior peel or ‘robust’ preparation. TCA peels allow different depths of penetration to be reached (Table 12.3). A study by Roenigk41 shows that regeneration of dermal collagen starts within 2–3 weeks. The increase in papillary dermal collagen and the production of elastic fibers continues for 6 months. Another study42 on mice artificially photoaged by exposure to UV rays compared the histological

■ ■ ■ ■

50% glycolic acid 30% TCA (m/v or m + v? – not specified) 50% TCA (m/v or m + v? – not specified) Phenol peel (Baker Gordon’s formula).

In all of the peel groups, the concentration of collagen increased from the 3rd day, fell around the 7th day and reached a positive peak around the 28th day. There was more of an increase with the TCA and phenol peels than with the glycolic acid. There was a significant increase in the concentration of glycosaminoglycans with the 50% TCA and phenol at 14 and 28 days. On the 60th day, the dermal concentrations both of collagen and glycosaminoglycans had returned to their original values in all of the groups. These findings cannot be considered as proof that these peels are not clinically effective, as the structure of the epidermis and dermis improved histologically, the collagen fibers were significantly rearranged in the papillary and reticular dermis and elastotic material disappeared in the deep TCA and phenol groups. At the same time, it was noticed that the elastic fibers rearranged themselves. These positive histological changes are more marked in the deep TCA and phenol groups than in the other peel groups. As for the global effect, the study shows an overall increase in dermal thickness with the deeper peels. In the long term, the histological changes brought about by TCA are temporary when the TCA penetrates superficially and long lasting when the TCA penetrates to the papillary dermis at least. Dermal fibroplasia causes hypertrophic scarring, scar adhesions and keloids. Black or dark skins are more likely to develop this type of reaction. The shoulder girdle and the lower thorax are both high-risk areas, as is the jaw area on the face. This type of scarring does not occur when necrosis goes no further than the upper reticular dermis.

Table 12.3 The depths of peelings, type of action and duration of change. Level of destruction

Type of action

Duration of change

Upper stratum corneum

Exfoliation

Very temporary

Intraepidermal

Partial destruction of the epidermis

Very temporary

Basal layer

Destruction of the basal layer

Temporary

Grenz zone

Destruction of the Grenz zone

Medium duration

Papillary dermis

Destruction of the papillary dermis

Long lasting

Upper reticular dermis (with vertical fibers)

Destruction of the upper reticular dermis

Permanent

Deep reticular dermis (with horizontal fibers)

Destruction of the deep reticular dermis

Permanent; risk of scarring

Hypodermis

Scarring

Permanent

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Apart from a few exceptional cases (e.g. Ehlers–Danlos syndrome), the destruction of the papillary dermis does not cause hypertrophic scarring. There is a risk of skin atrophy when all of the appendages of a treated area undergo necrosis. The skin does not have any source of supply to regenerate cells quickly. The keratinocyte clones can only come from the (distant) edges of the necrotic areas; they cannot be produced in sufficient numbers for rapid skin regeneration if the lesion is more than a few centimeters in diameter. Lesions smaller than 1 cm in diameter, even in the deep reticular dermis, do not pose a high risk of scarring unless there is a secondary infection or the patient scratches the scabs. When all of the appendages have undergone necrosis, the melanocyte reserve as well as the keratinocyte reserve suffers, and scarring will be hypopigmented or unpigmented.

Occlusion of TCA Following the example of phenol, it was suggested in the past that occluding TCA could potentially enhance penetration. A histological study by Stegman43 in 1980 throws some light on this question. Occlusion does in fact increase the depth of action of phenol, but actually reduces that of TCA. An occlusive dressing applied quickly after phenol helps it macerate and deepens its action. An occlusive dressing applied immediately after TCA creates a barrier to epidermal water evaporation and to the water in the solution itself. Under occlusion, this water accumulates in the uppermost layers of the skin, where it dilutes the TCA fairly rapidly. With phenol, this slight dilution enhances its penetration. An occlusive dressing applied 30 minutes after TCA does not dilute the acid, as it has had enough time to coagulate the proteins in the skin and neutralize itself by combining with the proteins before occlusion can dilute it. Applying a greasy substance, such as Vaseline® or an antibiotic ointment, immediately after a TCA peel is equivalent to occlusion, and can reduce the depth of necrosis caused by the TCA.

Increasing the permeability of the stratum corneum The thicker the stratum corneum, the less the TCA penetrates, and any method used to make the stratum corneum thinner before applying TCA deepens its action. Applying tretinoin for 2 weeks before a TCA peel thins the skin and causes the keratinocytes and corneocytes to dedifferentiate. Acetone degreases the skin and causes chemical changes in the membrane lipids, which increase the skin’s permeability and the depth of action of the peels. Applying a given concentration of TCA to a thin and

permeable skin will cause deeper necrosis than application to a thick and impermeable skin. Another way of increasing the depth of skin necrosis would be to use higher concentrations of TCA, but this method produces variable results because of the wide variation in penetration of TCA in an aqueous solution. The risk of scarring increases with the concentration of the TCA.

Notes 1. The alpha carbon atom is that adjacent to the COOH group (as with alpha-hydroxyl acids – cf Chapter 6). 2. Which means that at a pH of 4.76, 50% acetic acid in an aqueous solution is in the form of acetate. 3. ‘Glacial’ acetic acid is 100% acetic acid – it is so called because of its tendency to solidify near room temperature (the melting point of acetic acid is 16.7°C). 4. Through the accumulation of lactic and/or glycolic acid. Tubular necrosis develops rapidly. 5. Due to precipitation of myoglobin and oxalate crystals in the renal tubules. 6. Bismuth Ch. Toxicologie clinique, 5° ed. Paris: Editions Médecine–sciences, Flammarion, 2000. 7. Ketoacetic acid, oxoethanoic acid. 8. Oxalic acid (ethandioic acid) is HOOC.COOH, with pKa1= 1.23 and pKa2 = 4.19. 9. Glycolic acid is HO.CH2.COOH, with pKa = 3.83 (see Chapter 6). Glyoxylate is converted into glycolate by glyoxylate reductase. 10. Glycine (aminoacetic acid, aminoethanoic acid) is H2N. CH2.COOH, with pKa = 2.4. It is transaminated by an alanine–glyoxylate aminotransferase. The glycine can then be incorporated into proteins and used for serine synthesis or simply be degraded. 11. DCA was administered orally in the drinking water of rodents. No specific data have been reported in humans. 12. Kitamura N, Ota Y, Mimura K. Effects of diisopropylamine dichloroacetate on proliferation and differentiation of normal keratinocytes in vitro. Skin Pharmacol Appl Skin Physiol 1999; 12: 317–325. 13. Johnson K, with the Canadian Task Force on the Periodic Health Examination. Periodic Health Examination, 1995 update: 1. Screening for human papillomavirus infection in asymptotic women. CMAJ 1995; 152: 483–93. 14. Although using the new phenol formulas seems to be safer (see Chapter 36). 15. TCA is often found in drinking water as a by-product of disinfection. 16. Obtained by simple dilution of TCA crystals in water. 17. I beg any chemist reading this to forgive this explanatory short cut. 18. Trauchessec JM, Pissot F. Solution d’acide trichloracétique masse par masse pour peelings dermatologiques, nécessité d’une formulation explicite pour les solutions d’acide trichloracétique. 18° réunion du GRCD, Perpignan, 9 Septembre 1995: 28–38. 19. Trauchessec JM, Pissot F. Solutions d’acide trichloracétique

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20. 21.

22.

23. 24. 25.

26.

27.

28.

masse par masse pour peelings dermatologique. Nouv Dermatol 1996; 15: 252–5. One apple plus one apple equals two apples, whereas one apple plus one pineapple equals two pieces of fruit! According to Roenigk, applying TCA at 70% m/v on the face usually causes scarring, while in gynecology, treating vaginal or cervical condylomas does not produce any scarring. McCollough EG, Langsdon PR, Maloney BP. Chemical Peel with Phenol. Roenigk RK, Roenigk HH (eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996 UK, Oxford, Marcel Decker Ltd. Rereading the textbooks that I used at the beginning of my career as a ‘peeler’ now makes me realize why it was so difficult to get an overall grasp of the field and to understand the consistency of the technique. Brody H, Stegman S. Histological study by Harold Brody and Samuel Stegman, at 3, 30 and 90 days. TCA therefore does not have an ‘all or nothing’ action. McCollough EG, Langsdon PR, Maloney BP. Chemical Peel with Phenol. In: Roenigk RK, Roenigk HH (eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996, UK, Oxford, Marcel Decker Ltd. Easy TCA® and Unideep® consist of peel solutions as well as a post-peel cream whose ingredients help achieve better results and avoid complications. Only Touch® consists of a solution alone, but has to be combined with Easy TCA® or Unideep®, and thus benefits from the application of the post-peel cream of these peels as well. Chiarello SE, Resnik BI, Resnik SS. The TCA masque. A new cream formulation used alone and in combination with Jessner’s solution. Dermatol Surg 1996; 22: 687–90. Vergereau R, Trauchessec JM, Peyronnet B. Le new peel. J Med Esth Chir Derm 1990; XXII (68): 243–55.

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29. See the many previously published works on the semiology of TCA–SAS peels. 30. See Chapter 2. 31. Peyronnet B, Trauchessec JM, Vergereau R. Le peeling doux. J Med Esth Chir Derm 1991; XXIII (69); 33–7. 32. In fact, the commercially available ‘glyceryl monooleate’ is a mixture of esters of glycerol with a number of fatty acids (long-chain carboxylic acids), the major component of which is the monoester with oleic acid. 33. TCA Masque®, Accu Peel® cream and TCA cream peel®. 34. From the Greek chele, meaning ‘claw’. 35. Cabaní I. Nuestra experiencia en la aplicación de la nueva máscara de TCA. Medicina estética (SEME) 1995; 39: 25–9. 36. A clay is a friable sedimentary rock that can be molded when soaked in water. 37. Thanks to the metallic cations of the crystalline lattice. 38. Thanks to the oxygen atoms of the silica molecules. 39. Which would be pointless – even dangerous – if the TCA mask at 20% had the same effect as 50% TCA. 40. Prior application of a glycolic acid mask, and close and difficult monitoring of the contact time and downtime are necessary. 41. McCollough EG, Langsdon PR, Maloney BP. Chemical Peel with Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996, UK, Oxford, Marcel Decker Ltd. 42. Butler P, Gonzales S, Randolp M et al. Quantitative and qualitative effects of chemical peeling on photo aged skin: an experimental study. Plast Reconstr Surg 2001; 107: 222–8. 43. Stegman SJ. A study of dermabrasion and chemical peels in an animal model. J Dermatol Surg Oncol 1980; 6(6): 490–7.

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13 Trichloroacetic acid: indications and contraindications

Main indications for trichloroacetic acid Trichloroacetic acid (TCA) is an extremely versatile peel that can reach all depths, and can be applied to all skin types, on all parts of the body and in a great many indications. Using solutions that are properly prepared and following strict protocols ensures a safe and effective peel. Repeating several easy peels, such as Easy TCA®, can boost collagen and elastin production to the same degree as a deeper peel; repetition may even be preferable to using a more aggressive peel when the aim is to stimulate the skin and renew the epidermis, as is the case in the treatment of photoaging. On the other hand, when the desired effect is destruction of deeper layers of the dermis and epidermis to eliminate certain lesions, a single deeper peel may be a better indication than repeating several peels to the Grenz zone, as is the case when treating lentigines and mixed or dermal melasma.

Photoaging Early photoaging (Figure 13.1) is one of the best indications for a TCA peel. In short, it improves and evens out the complexion, reduces or gets rid of lentigines, improves elastosis and fine lines, improves skin tone, and generally brightens the skin. TCA peels have often been combined with tretinoin in this indication (see Chapter 2). Photoaging on the hands is an excellent and easy indication for TCA (see below and Figure 13.3).

Solar elastosis The papillary dermis is sometimes so atrophic that the epidermis appears to be lying directly on the middle dermis,

Folds and wrinkles Deep wrinkles and folds are not a good indication for TCA peels: ■ Folds cannot be treated by peels, and require surgery, dermal fillers or thread lifts. Deep nasolabial folds and marionette lines do not always respond to phenol. ■ Dynamic wrinkles respond well to a combination of botulinum toxin and peels: the peels restructure the epidermis and the dermis on an unmoving base and the clinical results are better when these two treatments are combined than when used alone. ■ Fine sun-related wrinkles respond well to TCA, but deeper ones respond better to phenol. ■ Wrinkles around the mouth and eyes are very poor indications for TCA, even in high concentrations; phenol is far more effective (see Chapter 36).

Figure 13.1 Early photoaging: a good indication for TCA.

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without the intervening Grenz zone. The epidermis then becomes ‘too big’ for the underlying dermis, and wrinkles appear – like baggy clothes that crease on a body that has grown too thin. In theory, only a very deep peel can treat solar elastosis, by producing enough good-quality collagen and elastin in the papillary dermis to fill the atrophied dermis and bury the sun-damaged fibers deep down (see Chapter 26). Repeating certain types of peel to the Grenz zone1 once a week may be effective enough to improve the appearance of the skin without the downtime that inevitably follows medium or deep peels. Of course, the deeper peels will be more effective: there is no comparison between the results of a phenol peel and those of an AHA, resorcinol or TCA peel! On the other hand, dermatologically and toxicologically, phenol is a risky option for treating anything but facial skin. Body skin only benefits from other agents. Solar elastosis appears in several forms. It starts with the appearance of limited areas of elastosis that as yet have no or little clinical expression. Its maximum expression is seen when the skin has a cobblestone appearance (Figure 13.2). The type of treatment depends on whether the elastosis is in its very early stages or if it is more advanced (Figure 13.2). Early elastosis, which is characterized by very fine lines and an uneven complexion, can be treated successfully with four Easy TCA® peels or one Unideep® peel, while advanced elastosis can only benefit from a deep reticular peel (fullface Lip & Eyelid® formula) and a major restructuring of the skin. TCA would have no effect on the deep wrinkles in Figure 13.2, no matter which concentration, adjuvants or other combined treatments were used. Solar elastosis often affects the legs if they are frequently exposed to the sun, which is the case with women who wear skirts. The skin between the knee and the malleolus is sometimes affected by visible elastosis that can be improved by combining abrasion and Easy Phytic® solu-

Figure 13.3 Overall rejuvenation of the hands after four sessions of Easy TCA® at a rate of one session every 2 weeks.

Figure 13.4

Figure 13.2 Solar elastosis (skin with a cobblestone appearance): this is not the best indication for TCA.

Lentiginosis and photoaging. (a) Before treatment, there are about 40 lentigines and/or actinic keratoses. (b) After four sessions of Easy TCA® peels to the Grenz zone, there are only about 10 lentigines/keratoses left. The signs of photoaging are visibly reduced: fine lines, quality of the skin, improved eyelid tension, etc.

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A

B

C

D

tion (see Chapter 11). The hands and forearms respond extremely well to Easy TCA®, with no side-effects (Figure 13.3).

Lentiginosis2 TCA is effective in treating solar lentigines: the concentration of the TCA is chosen depending on the assumed depth of the lentigo. Relatively superficial lentigines are easily treated with Easy TCA® (Figure 13.4). Lentigines of medium depth respond to Unideep®. Lentigines originating from the deepest dermal papillae and embedded deep in the dermis only respond to very concentrated TCA (Only Touch®), or even phenol (Lip & Eyelid® formula), applied locally and combined with Easy TCA® (or Unideep®) to even out the results and treat the smaller subclinical lesions (Figure 13.5). It should be noted that a TCA peel, even to the papillary dermis, does not always treat lentigines definitively and that several peels to the papillary dermis may be necessary for long-term results.

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Figure 13.5 Photoaging, actinic keratoses and lentigines. (a) Before and (b) after a peel to the papillary dermis with TCA (Unideep®) and phenol (Lip & Eyelid® formula) around the mouth and on the large lentigo on the left temple only. (c) Before and (d) on the 6th day after the peel. For more details, see Chapter 23.

Perioral wrinkles Very fine lines around the mouth can be improved by a combination of filling techniques (e.g. hyaluronic acid) and one or more TCA peels to the papillary dermis, but the results achieved with TCA never equal or even come anywhere near those achieved with phenol, which is preferred in chemical labioplasty or cheiloplasty (see Chapter 36) in combination with botulinum toxin, if possible.

Prevention of skin aging The wisest patients go to see their doctor before the clinical signs of aging appear and seek advice on how to prevent skin aging. The preventive treatments that might be suggested to these patients are straightforward and superficial procedures that do not disrupt their social lives too much. They may simply be prescribed cosmeceuticals: DHEAPhyto®, Actilift® (dimethylaminoethanol (DMAE) cream), Renutriv ACE Lipoic Complex® (an antioxidant) or Vit E

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Figure 13.6 Early photoaging: treatment of rosacea on the cheeks with a radiofrequency device (Ellman) and four applications of Easy TCA® (basic protocol). Daily care: Vit E Antioxidant® cream.

Antioxidant® (a hydrating antioxidant). These cosmeceuticals should be combined with sun protection against UVA, UVB. A series of AHA peels or TCA peels to the basal layer of the epidermis can be repeated on a yearly basis. If the signs of aging are beginning to show clinically, Easy Phytic® solution can be extremely beneficial. When the signs are more obvious, Easy TCA® is the best choice of peel (Figure 13.6). Very obvious photoaging can benefit from Unideep®, a papillary intraepidermal peel. An excellent treatment for preventing photoaging is a combination of a mesolift3 and a peel, sometimes called a ‘mesopeel’: a peel and a mesolift are used alternatively every other week or sometimes even in the same session when mesotherapy is combined with Easy TCA®. The need for a surgical facelift or a deep phenol peel can be put off for several years.

Melasma and chloasma Melasma (Figure 13.7) is a common acquired hyperpigmentation disorder of the face, neck and forearms. It is usually symmetrical. The density of color in the hyperpigmented area can vary, but is clearly delimited. Patients with a dark skin phototype are more prone and can get melasma earlier in life than light skin phototypes.4 Melasma appears almost exclusively on areas of skin that have been exposed to the sun. It can be of the following types: ■ Purely epidermal: there is a lot of melanin in the basal and suprabasal layers of the epidermis. It is occasionally found throughout the epidermis. A Wood’s light5 increases the contrast between the melasma and normal skin. This is the most common type of melasma. ■ Dermal: the melanin accumulates in the macrophages of the papillary and/or reticular dermis. A Wood’s light does not increase the contrast.

Figure 13.7 Melasma on the forehead: centrofacial. Other kinds of melasma include malar and mandibular.

■ Mixed epidermal–dermal: a Wood’s light accentuates the contrast in some areas and not in others, but an ‘epidermal’ area can hide an ‘underlying dermal’ area. The cause of melasma is still widely debated, and potential pathogenic factors include the influence of UVs, the hyperpigmenting effect of some cosmetics,6 genetic predisposition, hormone therapy and pregnancy.7 Estrogens and possibly progestogens can trigger melasma. Topical treatments for melasma usually include tyrosinase inhibitors, with or without tretinoin or one of its precursors. Azelaic acid is also a viable treatment option. A corticosteroid can be combined with it to counter any potential active inflammation. Lasers, intense pulsed light (IPL), dermabrasion and microdermabrasion have also been suggested, but often cause post-inflammatory hyperpigmentation. TCA can be an excellent treatment for melasma: it eliminates the melanin stored in the papillary dermis and epidermis (Figure 13.8). Mesotherapy has been recently reputed as an effective treatment of melasma.8

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Figure 13.8 Melasma on the forehead in a patient with skin phototype VI: (a) The condition before peeling. (b) Results of the following treatment: two sessions of Easy TCA® to the Grenz zone, combined with Blending Bleaching® cream. As the results were unsatisfactory, it was decided to use a deeper treatment. After two Easy TCA® peels, the patient was given two Unideep® peels to the papillary dermis, (c) still combined with Blending Bleaching® cream and Melablock® 50+. The peel to the papillary dermis was applied locally to the most resistant parts of the melasma. (d) End result.

If the melanin responsible for the melasma is too deep, TCA will only be effective after many repeated sessions. In any event, the TCA peel must be combined with effective sun protection and appropriate post-peel care in the long term. Simple aqueous solutions of TCA also require the skin to be prepared, in order to even out penetration and prevent common pigmentary changes. See Chapter 16 for the exact protocol for treating melasma.

Post-inflammatory hyperpigmentation and berloque dermatitis Post-inflammatory hyperpigmentation (PIH) (Figure 13.9) and berloque dermatitis9 usually respond well to TCA; they can be treated in the same way as melasma, but have a better prognosis as the original trauma disappears

after treatment, unlike melasma, which often persists or recurs.

Freckles Freckles (Figure 13.10) are small, clearly delimited, benign pigmented macules that appear on areas of sun-exposed skin in patients with a light skin phototype. They are never present at birth, but can start to appear from the age of 3 years, and there is an autosomal dominant pattern of genetic transmission. They result from melanocyte hypertrophy, although not from an increase in melanocyte numbers. In the basal and suprabasal layers, more melanin is synthesized and transferred between the melanocytes and keratinocytes. This increased melanin synthesis could result from melanocyte clones that have mutated following UV exposure. The structure of the epidermis remains normal, apart from the parabasal keratinocytes, which contain more melanin in relation to the neighboring unpigmented cells.

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Figure 13.11 Freckles before (a) and after (b) a peel to the papillary dermis (Unideep®). A peel to the papillary dermis improves the quality of the skin, removes the freckles and improves the fine lines, but does not treat wrinkles.

Post-acne scarring Figure 13.9 Post-inflammatory hyperpigmentation after a road accident (see Chapter 5).

TCA has some effect on shallow scars, but can only improve the general condition of the skin and cannot get rid of scars altogether. TCA can be combined with sandpaper abrasion (see the discussion of abrasive peels in Chapter 15) or scar subcision before the acid is applied. Even a phenol peel cannot always guarantee to heal acne scars. High concentrations of TCA can be directly applied on acne scars, levelly, with good results.

Dilated pores

Figure 13.10 Freckles.

A peel to the basal layer lightens the freckles, sometimes only temporarily. A peel to the Grenz zone removes many freckles and lightens others. A peel to the papillary or reticular dermis gets rid of freckles altogether (Figure 13.11). Easy TCA®, Unideep® (TCA) and Lip & Eyelid® (phenol) can all be used as treatments for freckles, although phenol will generally not be used as the TCA can get rid of them by itself. Other treatments have been suggested. As freckles grow darker on exposure to UV rays, using a sunscreen helps to lighten them. Tyrosinase inhibitors, antioxidants, and tretinoin and its precursors can be used in conjunction with the peels to improve or prolong results.

Although it has been claimed that TCA has a ‘circular contraction’ effect that ‘narrows the follicle opening’, it appears that it has a limited effect on dilated pores, or, at best, the results are difficult to predict. Patients should never be promised visible results for dilated pores. Any results should be considered a bonus and not taken for granted. Using an abrasive technique before applying Easy TCA® may give promising results, but this remains to be confirmed with more experience. High concentration TCA can be successfully used for treating dilated pores or pike acne scars.

Seborrheic dermatitis Seborrheic dermatitis, resulting from an excess production of sebum and overgrowth of the commensal yeast Pityrosporum ovale,10 improves rapidly but only temporarily after the application of TCA peels. Follow-up treatment after the peels consists simply of applying vinegar every morning before showering (for the antiseptic qualities of the acetic acid) and the use of antimycotic creams. In some cases, the reaction of the yeast and metabolites causes eczema, which can be treated with topical corticosteroids. It should be noted that Easy Phytic®

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solution rapidly improves the inflammation associated with seborrheic dermatitis, without having to resort to corticosteroids.11

Widespread flat warts Flat warts are localized skin-colored papules that mostly appear on the back of the hands, the forearms and the face. Clinically visible flat warts do not respond to moderate concentrations of TCA (10–30%), and higher concentrations (40–50% m/m) often produce only temporary or incomplete results. Figure 13.12 shows how flat warts on the back of the hand reacted to a combined treatment of Only Touch® and Easy TCA®. Smaller flat warts can disappear completely, as can subclinical flat warts. Medium-size warts will come back, and they will sometimes need shaving with a radiofrequency scalpel (Ellman), for example. Not only are larger warts impermeable to TCA, but also their very size prevents the TCA from getting round them to ‘undermine’ and treat them from underneath (Figure 13.13). They should be treated by shave excision at the same time as the others are being treated with a peel.

Figure 13.12 Appearance of the hand after two sessions of Only Touch® and three sessions of Easy TCA® (for further details, see Chapter 15). The flat warts have disappeared. Note that the flat wart treated with radiofrequency is still healing. The fine visible flaking all over the hand comes from an Easy TCA® peel applied to even out the Only Touch® and treat the subclinical lesions.

A

Sensitive skin Abnormal skin sensitivity is a clear sign of dysfunction of the skin’s protective properties against a hostile environment. Sensitive skin should be treated until its tolerance to external aggression returns to normal. Many products cause skin allergies that are not always easy to identify since they may manifest as ‘over-reactive’ or ‘oversensitive skin’.

B

Figure 13.13 (a) Multiple flat warts. (b) Localized frosting of the flat warts after multiple applications of Only Touch®. Note that the thicker dome of the flat warts is impermeable even to concentrated TCA. The wart in the middle is too thick, and should be shaved with (Ellman) radiofrequency.

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Figure 13.14 Keratoses: peel solutions penetrate the keratoses slowly. This photograph shows the slow penetration of phenol through keratoses during a full-face peel.

In the case of allergy, it is best to avoid using too many cosmetic products and stick to a few well tolerated creams.

Figure 13.15 Appearance of keratoses during treatment with 5-FU.

Actinic keratoses The treatment of actinic keratoses, like photoaging, is a common indication for chemical peels (Figure 13.14). The chemical elimination of actinic keratoses reduces the incidence of basocellular and/or spinocellular cancers.12 Other localized treatments (e.g. cryotherapy or laser) could also be suggested, but they are only applied to visible lesions and leave clinically undetectable microlesions to develop. A chemical peel, on the other hand, will treat all lesions, both visible and subclinical ones, and will improve long-term prognosis. In comparisons between TCA peels to the papillary dermis and the application of a 5-fluorouracil (5-FU) cream, the peels fare better, as applying 5FU gradually causes severe and rather nasty-looking dermatitis (Figure 13.15). Patients and friends can find the long-drawn-out treatment difficult to bear. A mediumdepth TCA peel, on the other hand, is generally a one-off treatment (few sessions at most).

Oncological indications As Vergereau et al12 reminds us, after a biopsy to confirm the diagnosis and depth of a lesion, TCA is indicated in the treatment of primitive malignant intraepidermal and intradermal tumors (depending on the depth of action of the TCA). Keratoses that have developed into microinvasive spinocellular or basocellular carcinomas can be treated

with TCA without leaving any scars: Only Touch® easily reaches the reticular dermis. Non-degenerated lentigo maligna (Hutchinson’s freckle or Dubreuilh’s melanosis) is also given as a potential indication for TCA, although phenol is no doubt more effective.

Acne All common types of acne can be treated with TCA. Severe acne, such as ‘acne necrotica’, ‘acne conglobata’ or ‘acne fulminans’, should first be treated medically and the inflammation eliminated before the cosmetic use of peels. Oral isotretinoin (13-cis-retinoic acid) is the gold-standard treatment for severe acne (Box 13.1), but new retinoids come to light regularly. Here too a combination of techniques proves worthwhile. Acne responds well to a TCA peel to the basal layer or the Grenz zone, whether it is comedonal, microcystic (Figure 13.16), papular or papulopustular. Deeper peels, to the papillary dermis, should not be used when acne is still active, because of the increased risk of infection (see Chapter 37). The number of open or closed comedones can be expected to decrease after several TCA peels. We shall see how the Easy TCA® technique allows comedones and microcysts to be opened immediately before the peel, which gives faster and better results. Seborrhea is often reduced after TCA

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high concentrations required make it relatively dangerous compared with the ‘chemical blepharoplasty’ technique using phenol, which is more effective and easier to control than highly concentrated TCA. It must be remembered that xanthelasma is associated with dyslipidemia in 50% of cases. It can also be symptomatic of hepatobiliary disorders (biliary atresia and biliary cirrhosis) when associated with cholesterol deposits that start to build up in the hands and feet before spreading. Monoclonal gammapathies have also been described in association with xanthelasma.

Stretch marks Figure 13.16 TCA will reduce the number of lesions and the inflammation of this type of microcystic acne. Opening the microcysts with a No. 11 scalpel blade or a needle and removing the blackheads with a comedone extractor immediately before applying Easy TCA® will produce faster and better results.

Box 13.1 Isotretinoin for acne Tablets dosed at 10 mg or 20 mg Total cumulative dose 120 mg/kg Daily dose 0.3–0.5 mg/kg For example – weight of 70 kg: Total cumulative dose 8400 mg • Daily dose of 0.3 mg/kg = 21 mg/day ⇒ accumulated dose for a month 600 mg ⇒ total duration of treatment 8400/600 = 14 months • Daily dose of 0.5 mg/kg = 35 mg/day ⇒ accumulated dose for a month 1050 mg ⇒ total duration of treatment 8400/1050 = 8 months

peels and seborrheic dermatitis improves significantly (although only temporarily). Acne in fact improves more quickly when treated with easy TCA than it does when treated with tretinoin, benzoyl peroxide13 creams, glycolic or azelaic acid creams, or ‘purifying’ creams used alone. These creams do, however, play an important part in the post-peel treatment of acne. Pigmented acne scars usually respond well to TCA. Shallow scars gradually soften. Ice-pick scars do not respond at all to TCA. A combination of sandpaper abrasion followed by Easy TCA® – a technique similar to the one described below for the treatment of stretch marks – can significantly improve post-acne scarring, even on the back.

Xanthelasma Eyelid xanthelasma has been presented as a good indication for TCA and dichloroacetic acid. Nevertheless, the

Countless suggestions have been made for the treatment of stretch marks, but none of them have really been effective. Some techniques are not deep enough and others not extensive enough. Superficial, intraepidermal, basal, Grenz zone and papillary techniques can only improve the appearance of stretch marks temporarily, but cannot reduce their size or depth. Some peels have been developed to give the atrophic base of the stretch marks a similar color to that of the surrounding skin; they contain resorcinol, which is oxidized to match the normal skin color. The results of these peels are good, but only temporary. Deep techniques, limited to the deepest part of the stretch marks, can do no more than tighten the little collagen that is left and slightly stimulate the few surviving fibroblasts: in spite of the fact that these localized treatments reach the deepest part of the stretch marks, the results are always disappointing. That is why I developed a technique for treating stretch marks consisting of sandpaper abrasion followed by Easy TCA® peel solution and post-peel cream. The excellent results achieved with this method are due to the fact that the atrophic base of the stretch marks contracts at the same time that the cells on the edge of the stretch marks being stimulated. The results seem to be permanent. See the section describing this technique in Chapter 15.

Other indications These include alopecia areata, liposuction scars, neurogenic excoriations and rosacea. TCA has often been tried on vitiligo, but without success.

General contraindications for TCA–SAS ■ ■ ■ ■

General run-down condition Epidermolysis or dermolysis bullosa Active bacterial, mycotic or viral skin infections Depression or personality disorders

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■ Tendency to scratch ■ IQ insufficient to understand the events surrounding the application of the peel solution ■ Expectations of miraculous and life-changing results ■ Refusal to go through with follow-up visits ■ Severe progressive neoplasic disorders ■ Immunodeficiency ■ Insulin-dependent diabetes: depending on the depth of the peel and the risk of infection. Type 2 diabetes is not a contraindication for peels. Patients with stable insulin-dependent diabetes can be given a peel to the Grenz zone ■ Prior treatment with isotretinoin, if the peel is to the Grenz zone ■ Ehlers–Danlos syndrome, keloid scars, if the peel is to the papillary dermis ■ Extensive telangiectasias: these should be treated before peeling

Notes 1. Easy TCA® in the basic protocol. 2. For more details, see Chapter 1. 3. A mesolift is a mesotherapy technique that involves injecting various products into the dermis: hyaluronic acid, vitamins, trace elements, DMAE, polylactic acid, etc. 4. In South Asian, South-East Asian or Middle Eastern patients, melasma can appear before the age of 10, while it is rarely seen in Caucasian patients before puberty. 5. It is not possible to do a Wood’s light examination on very dark skin types.

6. To date, however, it has not been possible to reproduce the melasma by applying these cosmetics intentionally. 7. The mask of pregnancy tends to lighten naturally and even disappear in patients with a light phototype unless they are taking estrogens and progestogens, which can cause the mask of pregnancy to persist. 8. www.astheticdermal.com 9. Berloque dermatitis is an acquired hypermelanosis resulting from contact photodermatitis caused by a sensitizing agent (perfume or metal in jewelry). Berloque, or berlock, dermatitis gets its (misspelled) name from the French word ‘breloque’ meaning a trinket or charm that is attached to a bracelet. These charms are often of poor quality and cause contact allergies in the shape of the trinket itself. 10. It should be noted that the precise pathogenic relationships between hyperseborrhea and yeast colonization are still controversial, even though ketoconazole can (temporarily) eradicate seborrheic dermatitis. It is suspected that it is caused by a more fundamental immunological disturbance. 11. The trial protocol currently being used is the following: apply a single layer of Easy Phytic® solution in the morning and leave it to act during the time it takes to brush the teeth. Take a shower. Repeat the application every day for 3 consecutive days. 12. McCollough EG, Langsdon PR, Maloney BP. Chemical Peel with Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996, UK, Oxford, Marcel Decker Ltd. 13. Vergereau R, Trauchessec JM, Peyronnet B. Le new peel. J Med Esth Chir Derm 1990, XXII (68): 243–55. 14. Recall that benzoyl peroxide, alpha-hydroxy acids and tretinoin thin the stratum corneum and enhance penetration of the acids.

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14 Trichloroacetic acid: classic semiology Preparing the skin Pre-peel care is discussed in Chapter 2. Further information can be found in Chapter 12. The safety of peels employing trichloroacetic acid in simple aqueous solution (TCA-SAS) has been greatly improved by systematic preparation of the skin before peeling. Preparing the skin helps improve microcirculation, increase glycosaminoglycan synthesis, increase the number of mitoses in the basal layer keratinocytes, stimulate production of epidermal growth factors, deactivate melanocytes and even out and deepen the effect of the TCA. One month before a peel with TCA-SAS (Soft Peel®), the patient should apply a cream consisting of hydroquinone (4 g), micronized hydrocortisone acetate (0.5 g), paraffin oil (16 g), or emulsifier based on polyglycol stearate (21.5 g) and excipient qs 100 g, twice a day. Tretinoin is then mixed into this cream in gradually increasing quantities. The concentration of tretinoin is increased every week to reach a final concentration of 0.3%.1 Dermatitis develops due to the tretinoin: irritation with flaking and redness signals that the skin has been properly prepared, and guarantees a successful peel. However, the need to use a technique to enhance and even out penetration of the TCA–SAS proves that the action of TCA–SAS is uneven and inadequate. The need to apply hydroquinone twice a day at a concentration of 4% as a preventive shows how aggressive the peel is to the skin and how it triggers postinflammatory pigmentary changes. In short, the introduction of skin preparation before a TCA–SAS peel and adding adjuvants greatly improved safety, and is still essential to compensate for the inadequate and uneven penetration of this type of peel, as well as to reduce the risk of complications, especially pigmentary changes. For the record, it is interesting to note that the first time I presented Easy TCA® at a congress of the Belgian Society of Cosmetic Medicine in Brussels in 1997, there was an outcry. The peel was shouted down, demonized and criticized even before it was presented, as it flew in the face of the all too recent dogma of aggressive skin preparation that then held sway. Anyone tempted to use it was told that their worst nightmares would come true if they did not prepare the skin beforehand. It was soon proved that the Easy TCA®2 technique is perfectly valid and that, apart

from certain specific cases such as the treatment of stretch marks or resistant melasma, this peel does not require any skin preparation. The doom-mongers, partisans of the dogma of preparation, gradually fell silent, and the sworn enemies of Easy TCA® started to talk about the relative merits of preparation and eventually the pointlessness of preparing the skin in many cases. Everything has finally fallen into place, and preparing the skin is now considered as an additional tool for many peels, a weapon that is optional in some cases, but that still remains essential when using TCA–SAS. Treatment with oral isotretinoin is sometimes essential in cases of severe acne, but is contraindicated before a peel to the papillary dermis. An Easy TCA® peel to the basal layer,3 on the other hand, can be performed without any risk of complications, and can produce excellent results for severe acne that has been treated beforehand with oral isotretinoin.

Application of TCA–SAS It is easy to summarize the application of TCA-SAS.

Day –30 to day 0 Pre-peel preparation (see also Chapter 2) involves the following: ■ ■ ■ ■

deactivation of melanocytes thinning and evening out of the stratum corneum stimulation of keratinocyte regeneration botulinum toxin, coagulation of telangiectasias, excision of benign tumors, cleaning the skin, etc. ■ obtaining photographs, informed consent and other legal documents.

Day 0 This involves the taking of photographs, settling in, disinfection and degreasing. The patient is photographed from five angles, with and without flash (see Chapter 34). The patient is placed in the dorsal supine position; good

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lighting is needed to monitor the skin and any changes in skin tone. The skin is disinfected with a sterile swab soaked in alcohol, and degreased with a sterile swab soaked in acetone. Good ventilation must be ensured so that the patient does not breathe in the alcohol or acetone fumes.

The depth of action of the same peel solution can therefore be varied simply by changing the applicator or the pressure of application.

Local anesthetic

The speed of application of TCA is not in itself important, because: ■ unlike alpha-hydroxy acid (AHA) solutions, TCA does not have to be neutralized ■ unlike phenol solutions, TCA is not toxic.

Local anesthetic is never needed when TCA is used to treat the epidermis to the Grenz zone. It may be necessary when the TCA reaches the papillary or reticular dermis.

Applying the TCA–SAS TCA–SAS can be applied with any type of applicator.

Effect of the type of applicator A rough-textured applicator (sterile gauze) abrades the skin, causing surface injury as it deposits the acid on the skin: this helps the TCA penetrate more deeply.

Effect of pressure of application The pressure of application also plays a role in determining the depth of action of the TCA. The harder the solution is applied, the more deeply will the TCA penetrate. A swab held in the hand has less abrasive force than a swab held with Kocher forceps. A smooth applicator does not abrade the skin while depositing the acid and the action of the TCA remains more superficial. Using a brush to apply the same number of coats of the same TCA solution with the same concentration produces a more superficial peel than using a swab.

Effect of speed of application

The speed of application depends on: ■ The patient’s sensitivity: a very sensitive patient will find it difficult to stand the burning sensation of the TCA on the whole face, and will be better off if the TCA is applied zone by zone. ■ The surface area being treated: Only Touch® can be applied quickly on lentigines, as only small areas are affected by the burning from the acid. Large areas (e.g. the back) should be treated by TCA zone by zone for the patient’s comfort. ■ The depth of the peel: applying TCA is painful, but an intradermal peel is far more painful than an intraepidermal peel. An intradermal peel should be applied zone by zone for the patient’s comfort, while an intraepidermal peel can be done in one go.

Symptomatology of TCA application Applying TCA causes protein coagulation more or less rapidly, depending on the formulation of the peel, its concentration, prior preparation of the skin, the pressure of

Table 14.1 Symptoms following TCA application 1. Erythema: the peel is intraepidermal

No or little risk of visible flaking

2. Scattered pinpoint frosting: the peel is near the basal layer (Figure 14.1)

Sunburn-type flaking (Figure 14.2)

3. Cloudy-white frosting: the peel has reached the Grenz zone (Figure 14.3)

Flaking: light, thin skin (Figure 14.4)

4. 4. 4. 4.

Flaking: more or less brownish skin, depending on phototype and photodamage (Figures 14.7 and 14.8)

Even pink-white frosting (Figure 14.5) and ‘epidermal sliding’ (Figure 14.6): the TCA is in the papillary dermis. The sliding (wrinkling) can be seen when the skin is pinched, and corresponds to the coagulation of anchoring fibers between the dermis and epidermis

5. Pure white frosting (Figure 14.9), gradual disappearance of epidermal 4. sliding: the TCA has reached the reticular dermis 6. Gray-white frosting, epidermal sliding has gone: the TCA is in the 4. reticular dermis 7. Gray frosting and/or yellowish patches (phenol): deep reticular dermis

TCA should no longer be used for peels to the deep reticular dermis

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application, the skin type, etc. A 35% m/m TCA coagulates proteins. Different symptoms appear gradually: see Table 14.1 and Figures 14.1–14.9. A low-concentration formula is applied in several coats; the doctor can progressively see each of the symptoms described in Table 14.1, and can stop whenever he wants. A high-concentration formula penetrates very rapidly, and the symptoms come in such quick succession that it is impossible to see them clearly. The technique is much quicker but the doctor cannot choose when to stop.

Figure 14.3 Cloudy-white frosting.

Figure 14.4 Flaking after cloudy-white frosting.

Figure 14.1 Scattered pinpoint frosting.

Figure 14.5 Figure 14.2 Flaking after scattered pinpoint frosting.

Even pink-white frosting (the differences in color come from the presence of melasma). The contours of the eyes have been chemically resurfaced locally.

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Figure 14.6

Figure 14.8

The skin wrinkles when pinched between the fingers.

Flaking after a papillary peel on a light skin phototype that has been badly damaged by the sun.

Figure 14.7 Flaking after a papillary peel on a light skin phototype with little photodamage.

Two endpoints are worthy of more attention: ■ Scattered pinpoint and cloudy-white frosting signal the most superficial peel to the dermis: this is the limit of effectiveness (see Chapter 15). ■ Even pink–white frosting signals a peel to the papillary dermis: this is the safety limit (see Chapter 23).

Figure 14.9 Pure white frosting from a peel to the reticular dermis.

peel solution is extremely easy – you do not need a university degree to take a cotton bud and get skin to frost gradually! The choice of indications and managing postpeel care are different matters entirely, and a thorough knowledge of medicine is essential to do these properly.

Notes Post-peel care Post-peel care is also discussed in Chapter 3. In short, post-peel care is extremely important and depends on the skin type, the depth of the peel and the dermatological problem being treated. It is more important than preparation when using Easy TCA® or Unideep®. Any ‘peeler’ very soon learns that applying a

1. 2.

3.

Preparing the skin with tretinoin before the peel accelerates post-peel healing. Easy TCA® was called ‘Easy Peel’ at the time. The name was changed when Easy Phytic® peel came out, in order to avoid any confusion between the two ‘Easy’ peels: Easy TCA®, a combination of a TCA peel and Easy Phytic®, uses AHAs and phytic acid. See Chapter 11 for more information on this peel. The peel produces scattered pinpoint frosting only.

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15 Easy TCA®: basic protocol and skin aging

In 1968, Paul Langerhans discovered the presence of a particular type of epidermal cell in humans, which is now named after him. The Langerhans cell (LC) is a mobile dendritic cell that has no desmosomes and is found in most multilayered malpighian epithelia. LCs make up 2–5% of epidermal cells. They come from the medulla and migrate towards and within the skin and stay within the epidermis for 2 weeks at the most. LCs have three functions: ■ constant monitoring of the antigenic environment ■ inspection of foreign molecules ■ custody of the foreign invaders while the lymphocyte system reacts with an appropriate immune response It is easy to understand how important LCs are when one imagines the impressive number of potential antigen contacts over the entire epithelial surface of the body. When the entire epidermis is destroyed by certain peels, this not only affects the keratinocytes and the LCs but also other dermal dendritic cells (DDCs) that are potentially antigenpresenting cells. New generations of sentinel cells migrate rapidly from the bone marrow to the epidermis, which is being rebuilt after the peel, but this process is not effective immediately. What is more, the first LCs to arrive as reinforcements on the battlefield of the skin are ‘overwhelmed’ as soon as they reach the dermis by the different types of antigen stimulation that they have to face on skin that has lost its impermeability and physical defenses. The stratum corneum can be compared to the ramparts of a medieval city and the Langerhans cells to the soldiers who have to defend it. The likelihood of unexpected bacterial and viral complications occurring will be even higher, as there are fewer cells in the skin capable of an immune response. It is important to consider these basic notions of biology to get a better understanding of what happens and anticipate which type of peel might be associated with a higher incidence of complications in the form of bacterial or viral infections. It then seems obvious why applying peel solutions capable of destroying the epidermis and part of the

dermis on a skin with active herpes, acne or other infectious disorders is strongly contraindicated. Any medical staff suffering from respiratory or nose-and-throat infections should be kept well away from the patient, and the doctor’s hands should always be surgically disinfected before applying medium or deep peel solutions. Superficial peels with alpha-hydroxy acids (AHAs), on the other hand, are known to cause very few bacterial or viral complications after peeling, as their direct action is limited to breaking up the spaces between corneocytes.1 Even if the peel penetrates too deeply in places, it is, quite logically, exceedingly rare for an AHA peel to cause complications in the form of infection, when the endpoint is focal or localized frosting. With AHAs, the stratum disjunctum (SD), the outermost layer of the epidermis that makes the skin feel rough, flakes immediately. The skin, having lost its topmost layer, immediately feels softer to the touch. The risk of bacterial or viral complications with medium or deep peels could lead doctors to think that, in order to avoid these problems, only superficial peels should be performed and patients with active acne or herpes should not be treated at all. With a medium or deep peel, herpes prevention – as far as it goes – consists in a sandwich treatment with aciclovir, which is not well tolerated by patients with sensitive stomachs. With acne, caution limits the range of treatment choice to careful superficial peels (which have limited effectiveness even after repeated sessions). We are forced to put off, sometimes indefinitely, performing ‘medium-depth’ peels on patients with acne or herpes that have not responded to preliminary medical treatment. With the development of Easy TCA® (ETCA), another possibility for treatment has opened up, however. In many indications, ETCA can produce the results of a medium peel with only the complication risks – usually non-existent – of a superficial peel. ETCA can be applied quite successfully to active acne lesions, and the presence of herpes lesions on the lips is only a formal contraindication to the peel applied following the basic protocol. It is still advisable to avoid treating patients with active herpes, however. Then again, if herpes were to develop in the course of an

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ETCA peel, it would be reasonable to think that it was fortuitous and not directly related to the treatment. To date, there has been no reported incidence of herpes spreading after the application of ETCA (basic protocol). With regard to acne, in 80% of cases, the first application of ETCA to active papulopustular facial lesions improves their number and severity by 50%, and the lesions seem to heal without scarring. ETCA is applied on the basis of one peel per week for 4 weeks that clear the lesions almost completely without having to resort to antibiotics. Deep wrinkles and acne scars do not disappear: they lie deep under the skin and even phenol or carbon dioxide laser resurfacing cannot always treat them. A combination of several different techniques is clearly needed in these indications. Although the face can be treated separately, the neck should always be treated at the same time – to at least the seventh cervical vertebra – to ensure a better ‘tightening effect’. Ideally, all ‘visible areas’ should be treated: face, neck, décolletage, forearms and hands.

General remarks Presentation A growing number of doctors consider ETCA to be the safest and easiest TCA peel, and it is used in over 50 countries worldwide. ETCA now comes in two different kits. The first kit (Figure 15.1) consists of 12 phials of base solution and three tubes of post-peel cream for 12 facial peels – enough to treat three patients on the basis of four peels per patient. The second kit (Figure 15.2) consists of two bottles of base solution for 24 peels – enough to treat six patients on the basis of four peels per patient, and a large tube of post-peel cream.

Figure 15.2 Easy TCA® kit for 24 peels.

The phials, introduced more recently, are safer for the patient and prevent any cross-contamination. With both kits, the doctor adds TCA to the base solution to activate the peel: the quantity of TCA to be added to the base solution may vary from country to country and from kit to kit. To avoid any confusion, it is best to refer to the volumes that are clearly indicated on the inside cover of each kit.

Post-peel mask cream The post-peel mask cream, which is highly antioxidant, contains vitamins, trace elements, growth factor, fatty acids and tyrosinase inhibitors. The doctor applies it only once, immediately after the required level of frosting has been achieved. Its formulation is responsible for a significant proportion2 of the beneficial results of ETCA. It stops the burning sensation almost immediately and greatly reduces the risk of post-peel complications (see Chapter 5, p41). Its components are as follows.

Vitamin C

Figure 15.1 ‘Classic’ Easy TCA® kit for 12 facial peels.

Magnesium ascorbyl phosphate (MAP) is more effective than ascorbyl palmitate (AP), as the protection of its active function by esterification protects the MAP against oxidation and provides an antioxidant effect that is of better quality and longer lasting than that of ascorbyl palmitate, a molecule in which the enediol function of the ‘2’ carbon atom is not protected by esterification. Vitamin C is a powerful antioxidant, effective in aqueous solutions, that scavenges free radicals and prevents the breakdown of protein chains. It protects other antioxidants, which is an advantage in situations involving oxidative stress, such as infected or uninfected wounds and in the post-peel healing period.

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Urea (carbamide) A keratolytic agent used in the treatment of dry skin, this increases skin permeability.

Silicion (trimethylsilanol monomannuronate) This is strongly linked to proteoglycans and mucopolysaccharides, hyaluronic acid, and chondroitin sulfate. Silicion plays an important role in skin healing and is essential in anti-aging treatments.

Citric acid A tricarboxylic AHA, this is an antioxidant, chelator and buffer.

Phytic acid An antioxidant and tyrosinase inhibitor, this protects against the risk of hyperpigmentation and post-peel inflammation.

Vitamin A The post-peel mask cream contains retinol microencapsulated in a cyclodextrin. Vitamin A is involved in the processes of cell division and differentiation that help the epidermis regenerate after the peel from the cells of the basal layer. Retinol induces the expression of retinoic acid-binding protein (RABP) and regulates cell migration in the skin epithelium, which is vital for skin regeneration after a peel. Encapsulating retinol provides better bioavailability of the vitamin and protects the skin against oxidation. Keratinocytes have the enzyme tools required to convert retinol into retinoic acid (the corresponding carboxylic acid), which is the molecule ultimately responsible for the effect of vitamin A.

Selenium This is a trace element that accelerates skin healing; it has been proved to penetrate more easily when combined with methionine. The post-peel mask contains a combination of selenium and methionine, which improves healing after laser resurfacing or a peel, and prevents seborrheic dermatitis. Selenium is a component of glutathione peroxidase (GPX), an antioxidant enzyme that helps fight against peroxidation. Selenium helps reduce inflammation by lowering the number of hydroperoxide intermediates in cyclooxygenase and lipoxygenase reactions. It prevents the production of inflammatory and immunosuppressive cytokines and stimulates cellular immunity as well as humoral immunity. Combining it with vitamin E rein-

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forces its protective action. Selenium and methionine have a tretinoin-like effect without having an irritative effect.

Vitamin E Tocopheryl acetate is the most stable ester of vitamin E. It is readily hydrolyzed by esterases into pure vitamin E after it has been absorbed by the skin. The advantage of the acetate form is that it forms a reservoir that gradually releases the vitamin E inside the skin. Vitamin E scavenges free radicals that could damage neighboring tissue. It blocks oxidative chain reactions by inhibiting the formation of lipoperoxides inside the cell, and in this way protects the nucleic acids and proteins.

Propylene glycol A disinfectant, moisturizer and vitamin stabilizer, this reduces corneocyte cohesion, enhancing penetration of the other active ingredients in the post-peel mask.

Phenoxyethanol An antibacterial agent, this is used to disinfect wounds and burns.

Coenzyme R (biotin, vitamin H, vitamin B8) The metabolic action of biotin is mediated through biotindependent enzymes that actively synthesize purines. It is a stable monocarboxylic acid, soluble in water and alcohol, and acts as a coenzyme as well as a growth factor, even in very small quantities. Biotin deficiencies cause scaly dermatitis, hyperkeratosis and alopecia. Topical application of biotin reduces the secretion of sebum.

Note The fact that the peel solution has been applied on the skin beforehand has a significant effect on the rate of penetration of the cream’s ingredients. The cream penetrates much more deeply after a peel than on untreated skin: the skin is far more permeable immediately after a peel; sebum and corneocytes no longer function as a barrier and the purely water-soluble ingredients can penetrate the altered epidermis rapidly. In this way, large quantities of stimulants and antioxidants can reach the dermis. The post-peel mask has a pH of 6.5: it is not a neutralizing cream.

Base solution ETCA solution, reconstituted by the addition of acid, has a pH <1, which is much lower than the solution’s pKa: it is mostly made up of free and potentially active acids.3 Its TCA concentration is 15% m/m and also contains the following ingredients:

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Ascorbic acid This has an anti-free radical action and protects the solution itself as well as the skin it is applied on. It is an acidifying agent and a buffer.

Citric acid This evens out penetration of the ETCA. It is also an acidifier and a buffer with anti-free-radical properties.

Cocamide (coconut fatty acid monoethanolamide) This protects the skin and improves the effectiveness of the saponins.

Sodium laureth sulfate A surfactant, emulsifier and wetting agent, sodium laureth sulfate is not the same as sodium lauryl (or dodecyl) sulfate, with which it is sometimes confused. It degreases the skin, emulsifies fats and holds skin impurities in suspension.

Saponins and excipients Saponins are natural extracts known as glycosides that have special foaming and soapy properties. As a glycoside, a saponin may have binding properties for water in the skin. Some studies show that saponins have an antimicrobial effect. They are also used to even out penetration of the acids through the skin and enhance skin healing.

Indications ETCA has a very wide range of indications and depths of action, both for the face and the body.

Indications for basic protocol These include comedonal, microcystic, papular and papulopustular acne, melasma, chloasma, post-inflammatory hyperpigmentation, photoaging, smoker’s skin, fine lines, keratoses, and superficial solar lentigines. ETCA can be applied to the face, hands, neck, décolletage and body.

Indications for abrasive protocol These include stretch marks, acne scars on the face and body, keratosis pilaris, and badly damaged décolletage.

Indications for combined protocols ETCA can be combined with other treatments: ■ a peel to the papillary dermis: Unideep® ■ a localized peel to the reticular dermis: Only Touch® ■ localized phenol for lip and eyelid wrinkles: Lip & Eyelid® formula ■ electric hair removal, skin cleaning, botulinum toxin, wrinkle filling, minor surgery, coagulation of telangiectasias, mesotherapy, slimming diets (to stop the face sagging), etc. ■ combinations with laser and flashlamps are not contraindicated but should be judged case by case, depending on the type of equipment used

Other protocols ETCA can be applied as a peel to the papillary dermis, when a sufficient number of coats are gradually applied to produce even pink–white frosting and ‘epidermal sliding’. The protocol developed to treat stretch marks has sometimes also been used successfully for facial rejuvenation.

Preparing the ETCA solution The base solution has to be activated by adding TCA at 50% m/m. If the distributor cannot supply the 50% m/m TCA solution ready for use, the pharmacist should be asked to prepare the following TCA–SAS solution at 50% m/m. TCA crystals 10 g distilled water 10 g pf 20 g of TCA aqueous solution In order to activate the peel,4 a precise quantity of this solution has to be injected into each phial (of the 12-phial kit) or into each of the two bottles of base solution for 12 peels (from the kit for 24 peels). This solution, prepared in advance, should be kept in the fridge.

Details for preparing the 12-phial kit for 12 peels The procedure is illustrated in Figures 15.3–15.6. The solution once made up cannot be kept, as it has been contaminated by the cotton buds used to apply it on the patient’s skin. One phial therefore corresponds to one peel per patient. This is the most hygienic method and avoids any risk of cross-contamination.

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Figure 15.3 Phials of base solution (12 pals classic kit).

Figure 15.5 The required quantity of TCA at 50% m/m is taken out. Detailed information is given in the actual kit.

Figure 15.4

Figure 15.6

The contents of a phial of base solution are transferred into a glass container.

The TCA is added at 50% m/m to the base solution in the glass container.

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Preparing the peel solution in the 24-peel kit In those countries where the solution comes in 2 bottles for two sets of 12 peels (Figure 15.7), the TCA must be injected into each bottle through the cap designed to this effect. Opening the bottle completely would accelerate oxidation of the solution. After the TCA has been added, the doctor takes out the quantity of peel solution needed for each procedure (Table 15.1), the mixture having been made for a total of 12 peels.

Table 15.1 Volume of ETCA solution for one peel (as a rough guide – see the different protocols for details) Procedure

Approximate volumes (ml)

Face only 1.2–1.5 Face and neck 1.5–2 Face, neck and décolletage 2.5–3 Face, neck, décolletage, hands and forearms 3–4 Hands and forearms 2

Preparing the patient As a general rule, no skin preparation is necessary during the weeks preceding the peel or even immediately before the procedure itself. It is not necessary to clean or degrease the skin, or to remove any make-up5 (except for impermeable make-up with a silicone base). If the doctor wants, the skin can of course be cleaned carefully, without irritating it or increasing its permeability. Skin Tech’s pre-peel cleansing mousse is recommended, as it is not acidic and does not increase skin permeability.

Applicator Different types of applicator can be used, but experience shows that the best results are achieved using a double cotton bud (Figure 15.8). A single cotton bud cannot with-

Figure 15.7 Bottle of base solution. The 24-peel kit contains two identical bottles: each bottle contains enough solution for 12 facial peels.

Figure 15.8 A single cotton bud cannot withstand sufficient pressure.

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Figure 15.10 Squeezing out the cotton buds.

Figure 15.9

the cotton buds on the rim of the glass container (Figure 15.10).

Soaking the cotton buds.

stand ‘scratching’ pressure6 and bends. Two cotton buds, on the other hand, can stand the right amount of pressure, and allow easy, quick and precise application.

Basic protocol Soaking and squeezing out the cotton buds Two cotton buds should be soaked in the ETCA solution that has been made up in the glass container (Figure 15.9). Any excess solution should be removed by squeezing out A

B

C

E

F

G

Application sequence for each coat The first coat of ETCA is applied in sequence on the face (Figure 15.11). This coat should be left to dry. If the application is even, following the recommendations described above, this first coat should not cause any problems. It must be allowed to dry completely before the second coat is applied. The doctor applies the number of coats needed to produce the first pinpoint frosting or, at the most, cloudywhite frosting. The number of coats necessary to produce the first pinpoint frosting depends on the skin type (Table 15.2).7

Figure 15.11

D

H

(a–h) Application of one coat of ETCA. The peel solution is applied in sequence on the face following the numbers shown in the images. For each different number, the double cotton buds must be soaked again in the peel solution. The eyelids are treated 1 mm away from the lashes.

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Table 15.2 Number of coats needed to achieve pinpoint frosting (a rough guide ) Skin type

Number of coats

Thin skin Skin treated with AHA, benzoyl peroxide, etc. Skin treated with retinoic acid Normal skin Thick and oily skin

1 only 1 only 1 only 1–2 2–4

Table 15.3 Thickness of pinched skin Thickness (cm)

Skin type

<1 1 >1

Thin Normal Thick

Figures 15.12 Pinpoint frosting.

Thin skin versus normal or thick skin Easy way to determine the thickness of the skin It is possible to determine the thickness of the skin by simply ‘pinching’ the cheek, where the cheekbone is most prominent (Table 15.3).

End of application of ETCA peel solution (basic protocol) The post-peel mask cream should be applied as soon as pinpoint frosting occurs (Figure 15.12).8 After the appearance of pinpoint frosting, applying another coat of ETCA solution produces cloudy-white frosting (Figure 15.13).

Figure 15.13 Cloudy-white frosting.

Table 15.4 Potential depths of action of ETCA Depth of ETCA peel

Clinical signs

Repetition of ETCA

Superficial: partial removal of the epidermis

Erythema without frosting

4 peels: 1 per week

Basic protocol: removal of the epidermis. The peel reaches the basal layer

Pinpoint frosting

4 peels: 1 per week

Basic protocol: removal of the Grenz zone. The peel reaches the Grenz zone

Cloudy-white frosting

4 peels: 1 per week

Medium protocol: removal of the papillary dermis

Even pink–white frosting

After 1 month

Abrasive protocol: removal of the reticular dermis

Skin liquefaction after 24 hours

After 1 month

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Figure 15.14 Dosage card from the ETCA kit. (a) One side of this card shows icons, beside each one of which the quantities of cream needed for each zone are indicated: to treat the face, 2 g are needed, while to treat the face and neck, 3 g are needed. (b) The lines on the other side of the card help to dose the post-peel cream correctly: 1 line is equivalent to 0.5 g of post-peel cream (therefore 2 lines = 1 g and 4 lines = 2 g).

A

B

If the pinpoint frosting occurs quickly (with very permeable skin), the post-peel mask can be applied even if the acid has not completely dried. If the pinpoint frosting appears slowly (with not very permeable skin), the post-peel mask should be applied after the skin has completely dried out.

Potential depths of action The potential depths of action of ETCA are summarized in Table 15.4.

Applying the post-peel mask The post-peel mask cream is not a neutralizing cream,9 and should be used in specific quantities according to the indications on the dosage card provided in the kit (Figure 15.14). The kit for 12 peels contains three 10 g tubes of post-

peel mask (Figure 15.15), while the kit for 24 peels contains a single 50 g tube of post-peel mask.

Basic protocol: end of application The peeling session is over after the post-peel mask cream has been applied. The inflammatory reaction is beginning: therefore the production of oxidants must be stopped quickly and the free radicals must be scavenged in order to break the vicious circle of self-perpetuating inflammation (see Chapter 5, p41). The post-peel mask cream reduces the risk of complications. The ETCA solution has permeabilized the skin: the components of the post-peel cream are rapidly absorbed and ready to act precisely where the free radicals have been produced. It scavenges the free radicals in order to reap the benefits of inflammation (stimulation of the regeneration processes) but not the disadvantages (uncontrolled and self-perpetuating inflam-

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cover the vast majority of cases treated in cosmetic medicine: aging, dyschromia, acne and sagging skin. Daily care creams should be used from the day after the first ETCA peel. See Table 3.1 in Chapter 3 for details of the creams required. These care creams have been specially formulated for very sensitive skin, as is the case between and after peels. There are many other cosmetics available on the market; however, their formulations have only occasionally been studied during the inter- and post-peel periods. Applying cosmetics that are not adapted for the post-peel period can cause fairly serious complications.

Obvious precautions Figure 15.15

The patient should avoid aggressive scratching or picking at the flaking areas of skin, and should call the doctor with any questions or if they are in the least doubt.

A 10 g tube from the ETCA kit for 12 facial peels.

Weekly repetition of ETCA mation), which are the cause of most post-peel complications. The patient should be warned not to wash the treated area until the next morning and to leave the post-peel mask to work for at least 12 hours. The next morning, the treated area should be washed with a mild soap or cleansing lotion and rinsed with water. No metal jewelry should be worn next to the skin on the treated areas for 48 hours.

The basic ETCA protocol (basic protocol to achieve scattered pinpoint frosting) is repeated four times,11 at weekly intervals for a facial peel and at 2-weekly intervals for a body peel. This repetition is in fact one of the peel’s builtin safety features; applying just one ETCA peel may not be enough and may cause complications.

Repetition of facial peels Post-peel tips Sun protection Melablock HSP® 50+10 should be applied before the patient leaves the surgery, as the skin is very sensitive after the peel. The day after the first peel, the patient must apply Melablock HSP® 50+ after putting on the prescribed daily care cream and before putting on any make-up. For sun protection to be effective, the cream must be reapplied every 3 hours between peels and for the first few weeks after the last peel. Thereafter, the patient should use Melablock HSP® 25+ spray. The patient should avoid exposure to direct sunlight both in the course of treatment and for 6 weeks after the last session. If the skin is highly photoreactive or if the patient lives in a very sunny climate, Blending Bleaching® cream should be applied twice a day from the day after the first peel. ETCA can be applied in all seasons and on all skin phototypes.

Daily care routine There is no need to know how to use many different cosmeceutical creams – fewer than 10 products are required to

A schematic illustration of the repetition of ETCA treatment for facial peels is shown in Figure 15.16. Eight days is the average frequency: the outside limits are a minimum of 5 days (if the condition of the skin allows) and a maximum of 15 days.

Repetition of body peels Body skin is not as permeable nor does it have the same capacity for regeneration as facial skin. For this reason, peels can only be repeated once every 2 weeks. A schematic illustration is shown in Figure 15.17. Two weeks is the average frequency – the outside limits are a minimum of 10 days (if the skin allows) and a maximum of 30 days.

Repetition of abrasive protocols Abrasive protocols are repeated once a month. After four sessions,11 a rest period of 4– 6 weeks allows the skin to regenerate fully and the results to be improved or maintained through the use of appropriate cosmeceuticals. Abrasive protocols alter the reticular dermis and therefore cause a definitive and irreversible skin reaction. The results achieved in each session can therefore be considered definitive, and the rest period of 4–6 weeks is a minimum.

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8 days

1st ETCA

8 days

2nd ETCA

3rd ETCA

Figure 15.16

6 weeks of regeneration

8 days

119

Repetition of ETCA on the face.

4th ETCA Daily care

2 weeks

1st ETCA

2 weeks

2nd ETCA

3rd ETCA

Figure 15.17

6 weeks of regeneration

2 weeks

Repetition of ETCA on body skin.

4th ETCA Daily care

8 days 8 days 8 days

1st ETCA

2nd ETCA

3rd ETCA

4th ETCA

8 days 8 days 8 days

1st ETCA

2nd ETCA

3rd ETCA

8 days 8 days 8 days

1st ETCA

4th ETCA

2nd ETCA

3rd ETCA

4th ETCA

Daily care

Figure 15.18 Diagram showing repeated cycles of skin regeneration. A maximum of three cycles is possible. More than 90% of cases are treated in one cycle. It is extremely rare to have to apply a third cycle.

The following peel can however be planned well ahead of the last one: 3 months, 6 months, 1 year, and so on.

The skin regeneration cycle We have just seen in detail how to induce a cycle of skin regeneration: four successive peels followed by (at least) 6 weeks of applying suitable care creams represents a cycle of skin regeneration.

What to do after the first ‘skin regeneration cycle’ A single cycle of regeneration is enough to achieve the desired results in the vast majority of cases, but when the results of the first cycle are deemed inadequate, another ‘regeneration cycle’ can be repeated after 6 weeks of applying cosmeceuticals at home, if it seems to the doctor that applying more peels will help improve the patient’s skin (Figure 15.18). Up to three ‘regeneration cycles’ can be repeated in some cases.

Maintaining results in the long term ETCA is more of a stimulating peel than a destructive one, and there is no risk of repeated peels making the skin less capable of regenerating in the future. One ‘regeneration cycle’ a year (four peels plus 6 weeks of post-peel care), combined with daily care creams, helps the skin stay healthy in the long term. This is the technique pompously known as ‘SYFE’ or ‘Stay Young For Ever’.

Treating photoaging and smokers’ skin Applying the peel The ETCA basic protocol can be used to treat the visible signs of aging: dull, dry, wrinkled skin and uneven skin tone. To combat the signs of photoaging, the basic protocol should be followed, as described above. Four (sometimes five) peels should be applied in all, at weekly intervals.

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Table 15.5 Anti-aging daily care creams Age under 40–45

Morning: Vit E Antioxidant ®

Evening: Re-Nutriv ACE Lipoic Complex®

Age over 40–45 with dry skin

Morning: DHEA Phyto®

Evening: Re-Nutriv ACE Lipoic Complex®

Age over 40–45 with oily skin

Morning: Actilift® (DMAE)

Evening: Vit E Antioxidant®

Sagging skin

Morning: Actilift® (DMAE)

Evening: Actilift® (DMAE)

Sun protection, light skin

Melablock HSP® 50+ every 3 hours

Sun protection, dark skin

Melablock HSP® 25+ every 3 hours

Daily care routine The ETCA sessions are just the start of the anti-aging treatment. The peels should be combined with appropriate daily care to combat the signs of aging effectively. Skin Tech’s care creams (Table 15.5) have been specially designed not only to be applied in combination with the peels but also for longterm application to maintain results (at least 6 months). Protection against ‘daylight’ plays an important part in the fight against photoaging, and a sunblock (Melablock HSP® 25+ or 50+) should be applied every day, every 3 hours.

5. 6. 7. 8. 9.

Notes 1. The breakdown of the corneodesmosomes has deeper repercussions in the skin (see Chapter 6). 2. Which some doctors judge to be more than 75%. 3. See Chapter 6 for more information on the relationship between pKa and peels. 4. The amount of TCA at 50% m/m that should be injected into each bottle of base solution is usually 4.8 ml. There are different types of presentation kits (Classic kit for 12 peels,

10. 11.

Classic kit for 24 peels and Starter’s kit for 4 peels), and it is preferable to refer to the information contained in each kit. See the discussion at the start of Chapter 14 regarding differences between ETCA and TCA–SAS peels. Recall that the penetration depth of TCA also depends on the pressure with which it is applied: it is recommended to apply the same amount of pressure as when scratching. This is why there is usually a lot of solution left when pinpoint frosting appears. The volume of solution allowed for is to treat oily, thick and resistant skin. With some protocols, it is recommended to produce cloudywhite frosting locally (see Chapters 16 and 22 on the treatment of melasma and entigines). Some attempts to copy ETCA have been made, where a product illegally called ‘Easy Peel’ was brought out consisting of a TCA–SAS solution with a neutralizing base post-peel cream. The many complications that occurred after use of these copies led to them being dropped. 50+ sun protection (EU standards) with induction of heatshock protein synthesis. See Chapter 3. Four times is, of course, an average. If the results are obvious, the treatment can be stopped after three sessions. If results are slow to appear and the skin is thick, up to six peels might be necessary.

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16 Treating melasma, chloasma and post-inflammatory hyperpigmentation The histological features of melasma and chloasma are discussed elsewhere in this book. The standard recommendations for treatment often only mention topical applications of tretinoin, hydroquinone and other tyrosinase inhibitors; corticosteroids and peels are considered as a last resort because of their potential to turn melasma into post-inflammatory hyperpigmentation (PIH). Conventional peels require conscientious pre-peel preparation to avoid this danger. Easy TCA® (ETCA), in combination with appropriate post-peel care, can be used to treat melasma without the constraints of pre-peel preparation (Figures 16.1–16.5).

■ Melablock HSP® 50+ (see Chapter 3): applied all over the face in the morning and then reapplied every 3 hours on the melasma itself

Preparing the skin It is not usually necessary to prepare the skin, but with long-standing or resistant melasma or with a skin phototype higher than Fitzpatrick IV, preparing the skin can be worthwhile and can improve results: ■ Blending Bleaching® cream (see Chapter 3): applied twice a day on the melasma itself and once a day on the rest of the face

Figure 16.2 On the third day after ETCA treatment, epidermal melanin has been eliminated.

Figure 16.1 Melasma on the neck. The position might suggest poikiloderma of Civatte, but there are neither telangiectasias nor any atrophy of the skin around the follicle.

Figure 16.3 Results after four ETCA peels and Blending Bleaching® cream.

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■ If the frosting is uneven, the ETCA solution can be applied there again at the same time as it is being applied to the whole face. The previous coat must be completely dry before another coat can be applied.

Applying the post-peel mask

Figure 16.4

The ETCA post-peel mask cream is applied to the whole face, starting from the melasma. A little more of the postpeel mask is applied to the melasma itself.2 The components of the ETCA post-peel mask cream work directly and specifically on pigmentation. If possible, the face should not be washed until the following morning.

Post-peel developments The acids dehydrate the keratinocytes and make the melasma appear darker the day after the peel and for several days (Figure 16.6). This is not a pigmentary change. The darkening of the melasma in the first few days after the first ETCA peel is, on the contrary, a positive prognostic factor, a sign that the acid is working.

Figure 16.5 Figures 16.4 and 16.5 Treatment of melasma with ETCA and Blending Bleaching® cream. Patients with light and dark skin phototypes.

Applying the peel solution A first coat of ETCA solution is applied to the melasma and left to dry completely (Figure 16.6). The desired endpoint is cloudy pink–white frosting that is exactly the same shape as the melasma plus 1 cm. If there is no frosting after the first coat, more coats of ETCA solution must be applied until cloudy pink–white frosting occurs. There is no set number of coats required, and there is no way of knowing in advance; each coat of ETCA solution must be left to dry completely before applying the next coat if the skin has not frosted sufficiently. More resistant skins only show cloudy pink-white frosting after three or four coats. Once localized cloudy frosting has been achieved on the melasma, the ETCA solution is applied to the whole face following the instructions for the basic protocol: see above. It is up to the doctor whether this last coat should go over the frosting on the melasma as well: ■ If the frosting on the melasma is pink and even, with some epidermal sliding,1 the ETCA solution should not be applied there again.

Repeating the peel The ETCA peel is repeated four times at weekly intervals (see Chapter 15). The doctor can change the total number of peels as well as the intervals between them, depending on the condition of the skin: the minimum recommended interval is 5 days and the maximum 15 days.

Daily post-peel care Post-peel care is essential to achieve optimum results and avoid complications. Lightening creams (Blending Bleaching® cream: Box 16.1) and sun protection (SPF 50+) should be applied from the morning after the first ETCA peel.

To boost the results Blending Bleaching® cream during the ‘regeneration cycle’: ■ on the whole face in the morning ■ on the melasma alone at midday and in the evening

Sun protection ■ Melablock HSP® 50+ every 3 hours (during the cycle) ■ sun avoidance (6 months–1 year)

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A

B

C

D

123

Figure 16.6 (a) Melasma before treatment. (b) Cloudy-white frosting after application of ETCA solution. (c) Flaking on third and fourth day. (d) Results after day five with the second ETCA combined with Blending Bleaching® cream.

Box 16.1 Blending Bleaching® cream Blending: evening effect • Glycolic acid • Tretinoin precursor Bleaching: lightening effect • Cocktail of tyrosinase inhibitors: Morus alba, kojic acid, lactic acid, licorice extracts, glabridin, liquiritin, mulberroside F • Reduction in the oxidation phases of melanin synthesis: vitamin E (tocopheryl acetate) • Natural anti-inflammatory effect: Glycyrrhetinic acid: slows down degradation of endogenous cortisol Transcutol™ • Concentrates the active ingredients near the melanocytes

Long-term maintenance (6 months–1 year) ■ Blending Bleaching® cream: 3 days per week ■ Melablock HSP 25+: morning and midday ■ four ETCA sessions are repeated once or twice a year as necessary

Potential problems Persistent dark ring on the edge of the melasma In this case the pink-white frosting has not gone beyond the edge of the melasma – it should go 1 cm beyond. The peel could not work on the melanin around the edges (Figure 6.7).

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■ ETCA should be applied to the rest of the face also. ■ Application of the following may be considered: – a strong corticosteroid immediately after the postpeel mask cream – tretinoin 0.05–0.1%

Appearance of pigmentary change after a few sessions ■ ETCA sessions should be continued until there is pinpoint frosting only ■ Blending Bleaching® cream should be applied every 3 hours, before sun protection and before the evening meal ■ Melablock HSP® 50+ should be applied every 3 hours ■ The patient should keep out of the sun completely ■ A topical corticosteroid should be applied for a few days if any inflammation is suspected

Figure 16.7 Persistence of a dark ring on the edge of the melasma.

Resistance The method of treatment should be changed.

Recurrence ■ It is important to check that the patient has kept up with post-peel care. ■ The four ETCA peels should be repeated once or twice a year. ■ The need should be stressed for: – sun protection with Melablock HSP® 50+ – Blending Bleaching® cream ■ A strong corticosteroid can be applied to the melasma immediately after the post-peel mask cream, after every peel, to reduce any inflammation. ■ The use of 5% hydroquinone (and 0.05% tretinoin) in combination with the Blending Bleaching® cream should be evaluated.

Slightly disappointing results

Post-inflammatory hyperpigmentation With a topical treatment alone, PIH usually has a good prognosis. Blending Bleaching® cream or a prescription cream with hydroquinone and effective sun protection should be used. PIH tends to improve gradually and naturally, and disappears completely if it is not too severe and as long as the melanocytes are not stimulated by UV photons. PIH, whether caused by trauma (e.g. a mosquito bite, scratch or wound), by laser or intense pulsed light (IPL) treatment, or by another peel, usually responds to four sessions of ETCA following the same guidelines as for melasma treatment.

■ Another cycle of four ETCA peels should be started after 6 weeks of Blending Bleaching® cream and Melablock HSP® 50+. ■ Post-peel care: the doses and frequency of Blending Bleaching®cream and Melablock HSP® 50+ should be increased.

Notes

Extremely disappointing results

2.

■ Unideep® (pure white frosting) could be applied locally on the melasma.

1.

Fine wrinkling of the skin when pinched: the acid coagulates proteins that ensure cohesion between the dermis and epidermis, and the epidermis slides on the dermis to which it is no longer firmly attached. The quantities of post-peel mask cream have been overestimated to allow for more cream to be applied in certain areas: each small tube contains 10 g of post-peel mask, and 8 g is enough to do four basic facial protocols.

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17 Treating acne

Treatment of comedonal acne1 Extraction of comedones (Figure 17.1) After disinfecting the skin, the comedones are extracted using a comedone extractor. The doctor will judge whether he prefers to extract all the comedones before the first of the four Easy TCA® (ETCA) peels or to extract only some of the comedones before each peel – patients usually prefer the second option as it is less aggressive.

A

Applying the peel solution As soon as the comedones have been removed, the ETCA solution is applied following the basic protocol (Chapter 15). The solution penetrates and disinfects the openings left by the comedones. This localized penetration has not been reported to have any negative effect. The irritation caused by extracting the comedones can, however, cause the ETCA solution to penetrate more deeply and produce ‘cloudy’ rather than ‘pinpoint’ frosting. To reduce the risk of cloudy frosting developing, the cotton buds should be squeezed out properly before applying the ETCA solution.

B

Figure 17.1 (a) Comedones before treatment. (b) Immediately after comedone extraction and ETCA peels.

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Maintenance treatment The skin is cleansed once a month. The four ETCA peels are repeated once a year. For daily care, see below.

Treating microcystic acne Opening cysts and applying the peel (Figure 17.2) The microcysts are opened and drained using the tip of a No. 11 scalpel blade. The doctor can choose whether to open all the microcysts before the first of the four ETCA peels or to extract some of them before each peel. Only the uppermost layers of the epidermis are cut; there is no bleeding, no pain and no scarring.

Applying the peel solution As soon as the microcysts have been opened, the ETCA solution is applied to the whole face. The peel solution disinfects the openings left by the microcysts, and may penetrate inside them, causing more intense frosting locally. There is no danger, and the doctor can limit the penetration if desired. The application protocol is the basic protocol for ETCA (see Chapter 15).

Treating papulopustular acne (Figures 17.3 and 17.4) Preparing the skin The comedones and the cysts and whiteheads are opened (comedone extractor, No. 11 scalpel blade; see above). The papules should not be touched. The open pustules are drained.

Applying the peel solution The basic ETCA protocol is used once again. More of the ETCA solution will penetrate into the inflamed lesions, where the distension caused by the edema makes the stratum corneum more permeable. To limit this penetration, the cotton buds should be squeezed out properly before applying the ETCA solution. Each coat of ETCA solution should be left to dry out completely before applying another coat.

Care between and after peels for all types of acne Care creams (Box 17.1) should be used from the morning after the first peel. The skin should be cleaned in the morning and evening with a cleanser.

Between peel sessions ■ In the morning, Purifying® cream should be applied to the whole face. ■ In the evening, Purifying® cream should be applied to the areas with acne only.

Figure 17.3 Figure 17.2 Micro cystic acne.

(a, b) Detail of the temple area of a young patient with papulopustular acne treated with ETCA and Purifying® cream.

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Box 17.1 Care creams during and after peels for acne Purifying cream® (Skin Tech) Glycolic acid (8%): softens the skin, prevents pores clogging up, stimulates epidermal turnover (pH 4) Retinol: tretinoin precursor, helps drain the pilosebaceous units Vitamin E: tocopheryl acetate: anti-free-radical, breaks the vicious circle of oxidation–inflammation Triclosan: antiseptic, anti-inflammatory, antimycotic Glycyrrhetinic acid: hydrates, antipruritic, anti-allergic

A

Tea tree oil: extract of an Australian shrub, as active as benzoyl peroxide, but without the pro-oxidant effect – antibacterial, antiviral, antimycotic, anti-inflammatory

Treating the side-effects of acne

B

Figure 17.4 (a) A patient with acne that did not respond to a 3-month course of tetracycline. The antibiotics were stopped and four ETCA peels were applied at weekly intervals combined with Purifying® cream. (b) The results at the end of the first ‘regeneration cycle’ – there is no scarring.

Long-term maintenance treatment The oil-free gel Purigel® should be applied once or twice a day according to medical advice. The four ETCA peeling sessions are repeated once or twice a year.

Combined antibiotic treatment: The doctor decides if it is necessary to have combined medical treatment. For example, if the papular acne does not improve after the first two sessions, they should be combined with 100 mg/day of minocycline.

■ Post-acne pigmentation (Figure 17.5), on the face can be treated in the same way as melasma, combining ETCA (basic protocol), Blending Bleaching® cream and sun protection (Melablock HSP® 25+ is sufficient). ■ Post-acne pigmentation, on the décolletage can be treated in the same way, but there is also an abrasive protocol especially for the décolletage: abrasion plus occlusion of the post-peel mask without the application of acid (see Chapters 20 and 21). ■ Post-acne pigmentation on the back does not respond readily to ETCA alone. The protocol developed for treating stretch marks produces excellent results, however – not only on the residual pigmentation but also on the depth of the acne scars. ■ Facial acne scars can be treated by dermabrasion followed by peeling (see Chapter 21).

Potential problems during acne treatment These are listed in Table 17.1, together with methods of dealing with them.

General remarks on treating acne with peels Speed of results When treating acne, as with melasma, getting early results fast is a positive sign that could indicate excellent end-results. If

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Table 17.1 Potential problems during acne treatment Problem

Solution

Temporary aggravation of the acne

Put the patient on oral antibiotics immediately

Recurrence

Keep up the maintenance treatment; do another four ETCA peels

Ineffectiveness

Establish an etiological diagnosis and suitable treatment

Comedones difficult to extract

Postpone extraction until the next ETCA peel, or open them with the tip of a No. 11 scalpel blade

Too many comedones

Extract them gradually – a few before each ETCA peel, instead of trying to remove them all at once

The patient is on isotretinoin

Do not go beyond pinpoint frosting and only use ETCA

Post-inflammatory hyperpigmentation

PIH may occur with abrasive treatments. The abrasive protocol includes preparing the skin with Blending Bleaching® cream

Folliculitis barbae

Unless it requires treatment with oral antibiotics, folliculitis of the beard can be treated in the following manner: Open the ‘whiteheads’ with the tip of the No. 11 scalpel. Drain the infection by squeezing gently and disinfect the skin. Apply ETCA to the whole face until pinpoint frosting occurs. Apply the post-peel mask. Daily care: after shaving, use white vinegar as an aftershave, before showering. Apply Purigel® after showering.

Intolerance of Purifying® cream

Patients with acne cannot always tolerate cream being applied on their oily skin. They can use the non-oily Purigel®

the acne or melasma improves after the first session, the patient can usually be guaranteed satisfactory and rapid results. If, on the other hand, the situation has not started to change after the second ETCA session, it is likely that results will be slow and only partial, and other treatments should be combined with the peels (antibiotics with acne and hydroquinone with melasma). It is best to warn the patient, who will understand that the doctor is in full control of the treatment.

Treatment of acne must remain multifocal ■ Normalize the rate of exfoliation/hyperkeratinization by enhancing elimination of dead cells and hydrating the skin properly: retinyl palmitate, glycolic acid and glycyrrhetinic acid.

Figure 17.5 Active acne and acne pigmentary sequellae on a phototype 5 patient. Result of treatment with Easy TCA®, 4 peels, 1 peel/week. Combination with Blending Bleaching® cream and sun protection.

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■ Eliminate or reduce infection: triclosan, tea tree oil and azelaic acid. ■ Help the pilosebaceous units drain: glycolic acid, lactic acid, retinyl palmitate, glycyrrhetinic acid and azelaic acid. ■ Eliminate or reduce inflammation: tea tree oil, triclosan, glycyrrhetinic acid and azelaic acid. ■ Reduce sebum production: thiosome. The protocols established for treating acne with ETCA in no way take away the doctor’s freedom to choose the treatment that is best for his patient based on his own knowledge and personal experience. ETCA helps combat acne lesions by exfoliating the skin chemically and through use of the post-peel mask cream. Daily care helps maintain the results of dermatological or systemic acne treatments. No peel can change the genetic

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make-up of a particular skin or individual: applying an acid does not reduce androgen production or change the sensitivity of sebocyte membrane receptors or the strength of 5α-reductase. The peel works on other parameters, such as intercorneocyte cohesion or unclogging the openings of the pilosebaceous units. Maintaining the results in the long term depends on prolonged treatment with Purifying® cream, which should be applied twice a day, starting from the day after the first peel and continuing up to at least 6 weeks after the last peel. Long-term maintenance of the results sometimes requires continued use of Purifying® cream or Purigel®, for several months.

Note 1.

There are of course other treatments for acne. This book only describes the use of peels in this indication.

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18 Treating multiple keratoses on the scalp

A balding scalp often shows signs of accelerated photoaging, with scattered lentigines and/or keratoses. Easy TCA® (ETCA) can help treat these problems using the following protocol.

Thirty minutes before the peel, the patient is given a paracetamol (acetaminophen) plus codeine tablet or any other relatively strong analgesic. The skin is cleaned (Skin Tech Pre-peel cleanser®), rinsed and dried. It is then disinfected with alcohol and degreased with acetone, which are left to evaporate.1

whole scalp and left to dry. The necessary number of coats are then applied to achieve an even frosting of the skin. The keratoses are relatively impermeable to acids and, generally, frosting is not strictly even (Figure 18.1). As soon as there are signs of epidermal sliding, the frosting is sufficient (Figure 18.2) (see Chapter 14). The acid works by ‘undermining’ – going underneath the keratosis. Each coat is left to dry before applying the next one. Up to five coats are sometimes required. Other peels can be used, depending on the case being treated. Unideep® is also indicated for the treatment of keratoses on the scalp: the Unideep® solution produces even frosting more rapidly. Only Touch® can be used in combination with a more superficial ETCA peel (cloudy-white frosting instead of even white frosting) on isolated keratoses on the scalp.

Applying the peel solution

Local anesthesia of the scalp

The whole area should be treated, and not only the local lesions. A first coat of ETCA solution is applied to the

If the doctor thinks that more than three coats will be necessary, nerve blocks should be applied to the front and back of the scalp.

Figure 18.1

Figure 18.2

Frosting – considered to be even because of the large number of keratoses.

Epidermal sliding: this appears when the skin is pinched after a peel to the papillary dermis.

Preparing the patient and scalp

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Anterior and lateral regions of the scalp The anterior half of the scalp is innervated by the frontal nerve. In its intraorbital journey, this nerve divides into the internal and external frontal nerves. The nerve branches emerge from the supraorbital foramen and innervate the front of the skull after traveling vertically upwards. Blocking these nerve branches anesthetizes the forehead as well as the first 6–10 cm of the area normally covered in hair. For more details, see Chapter 33. The lateral regions of the scalp are not innervated by the frontal nerve, but by branches of the lesser cervical plexus or the auriculotemporal nerve.

Posterior and vertex of the scalp The posterior region of the scalp that concerns us is innervated by the occipital nerve of Arnold, which is easily blocked by an injection of 2% lidocaine with adrenaline (epinephrine). The vertex of the scalp is innervated by all the nerve endings that sensitize the skull. This region is therefore sometimes difficult to anesthetize completely without doing a full circular nerve block of the scalp. If the doctor does not want to perform nerve blocks, or if they are inadequate for more sensitive patients, he can also do a tracer injection, 1 cm beyond the outside edge of the zone to be treated and a ring block on the whole area to be peeled. Ventilation or cooling (3M Cold Pack®) can help ease the pain of the acid.

Post-peel developments and care (Table 18.1) Flaking occurs after at least 1 week and lasts 4–5 days. On days 1–6, plenty of Renutriv ACE Lipoic Complex® should be applied to combat the formation of free radicals

and to hydrate the skin. Vaseline® should then be applied to help the flaking as soon as it starts. Effective sun protection is essential, as well as keeping out of the sun. The treatment is repeated four times at 2-weekly intervals, if flaking has finished. Results can be maintained in the long term with a combination of topical treatment (tretinoin, DHEA Phyto®, Renutriv ACE®, etc.) and a series of four ETCA peels a year, with local applications of Only Touch®.

A few tips How to accelerate penetration of the acid solution Gentle abrasion with sandpaper or intraepidermal erbium laser treatment help accelerate penetration of the ETCA solution considerably. When sandpaper abrasion is used, a topical anesthetic should be applied (a swab with 2% lidocaine with adrenaline (epinephrine)) after the abrasion, before applying the acid. With an erbium laser, a nerve block or ring block is necessary.

Relative impermeability of keratoses Keratoses are relatively impermeable, and the acid needs more time to get through them: patience is required, and frosting is (much) slower to appear. Enough ETCA solution has been applied when the skin immediately surrounding the keratosis has frosted.

How to determine the total number of coats required When the skin around the keratosis turns pink–white, it means that a sufficient number of coats has been applied. When the skin on the scalp is pinched between two fingers and epidermal sliding occurs (Figure 18.2), the papillary

Table 18.1 Daily maintenance creams Sun protection

Melablock HSP® 25+ or 50+, depending on skin phototype

Dry skin

Morning: DHEA Phyto®

Evening: Renutriv ACE Lipoic Complex®

Oily skin

Morning: Vit E Antioxidant®

Evening: Renutriv ACE Lipoic Complex®

Risk of post-inflammatory hyperpigmentation

Blending Bleaching® cream every 3 hours during treatment; then twice a day for 3 months

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dermis has been reached. As soon as an even frosting occurs, the ETCA post-peel mask cream should be applied and rubbed in. The peel is then over.

analgesic to be taken on leaving the surgery and in the evening before going to bed.

Post-peel pain

Example

The pain felt after a peel is bearable, but the patient can be made more comfortable if prescribed a medium-strength

Figure 18.3 shows an example of a scalp treated with ETCA peels.

A C

B

D

Figure 18.3 (a) Scalp before treatment. (b) After two ETCA peels to the papillary dermis. (c) After three ETCA peels to the papillary dermis. (d) A year after treatment: maintenance with topical 0.05% tretinoin.

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Note 1.

This is an exception to the normal procedure in the use of ETCA: the skin on the scalp has to be disinfected and degreased because it is much thicker and oilier than the skin on the face; the treatment has to reach the papillary dermis.

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19 Treating aging of the hands and forearms

The forearms and hands are treated in the same way.

Aging of the hands Over the last decade or so, facial rejuvenation treatments have been developed and refined. Major technical advances have changed the face of surgery as well as peeling and dermal filling techniques. The results of these treatments look more and more natural. Surgical scars, less visible now than they were in the past, can be softened even more by using peels or laser treatment after surgery. The blade has more respect for the architecture of the face, peels can maintain it perfectly well, and dermal filling techniques can even improve it. Cosmetic medicine helps to hide imperfections that cannot be put right by other means. The use of gentler or less aggressive techniques has drastically reduced the risk of permanent complications. In short, nowadays, a person’s age is not written on their face, and patients who are properly treated can easily claim to be 15 years younger than they really are. The risk of this little white lie being found out is minimal – on condition that the person doing the guessing only looks at the face. The quality of the skin on the neck and décolletage is often still a sure sign of time spent in the sun or on a tanning bed. Surgery can of course improve the tension of the skin on the neck, but only certain peels can improve the quality of the skin or make a telltale décolletage look younger. Even if the right combination of the most appropriate techniques has been used to excellent effect and a patient’s face, neck and décolletage do not show their real age, there is still one important area that can give the game away: the hands. They are often the weakest link in the treatment chain, a telltale sign of a patient’s real age and the fact that she or her has had other treatments. There are always mittens, of course, but who wears those nowadays? If you look at a patient’s hands, you notice that they start aging fairly soon, often between the ages of 30 and 40: small, almost colorless, sessile tumors may start to appear,

along with small patches of hyperpigmentation; the skin dehydrates and starts to wither. Between the ages of 40 and 50, the patches of hyperpigmentation grow and solar keratoses may start appearing. Between 50 and 70, in parallel with a decline in sex hormone production (more gradual in men than in women), signs of atrophy in the epidermis, subcutaneous fatty tissue, muscle and bone start to appear. Rheumatic disorders often develop that deform the joints. The veins, which have become more sinuous, stand out through the thinned epidermis. Very old hands are typically arthritic, atrophic (especially in women), dehydrated and covered in hyperchromic patches and hyperkeratoses. The often fragile capillaries easily cause bruising. Friction wounds are more frequent and more spectacular, as the dermal papillae are no longer as deep and the epidermis is not held as tightly to the dermis. Our calendar age is not the only thing responsible for the aging process, and we are ourselves directly responsible for several contributing factors: smoking, for example, either through vasoconstriction immediately after smoke has been inhaled or through excessive production of free radicals in the body, is one of the major causes of aging that might well be termed autogenous as it is directly linked to the behavior of the individual. Avoiding repeated traumas, a balanced diet of vitamins, antioxidants and fatty acids, keeping out of the sun, and good hormone levels all play an important preventive role in keeping the hands looking young. But what can we do when the damage is done, when the signs of aging are obvious and a patient wants to have younger-looking hands? What can be done to slow down the aging process once it has started? There is a 10-year age difference between the hands of the patients shown in Figure 19.1: the patient in (a) started the menopause and estrogen–progesterone hormone replacement therapy (HRT) 2 years previously; the patient in (b) has been in menopause on estrogen-only HRT1 for 13 years. The signs of aging due to dermal, epidermal, fat and muscle atrophy are clearly visible, and 10 years of (southern) sun on top have also left their mark on the skin.

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B

Figure 19.1 (a) Hand of a 50-year-old patient; (b) hand of a 60-year-old patient. A

All jewelry should be removed. Without disinfection or degreasing of the skin, three successive coats of ETCA solu-

tion are applied to the hands. Do not try to achieve frosting. Each coat should be left to dry completely before applying the next. If cloudy frosting appears after the first or second coat, no more coats should be applied. If there is any pain, the treated area should be cooled (e.g. with a cold pack). When the last coat of solution has dried, the post-peel mask cream is applied using the quantities indicated on the dosage card, and is left to work until the following morning. Flaking often occurs after at least 1 week and lasts around 4–5 days. The treatment is repeated four times, at 2-week intervals, unless the skin has not finished flaking.

A

B

Treatment of photoaging without lentigines Sometimes, all that is needed for the skin on the hands is to rebuild the dermis and epidermis. This type of skin regeneration is perfectly suited to Easy TCA® (ETCA): two examples of this treatment are shown in Figures 19.2 and 19.3.

Applying the peel

Figure 19.2 (a, b) The dermis and epidermis restructuring after four ETCA sessions, at a rate of one peel every 2 weeks.

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A A

B B

Figure 19.3 (a, b) The dermis and epidermis restructuring after four ETCA sessions, at a rate of one peel every 2 weeks.

Post-peel care Post-peel care should start the day after the first peel and continue for at least 6 weeks after the last peel. Post-peel care for aging hands is similar to that for facial aging.2 C

Solar lentigines on the hands Solar lentigines on the hands and overall photoaging usually come together and share the same etiology. Visible lentigines can be treated with a local application of Only Touch® solution (Figure 19.4). Lentigines that are too small to be noticeable and overall photoaging can be treated with ETCA. Only Touch®, used alone, is often associated with pigmentary changes, while ETCA prevents or treats them.

Figure 19.4 (a) Solar lentigines before treatment. (b) Frosting induced by local applications of Only Touch®. (c) Results after treatment. See Chapter 22 for details of application.

Both peels are therefore used together in the treatment of solar lentigines (Figure 19.5).

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A

A

B

B

C

Figure 19.5 (a) Appearance of the skin on the 8th day after Only Touch® combined with ETCA; the scabs should not be pulled off. (b) Appearance of the same hand on the 15th day: the scabs have gone.

Combined aging of the hands The hands have aged completely when superficial photoaging and solar lentigines are combined with atrophy of the integuments, subcutaneous tissue, muscles and bones. Peels do not correct hormone-induced atrophy, and often the only option is fat transfer combined with chemical peels (Figures 19.6 and 19.7).

Figure 19.6 (a) Before treatment. (b) 12 months after fat transfer. (c) 3 years and 6 months after fat transfer.

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B

Figure 19.7 (a) A hyperkeratotic lesion less than 1 cm in diameter, with a dry and atrophic epidermis. (b) After one local application of Only Touch®, combined with two ETCA sessions. (c) Dramatic improvement after two applications of Only Touch® and three of ETCA. An extra session of Only Touch® would be necessary to treat the problem completely.

C

Flat warts The hands of pre-menopausal patients do not show any signs of atrophic aging, but too much sun produces a whole range of spots, sessile tumors, flat warts and solar keratoses. Small flat warts can be treated success-

fully with Only Touch® combined with ETCA (Figure 19.8). Only small, flat warts respond to Only Touch®. Thicker, and therefore more impermeable, lesions do not respond, and should be treated by shave excision with high-frequency shaving.

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A

B

Figure 19.8 (a) Flat warts after treatment with Only Touch®. (b) Uneven but sufficient frosting achieved after local applications of Only Touch®.

Maintaining the results in the long term

Notes

Results can be maintained in the long term by using appropriate daily care and repeating the peels once a year.

2.

1.

I shall make no comment on the validity of this type of replacement therapy. See Chapter 3. DHEA-Phyto® cream (in the morning) and Renutriv ACE Lipoic Complex® (in the evening) are particularly effective on the hands.

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20 Treating the neck and décolletage

The neck is a difficult area to treat, and results vary widely; essentially, the neck remains a surgical indication. The skin on the décolletage responds all too readily to serious injury by forming scars that are often hypertrophic.

Slightly sun-damaged neck and/or décolletage (Figure 20.1) The décolletage is usually treated at the same time as the face and neck. It does not really matter which order these areas are treated in, other than out of consideration for the patient’s comfort, as treating the décolletage is usually less painful than the face. The basic protocol for Easy TCA® (ETCA) should be used.1 The peel should be repeated four times at weekly intervals on the face and at 2-weekly intervals on the neck and décolletage, which take twice as long to flake as the face.

A

Moderately sun-damaged neck and/or décolletage (Figure 20.2) A moderately damaged décolletage should be treated more aggressively than a slightly damaged décolletage. The ETCA is applied to the décolletage and neck until cloudywhite frosting appears and is followed by the post-peel mask. The face is treated to the desired depth afterwards.

Lentiginosis of the décolletage (Figure 20.3) This is treated with a combination of Only Touch® and ETCA (see Chapter 22). Regular maintenance treatment as well as sun protection are essential to avoid recurrence or the appearance of new lentigines.

B

Figure 20.1 (a, b) Improvement only in the quality of the skin on the neck after two series of four ETCA peels according to the basic protocol.

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Figure 20.3 Figure 20.2

Treatment of lentigines on the hands and décolletage with Only Touch® plus ETCA.

Only the top part of the décolletage has been treated with two sessions of four ETCA peels: there is a noticeable improvement in the texture of the skin in the treated area.

Moderate photoaging and acne scars on the décolletage (Figure 20.4) If photoaging is widespread, the ETCA abrasive protocol (see Chapter 21) can be used: the décolletage is abraded with sandpaper abrasion up to the very first bleeding pinpoints. The area is covered with post-peel mask cream and left under occlusion for 24 hours. No acid is applied in this

A

protocol, to avoid acid penetrating too deeply and potentially causing scars.

Severe photoaging of the décolletage (Figures 20.5–20.7) In some cases, careful application of a peel to the papillary dermis (e.g. Unideep®) may be necessary.

B

Figure 20.4 (a) Post-peel mask cream under occlusion after sandpaper abrasion. Appearance of the skin on the third day, just before flaking begins.

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C

A D

B

E

Figure 20.5 (a) Décolletage typical photo aging; (b) a treatment of décolletage photo aging with Unideep® ETCA peel to the papillary dermis. There is pink-white even frosting and ‘sliding’ sign; (c) Coldpacks (3M) can alleviate the burning sensation of acids; (d) treatment of décolletage photo aging with Unideep® (TCA peel to the papillary dermis). Endpoint of the treatment and application of the post peel mask; (e) skin desquamation of décolletage at day 3 after papillary dermis peeling Unideep®.

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Repeating peels on the décolletage ETCA (pinpoint or cloudy-white frosting) can be repeated every 2 weeks on the décolletage. Unideep® can be repeated after approximately 4 weeks. For Only Touch®, see Figure 15.18 in Chapter 15. The abrasive protocol can be repeated after about 4 weeks.

Care between and after peels Figure 20.6 Daily care is as follows: on days 1-6, Renutriv ACE Lipoic Complex®; on days 6 and 7, sterile white Vaseline®. The photograph shows the results after 8 days.

On the day after the first peel, patients should start using sun protection SPF 50+ and a care cream appropriate for their condition: see Table 3.1 in Chapter 3. Post-peel care is essential to maintain results in the long term. A follow-up peeling session should be planned for once a year.

Note 1.

Figure 20.7 Unideep®: results after 12 days. Sun protection SPF 50+ and daily care are essential to maintain the results in the long term.

Treatment should be stopped when pinpoint frosting has been achieved (see Chapter 15).

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21 Stretch marks and scars: dermabrasion and peeling

General remarks Stretch marks, acne scars on the back and severe photoaging on the décolletage are three common problems, and treatment results were disappointing in the past. The doctor would be disappointed at having to refuse treatment and admit to being powerless to help. In some cases where treatment was not refused, the doctor might end up regretting having used inappropriate techniques and having to deal with the resulting complications. Patients, for their part, would suffer from their doctor’s refusal to treat them, which meant having to put off indefinitely the blessed day when their problems might improve.

Origins of the treatment The high level of safety and effectiveness met with when first using the Easy TCA® (ETCA) peel led me to develop some effective application protocols for the treatment of stretch marks and scars. ETCA had proved effective in various areas, including acne, hyperchromia and skin aging, both on the face and on other parts of the body. ETCA consists of an acid solution and an active post-peel cream that the doctor applies to the treated area immediately after the acid solution has produced pinpoint or cloudy-white frosting and that is then left to work until the following morning. The active ingredients in the acid solution are citric acid, ascorbic acid, trichloroacetic acid (TCA), saponins and excipients. The basic protocol provides a peel to the basal layer of the epidermis or the Grenz zone. The postpeel cream is not a neutralizing cream, but, on the contrary, an active cream with a high concentration of vitamins C, E and H, tretinoin precursors, phytic acid, anti-free-radical agents, selenium, methionine, tyrosinase inhibitors, trace elements, fatty acids, and various plant extracts. This cream is used to provide a strong stimulus to the dermis, epidermis and regeneration processes and to protect against complications. Unlike a conventional TCA peel, the ETCA basic protocol does not use the acid solu-

tion to destroy the skin, but rather to make it more permeable for the post-peel cream to penetrate and take effect. The cosmetic problems dealt with in this chapter, however, do not respond well to chemical peels, even when they reach the papillary dermis. In an attempt to achieve better results, deeper peel procedures were tried that went as far as the reticular dermis. The peels were in fact dangerous at this depth; the reasons for this are discussed in Chapter 37. Other authors have suggested using a combined technique of chemical peeling and dermabrasion, but always in the order of a peel followed by dermabrasion. This technique is known as ‘chemabrasion’. We could use the term ‘post-chemabrasion’ for a peel followed by dermabrasion, and ‘pre-chemabrasion’, the technique described in this chapter, for dermabrasion followed by a peel, in order to distinguish between the two techniques. The treatment that I developed consists in using even superficial dermabrasion followed, in some cases, by ETCA acid solution and post-peel cream. Applying the cream under occlusion deepens the treatment, and the longer the occlusion is left, the deeper the treatment will be. Repeating the peels allows the epidermis to renew itself gradually (a chemical resurfacing effect) at the same time as ‘filling’ the dermis with fibroblast products, the fibroblasts having been stimulated by the treatment. Internal and gradual retraction reduces the width of the stretch marks (a filling–shrinking effect). The combination of sandpaper abrasion, with or without the application of the acid solution and occlusion of the ETCA post-peel cream,1 allows a whole range of different depths of action.

Classification of stretch marks The Deprez–Adato classification2 is based on the clinical appearance of the stretch marks (Table 21.1). Stretch marks in stages 2B to 4 seem to respond best to this treatment.

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Table 21.1 Deprez-Adato classification of stretch marks Stage Stage Stage Stage Stage Stage

1 2A 2B 3A 3B 4

Inflammatory Ladder rungs (–) Ladder rungs (+) Ladder rungs (++)

Non-palpable depression Palpable depression <1 cm wide <1 cm wide >1 cm wide

New, developing stretch marks Superficial, white stretch marks Atrophic stretch marks Atrophic pearly white stretch marks Atrophic pearly white stretch marks

Equipment needed for the abrasive protocol The sandpaper abrasion kit consists of 10 sheets of singleuse sandpaper (3M Wet-or-Dry® P220) sterilized3 with gamma rays and a yellow disinfecting and healing powder: bismuth subgallate.

Mechanism of action of the technique The mechanism of action could be as follows: the sandpaper abrasion and acid have a synergistic effect of physical and chemical resurfacing that improves the quality of the entire epidermis (Figure 21.1). When the post-peel cream penetrates the atrophic base of the stretch marks, it causes inflammation (controlled by the antioxidants) that stimulates fibroblast proliferation and metabolic production of the non-cellular components of the dermis (Figure 21.2). At the same time, the depth of injury to the skin could stimulate deep myofibroblast contraction and improve skin tension, as has been observed clinically after treatment.

Figure 21.1 The abrasion and acid resurface the normal skin surrounding the atrophic base of the stretch marks both physically and chemically.

Abrasion The whole area – not only the atrophic base of the stretch marks – must be abraded. Other techniques (laser and microdermabrasion) have failed because they tend only to stimulate the atrophic base of the stretch marks, where there are very few keratinocytes capable of proliferating and very few fibroblasts available to fill the dermis. Sandpaper abrasion produces even, physical resurfacing, leveling the skin and stimulating the healthy skin between the stretch marks to regenerate. The inflammatory reaction caused by the treatment stimulates the growth of healthy keratinocytes on the edge of the stretch marks. As these keratinocytes are stimulated, the epidermis can gradually rebuild in a clinically visible way.

Figure 21.2 Occlusion of the post-peel mask cream, on the other hand, causes severe inflammation of the dermis at the atrophic base of the stretch marks.

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Peel solution With the help of pre-peel abrasion, the ETCA solution rapidly penetrates to the papillary dermis and provides chemical resurfacing on top of the physical resurfacing of the abrasion itself. The combined physical and chemical effect accelerates stimulation of keratinocyte growth on the edges of the stretch marks. The subsequent occlusion does not deepen the action of the ETCA. We have seen elsewhere in this book that occluding TCA tends instead to soften the effect of the TCA.

to prevent it sticking to the outer, absorbent dressing. The dressing is removed for the last time around 6 days after the treatment (see below for details). The abrasion procedure is summarized in Box 21.1.

Box 21.1 Summary of abrasion The abrasion is carried out with 3M Wet-or-Dry® sandpaper, P220, sterilized with gamma rays. It should be gentle, steady, careful and even (intersect each pass) and be stopped as soon as the patient feels pain. The ‘keratinocyte touch’ should be positive: a gloved finger slides easily over the corneocytes (dead cells) that are still present in the area surrounding the abraded zone, but ‘brakes’ on the hydrated keratinocytes (stratum spinosum) that have been laid bare by the sandpaper. The first appearance of pinpoint bleeding signals that the sandpaper has reached the basal layer. Abrasion that goes any deeper can cause permanent complications.

Post-peel cream under occlusion The mechanism of action of the post-peel mask cream, under occlusion, is less easy to understand. This antioxidant and anti-inflammatory cream4 immediately stops the burning sensation and the inflammation caused by the acid during an ETCA peel (standard use as a peel to the basal layer or Grenz zone5), but when it is used under occlusion in the treatment of stretch marks, it appears to be responsible for the depth of the treatment. Clinically, it is plain to see that the longer the occlusion is left in place,6 the deeper is the treatment.2 We have also already seen that the postpeel mask cream can be applied without the acid solution after sandpaper abrasion and can deepen the treatment significantly, liquefying the skin under occlusion in the same way as phenol does (see the section later in this chapter on treating the décolletage). Sequenced photographs of the treatment show that the post-peel mask cream penetrates more readily through the atrophic base of the stretch marks after abrasion and application of the ETCA acid solution. Here, it causes inflammation, which triggers regeneration, and it appears to be limited to this area. The large majority of signs of active inflammation disappear very quickly, in around 2–3 days, but a non-irritative edema can persist for around 15 days at the base of the stretch marks.

Bismuth subgallate Bismuth subgallate (BSG) is a yellow powder that makes post-peel care easier and spares patients having to apply complicated localized treatments themselves, which could cause infection (see also Chapter 34). A generous amount of BSG is sprinkled directly onto the moist areas of skin where the epidermis has been destroyed. It can also be spread on with a gloved hand or sterile swab. Post-peel care has become much easier of late. The BSG is covered with a silicone sheet, such as Mepitel®, which is in turn coated in a thin layer of neutral, sterile Vaseline® and protected by a thick absorbent dressing that is held in place in a way that is comfortable for the patient. On the third day, the silicone sheet is carefully cleaned and put back in place. It is again coated in a thin layer of Vaseline®

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Three treatment possibilities after abrasion There are three possibilities for treatment after abrasion, depending on the depth of action required: ■ After abrasion and application of the ETCA solution, the post-peel mask cream is applied without occlusion. This method is used for acne scars on the face or back. ■ After abrasion, the post-peel mask cream is applied, under occlusion, but without prior application of acid. This protocol is deeper than the previous one and is used in rejuvenation treatments and in the treatment of acne scars on the décolletage. ■ In the deepest protocol, after abrasion and application of the ETCA solution, the post-peel mask cream is applied under occlusion. This is the protocol used to treat stretch marks and surgical scars, when the skin needs tightening.

Origin of stretch marks Stretch marks may result from the following, among other factors: ■ ■ ■ ■ ■

pregnancy – first or subsequent breastfeeding – of first or later children growth – at varying ages sport – a variety of sports may be responsible significant weight change.

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Position of stretch marks Figure 21.3 is a schematic illustration of the locations of stretch marks and the areas treated with ETCA/abrasion.

Summary of stretch-mark treatments Table 21.1 provides a summary of treatments for stretch marks (see also Box 21.2).

Box 21.2 Patients file DATE OF TREATMENT PRE PEEL Type of stretch marks: I – IIa – IIb – IIIa – IIIb – IV Age of stretch marks treated: 1 month – – – – 1 year – – – 5 years – – – 10 years – – – 20 years or + The pre-treatment photo is good quality: Yes/No Blending Bleaching® 2 weeks pre-peel: Yes/No Pre-peel painkiller: Yes/No PEEL  Disinfect with alcohol and degrease with acetone, leave to dry, mark out areas to be treated with marker pen  Gentle sand abrasion of whole area to be treated: • Sandpaper from Skin Tech’s abrasion kit: Yes/No • Other sandpaper: Which: Sterilized/Not sterilized Type of sterilization used: • Abrasion: Grade 1, Grade 2, Grade 3  Photograph the abraded zones before applying the peel solution  Gauze soaked in 2% lidocaine with adrenaline (epinephrine) – Occlusion for ...... minutes (10–15); dry the lidocaine  With two cotton buds apply a vertical coat eventually followed by a horizontal coat of Easy TCA® solution on each area: • Intensity of pain: 0 | ––––––––––––––– | ––––––––––––––– | +++ • Intensity of frosting: (Cloudy) – Even pink-white – (Pure white – Gray/white)  Apply the post-peel cream (0.5 g/10 cm × 10 cm surface area); plastic occlusion POST PEEL  Removal of the plastic dressing after ........... hours • Photograph 24 hours before application of bismuth subgallate (BSG) • Application of BSG: Yes/No • Application of silicone sheet: Yes/No • Thin layer of Vaseline® on BSG, protect with thick sterile gauze pad  Examination of skin on 3rd day: • Photograph – application of Vaseline® – protective dressing  Examination of skin on 6th day: Photograph – application of Vaseline® – light protective dressing 24 hours  Post-peel care from 8th day: • Leave the skin to regenerate for 3 weeks at least • Blending Bleaching® cream and Melablock HSP® 50+ • If atrophic stretch marks: DHEA Phyto® once a day • If inflammation: Renutriv ACE Lipoic Complex® Improvement in stretch marks since previous treatment: 0 | –––––––––––––– | –––––––––––––– | completely gone Improvement in stretch marks since start of treatment: 0 | –––––––––––––– | ––––––––––––––- | completely gone

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Disinfection and degreasing The doctor’s hands must be washed surgically or sterile gloves should be worn. The patient’s skin is disinfected with alcohol (75° alcohol and sterile gauze – firm pressure should be applied on the gauze) and degreased with acetone (pure acetone and sterile gauze – firm pressure should be applied on the gauze). The acetone starts to break down the membrane phospholipids. It makes no difference clinically which order the alcohol and acetone are applied in, but both products need to be applied several times. Sandpaper must be sterilized, ideally with gamma rays.7

Determining the ideal depth of abrasion

Figure 21.3 Picture used to take note of the general position of stretch marks and the areas treated with ETCA/abrasion.

Wearing gloves, the doctor rolls a sheet of sandpaper around a round object (e.g. a bottle of pre-peel cleanser). The skin is held taut with one hand, and intersecting, careful, gentle and repeated passes are made with the sandpaper. Pressure must be firm and even. If the pressure is too light,8 the skin will not be abraded properly. On the other hand, if the pressure is too firm, it will take off more skin and make it too permeable. When done correctly, the sandpaper abrasion gradually permeabilizes the skin, is not painful at first and is therefore done without anesthetic. The depth can be classified in four different grades (Figure 21.4).

Grade 0 sandpaper abrasion

Preparing the patient The patient is prepared psychologically: they are informed in detail about the treatment, developments and possible risks. Preparing the skin for 3–4 weeks before treatment tends to limit the risk of pigmentary changes, which are common after this treatment. The stretch-mark treatment causes severe inflammation and tends to stimulate melanocytes, albeit only temporarily. Phototypes I–III can be treated without preparation, but patients with a higher skin phototype must apply effective sun protection and Blending Bleaching® cream twice a day, especially if they live in a country with a very sunny climate (see Chapter 2). Applying products that stimulate synthesis of heat-shock proteins (HSP) helps all cells to resist this type of stress (see Chapter 2). Preparing patients also involves getting them to sign an informed consent form, explaining how the treatment and post-peel care will proceed, and giving them a paracetamol (acetaminophen) plus codeine tablet 30 minutes before treatment and 2 hours after treatment.

■ Subjectively: the patient feels almost nothing. ■ Objectively: the fingers slide easily over the superficial layers of corneocytes: the ‘keratinocyte touch’ is negative.

0 I II III

Figure 21.4 Sandpaper abrasion: grades 0–III.

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Table 21.1 Summary of stretch-mark treatments Pre-peel 30–60 mins before abrasion

• • • •

Phototype I-III: Blending Bleaching® 1 week before Phototype IV-V: Blending Bleaching® 3 weeks before Give the patient a paracetamol (acetaminophen) + codeine tablet Disinfect and degrease the skin

Abrasion (depth?)

• Too superficial: no pinpoint bleeding – no pain • Right depth: first pinpoint bleeding – first pain – K touch • Too deep: a lot of bleeding – very painful

The sandpaper can be found in Skin Tech’s Abrasion Kit

Abrasion depth check: pain + pinpoint bleeding + keratinocyte touch (K touch) Anesthetic

2% lidocaine with adrenaline (epinephrine) on gauze pad+ plastic film 15 min

No EMLA cream

ETCA solution (how many coats?)

• Right depth: even pink–white frosting • Too deep: pure white frosting

Acid or no acid? (décolletage, breast, ... )

Post-peel mask

0.5 g/10 cm × 10 cm area

Occlusion duration

• Superficial treatment: 6–8 hours • Medium treatment: 8–16 hours • Deep treatment: 16–24 hours

Occlusion or no occlusion? (back, breast ... )

Occlusion check: skin liquefaction or not Post-peel care To be done by the doctor

To be done by the patient

+24hrs:

• • • • •

• • • • • • • •

Remove occlusive film Gently cleanse with a dry gauze Apply BSG: thick coat to dry the skin (BSG powder can be found in Skin Tech’s Abrasion Kit) Apply a silicone sheet coated in Vaseline® to cover the BSG (see Figure 37.45) Protect with a thick gauze

Take paracetamol if painful No showers, no baths, no scratching No sports, no swimming Keep out of the sun (be careful, the sun can filter through clothes)

Between days 1 and 2: take paracetamol (acetaminophen) if painful Day 3:

• • • •

Day 6:

As day 3

As day 3

Days 7–8:

Skin is pink but usually healing well

If slow healing ⇒ prevention of problems

Weeks 1–5/6: • • • • • • • • • • • • •

Change dressing Clean the silicone sheet and reapply the dressing as on day 1, without adding any more BSG Avoid infection; administer antibiotics if necessary

Moisturize, protect, prevent PIH Prevent prolonged erythema: if erythema + 2 weeks, treatment with 1 week fluorinated corticosteroid Prevent PIH: Blending Bleaching® cream should be used before PIH begins, from day 8 Melablock HSP® SPF50+ (sun protection cream)• Prevent infection: administer antibiotics if necessary Prevent scratching: – if skin is very dry: Vaseline® – If skin is dry: Vit E Antioxidant® cream Check patient every week: – If PIH begins, even out with Blending Bleaching® and Melablock® HSP

• • • •

No showers, no baths, no scratching No sports, no swimming Keep out of the sun (be careful, the sun can filter through clothes)

• • • • •

08.00: Blending Bleaching® cream followed by Melablock HSP® (even if no sun exposure) 12.00: Blending Bleaching® cream followed by Melablock HSP® (even if no sun exposure) 17:00: Renutriv ACE Lipoic Complex®

• • • • • • •

20:00: Renutriv ACE Lipoic Complex® + DHEA Phyto® cream Call the doctor with any questions or problems such as pain, temperature, itching, redness Baths/showers are not allowed until the skin is completely healed (average day 7–8) Sports allowed from day 10–15

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Table 21.1 continued – If necessary add hydroquinone 4–5% to the Blending Bleaching® – Maybe do ETCA peel on area with PIH

• Sun not allowed for 3 months: sun protection for • 3 months (Melablock HSP® 50 or 25)

Repeat treatment after a minimum of 5 weeks or, as results are definitive, after 5 months or 5 years PIH: use Blending Bleaching® and Melablock HSP® 50 as soon as possible Treat with ETCA basic protocol (as described for hands in ETCA White Book) 1–2 weeks + Blending Bleaching® and Melablock HSP® For updates go to http://www.estetik.com-Treatment Tips.

This depth of abrasion provides only low-quality topical anesthesia and the peel itself will be painful and too superficial.

Grade I abrasion ■ Subjectively: the abrasion feels unpleasant, but still painless to the patient, as the sandpaper is still a long way from the free nerve endings that are in the lower part of the epidermis. ■ Objectively: the ‘keratinocyte touch’ is still negative – although the fingers can be felt to brake slightly as they slide from the healthy zone to the abraded zone, they still slide easily over the skin. Grade 1 sandpaper abrasion does not provide adequate topical anesthesia, and the peel is still painful and too superficial.

Grade II abrasion

Figure 21.5 Pinpoint bleeding – grade II abrasion. The arrows indicate the first pinpoint bleeding. This depth of abrasion is ideal for this treatment: it gives the right anesthesia and depth of action.

This is the correct level for effective abrasion combined with this peel. ■ Subjectively: the patient starts to feel pain from the sandpaper abrasion. Usually the abrasion should be stopped here, but the pain thresholds vary from patient to patient. It is therefore essential to look out for the objective signs. ■ Objectively: The ‘keratinocyte touch’ is positive – the finger feels a marked braking sensation as it passes from the slippery dehydrated corneocytes of the non-abraded surrounding skin to the living, well-hydrated keratinocytes exposed by the abrasion. The first pinpoint bleeding appears on the skin as the ‘highest’ dermal papillae, where the blood vessels of the papillary dermis are located, are abraded (Figure 21.5). Topical anesthesia will be of good quality, and the peel will reach the required depth.

Grade III abrasion ■ Subjectively: the patient usually finds the abrasion very painful, even unbearable, and will let the doctor know this – the abrasion is going into the papillary dermis, and care must be taken! ■ Objectively: there is a lot of pinpoint bleeding as the loops of blood vessels in the dermal papillae are now being abraded (Figure 21.6). Abrasion must be stopped. If it were to continue, the pinpoint bleeding would increase rapidly and appear as extensive surface bleeding. Topical anesthesia under these conditions would be rapid and of good quality, but the peel would be too deep and trigger permanent side-effects such as achromia and/or hyperpigmentation and/or scarring.

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the basal layer of the epidermis. Sensitivity varies from patient to patient, and other objective signs, discussed below, must be taken into account. The doctor should nevertheless ask patients to describe the pain they feel: ■ No feeling: the depth is assumed to have reached the stratum corneum. ■ Uncomfortable but not really painful: the depth is assumed to have reached the keratinocytes. ■ First pain felt: the depth is assumed to be close to the basal layer – stop abrasion! ■ Very painful: abrasion is definitely too deep or the patient is squeamish.

Figure 21.6 Pinpoint bleeding – grade III abrasion. Contact anesthesia will be just right, but there is a risk that the peel will be too deep. Care must be taken over how much acid is applied to the skin, in order to avoid complications such as scarring and/or pigmentary changes.

With a squeamish patient, before applying the acid, the doctor must check the anesthetic for effectiveness. When the abrasion is too deep (grade III), the doctor must monitor carefully how much acid is applied to the skin so as not to go beyond even pink–white frosting (see below).

2. Keratinocyte touch

Other abrasion techniques Other abrasion techniques have been tried, depending on the doctor’s experience and the equipment available: ■ microdermabrasion: it is impossible to get the microscopically even abrasion obtained with sandpaper; the corundum crystals also have to be cleaned after abrasion. ■ erbium laser: it is also possible to use laser abrasion after a local anesthetic, but this technique takes much longer, and is more difficult and more expensive; it has no additional advantages. The sandpaper abrasion technique has the advantage of being even over the whole area, and is cheap, fast and inexpensive.

Three signs that guide abrasion 1. Pain If the abrasion is completely painless, it has only reached the stratum corneum. When it goes deeper and the sandpaper comes into contact with the keratinocytes, it is uncomfortable but not yet painful, as the upper layers of keratinocytes are not directly innervated. When the patient says that the abrasion feels uncomfortable but not painful, the doctor must pay very careful attention, as it will become painful at any moment when the sandpaper gets closer to the free sensitive nerve endings in the deeper layers of the epidermis. Abrasion usually becomes painful when it reaches the keratinocytes next to

When sliding the fingers (even with gloves on) from a nonabraded area to an area that has been abraded, there should be a braking sensation if the abrasion has reached the right depth.

3. Bleeding If there is no pinpoint bleeding (grade I abrasion), the treatment is not deep enough. If there is too much pinpoint bleeding (grade III abrasion) or surface bleeding, there is a risk that the peel will be too deep and cause permanent complications.

Topical surface anesthesia Applying ETCA solution immediately after abrasion would be extremely painful without an anesthetic. There are several different types of anesthesia to be considered: ■ EMLA cream or other topical anesthetic cream: as pointed out in Chapter 33, EMLA cream should not be applied before a peel. For the same reasons, topical anesthetic creams should not be used before applying ETCA for stretch marks. ■ Anesthesia with lidocaine spray: lidocaine spray contains alcohol and is very painful on abraded skin. ■ Klein solution: injections of Klein solution have been tested, but the results are unsatisfactory: it anesthetizes the deeper layers not reached by the acid, but the surface anesthetic effect remains largely inadequate. ■ Topical application of 2% lidocaine solution with adrenaline (epinephrine), poured directly onto sterile gauze

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Figure 21.7 (a) Topical application of 2% lidocaine with adrenaline (epinephrine): the lidocaine is poured over the gauze. (b) Occlusion of the lidocaine for 10–15 minutes.

pads on the skin, provides an excellent anesthetic (Figure 21.7a). One percent lidocaine is not effective enough. Lidocaine without adrenaline is rapidly reabsorbed, and its effect is too short-lived after epidermal abrasion. Two percent lidocaine with adrenaline should be covered with an impermeable plastic film for 10–15 minutes to stop it evaporating too quickly and to enhance its effect (Figure 21.7b).

Checking the effectiveness of the topical anesthetic After 10–15 minutes’ occlusion, the lidocaine–adrenaline solution has penetrated the skin and reached the epidermis: the adrenaline induces vasoconstriction. Uniform vasoconstriction is a sign that the local anesthetic has worked. Applying a single 5 cm ‘line’ of ETCA peel solution with a cotton bud is enough to test the patient’s sensitivity. If the patient feels no pain at all where the acid has been applied, the ETCA solution can be applied to the whole area to be treated. If the patient still feels some pain, the doctor should replace the occlusion for another 5 minutes.

Applying the ETCA solution The plastic film from the anesthesia is gradually lifted, the skin is dried and the ETCA solution is applied with a double cotton bud until pink-white frosting, never pure white frosting, occurs (Figure 21.8).

Figure 21.8 Starting application of the ETCA solution

The first coat of ETCA solution may cause linear and uneven frosting, as can be seen in Figure 21.9. This application is not perfect, and more ETCA solution should be applied between the lines of frosting to even it out. In some cases, the first coat of ETCA solution does not trigger any frosting, so another coat must be applied perpendicular to the first. Epidermal sliding is easy to recognize, as the dermal and epidermal proteins have been coagulated by the TCA. The ETCA solution should not be neutralized or removed. It stays where it is, and will be covered with the post-peel mask cream.

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A

B

Figure 21.9 (a) Linear and uneven frosting following application of a first coat of ETCA solution; (b) uniformization of the frosting after passing a second careful coat of Easy TCA solution between the lines of frosting.

Applying the post-peel mask cream and occlusion As soon as frosting occurs, 0.5 g of post-peel mask cream should be applied per 10 cm × 10 cm surface area (Figure 21.10). The dosage card in the ETCA kit can be used to determine the right quantity. After applying the post-peel mask cream over the whole area that has been abraded and coated in ETCA solution, it should be covered with an impermeable, occlusive plastic film (Figure 21.11). The plastic film is secured with a hypoallergenic dressing and held in place for 24 hours. The actual depth of the peel and

the amount of ‘phenol-like’ skin liquefaction depend on how long the post-peel cream is occluded. From 8 to 12 hours’ occlusion does not liquefy the skin, and the results are often inadequate. More than 24 hours’ occlusion carries a higher risk of infection.

Removal of the occlusion How long the occlusion is left in place depends on the depth of action desired. Twenty-four hours seems to be a good compromise between effectiveness and the risk of complications. The occlusive plastic film is removed and

Figure 21.10 Application of the post-peel mask cream on the first quadrant to be treated.

Figure 21.11 Occlusion with impermeable plastic film.

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A

C

Figure 21.12 (a) The occlusive plastic film is left in place for 24 hours. After it has been removed, the skin can be seen to be inflamed (b) and covered in a thick runny, foul-smelling liquid. Softly remove this liquid before applying the bismuth subgallate powder (c). B

reveals skin that is extremely inflamed and covered in a liquid that can be thick, runny and have an unpleasant smell (Figure 21.12). This liquid consists of the remains of the cream, inflammatory serous fluids and dead cells. The smell, which can even be unpleasant for people standing close by, is the same for all patients. It is the same as the smell that follows occlusion of a full-face phenol peel.

Close-up of the skin after occlusion The treated area is severely inflamed. The atrophic base of the stretch marks stands out and signals the extent of the dermal reaction (Figure 21.13). The controlled inflammation caused by the treatment is essential, as it triggers the skin regeneration processes. In short, abrasion and the application of acid appear to stimulate the regeneration of normal keratinocytes on the edge of the stretch marks, and occlusion of the post-peel mask cream strongly stimulates the fibroblasts.

Figure 21.13 Severe inflammatory edema at the base of the stretch marks and in the surrounding skin.

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Applying bismuth subgallate Any excess liquid is mopped up with sterile gauze, although the skin is not dried completely. Some liquid is needed for the bismuth subgallate (BSG) powder to stick. Skin Tech’s Stretch Mark Kit contains P220 sandpaper as well as a sprinkler of BSG.9 A generous amount of the powder should be sprinkled directly onto the skin, leaving a thick layer (Figure 21.14). Gently passing a sterile gauze pad over the powder evens it out and makes it stick to the liquid left on the skin.

Different types of dressing have been tried in order to protect the BSG. Melolin® (Smith & Nephew) (Figure 21.15) is an excellent sterile dressing that has one ‘normal’ side and one side covered in a transparent plastic film that does not stick to wounds. The plastic is applied on top of the powder and the Melolin® is secured on the healthy surrounding skin. I used this method for many years until I could no longer get a supply of Melolin®. I then used Mölnlicke’s silicone or absorbent dressings (Mepilex®, Mepitel®, etc.) to good effect (Figure 21.16). Mepilex® and Melolin® are not always easy to find, and I therefore had to look for another type of cheap and readily available protective dressing. I then went back to using sterile white Vaseline®. Applying a thin coat of sterile white Vaseline® to the BSG turns it into a paste that is easily spread with a tongue depressor and sticks to the skin (Figure 21.17).

Figure 21.16 Figure 21.14

Mölnicke’s Mepilex®.

Application of bismuth subgallate to the left half of the abdomen.

Figure 21.15 Smith & Nephew’s Melolin®.

Figure 21.17 The BSG is covered with sterile white Vaseline® and protective gauze.

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Figure 21.18 Wide, thick gauze secured on the surrounding healthy skin.

The Vaseline® and BSG paste is then covered with a thick and absorbent sterile gauze that is secured on the healthy surrounding skin, as can be seen in Figure 21.18. In some patients, the BSG and Vaseline® can act as an occlusion and unexpectedly deepen the action of the peel. Any overpeeling can lead to complications with scarring or dyschromia.

Checking the dressing after 72 hours

Figure 21.20 Appearance of the skin after 72 hours, following removal of the dressing.

dressing come away naturally and quickly. The skin can look rather gruesome, as can be seen in Figure 21.20. The use of a silicone sheet coated in a thin layer of Vaseline® to cover the BSG, as described above, drastically reduces the risk of the dressing sticking to the skin and causing lesions. On the third day, the skin will be dry and flaking (Figure 21.21). To help the flaking proceed, a thick layer of sterile

The sterile gauze does not stick to the skin too much, and can usually be removed easily by drawing it back smoothly and carefully. If the dressing sticks in places, it should not be pulled off: instead, the doctor should cut around the part that is stuck to the skin and leave it in place (Figure 21.19). Vaseline® can be applied to this area to help the

Figure 21.19 The dressing is sticking slightly: it should not be pulled off – rather, the doctor should cut around the part that is sticking.

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Figure 21.21 Dryness and flaking on the third day.

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Figure 21.22 Application of Vaseline® on the third day.

Figure 21.24 white Vaseline® can be applied (Figure 21.22) and the skin protected with a new gauze dressing (similar to that shown in Figure 21.18).

Care on the 5th or 6th day The doctor sees the patient one last time to evaluate the condition of the skin and apply another thick layer of Vaseline® (Figure 21.23) and one last dry dressing (as in Figure 21.18). It is common to see lines of depigmentation on patients with a phototype higher than IV (Figure 21.24). This depigmentation tends to return naturally to the original

On the sixth day, areas of depigmentation are common in patients with dark skin phototypes.

skin color within a few weeks, even without Blending Bleaching® cream (Figure 21.25), which reduces the risk of post-inflammatory hyperpigmentation.

Protecting the skin At the end of the first week after the peel, the skin is thin and delicate, quick to hyperpigment, slightly itchy, and swollen. The edema can persist for more than 2 weeks at the base of the stretch marks. It is essential to apply appropriate care creams to the skin. ■ Hydration: Vit E Antioxidant® cream (see Chapters 2 and 3) or a thin layer of sterile white Vaseline® should be applied. ■ Prevention of pigmentary changes: Blending Bleaching® cream and Melablock HSP® 50 or 25 should be applied until the following treatment or for at least 6 weeks. ■ Prevention of infections: the patient should check for infection and prescribe antibiotics as necessary (the first week is the most dangerous). ■ Prevention of oxidation: the patient can apply an antioxidant cream if the extent of the inflammatory reaction appears to make this necessary. ■ Stimulation of the skin’s metabolism: the patient can apply a dehydroepiandrosterone (DHEA) cream if the extent of atrophy appears to makes this necessary.

Results of treatment Figure 21.23 A thick layer of Vaseline® is applied.

The results appear gradually after stretch-mark treatment, but they are permanent (Figures 21.26–21.28).

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Figure 21.25 (a) Depigmentation on the sixth day after the peel. (b) The pigmentation returns almost to normal 30 days after the first peel, after treatment with tyrosinase inhibitors.

Progression of results Stretch marks are the result of severe dermal and epidermal atrophy, lack of appendages and an extreme paucity

A

of cells. It would be impossible to get rid of them in a single treatment session. With each treatment, the quality of the skin improves visibly, and patients themselves can see this. Photographs do not do justice to the improvement

B

Figure 21.26 Before (a) and after (b) two treatments on day 30 in a patient with phototype V.

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Figure 21.27 Before (a) and after (b) two ETCA abrasive protocols.

Figure 21.28 Two treatment sessions on a phototype V patient: anterior chemabrasion as described in this chapter.

in skin quality, and in order to understand how this treatment works, detailed studies are necessary in the future. The first treatment usually brings great satisfaction to the patient in terms of how the stretch marks feel: they do not feel as deep, and the depressed atrophic base starts to fill out. Gradually, the atrophic base comes level with the surrounding skin, and in places its structure returns completely to normal. Regeneration continues throughout the following treatments. In one published study,2 69 patients of all phototypes and aged between 14 and 63 were treated for stretch marks in different places: abdomen, breasts, back, hips, etc. The patients were followed up for an average of 18 months, and the stretch marks treated were between light/recent and very deep/old. An average improvement of 70% in the appearance of the stretch marks was observed after an average of four treatments (4.2 exactly) and the results have been published.

Duration of results It is commonly acknowledged that the histological changes that take place in the deep dermis should be considered permanent. We can therefore assume that the results achieved are also permanent, and this corresponds to current clinical experience. The first treatments were carried out in 1996, and the results achieved then were still completely stable in 2005.

Post-peel details ■ This peeling technique is one of the most difficult: it requires sound experience in post-peel care and should not be the first peel that a doctor performs. ■ Post-peel monitoring is of vital importance, and the follow-up care during the first week after the peel must be rigorous: the doctor should see the patient several times during these first 8 days.

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■ If there is any doubt about the possibility of infection, antibiotics should be administered immediately. ■ Contact between the abraded skin and water is very painful and increases the risk of infection. The patient obviously cannot have a bath during the first week until the skin has completely restructured and is impermeable again. The patient can have a quick shower if an impermeable plastic covering is placed over the protective dressing. ■ Oral painkillers make both the patient and the doctor feel more at ease: a 500 mg tablet of paracetamol (acetaminophen) or paracetamol plus codeine taken half an hour before the peel and 2 hours after allows the patient to carry on as normal. The patient can take another painkiller before going to bed if need be. There should be no pain the following morning – only a feeling of slight discomfort. ■ The patient should keep out of the sun for 3 months after the treatment. Effective sun protection is essential, even under clothing. ■ There is a risk of an isomorphic response, especially in patients with progressive vitiligo or psoriasis and in patients where a minor trauma such as friction from clothing has induced the Köbner phenomenon in the past. The Köbner phenomenon can be induced by other disorders: reactive perforating collagenosis (transepidermal elimination of collagen), eruptive xanthoma (seen, e.g., in cases of secondary hypertriglyceridemia), erythema multiforme, macular or maculopapular exanthema associated with juvenile arthritis, and various types of lichen (e.g. planus or sclerosus). Caution should be exercised in all cases.

Complications Complications from this deep peel are relatively common, but can be prevented or treated. Caution and adherence to strict methodology should ensure safe treatment. The deeper the peel, the higher is the risk of complications. Complications include hyperpigmentation (Figures 21.29-21.31), depigmentation or scarring, depending on how serious the cause is: ■ Uneven abrasion: if abrasion is too deep, the acid penetrates too deeply and there is a risk of scarring. Even abrasion produces even results. ■ Uneven application of the peel solution: the solution must be applied evenly to achieve even results. It is especially important that the cotton buds be squeezed out properly, as the ETCA solution penetrates very quickly through the abraded skin. ■ Pulling off a dressing: if a dressing is stuck to the skin, it must not be pulled off; this would pull off the regenerating epidermis, and the skin would have to start the healing process again, leaving a hyperpigmented area. The dressing should be cut off around the area that is

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Figure 21.29

Figure 21.30 Figures 21.29 and 21.30 Two cases of post inflammatory hyperpigmentation linked to the lack of post peel use of antityrosinase/antioxidant cream and sun protection. Treatment applied used Blending Bleaching® cream and 2 Easy TCA peels without sandabrasion, using the ‘base protocol’.

sticking to the skin, and a coat of Vaseline® should be applied to help the dressing come away without causing injury to the skin. ■ Pruritus: this causes scratch lesions. ■ Infections: these can result from not cleaning hands and equipment properly, inadequate pre-peel disinfection or overlong occlusion (more than 24 hours’ occlusion usually causes infection). A pre-existing skin infection can also be the cause: treating acne scars when there are lesions that are still active. ■ Technical error. See Chapter 37 for more information.

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Facial scars Phenol Along with laser and abrasion treatment, a full-face phenol peel is certainly one of the best options for treating facial scars. It is not completely effective, however, and it is often necessary to use chemabrasion – that is, a combination of a phenol peel followed (immediately or the next day) by abrasion with a diamond fraise or sandpaper. See Chapter 30 for more information on the treatment of acne scars and phenol peel face lifts.

Dermabrasion plus ETCA (Figure 21.33) Figure 21.31 Scarring after anterior chemabrasion, resulting from an irregular abrasion and supposed poor follow-up. Treatment applied used topical and injected corticosteroids, antityrosinase and antioxidant cream, silicone sheet compression.

Treating scars Treating surgical scars and acne scars is never easy. A scar is the tip of a fibrotic iceberg buried deep under the skin: effective treatment is therefore by definition a deep treatment. Post-acne pigmentation scars are easy to treat (Figure 21.32).

A ‘pre-chemabrasion’ technique has been developed for the treatment of facial acne scars. The results are very good, and are similar to those achieved with phenol. The technique is the same as for stretch marks, apart from the following points: ■ The sandpaper abrasion must be taken a step further (grade III) on the face: confluent pinpoint bleeding appears on the abraded area of the scars. This physical resurfacing makes the skin appear smoother after abrasion. ■ The topical anesthetic (the same as used for stretchmark treatment) dries up the blood and anesthetizes the whole area before the acid is applied. The anesthetic is applied after abrasion and before application of the ETCA solution. ■ Application of the ETCA solution triggers pure white or even gray–white frosting. The solution penetrates to the reticular dermis.

Figure 21.32 (a, b) Post-inflammatory hyperpigmentation (acne) treated with ETCA (non-abrasive, basic protocol) combined with daily depigmenting treatment and sunblock.

A

B

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■ Occlusion is not necessary. ■ The next day, BSG can be applied to protect the skin and enhance healing, which begins within 8 days.

Body scars The treatment of body scars is more complex than that of facial scars. The same technique described for stretch marks is used: abrasion plus ETCA peel plus post-peel mask cream plus occlusion. The results, although not exceptional, are quite good, as can be seen in Figures 21.34 and 21.35. Scars that are in the same area treated for stretch marks by abrasion and ETCA respond well to this technique if they are stable and permanent. It is out of the question to use this deep peel on recent scars, as there is a risk that the scars will open. A

Acne scars on the back (Figure 21.36) Technique

B

An intraepidermal abrasion is performed with positive ‘keratinocyte touch’. Applying an acid solution immediately after abrasion would be very painful, and a surface anesthetic must be applied with gauze pads soaked in 2% lidocaine with adrenaline (epinephrine) (with 10–15 minutes under plastic film to prevent evaporation). The anesthetic can be seen to be working as the adrenaline penetrates and causes vasoconstriction. The ETCA solution is applied carefully, and cloudy-white frosting may appear with the first coat of acid solution. As soon as cloudy-white frosting occurs, 0.5 g of post-peel mask cream should be applied per 10 cm × 10 cm of surface area treated10 and the skin massaged. The doctor decides if he wants to deepen the action of the peel with 24 hours’ occlusion, as with stretch marks, or if he prefers to end the peel here, without occlusion.

Post-peel care Post-peel care is exactly the same as for the stretch-mark treatment. The peel should be repeated several times at 3- to 5-week intervals if necessary. Repeated epidermal repair and dermal stimulation gradually improve acne scars on the back. C

Figure 21.33 (a) Facial abrasion with 3M Wet-or-Dry® sandpaper, P220. (b) End of abrasion: confluent bleeding. (c) After application of ETCA solution, there is pure white or gray–white frosting. The post-peel mask cream is applied as soon as frosting occurs.

Scars or aging of the décolletage: easy protocol, without application of acid (Figure 21.37) Abrasion is applied to the skin until the first pinpoint bleeding appears. Local anesthetic is not necessary after

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B

C

Figure 21.34 (a) Abdominal scar before the first stretch-mark treatment. (b) Appearance of the scar 30 days after the first stretch-mark treatment: the quality of the skin has improved significantly; the small scars left on the sides by the stitches have disappeared/diminished, and the scar is flatter. (c) Improvement in the appearance of the scar and skin tension after the second stretch-mark treatment (abrasive–occlusive ETCA).

A

B

Figure 21.35 (a) Before stretch-mark treatment. (b) Before the third abrasive ETCA treatment. In spite of the poor quality of the photographs (due to the large pixel size of the first generation of digital cameras) it is easy to see the improvement in the scar across the abdomen as well as in the stretch marks.

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Figure 21.36 (a, b) Treatment of pigmentary changes from acne scars on the back (without occlusion).

Figure 21.37 (a, b) Improvement in acne scars on the décolletage in a young patient with vitiligo. There is no Köbner phenomenon on the treated area.

A

B

abrasion, as this protocol does not involve the application of acid. Immediately after the abrasion, the doctor applies 0.5 g of post-peel mask cream per 10 cm × 10 cm of surface area. An impermeable plastic film is then used as occlusion for 12–24 hours. The epidermis is usually destroyed locally. The area treated is moist after occlusion; abrasion and post-peel mask occlusion have made it permeable. Post-peel care is exactly the same as for the occlusive treatment of stretch marks: BSG is used.

Keratosis pilaris (Figure 21.38) Keratosis pilaris is abnormal keratinization of the hair follicles, and makes the skin feel rough. It occurs mainly on

the arms (especially the back of the upper arms) and thighs, but it can also develop on the cheeks of young children. A red, inflamed ring may surround the cone formed by the keratosis. After disinfection, light abrasion (grade I) with sandpaper should be applied. After abrasion, a topical anesthetic is applied as described in the protocol for stretch marks, followed by ETCA solution: pinpoint or cloudy white frosting appears, especially on the keratoses that take the brunt of the abrasion. The post-peel cream is applied and left to act until the next day. This procedure is repeated four or five times, at 2week intervals. To maintain results, the peels are repeated, and from time to time a simple, superficial abrasion is performed.

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Notes

Figure 21.38 Treatment of pilar keratosis: aspect of the skin after sandpaper abrasion and application of Easy TCA solution. Points of frosting can be seen.

1. The length of occlusion varies, as we shall see further on. 2. Adato M, Deprez P. Striae treated by a novel combination treatment – sand abrasion and a patent mixture containing 15% trichloracetic acid followed by 6–24 hrs of a patent cream under plastic occlusion. J Cosmet Dermatol 2004; 2: 61–70. 3. Sterilizing sandpaper for dermabrasion poses certain problems that are discussed later in this chapter. 4. See the detailed formula of this cream in Chapter 15. 5. We have seen above that the post-peel mask is a slightly acidic cream and cannot therefore be considered as a simple ‘neutralizer’. 6. Although there is no point going beyond 24 hours of occlusion. 7. Dry heat burns the sandpaper, damp heat twists it and in both cases the sandpaper’s silicone grains might come away from the paper and be ‘grafted onto’ the patient’s skin. With chemical disinfection, there is a risk of toxic molecules being imported onto the patient’s skin. 8. If the pressure is too light, too many passes are needed, which irritates and heats the skin more than abrading it. The risk of post-inflammatory hyperpigmentation is then higher. 9. See Chapter 35 for more information on bismuth. 10. 0.5 g of post peel mask can be measured out using the dosage card in the kit. This corresponds to ‘one line of cream’.

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22 Actinic keratoses and lentigines

Keratoses and lentigines need relatively deep treatment, but it is not essential to give the whole face a deep treatment when there are only a limited number of lesions: a local application of Only Touch® is enough in this case.

Description Only Touch® (OT) (Figure 22.1) consists of a saponified and stabilized solution, adjuvanted with alpha hydroxy acids (AHAs), vitamins and antioxidants. Once the doctor has reconstituted OT by adding trichloroacetic acid (TCA), it provides a solution that can be used to treat the skin locally to the reticular dermis in the treatment of small benign lesions less than 1 cm in diameter. Its pH is lower than 1 and the solution’s final concentration in TCA is approximately 45% m/m. It is therefore a very strong peel, to be used only for limited indications.

Indications OT is used to treat localized and benign solar lentigines (SLs) and/or actinic keratoses (AKs) in patients with skin phototypes I to III, or sometimes IV1 (Figures 22.2–22.4).

Lesions should not be more than 1 cm in diameter at the most. OT must not be used on larger surface areas – not even partially. Nor should it be used on lesions unless it is certain that they are benign. Nevi are not an indication for OT. Some doctors, by pushing the diameter limits, have tried to use OT to treat melasma. The melasma was partially treated in this way by gradually applying OT to small areas. However, this technique has proved ineffective, and there is a high risk of stimulating melanogenesis in the melasma, breaking the basal membrane and encouraging the development of dermal melasma. Under no circumstances should OT be considered as a treatment for standard or resistant melasma.

Preparing the skin OT is a deep TCA peel, and because of this tends to cause pigmentary changes. The patient must apply Blending Bleaching® cream (see Chapter 2) twice a day2 for 2–3 weeks before treatment in order to reduce melanocyte activity. After the Blending Bleaching® cream, sun protection cream (Melablock HSP® 50+ cream or 25+ spray) should be applied and then reapplied every 2–3 hours, depending on how much sun there is. This preparation reduces the risk of pigmentary changes after OT.

Preparing the solution

Figure 22.1 Only Touch®.

Using a 1 cm3 syringe, the required quantity of 80% m/m TCA3 is drawn up and injected into the bottle of OT base solution. It should be remembered that 80% m/m means 80 g of TCA crystals with an added 20 g of distilled water. After making up the OT solution, between 0.2 and 0.5 cm3 (the amount depends on the number of lesions to be treated) are drawn up. This solution is put in a small glass or ceramic bowl (under no circumstances should a metal container be used).4 A cotton bud is then soaked in this solution and partly squeezed out to make sure that

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Figure 22.2 Solar lentigines (a) before and (b) after treatment with a combination of OT and Easy TCA®.

there is no excess solution. Any ‘drips’ of OT on the face can lead to cosmetically disastrous results (Figure 22.14).

Applying the solution The product should be tested on a small area of skin before the first application. OT is applied with a cotton bud or, for very small lesions, with a wooden pick soaked in the solution.5 Great care should be taken to avoid any runs or drips of excess solution. Half a millimeter is usually enough for an application on both hands and forearms. With the chosen applicator the lesion that needs to be treated should be touched quickly, precisely and once only always combined with ETCA.

Quickly The contact time between the cotton bud soaked in OT solution and the skin should be as brief as a finger touch on a keyboard, a fraction of a second. Any longer (≥1 seconds), and too much acid will be left on the skin. The frosting then turns a gray or even a yellow color and signals prolonged sequelae (see Chapter 37). Prolonged contact or possibly repeated applications make the skin appear ‘frozen’ and means prolonged consequences. The scabbing can last for more than 3 weeks in this case, and hypochromic, achromic

Figure 22.3 Solar lentigines on the hands (a) before and (b) after combined OT and Easy TCA® treatment. Daily care consisted of DHEA Phyto® and Blending Bleaching® cream.

or even hypertrophic scars may develop (see the section on hyperpigmentation in Chapter 37).

Precisely AKs are less permeable to acid solutions than the normal skin surrounding them, and the frosting on the hyperkera-

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Figure 22.4 (a, b) An excellent indication for OT: the patient has a few scattered lentigines that do not justify a peel to the papillary dermis: a combination of OT and Easy TCA® is ideal.

A

B

tinized area appears (much) more slowly. OT should therefore be applied first only to the hyperkeratinized area and should not be allowed to run over onto the neighboring skin. If too much OT is applied in an attempt to achieve frosting more quickly, the neighboring skin may be damaged by the acid solution. Clinical experience shows that it is preferable to have uneven frosting on the AK during the first OT session, as a second application can be made a few weeks later, just before the fourth application of Easy TCA® that always accompanies the OT (see below).

Once only (on face)

6 weeks’ care 1st OT before 1st ETCA

2nd ETCA

®

Concentrated TCA has a strong potential to stimulate melanocytes, and post-inflammatory hyperpigmentation (PIH) is common when OT is used as monotherapy without the blocking action of Easy TCA® (ETCA) and without reducing melanocyte activity beforehand. PIH can also occur when the contact time between the cotton bud soaked in OT solution and the skin is too long – although not long enough to trigger scarring. Unlike ETCA solution, OT does not protect the patient’s skin against inflammatory and free-radical attacks after the peel. Applying OT correctly and combining it with ETCA helps to avoid almost all pigmentary changes, whereas applying OT on its own causes them in over 60% of cases. The method for combined application is simple: OT is applied as described above; ETCA is applied to the whole area, including the lesions that have just been treated with

3rd ETCA

2nd OT before 4th ETCA

Figure 22.5 OT peel combined with ETCA on the face.

2 weeks

The application of OT should ‘moisten’ the lesion. If it still looks dry immediately after the one dab of OT, more solution should be applied. The OT should be allowed to dry completely; frosting should now be clearly visible. Frosting on the face appears far more quickly than on the body (e.g. hands and forearms), and with a smaller amount of the product! One single dab of OT is enough most of the time to treat SL on the face. However, three or four dabs may be necessary to treat AK on the body. Excess solution and any unnecessary drips or runs should be avoided.

Combined with Easy TCA

1 week 1 week 1 week

2 weeks 2 weeks

6 weeks’ care 1st OT before 1st ETCA

2nd ETCA

3rd ETCA

2nd OT before 4th ETCA

Figure 22.6 OT peel combined with ETCA on the body.

OT, as soon as there is sufficient frosting from the OT. The protein coagulation caused by the OT does not allow the less concentrated ETCA to penetrate. It is unadvisable to apply ETCA before OT, as ETCA permeabilizes the epidermis and the OT would penetrate too deeply. The two peels are repeated at different intervals: ETCA is repeated once a week on the face and once every 2 weeks on the body; OT is repeated once every 3 weeks on the face and once every 6 weeks on the body. Figures 22.5 and 22.6 show how the two peels work together and how often they should be repeated.

Treatment of solar lentigines SLs are brown macules 1–3 cm in diameter that tend to converge and are found on 90% of Caucasians over 60 years old (Figure 22.7). They are often seen on people of

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Before any treatment, a differential diagnosis should be made between SLs and freckles, certain types of flat seborrheic keratoses, early pigmented AKs, lentigo maligna, junctional nevus and some acanthomas. There are different ways to treat solar lentigines on the face, hands, neck and décolletage, from laser to pulsed light, cryotherapy, dermabrasion and peels. Applying a combination of OT and ETCA to solar lentigines on the face is a simple, inexpensive and effective option (Figure 22.8). On the face, just a single dab of OT is enough to coagulate the skin locally to the reticular dermis. ETCA is applied immediately after OT, over the whole face, following the basic protocol (pinpoint frosting). The epidermis is more impermeable on the décolletage, and sometimes two dabs of OT are needed to obtain frosting. ETCA is applied over all of the neck and décolletage immediately after OT until pinpoint or cloudy white frosting occurs. Sometimes, SLs on the hands and forearms do not frost until after three or four applications of OT. When the frosting from the OT is satisfactory, three successive coats of ETCA are applied on the hands and forearms; there should be no further frosting from the ETCA, however. If any frosting starts with the second coat of ETCA, a third coat should not be applied.

Figure 22.7 Solar lentigines.

Treatment of actinic keratoses Actinic keratoses

Asian origin as well. They can, however, appear on the skin of much younger subjects after acute or chronic UV exposure. They can disappear partially or appear more diffuse when UV exposure stops. Melanocyte proliferation varies, but sometimes the melanocytes in the basal layer of the epidermis can increase to such an extent that the keratinocytes in the same layer seem to be replaced by melanocytes. The structure of the epidermis is hyperplastic and less permeable to the acids. Melanocyte abnormalities have been detected, and this suggests a potential relationship between SLs and lentigo maligna, but no clear link has been established to date between the two disorders. They are difficult to treat unless all the melanocytes involved are destroyed. Theoretically, this is an epidermal problem, but the treatment has to go deeper, as the basal layer does not form the classic, perfect sine wave that we see in the books. The basal layer of an SL typically takes on the form of a ‘golf club’ buried deep in the dermis; it merges with other ‘golf clubs’ and eventually creates a deep network. Conventionally, SL are treated with cryotherapy or laser (Q-switched ruby laser), but it is preferable to treat them with deep and very localized6 peels, which give excellent long-term results. Effective daily sun protection is essential.

AKs can be an early stage in the development of squamous cell epithelioma (SCE) or basal cell epithelioma (BCE). These are the most common types of skin cancer in humans, mainly caused by exposure to UV radiation. AK are usually 1–3 mm in diameter, but can sometimes reach 2 cm (Figure 22.9). Most AKs remain asymptomatic, but some can become pruritic or inflammatory. Growing AKs reach up to 3 cm in diameter and it is hard to distinguish them from Bowen’s disease.7 Pigmented AKs should be analyzed histologically to distinguish them from SL or melanoma in situ (lentigo maligna). Moreover, any recent change in the appearance of the AKs could indicate that they are becoming malignant. Until recently, AKs have been considered as potentially premalignant lesions, but some authors suggest they should be considered as an intraepidermal cancer, an early SCE. This classification8 has not been widely retained, as many SCE lesions appear without a ‘preclinical’ AK stage.9 Histologically, AKs are defined by the presence of abnormal keratinocytes in the basal layer of the epidermis; the thickness of the epidermis varies, and it can be anything between atrophic and extremely hypertrophic. On the lateral edges, there is often a clear border between the abnormal areas and the neighboring normal

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Figure 22.8 (a) Solar lentigines before treatment. (b) Localized frosting from OT. (c) Results after one OT treatment and four ETCA peels.

Figure 22.9 C

Actinic keratoses of different diameters.

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Figure 22.10

Figure 22.12

Precise application of OT solution to the lower limb.

The speed with which OT penetrates gives an idea of how keratinized the lesion is. If there is a lot of keratinization, the solution penetrates more quickly on the edges of the lesion.

areas. In the large majority of cases, the keratinocyte abnormalities do not spread to the appendages (whereas they do in Bowen’s disease), except in the case of proliferating AKs. When treating AKs, the risk of them turning into malignant SCE must be taken into account, although fortunately this rarely happens; effective treatment of AKs reduces the risk of developing SCE in the long term. Cryotherapy, curettage, surgery, electrodessication, 5-fluorouracil (5FU), carbon dioxide laser, photodynamic therapy (PDT), dermabrasion and chemical resurfacing with peels are all recognized as valid options in the treatment of AK .9 Given that a more aggressive treatment gives the patient better protection from recurrences, applying a peel such as

OT seems to be a good option for the treatment of AKs and SLs (Figures 22.10 and 22.11). Keratin is relatively impermeable to acids, and the frosting on the AK usually appears slowly and unevenly (Figure 22.12). The doctor has a natural tendency to apply more coats of OT too quickly, but there is then a risk of overpeeling and burning the skin deep down. Once through the keratotic layer, the acid can penetrate the dermis very rapidly, like a river in spate breaking the flood barriers that held it back. The acid must be given time to penetrate before being applied to the lesion again. The acid spreads once it has passed through the keratosis and reached the dermis, and can then work from underneath, undermining the keratosis. It is not necessary, therefore, to apply too much of the product. Besides, if the results are inadequate after the first treatment, the application can be repeated after 3–6 weeks, depending on whether the keratosis is on the face or body, respectively. ETCA should be applied on both the face and the body after OT to reduce the risk of pigmentary changes.

Post-peel care

Figure 22.11 OT can be used to treat numerous lesions, as long as the healthy skin between them is not touched.

At the end of treatment, the doctor can apply a corticosteroid cream to the lesions treated with OT to limit the inflammatory reaction. This application should not be repeated until after more than 72 hours. Between peels and for at least 6 weeks after the last peel, the patient should apply effective sun protection10 3 times a day after Blending Bleaching® cream. The patient should be warned not to touch or pull off the scabs: these are normal and to be expected (Figure 22.13). Vaseline® can be applied to the scabs to enhance healing. After 6 weeks of skin regeneration, the patient should use daily care products that are suited to his or her skin.

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much solution, too much pressure on the cotton bud or too long a contact time with the skin. Treatment consists in careful use of corticosteroids, tyrosinase inhibitors and effective sun protection (see Chapter 37).

Pigmented ring A full or partial pigmented ring is sometimes seen to persist when the solution has been applied between lesions. Treatment consists in applying OT to the ring during the next peel session. This can be avoided by letting the OT go slightly beyond the visibly pigmented zone at the end of the application. A

Persistence or recurrence of the lesion An SL or AK will persist without any change unless the acid goes deeper than the epidermis and penetrates the deep dermis. The lesion will recur if it has not been completely destroyed by the acid as a result of a technical error or because the lesion is unexpectedly deep. A differential diagnosis is necessary before any more OT can be applied. Lip & Eyelid® phenol solution can be applied locally, followed by 24 hours’ occlusion, in the case of recurrence or resistance to OT (see Chapter 30).

Depigmentation or scarring

B

Figure 22.13 (a, b) Normal scabbing 8 days after the application of OT.

Complications Prolonged erythema The erythema that always follows the application of OT usually lasts for 2–3 weeks. There may be prolonged erythema if too much OT has been applied as a result of too

Hypertrophic scars can be treated in the classic manner by corticosteroid injection and long-term use of a silicone sheet dressing (see Chapter 37). If OT has penetrated too deeply and has destroyed all the melanocytes in the area, it can cause hypochromic or achromic scarring. The situation depicted in Figure 22.14 may result from different causes: either because a pure TCA solution at 80% m/m was applied,11 or because the OT-type solution was applied too liberally and left too long on the skin. From the appearance of the patient’s skin in Figure 22.14, it seems likely that undiluted 80% TCA has been used or a low-grade copy of OT solution has been applied too liberally to areas larger than 1 cm2. Even if the long-term prognosis is good with the right treatment, surgery is sometimes the only solution when the damage is extensive.

Post-inflammatory hyperpigmentation Post-inflammatory hyperpigmentation (PIH) is relatively easy to treat and tends to fade naturally without sun exposure. For its treatment, see Chapter 37. It should be remembered that nevi, melasma and patients with phototype V or VI are not indications for OT (Figure 22.15).

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Figure 22.15 PIH after application of OT to nevi. Nevi are not an indication for OT.

Figure 22.14 A combination of post-inflammatory hyperpigmentation around depigmented areas, which are in turn centered around a scar, is common when a large excess of TCA is applied to skin of phototype IV or V.

■ Phototypes V and VI should not be treated – application of OT should be restricted to phototypes I to III, or IV. ■ Scabs should not be pulled off in the post-peel period. ■ Aggressive use of OT can cause scarring and/or pigmentation problems. Intense application of OT can cause patches of erythema that can persist for up to 3 months. This prolonged erythema can be treated by the application of topical corticosteroids and total sunblock.

Precautions ■ OT is a strong peel, and the indications and application method should be followed strictly. ■ Seborrheic keratoses and flat warts do not respond well to OT. They can be treated with shave excision followed by a single application of ETCA. ■ OT should not be used on lesions more than 1 cm in diameter. Larger lesions should not be treated, even partially, with OT. ■ Concentrated 80% m/m TCA must not be applied to the skin before it has been mixed with the base solution. ■ The contact time between the skin and the cotton bud must be brief. ■ OT should always be used in combination with ETCA, as well as Blending Bleaching® cream and sun protection (50+ then 25+) after the peel.

Treatment of AKs and SLs with ETCA OT may sometimes be too strong for the treatment of small AKs or SLs. Superficial lesions can also be treated with ETCA (Figure 22.16).

Phase 1 With a cotton bud, ETCA is applied only to the lesions to be treated. The peel solution is left to dry, following which additional coats are applied until pure white frosting is achieved. Each coat should be left to dry completely before the next coat is applied.

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B

Phase 2 After pure white frosting has appeared on the lesions, ETCA is applied to the rest of the face following the basic protocol. The protocol to the Grenz zone reduces the number of small superficial AKs or SLs, as well as lesions that are too small to be seen by the naked eye.

Treatment of AKs and SLs with a full-face peel to the papillary or reticular dermis AKs and SLs have been improved – sometimes temporarily – by peels to the papillary dermis (see Chapter 23). A full-face phenol peel is the most effective and long-lasting treatment for keratoses and solar lentigines (see Chapter 30). C

Figure 22.16 (a–c) Solar lentigines and photoaging treated with ETCA. The areas with lentigines are treated more deeply (pink–white or even pure white frosting) than other areas (pinpoint frosting). Daily care comprised Blending Bleaching® and DHEA Phyto®.

Notes 1. Using OT on patients with phototype IV or dark Asiatic skin should be discussed with the patient, because of the risks of pigmentary changes. 2. Three times a day for patients with phototype IV.

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3. Presentation boxes vary from country to country; it is best to read the instructions that come with the box. 4. It is also possible to inject the peel solution directly onto the tip of the cotton bud. They usually take a volume of 0.12–0.14 cm3 of solution, except for cotton buds from Asia, which are finer. 5. There is also a special applicator in the OT kit. 6. OT is a solution that is applied only on the lentigines to be treated and not on the surrounding skin. 7. Bowen’s disease, also called erythroplasia of Queyrat or prickle-cell carcinoma in situ, is a premalignant lesion.

8. The ‘KIN’ classification, in which the degree of intraepidermal invasion by abnormal keratinocytes is classified as (I) slight, (II) moderate or (III) severe. 9. Miller SJ, Moresi M. Actinic keratosis, basal cell carcinoma and squamous cell carcinoma. In: Bolognia JL, Jorizzi JL, Rapini RP (Eds.), Dermatology. St Louis, MO: Mosby, 2004: 1677–96. 10. Melablock HSP® 50+ between sessions and for at least 1 week after the last peel. Thereafter, Melablock HSP® 25+ is enough for the 6 weeks of skin regeneration. 11. Which can happen if the doctor does not prepare the solution himself and an inexperienced assistant is given this essential task.

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23 Trichloroacetic acid to the papillary dermis: Unideep®

Introduction Trichloroacetic acid (TCA) in a simple aqueous solution (TCA–SAS) is the peel most widely used to partially or completely remove the papillary dermis. Strict pre-peel preparation is required to even out penetration, reduce melanocyte activity and accelerate post-peel re-epithelialization. The main purpose of post-peel care is to counter complications (see Chapter 14). Unideep® was designed to make pre-peel preparation as easy as possible, at the same time as maintaining rapid reepithelialization and limiting the risks of post-peel complications. Unideep® is a by-product of Easy TCA® (ETCA) ‘technology’ and is a medium-depth peel that reaches the papillary dermis.

Description The Unideep® kit contains a bottle of base solution (which has to be activated by mixing it with 50% m/m TCA), two tubes of post-peel mask cream, two applicators, a glass bowl and an instruction leaflet (Figure 23.1). Unideep® is a saponified and stabilized TCA peel that contains 23% m/m TCA. It is a good peel for patients who

Figure 23.1 Unideep® kit for two patients: a bottle of base solution, two tubs of post-peel mask and two applicators.

want quick results with a lower risk of side-effects than TCA–SAS. The Unideep® solution coagulates proteins in the epidermis and the papillary dermis, but not the proteins of the vessel walls: the resulting frosting is an even pink–white rather than pure white. The skin is regenerated by the keratinocytes that have remained intact in the deeper dermal papillae, the pilosebaceous units and the sweat glands. These keratinocytes regenerate a new epidermis, while the dermal action of Unideep® stimulates fibroblast production: collagen, elastin and glycosaminoglycans. The post-peel mask cream should be applied twice: 50% immediately after the peel and the remaining 50% the morning of the first day after the peel. It stimulates the skin and breaks the vicious oxidative circle: ‘inflammation ↔ free radicals’, and accelerates healing time. It also helps to limit the vicious inflammatory circle that follows any medium-depth peel and counters post-peel pigmentary changes.

Indications The main indications for a TCA to the papillary dermis are the following: photoaging, non-active acne, hyperpigmentation, melasma, chloasma, keratoses and fine lines. Unideep® can also get rid of most freckles (Figure 23.2). A single peel is usually enough to achieve deep regeneration of the skin, but it may sometimes be necessary to repeat the peel for perfect results. Unideep® can be used: ■ as monotherapy ■ in combination with Only Touch® in the treatment of solar lentigines or actinic keratoses ■ in combination with phenol (Lip & Eyelid® formula) as an evening-out peel after treating deep wrinkles round the mouth or eyes (see Chapter 36). The downtime with lips and eyelid (1 week) is the same as for a peel to the papillary dermis. ■ as a local application (e.g. on the forehead only) in combination with a more superficial peel (ETCA) on the

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A

B

A

C

D

B

Figure 23.2 (a) Natural darkening of freckles 24 hours after the application of Unideep®: they will disappear 5–6 days after the peel. (b) Freckles 1 month after a Unideep® peel.

E

rest of the face so that the patient can keep up his or her social life more easily (Figure 23.3). It is sometimes difficult to choose between doing a single Unideep® peel and four ETCA peels. Overall, the two peels offer patients the same results. However, one Unideep® is sometimes more effective than ETCA when treating pigmentation problems originating in the dermis, whereas the opposite is true in the treatment of photoaging, when strong stimulation is needed to regenerate a healthier-

Figure 23.3 (a–c) Combination of peels: Unideep® has been applied to the forehead only, and ETCA has been used to treat the rest of the face that is not so badly damaged by the post-acne pigmentation. (d–e) Forehead view of a full face Unideep®.

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looking skin. The best indication for Unideep® is in patients with skin phototypes I to III. The risk of PIH must be discussed with patients with darker skin phototypes.

Method of application Preparing the skin The skin is cleaned with Skin Tech’s cleanser, disinfected with alcohol and degreased with acetone. To degrease the skin properly, it needs to be wiped with acetone several times. It is wise to reduce melanocyte activity in patients with a skin phototype higher than Fitzpatrick III. Patients who are prone to labial herpes should be given preventive treatment.

Figure 23.4 Unideep® applicator held in a clamp.

Preparing the applicator The ideal applicator is a cotton dental swab held in a clamp (Figure 23.4): this makes it easier to handle and to apply the right amount of pressure. The cotton swab in the kit is too long, needs to be cut in two equal halves for use as an applicator.

Preparing the peel solution Following the instructions in the kit, the doctor adds the required amount of TCA.

Anesthesia Most patients can easily tolerate this treatment without nerve block anesthesia if the peel is done slowly, cosmetic unit by cosmetic unit. More squeamish patients may prefer to have intravenous sedation, along with nerve blocks.

Analgesic medication The patient can take a paracetamol (acetaminophen) plus codeine tablet half an hour before going to the doctor. The patient may also benefit from taking a second tablet 1 or 2 hours after the peel, at the peak of the discomfort.

Cryoanesthesia Any pain can be eased considerably by simply chilling the skin before the first application and between the different coats. Cold packs (e.g. 3M’s products: Figure 23.5) or a ventilator can be used for this. If neither is available, a bag of ice or simply contact with a cold surface (e.g. an empty bottle) soon eases the burning sensation. Cold packs can be applied directly on the acid if they have been dried beforehand.

Figure 23.5 Cryoanesthesia with 3M’s cold pack.

Nerve blocks A local anesthetic (nerve blocks) may be necessary for sensitive patients. Application is completely painless with nerve blocks. There are more details on how to perform blocks in Chapter 33.

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Vocal anesthesia Vocal anesthesia or medical hypnosis is enough in many cases to alleviate the burning sensation of the acid in Unideep®.

is applied on the area that has just been treated before moving on to the next area. The face is done in three stages: forehead and temples, nose and cheeks, and the chin area (Figures 23.6 and 23.7). The post-peel cream soon stops the burning sensation.

Topical anesthesia For reasons outlined in Chapter 33, anesthesia with a topical cream should not be used before a peel to the papillary dermis.

Applying the solution Peel applied with nerve blocks and sedation The solution is applied to the whole face and left to dry. Additional coats are applied to achieve an even pink–white frosting and signs of epidermal sliding. The post-peel mask cream after the peel,1 is applied to the whole face.

Peel applied with nerve blocks With nerve blocks, application is painless and quicker. After nerve blocks have been applied to the area under treatment, the peel solution is applied to the face: it is applied on the forehead and temples first, until an even pink–white frosting is obtained; the post-peel mask cream

A

B

Figure 23.6 The first coat of Unideep® often produces uneven frosting that will even out with the second coat.

Figure 23.7 (a, b) Sequenced application.

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Figure 23.8 Epidermal sliding. A

Peel applied without nerve blocks or sedation Ideally, the patient has taken an analgesic (paracetamol plus codeine). The peel solution is applied to each cosmetic half-unit (e.g. half of the forehead) until even pink–white frosting and epidermal sliding2 occur (Figure 23.8), all the time making the best use of cryoanesthesia and vocal anesthesia. The post-peel cream soon alleviates the pain caused by the acid, and it is possible to do a peel to the papillary dermis without anesthesia.

Post peel mask application After frosting occurs, the solution should not be neutralized – rather, 5 g, or half a tube, of post-peel cream should be applied to the face (Figure 23.9). It should be rubbed in, and the solution and cream left to work until the next morning. The patient then applies the rest of the post-peel cream to the face, after washing with neutral soap or cleansing lotion.

B

Figure 23.9 (a, b) Two different types of flaking (on the sixth day).

Days 4–6 Follow-up and post-peel care Days 1–4 Renutriv ACE Lipoic Complex® is applied three times a day. The skin dries and starts to peel on the second or third day. The patient is seen on the third day to check the condition of the skin and to make sure that there is no secondary infection.

Pure Vaseline® is applied to facilitate flaking. The patient is seen on the seventh day.

From day 7 and for at least 6 weeks ■ Phototypes I to III: hydrating and antioxidant cream, combined with effective sun protection.

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■ Darker skin phototypes: to be treated very carefully: Blending Bleaching® morning, midday and evening, combined with effective sun protection and complete sun avoidance. The skin should be washed with pure water between the two applications of creams.

Specific precautions for dark phototypes

Precautions and complications

The techniques described are for patients with phototype I to III. To treat patients with a higher phototype (IV to VI), extra precautions are needed: the skin should be prepared by application of Blending Bleaching® cream twice a day for 2–3 weeks before the peel; sun protection cream (Melablock HSP® 50+) should be used, and exposure of the skin to daylight should be avoided. The peel should be applied carefully, and great care should be taken not to have any excess solution. After the peel, Blending Bleaching® cream should be applied as soon as possible, when flaking has finished, and continued for 6 weeks after the peel.

Potential complications from this type of peel are described in detail in Chapter 37.

Pigmentary changes

General precautions

Pigmentary changes can be treated with three or four ETCA sessions and Blending Bleaching® cream. Total sun protection is essential.

From the sixth week, for all allowed phototypes and for at least 6 months, the patient should use a care cream best suited to his or her skin (see Chapter 3). Results can be maintained in the long term by repeating the peel as and when the doctor thinks it necessary (once a year, once every 2 years, once every 3 years, ...).

Unideep® is a peel to the papillary dermis: it is essential to follow the indications and method of application. Misuse of Unideep® could produce the classic side-effects of medium-depth peels. The patient should be warned not to scratch. Concentrated TCA should not be applied to the skin without mixing it with the base solution.

Notes 1.

2.

Half of a tube of cream should have been applied by the end of the peel. The other half is given to the patient for an additional application on the evening of the peel and the morning after. The sliding occurs as the TCA coagulates the anchor proteins in the dermis and epidermis. Pinching the skin makes the epidermis slide over the dermis.

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24 Resorcinol: Unna’s paste/Jessner’s solution

Chemistry Resorcinol (Figure 24.1), also known as resorcin, metadihydroxybenzene, 1,3-dihydroxybenzene, and 1,3-benzenediol, has a molecular weight of 110.11 and a relative density of 1.272. It is slightly more acidic than phenol, with a pKa of 9.15. It is soluble in water, alcohol, ether and glycerol. It comes in the form of white needle-shaped crystals. Resorcinol crystals oxidize easily, and turn pink on contact with light, air or iron.

Figure 24.1 Chemical structure of resorcinol.

Properties of Resorcinol1 Antiseptic Resorcinol has antiseptic properties similar to those of phenol, and was used to dress minor wounds before the era of antibiotics. It has antifungal properties, and was also applied on chancroids and syphilitic ulcers. Its bactericidal effect is 30% of that of phenol.

Proteolytic and protein coagulant Resorcinol is a phenol derivative and its proteolytic power is about 1/40 of that of phenol. It breaks the weak hydrogen links of keratin and acts as a proteolytic agent, even at concentrations as low as 5%.2 At higher concentrations, it can also precipitate skin proteins and become a protein coagulant.

Antipruritic Resorcinol is used in many antipruritic formulations, especially in chronic kidney dialysis. It is mainly used in paste

form, usually called Unna’s paste, or in solution form, as Jessner’s solution or Combes’ solution.

Indications for resorcinol ■ Acne is a good indication for resorcinol. ■ Folliculitis: resorcinol is effective in this indication, even on the back. ■ Comedones: resorcinol eliminates comedones. ■ Scars: superficial scars can be slightly improved, but deep, ‘ice-pick’, scars or extended scars do not respond to this treatment. ■ Photoaging: solar keratoses, pigmentary lesions, epidermal atrophy and solar elastosis are indications for resorcinol if their histological origins are not too deep. ■ Dyschromias: resorcinol has been used with varying success to treat melasma, chloasma, post-inflammatory hyperpigmentation (PIH) and post-acne pigmentation. It can get rid of some freckles. Resorcinol is contraindicated in patients with phototypes IV to VI because of the risk of pigmentary changes.

Obsolete indications Manquat’s ‘Elementary Treatise on Therapeutics’ (1903) describes the heroic experiments of colleagues who tested, on their own persons, the effects of medication taken in ever-increasing doses until convulsions ensued (ingestion of 10 g of resorcinol in 15 minutes). The indications officially retained in 1903 were the following: ■ Antipyretic: resorcinol was considered a dangerous and rather ineffective antipyretic. ■ Antiseptic: the antiseptic use of resorcinol was recommended for surgery in place of phenol, as it is less toxic and less caustic. ■ Anesthetic: resorcinol acts as a mild local anesthetic. ■ Psoriasis and eczema: Unna used it in ointments of 10–20% to treat psoriasis, and from 2% to treat ‘pityriasis capitis’ and seborrheic eczema.

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Histological changes Epidermal After a resorcinol peel, the superficial stratum corneum comes away from the germinative layer in the stratum granulosum.3,4 The basal layer shows increased mitosis and accelerated turnover. The total thickness of the epidermis therefore increases, to the detriment of the stratum corneum, and the skin appears more hydrated.

Dermal The fibroblasts in the papillary dermis are stimulated and proliferate: they synthesize a large quantity of new collagen, which is deposited in bands beneath the epidermis (in the Grenz zone). The intercellular matrix is enriched in glycosaminoglycans. Further down, short-lived but rapid vasodilation occurs, that signaling the presence of dermal inflammation. Four months after the peel, the histological changes in the dermis, apart from vasodilation, are still visible. The intercellular space has a higher concentration of glycosaminoglycans, and there are more collagen and elastic fibers in the dermis.

Ingredients of resorcinol peels Many classic formulas use resorcinol combined with oldfashioned ingredients that may now sound somewhat strange and mysterious.

Wool fat (lanolin) Wool fat is obtained from extracts of soapy water in which sheep’s wool has been washed or extracted with solvents from grease wool. Lanolin is obtained by purifying the grease (or suint). This emollient is a yellow and viscous substance, consisting of fatty acids and fatty acid esters.

Benzoin Benzoin, or gum benzoin, is a resinous secretion obtained from cuts made in the trunk or branches of the Styrax benzoin tree. It contains coniferyl benzoate, benzoic acid, benzyl cinnamate, vanillin (a phenol aldehyde) and a number of triterpenes.5 Benzoin resin is a local irritant. A hundred years ago, it was considered to be an aphrodisiac when ingested. At the beginning of the 20th century, benzoin was mostly administered as an antiseptic in fumigation to treat chronic respiratory diseases: it was thrown in small pieces onto a heated metal plate.6 Tincture of benzoin is obtained from dissolving (1/5) benzoin in alcohol.

Ceyssatite and zinc oxide Ceyssatite is a white clay (from Ceyssat in France) whose absorbent properties, similar to those of kaolin, have been widely used in cases of hyperhidrosis and eczema. Ceyssatite and zinc oxide have an exfoliating and desiccant action that is absolutely essential for resorcinol to act evenly.

Kaolin Kaolin is a white clay mostly made up of silicon dioxide, aluminum oxide, iron oxide, titanium dioxide, magnesium oxide and sodium oxide. It was first found in China, in KaoLing. European kaolin is formed by the decomposition of feldspath in granite rock in Brittany or Limousin. Kaolin has good absorbent properties and is gentle on the skin; it is very well tolerated by very sensitive or reactive skins. It is used for its healing, antiseptic7 and anti-inflammatory qualities and its excellent coverage in Unna’s paste formula.

Benzoic acid Benzoic acid is a weak carboxylic acid.8 It is not very soluble in water (3 g/l at 25°C) and has a molecular weight of

Petrolatum (Vaseline®) This neutral, semisolid unctuous substance, tasteless and odorless, is derived by distilling or purifying petroleum. Thin layers are transparent. Petrolatum is the official generic name; Vaseline® is a (genericized) trademark.

Benzoin axunge Axunge is a greasy excipient used to reduce erythema. It is, in fact, simply lard – i.e. grease extracted from pig’s epiploon. Benzoin axunge is prepared by adding 5 g of tincture of benzoin per kilogram of melted axunge and stirring until the mixture has cooled.

Box 24.1 Benzyl and phenyl Benzene is a molecule Benzyl is a group that has to be attached to something else. It is methyl benzene whose methyl group (CH3-) has lost a (H-) Phenol is a molecule; the suffix -ol means that it has a (-OH) radical. Phenyl is a group that has to be attached to something else. It is a benzene minus a (-H) or a phenol without its (-OH) group.

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122. It comes in the form of a white silky-looking solid and is used as an antiseptic and antifungal agent or as a preservative in some fizzy drinks.

Resorcinol pastes Formulations of different pastes The formulations for resorcinol paste most often used in the past are shown in Table 24.1. The preparation of this paste involves a lot of work for the pharmacist, who has to use centrifugation and/or ultrasound. The resorcinol crystals have to be thoroughly ground in a mortar before making up the paste to make sure no big crystals remain in it.9 The resulting mixture will be more homogenous and easier to spread. Unna’s paste does not remain active very long, as it oxidizes rapidly. The doctor should therefore always use a freshly made paste. Another formulation contains resorcinol, olive oil, kaolin, zinc oxide, petrolatum and wool fat.

Table 24.1 Formulations of resorcinol paste

Resorcinol Zinc oxide Ceyssatite Benzoin axunge Benzoic acid Dermagor® cold cream

50%a,b

50%c

30%c

40 g 10 g 2g 28 g

60 g 15 g 3g

30 g 15 g 5g 50 g

2g 40 g

a

Trauchessec JM, Vergereau R. Les peelings. In: Bartoletti CA, Legrand JJ (Eds.), Manuel pratique de médecine esthétique, 2nd edn. 159–67. Paris, France, Société Française de Médecine Esthétique. b Rusciani L, Rossi G, Bono R. Les peelings chimiques. J Med Esth et Chir derm 1993; XIX (78) 78–80. c Cohen, Letessier, Préparations magistrales en Dermatologie. In: Arnette (Ed.), Collection des Manuels pratiques de médecine esthétique, 1989, Paris.

Preparing the peel Preparing the skin The best results are achieved when the skin has been prepared for 15 days beforehand; see Chapter 2. If the skin has been prepared with tretinoin or alpha-hydroxy acids (AHAs), if the patient has used products (benzoyl peroxide) or techniques (scrub, or abrasion with a massage glove) that increase the permeability of the stratum corneum, the resorcinol paste should not be left on too long.

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Allergy test An allergy test should be done before each resorcinol peel, by applying a small bit of paste on the skin behind the ear for 20 minutes: this provides a minipeel to evaluate the risk of allergy. This allergy test should be carried out like a localized peel: the skin must be allowed to dry and flake: the normal action of resorcinol on this thinner and more sensitive skin should not be confused with an allergy. Any hint of an allergic reaction (e.g. swelling, redness, itching, blistering or weeping skin) should rule out this peel immediately. There is one significant cloud on the horizon: the allergy test itself can make a patient who was not previously allergic to resorcinol allergic. It is therefore not wholly predictive.

Clean and degrease The skin should be disinfected (with alcohol) and degreased (with ether or acetone) before applying the paste.

Hydrating the patient The patient must be well hydrated to facilitate diuresis and elimination of the metabolites of the resorcinol. An intravenous drip of saline solution should be set up, but if this is not possible, the patient should be asked to drink several glasses of water before the resorcinol is applied.

Preparing the paste Resorcinol paste is compact and difficult to apply. It is easily softened by putting it in a bain-marie at 45° for around 10 minutes. If that is not possible, small blocks of paste should be applied to the patient’s skin. Heat from the skin will slowly ‘melt’ the paste and make it easier to spread, although the resorcinol may penetrate too deeply where contact time has been longer.

Analgesia and anesthesia No analgesia or anesthesia is necessary. A resorcinol peel is neither painful nor stressful – besides which, resorcinol has a mild local anesthetic effect.

Settling the patient in The patient lies down during the peel and for half an hour afterwards.

Applying resorcinol paste Application The eyelids are protected with Vaseline® or damp cotton (make-up remover) pads. A thick coat of paste is applied

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with a tongue depressor – enough to make a mask of even thickness. The paste should not be applied to the eyelids or mucous membranes. The paste has to be applied a little way into the hair, and should just touch the eyebrows. On the jaw area, as with phenol, the paste is applied up to 2 cm below the upper jaw. The paste should be rubbed gently to make it more homogenous. Resorcinol paste is often applied on the décolletage and back. Great care must be taken in these areas, however, as the extent of the surface area treated can induce toxicity. Large surface areas should be treated in several stages, and a rest period between two applications will help the body eliminate the metabolites from the detoxification of this phenol compound.

Contact time for a facial peel The contact times given and commented on below are a rough guide only, and should be modified to suit the patient’s skin type, the disorder being treated, the results desired, etc. First application (first day): contact time 10–25 minutes. A few minutes after the first application, the patient feels some heat and then a tolerable burning sensation. This sensation starts where the resorcinol has penetrated most rapidly. The cheeks are usually more permeable than the forehead. The areas where the patient first feels burning are the first to be cleaned of the resorcinol paste at the end of the peel. The sensation of acid ‘burning’ can sometimes become intense, and a yellow serous fluid may be seen to weep through the partially lysed epidermis. In this case, the patient should be given an analgesic for the first night: paracetamol (acetaminophen) plus codeine. After the first application, the skin becomes red in color, as if sunburned. Second application (second day): contact time 20–30 minutes. The resorcinol is left to work for longer: 10 minutes more than the first session, or even 15 minutes more on areas that did not react as well on the first application, mainly on the forehead. After the second application, the skin becomes brownish, and the patient’s social life is disrupted. Third application (third day): contact time 30–35 minutes. The third application must be carried out with extreme caution: if the ‘resorcinol membrane’ that is forming has modified the permeability of the skin, epidermolysis is present and the skin has been badly injured: rough handling (or paste that is too compact) could pull away the skin and sharply increase the risk of post-peel complications in the form of erythema and pigmentary changes. After the third application, a ‘resorcinol membrane’ has formed. It is made up of lysed and dried out corneocytes and keratinocytes, stuck together by any serous fluid seeping through the epidermis.

Contact time for a body peel The skin on the body is less permeable than the skin on the face, and the contact times will therefore be longer. On the first day, the contact time should be 30–50 minutes, on the second day 40–60 minutes, and on the third day 50–70 minutes. Once again, extreme caution is recommended in peels on non-facial skin because of its limited capacity to regenerate and because the extent of the area to be treated increases the risk of general toxicity.

End of the peel At the end of contact time, the paste is removed with a tongue depressor and a dry gauze pad. A small amount of paste can be left on the skin at the end of the peel so that a thin layer of resorcinol remains to give full results. It is not strictly necessary to take the paste off in the same order it was applied. It can be left to work longer in certain places to increase the strength of the peel locally – for example on the more resistant skin on the forehead. If the doctor wishes to remove all of the paste, the following solution can be used: tincture of Benzoin tincture of Quillaja10 rose water

50 ml 50 ml 100 ml

Immediate post-peel care The patient remains lying down for around half an hour after the peel. The back of the table is raised to take the patient gradually from a lying position to a sitting position, and he or she continues to be hydrated. The patient then goes home, with an analgesic or an anti-inflammatory to deal with any pain or unpleasant burning. 3M cold packs can help ease the sensation of heat. Resorcinol peels owe some of their effectiveness to the presence of siccative agents.11 Any topical hydration of the skin must therefore be strictly avoided until flaking has begun. Actual downtime will start after the second application of the resorcinol paste, and will last for 8 days. It is important to warn the patient about the downtime and explain clearly how the face will look during the week it is flaking. The ‘resorcinol membrane’ flakes from the fourth day. The more mobile areas of the face will flake first: around the mouth and eyes. The resorcinol membrane slowly cracks, making the skin look around 100 years old! It grips the skin in a straitjacket, making it difficult to speak and eat sometimes. The patient should anticipate a liquid diet for a few days: yoghurts, soups, broths, consommé, purées, etc. The patient must not pull off the strips of peeling skin. At the most, they can be cut off with scissors, without pulling the skin at all. The skin is pink and sensitive underneath the resorcinol membrane. As soon as flaking starts,

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the skin needs hydrating (vitamin E hydrating and antioxidant cream, or even Vaseline® if necessary). Effective sun protection (see Chapters 2 and 3) must be used permanently for 1–3 months. How long sun protection is used depends on the risk of hyperpigmentation (skin phototype IV, sunny climate, working outside, etc.).

Repeating the peel According to Unna, the resorcinol paste can be applied again as soon as flaking has finished. We are rarely called upon to repeat an application of resorcinol paste nowadays. The results of an Unna’s paste peel remain modest in relation to the complexity of the treatment and the downtime involved, and patients are not prepared to accept these conditions.

Jessner-type resorcinol solutions Formulations of different solutions Some authors use m/m instead of m/v, which changes the actual concentration of the active ingredients. It is also important to stress the need for the pharmacist to use the crystal form of the lactic acid and not the solution form. Lactic acid in fact comes in liquid form with a concentration of 85%. The pharmacist should use lactic acid crystals and not solution to prepare the Jessner solution. Moreover, different molecules, many of them unknown, are used to denature alcohol, to make it unfit for drinking, and there is a risk of potential chemical interactions with the acids. The alcohol used by the pharmacist must be pure, not denatured. Resorcinol solutions have been used at concentrations of 10–50% in alcohol or ether to treat keratoses. Resorcinol solutions have the distinct advantage of not having to be neutralized.

Eller and Wolf’s solution (1941)12 resorcinol (crystals) salicylic acid13 (crystals) lactic acid14 (crystals) rose oil alcohol 95°

17 g 8.5 g 8.05 cm3 0.05 cm3 ad 100 ml

Five to eight coats are applied one after the other with cotton, depending on the depth of peel desired and the skin type. Three coats produce frosting and six coats produce edema. Eller and Wolf recommended constant hydration of the patient before and after treatment.

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Urkov’s solution (1946) resorcinol salicylic acid lactic acid (solution) alcohol 95°

38 g 6.6 g 13 cm3 ad 100 cm3

After leaving the solution to rest for 24 hours and filtering it, UV exposure was what made it effective! Solutions not exposed to UV did not appear to work. The skin was also prepared by UV exposure, and the solution was applied five times, leaving each coat to dry before the next application. Urkov then applied an occlusive mask. This mask allowed the superficial layers to hyperhydrate by blocking transepidermal water loss (TEWL). The hyperhydration dissolved the salicylic acid that would have precipitated on the skin without occlusion and could not have penetrated, as only the acids in solution can readily penetrate the skin barrier. He then applied zinc stearate powder (which is antiseptic and anti-inflammatory). The erythema subsided in 5–6 days and exfoliation was superficial. The solution can be kept in the fridge for 10 days.

Jessner’s15 solution or Combes’16 solution (1950s) resorcinol (crystals) salicylic acid (crystals) lactic acid (crystals) ethanol 95° (not denatured)

14 g 14 g 14 g ad 100 ml

Jessner’s solution must be kept in a glass, light-protected, hermetically sealed bottle. It can be kept in the fridge for more than 2 years like this. When the solution oxidizes, it turns pink. Contact with the fingernails can turn them orange–yellow.

Other combinations Resorcinol solutions have been used in combination with glycolic acid, trichloroacetic acid (TCA) and 5-fluorouracil (5-FU). Many modified versions of Jessner’s solution have been presented, containing kojic acid, hydroquinone, etc. The effectiveness of these resorcinol solutions depends on skin preparation, skin sensitivity and thickness, the type of applicator and the force of application, the number of coats applied, the type of solution used, the quality of the solution’s preparation, etc. Moreover, products with a tyrosinase-inhibiting action (kojic acid, hydroquinone, etc.) only produce their effect in the long term. Single application of these products cannot treat melasma in any way. Only repeated applications, allowing the gradual absorption of products that inhibit melanocyte metabolism, can be considered as an effective treatment.

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Jessner’s formula Indications Jessner’s solution provides an exfoliating peel, effective in the treatment of acne and dyschromias of superficial origin.

Safety It is a relatively safe peel. Overpeeling is rare with this treatment, but phototypes IV to VI are still contraindicated because of the risk of pigmentary changes. Unlike resorcinol paste, Jessner’s solution does not cause dizziness, tinnitus or faintness. When applying the solution on large surface areas, however, it must be taken into account that the potentially toxic agents that it contains may be absorbed and are likely to be eliminated via the liver and kidneys. According to Rubin, applying Jessner’s solution on the face, neck and décolletage in a single session remains without danger of salicylism. Salicylism was described, however, again by Rubin, when doing Jessner peels together on the face, neck, arms and lower limbs.17

Standard application of Jessner’s solution (original formula) Preparing the skin Standard skin preparation increases the depth of penetration of Jessner’s solution and improves the results – at the same time as increasing the risk of complications. An allergy test is essential, especially because of the resorcinol in the formula. Cleaning and degreasing The skin is cleaned and degreased with alcohol and acetone. Care should be taken not to abrade the skin manually with the gauze pad while degreasing. Applying the solution Applying Jessner’s solution is about as painful as a TCA peel at 15%. It is applied gradually, leaving each coat to dry completely before applying the next coat. The strength of the peel depends on the number of coats applied; it is therefore possible to penetrate the skin gradually. Carelessly applying one coat immediately after the other would take the peel beyond the desired effect and increase the risk of complications. It takes time to do a peel with Jessner’s solution. The depth of action also depends on the force of application: the greater it is, the deeper will the acids penetrate. Patients with thin skin should be treated with lighter hand pressure than patients with thick skin. ■ Level 1: An even coat is applied to the area to be treated, regardless of the type of applicator (brush, cotton buds,

cotton balls, gauze pads, etc.18). It is always advisable to use disposable applicators to avoid any risk of transmitting infection. The first coat usually causes erythema and occasionally some pinpoint frosting. Some ‘pseudo-frosting’ can usually be seen after the ethanol has evaporated: this is caused by the ingredients of the solution, especially the salicylic acid, precipitating on the skin. Unlike genuine frosting, which is protein coagulation, ‘pseudo-frosting’ can be brushed off easily. The patient should be fanned with a hand-held or portable fan, to alleviate the ‘burning’ sensation and get rid of any unpleasant fumes. If the application remains at level 1, only a very slight drying of the skin will be observed afterwards. ■ Level 2: The skin is left to dry for 4–5 minutes between two successive coats. The second and third coats trigger more pronounced erythema and cloudy white frosting, as well as some pain and discomfort. The discomfort will last around quarter of an hour. Trauchessec19 applies the solution once a week until results are achieved. The first treatment consists of only one coat, the second of two, and the third of three coats of solution. After level 2, the patient’s skin feels dry and tight. The top layers of the epidermis, dried out by the solution, appear transparent but still stick to the underlying cells. Flaking occurs within 4–5 days. Locally, some areas may turn a brownish color where Jessner’s solution has penetrated more deeply than anticipated. After three coats, the stratum corneum separates from the skin, there is no blistering or epidermal necrosis, and the dermis is not directly affected. ■ Level 3: applying further coats deepens the effect of Jessner’s solution. The erythema becomes established and the frosting tends to spread over a wide area, sometimes over the whole of the treated area. Flaking is more pronounced, and the skin is brownish and comes away in long strips. This can last around 10 days. Downtime is common at this depth, even if there is rarely any scabbing.

Post-peel care The skin still feels tight and dry, but it should not be hydrated. When flaking has finished, the patient can wear make-up and should use effective sun protection. The patient must not help the flaking along at the risk of causing erythema and pigmentary changes.

Jessner’s as a preparation for a TCA peel Jessner’s solution can be used as a preparation for a deeper peel. Monheit technique The skin is prepared and cleaned in the usual manner. The Jessner’s solution is applied to level 1: erythema occurs,

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along with some localized pinpoint frosting at most. Five minutes should be left between each coat. The last coat is left to dry, and then TCA is applied – this will penetrate more quickly and more evenly20 because of the breakdown in the epidermal barrier function. It will also be more painful. This technique could be used on patients with thick and oily skin when better TCA penetration is needed.

Jessner’s as a preparation for an AHA peel A Jessner’s peel would improve and even out AHA penetration through the skin. Moy technique The skin is prepared and cleaned in the usual manner. Jessner’s solution is applied to level 1. The last coat is left to dry for 5 minutes, and then glycolic acid is applied until the erythema spreads. This is followed by neutralization. Because of the erythema already caused by Jessner’s solution, it is difficult to judge the progress of the AHA peel, and it is common for it to penetrate too deeply causing unexpected frosting. This more delicate technique should only be used for treating very thick and oily skins that can tolerate high concentrations of AHAs being left on the skin for long periods before neutralization.

Jessner’s for the neck and décolletage Jessner’s solution is applied in the usual manner, but at a rate of one peel every 2–4 weeks. Under no circumstances should the patient help the skin to flake, which could leave depigmented or hyperpigmented patches.

Jessner’s for keratoses To treat actinic keratoses with Jessner’s solution, the skin is first degreased carefully with acetone. Jessner’s solution is then applied once a week for around 8 weeks. This treatment is not very effective, however, as no more than 15% of the actinic lesions disappear.

Toxicity and side-effects J Andeer tested the toxicity of resorcinol at the end of the 19th century.6 He consumed gradually increasing doses of resorcinol and made objective and careful notes of the sensations he felt and the symptoms he developed. In this way, he tested a daily intake of 1 g of resorcinol, and gradually increased the doses until he was taking 10 g of resorcinol in 15 minutes. This triggered auditory, visual, muscular and proprioceptive symptoms, then convulsions with breathing difficulties and muscle contractions. He was fortunate

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enough to be able to report that all these phenomena disappeared after 5 hours of ‘resorcinol agony’. History does not tell us if he tried the experiment again to evaluate its reproducibility, but we know that other colleagues have tried the same kind of experiment on themselves with resorcinol and many other toxic agents as well. Although it belongs to the phenol group of chemicals, resorcinol has very different exfoliating properties and it is far less toxic than phenol itself. The routes of metabolic detoxification are mainly via the liver and kidneys. As a precaution, patients with liver or kidney deficiencies should be ruled out, as well as patients with arrhythmia and women who are pregnant or breast-feeding.

Toxicity Resorcinol is toxic by ingestion of an average dose of 6 g. Serious accidents have been described after ingestion of 3.5 g, however.6 It irritates the mucous membranes and the skin, and ingestion can cause methemoglobinemia, cyanosis, convulsions or even death. Cases of methemoglobinemia have been described after application on leg ulcers, but not after a peel on normal skin. The problem raised with the use of Jessner’s solution is more the fear of salicylism than the toxicity of the resorcinol itself. Cases of salicylism have been described after application of Jessner’s solution together to the face, chest, arms and legs.17 The size of the surface area treated, body weight and how well hydrated the patient is are all key factors: the risk of toxicity increases with the surface area treated. There is a greater risk in patients with low body weight and patients who are not well hydrated.

Secondary hypothyroidism Thyroid injury after chronic skin application of resorcinol has been reported several times. In 1977, Katin and colleagues21 published a case of hypothyroidism following regular application of a 2% resorcinol cream in a chronic dialysis patient suffering from pruritus. The mechanism of action seems to be as follows: the presence of a hydroxy group in the meta position in the resorcinol would block the metabolism of iodine by inhibiting the peroxidase needed to oxidize iodide into iodine, the only form that can be assimilated by the body.

Allergies Unna’s paste Allergies to resorcinol have been widely described. It is therefore wise to do a skin sensitivity test behind the ear 8 days before a resorcinol peel. Any contact with resorcinol can sensitize the patient (or the physician) to it, so the test

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must be repeated before each peel. The fact that the first peel does not trigger an allergic reaction is no guarantee that the next peel will not trigger one. Allergy to resorcinol is permanent – there is no point trying again. In the allergy test, a small quantity of Unna’s paste is applied to a patch of skin 2 cm × 2 cm behind the ear and left for 15 minutes. The test is read immediately and then again 48 hours and 5 days later – although Letessier3 recommends just one reading, after 4 days. It is important not to confuse an allergy with the skin’s natural response to the chemical peel applied behind the ear. A highly localized and normal skin reaction to the peel will occur: erythema followed by flaking. The appearance of any blistering or pruritus contraindicates any further contact with resorcinol completely and definitively. If a patient is allergic, Unna’s paste causes reversible facial eczema, with no cosmetic benefit.

Jessner’s solution The allergy rate to resorcinol is less than 0.1%.17

Hyperpigmentation Pigmentation disorders are relatively common after a resorcinol peel. Effective sun protection (see Chapter 3) must be used for 1–3 months after the peel. The people most prone to pigmentary changes are those who had pigmentation problems before the peel, those who take oral contraceptives or are on hormone therapy, and those who have a record of post-traumatic or postinflammatory hyperpigmentation or have a high density of melanosomes (phototypes IV to VI). Potential problems with pigmentary changes are treated in the usual manner, as described in Chapter 37. Pigmentation problems such as ochronosis after a resorcinol peel, also described in the literature, are more complicated to treat.

Prolonged erythema A few areas of mild erythema, which changes color with the cold, alcohol or emotion, can very occasionally last for several weeks. Erythema after a resorcinol peel is usually reversible without treatment, but requires preventive treatment against pigmentary changes, especially in high-risk patients (see the preceding paragraph and Chapter 37).

Dizziness and nausea Dizziness and nausea can occur during or after application of the paste. Some authors attribute these symptoms to peripheral vasodilation and the resulting low blood pressure. This explanation is not very satisfactory, however, as facial

vasodilation is in no way correlated with low blood pressure. Other facial peels produce at least the same degree of vasodilation without causing low blood pressure or faintness. What is more, there would have to be a great deal of peripheral vasodilation to make blood pressure so low that a patient in the lying position can feel it. Blood pressure readings taken after a peel are not low enough to explain this ‘dizziness’. It would appear instead that we are witnessing the actual symptoms of the beginnings of resorcinol poisoning, which fortunately soon resolve. We should not forget that resorcinol is a phenol compound. Using Unna’s paste and Jessner’s solution on large areas can theoretically lead to the usual phenol complications. If we consider that resorcinol is usually 40 times less toxic than phenol itself, we must also take into account that 100 g of Unna’s paste contains 40 g of resorcinol. That is the toxic equivalent of 1 g of phenol. The precautions of slow application (in 1 hour) that are taken with phenol are not observed for resorcinol and, with resorcinol, the area treated is often larger. Resorcinol is a small molecule that, like phenol, is easily absorbed by the capillaries. Rapid application of a thick and warm layer of resorcinol can introduce a relatively large quantity of the substance into the bloodstream and trigger the start of neurological toxicity typical of phenol compounds. As a result, the face can be treated in perfect safety, but when large areas are being treated, as is the case with a peel on the back, it is essential that the treatment consist of several separate peels.9 Arouette9 reports an unpublished clinical case of an extensive application of Unna’s paste bringing on coma in a few hours with full recovery.

Secondary infections A recurrence of herpes lesions should be anticipated, and preventive treatment should be taken if necessary. Scratch lesions22 can trigger impetigo on the face. Scratching is the only explanation for signs of infection after a peel with Unna’s paste or Jessner’s solution.

Scarring As with any superficial peel, and under normal conditions, the risk of developing scars is very low. Nevertheless, scabs and dry skin should not be pulled off.

Inadequate results If the results are considered inadequate, the patient might benefit from further peels. A maintenance resorcinol peel can be done every year, if indicated. According to Unna (quoted by Arouette9), ‘under some circumstances, it is necessary to do several successive exfoliations that can be performed without interruption’.

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Notes 1. For comparison with phenol, see Chapters 25 and 26. 2. Fintsi Y. Exoderm-lift – liquid formula. 1996. 3. Lettessier S. Chemical peel with resorcin. In: Roenigk RK, Roenigk HH (Eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1115-19. 1996, UK, Oxford, Marcel Decker Ltd. 4. Collins PS. Chemical face peelings. In: Evaluation and Treatment of the Aging Face. 34–67. 5. Terpenes are are a class of compounds whose chemical structures are based on a number of ‘isoprene units’, derived from the hydrocarbon CH2=C(CH3)–CH=CH2; they may themselves be hydrocarbons, but may also contain alcohol (OH), aldehyde/ketone (CO) and carboxylic acid (COOH) groups. Monoterpenes are C10 compounds derived from two isoprene units, sesquiterpenes (C15) are derived from three isoprene units, diterpenes (C20) from four and tritepenes (C30) from six. Terpenes are widespread in plants, where they are largely responsible for the odor, and they are the major constituents of plant-derived ‘essential oils’. Among the best known terpenes are β-pinene (turpentine), camphor, menthol and citronellal (all monoterpenes) and farnesol (a sesquiterpene that is a constituent of the essential oils of many plants). Certain terpenes have important biological roles: vitamin A, for example, is a diterpene, and steroid hormones have a structure related to triterpenes (and are biosynthesized by a similar route). 6. Manquat A. Traité élementaire de thérapeutique de matière médicale et de pharmacologie, 5° ed, tome 1. 1903: 240-60. 7. Kaolin (like ceyssatite) has absorbent properties that allow it to trap microorganisms. 8. Note the distinction between benzoic acid (C6H5COOH), in which a carboxylic acid group is attached to the benzene rign, and phenol (C6H5OH), in which the substituent on the benzene ring is a hydroxy group. 9. Arouette J. Dermabrasion, relèvements, peelings. In: Blackwell A. (Ed.), Collection des Manuels pratiques de médecine esthétique. 1989, Paris. 10. Quillaja bark is a natural soap containing 9–10% saponins,

11.

12. 13.

14.

15.

16. 17. 18.

19. 20.

21.

22.

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and is used in phytotherapy for dandruff, athlete’s foot, and irritated or sensitive skins. Used alone, a resorcinol peel at 5% triggers light exfoliation. The real peeling effect starts at 25% and becomes more obvious at 40%. Dr Eller and his assistant Shirley Wolf described this formula in New York in 1941. Salicylic acid (3–5%) triggers light exfoliation. A concentration of 15% is needed for a superficial peel. A concentration of 50% (beware of salicylism) produces a dermal peel. Such weak concentrations of lactic acid are ineffective in themselves, but may enhance penetration of the other ingredients. Max Jessner qualified as a dermatologist in Germany in 1922. He developed the solution that bears his name for the treatment of acne in the 1950s at New York University Hospital. Dr Jessner’s aim was to improve the performance of peels at the same time as reducing the risk of side-effects, by exploiting the synergy between the different ingredients. Dr FC Combes made wide use of Jessner’s formula in the 1960s, and is better known in the USA. Rubin MG. Manual of Chemical Peels, Superficial and Medium Depth. Philadelphia: JB Lippincott, 1995. Frosting is reached more quickly with a brush than with a double cotton bud, unless greater pressure is applied. Brushes should be used once only or disinfected with povidone–iodine. Single-use brushes are preferable: would you like to treat your skin with a brush that has already been used on acres of unknown skin? Trauchessec JM. Teoria y practica de los peelings. Med Estet 1996; 40: 11–21. This would not be the case with AHAs before a TCA peel (Coleman technique). AHAs do not penetrate evenly, and might cause the TCA to penetrate still more unevenly. Katin MJ, Teehan BP, Sigler MH, Schleifer CR, Gilgore GS. Resorcinol induced hypothyroidism in a patient on chronic hemodialysis. Annals of Internal Medicine 1977; 86(4): 447–9. As well as over-enthusiastic personal hygiene (e.g. using a sponge such as a Buf Puf®, non-prescribed cosmetic scrubs, a face cloth – which is a breeding ground for microbes – etc.).

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25 Phenol: chemistry, formulations and adjuvants

Chemistry of phenol As a class, phenols are compounds in which a hydroxy group is attached to a benzene ring. The name ‘phenol’ is also used to refer specifically to the simplest compound in this group, which is also known as hydroxybenzene, benzenol and carbolic acid (Figure 25.1). Phenol has a molecular weight of 94.11, a specific gravity of 1.071 and a boiling point of 182°C. It can react vigorously or even violently with other compounds, including formaldehyde, acetaldehyde and trifluroacetic acid, as well as aluminum chloride, nitrobenzene, some nitrates and nitrites, and other oxidizing agents. Phenol crystals are white or pink, and melt at 41°C. Most commercial phenol has a purity of 98%, but 100% pure phenol is obtainable.2

OH

Figure 25.1 Chemical structure of phenol.

CH3

CH3

CH3

CH

Phenol was formerly obtained from coal tar, but is now made by hydrolyzing chlorobenzene at 350°C or, most frequently, by air oxidation of cumene3 and treatment of the resulting cumene hydroperoxide to yield, phenol and acetone (Figure 25.2). Estimates of the amount of phenol produced worldwide vary, but since 1980 have usually been over 5 000 000 tons. Phenols may have more than one hydroxy group attached to the same benzene ring – for example, the three isomeric4 dihydroxybenzenes catechol (ortho-dihydroxybenzene or 1,2-benzenediol), resorcinol (meta-dihydroxybenzene or 1,3-benzenediol) and hydroquinone (paradihydroxybenzene or 1,4-benzenediol): see Figure 25.3. Molecules that have a single benzene ring with one or more hydroxy substituents are known as ‘simple phenols’ – examples are phenol itself and the three dihydroxybenzenes mentioned above, as well as the cresols (see below). There are also ‘diphenols’ (Figure 25.4) and polyphenols. Polyphenols are complex molecules containing several benzene rings with one or more hydroxy substituents. They are widespread in nature, often lending plants their color. Polyphenols (flavonoids and anthocyanins) constitute an important group of antioxidants used in anti-aging medications; flavonoids (Figure 25.5) are a distinctive group of polyphenols with a specific structure, containing two benzene rings, one of which is fused to an oxygen-containing ring.

OH

CH3 OOH

OH

OH

A A

OH

B

B

OH

C OH

Figure 25.2

Figure 25.3

Chemical structure of cumene (a) and cumene hydroperoxide (b).

Chemical structures of catechol (a), resorcinol (b) and hydroquinone (c).

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OH

OH

OH

OH CH3 OH

A

CH3

B

C CH3

Figure 25.4

Figure 25.6

An example of a diphenol: 2,3'-dihydroxybiphenyl.

Chemical structures of ortho-cresol (a), meta-cresol (b) and para-cresol (c).

OH OH

O

HO

OH OH

Figure 25.5 An example of a polyphenol: the flavonoid catechin.

Phenol derivatives Medicine has made wide use of phenols in many indications, as we shall see later in this book. Medical publications on peels abound in terms that are no longer in use and names of outdated molecules, which makes some texts difficult to read. It is therefore worthwhile taking a quick look at what these terms and compounds correspond to.

Cresols – Lysol® Cresols are simple phenols in which the benzene ring has one methyl and one hydroxy substituent. There are three isomers: ortho-, meta- and para-cresol5 (Figure 25.6). Coal tar cresol or cresylol is a mixture of the three isomers and is also called cresylic acid, hydroxytoluene and methylphenol. Coal tar and cade oil are mixtures of cresol and guaiacol (see below). Lysol® is the trade name of a solution of cresols in saponified vegetable oil, developed to counter the difficulties of putting cresol in solution form. It was an alkaline detergent containing 47–50% crysylol (= cresol = cresylic acid = cresylic phenol) as well as a little guaiacol, xylol, etc. Chemically, therefore, it was a poorly defined solution that nevertheless had the advantage of providing a clear solution when mixed with distilled water. Crude cresol comes from coal tar and consists of the three isomers: ortho-cresol 35–40%, meta-cresol 35–40% and paracresol about 25%. Cresol mixtures are used as

preservatives, deodorants and disinfectants. Ortho-cresol is a solvent and disinfectant. Meta-cresol is mainly used in insecticide chemistry or to produce antioxidants. Paracresol is mostly used in perfumery. Many foods contain cresols: butter, wine, tomatoes, asparagus, cheeses, bacon and smoked foods. Cresol is four times as toxic as phenol. Cresol mixtures are irritating to the respiratory tract and the skin. Although only anecdotal information is available on the potentially carcinogenic effects of cresols in humans, the US Environmental Protection Agency has classified these molecules as ‘possible human carcinogens’. Signs of intoxication include abdominal pain and vomiting. Other symptoms have also been described, such as heart, liver and kidney problems. Facial paralysis, coma and death are also possible with higher concentrations, even through simple skin contact.

Guaiacol Guaiacol (Figure 25.7) is also called o-methoxyphenol, 1hydroxy-2-methoxybenzene and catechol methyl ether. It is found in Valda® pastilles and expectorants, and is also used to make vanillin. It was originally extracted from a tree (Acacia catechu Willd), and then distilled from guaiac resin. Nowadays, pure guaiacol is synthesized from catechol, of which it is the methyl ether. Guaiacol salicylate has analgesic and anti-inflammatory properties. Its analgesic properties are due to the inhibition of cyclooxygenase and prostaglandin synthesis and the release of bradykinin. Guaiacol salicylate is anti-inflammatory as it stabilizes the lysoOH OCH3

Figure 25.7 Chemical structure of guaiacol.

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somal membrane and inhibits the action of the chemical mediators of inflammation.

Halogenated phenols Halogenated phenols are more powerful disinfectants than simple phenols, as they are more lipophilic. They are also more toxic to the central nervous system. The chlorinated phenols are the most active. Toxicity is specific to each compound.

Phenolic acids Phenol acids are phenols in which there is also a carboxylic acid group attached to the benzene ring. They include salicylic acid (ortho-hydroxybenzoic acid) and para-hydroxybenzoic acid (Figure 25.8). Acetylsalicylic acid (aspirin) and sodium salicylate are derivatives of salicylic acid. Like phenol, they have antipyretic and analgesic properties. The methyl, ethyl and propyl esters of para-hydroxybenzoic acid (parabens) are used as preservatives in pharmaceuticals, cosmetics and foodstuffs.

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and hexachlorophene (Figure 25.9) are members of this group of compounds. Septisol is a hexachlorophene soap used widely as a wetting agent in old phenol peel formulations.

Picric acid Picric acid (Figure 25.10) is 2,4,6-trinitrophenol. It is used in the treatment of burns in a 1% solution because of its stimulating effect on keratogenesis. The dry crystals are extremely sensitive to friction or shock6 and were widely used as an explosive before the discovery of TNT (trinitrotoluene). Picric acid can be synthesized from phenol, benzene or aspirin. It is soluble in water and alcohol. It turns the skin yellow. Applying swabs with 1.2% is not irritating but produces light flaking within 2–4 days. Using picric acid on open wounds and ulcers appears to stimulate epidermal regeneration. OH O2N

NO2

Bisphenols Bisphenols (not to be confused with the diphenols), are formed by two phenols linked with a bridge (–CH2–, –O– or –S–) in the ortho position, which makes the product easier to tolerate. Bisphenols are often chlorinated to increase their disinfectant power. Dichlorophene, tetrachlorophene O

O

OH

OH C

C OH

A

B

OH

Figure 25.8 Chemical structures of salicylic acid (a) and parahydroxybenzoic acid (b).

NO2

Figure 25.10 Chemical structure of picric acid.

Paracetamol (acetaminophen) Paracetamol (known as acetaminophen in the USA) is Nacetyl-para-aminophenol (Figure 25.11). It has the same detoxification pathways as phenol and also carries the risk of inducing methemoglobinemia. To be on the safe side, it should not be used as an intravenous analgesic during a full-face phenol peel, so as not to saturate the detoxification pathways. Paracetamol is also an intermediate in the pathway for detoxification of aniline derivatives, before hepatic glucuronide and sulfate conjugation allow them to OH

CI

CI

HO

CI

CI

CI

CH2

CI

OH

HN.CO.CH3

Figure 25.9

Figure 25.11

Chemical structure of hexachlorophene.

Chemical structure of paracetamol (acetaminophen).

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be eliminated in urine. The aniline derivatives acetanilide and phenacetin were once used as analgesics and antipyretic agents, but turned out to be excessively toxic, and were replaced by paracetamol, which had been shown in 1949 to be their major metabolite.

Different formulations of phenol peels Peels of the past Reviewing publications on phenol peels reveals a great many different formulations. The first surgical operation where phenol was used as a disinfectant took place in March 1865 (Lord Lister 1827–1912: Figure 25.12). At the very beginning of the 20th century, Manquat’s treatise on pharmacology7 described in detail the use of phenol as an anesthetic and disinfectant, at concentrations of around 5% in aqueous, oil or alcohol solutions. Preparation involved the use of various ingenious tricks to prevent the solutions from separating into multiple layers and to prevent the formation of isolated caustic droplets. After a relative lull, other formulations started to appear in medical publications. They reflect the constant search for the ideal solution and the increasingly clear understanding of the mechanisms that lie behind the excellent results achieved with today’s phenol peels. From this mass of publications. I have selected 13 major authors or groups of authors whose formulas will be surveyed in alphabetical order.

Figure 25.12 Lord Lister.

Ahronson presented a glycerinated phenol formulation: 88% liquid phenol is solubilized in anhydrous glycerol (glycerin) and a few drops of alcohol. This highly concentrated formula, used without occlusion, produces a peel that is not as deep as a peel with Baker–Gordon solution. Ayres achieved a medium-depth peel by combining phenol and trichloroacetic acid (TCA). These two formulas are no longer used today, as there are many other modern peel solutions that provide effective medium-depth peels using other molecules, such as TCA, that are not potentially toxic. Two Baker solutions are described. The first contains liquid phenol USP 5 cm3, distilled water 4 cm3, croton oil 3 drops and septisol 5 drops. The second contains liquid phenol USP 3 cm3, distilled water 2 cm3, croton oil 3 drops and septisol 8 drops. The water determines the concentration, which is variable. Baker’s solution has to be stirred constantly, as it is not stable and separates into layers if left to rest. Brown and Kaplan presented a more complex solution of phenol (at varying concentrations between 60% and 95%) mixed with saponified cresol in oil at concentrations of up to 10%. The application technique included a patch test behind the ear. This test made it possible to assess the necrotic effect of the solution on the patient. If the necrosis was too severe, the test was repeated with increasing concentrations of oil until the right solution for the patient was found. They recommended applying the solution area by area, leaving 2 hours between applications. The peel took 2 days to complete. Combes, Sperber and Reisch used an aqueous solution with a high concentration of phenol, combined with citric acid and sodium salicylate. Eller and Wolff, on the other hand, advocated an alcohol solution with a much lower concentration, around 25%, with salicylic acid. This was also applied in several stages (four at the most), with 1 or 2 hours between each application depending on how sensitive the skin was. Grade’s three formulas (aqueous phenol with croton oil), which had widely varying amounts of phenol and water, had to be left to rest for 6 weeks before use. This resting time was needed for ‘peroxides’ to form and buffer the solution. Klein presented a solution that was largely based on Baker’s, but with different concentrations. Karp’s three formulas are well known: the first was almost 80% glycerinated phenol, the second combined phenol with acetic acid, boric acid, salicylic acid and citric acid, but could only be applied locally, as it was too strong. Karp called his third formula ‘the phoenix’: it was an aqueous solution of glycerinated phenol combined with acetic acid and sodium salicylate. Litton proposed using a detergent other than septisol and recommended using glycerol. He was one of the first to describe an increase in the thickness of the Grenz zone after a phenol peel.

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Litton’s solution, as well as that of Truppman and Maschek, had the dual advantage over Baker’s of being stable in space and time. These aqueous and glycerinated solutions with concentrations of around 50% in phenol contained croton oil. Once prepared, they could be kept for several years when stored away from light and heat sources. Litton’s solution contains more croton oil than that of Truppman and Mascheck. Urkov used a simple alcohol solution of phenol, and treated deep wrinkles with electrocoagulation after the peel.8 He then applied an occlusive dressing for up to 3 days. His post-peel treatment was based on the ‘dry technique’. Verner Kellson’s aqueous solution uses two types of phenol: Lysol® (an oil solution of cresol) and phenol with various oils, including croton oil. The water has to be distilled, as Lysol® forms calcium cresate when mixed with tap water. The solution then becomes opalescent instead of clear.

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Table 25.1 Exoderm® formulas Formula 1a

Formula 2

Formula 311

Liquid phenol Phenol crystals Distilled water Alcohol Olive oil Sesame oil Glycerol Croton oil Resorcinol Septisol TCA 30%

Liquid phenol Phenol crystals Distilled water Alcohol Olive oil Sesame oil Glycerol Croton oil Resorcinol Septisol Salicylic acid Buffers

Liquid phenol Phenol crystals Distilled water Alcohol Olive oil Sesame oil Glycerol Croton oil Resorcinol Saponins Citric acid Buffers

a

Formulation certificate with bottles of Exoderm®, September 1995. The solution’s pH is 4.8.

Hetter formulas

Exoderm® My late friend, Yoram Fintsi, deserves special mention in this book, because, as well as being a close friend, he was one of the main catalysts for the current success of phenol peels, thanks to the formula he developed, Exoderm®. According to Fintsi, the Exoderm® formula was made in 1986 and then refined in 1990. Thereafter, Fintsi in Israel and Benhamou in France improved the formulation. Several formulations were put forward, one after the other, as shown in Table 25.1. The elements in common are listed above the dashed line. The first two formulas used septisol, a disinfectant soap with hexachlorophene, while the third formula – the one used today – simply contains saponins. The first formula contains TCA, the second salicylic acid and the third citric acid. The second two formulas are buffered to stabilize the pH. Fintsi commented on his own current Exoderm® formula in his article ‘Exoderm®, a novel, phenol-based peeling method resulting in improved safety’.9

In 1996, Hetter put forward a series of formulations based on the principle that by simply changing the concentration of croton oil, the depth of the peel could be varied (Table 25.2). Changing the concentration of croton oil is, indeed, one way of changing the strength of a phenol peel. It is not, however, the only way, and it is perfectly possible to do a phenol peel without croton oil. It is also possible to vary the depth of action of phenol without changing the concentration in croton oil. It is not, of course, a matter of questioning the intense cytotoxic effect of croton oil (see the section on adjuvants below), as Hetter10 stresses in 2000. Nor is it a matter of questioning Hetter’s legitimate refutation of the dogmas that claim, on the one hand, that lower concentrations of phenol wound more deeply (a lower concentration of phenol can penetrate more rapidly11 through an epidermis that is made more permeable by protein lysis and can therefore be more toxic) and, on the other hand, that phenol has an ‘all-or-nothing’ action, which is clearly untrue as also said by Dr Hetter. Attempts are currently being made

Table 25.2 Hetter formulas Very light peel

Medium light peel

Medium heavy peel

Heavy peel

4 cm3 88% phenol

4 cm3 88% phenol

4 cm3 88% phenol

4 cm3 88% phenol

6 cm3 water

6 cm3 water

6 cm3 water

6 cm3 water

16 drops septisol

16 drops septisol

16 drops septisol

16 drops septisol

1 drop croton oil

1 drop croton oil

2 drops croton oil

3 drops croton oil Take 3 cm3 of the above mixture and add 2 cm3 88% phenol and 5 cm3 water

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to market ‘completely non-toxic’ phenol peels. However, the phenol molecule is clearly defined, and so is its toxicity, as we shall see further on. A ‘phenol’ peel that is called ‘non-toxic’ cannot, by definition, contain phenol.

Lip & Eyelid® formula Lip & Eyelid® formula is a phenol peel that I first developed to increase dermatological safety and to achieve results without any occlusion on the sensitive skin of the eyelids. The same solution was then applied to the wrinkles around the mouth and then to the whole face, but with 24 hours’ occlusion in these two indications. It is an oil solution of phenol at over 60%. Four different oils are used in the various stages of the product’s preparation. The aim of the oily formulation is to slow down the penetration of the phenol through the skin and to improve dermal and epidermal maceration. It limits the toxicity of phenol by saturating the biochemical hepatic detoxification pathways more slowly. Split face treatment, comparing exoderm and lip & eyelid formula showed a higher efficacy of the last formula.

Storing phenol peel solutions Pure phenol is resistant to light, but the presence of impurities, even in small traces, turns it red due to oxygen fixation. This coloring does not change the properties of the product. Exoderm® solution must be stored away from light12 and humidity, however. It can be stored for 3 years in its original, unopened bottle. The contents of an opened bottle must be used within 1 year. Baker’s solution must be prepared for immediate use, unlike Litton’s solution, which can be kept for 3 years in the refrigerator. Medical publications report using the same solution successfully during a great many years. Lip & Eyelid® formula also remains stable for at least 3 years if kept in the refrigerator in the original, closed bottle.

Adjuvants of phenol peels General remarks Solutions with a high concentration of phenol cause rapid protein coagulation, which translates clinically into immediate frosting of the skin. This opaque coagulation acts as a shield that increases the skin’s impermeability, stops the surface phenol penetrating and prevents it from passing rapidly into the reticular dermis. A solution with a concentration higher than 80% therefore produces a more superficial peel than might be logically expected. Solutions with lower concentrations, of around 15–20% for example, are keratolytic and penetrate the skin more easily to a depth

where they are picked up by the drainage routes of the skin. The phenol is transferred rapidly for metabolization. A small quantity of free phenol, which can only act on the dermis for a short space of time, does not make for excellent results. If larger quantities of these low concentration solutions are applied to the skin in an attempt to get around this problem, the increased rate of reabsorption of phenol could saturate the detoxification pathways and the risk of intoxication is higher. At both higher and lower concentrations, effectiveness is blocked and adjuvants are needed to make it more effective. Everything that surrounds the phenol molecule, from pre-peel treatments to formulation methods, can be considered an ‘adjuvant’. Unlike superficial or medium peels, preparing the skin before a phenol peel is not intended to enhance or even out the penetration of the phenol, as it does not need help to penetrate the skin. Tretinoin or fruit acids are not necessary in pre-peel preparation, and perfect results are achievable without using them. Small, benign tumors can be treated with electrocoagulation immediately before the peel. Urkov, for his part, treated deep wrinkles with electrocoagulation after applying phenol and before applying the occlusive dressing. The skin must be cleansed and degreased thoroughly to get rid of any epidermal lipids and debris that can interact with or partially inactivate the phenol. Pre-peel and post-peel care, which are discussed in detail in Chapters 32 and 35, help to prevent or treat potential complications. Adjuvants can, for example, enhance the spread of the phenol within the epidermis, reduce skin surface tension, enhance liquefaction necrosis of the epidermis, help the phenol reach the dermis (where it causes a severe inflammatory reaction that generates collagen and elastin and blocks its action in the upper reticular dermis) and slow down and/or reduce the capillary absorption of the phenol (thus allowing time for sulfate and glucuronide conjugation of the toxin before its elimination).

Different chemical adjuvants The peel solutions should never be prepared simply by dissolving phenol in one of its potential solvents. Since phenol was introduced into treatment, doctors who use it have tried to: ■ Moderate (tame) its systemic toxicity. Different substances have been combined with phenol to reduce its adverse effects. It should be noted that the only demonstrated way to avoid cardiac toxicity lies in the application technique for a full-face phenol peel. ■ Improve its effectiveness. Different chemical adjuvants have been combined to modify the action of phenol. The application technique and pre-peel and post-peel care have very important roles. The latest formulations are therefore tamed and adjuvanted.

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The qualitative formulas of recent products are known, but the percentages and preparation methods are not revealed. Fintsi explained that adjuvanted and tamed phenol peels must be prepared according to a precise method and that he was afraid that if he revealed the exact proportions of the ingredients, doctors would try to make up the formula themselves without keeping to the necessarily strict order of preparation, and that this could lead to disastrous results. Logic must prevail in the attempt to understand how adjuvants work: it should be remembered that phenol has an anesthetizing action on sensitive nerve endings through protein coagulation; this anesthetizing effect develops within 10–15 seconds after application. This means that 15 seconds after application, the phenol is already in the dermis: it is therefore doubtful that combining it with products that penetrate more slowly, such as salicylic acid or citric acid, can improve the already rapid penetration of phenol. On the other hand, there is no doubt that phenol improves the penetration of these adjuvants, if they can survive without reacting chemically with the phenol solution itself.

Resorcinol See Chapter 24 for more details. Although resorcinol is known to have allergenic properties, there have been no allergies reported when it has been used in small quantities with phenol. However, the combined use of these two substances in the same peel solution does not appear to have any clinical value, as the phenol will have finished working before the resorcinol has started. Resorcinol cannot therefore modify the effect of phenol. No data are available on the potential clinical effect of resorcinol on skin that has just been coagulated by phenol.

Trichloroacetic acid TCA is an acid whose strength of action is proportional to the concentration used. However, it also depends on numerous other factors that are described in detail in the chapters on TCA.

Salicylic acid Salicylic acid is a keratolytic agent that dissolves the amorphous intercorneocyte matrix and thus diminishes the barrier function of the stratum corneum. It is sometimes combined with phenol, but does not improve its action. See also the comments on resorcinol and TCA above.

Figure 25.13 The shrub Croton tiglium – the source of croton oil.

Rubbing 2–10 drops of pure croton oil or croton oil with olive oil on the skin causes an intense burning sensation within 5 minutes that lasts for several hours and is followed by erythema. Clusters of small blisters then form and turn into pustules that dry, scab and drop off within a few days without leaving any scars. If, however, the croton is applied too vigorously, keloid scars may result.7 The crotonic acid (Figure 25.14)13 that it contains is an irritant that accelerates epidermal lysis and enhances the cutaneous penetration of the phenol. Some authors maintain that a phenol peel will only produce good results if croton oil is present. The croton oil enhances dermal penetration and epidermal protein coagulation, and thus lower concentrations of phenol can be used. We have seen, however, that many phenol peel formulations do not contain croton oil.

CH3

Croton oil Croton oil is extracted from the seeds of the shrub Croton tiglium (Figure 25.13), of the family Euphorbiaceae. In the past, these seeds were also called Moluccas seeds, Tilly seeds or small Indian pine nuts.

H CC

H

O



ch25

C

OH

Figure 25.14 Chemical structure of crotonic acid.

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The irritant action of croton oil is used to advantage in cancer research to enhance the penetration of carcinogens through the skin barrier. Croton oil is therefore a co-carcinogen. In 1994, Wilmer et al14 showed that keratinocytes can produce interleukin (IL)-type substances, growth factors and tumor necrosis factor (TNF). Phenol and croton oil induce keratinocyte production of IL-8 (at non-cytotoxic concentrations), TNF-α and also a growth factor. TNF-α is a cytokine synthesized (among others) by the keratinocytes in the stratum spinosum and the stratum granulosum. It stimulates the differentiation of keratinocytes into corneocytes and thus accelerates the full regeneration of the protective stratum corneum. Amazonian Indians used croton extracts as a vulnerary15 agent. It appears that an alkaloid, taspine, is (partially) responsible for the healing effect on wounds. Its mechanism of action is probably due to the chemotaxy of the fibroblasts being stimulated, which improves the efficiency of the first stages of healing, without affecting the following stages.16 At the beginning of the 20th century, the vesicant properties of croton oil were used to good effect on people with edema. Rubbing croton oil on large areas created numerous vesicles, the combined serous fluids from which produced enough liquid to relieve edema in the lower limbs of heart patients. Experiments were carried out involving the ingestion of croton oil: this produced intestinal inflammation with diarrhea and weight loss.17 Croton oil is a powerful toxin that taken orally in small quantities of around 20 drops can cause fatal hemorrhagic gastroenteritis.18

Septisol Septisol is a liquid soap with hexachlorophene, a bisphenol used as a disinfectant. It is also a surfactant. At low concentrations, hexachlorophene uncouples the oxidative phosphorylation of cells and causes morphological changes in membranes.19 It might be keratolytic.20 Intoxication of infants from hexachlorophene preparations (in France, in 1972) resulted in neurological (encephalitis) and cutaneous symptoms. These products have turned out to be dangerous after chronic use if not rinsed off or if applied to damaged skin or to large areas of the body with an occlusive dressing.

Saponins Liquid soap helps to reduce surface tension (Box 25.1) and therefore improves the penetration of active agents. It also improves maceration under an occlusive dressing. Anionic and cationic soaps, like alcohol, enhance the action of phenol.19 Formulation requirements are strict. If there is too much surfactant, the phenol ends up within a micelle and its action is reduced. If there is not enough, the solutions are not stable.

Box 25.1 Surface tension The forces of attraction and repulsion are more or less evenly distributed within a liquid. The surface molecules, however, are unable to balance the lateral intermolecular forces of attraction. The tension on the surface of a liquid acts like an elastic membrane, opposing penetration in the liquid. Agents called surfactants, wetting agents or detergents reduce this elastic surface tension and enhance penetration in the liquid. Wetting agents also have antiseptic properties. There are two large groups: • Cationic surfactants (cetrimide, lauralkonium, etc.): powerful bactericides and fungicides • Anionic surfactants (e.g. sodium lauryl sulfate): used to sterilize the skin before surgical operations

Cresol – Lysol® In the past, saponified cresol as well as Lysol® was used as a wetting agent to increase the penetration and therefore the strength of phenol. See the discussion of cresols earlier in this chapter.

Acetic acid For a description of acetic acid, see the beginning of Chapter 12.

Oil formulations21 versus aqueous formulations A cell membrane is a ‘fluid mosaic’ of phospholipids in two layers. The hydrophilic poles face outwards and the hydrophobic poles form the inside of the membrane. The lipid cell surface is strewn with proteins. If we compare a cell membrane to a chocolate cream sandwich cookie, the hydrophilic poles would be the cookies on the outside and the hydrophobic poles would be the chocolate cream in the middle. The surface proteins would be found in the small holes on the surface of the cookies. If we compared a cell membrane to a jam sandwich, the hydrophilic poles would be the slices of bread and the lipophilic, hydrophobic poles would be the jam. The surface proteins would be set in the air bubbles in the bread. At the beginning of the 20th century, the relative impermeability of cell membranes to many water-soluble components had already been attributed to the lipid nature of the membranes. Molecules that are soluble in non-polar solvents (e.g. olive oil, sesame oil and ether) enter cells more rapidly than water-soluble molecules with the same molecular weight.22 Fat-soluble molecules ‘dissolve’ in the lipophilic layers and readily penetrate the interior of the

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cell. The ratio of the solubility of a substance in olive oil in relation to its solubility in water provides the oil/water partition coefficient. Phenol has a good oil/water partition coefficient.19 The ability of a molecule to penetrate the cell membrane is proportional to its partition coefficient. Adding oils to phenol enhances its action in the epidermis and papillary dermis and slows down the penetration of the oil-bound phenol through the skin so that it reaches the deeper dermal layers more slowly. Phenol is also soluble in water and has a low molecular weight (94.11). Very small molecules that are water-soluble and non-polar pass through cell membranes much more quickly than one might expect given the molecular structure of the actual membrane and the partition coefficient. These small molecules appear simply to pass between two adjacent molecules in the membrane, without really dissolving in the pole taken up by the fatty acid. It is also possible that the proteins set in the membrane are highly permeable to these tiny water-soluble molecules. With increasing molecular weight, membrane permeability decreases and stops molecules with a molecular weight greater than 200 from getting through. Phenol’s low molecular weight and its high partition coefficient would allow it to pass through the membrane rapidly if it were not bound to oily components. Moreover, phenol coagulates membrane proteins. The vascular endothelium has two absorption pathways. There are 4 nm pores that form the intercellular spaces. These pores represent only 0.02% of the capillary surface. Diffusion is the main pathway, and the principles set out above also apply to the capillaries. The antiseptic derivatives of phenol have structural modifications (halogenation and alkylation) that, by increasing their liposolubility, improve their antiseptic action. Brown and Kaplan made use of the ‘buffering’ property of oils in phenol solutions. Their formulation contained up to 95% phenol combined with oils. A patch test behind the ear had to be carried out before the facial peel. If there was skin necrosis, they reduced the strength of the phenol by gradually adding oil in small quantities until the right dose was found for the patient’s skin. To increase the strength of the mixture, on the other hand, soap (saponified cresol) was added or the concentration of phenol was increased.

Glycerol Adding glycerin to phenol makes it less irritating. Glycerinated phenol at 10% is no longer an irritant.

Buffers Buffers keep the pH of a solution stable. Phenol is more aggressive in an acid environment. The presence of buffers keeps the solution at an appropriate pH. The pH of today’s

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phenol solutions is usually close to the skin’s physiological pH.

Alcohol and water Alcohol is used at different points during preparation to help products solubilize more efficiently in the aqueous solution. Phenol, for example, is more soluble in alcohol than in water. The purer the phenol crystals, the more soluble they are in water. Alcohol also enhances the action of phenol.21 Water is also used as a solvent for certain products or to modify the concentration of the phenol.

Notes 1. In this book, ‘phenol’ is used in this sense; the plural, ‘phenols’ refers to the group of compounds in general. 2. Material Safety Data Sheet. Fisher Scientific, USA. 3. Cumene (isopropylbenzene, 2-phenylpropane, cumol), molecular weight 120.2, is a colorless liquid with a strong depressant effect on the central nervous system. 4. Isomeric compounds (isomers) have the same empirical formulas but different chemical structures. 5. Also known as ortho-methylphenol and ortho-hydroxytoluene, etc. 6. Which is fortunately not the case with solutions. 7. Manquat A. Traité élémentaire de chérapeutique de matière médicale et de pharmacologie, 5° ed. 240–60, 1903. 8. Was this to make up for the inadequate results of this formulation? 9. Am J Cosmet Surg, 1997; 14: 49–54. 10. Hetter G. An examination of the phenol–croton oil peel: Part III. The plastic surgeon’s role. Plast Reconstr Surg 2000; 105: 725–63. 11. Quicker penetration is not synonymous with greater effectiveness. 12. To limit the risks of photochemical reactions. Storing the solution at low temperatures slows down the chemical reactions, and is the best way to store any chemical. 13. Crotonic acid is also known as 2-butenoic acid and has a molecular weight of 86.09. 14. Wilmer JL, Burleson FG, Kayama F, Kanno J, Luster MI. Cytokine induction in human epidermal keratinocytes exposed to contact irritants and its relation to chemicalinduced inflammation in mouse skin. J Invest Dermatol 1994; 102: 915-22. 15. Vulnerary – promoting the healing of wounds. 16. Porras-Reyes BH, Lewis WH, Roman J, Simchouritz L, Mustoe TA. Enhancement of wound healing by the alkaloid taspine defining mechanism of action. Proc Soc Exp Biol Med 1993; 203: 18–25. 17. Pol O, Ferrer I, Puty MM. Diarrhea associated with intestinal inflammation increases the potency of mu and delta opioids and the inhibition of gastrointestinal transit in mice. J Pharmacol Exp Ther 1994; 270: 386–91. 18. Klein DR, Little JH. Laryngeal edema as a consequence of chemical peel. Annual Meeting of the American Society for Esthetic Plastic Surgery, Las Vegas, 1982.

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19. Giroud JP, Mathé G, Meyniel G. Pharmacologie clinique. 1590–91. Expansion Scientific Français, 2003. 20. Ashen S. Unoccluded Baker–Gordon phenol peels – review and update. J Dermatol Surg Oncol 1989; 15: 998–1008.

21. See also Chapter 27. 22. Bene RM, Levy MN. Physiology, 3rd edn. Mosby Yearbook, Inc. 1993.

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26 Phenol: properties and histology

Miscibility with water Phenol is not completely miscible with water; to obtain a homogeneous solution, an excess of water is required.1

Neurolysis and local anesthesia Phenol has been widely used in a large number of disorders, including spasticity and chronic pain, because of its neurolytic and local anesthetic properties (5% solution). Topically applied phenol has a lasting local anesthetic action that can affect all the layers of the skin and occurs at the same time as frosting (Figure 26.1). Phenol has been used as a surface anesthetic to perform small operations. It is neurolytic;2 it coagulates the sensitive nerve endings at the base of the epidermis and in the superficial papillary dermis. During a phenol peel, the first application of acid causes an intense burning pain that can be alleviated by prior or immediate application of something cold. After

Figure 26.1 Immediately after application of phenol to the upper lip, the anesthetic effect is enough to be able to pinch the skin and draw blood without any feeling of pain (note the red spots in the photograph, taken during a chemical cheiloplasty).

frosting, the anesthetic effect takes hold and spreads beyond the frosted area by up to a centimeter. During a phenol peel, after an initial period of analgesia, patients complain of renewed pain that they all describe differently, however. The second wave of pain is more likely to come from the rapid onset of inflammatory edema; this distends the tissues and stimulates the deeper nerve endings. This pain wears off during the first night, when the edema is at its height and is no longer actively distending the tissues.

Carcinogenicity Phenol is not considered to be carcinogenic.3 On the contrary, long-term histological studies show that phenol (even when the formula contains croton oil) has a protective effect against skin cancers. A logical explanation of this protective effect may lie in the fact that the cells that take the brunt of UV rays are the keratinocytes closest to the stratum corneum, the ones that form, for example, the top of the dermal papillae. On the other hand, the keratinocytes that are in the lower regions of the dermal papillae are relatively protected compared with those higher up: the UV photons have been partially absorbed or diffracted by the epidermal layers above them. In addition, the sebocytes4 or keratinocytes that make up the shaft of the hair are anchored more deeply in the skin, at a depth where the harmful effects of the sun are not as severe. The cells that are most active in skin regeneration after a deep peel are those that are least damaged by the sun’s rays, the cells that have undergone the least UV-induced genetic mutation. After a phenol peel, the skin is much healthier than the skin that the acid coagulated, and statistically will develop fewer cancers. Moreover, phenol may well coagulate and get rid of any intraepidermal cancer in situ.

Protein coagulation Phenol coagulates proteins simply by combining with them, and this produces frosting similar to that occurring when the normally transparent proteins of an egg white become cloudy on cooking, as a result of their three-

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Stratum corneum disjunctum Stratum corneum compactum Keratinocytes

K

K GZ

K

K GZ

GZ

GZ

Epidermal basal layer Grenz zone

GZ

Papillary dermis Reticular dermis Hypodermis

Figure 26.2 Schematic diagram of the layers of the skin adapted to peelings.

dimensional structure being modified. The coagulated proteins and phenol can be separated by the action of alcohol.5 For the phenol and proteins to form a stable bond, the temperature must be raised. When phenol comes into contact with the skin or mucous membranes, it causes immediate proteolysis if the concentrations are high enough, with protein coagulation occurring at higher concentrations .

Disinfection Phenol is a powerful disinfectant that is more active in vivo than in vitro, because it coagulates the proteins of living organisms. It is bacteriostatic (at a concentration of 2 g/l) and bactericidal (at a higher concentration of 10 g/l). From 13 g/l (about 1.3%), it is tuberculostatic and fungistatic. It is not considered to be virucidal,6 although one commercial formulation containing 0.13% of glutaraldehyde and sodium phenate has a virucidal activity (according to AFNOR Norm T727). Some more lipophilic phenol derivatives have been declared virucidal against HIV and the hepatitis B virus.1 The fragility of the HIV envelope would explain this action, though the action against the hepatitis B virus is not so clear. Many patients report that labial herpes outbreaks are less frequent or even disappear altogether after a phenol peel. Phenol is found in bactericidal, tuberculostatic and fungistatic concentrations in all phenol peel formulas. Even after 24 hours’ contact, no phenol derivative has shown any sporicidal action.

Histology of phenol A study8 on guinea pigs showed that the reticular dermis reacts to injury as if it were made up of two distinct layers, whereas histologically there is no evidence that these two layers exist, and the reticular dermis appears to be homogenous (Figure 26.2 is a schematic illustration of the layers of the skin). When the uppermost part of the reticular dermis is attacked, it reacts by reorganizing the tissues, while the deeper part forms scars. It must be remembered that the deeper dermis contains fibroblasts that can react phenotypically as ‘conventional’ fibroblasts as well as myofibroblasts. Myofibroblasts are differentiated (in response to cytokines) fibroblasts that can both synthesize a strong collagen bundle and activate a cytoplasmic motor running on actin. This transforms them into ‘non-muscular’ motor cells that can activate a contractile capacity comparable to that of a smooth muscle cell. The myofibroblasts interact between themselves – as if they were holding hands across their thick and resistant collagen bundles; as if, after taking each other’s hands, they were bending their arms to draw closer to each other and thus contract the skin. Myofibroblasts (Box 26.1) are the skin’s final bulwark, the last defense against physical, chemical and biological attack: when a peel injures the dermis to a depth where there are fibroblasts capable of turning into myofibroblasts, it means that there are many keratinocytes (that have been destroyed) upon which the body can no longer count, to regenerate the skin and that skin regeneration will be slow and therefore dangerous for homeostasis.

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The activation of the myofibroblast actin-based contractile motor, which alone can draw the edges of the wound

together, increases the entire organism’s chances of survival. The deep reticular dermis therefore reacts like an entrenched guard that has nothing to lose and prefers to produce a scar rather than undergo extensive necrosis. When a peel injures the reticular dermis, the safety margin is therefore narrower and the risk of scarring is greatly increased. In 1985, Kligman studied and documented the long-term after-effects of a phenol peel in his remarkable study ‘Long-term histologic follow-up of phenol face peels’.9 Fintsi also studied the histological effects of phenol peels. It is still very difficult, however, to tally the clinical results and the histological changes of the different types of peels: the formulations, adjuvants and concentrations are different, as are the methods of preparation and application of the various active agents used. Each patient has different cell characteristics, either in the quality or the quantity of phospholipids, sterols and proteins embedded in the cell membranes. Doctors are guided by their own experiences and follow the application protocol they have gradually developed in the course of their practice. This disparity makes it difficult to compare the results of different studies. Some general principles can, however, be drawn: we can consider that all peels produce comparable histological effects. The differences arise from the extent of the inflammation caused and how this inflammation is controlled, as well as the relative depth reached. As far as

A

B

Box 26.1 Myofibroblasts Normally, fibroblasts do not exert much tension on the matrix of non-inflammatory tissue, but when all the layers of the skin are affected by an injury, local growth factors send fibroblasts to colonize the fibrin plug closing the wound and forming the temporary matrix. The fibroblast invasion and neoangiogenesis form the granulation tissue. The fibroblasts that have invaded the temporary matrix already exert a certain amount of traction on this tissue. The mechanical stress then stimulates the fibroblasts to produce more collagen and to turn themselves into ‘protomyofibroblasts’. The persistent stress induces the phenotypic transformation of the protomyofibroblasts into differentiated fibroblasts, the myofibroblasts, which secrete actin fibers and increase their contractile force at the same time as producing collagen and releasing proteases. Usually, the myofibroblasts disappear via apoptosis (programmed cell death) as soon as the scar is solid, but where stress persists, they do not disappear and gradually form a hypertrophic scar.

Figure 26.3 (a) Full-face phenol peel immediately after 24 hours’ occlusion. The darker patches are the areas that have not undergone liquefaction. This makes no difference to the overall result, as can be seen in (b), which shows the same patient 12 days after the full-face phenol peel with Lip & Eyelid® formula. The skin tone is completely even, even in the non-liquefied areas.

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medium and deep peels are concerned, effectiveness increases when the injury is close to the deep reticular dermis. The risk of retractile scars developing is greatly increased at this depth. There is therefore a fine line between achieving excellent results and the incidence of scarring. At the same peel depth, however, phenol peels produce the most significant changes and the most spectacular results (Figure 26.3).

Epidermal changes A phenol peel usually produces complete epidermolysis in keratinocytes and all other living cells in the epidermis. The Langerhans cells, which play an important role in the skin’s immune defenses, are also affected. There is a certain amount of dermolysis accompanying the destruction of the epidermis.

Superficial epidermal layers The epidermal layers are dissolved down to the basal layer in 24–36 hours under an occlusive mask. Thereafter, the architecture of the cells returns to normal and the histological coloring evens out. After a peel, the palisade structure of the keratinocytes is more even.

Basal layer Phenol restructures the architecture of the basal layer. It does not completely destroy the melanocytes: they are still found in the basal layer after peeling. In some histological studies, the density of melanocytes is sometimes higher overall. The melanocytes have, however, become incapacitated or partially incapacitated: melanin synthesis is reduced, as is the ability to transmit melanosomes to the neighboring keratinocytes. This histological observation explains any hypopigmentation or depigmentation following a phenol peel. How much the phenol damages the melanocytes largely depends on the formulation of the solution used and the application technique, which explains why total achromia occurs more often with some formulations than others. For example, with Baker’s formula, the risk of developing a ‘porcelain skin’ is higher than with Lip & Eyelid® formula. PIH is more frequent than achromia when using today’s phenol formula

Dermal changes On contact with the papillary dermis, phenol destroys the entire elastotic layer within it. Thereafter, the architecture of the dermis is spectacularly restored. Immediately underneath the basal membrane, in the Grenz zone, a dense new layer of collagen fibers is formed, arranged parallel to the

basal membrane and interspersed with good-quality elastic fibers in an effective network.10 Brown described this histological reaction as early as 1960. The new collagen and elastin that is formed covers the sun-damaged structures that have not been destroyed by the phenol and pushes them deeper down. The fibroblasts are strongly stimulated and secrete all the components of the extracellular matrix: ground substance, collagen, elastin, etc. The morphology of the fibroblasts varies widely depending on their location: ■ Papillary dermis: here the fibroblasts are small and have horizontal dendritic processes; each fibroblast is in contact with several collagen fibers. These observations explain the dense horizontal arrangement of the new collagen in the papillary dermis after a phenol peel. ■ Mid and deep dermis: the fibroblasts are larger and are in contact with just one bundle of collagen fibers. ■ Deep dermis and hypodermis: the fibroblasts are even larger here (four times bigger than in the papillary dermis), and the dendritic processes are long and form a continuous network. Collagen synthesis by the fibroblasts causes scars to contract. Myofibroblasts (see Box 26.1) are cells produced by fibroblast differentiation. They contain myofilaments that make them look like smooth muscle cells and are involved in the phenomena of scar retraction. Depending on the depth reached by a peel, different types of fibroblasts are stimulated and will react in a specific way because of their different genetic programming. All of these histological changes explain how the skin becomes thicker and the sometimes dramatic face-lift effect of deep peels. The blood vessels that are newly formed after a phenol peel provide an effective and lasting supply of nutrients to the new skin. After a deep peel, the body takes 4–6 weeks11 to regenerate a structurally normal skin. During these 6 weeks, the skin appears very red, as the many newly formed blood vessels are showing through an incomplete, thinned and pale epidermis. Six weeks is usually the minimum time that erythema lasts after a phenol peel. After this time, inflammation may persist and the skin can still appear red for several more months. Dermal lymphocyte infiltration associated with photoaging is reduced after a phenol peel. On the other hand, there is significant lymphocyte infiltration in the reticular dermis 2–5 days after a phenol peel. Overall, the wrinkled superficial layers are liquefied and replaced by structurally young and homogenous tissue. The inefficient elastotic dermal layers are renewed and/or pushed deep down by the synthesis of new fibers. The quality of the new collagen is not quite as good as the collagen that had been present since birth. However, it is produced in sufficient quantities, along with new elastin, to provide

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Other authors13 have confirmed these histological results after 15-20 years and even talk about permanent results in some patients. In 1985, Kligman10 showed that dermal reconstruction lasts for 20 years at least and that the risk of cancer is reduced. Clinically, the rejuvenated appearance of the skin can be maintained for a great many years (Figure 26.4).

Notes

Figure 26.4 The skin of a 78-year-old patient 10 years after a full-face phenol peel (Exoderm®) and 1 year after a medium-depth trichloroacetic acid maintenance peel (Unideep®).

better support to the newly rebuilt epidermis.12 The newly formed blood vessels supply the dermis with the nutrients it had slowly been deprived of because of the gradual vascular degeneration caused by photoaging.

Long-term histological follow-up after a phenol peel The changes described above last a long time. In histological sections taken 15 years after a phenol peel (Baker’s formula) the difference between the treated and non-treated skin is incredible, and this explains why, most of the time, only one phenol peel is necessary for long-lasting rejuvenation of the face.

1. Dauphin A, Darbord JC. Hygiène hospitatière pratique, 2° ed. 2. It is used in the treatment of pain in certain cancers to achieve neurolysis of the nerve routes responsible for transmitting the sensation of pain. 3. Material Safety Data Sheet. Fisher Scientific, USA. 4. Sebocytes are in fact keratinocytes that have been differentiated phenotypically into cells capable of producing sebum. When under attack, they can quickly dedifferentiate and turn back into keratinocytes and regenerate the skin. 5. By separating the phenol from the protein that it has coagulated, alcohol can enhance the action of the acid on another protein. 6. Giroud JP, Mathé G, Meyniel G. Pharmacologie clinique: 1590–1. Expansion Scientifique Français 2003. 7. Regelson W. DHEA, melatonin and hormone replacement. In: Updates, Anti-aging Medical Therapeutics, Vol 1. Health Quest Publications, 1997: 75-81. 8. Hayes DK, Berkland ME, Stombaugh KI. Viability of skin flaps subjected to simultaneous chemical peel with occlusive taping. Laryngoscope 1989; 99: 1016–19. 9. Kilgman AM, Baker TJ, Gordon HL. Long-term histologic follow-up of phenol face peels. Plast Reconstr Surg 1985; 75: 652–9. 10. Petes W. The chemical peel. Ann Plast Surg 1991; 26: 564–71. 11. Dembinstri M. Exoderm method, the non surgical face lifting. In: 44° Congrezzo Nazionale della Società Italiana di Chirurgia Plastica Ricostructiva ed Estetica, Bologna, Nov 1995. 12. Asken S. Unoccluded Baker–Gordon phenol peels – review and update. J Dermatol Surg Oncol 1989; 15: 998–1008. 13. Matarasso SL. Glogan RG. Chemical face peels. Dermatol Clin 1991; 9: 131–50.

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27 Phenol: skin penetration and detoxification

Skin penetration of chemicals The skin has many different functions: it can be the site of action of a product or the reservoir for a product; it can simply be a transit site or it can be an impermeable barrier. The skin’s main role is to form a barrier limiting the transfer of molecules in and out. It is especially adapted for this thanks to the multiple external layers of corneocytes. For the stratum corneum to be impermeable to both chemical and physical agents,1 it is essential for it to be intact. It is this layer that forms the main barrier to the penetration of active products through the skin. Corneocytes are made up of α-keratin filaments, buried in an amorphous matrix rich in disulfide bonds. There is a thick protein envelope of involucrin round each corneocyte, and the intercellular spaces are full of extremely hydrophobic lipids. The outer layer of the plasma membrane is hydrophilic. The outer layer of skin can be described as a hydrophilic ‘brick wall’ sealed with hydrophobic ‘mortar’.2 The whole forms an efficient barrier against both hydrophilic and hydrophobic molecules. This barrier is so efficient that chemicals can penetrate living or dead skin to the same degree, just as there is the same degree of penetration through the whole skin or the stratum corneum alone!2 Consequently, eliminating all or part of the stratum corneum drastically enhances the absorption of physical and chemical agents that could not have penetrated an intact protective stratum corneum. The ability of a product to penetrate the skin also depends on how it interacts with the corneocytes and the intercellular matrix. At the same molecular weight, a proteolytic product will penetrate the skin more readily than a product that is not proteolytic. The more liposoluble a molecule is, the greater its partition between the vehicle and the skin barrier and as a result its ability to penetrate is improved. Another factor to be taken into account is how solvents interact: ethanol diffuses better in the stratum corneum when it is mixed with oil rather than water.2 How well hydrated3 the stratum corneum is also plays an essential role in the skin’s absorption capacity. When the stratum corneum is hydrated, products can be absorbed up to 10 times more efficiently.2 Hydration swells

the corneocytes and makes them less dense and less resistant to diffusion. The fact that on facial skin the stratum corneum is not very thick means that molecules are absorbed more quickly. The skin on the face is more permeable than the skin on the limbs and the torso, but less permeable than the skin on the genital organs.

What happens to phenol after penetration (Figure 27.1) Lymphatic absorption The lymphatic system, which is highly permeable even to large protein molecules, slowly collects some of the phenol in the interstitial fluid. The total daily volume carried by the lymphatic system is approximately equal to the volume of blood of the same individual. This absorption route is very slow and therefore negligible from a toxicological point of view.

Capillary absorption Phenol penetrates rapidly through the skin and is immediately absorbed by the dermal blood vessels. The metabolization and/or excretion sites immediately pick up the phenol that has penetrated into the bloodstream.

Metabolization and elimination Twenty-five percent of phenol is metabolized into water and carbon dioxide and eliminated directly through the lungs. The remaining 75% is eliminated in free and conjugated form or undergoes oxidation. Phenol is oxidized to hydroquinone in the liver. Still in the liver, it is esterified by the transfer of the sulfuryl group of 3'-phosphoadenosine 5'phosphosulfuric acid to the hydroxy group of the phenol and produces phenylsulfuric acid: this is sulfate conjugation. Phenol also undergoes glucuronide conjugation through exchanges with glucuronic acid. The conjugated phenol is no longer toxic to the organism, and can be eliminated by

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Concentration? Adjuvants? Formulation, phenol Sequestered in applicator, etc.

100% phenol Epidermis

Oily? Dry? Thick? Thin? Prepared? etc. Thick? Hydrated? Rich in proteins? Rich vascularization? Occlusion?

Dermis

E = quantity of phenol sequestered in the epidermis

100 - E

D = quantity of phenol sequestered in the dermis

100 - (E+D)

Slow lymphatic elimination

L = quantity of phenol eliminated by the lymphatic system

100 - (E+D+L)=T

T = quantity of potentially toxic phenol

Capillary resorption slowed down by oils, edema, etc. About 70–75% (T) Hepatic detoxification

Phenol + 3′-phosphoadenosine 5′-phosphosulfuric acid → phenylsulfuric acid (sulfate conjugation) Phenol + glucuronic acid → phenyl glucuronide (alucuronide conjugation) Quinone and catechol subsequently undergo renal elimination

About 20–25% (T)

Pulmonary metabolism Elimination of H2O and CO2



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Renal elimination of conjugates Active transport of detoxified phenol in the proximal tubule

Elimination of non-conjugated free phenol Diuresis, hydration

Figure 27.1 Metabolization of phenol.

the kidneys. Other detoxification enzymes have been identified, such as phenol 2-monooxygenase, phenol O-methyltransferase and phenol β-glucosyltransferase.4 Active transport processes excrete organic acids such as glucuronide and phenol sulfate conjugates in the proximal tubule. All forms of free or detoxified phenol are therefore found in urine.

Hepatic and renal integrity Because of the way in which phenol is metabolized, hepatic and renal integrity is a prerequisite for a phenol peel. Applying phenol more quickly than it can be detoxified and eliminated by a deficient liver or kidneys could result in severe intoxication.

An interesting study in 1953 by Ruedmann and Deichmann5 concluded that hepatic and renal integrity were absolutely vital when using phenol. They wanted to draw the attention of practitioners to the potential dangers of applying phenol to large surface areas of the body, even though this type of treatment had previously presented only minor drawbacks. A patient did die, however,6 after a phenol solution with a concentration of 2.3%7 was applied under an occlusive dressing8 on one-third of the body surface area and on flesh burnt by kerosene.9 This death led the authors to study the metabolism of phenol by applying 1 g of phenol to 75% of the body surface area in a first group of human ‘guinea pigs’. Three other groups were given total doses of up to 4 g on the same body surface area (75%). A rest period of 90 minutes was left between successive applications of 1 g.

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Toxic phenolemia Doses of free and conjugated phenol show the following results: the levels of free circulating phenol do not vary much whether 1, 2, 3 or 4 g of phenol is applied on the skin or if a rest period of 90 minutes is left between each gram applied. The peak values in free phenol recorded were around 0.60–0.80 mg/100 ml. Benatar10 describes a reassuring 1962 study by Litton in which he recorded the following blood concentrations after applying 3 ml of 50% phenol on the face: after 1 hour, 0.68 mg/100 ml; after 2 hours, 0.19 mg/100 ml and after 3 hours, 0.10 mg/100 ml. According to the same author, phenol only becomes systemically toxic at a concentration of 23 mg/100 ml, which, for a total blood volume of 4 l, requires a total of 1 g in the blood at any given moment. Detoxification by conjugation is initiated immediately after applying phenol on the skin.

Aqueous or oil vehicle Phenol in aqueous solution is absorbed very differently to phenol in oil solution. Maximum blood levels reached 0.9 mg/100 ml when phenol was applied in an oil solution and 1.1 mg/100 ml in an aqueous solution. In 1950, Deichmann11 published a study on the reabsorption of phenol in an aqueous and an oil vehicle: 71 mg of phenol was absorbed by the skin of a rat in 1 hour’s contact with an aqueous solution of phenol at 4.7%, whereas only 15 mg was absorbed when the same concentration was present in (mineral) oil solution. Phenol penetrates the skin more slowly from an oil solution than from an aqueous solution. In this way, it also becomes less toxic. Applying 4 g of phenol to the skin does not make the blood concentration of the free form or conjugated form of phenol any higher than if 3 g were applied. Deichmann did not offer any explanation of this phenomenon, but the rest period of 90 minutes between each 1 g application most probably allowed enough time for the phenol to be detoxified. After 3 g, the phenol levels returned to normal within 48 hours. A little longer was needed to eliminate 4 g. On the third day, the blood levels of phenol reached doses lower than that of any normal individual, that is, around 0.15 mg. No sign of systemic intoxication was detected in the course of this study. It must be noted, however, that control mechanisms were not as sophisticated as they are today and continuous Holter-ECG recording monitors were, for example, not yet available then.

Effects of occlusion In the past, it was thought that applying a dressing was the cause of local necrosis. In fact, the necrosis occurred when very tight, thick dressings soaked in phenol were applied to the wounds. According to studies by Ruedemann and Deichmann,5 applying a dressing (unsoaked) after applying

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phenol actually reduces the speed with which the phenol is absorbed – although not the total quantity. There are two advantages to a dressing: it allows surface maceration and increases the contact time with the epidermis. In this way, it can improve the cosmetic results. Impermeable occlusion reduces the rate at which phenol is absorbed through the skin and increases the chances of hepatic metabolization, as the organism is not overloaded or saturated by a massive influx of phenol. Peaks of free phenol are lower under occlusion. The literature is unclear on whether occlusion improves the results of phenol. In 1980, McCollough and Hillman12 reported that the results of phenol (Baker’s solution) without occlusion were comparable to those of phenol under occlusion. They went on to say that not using occlusion improves patient comfort and lowers the risk of complications. What is true for Baker’s solution is not necessarily true for other formulas, however. In 1989, Baker published a study showing that occlusion with Vaseline® produces the same results as occlusion with impermeable tape. Stegman,13 Alt and Brody published studies that show that phenol is more active under occlusion. Occlusion can therefore be used to increase the depth of action of a peel when the practitioner wants the penetration to be deeper. This is the case with Lip & Eyelid®: occlusion is recommended when treating wrinkles around the lips and chin, but not for the treatment of eyelid wrinkles. Occlusion with Vaseline® appears to be as effective as an impermeable occlusive dressing. There is one small practical problem with using Vaseline®: heat from the skin makes it more liquid, and as it liquefies it tends to drip onto the eyes and neck, getting on to the clothes, hands and anything else the patient touches. The presence of Vaseline® also rules out spot application the day after the peel. The duration of occlusion has also been discussed at great length, with Baker recommending 48 hours’ occlusion. When I use occlusion, I leave it on for 24 hours. I have not noticed any difference with longer occlusion times – which seems logical, as after 24 hours all the phenol applied has had plenty of time to be reabsorbed by the skin; leaving it for more than 24 hours merely increases the risk of secondary infections. The importance of the question of occlusion becomes clear when it is considered that many surgeons take the occlusion off under anesthetic or sedation, which increases the cost and the risk for the patient. On the first day, there are very few nerve endings left that have survived the phenol, and taking the whole occlusive mask off in one go, pulling it downwards, is only very briefly painful. Another question is whether the occlusion should be applied immediately after the phenol or not. Phenol is a volatile compound, and applying occlusion immediately after it has been applied will stop it from partially evaporating and will therefore allow for longer maceration of a greater quantity of phenol. The sooner occlusion is applied after phenol, the deeper the effect will be.

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Urinary elimination The by-products of phenol are rapidly eliminated in the urine. After intoxication with phenol, these by-products make the urine a dark color – anything from light olive green to dark brown. The intensity of the color has no direct relation to the severity of intoxication.

Specific phenol sensitivities Very young children are particularly sensitive to phenol, and incidents of intoxication were recorded at the beginning of the 20th century after simply applying phenol dressings on the intact skin of infants and after ingestion of 0.25 g of phenol.14 In the early 1900s, Nothnagel and Rossbach described alcoholism as a situation that improves resistance to phenol. A logical explanation can be found in the ways in which alcohol and phenol are metabolized. Alcohol is oxidized to acetic acid in the body. Certain conjugation mechanisms bring acetic acid into play through acetylation of the phenol function. The detoxifying conjugation could be between the phenol and the acetic acid. Deichmann studied basal blood phenol levels before and after application of phenol to the skin. Basal blood phenol levels were lower than before treatment, showing that the body adapts to the detoxification process. Wine is known to contain numerous aromatic molecules, including polyphenols. Wine drinkers15 develop a more effective polyphenol detoxification metabolism than non-drinkers, which could explain their relative resistance to intoxication with phenol.

Notes 1. All peels remove the stratum corneum, at least partially, and make the skin permeable to chemical, physical and environmental attacks. Total sun block is essential after any kind of peel.

2. Guzzo CA, Lazarus GS, Werth VP. Dermatological pharmacology. In: Hardman JG, Limbird LE, Molinoff PB, Ruddon RW, Gilman AG, Chren MM, Bickers DR. Dermatological pharmacology. In: Hardman JG, Limbird LE, Eds., Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 8th edition, 1572–88. 2000, USA, NY, McGraw-Hill. 3. Young and well-hydrated skin is more sensitive to a peel than old and sun-damaged skin. 4. Kyoto University Ligand Chemical Database: http://expasy.hcage.ch/cgi-bin/get-enzyme-entry? 2.4.1.35/2.1.25/1.14.13.7. 5. Ruedmann G, Deichmann WR. Blood phenol level after topical application of phenol-containing preparations. JAMA 1953; 152: 506–9. 6. Deichmann WB. Local and systemic effects following skin contact with phenol: a review of literature. Ind Hyg Toxicol. 1949; 31:146–54. 7. This proteolytic concentration means the solution penetrates rapidly. 8. Occlusion stops phenol evaporating and enhances maceration in the flesh exposed by the burns. 9. Loss of skin impermeability means that the solution penetrates rapidly. 10. Benetar D. Lee peeling au phenol. J Med Esth Chir Derm 1988; XV(60): 319–23. 11. Deichmann WB, Miller T, Roberts JB. Local and systemic effects following application of dilute solutions of phenol in water and in camphor-liquid petrolatum on the skin of animals. Arch Ind Hyg Occup Med, 1950; 2: 454–61. 12. McCollough EG, Hillman RA. Chemical face peel [Symposium on the Aging Face]. Ontolaryngology Clinics of North America, 1980; 13: 353–65. 13. Stegman SJ. A comparative histologic study of the effects of three peeling agents and dermabrasion on normal and sundamaged skin. Aesthetic Plastic Surgery, 1982; 6: 123–35. 14. Manquet A. Traité élémentaire de thérapeutique de matière médicale et de pharmacologie, 5° ed, tome 1. 1903: 240-60. 15. It should be noted that when this observation was made in France, at the beginning of the 20th century, the majority of cases of alcoholism were due to wine.

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28 Toxicity of phenol: causes, prevention and treatment When phenol is dumped into river water, it is very toxic to aquatic fauna and lethal at a concentration of 1 ppm. The genuine toxicity of phenol and the almost apocalyptic descriptions of its side-effects, which can even lead to death by cardiovascular collapse, severely limited its cosmetic use until the second half of the 1990s, especially in Europe. English-language publications, for their part, state that, even so, a phenol peel is ‘one of the most frequently used techniques in the treatment of photoaging’.1 As we have seen in Chapter 27, phenol is rapidly absorbed by the skin and mucous membranes. It is also rapidly eliminated by the lungs in the form of water and carbon dioxide and by the kidneys in free form and in sulfate- and glucuronide-conjugated form. Detoxification starts immediately after phenol has been applied.2 Phenol vapor enters the pulmonary circulation very rapidly, and because of this respiratory absorption, doctors who use it (regularly) have to wear a mask. The treatment room must also be properly aired and ventilated to prevent the patient, who is already absorbing phenol through the skin, from absorbing any significant amount through the respiratory route. Keeping the patient well hydrated (with a saline drip) promotes diuresis and therefore renal elimination of free phenol as well as conjugated or oxidized phenol. Some authors recommend intravenous hyperhydration before and during the peel and sometimes forced diuresis with an intravenous injection of furosemide. This hyperhydration is not necessary when phenol is applied carefully.

concentration of the phenol, but is largely dependent on the total surface area of skin exposed to the product.’

Medications containing phenol There are many pharmaceutical products widely used in medicine and dentistry that contain phenol, sometimes in fairly high concentrations. Bonain’s local anesthetic mixture, combining menthol, cocaine and phenol, is well known, and is used, for example, as an intranasal analgesic treatment for certain facial pains. Other products containing phenol include hemorrhoid creams, chilblain solutions, ear drops or wax remover drops, psoriasis treatments, and mouth sprays with phenol in concentrations ranging from 3 mg/ml to 50 mg/g. Applying these products locally introduces only a small quantity of phenol into the organism at well-spaced intervals, and does not appear to cause intoxication.

Phenol soap Phenol soap with a concentration of 5 g/100 g introduces a small amount of the active product into the organism with each wash. Even if resorption, and therefore phenol toxicity, depends more on the surface area covered than on the concentration of the product,6 each wash only delivers a small quantity of phenol, which is soon rinsed off.

Gargles Data obtained from laboratory animals In rats, the oral LD50 is 530 mg/kg.3 In rabbits, 70% of the phenol applied to the skin is absorbed in 30 minutes and 99% within 24 hours.4 In 1944, Deichmann and Witherup5 published the results of their experiments on the toxicity of phenol in laboratory animals. Their conclusions were as follows: ‘the rate of absorption of phenol/skin surface unit is not closely dependent on the

Tercinol® is a phenol solution with a concentration of 15 g/100 g. It is recommended to dilute a teaspoon of concentrated solution in a glass of water and to gargle three or four times a day. One teaspoon is generally equivalent to 5 ml and therefore contains about 0.75 g of phenol. It is applied to irritated mucous membranes, and a small amount of the product will be swallowed every time it is used unless the user is an expert at gargling. Some 2–3 g could come into contact with the irritated mucous membranes every day. The package notice warns patients of the potential side-effects of phenol.

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Dental wick There are dental wicks that can contain up to 375 mg/g of phenol. They are introduced into the dental cavity being treated and are reapplied every 10 minutes. The explanatory notice simply recommends not touching the mucous membranes. Nevertheless, it is possible for the patient to accidentally ingest a total of 1 g, although the time lapse allows any phenol that might have been ingested to be eliminated without toxicity. The products with the highest concentrations of phenol benefit from its antiseptic and local anesthetic properties.

Mouthwash Argentofenol® is a disinfectant mouthwash recommended to be dabbed on the mucous membranes every other day. It contains up to 35% phenol. Phenol is still used in medicine and dentistry, sometimes at high concentrations. Sideeffects remain rare, as the product is relatively diluted, applied in small quantities or little surfaces and therefore readily eliminated, even when applied repeatedly during the day. There is plenty of time for the liver to detoxify and the kidneys to eliminate the phenol.

Phenol peel During a full-face phenol peel, 2.5–5 ml of phenol solution is usually applied on the skin. The conventional formulas (Litton and Baker) use concentrations of around 50%. Applying 3–4 cm3 of solution therefore leaves 1.5–2 g of phenol on the skin. It is important to be aware of the fact that the toxicity of phenol solutions appears to be paradoxical, as, up to a certain point, diluted solutions can be more toxic than concentrated ones. Publications report that simple aqueous dilutions of 2 parts phenol to 1 part water (i.e. solutions with a concentration of around 33%7) are usually the most dangerous. Some phenol peel formulations still use this concentration, however, confusing speed of penetration with cosmetic effectiveness.

Paradoxical toxicity At a concentration higher than 80%, phenol is a keratocoagulant. The first applications of phenol precipitate the skin proteins and thus create a biological barrier that prevents further applications of phenol from penetrating too rapidly. Concentrations lower than 80% are keratolytic,8 as they break the disulfide bonds between the keratin molecules and allow more of the solution to penetrate more rapidly. Reducing the concentration of a phenol solution can therefore make it more dangerous, both locally and systemically. Lowering the concentration of phenol in a peel solution is therefore not enough to make it non-toxic,

and quicker penetration should not be confused with improved results. Solutions with lower concentrations penetrate more rapidly through the skin and are more rapidly absorbed: they are therefore more toxic at the same time as being less effective from a cosmetic point of view. The distinction between keratolytic and keratocoagulant must be given careful consideration. It is clinically obvious that solutions that are assumed to be keratolytic cause protein precipitation, or coagulation. Roenigk9 published an interesting article on this subject: in spite of the concentration of approximately 50% (48.5% to be precise), phenol acts as a keratocoagulant in Baker’s solution because – according to him – of the combination with croton oil and septisol. Other protein coagulating peels do not use septisol or croton oil, however. Stone8 performed a histological study of the depth of penetration of various phenol formulas: the Gordon–Baker formula at 48.5% phenol, the Verner–Dickinson formula at 67% and liquid phenol at 88%. The results, in keeping with the principles set out above, show that Baker’s formula penetrates twice as deeply as Verner’s and four times as deeply as liquid phenol at 88%. Although phenol is absorbed rapidly by skin tissue, only a part of it will gradually reach the innermost regions, as the skin proteins flocculate almost immediately, and this creates a physical catchment area for the phenol as well as a natural dam that stops it penetrating the deeper layers too quickly.

Lessons from medical history General remarks The average fatal dose (death within 24 hours) in humans is 8–15 g by ingestion (according to Nothnagel and Rossbach in Manquat10). Individual predisposition largely explains the variations in the toxic dose. In 1903, Manquat10 reported two extreme cases: his colleague, Bouchard, had ‘by mistake injected’ (sic) two patients with enemas containing 48 g of phenol. Their temperatures fell to 35°C, went up to 41.8°C in the evening, returned to normal the next day and remained stable the following days. There is no information available on the long-term outcome of this accident: chemical intestinal necrosis, fistulization, secondary infection, survival, death, or liver and kidney toxicity? Ingesting just 0.5 g of phenol can lead to symptoms of toxicity, and sometimes an oral dose of 5 g is enough to cause death. The patient shows signs of corrosive esophagitis and gastritis, then signs of kidney damage, cardiac collapse, breathing difficulties and a feeling of inebriation followed by coma. Medical history tells us that the ‘Lister’ technique took the life of many patients. Lord Lister, born in England in 1827 (Figure 25.12 in Chapter 25), was the first surgeon to use phenol to disinfect the air in the oper-

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ating theater (1867). This technique saved many patients, but others started to die when phenol was first used to disinfect wounds or when catgut was disinfected with phenol oil. Phenol proved toxic when applied directly in too great a quantity to skin that was unprotected by the stratum corneum. Lysol®, used as a household disinfectant for toilets and bathrooms, is an oil mixture of cresols and other ill-defined phenols dating from before the First World War. Even if Lysol® is less toxic and less irritating than phenol, it was the method of choice for suicide11 and abortion12 at the beginning of the 20th century.

Phenol administration routes in the past Every possible route (apart from perhaps intra-arterial injection) was used to administer phenol: ■ Oral or rectal routes (0.5–1 g of phenol in enemas, 6–12 times a day in the case of typhoid fever); the rectal route was the preferred one ■ Topical route (diphtheria) ■ Intrapleural injection (3 g) ■ ENT route: gargles or ear drops ■ Intravenous route (treatment of varicose veins) ■ ‘Tissue’ route (neurolysis, etc.) ■ Inhalations (whooping cough). Authors at the beginning of the 20th century knew all about the toxic effects of phenol and described the symptoms in detail. It is obvious that the doses used caused frequent and serious accidents. Doctors then became more cautious, and would use a maximum concentration of 0.5 g of phenol in enemas, to be repeated every 3 hours, so as not to reach a total daily dose of 4 g. Doses of 4–20 g/day were considered dangerous or lethal. Manquat10 reported: ‘inside the body, we have nearly always administered phenol in enemas (0.5 to 1 gram of phenol to 200 to 500 grams of vehicle) that have sometimes been repeated every three hours (Desplats). A dose of 4 grams has brought the patient’s temperature down as low as 34° (Van Oye). Caution dictates that we should not go beyond 0.5 g per enema,’ and that ‘We sometimes prescribe a dose of 1 to 4 grams in a potion; patients have difficulty tolerating this preparation.’ Desplats recommended the following ‘lemonade’: ‘Phenic acid 2 to 4 grams Lemon water 100 grams Simple syrup 100 to 150 grams Water q.s. for one liter Take 100 grams of this solution every 3 hours.’ A simple calculation shows that patients at the beginning of the 20th century were supposed to ingest 800 g of this

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‘lemonade’ every 24 hours, that is 1.6–3.6 g of phenol per day. Toxic accidents, however, were mostly described when a dressing soaked in phenol left some of the product in a cavity that was having difficulty draining and the majority of serious cases was reported when phenol was injected into perirectal cell tissue.10 Reading these old texts provides access to a whole theory of symptoms that today are only seen in cases of industrial poisoning. All this – and even the fact that phenol was considered highly toxic by inhalation – did not stop Bethene and Court13 suggesting inhalation of liquid phenol fumes to treat whooping cough in 1954. The plasma concentrations reached were far higher than those described by Litton during full-face peels.

Symptoms of phenol intoxication Gastrointestinal symptoms Ingesting more than 0.5 g of phenol triggers anorexia, nausea and belching. Symptoms of gastroenteritis (colic, vomiting and diarrhea) occurs with slightly higher concentrations. Massive ingestion destroys the mucous membranes in the upper digestive tract. It has been reported that gastric problems can occur after applying phenol dressings externally. Experience of conventional14 phenol peels also shows that a small percentage of patients complain of nausea or even vomiting shortly after a deep peel. This nausea and vomiting occur within a few hours after the application of an occlusive mask.15 The cause-and-effect relationship between these symptoms and excessive phenolemia has not been officially established.

Neurological symptoms Generally, there are no neurological symptoms when doses of less than 1–2 g have been ingested. The neurological symptoms are headaches, tinnitus, hypoacusis, paresthesia, muscular hypotonia and stupor. If the dose is fatal, the patient falls into a coma after a feeling of inebriation and dies without convulsions. Phenol stimulates the motor neurons of the anterior horn.16

Cardiovascular symptoms Cardiovascular complications have been known about since the 19th century: the pulse was described as becoming irregular and weak, slowing down to become extremely weak or imperceptible. Hemoglobinuria and methemoglobinemia were also described. Details of these complications are considered later in this chapter, as well as techniques for avoiding and treating them.

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Lessons from toxicology centers In 1993, a retrospective study was conducted over 5 years at the Poison Center Philadelphia.17 It involved 96 cases of poisoning with Creolin®, a disinfectant containing 26% phenol. This concentration is known to be potentially toxic, as it enhances penetration through keratolysis. Exposure was oral in 60 cases, dermal in 2 cases, and both oral and dermal in 12 cases. Only 1 case of inhalation was recorded. ■ Oral exposure. Eleven patients (14%) experienced rapid CNS depression that was rapidly reversible. Fourteen patients experienced vomiting, coughing and stridor. ■ Dermal exposure. Seven patients (100%) also had respiratory symptoms. On contact with the skin, phenol precipitates keratin and forms a white film, followed by redness and then necrosis. A 5% solution causes a burning sensation and then local anesthesia.18 ■ Antidotes to phenol. Isopropanol (isopropyl alcohol) and polyethylene glycol seem to be the most effective local antidotes, both histologically and because they slow down blood penetration.19 Immediately rinsing the area of skin that has come into contact with the phenol with plenty of water gets rid of some of the toxin and prevents precipitation of some of the epidermal proteins. ■ Mixed exposure (oral plus dermal). Four people experienced vomiting, coughing and stridor. Skin and mucous membrane burns were recorded in approximately 25% of the poisonings. It is remarkable that no cardiovascular complications were recorded in this study. Medical publications report that when a person is exposed rapidly to a sufficient quantity of phenol (in general, 3–4 g of phenol applied quickly to the face), abnormal heart rhythms may occur. These abnormalities appear 15–20 minutes after the beginning of the peel and are often rapidly reversible. If any arrhythmia had developed during these cases of poisoning, it would no doubt have occurred rapidly and disappeared again by the time the patient arrived at the hospital. This argues in favor of the autonomous reversibility of arrhythmias with phenol. The authors cautiously conclude: ‘The absence of serious toxicity and major chemical burns in this series does not eliminate concern with the corrosive and systemic risks of phenol poisoning’. It should also be noted that phenol was widely used for 112 years between 1867 (Lister) and 1979 (in a study by Truppmann and Ellenby20) without any cardiovascular monitoring and with relatively few serious or fatal complications considering that very often it was applied in nonmedical circumstances (by lay peelers). Baker6 himself asserted that in 5000 cases of full-face or partial treatments, he did not note any abnormal heart rhythms – or any sys-

temic toxicity – that could be attributed conclusively to phenol. McCollough and Maloney21 pointed out that in 25 years of using phenol, they came across a certain number of arrhythmias of toxic origin, but that none of these cases needed any specific treatment apart from waiting for the sinus rhythm to return and adding on 15 minutes to be on the safe side. Asken22 confided that in 15 years of performing phenol peels using the Baker–Gordon method, he never came across a case of arrhythmia that needed treatment. I personally, however, was faced in 1997 with a relatively severe arrhythmia when applying a full-face phenol peel. How this arrhythmia developed is described later in this chapter. The fear of arrhythmic complications is the main brake on the use of phenol peels today. It is therefore worthwhile studying this problem in detail. The conclusions that can be drawn from reading about these complications in medical literature help us to understand how to apply phenol with greater safety, though the possibility of arrhythmias occurring cannot be avoided.

Cardiovascular complications (Figures 28.1–28.7)

Figure 28.1 Sinus rhythm.

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Figure 28.4 Bigeminy.

Figure 28.5 Trigeminy.

Figure 28.6 Quadrigeminy

Figure 28.2

Figure 28.7

Supraventricular tachycardia.

Ventricular tachycardia.

Figure 28.3 Premature ventricular contraction.

For more than 50 years, lay peelers used phenol in full-face peels for cosmetic purposes without any medical monitoring. Cases of deaths related to phenol peels date from this era and up until the 1960s. In 1973, Litton, Fournier and Capinpin23 published the results of a survey covering cardiovascular complications during phenol facial peels. In the 493 questionnaires

returned by plastic surgeons, only 3 cases of cardiac arrhythmias were reported. It should be noted, however, that heart monitoring was only (very) rarely used in this era and in this indication. Reading all the works on the cardiac toxicity of phenol clearly shows that arrhythmias (easily triggered by the rapid application of large quantities of phenol) were only rarely diagnosed or published, and the fact that they tend to resolve spontaneously allowed practitioners to sleep peacefully. Truppmann and Ellenby routinely used cardiac monitoring when doing phenol peels, and detected many arrhythmias. In 1979, they published the results of a study on 48 patients treated with phenol peels.20 Saponified and non-saponified Baker or Litton formulas were studied. They report that 23% of patients treated with phenol showed arrhythmia, on average 17.5 minutes after the phenol was first applied. These arrhythmias were often premature ventricular (Figure 28.3) or supraventricular contractions, bigeminy, or supraventricular (Figure 28.2) or ventricular tachycardias (Figure 28.7). Tachycardia, which in extreme cases can sometimes reach 220–230 beats per minute, can turn into ventricular fibrillation and lead to cardiac arrest. These seem to be the first documented reports of cardiac arrhythmias that can definitely be attributed to phenol in

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humans. The authors also state that when they applied phenol slowly, taking more than 1 hour, no incidence of arrhythmia was detected. The types of arrhythmia encountered were the following: ■ 10 patients out of the 48 treated with facial peels showed arrhythmia ■ 4 patients showed premature ventricular contraction; aged 30, 36, 59 and 71 ■ 2 patients showed bigeminy; aged 24 and 43 (Figure 28.4) ■ 2 patients showed paroxysmal tachycardia; aged 55 and 67 ■ 2 patients showed ventricular tachycardia; aged 36 and 73 In order to refine their conclusions, the authors studied the potential influence of different parameters: ■ products used in anesthesia: no correlation could be found ■ oxygenation before and during the peel: no correlation could be found ■ saponified or non-saponified formula: no correlation could be found ■ preexisting arrhythmia: no correlation could be found (other authors24 have confirmed this lack of correlation). ■ age of the patient: no correlation could be found ■ speed of application: 50% of patients who received a phenol peel in less than 30 minutes developed arrhythmia, with the average time for arrhythmia to occur being approximately 17.5 minutes; no patient developed arrhythmia when the peel was applied over a minimum period of 60 minutes ■ surface area treated: No arrhythmia occurred before phenol was applied on at least half of the face Lotter in 1980 and Litton in 1981 published the results of two counter-surveys. Lotter25 highlighted the fact that only 23% of doctors performing phenol peels use cardiac monitoring to check the progress of the application. Litton recorded in his study26 that after reading Truppmann and Ellenby’s article,20 13% of plastic surgeons who had answered his questionnaire now reported arrhythmias under phenol and that 51% of practitioners now monitored phenol peels with a cardioscope. The question asked of the plastic surgeons was: ‘Have you seen any cardiac complications during a phenol peel?’ The answers were as follows: yes: no: tachycardia: arrhythmia: premature ventricular contraction

5% 87% 6% 1% 1%

Of the doctors questioned, 51% said they used monitoring, while 42% never used it and 7% only sometimes monitored their patients. The conclusion that can be drawn from these studies is: Putting the patient on cardiac monitoring is a legitimate precaution that allows the doctor to act immediately in case of cardiovascular complication. On the other hand, not monitoring the patient does not necessarily make the prognosis for complications any worse, and most of the time they seem to resolve spontaneously. In response to these studies, Baker27,28 claimed that, in the course of 5000 phenol peels, he never came across a case of arrhythmia. His observation was based on the following evidence: ■ Complications can take practitioners by surprise during any cosmetic procedure – and facial peels are no exception to this rule. ■ The most common complications involve pigmentation, and through careful patient selection these complications can be avoided. ■ Hypertrophic scars are extremely rare after a chemical peel. ■ Systemic toxicity is also ‘extremely’ rare. Nevertheless, Baker recommended that all patients should be monitored during full-face phenol peels – which seems obvious to us nowadays. Baker stated that he only observed ‘normal’ irregularities during his phenol peels and never had a patient die. He considered the cases of premature supraventricular contractions and the two cases of paroxysmal tachycardia reported by Truppmann and Ellenby20 to be epiphenomena, not very serious and fairly frequent during minor procedures, especially if an anesthetic containing adrenaline (epinephrine) is used. The two cases of bigeminy reported by Truppmann and Ellenby did not bother him either, as he often came across bigeminy during routine procedures and drew the logical conclusion that phenol should not be blamed automatically for everything. He was, however, alarmed by the two cases of ventricular tachycardia in the patients who received a ‘rapid’ application of phenol in less than 1 hour, and stressed the importance of taking time over the peel. Baker also recommended taking at least 1 hour to apply any phenol peel. Finally, he concluded that phenol peels produce results that no other surgical technique can rival and that an experienced practitioner, aware of the complications and risks, can, by carefully selecting his patients, apply phenol peels without any fear of dire consequences. In 20 years of using phenol, he did not observe any cardiac complication that could be directly attributed to phenol with certainty.28 Nevertheless, all of these opinions, even when they come from such well-known medical experts, cannot aspire to the status of scientific facts. Gross29 decided to reproduce the study by Truppmann and Ellenby, using the same non-saponified formula in 100

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consecutive peels on the face and neck (up to the clavicles in the anterior region and up to the 7th cervical vertebra in the posterior region). Given the number of arrhythmias that occurred after the 54th patient, the method of application had to be changed. Out of 54 patients, 31 (57%) developed cardiac arrhythmia (supraventricular and/or ventricular). Unfortunately, Gross did not reveal the quantities of phenol used. Logically, it was used in large quantities, since the surface area treated included the face and neck up to the 7th cervical vertebra. Moreover, the premedication contained substances that change the heartbeat, such as beta-blockers. The rest of the patients were therefore treated in two sessions with a 24-hour interval in between: the face was treated in the first session and the neck in the second. In this series, ‘only’ 22% of the patients developed arrhythmia. No correlation was found between the age of the patients, their gender, the preexistence of cardiovascular diseases and the incidence of arrhythmias. On the other hand, the blood concentrations reached in this study seem to be very high, up to 33.29 mg/100 ml. These figures differ enormously from those in Deichmann’s or Litton’s studies (see below). We know that the systemic toxicity of phenol can manifest from 23 mg/100 ml.30 The arrhythmias seem to occur in the following order: tachycardia and premature supraventricular contractions that develop into atrial fibrillation (pulsus irregularis perpetuus). Arrhythmias lasts on average 2–19 minutes and are spontaneously reversible, depending on the clearance of the phenol and the gradual lowering of blood concentrations after hepatic detoxification and renal elimination. This study did not show any relation between blood levels and the occurrence or severity of arrhythmias. Each patient appears to have his or her own particular sensitivity to phenol. In conclusion, Gross recommended dividing the face into different sections and leaving a rest period of 20 minutes between each zone (cf Chapter 33). Baker’s point of view is fully shared by Cortez,31 who, in a retrospective study of hundreds of phenol peels that he carried out between 1983 and 1990, did not observe any cardiac toxicity when the precautions for use were followed. A study by Wexler et al4 on rabbits found a correlation between the rapid onset of arrhythmia and the speed with which phenol is absorbed through the skin: 70% of phenol is absorbed in 30 minutes in rabbits. Forced diuresis (intravenous furosemide) while the peel is being applied prevents cardiac arrhythmia by increasing renal elimination of free phenol, even before the conjugation and oxidation processes of detoxification could protect the organism. In addition, slow application of the solution in at least 1 hour meant that no arrhythmia was observed, as this leaves enough time for the phenol to be detoxified. A study on humans, limited to 10 patients, was published in 1990.32 Continuous electrocardiogram (ECG) recordings (halters) were taken before, during and after the

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peels. Many ectopic beats were recorded, but no direct relation with the application of phenol was established, although one case of arrhythmia was found to be suspicious. With the documents in my possession, however, I am unable to analyze the different factors that might have influenced this study with any precision. In 1985, Warner and Harper33 published an article reporting a suspect case of multifocal premature ventricular contractions and bigeminy in a child34 weighing 36 kg who received a dose of 2.4 g of 40% phenol in 0.8% of croton oil, hexachlorophene and water.35 This large quantity36 was applied to 1.9% of the body surface area (we know that the absorption surface is at least as important if not more than the total quantity of phenol applied) and under general anesthetic. Arrhythmias from phenol usually occur rapidly, in approximately quarter of an hour, and in this case they occurred after 55 minutes. Phenolemia was not measured and, according to the authors, there was nothing in the case history that could have attributed the arrhythmia to phenol. The child had already had several phenol peels in the past for dermatological problems and had never experienced any problems, but because of Truppman’s and Ellenby’s descriptions, the authors assumed that phenol was the culprit. Another study37 compared the toxicity of trichloroacetic acid (TCA) and phenol (Baker’s solution); the conclusion was that ‘it would appear advisable’ to set up a cardiac monitor during a full-face peel with Baker’s solution, whereas TCA does not cause any type of arrhythmia. Previous studies have shown that cardiac monitoring is an essential prerequisite when doing a phenol peel on the face, even if serious arrhythmia can be avoided by applying the product in at least 1 hour. Applying phenol without any cardiac monitoring is not good medical practice, and any subsequent complications could be considered professional malpractice based on negligence. It should be remembered that vagal reactions are not uncommon during any treatment that is stressful for the patient and that they need to be detected in order to be treated correctly.

Prevention of cardiac arrhythmias By observing the following seven points, the risks of cardiovascular complications can be significantly reduced:4,38 1. Pre-peel checkup: ECG, liver and kidney (blood analysis) 2. Application over more than 1 hour 3. Monitoring (ECG and pulse oximetry)39 4. Good general health 5. Good patient selection 6. Good hydration40

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7. Lidocaine as a preventive (?):41 this point is highly debatable, since arrhythmia can be avoided simply by taking more than 1 hour to apply the phenol. Simple lidocaine used to do nerve blocks before the phenol peel should be considered a cautious technique.

Treating arrhythmia during a peel There are several articles describing the appropriate treatment for heart arrhythmias occurring in the course of a phenol peel.20,24,26,33

At the first signs of arrhythmia If the ECG shows the least sign of arrhythmia – even slight, seemingly insignificant and supraventricular – the application of phenol should be stopped immediately and the intravenous drip speeded up to hydrate the patient more and force diuresis to eliminate not only the conjugated phenol but also free phenol. Under these conditions, the arrhythmia should show rapid signs of improvement and not get any worse. Fifteen minutes after the last arrhythmia, the phenol can be reapplied again carefully. It is essential for the anesthetist, the doctor doing the peel and/or an assistant to read the ECG constantly. A certain amount of competence in ECG reading is therefore recommended before doing a full-face phenol peel. There would be no point plugging in an ECG monitor and being unable to detect basic heart rhythm abnormalities! Some authors4 recommend the use of furosemide to increase diuresis, but furosemide can cause abnormal ionic plasma levels, which can, in turn, cause arrhythmias or make them more likely. Be that as it may, furosemide rapidly increases the elimination of free phenol in urine, even before the processes of hepatic conjugation, which come into play very rapidly all the same, have been able to detoxify it. Experiments undertaken by Wexler et al4 show the following results in animals. When 2 ml of Baker’s solution is applied quickly on the skin of rabbits weighing 3 kg and sedated with pentobarbital, on a surface area proportionally 5–8 times larger than the human face, numerous heart arrhythmias are observed. It is interesting to note that the doses required to induce arrhythmias in rabbits are high. Forced diuresis with furosemide significantly reduces the arrhythmias. By applying the product slowly, arrhythmia is avoided altogether, in spite of the extremely high doses and the extent of the surface area treated.

‘Benign’ arrhythmias Simple, isolated supraventricular extrasystoles can occur frequently during any type of procedure, simply because

the patient is under stress. The right reaction to these benign arrhythmias is to stop applying the phenol and wait for the sinus rhythm to return ‘naturally’. These seemingly benign extrasystoles can in fact be a sign of becoming more serious arrhythmias. It is best to be prepared and have all the necessary equipment ready to hand and to keep a very close eye on the ECG in order to pick up any more significant changes in rhythm. It is a bit late at this stage to be wondering whether the lidocaine is at hand or if the battery in the laryngoscope is charged!

More serious arrhythmias Bradycardia In the case of bradycardia, intravenous atropine is indicated. In cases of severe phenol poisoning, it has been reported that the pulse rate can at first increase and then drop off afterwards.

Tachyarrhythmias Arrhythmia can evolve rapidly: within a few seconds, benign supraventricular arrhythmias can turn into other types of rhythm disorders, such as nodal tachycardia, atrial fibrillation and multiple ventricular extrasystoles, in doublets or triplets. It is important to act quickly – which is easy as everything that is needed to deal with these arrhythmias (fortunately very rare) is ready to hand and the patient is on a drip. The patient should be put on oxygen to maintain good blood oxygen levels. Treatment consists in the slow intravenous injection of 50 mg of lidocaine without adrenaline (epinephrine). Usually, the arrhythmia rights itself in less than 10–15 minutes. A total maximum dose of 100 mg, in two slow intravenous injections of 50 mg (in 1 minute), provides a strong and rapid antiarrhythmic effect (50 mg of lidocaine may be sufficient to get the patient back into a regular sinus rhythm). If lidocaine does not bring the rhythm back to normal, bretylium tosylate may be indicated42 (if in an area equipped for resuscitation).33 Other antiarrhythmics are now available and can of course be used, depending on the type of arrhythmia and the competence of the doctor injecting them.

Blood pressure In cases of severe phenol poisoning, blood pressure can rise slightly and then drop significantly afterwards.43

Collapse and cardiac arrest To the best of my knowledge, collapse, ventricular fibrillation or flutter, torsade de pointes, and other extremely serious arrhythmias have not been described during peels, but

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could occur with severe phenol poisoning, usually caused by accidental intravascular injections of phenol. In Truppmann’s and Ellenby’s study, none of these serious arrhythmias were described, and cardioversion and defibrillation were not necessary if more than 1 hour was taken to perform the peel. If medication proved insufficient and the arrhythmia led to collapse, external heart massage and/or an electric shock of 200 J would resuscitate the patient. Once again, however, there is no risk of this level of arrhythmia when a phenol peel is applied correctly, and as we have seen already, a full-face phenol peel performed in more than 1 hour does not trigger any arrhythmia. The only case of arrhythmia that I have come across44 occurred when, for once, I allowed myself to be influenced by a colleague who is highly respected in the world of phenol peels and who claimed that he performed all his full-face peels in 30 minutes, without any ECG monitoring, as he had never had any patients feel unwell. The absence of an ECG obviously meant that he could not pick up on any arrhythmias. His experience could lead us to the conclusion that the arrhythmias potentially caused by a full-face phenol peel remain benign and resolve without treatment. However, this conclusion would be hasty and irresponsible. In 1994, Lalanne et al24 described two cases of cardiac arrest after the injection, in 3 minutes, of 1.4 and 1.8 g of phenol in an aqueous solution with a concentration of 6% (2 × 15 ml). The injections were strictly extravascular, but were near the aorta. The injections were made into the semilunar ganglia and were given as painkillers to patients with inoperable pancreatic cancer. These patients were in a poor state of health generally, on numerous drugs and under general anesthesia.45 There is an accumulation of numerous risk factors here, and the phenol peels were applied under completely different conditions. The complications occurred almost immediately, 2–3 minutes after the injection, and started with a drop in arterial oxygen saturation to 92%. The arrhythmia began with polymorphous ventricular extrasystoles that rapidly turned into ventricular tachycardia, ventricular fibrillation and cardiac arrest. The treatments described above got the patients back to normal rhythms. In 1993, Gaudy et al46 described the same type of accident, in which 30 ml of 6.6% phenol solution (around 2 g) was injected for palliative splanchnic neurolysis in a patient with cancer of the pancreas. It seems obvious that, in spite of the fact that the injection was extravascular and given by a competent practitioner, there was massive vascular absorption, which can cause accidents that are fortunately reversible after treatment. It is most likely that the injections were made in edematous tissue that had been damaged by surgery beforehand and that this enhanced penetration. When intoxication has been severe and death narrowly avoided, jaundice and oliganuria43 follow – a sign of the hepatic and renal toxicity of phenol. These cases do not fall

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within the strict framework of a phenol peel carried out correctly: hepatic and renal toxicity are complications linked to acute poisoning.

Other types of toxicity Toxicity by inhalation Phenol vapors are heavier than air (vapor density 1.2). The best way to ventilate a room where a phenol peel is being performed is therefore at ground level and not higher up. This is important, as phenol vapors can travel considerable distances at ground level. Care should be taken with electric heaters, as there is a risk of the vapors coming into contact with a source of heat that can start a fire: the mixture of phenol vapors and air has a flashpoint of 79°C (174°F).43 The olfactory sensitivity threshold is 0.047 ppm: phenol vapors are hard to eliminate from a surgery – it can take hours. The presence of 250 ppm in inhaled air poses an immediate danger to health and life. Acute poisoning from phenol vapors can produce the same symptoms as oral poisoning. Chronic exposure47 to phenol vapors produces the following symptoms: vomiting, difficulty swallowing, excessive salivation, diarrhea, anorexia, headaches, dizziness, weakness and myalgia, mental disturbances, dark urine, and sometimes skin eruptions. Postmortem examinations of animals given fatal doses of phenol vapors show the presence of myocardial necrosis and acute pneumonia, as well as vascular, liver and kidney damage.43

Ophthalmic toxicity Direct contact with phenol crystals, concentrated solutions or vapors (45 ppm) causes serious damage to the eyes: hyperalgesic chemical conjunctivitis, severe iritis, and possibly corneal opacification with loss of vision and edema of the eyelids. In some cases of poisoning through direct accidental eyelid contact, the seriousness of the injury to the eyelids has required surgery.48 The results of phenol coming into direct contact with the eye can vary from complete recovery of vision to loss of the eye, depending on the severity of the lesions. Chronic, repeated or prolonged exposure to phenol vapors can cause conjunctivitis. A gray discoloration of the sclera along with brown patches of pigmentation at the insertion of the rectus muscle tendons of the eye have been described after chronic exposure.43 Any direct contact between phenol and the eyes requires raising the eyelids and rinsing immediately with copious amounts of water or saline solution. The eye should be flushed with saline solution for 30–60 minutes, while waiting for the opinion of an ophthalmologist. Ophthalmic Vaseline® or a Vaseline®-based antibiotic eye ointment should always be put in the eyes before applying phenol, as Vaseline® largely deactivates phenol.

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Hepatic and renal toxicity Some cases of hepatic and renal toxicity after severe poisoning with phenol derivatives have been reported in the literature, but I have not been able to find any such record in medical publications dealing with phenol peels.

19.

Notes

21.

1. Glogau RG, Matarasso SL. Chemical peels: trichloracetic acid and phenol. Dermatol Clin 1995; 13: 263–76. 2. Ruedemann R, Deichmann WR. Blood phenol level after topical application of phenol-containing preparations. JAMA 1953; 152: 506–9. 3. Rats seem to be resistant, as this LD50, applied to an average human weight of 65 kg, would give a figure of 34.45 g of phenol. 4. Wexler MR, Halon DA, Teitelbaum A, Tadjer G, Peled IJ. The prevention of cardiac arrhythmias produced in an animal model by the topical application of a phenol preparation in common use for facial peeling. Plast Reconstr Surg 1984; 73: 595–8. 5. Deichmann WB, Witherup S. The acute and comparative toxicity of phenol and o-, m-, and p-cresols for experimental animals. J Pharmacol Exp Ther, 1944; 80, 233–40. 6. Baker TJ. Chemical Rejuvenation of the Skin. 7. Arouette J. Dermabrasion, relèvements, peelings. In: Blackwell A (Ed.), Collection des Manuels pratiques de médecine esthétique. 1989, Paris. 8. Stone PhA. Peelings au phénol Baker–Gordon et modifies. J Med Esth Chir Derm 1996; XXII(90): 93–7. 9. McCulloch EG, Langsdon PR, Maloney BP. Chemical Peel with Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996, UK. Oxford, Marcel Decker Ltd. 10. Manquat A. Traité élémentaire de thérapeutique de matiére médicale et de pharmacologie, 5° ed, tome 1. 1903: 240–60. 11. After voluntary ingestion of Lysol®, death occurs within 3–4 hours; at autopsy, corrosive esophagitis and gastritis were of course noted. 12. Back-street abortionists readily used irritant solutions, phenol and Lysol® solutions among them, as uterine enemas to induce abortions. It is likely that this method was just as dangerous for the mother as for the fetus, because of the rich vascularization of the uterus. Autopsy would show a high concentration of phenol in the right side of the heart, which drains all the veins of the body and therefore the phenolladen blood. 13. Bethene, Court. BMJ 1954; i: 1494. 14. As opposed to ‘tamed’ formulations. 15. Vomiting can cause reversible petechiae (see Chapter 37). 16. Dauphin A, Darkord JC. Hygiène hospitalière pratique, 2° ed. Association de Pharmacie Hospitalière de l’lle de France. Editions médicales internationales. 17. Spiller HA, Quadrani-Kushner DA, Cleveland P. A five-year evaluation of acute exposure to phenol disinfectant (26%). J Toxicol Clin Toxicol 1993; 31: 307–13. 18. Giroud JP, Mathé G, Meyniel G. Pharmacologie clinique:

20.

22. 23. 24.

25.

26.

27. 28. 29. 30. 31. 32. 33.

34. 35.

36. 37.

38.

39.

40. 41. 42.

bases de la théapeutique. 2nd Edn. 1978, France, Paris, Expansion Scientific Français. Hunter DM, Timerdery BL, Leonard RB, McCalmont T, Schwartz E. Effects of isopropyl alcohol, ethanol and polyethylene glycol/industrial methylated spirits in the treatment of acute phenol burns. Ann Emerg Med 1992; 21: 1303–7. Truppman E, Ellenby JD. Major electrocardiographic change during chemical face peeling. Plast Reconstr Surg 1979; 63: 44–8. McCulloch EG, Langsdon PR, Maloney BP. Chemical Peel with Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996, UK, Oxford, Marcel Decker Ltd. Asken S. Unoccluded Baker–Gordon phenol peels – review and update. J Dermatol Surg Oncol 1989; 15: 998–1008. Litton C, Fournier P, Capinpin A. A survey of chemical peeling of the face. Plast Reconstr Surg. 1973; 51(6): 645–7. Lalanne B, Baubion O, Sezeur A, Tricot C, Gaudy JH. Circulatory arrest after splanchnic neurolysis with phenol in unrespectable cancer of the pancreas. Ann Chir. 1994; 48(11): 1025–8. Lotter cited in Botta SA, Straith RE, Goodwin HH. Cardiac arrythmias in phenol face peeling: a suggested protocol for prevention. Aesthetic Plastic Surgery. 1988; 12(2): 115–17. Litton C, Trinidad G. Complications of chemical face peeling as evaluated by a questionnaire. Plast Reconstr Surg 1981; 67: 738–43. Discussions following Litton and Trinidad. Baker TJ. The voice of polite dissent. Plast Reconstr Surg. 1979. Gross BG. Cardiac arrhythmias during phenol face peeling. Plast Reconstr Surg 1984; 73: 590–4. Benatar D. Le peeling au phénol. J Med Esth Chir Derm 1988; XV(60): 319–23. Cortez E. Chemical face peeling. Otolarynyol Clin North Am 1990; 23: 947–60. 1990 study. Warner MA, Harper JV. Cardiac dysrhythmias associated with chemical peeling with phenol. Anesthesiology 1985; 62: 366–7. We have already seen that infants are more sensitive to phenol than adults. This keratolytic concentration makes for rapid penetration, and blood vessel uptake of the phenol is quicker in a formula that does not contain any oils other than croton. More than is usually applied during a facial peel. Stagnone GJ, Orgel MG, Stagnone JJ. Cardiovascular effects of topical TCS 50% and Baker’s phenol solution. J Dermatol Surg Oncol 1987; 13: 999–1002. Botto SA et al. Cardiac arrhythmias in phenol face peeling: a suggested protocol for prevention. Aesthet Plast Surg 1988; 12: 115–17. Both are essential, as the onset of arrhythmia is often preceded by a significant drop in oxygen saturation. Besides, arrhythmia cannot be detected by a pulse oximeter. 500 ml of saline solution before the peel to trigger diuresis. The lidocaine used to carry out any facial nerve blocks should be taken into account. Note that 2 ml intravenous vials contain 100 mg. 5 mg/kg should be injected and repeated after 15–30 minutes,

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10 mg/kg if necessary. The total maximum dose is 30 mg/kg. 43. Material Safety Data Sheet. Fisher Scientific, USA. 44. This arrhythmia occurred before the research that allowed me to write this book was undertaken. 45. General anesthesia is not always considered to be an additional risk factor during phenol peels.

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46. Gaudy JH, Tricot C, Sezeur A. Troubles du rythme cardiaque graves après phènolisation splanchnique peopèratoire. Can J Anaesth 1993; 40: 357–9. 47. This has no relation to what a doctor performing phenol peels, even on a regular basis, can inhale. 48. A phenol peel always causes severe edema in the eyelids. Scarring, however, is very rare.

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29 Phenol: choice of peel and combination treatments

A phenol peel is mainly indicated to treat facial skin for severe photoaging. It is the only type of peel that can get rid of deep wrinkles1 and regenerate elasticity and firmness in

the treated skin in one single treatment. Phenol peels are therefore usually aimed at people who are (well) past their 40s. There is no real age limit, and phenol has been used on patients of advanced years (Figure 29.1), as well as on other much younger patients. Old age is not in itself a contraindication to phenol,2 and it is remarkable to note that the skin regenerates perfectly well at any age: the oldest patient that I have ever treated was 82 when she had a phenol peel – and I know for a fact that I do not hold the record

A

B

Influence of the age and gender of the patient Age of the patient

Figure 29.1 An 82-year-old patient (a) before and (b) after a full-face phenol peel.

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for the oldest patient. Phenol has also been used on children to treat specific disorders. Young adults have also been treated with phenol for acne scars or scars of other origins. However, because of its toxicity and the profound changes it makes to the skin, phenol should not be used without a good reason. Phenol should not be used to treat something that alpha-hydroxy acids (AHA) or trichloroacetic acid (TCA) can treat just as well. The strength of a peel should always be adapted to the problem being treated: there is no point applying a peel that is too superficial or too deep.

Male skin and female skin Thickness of the skin A man’s skin is often more resistant, thicker and oilier (Figure 29.2) than a woman’s skin. Sagging skin is more common than photoaging in men, and men are often better candidates for a face-lift than a peel. It is the type of skin more than the gender that determines the results of a phenol peel. If aging has resulted in a thick skin sagging, without dyschromia (see also Figure 29.7), and if the folds are

more pronounced than the wrinkles and fine lines, a peel is not at all indicated either in a man or a woman, as, even if phenol produces a ‘three-dimensional face-lift’ effect, the extent of the retraction is no substitute for surgery (Figures 29.2 and 29.3). When aging has resulted in sun-damaged thinning skin with wrinkles and age spots, a peel is an excellent indication and produces surprising results, in both men and women (Figure 29.4). Men with light skin phototypes and thin and sun-damaged skin respond very well to phenol. The gender-based distinction is purely statistical: in general, women can be said to respond better to phenol than men, but this does not rule men out from treatment. The only problem that proves really awkward after treating a man’s skin is post-peel erythema (Figure 29.5): women can easily use make-up to hide it, but this is difficult for men. Men can, however, wear a tinted sunblock to hide the redness.

Shaving The question of shaving often comes up, and it is true that stubble can pose a technical problem for a patient who wants to shave at all costs. This is a minor concern, however, as the patient only has to wait for 10 days before shaving after a phenol peel. On the 11th day, the doctor might allow the

Figure 29.2

Figure 29.3

A patient 8 years after a full-face phenol peel: the quality of the skin has remained much improved, but the wrinkles and sagging did not really benefit from the peel. A face-lift would be indicated for this patient.

Two years after a full-face phenol peel on a patient with thick and oily skin, the quality of the skin has improved but the folds and sagging remain unchanged. A face-lift would have been a better indication for this patient.

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Figure 29.4 (a) Photoaging before a phenol peel. (b) Three weeks after Lip & Eyelid® formula (full-face phenol peel).

patient to shave carefully, after evaluating the condition of the patient’s skin. Wearing a beard can even be an advantage and make the demarcation line less visible (Figure 29.5).

Make-up Patients regularly ask about make-up. Patients who usually wear foundation can go back to using it when the skin has finished flaking, around the 8th day and with the doctor’s permission. The first time make-up is used signals the long-awaited return to a normal social life. There are some patients who do not usually wear makeup, and it is important to tell them that it will probably be essential for them to wear foundation after the peel to hide

the erythema, which can last up to several months. The reddest areas should be covered with a green (to counteract the redness) make-up stick before foundation is put on. If the patient refuses to use make-up, she should be advised to use a tinted sunblock, and this should be discussed with her before the peel.

Influence of the patient’s phototype Although phenol has been used successfully on patients with a ‘Mediterranean’ skin type or on Asian patients with

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Figure 29.5

Figure 29.6

A patient 15 days after a full-face peel: wearing a beard can limit the effect of the demarcation line caused by the erythema.

Ten days after a Lip & Eyelid® peel around the mouth on a tanned patient: the phenol has taken away the tan. Easy TCA® (four sessions) or Unideep® (one session) will even out the skin tone.

a fair skin, it is nevertheless aimed at patients with a light skin phototype. Patients with Fitzpatrick skin type I to III are excellent candidates. Patients with Fitzpatrick skin type IV and patients with severely sun-damaged skin will have to accept the possibility of a visible demarcation line3 on the neck. This demarcation line (Figure 29.6) can be made less obvious both by a good peeling technique and by combination with other peels on the neck.4 Darker skin types are not such a good indication, because of the change in skin tone after the peel. Most patients with a lot of wrinkles, however, prefer to exchange their wrinkles for a difference in skin color that can easily be disguised with makeup. Skin phototype is even more important when using phenol locally; a local5 phenol peel can only really be applied on light skin phototypes that will not show any significant and visible difference in color on the eyelids and around the mouth. The same applies to patients with a lot of freckles, keratoses or lentigines, which only disappear from the areas treated with phenol but still remain in the surrounding areas. The difference in skin quality is also very visible. These patients should only be treated with a full-face peel. It is nevertheless possible for these patients to have a local phenol peel combined with a full peel to the papillary dermis. Combining Lip & Eyelid® with Unideep® provides a phenol peel and a peel to even out skin with lentigines, keratoses or freckles.6 The two peels should be done in the same session: the phenol first, followed immediately afterwards by Unideep® on the rest of the face, around the area treated with phenol.

Phenol peel versus other medical or surgical techniques Peel versus face-lift There is not much point asking this question, as a full-face peel is no substitute for a full face-lift, and vice versa (Figures 29.7 and 29.8). The indications are different; peels and

Figure 29.7 The sagging – more pronounced than the photoaging – contraindicate a phenol peel, which would have no effect on this patient.

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Figure 29.8 Excellent three-dimensional tightening effect from a phenol peel: (a) before treatment and (b) 3 months afterwards.

face-lifts complement rather than compete with each other.7 When the damage is localized, the doctor alone can advise his or her patient on which treatment or combination of techniques to use. A face-lift cannot treat wrinkles on the upper lip, but laser treatment, dermabrasion or Lip & Eyelid® formula can get rid of them. These treatments should be carried out on the same day as the sur-

gical face-lift while the patient is still under anesthetic. Wrinkles around the lips sometimes benefit from a combination of dermabrasion and phenol: Lip & Eyelid® formula is locally applied on the day of the face-lift and left under occlusion for 24 hours; the following day, the surgeon evaluates the results of the peel on the upper lip; if some wrinkles still persist, they can be touched up with the peel solution.8 It is also possible, on the first day, to

Figure 29.9 (a) Photoaging, thin skin and slight sagging: a good indication for a full-face phenol peel. Aging of the neck: a neck- and face-lift is indicated before the phenol peel. (b) Results of a full-face phenol peel (Lip & Eyelid®), 14 days after the peel. There is spectacular improvement in the skin. Oddly enough, some of the lentigines have been replaced by telangiectasias. They must be treated quickly, to avoid extravasation of iron pigments and potential multiple localized tattoo marks.

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perform dermabrasion9 after a focal application of phenol on the lip. If surgical blepharoplasty is not combined with a facelift, Lip & Eyelid® formula can be applied on the eyelids at the same time as the face-lift. The patient in Figure 29.9 is a typical case where the facial photoaging10 would benefit far more from a full-face phenol peel than from a neck- and face-lift. Nevertheless, phenol, with difficulty, tightens and rejuvenates the neck, which will only benefit from surgery followed by a peel to the papillary dermis or several peels to the Grenz zone (with ETCA) to improve the quality and the color of the skin after the surgical face-lift. When the wrinkles are on the eyelids and around the mouth, the problem is therefore easily solved. In the case of sagging and wrinkled skin, it is clear that the best results can be achieved with a combination of treatments that should be carried out at different times (see below). The large majority of patients are in this situation, and the degree of facial ptosis will be the deciding factor in whether to suggest a face-lift or a phenol peel. A face-lift gives better results for facial ptosis (Figure 29.10); a peel gives better results for wrinkles and dyschromias. A surgical face-lift can only tighten damaged skin that will not have enough elasticity to remain tight definitively.

Figure 29.10 This is the same patient as in Figure 29.8. Two years after full-face Exoderm®, the improvement on the cheeks is still well maintained. However, sagging has partially recurred, the results on the upper lip are inadequate and the color of the skin is slightly uneven. The patient, who is keen on boating in sunny climates, has not kept out of the sun as recommended. Treatment will consist of a spot application of Lip & Eyelid® formula on the upper lip (using an occlusive technique), combined with one Easy TCA® peel per week for 4 weeks to even out the skin tone. Daily care comprises Blending Bleaching® cream and Melablock HSP® 50+.11

Phenol peel combined with a surgical face-lift We have seen above that there is no problem with performing a localized phenol peel at the same time as a surgical face-lift if the two treatments are aimed at different areas. When both treatments are indicated for the whole face,12 the face-lift should be done first, followed by a rest period of around 6 months before the deep peel (Figure 29.11). The peel will have the additional advantage of softening the scars from the face-lift at the same time as

Figure 29.11 (a) A patient after surgical face-lift. (b) The same patient: phenol peel (Lip & Eyelid®) after a face-lift.

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restructuring the histology of the epidermis and the dermis and removing the marks and fine lines that did not respond to the face-lift. With a phenol peel, a demarcation line is left under the jaw13 that is partially hidden by shadow. A face-lift after a phenol peel could raise this demarcation line to the cheeks: any face-lift should therefore be done before a phenol peel. More importantly still, using a phenol peel (or even a deep TCA peel14) at the same time of operation on an area that has just been treated with a surgical lift can potentially cause extensive facial necrosis. The general principle is not to undermine the skin’s inner vitality with surgery at the same time as injuring the outer layers of the skin with a peel. In other words: a face-lift should not be done on the same day as a full-face deep phenol peel. A study15 from 1989 looked at the viability of dorsal skin flaps (on guinea pigs) subjected in vivo to transposition and suture immediately followed by a single application of phenol (Baker’s solution) and 24-hour occlusive tape dressing. Thirty-six skin flaps were raised and sutured back into place, and only 18 were treated with phenol. Analysis of the results clearly shows that combining a surgical lift and phenol at the same time of operation is not a wise choice, as the average necrosed surface area without phenol was 3.1 cm2, compared with 6.3 cm2 for the peeled flaps. Another study16 on animals came to the conclusion that raising a skin flap causes changes in the tissue of the reticular dermis and the underlying tissue, which makes it more sensitive to any subsequent injury. The risk of compromising the viability of a raised skin flap is therefore too high to opt for a simultaneous face-lift and deep peel. On the eyelids, however, the fat hernia around the orbit was removed through the transconjunctival approach and combined – in expert hands – successfully and safely with a local phenol peel.17 McCollough and Maloney18 combined surgical blepharoplasty with a phenol peel, but left the skin to rest for 3 months before doing the eyelid peel.

Phenol peel and Aptos® threads There is a new technique that involves inserting barbed or spiral threads under the skin to tighten sagging tissue (Figures 29.12 and 29.13). These are known as Aptos® threads or Russian threads, as in their current form they were designed by a Dr M Sulamanidze from Moscow.19 The Aptos® threads are inserted deeper than the phenol penetrates: there is therefore no risk of interaction between the phenol, and the thread that would, in any case, resist it chemically. There are, however, three problems: ■ The entry points of the threads must not come into contact with the phenol, as there is a risk that the inflammation will push them out.

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Figure 29.12 Aptos® thread.

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Figure 29.13 (a) Aptos® springs. (b) Springs.

■ The inflammation caused by the phenol peel affects all the layers of the skin: this reaction, combined with the inflammation caused by the thread itself, could make the tissue in which the threads have to anchor themselves more fragile and cause them to rapidly unhook. ■ Phenol is, of course, a disinfectant, but a phenol peel coagulates all of the skin’s immune structures, and the skin becomes very prone to infection. The risk of secondary infection from the thread is increased. It is therefore preferable not to insert Aptos® threads at the same time as performing a phenol peel. Moreover, phenol partially tightens the skin, and it may well be more worthwhile using Aptos® threads as a second line of treatment, when the phenol has taken full effect, after at least three months. The presence of threads inserted in the skin several months previously is not a contraindication for a phenol peel, and it is possible to decide on the opposite course of action if the doctor thinks this is a better option for the patient: Aptos® threads can be inserted first and a phenol peel can be done afterwards.

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Phenol peel versus carbon dioxide laser resurfacing Several studies have been carried out comparing the results of a full-face phenol peel and resurfacing with a carbon dioxide (CO2) laser, sometimes known as a carbon dioxide laser peel. A study by Langsdon, Milburn and Yarber20 looked at four women volunteers with sun-damaged facial skin and wrinkles. A phenol peel was applied to the left half of the face and a Sharplan Silktouch Flashscanner CO2 laser was used to treat the right half. The clinical results were similar in both cases, although the laser appears to give better results in areas where the skin is very thick (e.g. the chin). The laser, however, causes more hypopigmentation and complications, and the post-peel period is more comfortable for the patient with phenol than with laser. Histologically, the depth of action of phenol is deeper than that of the laser and reaches the reticular dermis. The authors concluded that both ablative laser and phenol peels remain useful clinical tools. The records show that the battle has been won by phenol because of the high number and the severity of complications caused by CO2 lasers. Fintsi also presented a split-face study, applying phenol (Exoderm® – Fintsi’s formula, congress presentation, Stiges, Spain) on one half of the face. One of his colleagues, a laser specialist, applied a CO2 laser to the other half of the face. The results were clinically obvious, and it was clear that they were better on the half of the face treated with phenol – so much so that the patient asked for another phenol treatment to even out the two sides. We could perhaps conclude, however, that the CO2 laser might be a better indication for very thick and oily skins, especially on the chin and nose.

Notes 1. The nasolabial folds only respond to phenol if they are light and the skin is thin. 2. The contraindications are described in Chapter 31. 3. For pictures, see Chapter 37.

4. TCA, for example: one session of Unideep® (a peel to the papillary dermis) or four sessions of Easy TCA® (less aggressive). These peels should be combined with a depigmenting cream such as Blending Bleaching®. 5. Chemical eyelid or lip surgery (see Chapter 36). 6. These disappear after Unideep®, a TCA peel to the papillary dermis. 7. Stuzin JM, Baker TJ, Gordon HL. Treatment of photoaging. Clin Plast Surg 1993; 20: 9–25. 8. When wrinkles persist, the doctor might also decide on a second period of occlusion. 9. Using sandpaper or a diamond fraise. Microdermabrasion is not recommended here. 10. Atrophic, sallow skin, numerous lentigines and benign tumors, solar/senile keratoses, Hutchinson’s freckle, wrinkles and fine lines, and wrinkles around the mouth and eyes. 11. HSP sunblock: heat-shock proteins – sunblock containing stimulants to produce these proteins that protect against heat damage. 12. For example, when the patient presents with severe photoaging and sagging skin at the same time. 13. For pictures see Chapter 37. 14. I am talking here of a TCA peel to the reticular dermis. A TCA peel to the papillary dermis (e.g. Unideep®) is, on the contrary, applied immediately after a surgical lift. 15. Hayes DK Stambaugh KI. Viability of skin flaps subjected to simultaneous chemical peel with occlusive taping. Laryngoscope 1989; 99: 1016–19. 16. Hayes DK, Berkland ME, Stambaugh KI. Dermal healing after local skin flaps and chemical peels. Arch Otolaryngol Head Neck Surg 1990; 116: 794–7. 17. McKinney P, Zukowski ML, Mossie R. The fourth option: a novel approach to low lip blepharoplasty. Aesth Plast Surg 1991; 15: 293–6. 18. McCulloch EG, Langsdon PR, Maloney BP. Chemical Peel with Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996, UK, Oxford, Marcel Decker Ltd. 19. Some attempts at copies can be found on the market: some of these copies are extremely crude, others tend to break easily and others are too thick and can be felt through the skin. 20. Langsdon PR, Milburn M, Yarber R. Comparison of the laser and phenol chemical peels produce similar results in facial skin resurfacing. Arch Otolaryngol Head Neck Surg 2000; 126: 1195–9.

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30 Phenol: indications

A phenol peel is the deepest type of peel, the one that gives the most dramatic results but that is also the most dangerous. Its indications are precise and limited to cases that cannot be treated by other peels. If an alpha-hydroxy acid (AHA) or trichloroacetic acid (TCA) peel can solve a skin problem, it will be chosen over a phenol peel without hesitation. The main indication for a phenol peel is severe photoaging.

Treating wrinkles: phenol plus botulinum toxin Fine lines, wrinkles, furrows and folds do not respond to phenol in the same way. Wrinkles and fine lines caused by sun damage are far more responsive (Figure 30.1) than expression lines or, above all, skin folds due to excess skin.

Expression wrinkles are also an excellent indication, on condition that movement is blocked by botulinum toxin approximately 8 days before the peel. Without this highly effective synergetic combination, kinetic wrinkles will of course disappear during the first few weeks after the phenol peel, but will come back afterwards, much to the annoyance of patients.1 ‘Compression’ wrinkles that form during sleep are particularly problematic and difficult to get rid of: they come from an excess of skin combined with loss of elasticity, and form during the night as a result of continuous pressure from the head on the pillow that ‘chisels’ the skin. Filling techniques can be tried, can be disappointing in this indication in the long term. The only real solution is to change unconscious sleeping habits, which is almost impossible. Special pillows have been designed specifically to combat this problem.

Folds and furrows

Deep wrinkles These can respond very well to a phenol peel (Figure 30.2). Deep cheek wrinkles (Figure 30.3) caused purely by sun damage are one of the best indications for a phenol peel.

These usually result from excessive skin laxity. Deep folds and furrows are not a good indication for phenol. They result from intrinsic aging and can sometimes be filled before a phenol peel. There is no need for a long time interval between

Figure 30.1 Full-face phenol (Lip & Eyelid® formula): (a) before and (b) 30 days after the peel. The combination of botulinum toxin and phenol work together on the forehead, crow’s feet, frown lines and sometimes wrinkles on the upper lip.

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filling and peeling; the two treatments can even be done at the same time if the filler is resorbable:2 furrows and folds can be filled immediately before the phenol peel. It is easy to understand how the severity of the inflammatory reaction after the phenol peel does not help the implant in the long term, but the clinical results of this combination speak in its favor. Folds and furrows can also be filled after a phenol peel, after the inflammatory erythema has subsided. An injection given too soon after the peel, during the erythematous phase, can easily cause bruising.

Expression lines

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Figure 30.2 (a) Before full-face phenol. (b) 15 days after full-face phenol (Exoderm®). Kinetic wrinkles are starting to come back. (c) 30 days after full-face phenol: the phenol has solved all the skin problems apart from the expression lines, which have come back.

Expression lines on the forehead and between the eyebrows and crow’s feet have a natural tendency to recur partially and rapidly, even after a phenol peel. A botulinum toxin injection before the peel stops expression lines imprinting themselves on the skin as it renews itself, and this combination is very satisfactory, improving results significantly. The botulinum toxin should be injected 1 week before the peel so that new collagen can be synthesized on an immobile dermis. The injection can also be given 8 days after the phenol peel, if not done beforehand. Injecting botulinum toxin during the post-peel period of erythema and edema increases the risk of the toxin moving as well as the risk of temporary cosmetic complications caused by the toxin. The duration of the toxin’s effect does not seem to change much, however.

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Figure 30.3 (a) Sun-damaged cheek skin. (b) Complete restructuring, 30 days after a full-face phenol peel (Lip & Eyelid® formula).

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Figure 30.4 Rejuvenation of the eyes: (a) before; (b) 30 days after a full-face phenol peel (Lip & Eyelid® formula).

We will look at the chemical blepharoplasty and/or cheiloplasty (labioplasty) technique in detail in Chapter 36.

Wrinkles on the lower eyelids, drooping upper eyelids and loss of elasticity are excellent indications for a local application of phenol (Figures 30.4 and 30.5). Wrinkles around the upper and lower lips respond very well to a local application of Lip & Eyelid® formula (Figure 30.6).

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Wrinkles around the mouth and eyes

Figure 30.5 Chemical blepharoplasty (Lip & Eyelid®): (a) before; (b) after.

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Figure 30.7

Figure 30.6 Long-term removal of wrinkles around the lips after a phenol peel: (a) before; (b) after 1 year; (c) after 3 years. The contour of the lips has been plumped with an injection of a slow resorbable filler, 1 year after the phenol peel.

(a) Occlusion of localized phenol to treat the radial wrinkles of the outer canthus of the upper eyelids in a 75-year-old Caucasian patient. This treatment should be combined with a botulinum toxin injection (8 days before the peel) and a TCA peel to the papillary dermis (Unideep®) in the same session to even out the skin tone of the rest of the face. (b) Three weeks after this combination of treatments, the radial wrinkles have disappeared. There is no visible demarcation line.

Laxity and skin elastosis Radial wrinkles on the upper eyelids ‘Radial’ wrinkles on the outer canthus of the upper eyelid respond well to localized treatment with phenol using the occlusive technique (Figure 30.7).

Other wrinkles Other wrinkles, such as cheek wrinkles (see Figure 30.9) or forehead wrinkles, are excellent indications for a full-face phenol peel, but are usually not treated locally, as not only are the results less obvious than after a full-face peel but also the difference between the treated area and the surrounding skin can be too obvious. This type of local treatment is reserved for very particular cases, when there is no risk of tone and structure differences between the locally treated area and the surrounding skin.

Thin, elastotic and distended skin is ideal for a phenol peel (Figure 30.8). Results are better than with a surgical facelift. On the other hand, a phenol peel, even under the best conditions, cannot completely lift jowls. Although phenol is indicated in many cases of facial sagging, large amounts of excess skin still have to be resected surgically. Surgery does not, however, change the texture of the skin, and applying a phenol peel after surgery rejuvenates skin texture, removing all the wrinkles and marks that surgery has no effect on. When the skin is thin, a full-face phenol peel can often produce sufficient retraction to make a surgical face-lift unnecessary. The same applies for upper blepharochalasis: a surgical blepharoplasty is still the best choice in this indication, but excellent results can be achieved with a single application of Lip & Eyelid® formula, and drooping skin can be retracted satisfactorily, as described in Chapter 36. Oddly enough, eyelid retraction is automatically restricted to ‘normal’ tension, and I have never had any cases of ectropion, entropion or lagophthalmia.

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Figure 30.8 (a, b) Pronounced photoaging, combined with slight sagging, is an excellent indication for a full-face phenol peel.

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Dyschromias We have seen that phenol has a marked effect on dyschromias, and it incapacitates melanocytes, even if it does not destroy them histologically (Figure 30.9). Even if many melanocytes are still physically present in the basal layer,3 they can no longer produce melanin (partially or completely).

Melasma and post-inflammatory hyperpigmentation Phenol is a good indication for all types of hyperpigmented lesions: lentigines, pigmented keratoses, chloasma, melasma, freckles and post-inflammatory hyperpigmentation (PIH).4 All the same, phenol is not the first choice of

Figure 30.9 Before (a) and after (b) a full-face phenol peel (Lip & Eyelid® formula): a combination of yellow skin, wrinkles, fine lines and lentigines in a patient who smokes. Thirty days after the peel the erythema is normal. The patient is not wearing any make-up. Botulinum toxin was injected 8 days before the peel (forehead, frown lines and crow’s feet).

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treatment, as other, less aggressive, peels will do most of the time. Hyperpigmentation problems have to be treated differently, depending on how deep they are: epidermal hyperpigmentation can be treated with a more superficial peel than dermal hyperpigmentation, which will only respond to a deeper peel. Phenol may be indicated to treat severe and resistant melasma definitively. Some patches may recur after a period of lightening. Patients must be warned of this possibility. The problem can largely be avoided by recommending that the patient uses Blending Bleaching® cream5 for several months after the phenol peel. Asken6 has drawn attention to the following fact: the distribution of melanosomes is particularly uneven in melasma – a phenol peel may accentuate this uneven pigmentation even more.

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Wood’s lamp It is useful to evaluate the depth of pigmentation: a Wood’s lamp can be used to do this, as shown in Figure 30.10. The worse the pigmentation appears when exposed to the Wood’s light (i.e. the more patchy the skin appears), the more superficial the melanin is and the treatment will soon take effect. Superficial pigmentation does not need to be treated with phenol, and can be treated effectively with less aggressive peels.

Asian skin Light Asian skin is not a contraindication to phenol. Between 1986 and 1992, phenol was applied to 710 lightcomplexioned Asian patients and proved to be highly effective and very safe to use.7

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Figure 30.10

Freckles Histologically, freckles are characterized by a normal number of melanocytes in the basal layer. The melanocytes are, however, larger and more ‘dendritic’, and give up their melanosomes more readily to the keratinocytes. Freckles disappear completely and definitively with phenol. A TCA peel to the papillary dermis8 will also get rid of freckles. A local phenol peel is contraindicated on light skin phototypes – which in principle are a good indication for phenol – with freckles, as they will disappear where the phenol has been applied and will persist in the surrounding areas. A combination of local Lip & Eyelid® and Unideep® (TCA to the papillary dermis) is suitable to avoid this freckle demarcation line.

Lentigo maligna Lentigo maligna9 is a flat, multicolored, pigmented lesion with an irregular shape that may be precancerous. It has a slow radial growth phase and its diameter can vary from a

(a) Wood’s lamp and (b) patient with melasma seen under this light.

few millimeters to several centimeters. It is usually found on the face, temples or cheekbones, in patients over 50 years old. The average age of onset is 65 and the incidence increases with age. Lentigo maligna is formed by melanocyte proliferation that is purely intraepidermal. Histologically, there is an increase in the number of atypical melanocytes in the basal layer of the epidermis. Some of the melanocytes may have multiple nuclei. These atypical melanocytes are found at a distance from the clinical border of the lesion. The epidermis is atrophic and the dermis elastotic. This lesion is, in fact, associated with chronic sun exposure over many years, mainly in patients with a light skin phototype. Adnexal spread is not uncommon, and numerous melanophages are found in the dermis. This lesion can, however, degenerate into a superficial melanoma, whose prognosis is good, as, more often than not, it does not produce metastases. When lentigo maligna

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ied. Cryotherapy should theoretically produce good results because melanocytes are particularly sensitive to cold, but this treatment has a 50% recurrence rate. 5-Fluorouracil (5-FU), used alone, gives poor results. With carbon dioxide and argon lasers, radiotherapy and electron-beam therapy, there have been many recurrences. Curettage, dermabrasion and electrodessication have produced few positive results and a high rate of recurrence. Topical hydroquinone and tretinoin have no effect on the lesion. It is not my intention to suggest that a phenol peel is the ideal treatment for lentigo maligna, but only to say that, unlike the majority of other treatments suggested, I have never seen a recurrence of flat lentigo maligna after a phenol peel, be it full-face or local (Figure 30.11).

Keratoses Extensive multiple keratoses (solar or senile) on the entire face should be treated with a full-face peel, whereas isolated keratoses can be treated by other methods (see Chapter 22). According to McCollough and Maloney,10 laser treatment has no advantage over chemical treatment. Vergereau, for his part, published a study confirming the advantage of applying Only Touch® TCA over laser, dry ice or coagulation. Several forms of keratoses can coexist.

Seborrheic keratoses

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Seborrheic keratoses (Figure 30.12) are very common and are found on areas of skin that have been exposed to the sun as well as unexposed areas. The lesions are always benign, but can sometimes be difficult to distinguish from malign melanomas. Beyond a certain thickness, the keratotic layer makes them unresponsive to peels, even to phenol. They can be treated by shave excision with a snare and radiofrequency (Ellman unit) immediately before applying

Figure 30.11 Lentigo maligna combined with severe photoaging: (a) before and (b) after a full-face phenol peel.

is diagnosed at the age of 45, the statistical risk of it developing into melanoma is 47% over the lifetime of the patient. When it is diagnosed at the age of 67, the risk of it turning into a malignant melanoma is 22%. In both cases, the 5-year survival rate is 90%. That is why dermatological monitoring and sun protection are usually all that is recommended. If the lesion is extensive, surgical excision and maybe a skin graft are sometimes necessary. The excision must be wide and the excision margin at least 1 cm beyond the clinical border of the lesion: the cure rate is then 91% with a 9% recurrence rate in 4 months. Mohs microsurgery is also widely used. Many other treatments have been stud-

Figure 30.12 Seborrheic keratoses

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the phenol. When treating seborrheic keratoses by shave excision without combining it with phenol, a TCA peel to the basal layer or to the papillary dermis can be applied to even out the structure of the skin once it has completely healed.

Actinic keratoses Actinic (or solar) keratoses11 form mainly on areas of skin that have been exposed to the sun: the face, the pinna of the ear and the hands, for example. They are tumors that are often precancerous: 10–20% (25% according to some authors) develop into skin cancer, often of the spinocellular carcinoma variety. Many patients with actinic keratoses or even subclinical epithelioma in situ could benefit from a phenol peel on the face,12 possibly preceded by curettage of the largest lesions. Patients who have been treated with 5FU are often reluctant to put up with the necrotic appearance of their skin after each treatment. A phenol peel gets rid of the actinic keratoses at the same time as making the skin look younger overall. Many authors describe very longterm results, if the patient is prepared to change his or her attitude to sun exposure after the peel and, as well as keeping out the sun, is prepared to use SPF 50+ sunblock every day thereafter. In case of recurrence, inadequate results or the appearance of new lesions, the patient can be treated again 4–6 weeks after the first peel. Patients treated with phenol are at far less risk of developing cancer later on.4

Superficial cancers Phenol necroses the epidermis and part of the dermis and eliminates intraepidermal skin cancers in situ. Carcinomas form from cells in the epidermis. To my knowledge, no scientific article has ever reported skin cancers being caused by the application of peeling agents. If the literature is to be believed, a phenol peel treatment has the added advantage of lowering the frequency of other precancerous lesions forming and probably other cancers in situ in sun-damaged skin. From a toxicological point of view, topically applied phenol13 is not recognized as a carcinogenic or teratogenic agent. It is still necessary, however, to make a definite diagnosis before applying chemical agents to suspect pigmented lesions.

usually brings about an improvement in the appearance of telangiectasias. However, in some cases, the extent of postpeel neovascularization can make them worse or cause new vasodilations to appear. ‘Raised’ telangiectasias may become more visible in patients with thin and transparent skin. Facial telangiectasias can be electrocoagulated immediately before the phenol is applied, while the patient is under nerve-block anesthesia for the peel. An Ellman radiofrequency unit is completely satisfactory in this indication.

Xanthelasma Xanthelasmas are permanent and often symmetrical yellowish plaques that appear on the inner canthus of the eyes (Figure 30.13). All four eyelids can be affected by this nonpremalignant dermatitis. They can be soft or hard. In 50% of cases, they are associated with hyperlipidemia. Women are affected twice as often as men. Xanthelasmas are formed by a build-up of xanthoma cells: macrophages swollen with free or esterified cholesterol and mainly located in the superficial layers of the reticular dermis. Phenol can therefore reach them (Figure 30.14). Other treatment options include surgical excision, carbon dioxide laser, argon laser, electrocoagulation and cryotherapy. Dichloroacetic acid has also been used in this indication, dissolving the xanthelasma and healing with minimal scarring.

Acne and acne scars Active acne is not an indication for phenol, because of the risk of secondary infection among other things and because

Superficial telangiectasias A phenol peel is not used to treat telangiectasias, even though the more superficial ones usually disappear through protein coagulation along with the superficial layers of the skin. Deeper telangiectasias can become even more deeply embedded in the dermis as the new layer of dermal collagen and elastin form. Therefore, a phenol peel

Figure 30.13 Xanthelasma. (Courtesy of Dr Munelly, UK.)

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Figure 30.14 (a) Eyelid xanthelasma before a local phenol peel (b) Five days after the peel: normal erythema. (c) Nine days after the peel: the xanthelasma has gone

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there are other less aggressive and highly effective treatments.14 Acne scars15 that are deep, adherent, crater-like, sometimes atrophic, sometimes hypertrophic and keloid16 are a complex problem, and it is clear that no easy treatment exists to date that can claim to get rid of them completely and definitively. Applying a phenol solution will of course bring about a cosmetic improvement, but may well be disappointing to both doctor and patient in some severe cases. The patient in Figure 30.15 is an interesting case from many points of view. A phenol solution (Exoderm®) was applied correctly and deeply enough to treat the many acne scars (Figure 30.16). An occlusive dressing was then applied for 24 hours. On examining the skin at the end of occlusion, the scars had only improved very slightly, and an extra coat of phenol was applied to the cheeks after 24 hours, without occlusion this time. On examination after seven days, the results appeared inadequate (Figure 30.15) and another spot application was made without much success. When discussing treatment possibilities for acne scars with a would-be patient, the doctor should be extremely cautious. Skin that is very scarred can, however, be completely renewed, evened out and smoothed using a combination of treatments such as subcision,17 dermal filling,18 dermabrasion, punch excision, punch elevation, possibly micro skin grafts or even injections of cultured stem cells or fibroblasts (Isolagen).

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Figure 30.15 Acne scars treated with a full-face phenol peel (Exoderm®). On the 8th day, there is a distinct improvement in the structure of the skin: wrinkles have disappeared, along with small active acne lesions. However, the improvement in the acne scars remains limited.

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Figure 30.16 (a) The application of phenol on this patient produced normal skin frosting, but did not reach the deeper acne scars, which are still the same color. (b) An extra coat of phenol causes ‘buff-colored’ patches to appear – a sign that the product has reached the maximum depth of penetration.

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Figure 30.17 (a, b) A patient treated with an Exoderm® peel (full-face phenol occlusive peel), followed by mechanical dermabrasion (postchemabrasion). (Courtesy of Dr Y Fintsi.)

Treating severe acne scars therefore requires specific technical ‘preparation’ before applying phenol to allow complete and definitive renewal of the architecture of the skin, as well as to even out the tone of skin that has been damaged by the acne itself and by the treatments given before the phenol peel. It is therefore imperative to cure the acne before treating the consequences and not to forget that taking isotretinoin (Roaccutane®) in the year before or after a phenol peel poses a major risk of atypical scarring, often on the cheeks. Results are excellent, however, on more superficial scars: permanent removal of scars, tightening effect on the skin and overall normalization of skin tone. Some authors19 prefer to treat acne scars with dermabrasion, on condition that the hand guiding the wheel is expert enough to be able to control the depth of skin abrasion precisely and to vary the depth depending on the area and the size of the scars being treated. Dermabrasion may be prescribed as monotherapy or in combination with other

techniques (Figure 30.17). The results of microdermabrasion as monotherapy for treating severe acne scars are disappointing.

Other scars Atrophic scars resulting from a face-lift A surgical face-lift always leaves scars. If there are no serious complications, these scars are not really visible and patients do not complain. Secondary infections are not common but they are not rare either, and in some patients the skin surrounding the scar behind the ear becomes necrotic. The scar shown in Figure 30.18 is the result of a secondary infection after a surgical face-lift. Note the central atrophy

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Figure 30.18 Atrophic scar after a face-lift, resulting from a local secondary infection.

and depigmentation surrounded by a hyperpigmented ring. There is a telangiectasia in the middle of the scar. The patient wanted to have a phenol peel, but was refused because of the risk of the face-lift scar not healing properly. The telangiectasia can be treated separately, however, and the peripheral post-inflammatory hyperpigmentation, which shows up the central atrophic hypopigmentation, could be treated with a more superficial peel (Easy TCA®) combined with a topical depigmenting treatment (Blending Bleaching® cream). The visual impact of the scar would be reduced if the skin tone were evened out. Normal face-lift scars are not usually too unsightly, but some patients want a treatment to soften them or get rid of them completely. A full-face phenol peel is the best option (Figure 30.19), but a local application of phenol precisely on the scar is also a possibility, in combination with another more superficial peel (to the papillary dermis, the Grenz zone or the basal layer). Standard scars from an upper blepharoplasty do not seem to respond as well to a

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Figure 30.19 (a) A face-lift scar that is not too unsightly. However, the skin tension lines converging on the scar emphasize it. (b) Thirty days after a full-face phenol peel (Lip & Eyelid® formula), without any make-up, the tension lines have gone and the face-lift scar is less visible.

phenol peel. Scars on the body are not an indication for phenol.

Traumatic scars These can be treated with localized application of phenol and a series of Easy TCA® peels (Figure 30.20).

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Figure 30.20 (a, b) Post-traumatic scar and post-inflammatory hyperpigmentation, 6 years after a road accident. (c) Local application of phenol to the scar. Frosting occurs immediately. An impermeable occlusion will be applied for 24 hours and followed in the standard manner with an application of bismuth subgallate powder. The patient will also have four sessions of Easy TCA® peels, at a rate of one peel per week, to produce cloudy white frosting on the hyperpigmentation. Daily depigmenting care is Blending Bleaching® cream. (d) Results after the third Easy TCA® peel and one application of localized phenol to the scar between the eyebrows. The edges of the scar are less marked, the base of the scar appears less atrophic and the skin tone has evened out.

Dermabrasion scars These too can be treated with a local phenol peel combined with Easy TCA® (Figure 30.21).

Nevus Another less well-known indication for a phenol peel is the treatment of generalized verrucous epidermal nevi, a disorder that can be associated with a certain number of bone, ophthalmic or neurological malformations. Treatment consists in shave excision of the lesions followed by an application of phenol to the hyperpigmented areas of the face.20 Giant hairy nevi have been treated with phenol: 40% solution, combined with croton oil (0.8%) and hexachlorophene soap.

It should be remembered that some nevi fade after a phenol peel and that others, after a period of fading, become hyperpigmented.

Other indications Dilated pores Dilated pores are not the best indication for phenol, and the abrasive technique21 combined with Easy TCA® seems more effective.

Neurolysis and chemical sympathectomies Phenol is sometimes used in paraaortic injections in the semilunar ganglions to achieve neurolysis as an analgesic

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Figure 30.21 (a, b) A scar resulting from lip dermabrasion: the upper left half of the lip is still wrinkled because the mechanical dermabrasion was too superficial, whereas the upper right half of the lip is scarred as a result of the dermabrasion being too deep. The patient is seen in an attempt to correct this unsightly scar and a local phenol peel is suggested. Lip & Eyelid® solution will be used locally and combined with four Easy TCA® peels to even out the results. (c) Frosting on the upper lip after application of Lip & Eyelid® solution. The scar reacts with frosting of a different color where the tissue is most fibrous. (d) Three weeks after treatment, the wrinkles on the upper left half of the lip have disappeared. The scar on the upper right half of the lip has softened and evened out, and the color is similar to that of the surrounding skin.

technique in cases of inoperable cancers (30 ml of a 6% phenol solution can be injected in this indication) (see also Chapter 28). There are descriptions in the literature of the use of phenol in chemical sympathectomies in the treatment of palmar hyperhidrosis, Raynaud’s syndrome and obliterative arteriopathy.

Urinary incontinence Phenol has been used in injections beneath the bladder trigone in the treatment of urinary incontinence due to spina bifida (30 ml of 6% phenol). Aqueous solutions of phenol have been injected as a sclerosant in cases of hydrocele.22

Spasticity and chemical neuroablation Publications indicate 5% phenol injections to treat spasticity in pediatrics. The use of chemical neuroablative techniques dropped off rapidly with the arrival of more specific treatments. Injecting neurolytic solutions (e.g. phenol23 or alcohol solutions) causes non-specific damage to all the structures that come into contact with these products, namely both motor nerves and sensory nerves, muscles, aponeuroses, and subcutaneous tissue. The effects of chemical neurolysis last several months, and subsequent injections often do not produce the same results. It is now

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acknowledged that the risk of complications linked with these injections is too high, considering that there are other techniques that are less dangerous, more specific and more effective. Injecting phenol for the purpose of chemical neurolysis is now only indicated for patients suffering from pain that is unresponsive to any other treatment and whose life expectancy is not longer than 3 months. Recently, there have been reports of phenol being used to produce chemical neurolysis and a ‘botulinum toxin-like’ effect.

Hemorrhoids Martindale23 reports the use of injections of an oil solution of phenol as a sclerosant for hemorrhoids. The phenol is injected into the tissue surrounding the internal hemorrhoids as a hardening agent and painkiller.

Various Phenol has been injected into the soft tissue of the lower back to relieve chronic pain. Phenol ablation is sometimes preferred to surgery to treat ingrown toenails or onychogryphosis.

Notes 1. See the section on inadequate results in Chapter 37. 2. It is possible, for example, to inject hyaluronic acid immediately before the phenol peel. 3. Given that the exact role of melanocytes is not yet completely understood – although we know that it is not just restricted to the production of melanin – it is interesting to note that they are still where they should be: in the basal layer of the epidermis. 4. Cortez E. Chemical face peeling. Otolaryngol Clin North Am 1990; 23: 947–50.

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5. Blending Bleaching® cream should be applied twice a day from the 10th day after Lip & Eyelid®, if the skin is ready. 6. Asken S. Unoccluded Baker–Gordon phenol peels – review and update. J Dermatol Surg Onol 1989; 15: 998–1008. 7. Zhao QM. Clinical observation of face peeling for ephelides and phenol excretion in wine. Article in Chinese 1992; 8: 179–81, 247. 8. Unideep® is therefore a good treatment for freckles. 9. Lentigo maligna is also known as Dubreuilh’s melanosis and Hutchinson’s freckle. Different authors consider it either as a malignant melanoma in situ or as a premalignant melanocytic dysplasia. 10. McCulloch EG, Langsdon PR, Maloney BP. Chemical Peel with Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996, UK, Oxford, Marcel Decker Ltd. 11. See also treatment with localized TCA (Only Touch®) – Chapter 22. 12. Usually, phenol peels are not recommended for non-facial skin. 13. The same applies to alpha-hydroxy acids (AHAs) and TCA. 14. Active comedonal, microcystic, papular or papulopustular acne are good indications for Easy TCA® or Easy Phytic®. Many dermatological treatments are equally effective. 15. See also Chapter 21. 16. They often result from pustular or nodulocystic acne or acne conglobata. 17. With a Nokor needle or Sulamanidze’s wire scalpel. 18. Ideally combined with subcision. 19. Farrior RT. Dermabrasion in facial surgery. Laryngoscope 1985; 95: 534–45. 20. Basex J, el-Sayd F, Sans B et al. Share excision and phenol peeling of generalized verrucous epidermal nevus. Dermatol Surg 1995; 21: 719–22. 21. ‘Pre-chemabrasion’ – see Chapter 21. 22. Martindale W, Reynolds JEF. The Extra Pharmacopoeia, 30th edn. 1993, USA, PA, Rittenhouse Book Distributors. 23. ‘Phenolization’: 5–7% phenol in aqueous solution.

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31 Phenol: contraindications, precautions and safety

Contraindications and precautions Insulin-dependent diabetes Insulin-dependent diabetes is an absolute contraindication to a phenol peel. Diabetes significantly increases the risk of secondary infection; the vascular and/or immune disorders associated with this illness mean that complications are more of a probability than a possibility. Stabilized, noninsulin-dependent type 2 diabetes is not an absolute contraindication to a phenol peel. The doctor must take particular care with these patients to avoid secondary infections.

Florid herpes Active herpes is an absolute contraindication to a phenol peel. A history of herpes is not a contraindication to phenol, but requires treatment to prevent herpes recurring. For more details, see Chapters 32 and 37.

Other obvious, absolute contraindications Who would dream of doing a phenol peel on a woman who is pregnant or breastfeeding? Or on a patient with an obvious malign lesion? Or a patient recovering from a serious illness? A patient with immunodeficiency?1 On a patient with Ehlers–Danlos syndrome?2 On one with scleroderma or collagen disease? The doctor must use his professional skill and experience to rule out any patient who poses an increased risk.

Pre-existing heart condition A phenol peel should of course not be performed after myocardial infarction or cardiac decompensation. Unstable angina also rules out a phenol peel, as the stress associated with a peel could trigger an angina attack. No clear link has ever been established between a personal medical history of a heart condition, if currently stabilized, and the incidence of cardiovascular complications during a phenol peel. Apart from arrhythmias, to the best of my knowledge there is no mention in the literature of any serious heart problems occurring as a complication of a phenol peel.3 Of course, we cannot know for certain that such complications are always reported in scientific journals, even though any serious complications following cosmetic interventions always make headline news in the popular press and on TV. As far as I know, however, recently there have been no serious health problems resulting from a phenol peel.

Pre-existing kidney or liver disease Liver or kidney deficiency increases the risk of toxicity, as the normal detoxification and elimination processes will not be functioning properly (see Chapter 28).

Patient history Recent postoperative wounds We saw in Chapter 30 that it can improve the appearance of stabilized surgical scars on the face. Phenol should not be used to treat recent postoperative wounds that have not yet stabilized, however, as there is a significant risk of necrosis.

History of local radiotherapy

Local anesthesia with adrenaline (epinephrine) Adrenaline (epinephrine) is a cardiac irritant that increases the risk of arrhythmias. For more details, see Chapter 37.

In addition to all the structural changes that can follow exposure to ionizing radiation, there is a possibility that the pilosebaceous units might atrophy. This would delay epidermal regeneration and promote the formation of nasty scars.

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History of keloid formation It is better to select a peel whose depth of action does not go beyond the papillary dermis.

Use of isotretinoin Recent use of isotretinoin (Roaccutane®) is an absolute contraindication to phenol. For more information, see the section on scarring in Chapter 37.

Use of MAO inhibitors Monoamine oxidase (MAO) inhibitors are contraindications to the use of the majority of analgesics and psychotropic drugs required for patient comfort. This would make a phenol peel almost unbearable for a patient on MAO inhibitors, who is, by definition, psychologically unstable.

Refusal or inability to wear make-up Patients who absolutely refuse to wear make-up during the post-peel period are not the best candidates for a phenol peel, as the erythema and potential dyschromias, even if temporary, are best covered up with make-up.

Patients at risk of dyschromia Patients with dark skin should be warned about the demarcation line between the treated and untreated areas, both with a full-face peel and a localized phenol peel. Patients on estrogen–progesterone hormone-replacement therapy (HRT) will need close monitoring for pigmentary changes. McCollough and Maloney4 ask their patients to try to stop HRT or the contraceptive pill for at least the first 6 months after a peel. If they cannot stop HRT during this time, they are warned of the risk of pigmentary changes. Patients who work outside most of the time should also be warned of the high risk of hyperpigmentation and of the absolute necessity not only to wear an effective sunblock but also to change their general attitude to the sun.

Patients with mental or behavioral risks The patient has to understand the peel procedure and the limits of a deep peel. He or she must agree to comply with strict rules of procedure before, during and after the peel. Any cosmetic procedure, in which the patient is required to take an active part, and especially a deep peel, is strictly contraindicated for patients who do not have a minimum level of intelligence. The patient has to be capable of understanding and accepting the necessity to wear sunblock and

make-up after the peel and be aware of the time needed for the skin to regenerate completely. Squeamish patients will overwhelm the doctor with complaints, worries, questions and reproaches. It is better to test a patient’s mental and physical resistance by first suggesting a painless peel without complications and then progressing onto a medium-depth peel before considering a phenol peel. Individual tolerance can be tested in this way, and the patients themselves gradually learn what a peel is and what it can do for them. Patients should be shown a series of photographs showing what the face looks like day by day during the first week after a peel. Ideally, the patient’s immediate family should also see these photographs. Without this precaution, paranoid patients, friends and family may not believe it when the doctor tells them that everything is proceeding as normal.

Isolated patients Being alone is of course not in itself a contraindication to a phenol peel. The dramatic results of a peel could bring couples back together,5 but a few rules are necessary for the patient’s safety. The phenol formulas of today allow patients to remain on their feet: the patient can go home almost immediately after a phenol peel. However, it does causes significant edema that can sometimes make it difficult for patients to open their eyes. It is therefore out of the question for a patient who lives alone to go home after the peel. The patient needs help to go about his or her daily life during the first 3 days after the peel. Clinics with hospital beds can keep patients in during the first few days or even the first week after a peel.

Neck peel A phenol peel is better intended for facial skin, and there are other treatments for the rest of the body.6

Specific precautions If a phenol peel on the neck proves necessary, the following precautions must be taken: ■ No impermeable dressing should be applied: no occlusion. ■ The solution should be applied sparingly on the skin of the neck. ■ Any movement or friction likely to cause scarring should be avoided after the peel. ■ The phenol must not be allowed to macerate in the folds of the neck. This maceration is equivalent to occlusion. ■ After treating the face, the solution should be applied extremely slowly on the neck, or, preferably, should be postponed until the following day so as not to overload

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the body’s metabolization and elimination pathways. It is especially important in this case to avoid the toxic complications associated with phenol being applied too rapidly on too large an area.

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taken into account, as well as the results of the essential preliminary clinical check-ups.

Local and systemic safety

Skin regeneration

The following is a summary of some of the safety rules:

After an intraepidermal peel, to the basal layer or the Grenz zone, the skin regenerates from leftover islets of keratinocytes. In the case of a deep peel, the skin regenerates from its appendages.7 The face has more pilosebaceous units than the neck, and facial skin regenerates more quickly, with less risk of scarring.

■ The product should only be applied to the face. There is a large number of pilosebaceous units here that help the epidermis regenerate properly. ■ It is better not to treat the neck with phenol, both for local, dermatological reasons and so as not to increase the absorption area. ■ Using the right formulation and the proper application technique ensures perfect results every time. A ‘number 1’ phenol formula should not be applied using the application procedure for a ‘number 2’ formula. In some cases, this precaution is not essential, but in others it is. ■ All contact between phenol and the eyes should be avoided. ■ No phenol should be applied in cases of liver or kidney deficiencies or serious heart disease. ■ Phenol is contraindicated for patients with Ehlers–Danlos syndrome, collagen disease, insulin-dependent diabetes and active infections (acne, herpes, etc.). ■ Phenol should be applied extremely carefully and in accordance with all the safety rules (equipment, skill). ■ Doctors should inform their professional insurers that they perform this type of peel. ■ The toxicity of phenol is paradoxical, and low-concentration solutions are potentially more toxic than highconcentration solutions. ■ A phenol solution should contain oil to slow down absorption and allow enough time for the liver to detoxify it and the kidney to eliminate it. The solution must be stable, tamed and adjuvanted. ■ As well as improving the cosmetic results, using occlusion also slows down the absorption rate of phenol and reduces its toxicity. Occlusive masks must be applied carefully to avoid air bubbles or pools or phenol forming. ■ The doctor must be aware of all the potential complications, watch out for any signs and be ready to treat them should they occur. ■ Phenol should be applied slowly, in a minimum of 1 hour, on healthy patients with normal liver and kidney function who can be expected to achieve good cosmetic results. ■ The patient should be hydrated, ventilated and monitored (pulse oximeter and electrocardiogram). A venous drip should be set up beforehand, and if necessary glucose serum can be administered to avoid hypoglycemia. ■ The risks of general anesthesia and products that could irritate the myocardium can be avoided by using local nerve blocks or deep sedation.

Solution to the problem of neck peels The answer is to do a peel to the papillary dermis on the neck and décolletage. This peel can be carried out at the same time as the phenol face peel or in the weeks following the face peel.

Sun exposure Complete sun avoidance and effective sun protection is a must for 2 or even 3 months (see Chapters 2 and 3). Postinflammatory hyperpigmentation (PIH) is not at all uncommon, even after a phenol peel. After the immediate post-peel period, which requires close and almost daily monitoring, it is advisable to see patients again after 15 days, 30 days and 2 months and to warn them of the need to treat any early signs of hyperpigmentation immediately. It should be noted that PIH frequently resolves itself without treatment after a phenol peel.

Cost One of the drawbacks of a deep peel is the high cost, which means that this technique is not within everyone’s reach. The results that can be achieved offer excellent value for money, however, and no patient who has benefited from this treatment has ever complained about the cost.

Disorders that may be aggravated Telangiectasias, seborrheic dermatitis, eczema, acne rosacea, lupus and other autoimmune disorders are among the forms of dermatitis that may be aggravated by a phenol peel.

Safety factors Patient selection Choosing the right patient is a key safety factor. The few, but strict, indications and contraindications should be

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Notes 1.

2. 3.

Because of the risk of secondary infection, patients with immunodeficiency (e.g. HIV) should be ruled out from a full-face phenol peel, as well as patients with hypogammaglobulinemia. See the section on scarring in Chapter 37 Fiatsi Y. Exoderm®, a novel, phenol based peeling method resulting in improved safety. Am J Cosmet Surg 1997; 14: 49–54.

4.

5. 6. 7.

McCulloch EG, Langsdon PR, Maloney BP. Chemical Peel with Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996, UK, Oxford, marcel Dekker Ltd. Doctors should not suggest a peel as the answer to a patient’s personal problems. A peel repairs the skin, not the soul. Vigneron JL. Les peelings en dehors du visage. J Med Esth Chir Derm 1993; XX(75): 53–6. Rusciani L, Rossi G, Bono R. Les peelings cliniques. J Med Esth Chir Derm 1993; XIX(78): 75–80.

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32 Phenol: pre-peel preparation

The preparation procedure for a local phenol peel has some aspects in common with those for a full-face phenol peel – however, a local application of phenol is far easier.

benign skin tumors, remove small sebaceous cysts and fill any deep furrows.

Medication Eight days before the peel Photographs Before any treatment, top-quality photographs (Tiff format) should be taken of the face, profile and three-quarter profile (Figure 32.1), with and without flash. A flash changes the appearance and color of the skin: dyschromias are less apparent and reliefs are flattened. Pigmentation and relief is more clearly visible on photos taken without flash, especially in natural low-angled light (Figure 32.2). Any pre-existing abnormalities will be recorded to avoid any potential medical and legal problems later. In this way, a ‘round eye’ appearance after surgery, lagophthalmia or ectropion should be photographed and this noted in the file. Nevi and other lesions should be photographed in particular. The whole peel procedure could also be filmed. The patient, preferably accompanied by a member of his or her family, will have seen sequenced photos showing the aftereffects of a phenol peel, day by day.

Preparing the skin Many phenol peel techniques require skin preparation before the peel to ensure that penetration is even and to reduce complications (see Chapter 2). No specific preparation is necessary before Lip & Eyelid® formula.

Botulinum toxin Botulinum toxin should be injected 1 week before the peel into forehead or glabellar wrinkles, crow’s feet, lip wrinkles or radial wrinkles around the outer canthus of the upper eyelid. Blocking the muscles allows the skin to regenerate more evenly. The results will be of better quality and longer lasting. This is also the ideal moment to shave off any

The patient should be given a prescription for: ■ a strong analgesic to be taken before the peel to test for tolerance. Paracetamol (acetaminophen) plus codeine is usually strong enough and well tolerated ■ a benzodiazepine (e.g. 2 mg lorazepam) ■ aciclovir (or, better, valaciclovir) if the patient has a history of herpes ■ sterile white Vaseline® for post-peel care ■ an antipruritic (e.g. promethazine) ■ domperidone: to settle the stomach in case of post-peel nausea ■ make-up that matches the patient’s skin color: Couvrance® or Covermark® are both well tolerated by patients from the 8th day ■ beware of patients on monoamine oxidase (MAO) inhibitors: they are contraindicated in combination with many other drugs, including some analgesics or sedatives that have to be used for the patient’s comfort during and after the peel ■ some single-dose carmellose sodium eye drops to be used freely after the phenol peel to alleviate any eye irritation, which is common during the hours following a full-face phenol peel.

Legal documents The patient should be given the following documents to read and sign: informed consent (Box 32.1), authorization to take and use photographs (Box 32.2) and a general questionnaire on health and coagulation (Box 32.3).

Clinical examination The patient should be given a full clinical examination and questioned closely; the results should be noted down in the

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A

B

C

Figure 32.1 (a) Right profile. (b) Three-quarters right. (c) Full face. (d) Three-quarters left. (e) Left profile.

D

E

Figure 32.2 The same patient taken during the same consultation: (a) without flash and (b) with flash: relief and lip wrinkles are flattened by the effect of the flash. The nasolabial folds, on the other hand, are more clearly visible with flash.

A

B

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Box 32.1 Example of an informed consent form (originally drawn up by the Sociedad Española de Medicina y Cirugía Estética, Barcelona, SEMCC) Place and date Mrs/Mr ………………………………….. Address: ……………………………........ Date of birth: ……………........................ Tel: ……………………………………… Authorizes Dr …………………… to perform on my person/on …………………… for whom I am legally responsible. A CHEMICAL PEEL OF THE TYPE ………………………………………… I declare that I have been properly informed of the details of this treatment, of the composition of the solution that will be applied on my skin, of its immediate effects, of the process of skin recovery, of the post-peel care after treatment and of the precautions to be taken during the months following the peel. I have also been informed that, because of the variability of individual reactions, it is not possible to be given a precise date when normal activities may be resumed. I have also been informed of the usual risks of local anesthesia, sedation and the treatment itself and I accept them. The doctor has informed me of alternative methods of treatment to the above-mentioned chemical peel, and I choose this latter course of treatment with full knowledge of the facts. Should any unforeseen situation or complication arise that requires medical intervention not described in the explanations given beforehand, I authorize the medical team to make any decision that they deem necessary or useful. I have been fully informed of the fact that the doctor cannot guarantee perfect results after the first application, and accept the possibility of having a touch-up. I acknowledge that I have been given valid answers to all my questions, either in the written documentation that I have received written in language I can understand and that I have read carefully or orally by the doctor during consultations prior to treatment. Date and signature preceded in handwriting by the words ‘read and approved’.

Box 32.2 Example of a photographic consent form Place and date Mrs/Mr …………………………………... Address: ……………………………......... Date of birth: ……………........................ Tel: ……………………………………… I authorize Dr …………………… to use the photographs taken before and after treatment in:    

Medical science congresses or conferences Scientific articles or papers to be published in medical reviews Media publications I do not authorize the use of photographs

I have ticked the points I agree to and deleted the point or points that I do not agree to. This document comes in two copies: one for the patient and one for the doctor. Signature, preceded in handwriting by the words ‘read and approved’.

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Box 32.3 Example of a general questionnaire and coagulation questionnaire Are you taking medication that contains aspirin or an anti-inflammatory?: Yes/No Are you currently taking medication to thin the blood?: Yes/No Do your gums bleed when you brush your teeth?: Yes/No Have you ever had any problems with bleeding: During dental treatment?: Yes/No During child birth?: Yes/No During surgery?: Yes/No Have you ever had blood in your stools?: Yes/No Do you bruise easily?: Yes/No Do you feel that you bleed a long time when you cut yourself?: Yes/No

patient’s file. The patient should be given a cardiovascular examination before the peel if there is any doubt as to their cardiovascular health, or merely as a precaution; the doctor then has the opinion of a specialist to confirm that there is no cardiovascular contraindication to the peel. The patient should be asked to have a biological examination. The results must be checked before the start of the peel. It is essential to check the patient’s blood count1 and liver and kidney function, to make sure there is no bacterial or viral infection, diabetes or immunodeficiency.

The night before and the morning of the peel The evening before the peel, patients should take lorazepam if they are worried about not getting to sleep. Patients who are very nervous or anxious can take another lorazepam tablet on the morning of the peel, together with 10–20 mg of domperidone.

Are your periods abnormally heavy?: Yes/No Do you have any other problems with bleeding?: Yes/No Do any members of your family have problems with bleeding?: Yes/No Are you on any medication at present?: Yes/No If ‘yes’, which (give details below): ..................................................................................... Have you ever been treated for heart trouble?: Yes/No Do you get palpitations?: Yes/No Have you ever had any treatment for the lungs?: Yes/No Do you have asthma?: Yes/No Have you ever had phlebitis?: Yes/No

One hour before the peel The patient should arrive at the clinic half an hour to an hour before the peel and not have eaten for more than 4 hours. ■ If the peel is to be done without deep sedation, the patient should immediately be given premedication, as per the doctor’s usual practice: for example, one sublingual tablet of Temesta 2.5 mg (lorazepam) if the patient has not taken any that morning and 15 drops of tilidine (a major analgesic) or any other strong analgesic the doctor usually prescribes. It is best to use an analgesic that the patient can tolerate easily. ■ If the peel is to be performed under deep sedation or neuroleptanalgesia, the anesthetist should deal with premedication.

Have you ever had a pulmonary embolism?: Yes/No Have you ever had an operation?: Yes/No

Advantages of benzodiazepine

For what? (give details below):

Using benzodiazepine as premedication is very worthwhile. There are four obvious advantages:

..................................................................................... Have you ever had a local anesthetic?: Yes/No If you did not tolerate it, what happened? (give details below): ..................................................................................... Are you allergic?: Yes/No To what?: .....................................................................

■ Anxiety and fear of pain increase the perception of pain. Benzodiazepines play an auxiliary role as an analgesic. ■ Benzodiazepines cause a certain amount of amnesia. More than 2.5 mg of sublingual lorazepam can produce partial amnesia that lasts for more than 10 hours. Midazolam produces short-term but deep amnesia that makes the patient forget any pain he or she may have felt in the course of the treatment.

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■ Benzodiazepines are neurostabilizers that can counteract the initial toxic neurological effects of local anesthetics or phenol. ■ A long-acting benzodiazepine greatly improves patient comfort. It makes the patient feel drowsy, which reduces facial movements and therefore helps keep the post-peel occlusive mask in place. Also, when a patient has taken 2.5 mg of sublingual lorazepam as premedication, they will feel much less pain immediately after the peel. A calm patient is a patient who does not complain, does not fidget, does not speak, does not smoke and does not scratch.

Preparing the occlusive mask Sleek®, Micropore®, Blenderm® or Leukoflex®?

Figure 32.3 Four different types of occlusive dressing that can be used for occlusive phenol.

The occlusive mask applied at the end of the peel will consist of either a single or a double layer, depending on what type of dressing is used. Sleek® and Leukoflex®2 can be used in a single layer. Leukoflex® has an advantage over other brands in being transparent. Micropore® can be applied in two layers, or a layer of Blenderm® can be applied on top of the first layer of Micropore® (Figure 32.3). Whichever dressing is used, the tape should be precut into 3–5 cm strips (Figure 32.4) and placed within easy reach, ready for the occlusive mask (Figure 32.5) to be applied at the end of the peel.

Settling the patient in The patient is placed in a comfortable position to be maintained for over an hour without moving,3 covered in a warm electric blanket or a metallic survival blanket.

Protecting the eyes

Figure 32.4 The most common technique involves the use of occlusion for 24 hours. An assistant prepares the strips of occlusive tape, cutting them to the right size (about 3–5 cm long) so that the occlusive mask can be applied immediately after the peel.

A small quantity of sterile ophthalmic Vaseline® should be put in the conjunctival cul-de-sacs. The Vaseline® deactivates the phenol and protects the eyes from accidental contact. Terramycin® ointment or ophthalmic gentamicin can be used instead of ophthalmic Vaseline®. A syringe of physiological saline (200 cm3 at least) should be prepared, to be kept at hand to rinse the eyes out immediately in case of contact with phenol (which is highly unlikely if the peel is applied correctly).

Ventilation Keeping the treatment room properly aired and ventilated4 and fanning the patient’s face help make the patient more

Figure 32.5 After cutting, the pieces of occlusive dressings are installed on a sterile base, easy to take.

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Figure 32.6 Ventilation during a local application of phenol (chemical cheiloplasty: see Chapter 36).

comfortable when the doctor goes through the essential phase of carefully cleansing the skin with acetone and alcohol before the peel (Figure 32.6). It is most unpleasant for a patient to have to inhale the fumes when these products are being wiped on the lips, cheeks and chin. Good ventilation prevents sweating, especially in hot climates: sweat overhydrates the superficial layers of the epidermis, which can lower the concentration of the active products locally and increase skin permeability. Ventilation also creates drafts that will stop the phenol vapors from stagnating in the immediate vicinity of the patient and doctor.

Intravenous drip and monitoring Diuresis Osmotic balance across the plasma membrane is regulated by the concentration of proteins (albumin more than globulins). Relative dehydration would increase plasma oncotic pressure and capillary absorption of water and water-soluble molecules. Phenol is soluble in water, and its absorption rate could be accelerated by the slightest dehydration. Intravenous access should always be set up to help diuresis by infusing 1 l of physiological saline or glucose solution throughout the procedure and for 1 hour afterwards. Proper diuresis is usually considered to be an effective way of reducing the toxic effects of phenol by helping renal elimination.

Cardiorespiratory monitoring Every patient must be properly monitored with pulse oximetry and electrocardiography (ECG). Even if the peel is done by the book and even when the simplest and least aggressive techniques are used, stress can cause vagal reactions, low blood pressure and tachycardia. Pulse oximeter monitoring can pick up on any drop in oxygen saturation that could accentuate myocardial irritability and cause arrhythmias. Without monitoring, a simple vagal reaction can go undetected, and if it is not treated correctly, the patient can

pass out or even stop breathing. The pulse oximeter is not very effective at detecting arrhythmias; continuous ECG monitoring is essential, even though some authors5 recommend simply checking the heartbeat and vital signs when more than half the face is treated with a phenol peel. This vague recommendation could be taken as encouraging an amateurish approach, while close and continuous monitoring is essential as a simple precaution. Other authors,6 on the other hand, recommend monitoring the patient up to 4 hours after a phenol peel, which seems excessive given the results of toxicological studies showing how quickly phenol is metabolized and detoxified. The blood levels of phenol recorded by Deichmann and Litton during a fullface phenol peel show a rapid drop in plasma values 2 hours after the beginning of the application. The blood level of phenol always remains below toxicity thresholds when phenol is applied slowly. It is therefore not unreasonable to stop monitoring the patient shortly after the occlusive mask has been applied. By then, approximately 2 hours after the beginning of the application, the liver is detoxifying the phenol effectively, the kidneys are eliminating it and plasma levels are already going down.

Corticosteroids, atropine and antibiotics Some authors recommend injecting 125 mg of solumedrol intravenously before starting a phenol peel: injecting a steroid is said to reduce post-peel edema and to prevent some of the complications described above. However, I have not noticed any advantage from this injection. The aftereffects of the peel are similar with or without corticosteroids. However, it is worth considering an intravenous injection of prednisolone for patients who smoke and do not have any history of gastric ulcers. Smokers have an increased risk of laryngeal edema immediately after a full-face phenol peel. Atropine should not be injected automatically before a full-face phenol peel. It should be at hand, however, to treat any incidence of bradycardia. As a precaution, it has been recommended to inject a broad-spectrum antibiotic before a phenol peel, although this is not essential for the correct peel procedure.

Cleansing, degreasing and disinfecting Once the patient is settled in comfortably in the dorsal decubitus position and put on a monitor and drip, the doctor can start cleansing the skin either before or after the anesthetist has started injecting the sedatives. The skin is cleansed and disinfected with a mixture of chlorhexidine,7 water and alcohol in equal parts (5 cm3 of each). It is then rinsed and dried thoroughly. The whole area is carefully

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degreased with a swab lightly soaked in acetone (or ether) until all traces of oil or skin debris have gone. The skin must be degreased very carefully, applying medium pressure8 and paying special attention to the base of wrinkles and acne scars. The patient should be properly ventilated (with an electric or hand-held fan) to avoid inhaling the acetone and alcohol vapors. All told, it takes around 10 minutes to cleanse the skin thoroughly. Applying medium pressure helps extract and eliminate some of the residual sebum from the sebaceous glands, but should not take off the stratum corneum: the doctor must be careful not to abrade the skin with the swab before a phenol peel. Acetone has various functions: it degreases, cleans and helps the phenol penetrate; it also breaks down the barrier function of the epidermis.9 This preliminary phase of careful cleansing, disinfecting and degreasing is essential to get perfect results. Phenol does not penetrate as evenly and as well through skin that has not been properly cleansed.

2. 3.

Asepsis

4.

It is easier and more precise to hold the phenol-soaked cotton-tipped applicator with a bare, ungloved hand. It is therefore imperative for the doctor to disinfect his hands surgically to avoid infecting the patient’s skin. The assistant who cuts the occlusive dressing and helps the doctor put them in place should also disinfect his hands in the same way, for the same reasons. There are two reasons why a mask should be worn: firstly to avoid contaminating the patient’s skin with respi-

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ratory bacteria, responsible for many of the cases of secondary infection described, and secondly to protect the doctor from partially inhaling the phenol vapors. Standing above the phenol vapors for over an hour, the doctor inhales a fair amount of this volatile chemical, which can have unpleasant side-effects such as dysgeusia or nausea. Any person with any kind of infection should be kept away from the treatment room: it is out of the question to perform a phenol peel when suffering from a sore throat, tracheitis, impetigo or a fungal infection on the hands.

Notes 1.

5. 6. 7. 8. 9.

To screen for anemia, an obvious contraindication for a fullface phenol peel. Leukoflex® is included in the Lip & Eyelid® formula kit. Particular care must be taken with patients who suffer from lumbago, as they sometimes find it difficult to remain in a dorsal supine position on a hard surface for a prolonged period of time. By mechanical ventilation with an electric fan, air conditioning, fanning by hand, etc. Benatar D. Le peeling au phénol. J Med Esth Chir Derm 1988; XV(60): 319–23. Konior RJ, Kerth JD. Selected approaches to the aging face. Otolaryngol Clin North Am 1990; 23: 1083–95. If there is no chlorhexidine, simple disinfection with 70% alcohol is sufficient. The pressure should be equivalent to scratching. Simply applying acetone increases DNA synthesis as well as synthesis of skin lipids

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33 Full-face phenol: nerve block anesthesia and/or sedation

Properties of cold Cold has interesting anesthetic properties1 that develop when the surface of the skin reaches 5°C. The temperature of the dermis and hypodermis is then 15°C. Even if the skin can withstand this temperature for a long time without any obvious damage, in practice it is unthinkable to use cryoanesthesia alone for a full-face phenol peel. Limited areas can, however, be cooled before applying the acids2 to make the application more bearable, when no other anesthetic is being used. To do this, the practitioner can use 3M® cold packs (Figure 33.1) or surgical gloves filled with an aqueous solution mixed with antifreeze (75% water and 25% antifreeze). The skin must not be frozen, of course. Some doctors use a facial anesthetic technique that consists in injecting Klein solution3 cooled to just a few degrees celsius under the skin of the face. This painful technique does not produce sufficient surface anesthesia, and changes all the parameters of how the phenol penetrates through the skin. The skin itself, as opposed to the subcutaneous tissue,

Figure 33.1 3M® cold pack. This photo shows the forehead being cooled prior to a trichloroacetic acid peel to the papillary dermis (Unideep®).

is only partially anesthetized by this type of injection, and the peel is still very painful. It is also impossible to inject this solution in the lips, nose, eyelids, etc. Doctors who use lasers are familiar with the Dermacool® device: it generates cooled air that can be directed locally using a handpiece. This cooling device is sometimes used for local applications of phenol.

Anesthetic properties of phenol Phenol was used widely in the First World War as an antiseptic and a local anesthetic in surgery. Depending on the concentration and the different adjuvants used, phenol can induce coagulation or lysis of the membrane and interstitial proteins, which clinically manifests as the whitening of the skin that occurs when phenol is applied. An application of phenol immediately triggers intense pain followed by local anesthesia that takes effect within about 15 seconds, as the skin whitens. The pain caused by an application of phenol is therefore very brief. The local anesthetic effect lasts for 20–30 minutes, shortly after which the processes of dermal inflammation intensify and trigger a painful, pulsing heat that, depending on the patient’s own perception, is relatively intense. This pain gradually subsides over the following few hours and goes completely once edema sets in and the inflammation has stabilized, usually the morning after the peel. Phenol can therefore be applied on very small surface areas without any anesthetic: it is enough to tell patients that they will feel an intense burning for 15 seconds, immediately after the phenol has been applied on the skin. The patient should be given painkiller tablets to alleviate the post-peel pain, which can last until the following morning. The eyelids and upper lip can be treated with Lip & Eyelid® formula, without any analgesic other than a paracetamol plus codeine tablet to be taken 1 hour before treatment. Patients should also be given a clear description of the pain they will feel. By the time they have counted to 15, the pain will have gone.

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Type of anesthesia for a full-face peel Unlike a local application of phenol, a full-face phenol peel cannot be done without anesthetic.4 There are several different possibilities.

General anesthesia According to the medical literature, general anesthesia (GA) should not be considered as an additional cardiovascular risk factor during a phenol peel. However, there are other effective techniques that are less complex and also less dangerous.5 What is more, it is in the hours following treatment that the pain is at its height – a long time after the GA has worn off. GA is a needless source of stress. GA does not make the patient more comfortable or any safer. On the contrary, it adds the inherit risks of general anesthesia to those of the phenol peel. GA is not the ideal choice for a full-face phenol peel. It is never indicated for a local phenol peel.

Facial nerve blocks Facial nerve blocks (FNB see p. 265) are quick and easy to administer, are not painful and cause few complications in the hands of an experienced doctor. A drop of 2% lidocaine can be injected very superficially with a fine-gauge needle 32G in precisely the same place that the nerve itself is injected with a 25G5/8 gauge needle. It is not possible to see the backflow of blood before injection with a 32G needle.

Allergy to local anesthetics Allergies to local anesthetics (LAs) are rare, and the term ‘allergy’ is often used to describe numerous problems that are more likely an overdose or a vagal reaction. Publications report that the frequency of allergic reactions to LAs is no more than 1% of all the side-effects met with.6 Lidocaine is an amide local anesthetic that does not cause many allergies. Procaine, on the other hand, is an ester-type local anesthetic: when it is injected into the organism, it is transformed into N,N-diethylaminoethanol and para-aminobenzoic acid (PABA) when the ester link that binds these two components of procaine is broken. PABA is a wellknown allergen. Methyl para-hydroxybenzoate, whose structure is similar to that of PABA, is also called PAB or methylparaben. It is a preservative that binds, like a hapten, to the immunoglobulin E (IgE) on the surface of mast cells and basophils and may be the cause of the few cases of anaphylactic shock that have been described. Other patients may be allergic to metabisulfite conservative, found in preparations containing adrenaline (epinephrine).

Toxicity of local anesthetics When nerve fibers depolarize, the sensation of pain is carried from the periphery to the brain. LAs are molecules that stabilize the membranes of excitable cells that are susceptible to depolarization. Their general toxicity is directly linked to this property. In cases of overdose, excessive cell membrane stabilization in the central nervous system (CNS) and the cardiovascular system produces severe side-effects. Different factors influence the risk of intoxication with LAs. For example, capillary absorption is more rapid in the face than on the body. The large number of facial blood vessels is one factor that speeds up absorption. Other factors that can cause intoxication include lack of adrenaline, low body weight (<45 kg), advanced age and competition with other molecules that use the same detoxification pathways. Intoxication with lidocaine is dose-related: unless there is a gross error when injecting, the symptoms are gradual and do not start with loss of consciousness or convulsions. The toxicity of bupivacaine, on the other hand, can trigger cardiovascular symptoms together with neurological symptoms. The first signs of local anesthetic CNS toxicity are drowsiness, yawning and a general feeling of malaise. The patient may complain of feeling lightheaded, anxious or dizzy. They may appear confused, pale, disoriented and complain of visual, auditory or gastric symptoms. When blood levels of lidocaine increase and reach 4–7 µg/ml, muscle spasms or tremors may start. The patient may have difficulty speaking and suffer from hallucinations, nystagmus and dizziness. Loss of consciousness follows, as blood levels of lidocaine reach or go beyond 8 µg/ml. Muscle spasms and tremors can develop into convulsions. Severe respiratory depression can lead to respiratory arrest, and the patient goes into a coma and dies if not properly ventilated. Death can come from both respiratory arrest and arrhythmia. The cardiovascular system is actually more resistant to LAs than the CNS, and cardiac toxicity starts at much higher blood levels of lidocaine. The first stages of cardiovascular toxicity are spontaneously reversible; they manifest in changes in blood pressure: stable or higher to start with, due to vasoconstriction or the increase in cardiac sympathetic tone, it then drops because of the decrease in cardiac output without any change in peripheral resistance.7 Circulatory collapse occurs as a result of negative inotropic effects, bradycardia caused by the reduced excitability of the myocardial cells, decreased intracardiac nerve impulse conduction and the direct myorelaxant effect on the vascular fibers that causes peripheral vasodilation. Cardiorespiratory resuscitation should be carried out immediately. Caution therefore dictates setting up venous access for fluid administration, an electrocardiograph, a pulse oximeter and a sphygmomanometer. The first thing a doctor faced with LA toxicity must do is to ensure good ventilation, at the same time as monitoring the heartbeat. An upset stomach, one of the first signs of

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intoxication, can trigger vomiting. If the patient is not placed correctly in the ‘safety’ position, the airways can become blocked, causing respiratory arrest and convulsions or inducing hypoxemia, hypercapnia or acidosis, all conditions that can aggravate arrhythmias. The low quantities of lidocaine needed to do the facial nerve blocks for the hour that the peel will last make CNS and cardiovascular toxicity to LAs almost impossible. It is nevertheless essential to recognize the symptoms and to be able to treat them. Choosing the right LA agent is also a safety factor, and we will see below why simple lidocaine without adrenaline is the best choice of molecule for a phenol peel, both local and full-face.

Bupivacaine Bupivacaine is an amide-type anesthetic and rarely causes allergic reactions. It is stronger than lidocaine and has a longer duration of action (anesthesia for about 3–6 hours). It also has a slow onset of action, and it takes 20–30 minutes for the anesthetic effect to develop. Mixing bupivacaine with lidocaine speeds up the onset of action, as lidocaine anesthetizes almost immediately. It is therefore very tempting to combine the two products to achieve immediate anesthesia with the lidocaine as well as a longer duration of anesthesia with the bupivacaine, which starts to take effect almost as the lidocaine stops. Bupivacaine is far more toxic than lidocaine, however, and no more than a total of 10 cm3 should be used for all of the nerve blocks on the face.8 The threshold value for the onset of neurological toxicity in humans is 6.4 mg/kg for lidocaine and only 1.6 mg/kg for bupivacaine. The threshold value for the onset of neurological side-effects in a patient weighing 50 kg would therefore be 80 mg. A 10 cm3 phial contains 50 mg of bupivacaine. Intravascular injection is instantly toxic to the heart and can induce ventricular arrhythmias, ventricular tachycardia, ventricular fibrillation and cardiac arrest. Moreover, injecting small quantities of bupivacaine in the head or neck can cause symptoms of systemic toxicity similar to those caused by the accidental intravascular injection of much larger quantities. If it is not possible to avoid using bupivacaine, it is essential to do an aspiration test before each injection. There are many drawbacks to using this product in a full-face phenol peel: its slow onset of action requires patience, and the nerve block takes about 30 minutes to set up but lasts 180–360 minutes. This product is painful to inject. The doses required to produce a nerve block of the whole face are lower than the neurotoxic doses, but not by much. As we saw above, the dose required for the face is at least 50 mg, while the toxicity threshold starts at 80 mg and the maximum allowed dose is 150 mg. As we saw in Chapter 28, Lalanne’s9 experiment clearly shows that perivascular injections, even when the blood vessels have been properly dissected and are in plain view, can be followed by

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vascular absorption and trigger serious rhythm disorders. It is therefore advisable not to use bupivacaine for facial nerve blocks, especially in a full-face phenol peel, when any molecule likely to irritate the heart must be avoided. Besides, the most painful part of a phenol peel is the 20 seconds immediately following the direct application of phenol to the skin. The pain caused by post-peel inflammation is soon alleviated with painkiller tablets and lorazepam.

Ropivacaine Ropivacaine is an amide-type LA, a vasoconstrictor at less than 1% and a vasodilator at more than 1%.10 The fact that it is the pure S-enantiomer reduces its toxicity. Like phenol, it is metabolized by the liver and eliminated by the kidneys. When administered by dermal injection, it has a rapid onset of action (less than a minute) and the duration of action is longer than or equal to that of bupivacaine. Combining it with adrenaline does not prolong its duration of action, and a concentration of 0.75% provides longer anesthesia than a concentration of 1%. Neurological and cardiovascular tolerance to ropivacaine is much better than to bupivacaine. What is more, there is a considerable difference between the neurotoxic and cardiotoxic doses. The toxicity of ropivacaine is intermediate between that of lidocaine and bupivacaine. Direct intravascular injection of ropivacaine is still dangerous, however.

Prilocaine Prilocaine is an amide-type LA, with a very low allergenic potential and low toxicity11 and is non-vasodilating. Unfortunately, prilocaine is metabolized into ortho-toluidine, a chemical that can induce methemoglobinemia. In doses higher than 500 mg, it can cause cyanosis and reduce the oxygen-carrying capacity of the blood.

Mepivacaine Mepivacaine is intermediate between bupivacaine and lidocaine in its kinetics of action. The FNB is set up more slowly than with lidocaine, in 10–15 minutes, although it lasts 90–180 minutes. Mepivacaine has no real advantage over lidocaine, as, at the same dose, its duration of action is only slightly longer. Mepivacaine does not cause vasodilation but, unlike lidocaine, it does not have an antiarrhythmic action.

Lidocaine Lidocaine is an amide-type LA with a very short onset of action. It produces an immediate FNB that lasts from 25 to 45 minutes, depending on whether it is combined with adrenaline.

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Unlike other LA, lidocaine has an anticonvulsant action through the competitive inhibition of the subcortical receptors (0.5–4 mg/ml). It stabilizes the heartbeat:12 an intravenous injection of lidocaine is an effective treatment for heart arrhythmias resulting from phenol intoxication. The toxicity of lidocaine is increased by beta-blockers and cimetidine, as they decrease blood flow in the liver, slow down detoxification and increase plasma levels. Calcium channel-blocking agents increase the risk of arrhythmia by altering the electrical activity of the myocardial cells. Digitalis glycosides also alter atrioventricular conduction and increase the risk of rhythm disorders. Diphenylhydantoin can increase the free fraction of lidocaine by competing with the plasma proteins at the binding site. Stabilization of the CNS with benzodiazepines can mask the first signs of lidocaine intoxication. However, the body easily eliminates the low doses of lidocaine used in a series of FNB, and there have been no reported cases of lidocaine intoxication during a full-face phenol peel performed with FNB.

■

■

■

Combination with adrenaline (epinephrine) Adrenaline stops LA spreading and shortens the onset of action; it prolongs the duration and improves the depth of local anesthesia. Adrenaline slows down capillary absorption of LAs, and therefore makes metabolization and detoxification easier. Adrenaline is contraindicated in cases of diabetes, hyperthyroidism, serious heart arrhythmias and coronary insufficiency or in combination with beta-blockers or monoamine oxidase (MAO) inhibitors. Lidocaine with adrenaline has a very rapid onset of action. Its duration of action is longer than that of lidocaine without adrenaline. However, inadvertent injection of a lidocaine–adrenaline solution into the vessels located near the nerve trunks increases the heart rate (immediate sinus tachycardia at over 130 beats per minute, spontaneously reversible in around 15 minutes) and increases ventricular excitability (risk of fibrillation). It can trigger angina attacks that may lead to a heart attack. It is therefore preferable not to use adrenaline before a full-face phenol peel.

Topical anesthesia: EMLA This ‘Eutectic Mixture of Local Anesthetics’ is used successfully in many brief but painful minor operations. EMLA has been tried as a local anesthetic for phenol peels. However, the following arguments should restrict its use in this indication: ■ There is no denying that EMLA anesthesia for a phenol peel is not as easy as it appears. It is a time- and spaceconsuming local anesthetic procedure: a large quantity

■

■

■

of EMLA must be applied to the whole face, in a thick and even layer, without occlusive dressing, for 1 hour and without any contact with the eyes. The skin on the face has a greater absorption capacity than the rest of the body, and the duration of anesthesia may not be long enough to finish applying the phenol in time and in optimal conditions of comfort, as it takes over an hour to apply phenol. Mixing lidocaine base and prilocaine base in equal parts, at room temperature, gives a ‘eutectic’ mixture. This mixture is emulsified in a base that consists mainly of water and polyoxyethylene castor oil, and the anesthetics are added to the oily phase. Phenol has an excellent oil/water partition coefficient. The oils lower the toxicity of phenol, but also slow down its rate of penetration as well as absorption of the local anesthetics. There is a competition between the phenol solution and the EMLA, which changes the activity and penetration of the combined molecules. Applying an occlusive dressing, necessary for the EMLA cream to work, causes significant changes in the hydration of the stratum corneum and increases permeability. Under occlusion, the corneocytes swell with water and become more permeable. The potential interactions are so complex that it is not possible to predict the results of combining EMLA and phenol peel formulations. With EMLA, liposoluble anesthetic molecules penetrate the stratum corneum and the rest of the epidermal barrier and soon reach the skin nerve endings. The phenol, which is also liposoluble, can get through the epidermis more quickly. On the surface: the shorter contact time between the epidermis and the phenol could reduce epidermal liquefaction. Deep down, a higher concentration of phenol in the reticular dermis could cause the formation of retractile scar tissue. The concentration gradient created in the perivascular spaces of the dermis speeds up the absorption of phenol. The risk of systemic toxicity can also increase. EMLA causes vasoconstriction followed by vasodilation. Vasodilation can sometimes be seen after only 30 minutes of EMLA under occlusion. How will these vasomotor changes affect the effectiveness or absorption of phenol – and therefore its toxicity? There have been studies to prove that EMLA is not toxic. Quantities of up to 150 g of cream applied on 1300 cm2 of intact skin and left under occlusive dressing for 7 hours did not produce toxic levels. Other studies show that injured skin allows EMLA to penetrate much more rapidly. Blood levels, although subtoxic, are then much higher than when EMLA is applied on normal, healthy skin. When 10 g of EMLA is applied to healthy skin, maximum blood levels of the anesthetics are reached after 2–3 hours. Phenol substantially changes the structure of the skin and causes intense vasodilation: how will it affect the absorption of the anesthetics in the EMLA?

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■ The facial skin is more permeable than the skin on the rest of the body. It allows the EMLA to penetrate twice as quickly as the skin on other parts of the body.13 Proper anesthesia of large surface areas requires approximately 1–1.5 g of EMLA/10 cm2. The surface area of the face is around 500 cm2 (5% of the body surface area) and the maximum acceptable dose in an adult with a healthy skin is 50 g. ■ Because of the high cost of such large quantities of the product, practitioners have sometimes resorted to using copies that are not always standardized. It should be noted that there is an increased degree of uncertainty with the use of non-standardized products. ■ It is recommended not to use EMLA as an anesthetic before doing epicutaneous allergy tests, as EMLA blocks the vasodilation induced by certain mediators, such as histamine and antigens.14 ■ The presence of prilocaine is a (relative) contraindication to combining EMLA with products with a potential to cause methemoglobinemia. Combined use with paracetamol (acetaminophen), for example, is to be avoided. Paracetamol is a derivative of phenol (N-acetylpara-aminophenol) and is subject to the same detoxification pathways as phenol. Paracetamol inherits its properties of causing methemoglobinemia from phenol. Large doses of EMLA (>600 mg of prilocaine, or four 5 g tubes) should therefore not be applied prior to phenol. ■ Eye contact with EMLA must be avoided, as it causes intense and painful irritation. Using EMLA on the eyelids significantly increases the risk of eye contact. The vehicle for EMLA contains carbomer 934, which only gels in an alkaline environment. The alkalinity of the mixture also contraindicates its use on the eyelid skin. ■ The pH of EMLA cream is 9.4 (the excipient contains sodium hydroxide). Phenol is more active in an acid environment. Impregnating the skin, for 1 hour, with a mixture at pH 9.4 will change the physiological balance of the skin, its acidity, its permeability and the activity of phenol. ■ A few (unsuccessful) attempts to use EMLA as a topical anesthetic before a trichloroacetic acid (TCA) peel have been published, but the authors reported that they were not impressed by the results. Therefore EMLA should not be used as an anesthetic before a phenol peel.

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small quantities would not be dangerous during a phenol peel. Its short duration of action is the only drawback, but we have seen above that paracetamol plus codeine and cold packs are enough to alleviate the post-peel pain in the hours following a phenol peel.

Sedation plus FNB with lidocaine without adrenaline (epinephrine) This is the best technique for doing a full-face phenol peel. The patient and the doctor are at ease, under the benevolent protection of the anesthetist. Applying phenol to the whole face is completely painless and the patient does not experience or remember any stress or pain. Sedation and intravenous analgesia make up for the speed of sensory recovery after FNB with lidocaine without adrenaline.

How to apply facial nerve blocks Before a full-face phenol peel, the patient is always put on a drip, electrocardiographic monitoring, pulse oximeter and blood pressure monitor. The doctor has everything he needs at his disposal in case of any allergic, vagal or other reactions. Although bupivacaine, ropivacaine or mepivacaine can be employed for FNB, these products should not be used for the reasons set out above, and anesthesia should consist of FNB with lidocaine without adrenaline and with deep sedation. It takes approximately 15 minutes to do all the nerve blocks needed to anesthetize the whole face. If the skin has not been cleaned and degreased before the FNB, the phenol will not be applied until about half an hour after the beginning of the first nerve block on skin that is already recovering sensation. The FNB should therefore be done after the skin has been cleaned and degreased. The FNB should be done in a clockwise (or anticlockwise) sequence, as and where the phenol needs to be applied. This has the added advantage of diluting the doses of lidocaine in time and leaving a rest period between each zone. The hepatocytes, which initiate phenol detoxification by glucuronide and sulfate conjugation as soon as it is applied to the skin, benefit from these pauses between the different blocks. Administering the nerve blocks sequentially also helps reduce the risks of systemic phenol toxicity.

Frontal and upper eyelid block The best choice of LA for FNB: lidocaine without adrenaline (epinephrine) Lidocaine without adrenaline is therefore the best choice of LA for FNB before a full-face phenol peel. Lidocaine stabilizes the heartbeat, so accidental intravascular injection of

A frontal FNB anesthetizes the supraorbital nerve, the supratrochlear nerve and the external nasal nerve (Figures 33.2a–c, 33.3a,b). The quantities required to anesthetize the whole of the frontal region are two times 1.5 cm3 of 2% lidocaine without adrenaline. The phenol can be applied to this area soon after the anesthetic has been injected (with onset in around 1 minute).

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A A

B

B

Figure 33.3 (a,b) Frontal and upper eyelid block.

Mid-face and outer eyelid block (Figures 33.4a,b, 33.5) C

Figure 33.2 (a–c) Frontal and upper eyelid block.

The mid-face block anesthetizes the lower eyelid, part of the cheek, part of the nose and the upper lip. This second phase is done after the phenol has been applied to the frontal area. The infraorbital nerve can be reached from the outside (Figure 33.4a,b) or from inside the mouth. The internal route is preferable, as it is easier to anesthetize the upper lip, the nostrils and the tip of the nose (Figure 33.5). It is best to anesthetize the upper eyelid from the outside, however.

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B

Figure 33.4 (a, b) External route for blocking the infraorbitary nerve.

Figure 33.5 Internal route for blocking the infraorbitary nerve.

The small, outer eyelid nerve block (0.5 cm3 of lidocaine without adrenaline) anesthetizes the zygomatic and lachrymal branches of the facial nerve (Figures 33.6 and 33.7). Approaching the infraorbital nerve internally allows the injection to ‘fan out’ towards the tip of the nose. This technique provides perfect anesthesia of the upper half-lip, the nostril and half of the tip of the nose on the same side: 1–1.5 cm3 of 2% lidocaine without adrenaline is injected in each side.

Lateral regions The temporal region can be anesthetized by blocking the auriculotemporal nerve (Figure 33.8a,b). After raising a

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A

B

Figure 33.6 The small, outer eyelid nerve block (0.5 cm3 of lidocaine without adrenaline) anesthetizes the zygomatic and lachrymal branches of the facial nerve.

Figure 33.7 The small, outer eyelid nerve block (0.5 cm3 of lidocaine without adrenaline) anesthetizes the zygomatic and lachrymal branches of the facial nerve.

skin wheal with a 32G needle just in front of the opening of the ear, a 25G1/2 needle is introduced perpendicularly, immediately in front of the tragus and behind the mandibular condyle (Figure 33.8). It is essential to do an aspiration test because of the proximity of the superficial temporal vessels. The injection should be done slowly and should not meet with any resistance. Resistance would signal that the injection had gone into the intracapsular joint or the posterior meniscus of the temporomandibular joint. If the peeling is performed under deep sedation, this area is usually not blocked. The lower cheek region now needs to be anesthetized (Figure 33.9a,b). This area is not sensitized by the trigeminal nerve but by the ascending branches of the superficial cervical plexus. Sensitivity in the lower cheek can easily be blocked by injecting a ‘line’ of lidocaine under the skin along the lower jaw (Figure 33.9). The pulse of the facial artery should be palpated over the jaw before injecting the lidocaine. The lidocaine should be injected in a line parallel to the lower jaw, on both sides of the pulse, over a few centimeters. The anesthetist should inject a small dose of analgesic before phenol is applied on this area, which is less sensitive and not protected by a nerve block.

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Figure 33.8 (a, b) Block of the auriculotemporal nerve.

A

B

Figure 33.9 (a, b) Palpate the pulse of the facial artery over the jaw before injecting the lidocaine. The lidocaine should be injected in a line parallel to the lower jaw, on both sides of the pulse, over a few centimeters.

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Figure 33.10 Mental block: external route.

Figure 33.11 Mental block: internal route (better).

Mental block A drop of lidocaine is deposited in the gingival crevice so that the injection will be painless. Bilateral injection of 0.5–1 cm3 of 2% lidocaine without adrenaline (canine teeth or premolar–canine junction) anesthetizes the whole of the chin region (Figures 33.10, 33.11). The lidocaine should be injected in a line and slightly fanned. The older the patient, the further back the injection has to be, as the mental nerve foramen recedes as the bones age. The nerve block anesthetic is applied gradually to the whole face: the forehead and the right midface region followed by the right lateral region. The chin is then blocked and treated before blocking the left midface region and finally the left lateral region. The lateral regions are often treated without nerve blocks; they are more complex and patients can easily tolerate an application of phenol to the sides of the face thanks to analgesics, sedation or the anesthetizing effect of the phenol itself. The quantities of lidocaine injected are thus diluted in time, and peak levels of lidocaine are not reached under these conditions. The phenol must be applied in over 1 hour to the whole face: there is no justification for blocking all the sensory nerves in the face at the same time before starting to apply the phenol. This would also increase the risk of toxic peaks of lidocaine in the blood.

Evolution of pain in the course of the peel In the course of a phenol peel performed under FNB with lidocaine without adrenaline and with no analgesic sedation, the patient gradually feels a painful, but bearable, sensation of heat develop in the treated areas. The patient will complain of this unpleasant sensation on the forehead as treatment of the midface region is ending. While the second midface region is being treated, the patient feels this heat in the first midface region. The burning sensation on the forehead is subsiding at this stage of the treatment, and so on and so forth. At the end of the peel, the effect of the FNB has worn off and if the patient has not been given an analgesic before or during the peel, he or she will usually feel a painful burning sensation over the whole face. This can soon be alleviated with a strong analgesic administered by mouth. It is important to check beforehand that the patient can tolerate the analgesic. At the end of the peel, the barrier function of the epidermis is completely incapacitated and it is possible to achieve rapid and effective analgesia by applying a few grams (at most) of EMLA on the areas where the burning sensation is most painful and where treatment has finished. EMLA should be used only rarely in this indication. This recommendation does not conflict with the previous recommen-

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dations, as the speed with which analgesia is produced in this way means that only very small quantities of EMLA need to be applied to the face after a deep peel – far from toxic plasma levels. Also at this point in the procedure, the interactions between the small quantities of EMLA applied and the quantity of active residual free phenol left on the surface of the skin will be insignificant.

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The burning sensation on the skin is much improved by applying a cooling mask (Figure 33.12) in the hours or days following the peel.

Sedation Premedication 30–60 minutes before the peel, a 100 mg tablet of hydroxyzine or intramuscular promethazine is usually sufficient. The patient can also benefit from the rapid sedative properties of sublingual lorazepam, as discussed earlier in this chapter. Atropine should not be injected automatically, but should be available in case of bradycardia. Analgesic sedation consists of minimal doses of midazolam or intravenous fentanyl, with blood pressure, cardiac and pulse oximeter monitoring.

Fentanyl

A

This is a strong, short-acting analgesic. The anesthetist ‘titrates’ the analgesic slowly with repeated intravenous injections of 25 µg when the patient complains about the pain. A total dose of 100 µg can be given safely. Some authors administer 50 µg at a time to reach a maximum dose of 250 µg in 1.5 hours.15

Midazolam This is a strong sedative with a short onset of action that can be administered intravenously, rectally, intramuscularly or sublingually. Midazolam can be used as premedication: 4 or 5 drops are given sublingually as soon as the patient arrives at the clinic. It has a short half-life. The anesthetist injects a dose of 1 mg intravenously under pulse oximeter monitoring, even if the risk of respiratory depression is very rare with a 5 mg dose. In case of overdose, flumazenil (Anexate®, which comes in 1 mg/10 ml phials) takes less than 1 minute to compete with the central receptors occupied by the midazolam: 0.2 ml is injected intravenously (15 seconds). Additional doses of 1 ml can be reinjected every minute until the patient regains consciousness. Flumazenil has very low toxicity, and doses of up to 100 mg have been injected intravenously without any signs of overdose.

B

Figure 33.12 A cooling mask (a) can be put in a freezer and placed on the face as soon as the peel is over (b).

Fintsi16 recommended simple intravenous sedation without FNB: he used promethazine and morphine sulfate (5–15 mg) and titrated the doses until the burning sensation subsided. According to him, nerve block anesthesia is not essential with this procedure, but, without the FNB, the patient is in pain during the peel and this makes it uncomfortable for both the patient and the doctor. The patient only has a vague memory of the pain. Asken15 reported on a study by Litton showing an accelerated heartbeat slowing down when deep sedation is combined with nerve block anesthesia.

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Notes 1. Cold temperatures slow nerve conduction. What is more, the vasoconstriction caused by cold temperatures slows down the rate at which local anesthetics are absorbed, and their effect is prolonged. 2. This is applicable to all types of peels. 3. Klein solution: a mixture of saline solution, lidocaine, adrenaline (epinephrine) and sodium bicarbonate normally used as a local anesthetic in liposuction procedures. 4. Various phenol peel formulas can be found on the market that boast of the possibilities of doing a full-face peel ‘without anesthetic’. In some cases, this means ‘without general anesthetic’ and in others the patient is put on strong analgesics, sedation and premedication. Some low-dose phenol peels (around 30%) are no more painful than a trichloroacetic acid to the papillary dermis, but they are not much more effective either. 5. There is no such thing as a ‘small’ general anesthetic. 6. Which in no way means that 1% of patients are allergic. I have never myself come across any patient who is allergic to lidocaine in almost 30 years of my medical career. 7. Correct treatment consists in filling the blood vessels, raising the legs and putting the patient on oxygen.

8. It must be remembered that the large number of facial blood vessels speeds up the absorption of LAs 9. Lalanne B, Baubion O, Sezeur A, Tricot C, Gaudy JH. Circulatory arrest after splanchnic neurolysis with phenol in unrespectable corner of the pancreas. Ann Chir 1994; 48(11): 1025–8. 10. Which explains why the effect is not prolonged even when the injected dose is increased. 11. The toxicity of prilocaine is 40% of that of lidocaine. 12. Dose-related action. High doses are toxic. Toxic convulsions occur when blood levels of lidocaine reach 10–22 mg/ml. 13. Juhlin L, Hagglund G, Evers H. Absorption of lidocaine and prilocaine after application of a eutectic mixture of local anesthetic (EMLA) on normal and diseased skin. Acta Derm Venerol (Stock) 1989; 69: 18–22. 14. Ferrari FP, Rosario Filho NA, Schmidt AV. Allergy skin testing after topical anesthesia. J Pediatr (Rio J). 1996; 72(4); 215–20. 15. Asken S. Unoccluded Baker–Gordon phenol peels – preview and update. J Dermatol Surg Oncol 1989; 15: 998–1008. 16. Fintsi Y. Exoderm®, a novel, phenol based peeling method resulting in improved safety. Am J Cosmet Surg 1997; 14: 49–54.

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34 Full-face phenol: application

Preparing the solution Lip & Eyelid® formula Lip & Eyelid® formula is an oily solution of phenol, often called phenol oil. The solution is ready for use and there is no preparation involved. The flask contains 3 ml of solution, which is the quantity usually needed to treat the whole face or do around 15 eyelid treatments.1 It is easy to plunge the applicator straight into the container and to squeeze it out correctly on the neck of the flask. Lip & Eyelid® formula remains stable for many years.

Baker–Gordon solution The four ingredients must be mixed immediately before the peel: liquid phenol (88%) croton oil septisol distilled water

3 ml 3 drops 8 drops 2 ml

Other formulas also have to be prepared immediately before the peel: for more information, see Chapter 25. Mixing the four ingredients of Baker’s solution produces an unstable emulsion rather than a truly stable solution. It is recommended to keep strictly to the formula, as any attempt at customizing it can lead to unexpected results and relatively serious complications. Because the emulsion (soap + oil + phenol + water) is unstable, the solution has to be freshly prepared. It must be shaken continuously throughout the peel to keep the emulsion as homogenous as possible. This essential task should be given to an assistant who will be responsible for holding the container throughout the peel. If the Baker–Gordon solution is left unattended, without being shaken, it separates into different phases. Each of these phases has a specific concentration of phenol and produces different peel depths. If the solution is not shaken continuously, each phase could be

applied in turn to the patient’s skin and the results would be uneven: inadequate in some places and too deep in others. This could cause scarring, hypopigmentation or hyperpigmentation. Not shaking the solution could certainly cause certain post-peel complications.

Litton’s solution If stored in the right conditions, away from sources of air, light and heat,2 Litton’s solution remains stable for several years. After shaking the flask,3 the quantity required for the peel is drawn out (usually 3–5 ml, depending on how thick the applicator is and how much of the product it retains).

Applying the peel solution Preparing the applicator The applicator should not be too thick, so as not to retain too much of the product and to reduce the risk of drips. The doctor usually prepares it ‘by hand’ before starting application and after disinfecting his hands. Ideally, the applicators should be prepared beforehand and left in sterile covers. The simplest and most efficient applicator consists of a wooden skewer approximately 15 cm long with cotton wound uniformly around one end to form a cylinder of even diameter (Figure 34.1). Other types of applicators can be used, depending on the doctor’s experience. Some authors suggest applying phenol with a brush to get a more superficial phenol peel.4 The bristles of the brush must be tested for resistance to phenol. Synthetic brushes can react chemically with the phenol. This reaction denatures them and can change the composition of the phenol solution. A gauze pad should not be used to apply a phenol peel, as the rough texture of this applicator could allow the phenol to penetrate too rapidly; besides, the large quantities of solution that gauze can absorb may cause drips and runs or deposit uneven quantities of the product on the skin too quickly; the most serious complications can only be avoided by slow and even application.

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A

B

C

Figure 34.1 (a–c) Wooden skewer, approximately 15 cm long, with cotton wound uniformly around one end to form a cylinder of even diameter.

The use of cotton balls is not advised, as they are not easy to handle in ‘delicate’ areas such as the eyelids and also because of the risk of runs. Cotton buds are not suitable for large surface areas, as they do not allow even application. In a very localized phenol peel (i.e. eyelids or upper lip), however, phenol is applied with a single cotton bud, as it is more precise and uses up less of the product. The applicator should only ever be used once.

Some quick reminders about skin preparation No skin preparation is necessary during the weeks preceding the use of Lip & Eyelid® formula. For other formulas, refer to the recommendations that come with the product. Muscle mobility will have been blocked by an injection of botulinum toxin 8 days before the peel. Small benign tumors, in low numbers, can be treated by shave excision immediately before the peel and will therefore benefit from the local anesthesia induced by the nerve blocks. If there are a large number of tumors, they can be excised after

frosting is obtained to avoid creating too many rapid transcutaneous penetration routes in the treated areas. Telangiectasias can also be electrocoagulated immediately before the phenol is applied. Urkov applied phenol and cauterized deep wrinkles at the end of the peel, before putting on an occlusive mask.

Precautionary details The flask of peel solution is put on a table, within reach of the doctor, and the top should be easy to take off and put back. Replacing the top on the bottle after each use (the assistant’s responsibility) helps reduce the amount of phenol in the air and prevents accidental spills. There is a general rule for all peels: the doctor should avoid holding any vessel containing a chemical peel in his hand for a long time and should not hold the product in front of his face. The air space above the face should not be violated. On the same table, a 20 ml syringe of sterile physiological saline and a row of make-up remover pads (preferably ster-

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ile) are placed at hand. The doctor will use some of the pads to spread the phenol evenly on the skin, and the assistant will use the rest to immediately sponge away any tears, often a unilateral reflex reaction. The patient is on a drip and monitors; the eyes are protected with ophthalmic Vaseline®.

Setting the lower limits of the peel Before treatment, the lower limits of the peel must be established with the patient in a sitting position. The practitioner, with hand outstretched, places four fingers on the edge of the lower jaw, halfway between the chin and the angle of the jaw, and lifts the skin upwards. A surgical skin marker is then used to draw the line marking the lower limits of the peel on the stretched skin: the line should start at the angle of the jaw and go towards the chin. The lower demarcation line will be hidden in the shadow of the jaw (Figure 34.2). If the demarcation line is drawn when the patient is lying down, the peel will not go far enough under the jaw, and the line between treated and untreated skin may be more visible.

Application technique The applicator is soaked in Lip & Eyelid® solution and carefully squeezed out on the inside of the neck of the bottle to get rid of any excess and avoid drips. The solution must be applied slowly and conscientiously to each square millimeter of the facial skin. The right hand5 holds the handle of the applicator between the thumb, index finger and middle finger. By moving the thumb smoothly over the other two fingers,6 the applicator can be rolled over the

Figure 34.2 End of the third phase of treatment, up to the lower demarcation line. The phenol has gradually penetrated through the keratosis that was still visible at the end of the second phase of treatment.

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skin: it is not a rubbing movement but a rolling one. The applicator is pressed on the skin with the same amount of pressure that would be used for scratching. The solution is applied uniformly and the pressure is firm and even. The phenol is applied first in the base of the wrinkles. The gloved left hand holds the skin taut to make it easier to treat apply the phenol and to help it penetrate. Care should be taken to avoid maceration in the bottom of skin folds. A first layer of phenol is gradually applied to the whole region that has been anesthetized. To even out penetration of the phenol that has just been applied, the area should be immediately gone over again with a make-up remover pad, moved perpendicular to the direction of application. The same cotton pad can be used throughout the peel, as it does not come into contact with the eyes. If the phenol is applied horizontally, the pad should be applied vertically and vice versa.

Bad practice A few doctors have been known to talk (sometimes proudly) of conduct that has more to do with greed than good medical practice: they try to economize on the volume of peel solution by whatever means they can. Technically, it is of course possible to use less solution for a full-face peel, but this kind of misplaced economy is not to be recommended. The efficacy of a phenol peel is also dependent on the total quantity of phenol that is applied to the skin and that reaches the dermis.7 If too little phenol is applied, the results will be inadequate and in the long run it will cost the doctor more to do touch-ups than to apply the right amount of good quality solution in the first place. As in many other areas, false economies do not make a fortune.

Around 3 ml of solution is applied on the skin in successive coats to complete a full-face peel in over an hour. The endpoint is the appearance of an even ‘gray–white’ frosting (see below). An assistant constantly sponges away any small reflex tears with a cotton ball or make-up remover pad, which is thrown away and replaced after each use to make sure that the next time the eyes are wiped, no phenol is carried into them with the tears that have just been sponged away. Any touch-ups can be done the next day on the same patient with the solution left in the bottle. Even though a phenol solution is antiseptic, it is out of the question to use this remaining solution on any other patient. Practitioners often ask themselves the basic question of ‘how many coats’ to apply on the skin. Phenol has reached its peak effect when a gray–white frosting appears. Some

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patches of buff yellow may also appear when the maximum depth has been reached (Figure 34.5). Pink–white or pure white frosting occurs when the phenol has penetrated the papillary dermis, and the results would be comparable to those of a trichloroacetic acid (TCA) peel, which is not as good as can usually be achieved with phenol. Some phenol peel formulas need several coats of solution to achieve this type of frosting. Lip & Eyelid® formula is usually applied in a single coat, and it only requires a little patience for the pure white frosting to turn gray–white.

Clinical signs of the phenol application Frosting Applying Lip & Eyelid® formula to the skin triggers frosting8 (Figures 34.4–34.6) that is more or less intense and occurs more or less rapidly depending on the skin type. A thinner

Figure 34.4 Phenol penetrates more slowly on keratoses. A little patience is required.

Figure 34.5 Figure 34.3 Pure white frosting after an application of Lip & Eyelid® formula to the right midface region. The frosting on the forehead has already faded during the rest period.

When Lip & Eyelid® is being applied, a pure frosting appears temporarily. It is soon replaced by gray–white frosting that turns a buff yellow color in places, as can be seen here. The appearance of buff yellow patches is a sign that the phenol has reached maximum penetration.

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Figure 34.6 All the colors associated with a phenol peel can be seen here. The chin has pure white frosting just after the phenol has been applied. The cheeks have gray–white frosting after the same amount of phenol as applied on the chin has penetrated more deeply. The forehead is a pink color, where the frosting is fading, with patches of buff yellow.

skin frosts more quickly than a thick and oily skin (Figure 34.4). The rapidity of the onset of frosting is not always related to the depth of the phenol peel. As soon as the skin comes into contact with an aqueous9 solution of highly concentrated phenol, protein coagulation is abrupt (pure white frosting) but relatively superficial, and this stops the rest of the phenol applied on the skin from penetrating deeply. With an oily solution, on the other hand, frosting occurs more slowly and the color is less intense, which is a sign of deeper penetration. Rapid frosting is often pure white in color, whereas slower frosting gradually turns into a gray–white color that indicates deeper penetration of the phenol into the skin. The appearance of buff yellow patches signals even deeper penetration (Figure 34.5). It is therefore relatively easy to judge the depth of action of phenol: frosting that remains pure white shows that penetration is not as deep as with frosting that turns gray–white. The appearance of buff yellow patches shows that maximum penetration has been reached. Any additional application of phenol would be associated with a major risk of local complications.

Edema Severe edema (Figure 34.7) occurs quickly after phenol has been applied. The skin soon feels like cardboard because of the speed and extent of the edema that sets in and stretches it.

Gradual application Nerve block anesthesia is performed sequentially (anesthetize one nerve trunk and apply phenol on the anes-

Figure 34.7 Edema is clearly visible on the left side of the face, which was treated before the right side. The arch of the left eyebrow is more prominent than the right. The left side of the nose is swollen, as well as the upper left half lip. The edema line is very visible on the neck. Edema usually occurs at the same time as the frosting fades. The erythema goes beyond the limits of the edema, which in turn goes beyond the limits of the phenol application.

thetized area; anesthetize the next trunk and apply phenol on the corresponding area, etc.). This means dividing the face into as many areas as there are nerve trunks to block. The full-face phenol peel is thus done gradually, area by area. Particular care must be taken not to leave thin strips of skin untreated on the borders between the different areas: this would make the face appear ‘striped’, as the strip of untreated or undertreated skin would show up clearly between the areas regenerated by the phenol. It is easy to be misled by the erythema and edema that develop around 10 minutes after frosting and that extend beyond the area that has been in physical contact with the phenol. When treating the next area, the applicator should be taken slightly into the area of erythema and edema. The different cosmetic units are treated in turn, after each corresponding nerve block.

First phase The first phase covers the forehead, the upper eyelids and a temporal ‘extension zone’ on the right hand side (Figure 34.8). A frontal block and an outer eyelid block (see Chapter 33) are done on each side of the face. The phenol is applied vigorously in the base of each forehead wrinkle before treating the whole of the forehead. There are three borders

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Figure 34.9 Day 1 after a localized Lip & Eyelid® peel of the four eyelids. The upper eyelid tarsus was not treated with phenol: it does not show any skin change, just edema and severe erythema.

Figure 34.8 A single coat of Lip & Eyelid® has just been applied to the first zone. The frosting will turn gray–white without another application.

to this first phase: the anterior hairline, the eyebrows and upper eyelids, and the temporal region. Anterior hairline Phenol is not toxic to the pilosebaceous units. To avoid creating a visible demarcation line between the skin of the forehead and the hair, the applicator is taken 1 cm into the anterior hairline. Eyebrows The phenol is applied to the eyebrows against the lie of the hairs to ensure proper contact with the skin. Its action is not deep enough to remove any permanent make-up.10

The skin of the forehead is thoroughly anesthetized by the nerve blocks, and the phenol application should extend slightly into the temporal zone. Patients should be warned that they will feel a burning sensation on the temples for 15–20 seconds as the phenol is applied to this unanesthetized area. The temporal regions are treated gradually up to a virtual horizontal line that goes through the center of the pupils. The extension zone includes part of the wrinkles of the crow’s feet: the phenol is first applied at the base of these wrinkles; the left hand stretches the skin to make it easier to reach the base of the wrinkles with the applicator. The peel solution is then applied to the rest of the area.

Rest period The phenol is applied slowly and carefully. A rest period of 10–15 minutes is obligatory after the end of the first phase

Upper eyelids (Figure 34.9) After the eyebrows, the doctor treats the upper eyelids. Any excess of phenol is avoided by using an applicator that has already been used to treat an adjacent area and that has not just been soaked in phenol. The upper eyelid tarsus does not have to be treated: this would cause severe palpebral edema. When the eyelids are being treated, the assistant should be ready to rinse the eyes out with a syringe of sterile physiological saline (prepared before the peel) and sponge away any reflex tears. Temporal ‘extension zone’ (Figure 34.10) At the border between the frontal and temporal zones, it is worth making the most of the anesthesia that the phenol has induced and that extends about 1 cm beyond the frosting.

Figure 34.10 End of first phase of treatment. The white line is the virtual borderline passing through the pupils. The area marked out by the colored line is the temporal ‘extension zone’.

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of treatment. It takes around fifteen minutes to treat the frontal region, the upper eyelids and the temporal ‘extension zone’. Twenty-five minutes after the beginning of the treatment, the second phase can be started. Well-equipped clinics can make the most of the obligatory rest period to treat two patients at the same time, in two different rooms.

Second phase The second phase covers the central right-hand side: lower eyelid, midface region, half of the nasal pyramid, upper half lip, periauricular ‘extension zone’, earlobe and tragus (Figure 34.11). Lower right eyelid Phenol is applied up to 1–2 mm from the eyelashes. Nerve blocks do not always succeed in fully or properly anesthetizing the eyelid skin. If intravenous sedation is not being used, patients should be warned that they might feel an intense but brief burning sensation. If the peel is done step by step, very slowly, the anesthesia caused by the phenol itself, together with reduced sensitivity caused by the analgesics, are sufficient to apply phenol on the eyelids without causing much pain. ‘Vocal’ anesthesia is essential in this area, and I usually use the following ‘trick’ for the eyelids: the area is supposedly anesthetized by the nerve blocks; I tell the patient that I am going to test the depth of the anesthesia and that if it is not deep enough, it can be improved. Inadequate anesthesia is signaled by a burningtype pain that lasts around 15 seconds. The phenol is applied to the eyelid as if it were properly anesthetized. The patient interprets any pain as a simple test and finds it bearable, whereas in fact the phenol has been applied. The phe-

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nol itself produces sufficient anesthesia for treatment to continue without pain. As soon as the eyelid frosts, application can be completed painlessly. The practitioner and assistant should watch out for any reflex tears while the eyelids are being treated. Nose and right midface region The right side of the nasal pyramid is treated, as well as the skin just on the edge of the right nostril. As the face ages, the subcutaneous fat in the nose atrophies, and this, together with degeneration of the ligaments or connecting fibers, leads to loss of tip support. The resulting nasal tip ptosis contributes to the classic impression of increased nose size with aging. There are surgical nose lift techniques as well as a filling technique11 that raises the tip of the nose. A phenol peel is a valuable alternative: the tightened dermis often gives the tip of the nose a clinically visible lift. Upper right half lip The upper lip requires careful treatment: several coats of Lip & Eyelid® should be applied. Before treating the whole lip, the solution is applied vigorously in the base of each wrinkle, the skin of the lips is stretched between two fingers of the gloved left hand to open the wrinkles and make the atrophic base accessible (see Figure 34.12). Dermabrasion can be performed after the phenol has been applied,12 when frosting is still apparent, if the doctor considers that phenol alone is inadequate. The term ‘chemabrasion’ can be reserved for this technique.13 After 24 hours of occlusion, if some lip wrinkles still persist, either the base of the wrinkles can be treated again with phenol or the whole lip can be treated with chemabrasion. To avoid creating a demarcation line on the vermilion portion of the lip, the phenol must go 1–2 mm into the red lip. If the phenol does not penetrate the red lip, not only will there be a demarcation line, but fine lines will also persist and lipstick can bleed into the white lip area. Aging of the lips, combined with fat and jawbone atrophy, often starts with upper-lip ptosis that hides the teeth. In young subjects (under 30 years old),

Figure 34.12 Figure 34.11 The second zone being treated with Lip & Eyelid® formula.

As for the upper lip, the base of the wrinkles on the chin should be treated first before applying the phenol to the whole chin area.

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1–2 mm of the upper teeth can often be seen when the face is at rest and the mouth slightly open. Surgical techniques that reduce the height of the upper lip have been described, such as ‘moustache plastic surgery’:14 a simple technique performed under local anesthetic that requires special care in the suturing to do a perfect edge-to-edge repair of the epidermis. After a phenol peel, the upper white lip retracts slightly, and this is often enough to make the whole area look younger and the upper lip appear plumper without resorting to filling techniques. Pretragal ‘extension zone’, earlobe, right tragus (Figure 34.13) A pretragal nerve block can be done to anesthetize this area, although it can easily be treated without a nerve block, gradually, up to the virtual line between the corner of the mouth and the earlobe. Lip & Eyelid® can be applied more vigorously in the pretragal folds, using the left hand to stretch the skin and expose the base of the wrinkles to the phenol. The earlobe and the tragus must be treated so that the results are even over the whole area. If the earlobe and tragus are not treated, an area of sun-damaged skin would be clearly visible on either side of the rejuvenated face.

Rest period After these areas have been treated, the 10–15 minute rest period between the two phases can be used to apply the occlusive dressing to the first zone that was treated.15 The third phase starts around 50 minutes after the start of the treatment.

Third phase This essential phase of the peel covers the rest of the righthand side: half chin and lower lip and the right jaw ‘extension zone’ to the neck (Figure 34.15). Lower half lip and right half chin The corner of the mouth requires careful treatment, as the wrinkles here are deep and atrophic. The fingers of the left hand stretch the skin to expose the atrophic base of the wrinkles to the phenol. The lower lip is treated in the same way as the upper lip (see above). The skin on the chin is often resistant to treatment, and several coats may be required. Acne scars and deep wrinkles are particularly resistant in this area, and sometimes require chemabrasion during the peel itself or after 24 hours of occlusion. Right jaw ‘extension zone’ There is one small lateral region that has not been treated. This region can be anesthetized with a lateral nerve block (see Chapter 33) or can be treated slowly and gradually. This latter option is always chosen when the full-face peel is performed under deep sedation. Lower limits of the peel and the neck Phenol is applied up to the lower limits set before the start of the peel; this forms the demarcation line (Figure 34.14). The skin on the neck is structurally different to that on the face: it has fewer appendages and pilosebaceous units. After a deep peel, the skin regenerates from these appendages. A phenol peel on the neck carries an increased risk of scarring. What is more, the usual post-peel facial edema tends to extend downwards to the neck, and if the neck is treated

Figure 34.13 End of second phase of treatment. The white line shows the virtual line from the corner of the mouth to the earlobe. The colored line shows the pretragal and cheek ‘extension zone’. The lower part of the extension zone shows a darker patch of skin that comes from the slow penetration of the phenol through keratoses.

Figure 34.14 End of the third phase of treatment, up to the lower demarcation line. The phenol has gradually penetrated through the keratosis that was still visible at the end of the second phase of treatment.

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Figure 34.16 Application of Lip & Eyelid®: fourth phase.

Figure 34.15 End of the third phase of treatment. The occlusive dressing has been placed on the frontal region during the second rest period; the second zone will be covered with an occlusive dressing during the third rest period. The color of the frosting will gradually turn gray–white without any additional application of phenol.

at the same time then the edema that builds up in this area can make patients feel as if they are suffocating – a very unpleasant sensation. Therefore the neck could – possibly16 – be treated at a different time to the face. The best treatment for a sagging neck is still a surgical lift of the lower half of the face, and a ‘medium-depth’ peel can improve the photoaging: a phenol peel on the neck can be avoided in the majority of cases. Nevertheless, some authors (including Baker) treat the neck at the same time as the face: they apply the product up to the clavicles on the anterior neck and up to the 7th cervical vertebra on the posterior neck. Other authors suggest treating the face on the first day and the neck the day after to reduce the risks of toxicity associated with applying greater quantities of phenol to a larger surface area.

Rest period After these areas have been treated, the 10–15 minute rest period can be used to apply the occlusive dressing to the second zone that was treated .

Fourth phase This phase of the peel covers the left-hand side: lower eyelid, midface region, half of the nasal pyramid, upper half lip, periauricular extension zone, earlobe and tragus (Figure 34.16). See the details of application in the second phase.

Rest period After these areas have been treated, the 10–15 minute rest period can be used to apply the occlusive dressing to the third zone that was treated.

Fifth phase This phase marks the end of the peel, with an application of phenol to the left-hand side, to half of the chin and the upper half lip, and to the jaw ‘extension zone’ to the neck (Figure 34.17).

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Figure 34.17

Figure 34.18

End of application of the phenol peel. Occlusion dressing is nearly complete.

Appearance of the face at the end of the peel (Lip & Eyelid®). The mask (here Leukoflex®) is complete. The appearance of ptosis of the right eyelid comes from the edema that started earlier in this area as a result of the ‘phased’ application of the peel solution.

Finishing the occlusive mask The occlusive mask is applied to the rest of the treated areas (for details, see Chapter 35). At the end of the peel, the edema on the face will not be even, as it will have developed phase by phase (Figure 34.18). The patient may complain of a pulsing heat, which can soon be alleviated by applying a cold pack. New, longacting analgesics can be used to reduce the pain.

Notes 1. With one flask, it is possible to treat the upper or lower eyelids of 15 different patients, as approximately only 0.2 ml is needed to do a peel on two eyelids. 2. The refrigerator is an ideal place to keep peel solutions. 3. For phenol as well as other peel solutions: even if a solution is said to be stable, there is no harm in shaking the bottle to avoid all risk. 4. Though using phenol to do a superficial peel means both patient and doctor taking a pointless risk where less toxic agents are available (TCA, AHA, salicylic acid, etc.). 5. Left-handers will understand that they must reverse the hands used. 6. Making the gesture that universally means ‘to pay’.

7. Cortez E. Chemical face peeling. Otolaryngol Clin North Am 1990; 23: 947–60. 8. As with TCA, the frosting is caused by protein coagulation: the three-dimensional structure of the proteins is changed and they become opaque. The same phenomenon is responsible for egg whites becoming opaque when cooked. 9. Which is not the case with Lip & Eyelid® formula, which is, on the contrary, a very oily solution. 10. However, the eyebrows may become a little lighter. 11. Due to Dr Sammy Passy, Brazil. 12. It is preferable to apply the phenol before dermabrasion, as the dermabrasion might cause the phenol to penetrate too quickly and too deeply through skin whose permeability has been significantly altered by the abrasion. Also, the diffuse bleeding that accompanies the abrasion would partially neutralize the phenol. 13. Asken S. Unoccluded Baker–Gordon phenol peels – review and update. J Dermatol Surg Oncol 1989; 15: 998–1008. 14. Regis-Milano G. La plastie en moustache. XIX° réunion du GRCD, Paris, Janvier 1996: 17–18. 15. Information on the choice and preparation of the occlusive post-peel mask can be found in Chapter 35. 16. See Chapter 31 for more information on the risks of treating the neck with phenol. The increased absorption area also carries an additional and unnecessary risk of toxicity for the patient.

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35 Phenol: post-peel care

Immediate post-peel care The care required for the skin and patient after an application of phenol largely depends on the formulation and the doctor’s experience.

Hospitalization or ambulatory peel? The first question to ask is whether or not the patient should be hospitalized. Some hospitals or cosmetic clinics like to combine a phenol peel with other treatments: surgical or medical, nutritional or cosmetic. In these cases, patients remain in the hospital, clinic or spa for 8–15 days. Some peels require complex and repeated sessions of postpeel care that can only be given if the patient is hospitalized for 8–10 days. It is clear that hospitalization can contribute to patients’ wellbeing, making life easier and helping them avoid any contact with the public, friends or relatives during the first week of – unsightly – skin regeneration. Some practitioners, for fear of the potential toxicity of phenol and the possibility of heart rhythm disorders, prefer to hospitalize patients the first night after the peel until the occlusive mask has been removed 24 hours later. This brief period of hospitalization can also be beneficial to the patient, who can be given a titrated intravenous analgesia until the morning after the peel. Some more recent techniques provide a phenol peel of the same quality and are completely ambulatory. Patients are taken home by a friend or relative. They can leave the clinic a few hours after the end of the phenol application,1 on condition that someone stays with them around the clock for the first 72 hours and that the patient can get to the doctor’s surgery quickly,2 whenever advised or necessary. The severity of the edema on the first day means that the patient is completely dependent on others, and it is important that any localized treatment can be given rapidly. Cardiac toxicity has been discussed in Chapter 28: in summary, when the peel is performed slowly, in over 1 hour, there is no cardiac toxicity. If phenol is applied too quickly on too large an absorption

area, arrhythmias develop rapidly: this is a problem that occurs while the phenol is being applied. Detoxification starts immediately. A few hours after the peel, the risk of phenol-induced arrhythmia is practically non-existent, if the liver has been able to detoxify the phenol and the kidneys eliminate it normally (see Chapter 28). Peels of the Baker–Gordon or Litton type are often performed with hospitalization. Exoderm® or full-face Lip & Eyelid® peels are usually ambulatory procedures. With the exception of some techniques, hospitalization, even if brief, no longer seems to be a necessity but is more of a comfort factor for both patient and doctor. Patients are often happy to be able to go home and be in familiar surroundings.

Occlusive or open technique? Publications on peels mention different possibilities, and once again it is the formula used that determines the application procedure and the need for an occlusive or open technique. Both techniques have been described as giving excellent results. The following discussion weighs up the pros and cons of occlusion.

Ease and speed The doctor may find it easier and quicker not to apply an occlusive mask, but this is a hasty conclusion: applying an occlusive mask is a simple procedure and can be done in the obligatory rest periods between each treatment area. No time is wasted.

Comfort The occlusive mask improves patient comfort: the skin liquefies beneath the mask, and the liquefied integuments do not drip on the skin. The occlusive mask prevents the skin from sticking to clothes or pillows. When an occlusive mask is put in place, the patient can apply a cooling cold pack to alleviate the painful burning sensation, whereas with the open technique, direct contact with the skin is not possible.

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Safety With an occlusive mask, patients do not have to treat themselves or be treated by anyone else; nothing has to be applied to the skin, which reduces the risk of involuntary errors, allergies or secondary infections. The mask prevents patients from touching their skin and importing bacteria from their fingers. The mask prevents contact between the skin and any insects or pets carrying infectious agents, which may be dangerous to a skin deprived of its immune defenses. With transparent occlusion (Leukoflex®), it is possible to evaluate how the treated skin is developing through the mask. When phenol is applied to healthy skin,3 occlusion slows down the absorption rate but does not alter the total quantity absorbed.4 The liver therefore has more time to detoxify the phenol and the kidneys have more time to eliminate it. This increases the peel’s safety margin.

Effectiveness Unlike trichloroacetic acid (TCA), whose effect is restricted by occlusion,5 the effectiveness of phenol is improved by maceration. Stegman proved that applying an occlusive mask allows the phenol to penetrate more deeply and improves the cosmetic results.6 Asken1 reported that it is possible to increase the penetration and effectiveness of phenol with occlusion, but that the same results can be achieved by vigorously cleansing and degreasing before the peel or by repeatedly applying hydrating and covering agents (Vaseline®- or siliconebased products) after a phenol peel.7 This principle is applied in certain phenol peel protocols that vaunt the merits of replacing 24-hour post-peel occlusion with continual application of hydrating products. Using cream- or Vaseline®-based occlusion rules out any possibility of a touch-up after 24 hours and deprives the doctor of a valuable weapon in his treatment arsenal. Cortez,6 Beeson et al8 and McCullough and Maloney9 have achieved excellent results without occlusive masks, although Cortez applies a hydrating cream such as Eucerin® that patients must continue applying themselves throughout the first night and up to 5 days after the peel. The face is washed with a showerhead with warm water every 4–5 hours, before each coat of cream is applied. On the 5th day, the Eucerin® is replaced with white Vaseline® until the 10th day. This procedure, more complicated for the patient, often results in bacterial infections, which is why other authors9,10 have replaced the hydrating cream with an antibiotic cream such as bacitracin. Fungal resistance or secondary infections are not uncommon, however, and there have been reports of allergic reactions to antibiotic creams applied on skin that is completely permeable. McCullough and Maloney9 recommend the following method. During the first day and night, swabs of cold phys-

iological saline are applied. Thereafter, patients rinse their faces under the shower four times a day and apply a bacitracin-type antibiotic cream up until at least the 8th day. Healing takes 10–14 days.11 Any scabs are rinsed under the shower and softened by the water, then coated in bacitracin. Another occlusive technique consists in applying sterile white Vaseline® after the phenol: the Vaseline® provides perfect occlusion, but can sometimes be unpleasant, as heat from the skin liquefies it, making it to drip and shifting bits of skin debris. The patient is then led to wiping the skin frequently and the risk of secondary infection is increased. Prolonged use of Vaseline® after a peel is known to cause acneiform or milia lesions to appear. Whichever technique is used instead of the occlusive mask, there is an increased risk of infection, injury, allergies or errors, and a transparent occlusive mask is recommended during the first 24 hours to improve the peel’s effectiveness, reduce the need for patient participation in post-peel care and lower the risk of secondary infection.

How to use the occlusive mask Pitfalls to avoid The occlusive mask must be perfectly even. The main pitfalls to avoid are as follows. Air bubbles, pockets of maceration, tension lines The presence of air bubbles reduces local maceration and therefore effectiveness. Pockets of maceration increase local penetration of phenol (risk of dyschromia and scarring). Any tension lines in the mask are transferred onto the skin; they can cause unnecessary pressure and may generate areas of necrosis. Some protocols, however, take advantage of the benefits of intentional, well thought out and controlled tension on the skin while it is regenerating: for example the Molding Mask (Dr Roige, Spain). Post-peel care in this case includes the precise positioning of support strips. Occlusive mask coming unstuck The occlusive mask sometimes comes unstuck around the edges of the mouth, and lip wrinkles are among the most difficult to treat. Lack of maceration where the mask has come unstuck can lead to inadequate results (Figure 35.1). The mask comes unstuck all the more easily if the patient talks, laughs, eats, chews or smokes. The patient should therefore be kept in complete isolation for the first 24 hours, without social contact, except for close friends or relatives, who should be encouraged to help the patient avoid facial expressions and communicate without talking. Smoking is strictly contraindicated on the first day because of the lip movements required for puffing on a cigarette

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occlusive layer is covered with a second layer of adhesive tape. The Steridrape® is thin, very adhesive and completely impermeable, and is perfectly suited to the skin. It is quick to put on, as it only consists of 10 pieces and is easy to adapt to faces that are especially wide or narrow. Classic mask: waterproof tape Choice and preparation of these tapes are discussed in Chapter 32. At the end of the peel, the doctor has several rows of precut strips that can be picked up with the fingertips. They are placed gradually on the skin, with several millimeters overlap between them, as on a tiled roof. Only one layer of Sleek® is necessary. Garcia (Spain) has suggested replacing Sleek® with a first layer of Micropore®, over which a second layer of Blenderm® is applied. Santos (Brazil) uses a double layer of Micropore®. I recommend using Leukoflex®, an impermeable and transparent dressing, which is applied in a single layer and through which the skin can be seen on the first day.

Figure 35.1 An occlusive mask that has come mostly unstuck after 24 hours; the results of this peel will be inadequate.

and inhaling the smoke. These movements soon make the mask come unstuck around the mouth. However, it is preferable to have a patient smoke calmly and cautiously rather than getting irritable and pulling off the mask too soon in their haste for a cigarette or frantically and carelessly inhaling smoke in secret. Vigorous chewing motions also make the mask come unstuck. The patient should therefore be put on a carbohydrate and protein liquid diet so as to avoid chewing movements. A feeding cup should be used instead of a straw to avoid sucking movements. If the mask comes unstuck before the end of 24 hours, the patient should substitute the Leukoflex® occlusion with Vaseline®.

Specific areas The anterior hairline is a special area. A first strip of Leukoflex® is placed directly on the patient’s skin, at the edge of the hairline. Any hair sticking out over this edge should be cut off so that it does not get pulled out when the mask is removed 24 hours later. A hairnet is placed on the patient’s hair. An impermeable or plastic shower cap should not be used, as it holds the sweat on the scalp and makes the occlusion very uncomfortable for the patient. The (loose) elastic edge of the hairnet is positioned on the first strip of Leukoflex®. A second layer of Leukoflex® holds the elastic of the hairnet in place; the net thus forms an integral part of the occlusive mask and can be used to pull the whole dressing off smoothly and painlessly when the time comes to remove the mask. A simple gauze pad can be used instead of a hairnet (Figure 35.2). The gauze should be cut close enough to the dressing for the patient to be able to brush or comb the hair, and at the same time there must be enough gauze to hold onto to remove the occlusive mask later. Around the eyes, the occlusion should completely cover the eyebrows

Making the occlusive mask The occlusive mask can be put on the lower part of the face with the patient in a half-sitting position at the end of the peel to make it hold better. Precut Epstein mask Epstein recorded the facial measurements of 24 patients; from there, he worked out the average size and designed an adhesive mask that he considers ideal and that includes 10 pieces of precut, standard-sized Steridrape®.8 This first

Figure 35.2 Close-up of the top of the occlusive mask, near the anterior hairline. The sterile gauze included in the mask serves as a ‘handle’ for removing the occlusion after 24 hours.

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but leave enough room for the eyes to open normally (Figure 35.3). The eyelids, where occlusive dressing is not used, should be coated in ophthalmic antibiotic ointment or sterile Vaseline®. The nose must be properly covered – several thin strips of occlusive dressing are needed to do this. The area underneath the jaw, treated up to the pre-set limits, should only be partially occluded. Partial occlusion of the area under the jaw serves to create an area of feathering that ends on the demarcation line on the neck. The earlobes should not be occluded.

Medical post-peel treatment A drop of artificial tears should be placed in the eyes at the end of the peel and several times a day over the following few days to reduce eye irritation, common after a phenol peel. An ophthalmic antibiotic cream should be applied to the eyelids. The patient must eat and drink as soon as possible after the peel to enhance elimination of the phenol. A sedative is recommended to reduce anxiety, which can amplify the feeling of pain: lorazepam (2.5 mg) is highly indicated and well tolerated by patients. Medication to regulate gastric emptying (domperidone) can be administered intramuscularly or orally before the patient leaves to prevent any nausea in the first few hours after the peel. In patients with a history of herpes labialis, antiviral prevention should be kept up. Patients should be given a telephone number or other means of communication so that they can contact the doctor at any given moment. They should also have a strong analgesic to hand: paracetamol (acetaminophen) plus codeine is a good and most effective option and alleviates the pain during the first few days.13 Applying cold packs can also alleviate the sensation of heat after the peel.

Figure 35.4 The same patient as in Figure 35.3: appearance of the face after 24 hours of occlusion (Lip & Eyelid® formula).

skin has absorbed all the phenol and the risk of infection increases proportionally with the duration of the occlusion.

Post-peel care after 24 hours

Removing the occlusive mask

After 24 hours, the occlusion has reached its full effect (Figure 35.4). Maceration is finished and the superficial layers of the skin have been liquefied. It is not necessary for the occlusion to be kept on any longer, as after 24 hours the

A phenol peel causes a liquid to form that unsticks and gradually lifts the occlusive mask during the first 24 hours, which means that it is often easy and relatively painless to remove, though this is not always the case. Removing the occlusive mask can certainly be painful (though only briefly) if the mask is ‘pulled off’ rather than pulled down. When the mask is made correctly, the first few centimeters are left loose on the anterior hairline. It is easy to take hold of the mask here and to pull it down hard, removing it in one swift movement. The patient might cry out at this point, but it is more from surprise than from pain. The patients who find the first 24 hours the most painful are also the ones who find it more difficult to bear the occlusive mask being pulled off: they have a lower pain threshold and can be given a strong analgesic or sublingual midazolam 30 minutes before the mask is removed. Some practitioners suggest (needlessly in my opinion) removing the mask

Figure 35.3 Close view of the occlusive mask in the eyes area. Eyebrows are covered but eyelids are not.

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Figure 35.5 Appearance of the face after the occlusion has been removed after 24 hours (Lip & Eyelid® formula).

under anesthetic or sedation, which increases the overall risks and the cost for the patient.

Appearance of the face Underneath the mask, the skin is coated in a thick liquid14 with a distinctive smell; this liquid results from the liquefied epidermal layers mixed with inflammatory lymph (Figure 35.5). Good epidermal liquefaction seems to make for a good prognosis, although the final results will not necessarily be proportional to the amount of liquid found beneath the occlusion. After removing the mask, the face is very swollen and looks severely burnt, but for all that the patient does not feel much pain.15 The skin appears crumpled in places, as the edema develops rapidly beneath the rigid mask and the skin cannot stretch. This crumpled appearance soon disappears. The residual liquid is wiped from the rest of the face with a sterile cotton pad.

Touch-ups When the mask is removed, wrinkles and marks should have disappeared completely. Any persistent marks or wrinkles can be touched up immediately after the mask has been removed (Figure 35.6) by applying some more Lip & Eyelid® solution in the base of the wrinkles or on any resistant marks. Wrinkles on the upper lips are usually the most

Figure 35.6 Immediate touch-up of the upper lip and chin after the occlusive mask has been removed after 24 hours.

resistant. Small touch-ups do not require anesthesia: the pain does not last long, as the phenol has produced neurolysis of the sensory nerves. Patients should just be warned that they might feel a brief burning sensation, and the undertreated areas should be treated again slowly. More extensive touch-ups (e.g. the whole of the midface region) might require short-term nerve block anesthesia in sensitive areas. After 24 hours of occlusion, persistent wrinkles on the upper lip can be treated with chemabrasion: Lip & Eyelid® solution is once again applied to the whole of the lip, with special emphasis on the base of the wrinkles. Frosting occurs relatively quickly. When the frosting has stabilized, the skin can be abraded with a diamond fraise or sandpaper on the frosting itself. The doctor then decides whether to reapply the occlusive dressing; the duration of occlusion depends on the results achieved with the chemabrasion: if the results are still no better than after the first treatment, the ‘secondary’ occlusion should be left on longer. The skin now needs to be protected and regeneration encouraged.

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The advantages of moist or closed occlusive dressings have been extolled since ancient times. Ayurvedic doctors, the Egyptians, the Chinese and the Greeks all maintained that a closed dressing, often coated in honey, enhanced wound healing. At the beginning of the 20th century, doctors who treated burns with gauze pads soaked in picric acid knew and made the most of the virtues of healing ‘under a scab’. Thomas Bayton (1797) was the first to rediscover the benefits of occlusion in treating venous ulcers after centuries of medical obscurantism. The latest studies confirm that exposing a wound to the air slows down healing and that occlusion accelerates healing and reduces the risk of infection and pain. The term ‘moist technique’ could lead to some confusion. A moist technique does not involve applying dressings soaked in physiological saline, for example. The presence of textile or skin debris can actually cause infection and delay wound healing. Nor does a moist technique involve using antibiotic creams. What is referred to as a moist technique is actually any procedure that allows the skin to regenerate in conditions that are close to the skin’s physiologically moist environment. Post-peel regeneration is radically different to the regeneration that follows mechanical abrasion or ablative laser treatment. Unlike ablative laser treatment or dermabrasion, a peel does not physically remove the skin, even though it devitalizes it completely. The skin can be considered as the base of a ‘moist’ dressing, even though using powder makes it appear rather dry (Figure 35.7). Sprinkling powder on skin that has been devitalized by phenol but that still serves as a

protective layer creates the ideal conditions for rapid skin regeneration without infection.16 We will discuss the type of powder that can be used below. One of the advantages of using a powder mask is that the patient does not have to treat the skin at all. This reduces the risk of secondary infection, errors or allergies, and also means that the new epidermis, which is in the horizontal growth phase, will not be pulled away by the constant cleansing of the skin that goes hand in hand with the use of antibiotic creams. As the skin begins to regenerate, the keratinocytes are not yet anchored by desmosomes and the dermal papillae have not yet formed. This new, growing epidermis is an important source of cells with a great potential for regeneration and should not be removed by untimely cleansing. Sprinkling bismuth subgallate on what remains of the skin after removing the 24-hour occlusive mask anchors the dead cells in a sort of membrane and actually forms a kind of natural dressing that is dry on the outside but physiologically moist on the inside. Occlusive dressings have often been disparaged for fear of secondary infection that could delay healing. A phenol peel has one big advantage over laser or abrasion in that phenol is a powerful disinfectant in vivo even more than in vitro. Infections are less common with phenol than with TCA, for example. Sprinkling on an antiseptic is preferable to applying an antibiotic cream. Indeed, antiseptics discourage the growth of any microorganisms in the wound, whereas antibiotics only work against certain strains of bacteria. Bacterial resistance to antiseptics is much lower than it is to antibiotics. There have been no reports of cross-resistance to different antiseptics, whereas this phenomenon has been widely reported with antibiotics. Allergies are far more common with antibiotics than with antiseptics. The presence of a large amount of exudate can,

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Bismuth subgallate mask or antibiotic cream?

Figure 35.7 (a) On the 7th day after a Lip & Eyelid® peel, the film formed by the necrosed skin, the bismuth subgallate or Vaseline®, does not stick to the skin. (b) It comes off in one piece like an occlusive dressing under which the skin receives moisture.

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on the other hand, render many antiseptics ineffective, but a phenol peel does not generate much liquid and any excess inflammatory liquid is soaked up when the skin is powdered. It is therefore far more advantageous to use a powder mask than antibiotic creams. When I have used antibiotic creams on my patients, secondary infections have been very common, while this has rarely been the case with a mask of bismuth subgallate powder. Publications on peels describe several different powders.

Thymol Thymol (thymic acid) is extracted from essence of thyme. It is four times more bactericidal than phenol and ten times less toxic. Thymol iodide is used on burns in the same way as iodoform, but has the advantage of not being absorbed and not having any odor. It is less irritating on wounds and mucous membranes than dithymol diiodide or aristol. Thymol iodide powder, an antiseptic that is used often after a phenol peel, physically alters the selective permeability of plasma membranes. It is nevertheless a protoplasmic poison that denatures enzyme proteins and is also an allergen.

Bismuth subnitrate Bismuth subnitrate is an inert powder that has healing and absorbent properties. It sticks well to the skin. It is not very toxic by the systemic route, but can be more so by the local route as a result of combining with proteins.

subgallate comes into contact with the eyes, eye drops should be used.

Zinc stearate Urkov used zinc stearate as a healing powder for 5 days after removing the occlusive mask.

Making the bismuth subgallate mask Before sprinkling the powder on the face, a drop of artificial tears should be put in each eye and protective cotton pads placed on the eyes (Figures 35.8 and 35.10). The patient is placed in the dorsal decubitus position with eyes closed. The face must not be completely dried before sprinkling the powder on the face so that it sticks to the exudate (Figures 35.8–35.10). If the powder does not stick properly on the skin, it should be sprayed with thermal water to help the powder stick. The mask must not be too rigid, however.17 Bismuth subgallate comes in two formats: the Lip & Eyelid® kit contains 12 separate sachets for deep localized peels (Figure 35.11a). A large bottle is also available (Figure 35.11b) that allows for easy application by sprinkling the powder directly on the skin. An assistant should gently compact the powder with sterile gauze.

Gallic acid–iodoform Gallic acid was used in the past to treat wounds, as was iodoform. Iodoform was discovered in 1822 and used by Hebra for its local anesthetic action – in the form of an iodoform gauze – on burns.

Bismuth gallate Bismuth gallate (formerly known as Dermatol®) is antiseptic, astringent and siccative. Gallium nitrate reduces metalloproteinase activity in wounds and promotes the migratory phenotype of keratinocytes that can move more easily over the temporary protein matrix and close the wound more quickly. It reduces keratinocyte ability to synthesize the desmosomes that anchor the cell locally and limit its movements.

Bismuth subgallate Bismuth subgallate is also known as bismuth 3,4,5-trihydroxybenzoate dihydroxide, basic bismuth gallate and gallic acid bismuth basic salt. Its molecular weight is 394.09. It has low toxicity; not much bismuth is absorbed. If bismuth

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Figure 35.8 The eyes are protected before powdering with bismuth subgallate.

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Figure 35.11 (a) The Lip & Eyelid® kit contains 12 sachets of bismuth subgallate. (b) A sprinkler is also available. This makes it easier to apply the powder.

Figure 35.9 Bismuth subgallate powder mask: end of making the mask. Note that the peri ophthalmic area is covered with petrolatum jelly.

A mask that is too thick may also crack after the third day and form jointed plates that can leave visible lines imprinted on the skin and sometimes even wrinkles that were not there before the peel. The mask should be monitored closely from the 3rd day. As can be seen in Figure 35.12, a powder mask that is too dry should be treated locally with an application of sterile white Vaseline®.

Following days Days 1–6 (Figure 35.13)

Figure 35.10 Eye protection before sprinkling the bismuth subgallate powder on the skin.

The bismuth subgallate mask should not be too thick. Too much powder makes the mask rigid, which is unpleasant for the patient and is sometimes difficult to remove later.

During the first two days, the patient puts artificial tears in both eyes. During 48 hours, it is the patient that puts the subgallate powder on the areas that need it, that is, where the powder appears moist. Where the powder has not stuck, because of a lack of skin liquefaction, a little Terramycin® ointment or sterile white Vaseline® should be applied. The patient and doctor should be in contact – even if it is only by telephone – every day, as the appearance of the face is very worrying for both the patient and friends and relatives (Figure 35.13). The person in contact with the patient must be able to answer any questions, allay any fears and possibly examine the patient: it is essential that the patient should be regularly reassured by the doctor that things are proceeding as normal (Figure 35.14).

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Figure 35.12 (a) A bismuth subgallate mask that is too dry. (b) Application of sterile white Vaseline® around the eyes and mouth.

Figure 35.13 (a) Bismuth subgallate mask on day 1. (b) Day 3: the edema is going down quickly. (c) Day 3: close-up of the mask on the eyelids. The upper eyelids are coated in an antibiotic ointment instead of the powder.

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Figure 35.14 The lower demarcation line on the neck should be given special attention and should be coated with Vaseline® in case movement is awkward (patient on the 3rd day). (b) The same patient after repeated applications of Vaseline® on the 4th and 7th days. The edema that could be seen in (a) has gone.

The pain usually intensifies suddenly on the 3rd and 4th days: patients generally consider the night of the 3rd day to be the most ‘unpleasant’ of the whole week. Strong analgesics might be necessary: paracetamol (acetaminophen) plus codeine, which the patient should have at hand, is sufficient to ease the pain in most cases. Cold packs – chilled but not frozen – can help alleviate the sensation of burning or pulsing heat. Many patients complain of severe itching that can be relieved with a sedative antihistamine such as promethazine. In some cases, the antihistamine can be combined with lorazepam. A patient who is asleep on promethazine and lorazepam does not scratch! No other specific treatment should be applied on the face during the first week. The patient should be seen again on the 4th or 6th day, and the doctor should take special

care to check for any secondary infections (Figure 35.15). The doctor should apply a thick coat of sterile white Vaseline® to the patient’s skin and gently rub it in when he sees the patient on the 6th day (Figure 35.16). The doctor can also help flaking along, but must take care not to damage the skin. Anything that is not stuck to the regenerating skin can be removed. Once the patient is back home, he or she continues to apply a thick coat of sterile white Vaseline® to the face and gently rubs it in after carefully washing the hands with antiseptic soap. A thick coat of Vaseline® creates an impermeable dressing that prevents transepidermal water loss (TEWL). The water accumulates between the Vaseline® and the skin – that is, in the bismuth subgallate powder. It hyperhydrates the powder mask, helping it come away without the patient having to do anything other than pick up the strips (skin plus powder) that fall away by themselves. Throughout the first week, the patient should be told quite firmly to sleep on his or her back instead of on the side, so that the skin on the face does not stick to the pillow (see Chapter 37).

Day 7 (Figure 35.17)

Figure 35.15 An infection may occur in the form of a papular reaction on the neck. Oral antibiotics are essential in this case.

The doctor can use forceps to remove any small bits of the mask that are still on the face. On some patients, the powder mask has not come off by the 7th day, and the doctor should then remove it, taking care not to damage the skin. The skin sometimes appears a bit crumpled under the mask, but the crumpling, caused by the pressure of the mask, can be seen to disappear within moments. If the skin is in good enough condition, camouflage make-up (Avene® or Cover Mark®) can be applied immediately after sun protection. Sun avoidance and the use of a

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Figure 35.16 (a) Day 6 after Lip & Eyelid® formula: appearance of the patient on arrival at the medical center. The doctor should apply the first coat of Vaseline® and can help flaking along, taking care not to damage the skin. (b) Immediately after an application of Vaseline® and doctor-assisted flaking.

total sunblock must be kept up for 3–6 months. Patients who are averse to the idea of having to put any product whatsoever on the skin should be ruled out from a phenol peel. Flaking does not stop on the 7th day, and it is common to see it last several weeks. Applying hydrating cream (Vit E Antioxidant® or Renutriv ACE Lipoic Complex®) helps to reduce any itching caused by the persistent flaking.

Following weeks The patient applies a hydrating cream with vitamin E (see Chapters 2 and 3) four or five times a day to stop the skin drying out and becoming itchy and to prevent scratching and/or complications. The patient can continue to apply a thin layer of Vaseline® as long as it is needed to improve dryness or itching. On the 10th day, the patient can usually return to normal activities, making sure that the skin is protected with an effective sunscreen and wearing make-up to hide the very pink color of the skin. A colorless sunscreen can be mixed with the patient’s usual foundation as well as a col-

ored sunscreen (metablock HSP 50 color). Erythema remains severe for the first few weeks, but gradually fades within 4–8 weeks. Patients with dark skin or who live in sunny climates should apply Blending Bleaching® cream once or twice a day to reduce the incidence of pigmentary changes.

Sun avoidance Sun avoidance should be ‘aggressive’ and ‘permanent’ during the first 3 months after the peel. Patients who work outdoors are most likely to suffer from uneven skin color or post-inflammatory hyperpigmentation. ‘Permanent sun protection’ does not mean that patients should keep out of the sun for the rest of their lives, but that they should actively protect their ‘new’ and more sensitive skin. Patients have a natural tendency to avoid sun exposure for some time after a peel. After strict sun avoidance for up to 2–3 months, outdoor activities can be resumed with total sunblock, although sunbathing is forbidden during the first year after a peel.

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Touch-ups Phenol peels do not always produce the results hoped for, but fortunately it is rare that the results are so inadequate as to require extensive touch-ups or a complete re-peel. An extensive touch-up can be done 6 weeks after the peel. Fintsi18 reported an incidence of 30% of local touch-ups after Exoderm®. In his study, 21 cases out of 558 had to be given more extensive touch-ups: 20 times for acne and once for a hyperpigmentation problem.

Notes

Figure 35.17 The usual appearance of the skin, 7 days after a phenol peel. The skin is thin, sensitive and red. The demarcation line is particularly visible between the face and the neck. A TCA peel (Easy TCA®) has actually been applied to the neck and décolletage on the 3rd day after the peel and these areas are now flaking (see also Figure 30.8).

During the first few months, wearing sunglasses (that do not press too hard on the temples or the nasal pyramid) prevents reflex squinting against excess light. It is possible, like Cortez,6 to recommend using a cream with 0.05–0.1% tretinoin for 3 months after the peel, although this is not recommended for use before then, as recent studies show that although retinoids improve post-peel skin regeneration when used before the peel, it seems that they can delay regeneration when they are applied too quickly after a peel or dermabrasion. The patient should be seen again during the 3rd week to make sure there are no pigmentary changes or other complications and to treat them if necessary. It is sometimes necessary to use a depigmenting cream during the first 6 weeks, especially in patients who live in very sunny climates.

1. According to Asken, the patient can go home 6 hours after the peel (Asken S. Unoccluded Baker–Gordon phenol peels – review and update. J Dermatol Surg Oncol 1989; 15: 998–1008). 2. The patient should be able to get to the doctor within 1–2 hours at the most. 3. As opposed to the use of phenol in the past as a disinfectant for wounds, when occlusion does not slow down the rate of penetration of phenol. 4. Ruedemann R, Deichman WR. Blood phenol level after topical application of phenol-containing preparations. JAMA 1953; 152: 506–9. 5. Occlusion dilutes the TCA and reduces its effectiveness. 6. Cortez E. Chemical face peeling. Otolaryngol Clin North Am 1990; 23: 947–60. 7. Applying Vaseline® or silicone after the peel acts as occlusion. It is in fact cosmetic occlusion rather than physical occlusion. 8. Beeson WH, McCollough EG. Chemical face peeling without taping. J Dermatol Surg Oncol 1985; 11: 985–90. 9. McCulloch EG, Langsdon PR, Maloney BP. Chemical peel with phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996, UK, Oxford, Marcel Dekker Ltd. 10. Konior RT, Kerth JD. Selected approaches to the aging face. Otolaryngol Clin North Am 1990; 23: 1083–95. 11. With Lip and Eyelid® formula (for a full face), healing takes 7–8 days. 12. This is a sterile adhesive plastic used in surgery to cover a field of operation and through which the surgeon can make incisions. 13. Paracetamol must not be injected intravenously during the peel, however, to avoid any competition among the enzymes responsible for liver detoxification. 14. Patients often complain that some liquid has leaked out from the bottom of the occlusive mask and that they have had to cover their necks. 15. Recall that phenol is a neurolytic agent. 16. Moreover it is recommended not to remove the skin on top of a blister for the same reasons. 17. A mask that is too thick or rigid is extremely unpleasant for the patient and could make the skin unusually tight and promote infections. If the mask is too thick or rigid, it must be covered immediately in sterile white Vaseline® to soften it. 18. Fintsi Y. Exoderm-lift – liquid formula. 1996.

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36 Phenol: chemical blepharoplasty and cheiloplasty

Chemical blepharoplasty Introduction Surgical blepharoplasty is a technique that has become progressively easier as it has been taken out of the strict framework of surgery requiring hospitalization. Once performed readily under general anesthesia, it soon moved onto local anesthesia combined with neuroleptanalgesia, then deep sedation, and is now often carried out under simple local anesthesia with lidocaine. Lip & eyelid formula allows a treatment without any kind of anesthesia. Surgical blepharoplasty, when performed by a skilled surgeon, should give excellent results that last several years, after which patients go back to the doctor, as they are no longer happy with the results. A second blepharoplasty is then decided on and the results will be no different to the last. It is common to come across patients who have ‘benefited’ from three successive surgical blepharoplasties over 15 years. It has to be admitted that the cosmetic results of multiple surgical blepharoplasties are not always of good quality and patients who have been operated on too often are as easy to spot as patients with rotation flap hair transplants or large cylindrical punch grafts. Surgical blepharoplasty can change the look of the palpebral aperture, especially when patients want their eyes to look more ‘cat-like’. A second blepharoplasty can make the tarsal region of the upper lid slightly darker. A third blepharoplasty can be disastrous: the palpebral aperture loses its elasticity and narrows, the eye becomes smaller and less mobile, the skin above the tarsus of the upper eyelid takes on a very dark color that stops abruptly on the scar because of the altered distribution of dilated vertical blood vessels (Figure 36.1). Lagophthalmia entropion or ectropion can develop. I performed my first chemical blepharoplasty with localized phenol in the 1990s to treat blepharochalasis that had developed just a few years after a surgical blepharoplasty of the four eyelids. The blepharoplasty had been done perfectly correctly, well before the patient had reached 40, and 4 years later there was once again a significant excess of skin on the upper eyelid that made the patient’s eyes look heavy and sad. The patient preferred to have non-surgical treatment.

Figure 36.1 Typical abnormalities of the upper eyelid after several surgical blepharoplasties.

Clinically, it was reasonable to investigate the problem with her. Apart from surgery, what treatment options were there to lift the ‘curtain’ of the upper eyelids? After a quick look at the question, a peel seemed to be the only option. Alpha-hydroxy acids (AHAs) were ruled out immediately because of the risks involved and the fact that they are ineffective on the eyelids. Trichloroacetic acid (TCA) was ruled out, as the high concentrations needed to get the skin to retract would be dangerous and in any event ineffective. There was therefore only one option left: phenol. I have not encountered many problems with regular use of full-face phenol peels and, on the contrary, have found them to be very successful. The results achieved locally on the eyelids have often been remarkable (Figure 36.2).

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increased risk because of their depth of penetration in the thin eyelid skin. After using several different formulas, I gradually came to develop a phenol oil that meets my own high standards of safety and effectiveness. Adapted for the treatment of the eyelids and lips, this solution is called Lip & Eyelid® Formula. The eyelids and the lips do not, of course, have the same thickness, resistance, permeability or reactivity; they are very different, and this is why the application protocol is also different in each case.

Figure 36.2 Full-face Lip & Eyelid® peel: close-up of the eyelids 30 days after treatment – note the significant retraction of the eyelid.

Phenol therefore seemed to be an excellent option for treating drooping eyelids. In fact, the general toxicity of phenol is non-existent when treating limited areas, and a local anesthetic is all that is needed given the anesthetic properties of the phenol itself.

Application to the eyelids (Figures 36.3–36.5) The choice of applicator is important: the large cotton buds normally used in a full-face phenol are not precise enough and absorb too much of the product. Cotton wool or gauze

Anesthesia Chapter 33 is devoted to the details of anesthesia for a phenol peel. Lip & Eyelid® formula can be applied without any anesthetic on small areas, however. Patients feel an intense burning sensation a few seconds after application. They will have been told that the burning sensation only lasts for 15 seconds and that they can have a nerve block if they want. Vocal anesthesia plays an important part, and the patient can take a paracetamol (acetaminophen) plus codeine tablet 1 hour before the treatment. Nerve blocks are often used to increase patient comfort: 2% lidocaine without adrenaline (epinephrine) is used, and its duration of action is sufficient. The patient should be given paracetamol plus codeine tablets for the post-peel pain, which is inevitable during the first 24 hours because of the severity and rapidity of inflammation caused by the peel.

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Protecting the eyes A small quantity of ophthalmic Vaseline® is put in the conjunctival cul-de-sacs to protect the cornea, before the bottle of phenol has even been opened. The Vaseline® actually deactivates the phenol. The patient has eye drops (artificial tears) to put in the conjunctivae as soon as the phenol has been applied and several times a day over the following days.

Phenol solution There are many different phenol formulations, and different combinations have been tested with varying results. The Baker–Gordon or Litton formulas potentially pose an

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Figure 36.3 (a) Lip & Eyelid® to the lower eyelids and an application of Only Touch® (lentigo to the forehead and right cheek) plus Easy TCA® as an evening-out peel. (b) Lip & Eyelid® on all four eyelids. The tarsus of the lower lid is not treated.

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Figure 36.4 Lip & Eyelid® to the upper eyelids.

soaked in solution is not suitable because of the risk of drips on the neck, or, even worse, in the eyes (let us not forget that phenol is a protein coagulant and any contact with the cornea could damage it irreversibly). A double cotton bud would not be precise enough either and the ideal applicator is a single cotton bud: it is light, precise and simple – all of which are good qualities when it comes to using phenol. Using a 1 cm3 syringe, 0.2 cm3 is drawn up from the 3 cm3 bottle of Lip & Eyelid® and the

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cotton bud is soaked by ‘injecting’ 0.10–0.14 cm3 of the peel solution directly onto it. After disinfecting the area with alcohol and carefully degreasing with acetone, Lip & Eyelid® is applied carefully on the lower lids with the cotton bud. Distinct frosting occurs rapidly and marks the end of the phenol application. The tarsus of the upper eyelid is not usually treated. Applying Lip & Eyelid® on the eyelid tarsus induces severe edema that is very uncomfortable for the patient and does not significantly improve results. To treat the second eyelid, the remaining 0.06 cm3 should be ‘injected’ onto the end of the same cotton bud. A bottle of Lip & Eyelid® formula provides enough solution to treat two eyelids on 15 patients. The same quantity of solution is needed to treat the upper eyelids. An assistant should be present whose sole duty is to mop up any tears as soon as they appear to prevent any diluted phenol dripping onto the face or going up into the conjunctivae by capillarity. A fresh cotton pad should be used for each tear. An evening-out peel is necessary to prevent demarcation lines, it should be applied on the rest of the face when the Lip & Eyelid® application has finished and before any occlusion is applied. Patients with a light skin type could be given four weekly sessions of Easy TCA® (to the Grenz zone) or a single session of Unideep® (to the papillary dermis).

Occlusion versus open technique Occlusion causes the phenol to macerate, which is often unnecessary on the eyelids. The lower eyelid can be covered with impermeable tape (there is a roll of tape in the peel kit) if a greater depth of action is required (Figure 36.6), if

Figure 36.5 The upper and lower eyelids have been treated with Lip & Eyelid®, and the frosting has already faded. The rest of the face has been treated with a Unideep® as an evening-out peel: note the even pink–white frosting from the Unideep® and the post-peel Unideep® cream on the forehead.

Figure 36.6 Occlusion can be applied if necessary, although this is rarely the case. Here, occlusion has been applied using Sleek® (see Chapter 32).

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Figure 36.7 (a) After 24 hours of occlusion, the dermis has been destroyed. Note the significant amount of skin liquefaction. (b) Destruction of the dermis after 24 hours of occlusion.

the wrinkles are deep or if there is xanthelasma for example. No occlusion is applied otherwise. Occlusion of the upper eyelid, which is only indicated to increase the depth of action of the peel, will always be essentially extratarsal (Figure 36.6). In the large majority of cases, a chemical blepharoplasty is done without occlusion. After applying the phenol, the doctor applies an evening-out peel, either Easy TCA® or Unideep®, to the rest of the face. Both of these peels consist of an acid solution and a post-peel cream that stimulates healing, is antioxidant and tyrosinase-inhibiting. This special postpeel cream should be applied once only by the doctor at the end of the facial peel. When the phenol is used without occlusion and without impermeable dressing, the Easy TCA® or Unideep® post-peel cream is applied on the area treated with Lip & Eyelid® at the same time as it is applied to the rest of the face.

first been soaked with the products of epidermal liquefaction, dries on the skin, it can form crusted plates that hinge on the skin and that (in my experience) have occasionally created wrinkles that did not exist before the peel. I therefore do not put any powder on the mobile part of the upper eyelid, and rather use a ‘moist’ technique, namely an antibiotic ointment (e.g. ophthalmic Terramycin®) during the first week after the peel) or just Vaseline®. Applying this type of ointment is in any event equivalent to occlusion.1 Without occlusion The patient’s skin, dried out by the phenol, provides an ideal physiological dressing. The doctor can, however, try applying some bismuth subgallate (with a cotton bud), as beads of serous fluid can often ooze unseen through the

Immediate post-peel care Immediate post-peel care With occlusion Any occlusion is removed after 24 hours and the dermis is usually laid bare (Figure 36.7) and needs protecting. Applying bismuth subgallate, although highly effective at wound healing in general and in phenol peels in particular, has always caused minor problems for me on the mobile region of the upper eyelid. The powder easily falls into the eyes (Figures 36.8 and 36.9). When the powder, which has

Figure 36.8 Bismuth subgallate powder on lower eyelid.

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Figure 36.10 Day 3: the bismuth subgallate is dry.

Figure 36.9 Application of bismuth to all four eyelids: chemical blepharoplasty and evening-out peel (Unideep®). The Unideep® post-peel cream is applied to the face immediately after the peel, the evening of the peel and the following morning. This photograph was taken on day 1.

skin that has been ‘mortified’ by the phenol. If the powder sticks to the treated area, it can be concluded that it was necessary. If it does not stick, it was not necessary and there is no point trying to force it to stick. In this case, the patient should be seen again the next day to check whether the powder is now required by trying to apply it again. Bismuth subgallate (or Vaseline® or an antibiotic ointment) will protect the skin for around 6 days. After that, the patient should apply Vaseline® (ophthalmic if possible) several times a day so that the bismuth subgallate powder comes away from the skin by itself, without any outside help.

Subsequent post-peel care Patients should be given a small sachet of bismuth subgallate (there are some small sachets in the Lip & Eyelid® kit), which they should apply with a cotton bud to any area that appears moist. The patient should be seen as often as necessary, usually on the 1st, 3rd, 6th and 10th days. The

treated area is usually dry within 48 hours, at the most. If additional bismuth subgallate powder will not stick to the skin, it is not necessary (Figure 36.10). Patients should not touch their skin with their bare hands to avoid any risk of infection. In cases where the doctor has opted for a ‘moist’ post-peel technique and has applied an antibiotic ointment or Vaseline®, the patient should wash the area with thermal water spray or with a showerhead before each application of cream. The different layers of antibiotic ointment or Vaseline® should be not allowed to accumulate without washing in between. Patients sometimes feel some considerable discomfort that they describe as a pulling sensation, a tightening of the skin, caused by the powder mask. This sensation is usually localized around the edge of the mask, where it meets the skin that has not been treated with phenol. Applying Vaseline® with a cotton bud to the edge of the treated area can help alleviate this feeling of tightness (see the yellow dots in Figure 36.10: on day 5, the subgallate is dry). From the 5th day onwards (or the 4th day if needs be), and as long or as often as necessary, sterile white Vaseline® or ophthalmic Vaseline® should be applied on the bismuth subgallate so that it comes off without any outside help (Figure 36.11). The borderline between the area treated with Lip & Eyelid® and the area treated with the more superficial peel may feel painful or just uncomfortable. The doctor should apply a little Vaseline® on this area to soften it, even if it is only a few days since the peel was applied.

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Figure 36.11 From the 5th day, Vaseline® should be applied on the bismuth subgallate so that it comes off without any outside help.

Post-peel developments Eyelid edema Severe eyelid edema, which goes down quickly and lasts 7 days at the most, appears immediately after the solution has been applied (Figure 36.12). It peaks on the morning of the 1st and 2nd days. The edema goes down during the day when the patient is no longer lying down. It spreads to the upper cheek on the 2nd day, the lower cheek on the 3rd day, the lower jaw on the 4th day, and on the 5th day is barely noticeable. It is not uncommon for the patient to be unable to open their eyelids on the morning of the 1st day. If the edema lasts longer than 10 days, it is not normal. Erythema Erythema develops equally rapidly, a few minutes after Lip & Eyelid® has been applied. It peaks during the first few weeks (Figure 36.13), and fades, more or less slowly depending on the patient, in 3 weeks to 3 months. The erythema takes longer to fade on lighter, more transparent skin. It always resolves, however, and is easily covered up with make-up (a green make-up stick should be applied first, followed by camouflage make-up, e.g. Couvrance® by Avène). The bismuth subgallate powder comes away from the skin automatically (Figure 36.14) with the Vaseline® that prevents transepidermal water loss (TEWL) evaporation. The downtime is 8–10 days maximum.

B

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Figure 36.12 Normal edema over the first 2 days that has spread to the cheek area. (a) Chemical blepharoplasty of the four eyelids. (b) Chemical blepharoplasty of the upper eyelid only. (c) Chemical blepharoplasty of the lower eyelids only.

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Figure 36.13 Normal erythema on the 13th day.

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Figure 36.14 Vaseline® has been applied the night before, on the 5th day, to remove the subgallate powder.

Effectiveness and indications The results of a chemical blepharoplasty may be inadequate if there is a large amount of excess skin or for lower eyelid fat pads. In these cases, surgical blepharoplasty is indicated. Applying Lip & Eyelid® to the eyelids treats wrinkles and fine lines, dyschromia, keratoses, and sagging eyelids (Figure 36.15), but only improves eye bags when they are caused by sagging skin rather than the presence of subcutaneous fat. Surgery is indicated in this case.

D

Figure 36.15 Examples of the results of chemical blepharoplasty. (a,b) Chemical blepharoplasty of the upper eyelids and Easy TCA® as an evening-out peel. (c,d) Chemical blepharoplasty of the lower lids and Easy TCA® as an evening-out peel.

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Complications Lip & Eyelid® is one of the safest phenol peels on the market, but incorrect application can lead to the usual local side effects of chemical peels.

Pain Taking a painkiller tablet half an hour before treatment alleviates the pain resulting from the inflammatory edema. A second tablet, taken before going to bed, ensures the patient gets a good night’s sleep. The following morning, the pain will have almost completely gone. It is common for some pain to recur on the third day.

Figure 36.16

Risk of pigmentation disorders and pre-peel preparation Even if it is generally accepted that phenol has more of a depigmenting than a hyperpigmenting effect, the doctor must be prepared for any reactional hyperpigmentation. If the skin being treated is a very ‘melanin-reactive’ phototype or might have a severe inflammatory reaction, the melanocytes should be ‘sedated’ with tyrosinase inhibitors and antioxidants (Blending Bleaching® cream) before and after Lip & Eyelid®, both on the areas to be treated and on the surrounding areas. The cream should be applied twice a day for 2 weeks before the peel and as soon after the peel as possible. The skin can usually tolerate Blending Bleaching® cream from the 10th day after the peel. Melanocyte ‘sedation’ should be continued for a minimum of 6 weeks. If the peel is being performed on a skin phototype I to III and if the patient follows advice to keep out of the sun and use sun protection, there should be no post-inflammatory hyperpigmentation, but there is an increased risk of prolonged erythema on lighter skin types. The sun should be avoided completely, and effective sun protection (Melablock HSP® SPF 50+) should be used for up to 3–6 months. Exposure to UV light should be gradual thereafter. Even when the peel is applied correctly, there is still a risk of pigmentary changes, which are always reversible with Blending Bleaching® cream. Avoiding pigmentary changes is mainly a matter of pre- and post-peel care. Local depigmentation, which can only be treated with a full-face application of Lip & Eyelid®, can be avoided by careful patient selection.

Demarcation line There is clearly a risk of a demarcation line on skin with severe dyschromia or sun damage, a lot of wrinkles, freckles, keratoses, or lentigines, as the skin treated with Lip & Eyelid® will look rejuvenated and stand out clearly from the surrounding damaged skin. In these cases, it is espe-

Benign delayed healing after chemical blepharoplasty.

cially important to combine the peel with Easy TCA® or Unideep® to minimize the demarcation line if the skin phototype has been properly selected (see above). A healthy skin without dyschromia, of phototype I to III, IV at the most, does not pose the risk of a marked demarcation line. The demarcation line can be seen most clearly on the edges of the occlusion. When using the occlusive technique, it is best not to cover the whole of the treated area, but to leave an area unoccluded in order to create a graduated area of penetration. If results prove inadequate, they can be touched up or avoided altogether through proper patient selection.

Delayed healing When a chemical blepharoplasty is performed without occlusion, the increased depth of action of the phenol sometimes translates into a persistent moist scab in the inside corner of the upper eyelid (Figure 36.16), where the phenol has macerated more intensely. Applying an antibiotic cream or ointment remedies the problem, and it should resolve before the 15th day. There are no sequelae from this slow healing. If the scab persists for more than 2 weeks, the doctor should remain alert and monitor the patient more closely.

Other complications Poor application technique can lead to inadequate results. The technique should be corrected and Lip & Eyelid® should be reapplied after 6 weeks. The second peel will heal more quickly than the first. I have never experienced scarring, entropion or ectropion with this treatment, but in theory they are possible. Prolonged erythema of several months can be treated, if it bothers the patient, with alternating applications every 2

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weeks of corticosteroids (hydrocortisone) and antioxidant creams (Renutriv ACE Lipoic Complex®). Bacterial infections should not occur if the technique is correct and postpeel care is conscientious. Herpes prevention is essential in patients with a history of herpes. Post-peel anxiety is common, not to say usual, and the extent of anxiety depends on the patient’s state of mind before the peel. Patients should be able to contact the doctor whenever they feel the need.

Record of results A photographic record of results is shown in Figures 36.17 and 36.18. E

Figure 36.17 Developments and results: (a) before; (b) +24 hours; (c) +3 weeks; (d) +6 weeks; (e) +14 months.

In conclusion Chemical blepharoplasty of the upper and/or lower eyelids with Lip & Eyelid® formula is a relatively simple technique

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Figure 36.18 Long-lasting results: (a) before treatment; (b) 1 year after a localized peel with Lip & Eyelid® on the lower lid; Unideep® was employed as an evening-out peel

that does not cause bleeding and is very quick (a few minutes). It does not change the appearance of the eyes, but, on the contrary, restores their original qualities. It is easy to perform without local anesthetic or with nerve blocks of lidocaine without adrenaline. Results are inadequate for treating fat pads, but are excellent, if not perfect, in all resurfacing indications. The low rate of local complications and the lack of general complications make it an ideal technique to rejuvenate the eyes, when the patient does not want laser treatment or surgery and if the doctor is experienced in performing peels in general and in using phenol in particular. It is obvious that a chemical blepharoplasty should not be the first peel performed by a doctor who is inexperienced in this branch of medicine or cosmetic dermatology.

Chemical cheiloplasty A chemical cheiloplasty or labioplasty treats wrinkles around the lips. The principle of the treatment is identical to that of a chemical blepharoplasty, but it is easier to treat wrinkles on the upper lip than on the eyelids. It is also less stressful for an inexperienced doctor. The skin on the lips is more resistant than the skin on the eyelids. It has more appendages and is more apt to heal well.

Chemical resurfacing of the upper lip in combination with Easy TCA® Lip & Eyelid® can be applied to the upper lip without nerve block anesthesia. A first quick coat of peel solution induces

B

local anesthesia within 15 seconds. Subsequent applications of phenol will therefore be painless. Easy TCA® is applied without anesthetic, and Lip & Eyelid® and Easy TCA® can be combined when the wrinkles are mainly located around the lips and the skin on the rest of the face does not require a peel to the papillary dermis, which is often the case. The procedure is then very quick. Figure 36.19 shows an example of this approach. When there is more extensive sun damage, it is preferable to combine Lip & Eyelid® with Unideep®. Figure 36.20 shows an example of a case of upper lip wrinkles in a patient who does not require a peel to the papillary dermis on the rest of the face. Upper lip wrinkles are more common in smokers and in patients whose mouths are very mobile and who use the orbicular muscle of the mouth too often or too vigorously: an injection of botulinum toxin reduces upper lip mobility and produces better results in combination with a deep peel. Because of the severe inflammation resulting from a deep peel, the toxin is injected before the peel (at least 24 hours previously). 15 units of Dysport® or 4 units of Botox® are usually enough, injected at four different points on the upper lip (Figure 36.20).

Chemical resurfacing of the upper lip in combination with a peel to the papillary dermis When sun damage is more severe or if the patient has asked for an evening-out peel at the same time to minimize sometimes long journeys, Lip & Eyelid® can be combined with Unideep® (Figure 36.20).

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Figure 36.19 Chemical cheiloplasty of the upper lip in combination with Easy TCA® as an evening out peel. (a,b) Before treatment. (c) Application at the base of the wrinkles. (d) Fading frosting. (e) Even application to the whole treatment area: appearance of gray–white frosting (Easy TCA® is applied after the lip has frosted and before occlusion). (f) Occlusion, beginning of occlusion. continued

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Figure 36.19 continued (g) Occlusion +24 hours. (h) Skin liquefaction after 24 hours, when the occlusion has been removed; note the edema on the upper lip. (i) Bismuth subgallate. (j) Results after 30 days (flash photography, with the patient wearing make-up). (k) Results after 60 days (photograph without flash, with patient not wearing make-up). (l) Result of a chemical cheiloplasty. The yellow dots show where the botulinum toxin was injected 8 days before the phenol peel.

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Figure 36.20 (a) Appearance of the patient’s upper lip before the peel. The rest of the skin is quite badly sun-damaged and requires an application of Unideep®, a TCA peel to the papillary dermis, if not a full-face phenol peel. (b) After disinfecting and degreasing the whole face, Unideep® is applied gradually in sequence. (Unideep® is applied in sequence, like phenol, but without the rest periods: see Chapters 23 and 34). (c) Lip & Eyelid® is applied to the right half of the upper lip. (d) Immediately after Unideep® has been applied, the patient feels a slight burning sensation that can be alleviated with a cold pack placed directly on the acid before it has dried. The cold pack must be completely dry so that it does not dilute the peel solution. continued D

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Figure 36.20 continued (e) The forehead was treated first and the frosting has faded. Some pinpoint frosting (gray–white) remains in places where the peel has penetrated more deeply (there is a chance of infection or scratching etc. later on). The pinpoint frosting is similar to that produced by One Touch® peel. The midface and cheek region have been treated as described above. Unideep® is applied to the chin at the same time as the jaw area, where the patient also benefited from a cold pack. The Unideep® post-peel cream has been applied to the whole treated area, apart from the lips, which are to be occluded. (f) The base of the lip wrinkles is treated (Lip & Eyelid®). (g) This is followed by an application of Lip & Eyelid® to the whole of the left half of the upper lip. (h) Unideep® is applied to the left midface region and the cheek. The post-peel cream is applied. The chin region as well as the jaw area are treated with Unideep®. This photograph shows an impermeable keratosis that will be treated with a single application of Only Touch®.

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Figure 36.20 continued (i) Application of Only Touch®. (j) Immediate induction of local frosting. (k) The upper lip is occluded with the impermeable tape provided in the Lip & Eyelid® kit. It must go at least 1 cm beyond the area treated with phenol. The patient should be told not to make any mouth movements for the next 24 hours. At the end of treatment, a cooling mask is applied for around 15 minutes. The patient can go home, having made an appointment for the next day to remove the occlusive mask on the lip.

Although both peels can be done without nerve blocks, patients often appreciate them, as they make the whole procedure more comfortable, especially when TCA is being applied. Patients who are very squeamish may benefit from sedation.

Results Results, as we have seen elsewhere in this chapter and this book, can sometimes be perfect. Others are less perfect, although still appreciated by the patient. Results can last 3–10 years. More superficial peels should be done on a yearly basis to maintain the results.

K

Complications See Chapter 37.

Summary of the ‘chemical resurfacing’ technique Pre-peel ■ If risk of pigmentary changes: – Skin phototype I to III: Blending Bleaching® twice a day, 2–3 weeks before the peel

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– Skin phototype IV: blending and bleaching cream and 4% hydroquinone, 3-4 weeks before the peel If risk of herpes: valaciclovir or aciclovir. Do not treat very squeamish or low-IQ patients Tell the patient how the skin will look during the first week: – Crust of yellow powder – Swollen face – Social life impossible Give the patient a painkiller tablet 30 minutes before the peel

Preparation and application of the peel ■ ■ ■ ■ ■

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Degrease the skin with acetone (ventilation) Disinfect with alcohol (ventilation) Protect the eyes with sterile ophthalmic Vaseline® If the evening-out peel is Easy TCA®: – Start with phenol and apply Easy TCA® after the phenol. If the evening-out peel is Unideep®: – Start with Unideep® (see the details of application earlier in this chapter) – Inject ±0.14 cm3 of Lip & Eyelid® solution directly onto a cotton bud – Apply Lip & Eyelid® to the whole treatment area With nerve block anesthesia: start at the base of the wrinkles and then apply to the whole area Without nerve block anesthesia: apply a quick coat of Lip & Eyelid® to the whole area; warn the patient how long the burning will last (15 seconds) Apply in the base of the wrinkles and to the whole area.

The evening of the peel ■ The treated area must not be washed ■ If the evening-out peel was Unideep®: apply the rest of the tube of post-peel cream ■ If the evening-out peel was Easy TCA®: no particular treatment

The following morning ■ The face can be washed with water, but the area treated with Lip & Eyelid® should not be washed ■ If the evening-out peel was Unideep®: apply the rest of the tube of post-peel cream ■ If the evening-out peel was Easy TCA®: no particular treatment ■ In all cases: start sun protection: Melablock HSP® 50+

See the patient again after 24 hours ■ If occlusion: remove occlusion ■ If no occlusion: no treatment (maybe remove Vaseline®) ■ Occlusion or not: powder with bismuth subgallate ■ If the subgallate does not stick: spray with thermal water to enable the powder to stick ■ If it still does not stick: antibiotic cream or sterile Vaseline® to be applied four times a day; rinse the skin under the showerhead before applying another layer of cream ■ Patients should wash their hands thoroughly before touching their skin ■ If there is an unpleasant sensation of tightness in the area treated with phenol: apply neutral sterile Vaseline® to the edges of this area

Eyelids immediately after the peel

The 3rd day

■ (In general) no occlusion; only Unideep® or Easy TCA® post-peel cream is applied to the eyelids ■ Eye drops (artificial tears) several times a day ■ A painkiller tablet for the evening or night (more if painful) ■ Lorazepam 2 mg to be taken before going to bed

■ Normal recurrence of pain for several hours: paracetamol plus codeine tablet

Upper lip and chin immediately after the peel ■ 24 hours of occlusion: the transparent occlusive dressing can be found in the Lip & Eyelid® kit ■ If the occlusive dressing comes off accidentally before 24 hours, apply Vaseline® as emergency occlusion ■ A painkiller tablet for the evening or night (more if painful) ■ Lorazepam 2 mg to be taken before going to bed

See the patient again on the 4th day ■ Check that there is no bacterial, viral or fungal infection ■ If infection: treat by mouth, not topically ■ Apply sterile white Vaseline® to any cracks (very locally)

After the 6th day ■ The patient applies white Vaseline® several times a day to help the powder come away.

See the patient again on the 7th day ■ Help remove the bismuth membrane

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– Do a few sessions of Easy TCA® (pinpoint or cloudy white frosting) – May be combined with a corticosteroid such as clobetasol

After the 8th day ■ The patient can wear make-up or carefully shave ■ Sun avoidance and protection: SPF 50+ UVA–UVB (Melablock HSP®) for 3–6 months ■ Blending Bleaching® cream (as soon as the skin can tolerate it) twice a day ■ Tyrosinase inhibitors, antioxidants and vitamins to block excess melanin synthesis ■ Renutriv ACE Lipoic Complex® (antioxidant) 2–3 times a day

See the patient again after 15 days and 1 month ■ If there are pigmentary changes (after approximately 1 month):

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See the patient again after 3 months for the end of treatment

Note 1.

See Chapter 32 for further remarks on the use of Vaseline® immediately after a peel.

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37 Complications of chemical peels

General remarks We must humbly accept the fact that there is still no magic formula that even the most experienced practitioner could use on all skin types without taking precautions and without risk and whose results would be both spectacular and permanent. Some formulations are of course more simple and less dangerous to use than others, but there is no guarantee of automatic success and complete safety. The practitioner must follow the rules of application for each peel, be aware of its limitations, risks and indications, and know how to avoid and treat any complications. ‘Artistic’ improvization usually leads to disastrous results. It is vital to read the instructions for use for each peel before applying it. A thorough knowledge of the symptomatology and physical and chemical mechanisms of peels is essential for the practitioner to be able to work confidently, safely and efficiently. It is child’s play for any competent doctor to apply liquid to a patient’s skin, but the true skill lies in anticipating the complications, being able to prevent them and, if prevention fails, being able to treat them. Patients deserve to be treated with respect, optimum safety and conscientiously by true professionals. Any peel, even a superficial one that is neutralized quickly and even in the most experienced hands, can lead to complications that are not necessarily serious or permanent, but that are more than what a particular patient is prepared to put up with. The deeper a peel penetrates, the sooner it is effective and the greater the risk of serious and permanent complications. We will look at each complication in detail, how to prevent it and how to treat it. Systemic complications,1 exclusive to phenol peels, are dealt with in Chapter 28. The magnitude of the risk depends on the following factors: ■ the type of peeling agent used, its concentration, how it is applied, and the depth it reaches ■ the doctor’s (lack of) experience, the monitoring and treatment equipment used ■ skin preparation (when necessary) and post-peel care recommended by the doctor

■ the patient’s own sensitivity and compliance with the pre- and post-peel treatment ■ the patient’s medical and treatment history ■ the area to be treated (e.g. the neck poses a greater risk than the forehead) ■ countless individual and impromptu factors. It is therefore essential to be knowledgeable, consider, weigh up, compare, photograph, note, record, film, explain, palpate, measure, monitor, diagnose, check, etc.

General safety factors If there were a secret to safety, it would lie in a thorough knowledge and understanding of this type of treatment. For doctors to give patients a wide range of choice, they must know how to use at least the three main types of conventional peels correctly: alpha-hydroxy acids (AHAs), trichloroacetic acid (TCA) and phenol (for phenol, the doctor should at least know how to apply it locally). For each type of peel, the doctor must be perfectly acquainted with its indications, results, limitations and complications to be able to choose the right product for a given patient and to be able to apply it correctly. The patient should be informed of alternative techniques, their possibilities, contraindications, side-effects and cost. The application technique must be flawless and in keeping with the particular procedure for each peel, appropriate to the patient’s skin type and the results expected. The doctor must be aware of and acquainted with the risks of complications and the means to prevent and treat them. It is better to avoid complications through prevention rather than treat them. Each patient is different and each peel must be suited to each patient, which in no way means trying dangerous experiments with different formulas on a caseby-case basis. On the contrary, it is a matter of choosing among tried and tested treatments the one that is most suitable for the patient’s skin structure and that will give the best results with a minimum of inconvenience. For example, the practitioner should be able to decide whether it is

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preferable to carry out several more superficial treatments or, on the contrary, to do a single phenol peel. If the latter option is chosen, which formula should be used: Baker–Gordon, Grade’s or Litton’s, Verner, Hetter, molding mask, Cora Valenti, Exoderm® or Lip & Eyelid? Should an occlusive mask be applied? Should the peel be neutralized? Should occlusion be left on for 24, 36 or 48 hours? Is post-peel care necessary? If so, what? If TCA is the treatment selected, should it be medium or deep or is it better to do several sessions with Easy TCA® or Unideep®? If an AHA peel seems the best choice, should it be glycolic acid, mandelic acid or lactic acid? Or Easy Phytic® peel? Should the peels be combined with other treatments, such as botulinum toxin, dermabrasion, filling, surgery, coagulation of telangiectasias, shave excision, mesotherapy, etc.? Which order should the combined treatments be performed in? Peel before toxin or vice versa? Peel before a face-lift or vice versa? Peel before mesotherapy or vice versa? Most peels carry a risk of one of the complications dealt with in this chapter. The likelihood of these complications occurring largely depends on the type of peel and the patient. Classifying peels as very superficial, superficial, medium or deep is purely theoretical and should not make the doctor any less vigilant. A low-concentration TCA or a simple glycolic acid peel can penetrate deep into the dermis if the peel is applied repeatedly and vigorously, or, as far as glycolic acid is concerned, if the peel is not neutralized in time. Depending on the agent and technique used, complications can be systemic or local, permanent or temporary, serious or not.

Figure 37.1 Wrinkles on the cheeks that will not respond or respond poorly to superficial or medium peels.

Inadequate results

Poor product knowledge

Inadequate results are an acceptable complication when the patient has been forewarned and the practitioner is prepared to compensate and do a proper touch-up. It is unacceptable when the patient has not been warned of this possibility and the doctor does not provide the care the patient deserves.

Attempting to use glycolic acid or TCA to achieve a visible lifting effect on ‘Sharpei skin’ is inviting disappointment: cosmetic and plastic surgery alone can achieve a lifting effect. It is better to warn patients of the possibility of inadequate results with any peel, even a deep one, if their skin is very thick, oily and sagging. It is likely that a deep peel would have to be repeated (locally or completely) to achieve the desired results. In these cases, it is worth considering a combination of a surgical face-lift and a peel. Sagging, thick skin is not a good indication for peels in general (Figure 37.2). Peels can get rid of fine lines, hyperpigmentation and keratoses and improve the quality of sun-damaged skin.

Reasons for inadequate results Wrong indication If the doctor’s aim is to improve the texture of the skin, treat hyperpigmentation and even-out the complexion, a single peel to the papillary dermis or four Easy TCA® peels to the basal layer Grenz zone are good indications. On the other hand, it would be dreaming to expect to get rid of surgical or acne scars or the wrinkles on the cheek of the patient in Figure 37.1 with glycolic acid or even TCA. Scars are treated with deep peels, often in combination with other treatments (punch elevation, dermabrasion, subcision, laser, filling, etc.). Wrinkles are treated with phenol.

Lack of pre-peel preparation, proper cleansing and/or degreasing the skin The presence of a lipid film on the skin partially deactivates many peels and limits their penetration. An unprepared stratum corneum may be too thick – too impermeable – in places. This relative local impermeability means that the acids

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Figure 37.3 Reappearance of dynamic wrinkles 10 days after a full-face phenol peel.

filling treatments, shave excision, prior surgical removal of small benign tumors, punch elevation of scars, stimulating facial mesotherapy, peels of different depths, etc. The doctor can only learn by experience what results to expect, which techniques should be combined and how best to use the chosen peel on a particular patient. Therein lies the art of peeling.

Histology of lesions undergoing treatment Figure 37.2 Sagging skin that does not respond well to peels.

do not penetrate evenly and the results will also be uneven. Pre-peel preparation is essential for certain peels,2 but unnecessary, or even dangerous, for others.3 It is essential to follow the recommendations for each peel solution to the letter.

Facial expressions After a deep peel, facial expressions imprint lines in the newly regenerating dermis and epidermis (Figure 37.3). Injecting botulinum toxin (before or after a peel) prevents dynamic wrinkles reappearing after a peel. Smoking should be forbidden after a deep peel to prevent the rapid reappearance of ‘accordion folds’ around the mouth. As well as the sucking movements required, smoking reduces the oxygen supply to the newly regenerating skin at the same time as dramatically increasing the number of free radicals. Smoking accelerates skin aging and slows down healing.

Lentigines, for example, result from a problem in the basal layer of the epidermis. Let us not forget, however, that the epidermis extends to varying depths into the dermis to form the dermal papillae. If a lentigo originates in a relatively superficial papilla, a peel to the Grenz zone will solve the problem,4 but if the lentigo originates in a deep papilla, it would take a very deep peel to dislodge it. Histologically, lentigines often have a deep ‘golf club’ structure that makes them difficult to reach. In this way, some problems that are histologically epidermal can only be treated by deep peels. In the diagram in Figure 37.4, a peel to the Grenz zone can resolve problem ‘A’, whereas problem ‘B’ will only respond to a peel to the reticular dermis. This reticular peel can be

Grenz zone

A

B

Combined techniques Non-surgical facial rejuvenation often requires a combination of different techniques, such as (micro)dermabrasion,

Figure 37.4 Lentigines at different depths,

Reticular dermis

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localized (e.g. with Only Touch®) or full-face (phenol peel). Repeated intraepidermal peels, no matter how often they were performed, would do nothing to solve the problem. Stretch marks, to give another example, are characterized by epidermal and dermal atrophy. They can only be improved by combining epidermal resurfacing with strong and deep dermal stimulation.

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Prevention of inadequate results This involves:

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■ proper targeting of patients ■ following the indications and application method of the chosen peel ■ thorough knowledge of the products used ■ possible combination with other treatments

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In all cases, caution dictates that the patient should be promised less dramatic results that might be hoped for. In this way, in the best-case scenario, the patient will get a nice surprise and be happy with the better than expected results. In the worst-case scenario, the doctor will not have made promises he cannot keep. Patients should be made fully aware of the limitations of their treatment. They should be shown photographs – and not necessarily the ones showing the best results. It is always essential to talk with patients before treatment to find out what they want and make sure they get the results they are looking for. It would be pointless to suggest a series of superficial peels to patients who want to get rid of crow’s feet, when a botulinum toxin injection would provide them with the quick results they want. False hopes always create problems for the doctor that raised them. Some patients’ disappointment can turn into a nightmare for the doctor.

Treatment Touch-up or different technique If the selected peel turns out not to be strong enough, a different peel should be used or it should be combined with other treatments. Local or general touch-ups can be done as soon as the condition of the skin permits, that is, when the skin has completely regenerated and when all erythema and flaking has finished. The ‘rest’ time between two peels is usually between 4 and 6 weeks.5 Many peels only produce results after fairly frequent repetition.

Repeating peels ■ Very superficial (stratum corneum) and superficial (intraepidermal: Easy Phytic®) peels have to be repeated to produce visible results. Results usually only show

■

after a certain number of sessions, as they are stimulating rather than destructive. Peels to the basal layer can be repeated four or five times (Easy TCA®) on an average of one session a week. The doctor should always wait for the skin to recover before re-peeling. Skin that is actively flaking should not have another peel applied to it. Some patients need a fifth peel (oily skins, resistant hyperchromia, squeamish patients who do not allow the doctor to apply the solution properly, etc.). TCA peels to the papillary dermis (Unideep®) should not be repeated until at least 1 month later and on condition that the skin has completely recovered from the previous session. Localized TCA to the reticular dermis (Only Touch®): in some cases, lentigines or keratoses do not disappear after the first session of Only Touch®. The application protocol for Only Touch® provides for a second application where necessary. The Only Touch® peel should be combined with Easy TCA® to avoid pigmentary changes and can be applied before the first and the fourth Easy TCA® peels. If some lesions resist or recur, a complete cycle of Only Touch® plus Easy TCA® can be started again after a 6-week rest period. Resistant lesions on the face can be treated locally with a spot application of Lip & Eyelid®. However, applying very localized phenol often produces long-lasting (3–6 months or more), localized erythema. This erythema tends to resolve naturally, but should be accompanied with protective measures against postinflammatory hyperpigmentation. Phenol (Lip & Eyelid® formula): if a full-face phenol peel does not produce adequate results, a second peel can be applied to the areas that did not respond to the first peel. The touch-up can be localized or full-face, if the condition of the skin permits and if there has been a long rest period. Skin regeneration after the second peel is much quicker, there is less edema and post-peel erythema is of a much shorter duration (2 weeks at the most). If a third phenol peel were indicated (in extremely rare cases of very thick skin, patients who smoke, or rapid resumption of facial expressions), it would most often be localized. The author has only once had to do a third phenol peel on the lip and cheek area after inadequate results on skin that was extremely oily and thick. Recovery was even faster after a third application of phenol and there was hardly any erythema. It should be noted that if a second phenol peel can boost inadequate results, a third phenol peel only brings a very slight improvement over the second.

Melanocyte toxicity Melanocytes are located in the basal layer of the epidermis and form part of the dermoepidermal interface. Skin color

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depends – among other things – on the melanocytes’ capacity to give up their melanosomes to neighboring keratinocytes and thus provide a homogenous photoprotective layer of pigments on the surface of the epidermis. It has been shown6 that melanocytes have three different ways of transporting melanin to keratinocytes: ■ melanocyte phagocytosis: transfer of melanin plus cytoplasm plus melanocyte dendrites to the keratinocyte ■ membrane fusion between melanocytes and keratinocytes, leading to direct exchanges between melanocytes and keratinocytes ■ exocytosis of melanosomes by melanocytes to the extracellular environment, where they are picked up again by keratinocyte endocytosis Each melanocyte communicates with 35–40 keratinocytes through its dendrites and forms one ‘melanization unit’. If the melanocyte transmits eumelanosomes, the keratinocytes receive effective sun protection. On the other hand, if pheomelanosomes are transmitted to the keratinocytes, they will not be properly protected against UV rays. Keratinocytes can synthesize active substances that alter the proliferation, differentiation and certain biological functions of melanocytes.6 An agent’s melanocyte toxicity is an advantage when treating melanin hyperpigmentation. On the other hand, it is an adverse effect when melanocyte toxicity results in partial, complete, localized or generalized depigmentation. Complete, generalized and permanent depigmentation results in ‘porcelain’ skin and, according to Litton,7 occurs in 3% of phenol peels with his formula. This complication has not been described to date with the Lip & Eyelid® formula.

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■ the patient has used abrasive or hair-removing techniques that alter the relative impermeability of the skin before the peel In general, the appearance of frosting during an AHA peel is a sign of overpeeling, and pigmentation problems may well occur. An AHA peel should always be neutralized after erythema and before frosting.

TCA TCA is not considered toxic to melanocytes. High concentrations of TCA can, however, coagulate melanocytes and destroy them. Areas of depigmentation can therefore appear if TCA has been too aggressive locally. Aqueous solutions of TCA in particular can penetrate more deeply than they should, as they are neither homogeneous nor stable. An even, intraepidermal TCA peel to the basal layer or Grenz zone does not cause depigmentation. Easy TCA®, in the basic protocol, does not produce depigmentation. A TCA peel to the papillary dermis, if applied evenly, does not usually cause permanent, pathological depigmentation. If the TCA penetrates too deeply into the dermis, depigmentation is sometimes accompanied by scarring. Three different degrees of TCA penetration cause three different complications: scarring results from the deepest penetration; depigmentation without scarring results when the TCA penetrates too deeply (but not deep enough to cause scarring) and is melanolytic; and a hyperpigmented halo results from an untreated, peripheral inflammatory reaction (Figure 37.44).

Phenol

Melanocyte toxicity of different types of peels AHAs AHAs are not considered toxic to melanocytes. Therefore, there is little fear of depigmentation when these peels are applied according to the rulebook. When these peels are neutralized, their effect stops, and AHAs cannot therefore do any irreversible damage to melanocytes. If they are not neutralized soon enough, they can, however, cause melanocytic lesions and areas of depigmentation as a result. Uneven penetration of AHAs can damage melanocytes locally. Uneven penetration can occur when: ■ There is no skin preparation (except for Easy Phytic® peel8) ■ the doctor does not apply the peel evenly ■ the patient has applied products locally that reduce the thickness of the stratum corneum: tretinoin, glycolic acid, benzoyl peroxide, etc.9

Phenol is considered toxic to melanocytes, although pigmentary changes can sometimes occur after a phenol peel (see later in this chapter). Phenol is by far the most effective agent when it comes to treating many facial hyperpigmentations. In general, a slight loss of pigment should be considered as normal after a phenol peel, and not as a complication. For a given concentration, depigmentation is proportional to the total quantity of phenol applied to the skin. That is to say that several coats of the same product will cause depigmentation more often than a more smaller number of coats. The presence of adjuvants can also be a risk factor for depigmentation: croton oil is a common adjuvant in phenol formulas and enhances penetration of the phenol. If there is too much croton oil, the phenol can penetrate more deeply and cause depigmentation. The use of thymol iodide as a post-peel mask is another risk factor, as thymol is a phenol derivative that can have a toxic effect on melanocytes in the period immediately following the phenol peel. This risk can be avoided by using bismuth subgallate as a post-peel mask. Phenol is not melanolytic, however: it does not physically destroy

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melanocytes. Melanocytes are not simply melanin-producing organelles, but play an active part in many of the biological processes in the skin:

the areas of the body that have never been tanned can provide a clue to the patient’s ‘base’ color, and the area treated with phenol may well return to this original color.

■ ■ ■ ■

Melanocyte toxicity depending on skin phototype

production of cytokines mediators of inflammation enzyme production synthesis of molecules in the extracellular matrix

Histological sections taken after phenol peels show that melanocytes are still present, though many of them are inactive. Clinically, fewer melanocytes are rendered inactive with the latest formulas (e.g. Lip & Eyelid®). This means that long-term prognosis for sun exposure can be better with these peels than with older phenol formulations and that a few months or even a year after the peel, it is often difficult to see a demarcation line.10 The melanocyte toxicity of phenol means the practitioner must choose the product most suited to the patient’s complexion. When persistent (absolute or relative) depigmentation is likely after a phenol peel and it is essential to warn patients that the texture of their skin will be rejuvenated, but that in all likelihood they will have to wear foundation on a permanent basis to hide the difference in color between the treated and untreated skin. The risk of depigmentation can pose a problem with badly sun-damaged skin, but, at the same time, this is one of the best indications for phenol. The extraordinary results achieved on photoaged skin are often accompanied by a more visible demarcation line between the areas of healthy, treated skin and the old, untreated skin. Combined use of phenol on the face and Easy TCA® or Unideep® on the neck help attenuate this demarcation line (Figure 30.1). The melanocyte toxicity of phenol poses different problems depending on whether the treatment has been applied to the whole face or just locally (e.g. the upper lip). Depigmentation of the whole face is easier to hide with make-up than localized depigmentation, and this should be discussed with the patient. Usually, older patients whose upper lip is very damaged will accept this local depigmentation, easily disguised with camouflage make-up, whereas younger patients find it more difficult to accept being condemned to wearing make-up every day, and often prefer other treatment options.

Prevention The selected peel must be applied in strict accordance with the instructions for use. The practitioner should always bear in mind that the deeper the peel, the more effective it is, but also the more dangerous it is and that phenotype does not always correspond to genotype: an individual who appears to have a light complexion may react dermatologically like a much darker phenotype. With this in mind, family anamnesis might well prove worthwhile. Examining

Black patients Black patients can be treated with correctly neutralized glycolic acid or with Easy Phytic® solution. Easy TCA® can also be used (pinpoint or cloudy-white frosting): TCA should never be allowed to penetrate reticulary dermis (see Chapter 16). Phenol should not be applied on patients with a skin phototype above IV.

Asian patients Asian patients might pose a problem of residual depigmentation with deep peels. Dark Asian skins are treated like black skins. Lighter Asian skins can be treated with deeper peels. Fintsi69 and Professor Damiano Kim (Korea) applied phenol successfully to light Asian skins. AHAs, Easy Phytic® and Easy TCA® can be used in all cases. TCA in simple aqueous solution (TCA–SAS) often triggers postinflammatory hyperpigmentation on Asian skin. Unideep® should be used with caution on Asian skin phototypes.

Dark-skinned patients Mediterranean or Latin American skin types can be treated with AHAs, superficial TCA or Easy TCA®. A TCA peel to the papillary dermis can be used with caution, avoiding overpeeling and post-peel inflammatory reactions. Patients with skin phototype IV can be treated with phenol if the patient is warned of the possibility of depigmentation in the treated skin. Results can be very satisfactory, as the difference in color between the treated and untreated areas may not be too marked.

Red-haired patients Red-haired patients, whose skin is often covered in freckles, do not pose any problems with AHA peels or Easy TCA®. A TCA peel to the papillary dermis gets rid of most of the freckles and Easy TCA® in the basic protocol lightens them. In principle, the texture of their skin makes them good candidates for phenol, as they get wrinkles sooner than darker skin phototypes and do not often suffer from postinflammatory hyperpigmentation after a medium or deep peel. All the freckles will disappear, however, leaving the skin depigmented and a demarcation line on the neck. Red-haired patients are the ones most at risk of complete

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depigmentation after phenol: porcelain skin that will often take on the color of areas that have never been exposed to the sun.

Treating melanocyte toxicity As yet there is no easy and effective treatment to return color to a skin that has lost it. No doubt in the future melanocyte grafts will be a possibility. For now, make-up is the only solution.

Erythema Post-peel erythema can be perfectly normal (Figure 37.5) or a warning sign of a more serious complication. Erythema can occur as a reaction even after simply cleansing thin and sensitive skin before a peel. If an erythema develops after the skin has been cleansed gently and without acid products, it may be concluded that it is hypersensitive and should be treated with caution. Chronologically, the skin’s first response to an application of acid is usually erythema. This erythema is caused by the inflammatory vasodilation of the blood vessels in the dermis in response to chemical injury. The vasodilation triggers transient dermal edema. This edema is largely responsible for the rapid disappearance of fine lines after

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superficial peels. The dermis fills with extravasated fluids as a result of vasodilation, and this stretches the epidermis. The fine lines disappear temporarily. Erythema may therefore be the only clinical sign of a superficial peel. The deeper the peel, the more erythema is replaced by frosting due to protein coagulation. The speed with which erythema is replaced by frosting largely depends on the strength of the acid used. Some very strong acids trigger frosting even before erythema becomes apparent.

AHAs and erythema AHAs in aqueous solution Essentially, AHAs trigger erythema – a sign that the peel should be neutralized. Erythema appears more quickly when the skin has been prepared (certain products increase the permeability of the stratum corneum) during the weeks before the peel. ■ Very localized, isolated erythema signals an area where the AHAs have penetrated rapidly. The doctor should keep a close eye on this area and neutralize it with sodium bicarbonate or another alkaline solution, while leaving the peel to work a little longer on the rest of the treated area that has not yet reached the stage of erythema. Great care should be taken not to let the acid penetrate too deeply locally and trigger frosting, which can lead to complications. After neutralizing, it can help to apply a little cortisone cream on an area of erythema. ■ Even and light erythema is a clear sign that it is time to neutralize the peel with an alkaline solution prepared before the peel has been applied. After the acid has been properly neutralized, the erythema should be transient and last one hour at the most. ■ If the practitioner ignores the erythema and does not neutralize, the AHA peel can cause localized pinpoint frosting that will gradually converge and become relatively uniform. An AHA peel that is not neutralized causes scabbing and, in the most serious cases, dyschromia and scarring. Patients often give up on the treatment if the peel is not properly neutralized. Erythema from overpeeling can last for several weeks or months and leave areas of skin that are ‘smoother’ than the surrounding skin.

Easy Phytic® solution

Figure 37.5 Normal erythema after a full-face phenol peel.

This peel deserves special attention because of the fact that it does not need neutralizing (see Chapter 11). It triggers light and uniform erythema that lasts for a few hours at the most. Neutralizing this peel would reduce its effectiveness and take away any benefit. If any abnormal frosting occurs, the peel should be neutralized immediately.

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TCA and erythema TCA in simple aqueous solution (TCA–SAS) The appearance of light, uniform and widespread erythema after a TCA–SAS peel does not usually lead to any problems and has a natural tendency to resolve gradually without treatment. The appearance of localized erythema, especially on the cheekbones, should alert the doctor, as it can be a sign of local overpeeling or one or more of the following: ■ ■ ■ ■ ■ ■ ■

Highly concentrated TCA triggers immediate ‘pure white’ frosting without any hint of pink or gray, which signals coagulation of the skin proteins and the walls of the dermal blood vessels. Although the erythema from TCA is often less severe than that from phenol, it can be vivid and last 15 days to several months. TCA–SAS peels sometimes produce prolonged and spectacular erythema, as can be seen in Figure 37.7. These simple aqueous solutions do not penetrate evenly, and uneven pathological erythema often results. Erythema after a peel to the papillary dermis with TCA in simple aqueous

too high a concentration of TCA an inhomogeneous TCA solution too many coats of acid applied locally too aggressive or uneven pre-peel preparation scratch lesions becoming infected the start of a viral infection an incorrect application technique

Applying TCA to the skin produces, in sequence, the following clinical signs: erythema, pinpoint frosting, cloudywhite frosting, converging cloudy frosting, even pink–white frosting, pure white frosting and finally gray–white frosting. The speed with which one sign replaces another is dose-dependent. These signs should appear in sequence when a low-concentration TCA peel is applied in successive coats. A more concentrated TCA peel will trigger converging clouds of frosting at the same time as erythema around the frosting (Figure 37.6). Higher concentrations trigger pink frosting instead of erythema and erythema, only then appears as the frosting fades in the treated areas.

Figure 37.7 Figure 37.6 Normal erythema around an area of frosting during a TCA peel to the papillary dermis (Unideep®) on the décolletage.

Uneven, pathological erythema after TCA in aqueous solution – a peel to the papillary dermis. (Courtesy of Dr A Carvajal, Colombia.)

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Figure 37.8 Normal and transient erythema 30 minutes after Easy TCA®.

solution is usually expected to last 1–2 months. A peel to the top of the reticular dermis can last 1–3 months. Persistent erythema is often followed by inflammatory hyperpigmentation that is aggravated by sun exposure. Effective sun protection (see Chapter 3) is therefore essential as long as the erythema persists. Indurated erythema might lead to scarring, and preventive treatment should be started (see the section on scarring later in this chapter). When intraepidermal TCA peels or TCA peels to the basal layer are repeated too often,11 erythema can last even longer. Using tretinoin during the weeks before or after a TCA peel is also likely to trigger or exacerbate erythema.

Easy TCA® Basic protocol (pinpoint or cloudy white frosting) Light erythema develops immediately after the peel and disappears in around 30 minutes (Figure 37.8). The skin may appear ‘sunburned’, and this can last up to a maximum of 48 hours in patients with thin and sensitive skin. Because of the action of the post-peel cream, there is often no observable erythema during the days following this peel if it has not gone beyond pinpoint or cloudy white frosting. The post-peel mask scavenges free radicals and breaks the vicious inflammatory circle that sets in after any peel. Scratch lesions can, as with TCA–SAS solution, cause localized erythema resulting from local infection (Figure 37.9), which should be treated. Treating stretch marks This more aggressive protocol involves sandpaper abrasion prior to the application of Easy TCA® solution and 12–24 hours’ occlusion of the post-peel mask cream. It causes severe erythema within the first few hours of occlusion. After the occlusion has been removed, the skin looks

Figure 37.9 Localized erythema around scratch lesions after an Easy TCA® peel to the papillary dermis.

swollen and red (Figure 37.10). During the first week, overall developments are comparable to those of a phenol peel. The erythema can last for several weeks and the next peel can only be performed after the erythema has completely resolved. As with TCA–SAS, persistent localized erythema is a sign of local complications and should be monitored, while uniform erythema has a natural tendency to resolve gradually without treatment (Figure 37.11).

Figure 37.10 Erythema 24 hours after treatment of stretch marks: abrasionocclusion protocol.

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Figure 37.11 Erythema totally disappeared 5 weeks after Lip & Eyelid® formula of upper eyelid and unideep (TCA peel to papillary dermis) in the rest of the face.

Unideep® Unideep® is a TCA peel to the papillary dermis. Adapted from Easy TCA® technology, it consists of a peel solution and a post-peel mask. Thanks to the post-peel mask, the erythema following the peel does not last as long as the erythema after a peel with TCA–SAS to the same depth. The erythema following Unideep® lasts around 5–8 days (Figure 37.12), and the only treatment that it requires is an application of antioxidant cream (e.g. Renutriv ACE Lipoic Complex®) and Vaseline® (see Chapter 23). If there is persistent localized erythema, there might be a local complication, and treatment is necessary. Effective sun protection must be used.

Figure 37.12 Erythema 5 days after Unideep® on the face, apart from the area around the mouth, which was treated with occlusive Lip & Eyelid®.

Figure 37.13 Normal erythema after Only Touch® and Easy TCA® for lentigines: (a) before; (b) 2 weeks after treatment.

A

B

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Only Touch® Only Touch® is an adjuvanted, stabilized and concentrated TCA peel, used to reach the reticular dermis locally. It should be applied in strict accordance with the recommendations for use (see Chapter 22). The erythema that always follows an application of Only Touch® usually lasts 2–3 weeks and gradually resolves without treatment (Figure 37.13). Only Touch® should be applied carefully, avoiding any excess product and limiting contact time between the applicator and the skin: the skin should just be touched lightly, with the same pressure as for pushing the buttons on a telephone to dial a number. If contact time is any longer, the acid solution will penetrate too deeply. Too much solution and too long a contact time can cause small, erythematous lesions that do not last longer than 3–4 months and that gradually resolve with treatment. The erythema caused by Only Touch® can easily turn into post-inflammatory hyperpigmentation if the product is used alone,12 but post-inflammatory hyperpigmentation is rare if Only Touch® is combined with an ‘evening-out’ Easy TCA® peel. Any erythema warrants effective sun protection. Any erythema lasting longer than 2 weeks must be treated.

Figure 37.14 Normal erythema and edema 24 hours after full-face phenol.

Phenol and erythema Full-face phenol Phenol peels are always accompanied by severe erythema (Figures 37.14 and 37.15). The erythema appears immediately around the edges of the frosting caused by the phenol and can then be seen on all of the treated area, as soon as the frosting fades. This immediate erythema results from inflammatory vasodilation that follows chemical injury and is normal. After 24 hours, the patient appears severely burnt, as can be seen in Figure 37.14. The classical phenol formulas often cause erythema that last more than 3 months, or sometimes even several years. It can be permanent (in some rare cases). Lip & Eyelid® causes erythema that lasts 1–3 months on average. This erythema results from the combined effects of: ■ temporary thinning of the epidermis (4–6 weeks) ■ a reduction of the overall quantity of pigments in the epidermis (permanent after phenol) ■ an increase in the vascular network of the dermis (rarely permanent) The first two changes make the third more clearly visible through the transparent skin. Within a few weeks or months, the restructured epidermis will cover up the hypervascularization, which tends to gradually diminish.

Figure 37.15 Normal erythema 15 days after full-face phenol.

Local phenol The eyelids, upper lip and the area around the mouth can all be treated locally, in combination with an ‘evening-out’ peel on the rest of the face. The usual erythema caused by phenol appears locally and lasts from 3 weeks to 3 months (Figure 37.16). The localized erythema, surrounded by skin of a normal color,

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Figure 37.17 Normal erythema 7 days after Lip & Eyelid® around the mouth and chin. The whiteness comes from an application of antioxidant cream and the shine from Vaseline®. The rest of the face has been treated with Unideep® (TCA peel to the papillary dermis)

Figure 37.16 Normal erythema 15 days after localized phenol (Lip & Eyelid® formula). Rest of the face treated with Unideep®.

is more visible than with a full-face peel, where the demarcation line is in less visible areas. It is essential to warn the patient of the need to wear camouflage make-up. Persistent, localized erythema in the treated area means that complications are likely and should be closely monitored. Figure 32.17 shows erythema of the whole area treated with phenol. This is not a dangerous, ‘localized’ erythema.

Prevention The basic rule is ‘the deeper the peel, the more severe and longer-lasting is the erythema.’

Rules of conduct ■ Avoid situations that subject the facial skin to extreme changes in temperature. ■ Avoid vasodilating agents such as spicy food or alcohol. ■ Avoid exposure to ‘daylight’. ■ Use effective sun protection (see Chapter 3). ■ After a peel, avoid using photosensitizing products (hairspray, perfumes, etc.) or products that induce erythema (e.g. tretinoin).

■ Avoid secondary infections and skincare products that are too aggressive. Beware of ‘scrubs’ used too soon after a peel. Some patients cannot tolerate flaking, and try to pull off the strips of flaking skin. Others try to get rid of the ‘dead skin’ with abrasive creams. In both cases, the skin can be damaged and localized erythema or hyperpigmentation can occur. With Easy TCA® (pinpoint frosting), there may be some light exfoliation before the end of the first week after the peel. ■ Do not repeat peels more often than necessary, and wait for the erythema from the previous peel to subside before applying the next peel. ■ Apply the peel evenly, using a stable and homogenized formulation. ■ Avoid peeling techniques that do not allow monitoring of how the skin is reacting throughout the procedure (e.g. ‘opaque masks’ or thick, colored pastes). ■ If patients have been asked to prepare their skin, make sure that they have done so regularly and evenly.

AHAs: erythema prevention The practitioner should monitor the whole peel procedure closely and carefully and make sure that the acid is neutralized at the right time (except for Easy Phytic®, which does not require neutralization). Any frosting will result in prolonged erythema. The neutralizing solution should be prepared before the start of the peel.

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TCA: erythema prevention TCA–SAS The peel should not be applied more often than the patient’s skin can tolerate it. After a peel to the papillary dermis, erythema cannot be avoided. Flaking should not be forced prematurely by pulling off strips of flaking skin. On the 8th or 10th day after a peel to the papillary dermis, persistent erythema and/or slightly infected areas without any trace of flaking suggest that the skin has been pulled off or that the patient has been scratching, sometimes completely unconsciously at night. A TCA–SAS peel can be repeated after 4–6 weeks at the earliest, once the erythema has completely disappeared. Effective sun protection is essential. Easy TCA The very light erythema that follows Easy TCA® disappears very rapidly. It is the only peel where it is not strictly forbidden to help flaking along. Bleeding should, of course, be avoided, as this would trigger erythema. The erythema soon subsides and does not cause any adverse sequelae unless there is a secondary infection. The maximum frequency for repeating the basic protocol (pinpoint frosting) is four peels at 5-day intervals. The ideal frequency is four peels at 8-day intervals. Effective sun protection is essential. Only Touch® Local erythema is inevitable after a peel to the reticular dermis. Pulling off scabs must be avoided at all costs. Only Touch® can be combined with Easy TCA® to reduce erythema and hyperpigmentation. The maximum frequency for repeating the peel is when the erythema has completely disappeared. Effective sun protection is essential. Unideep® Erythema clears up rapidly after this peel to the papillary dermis – usually within 8 days. The maximum frequency for repeating the peel is 3–4 weeks and once the erythema has completely cleared. Effective sun protection is essential.

Phenol–Resorcinol Erythema is inevitable after a phenol peel (Figure 37.18). It can sometimes be less severe and of a shorter duration if a corticosteroid is injected intravenously at the beginning of the peel. Its intensity varies from patient to patient, from light and imperceptible to severe and deep. Resorcinol is a potentially allergenic phenol derivative: persistent, pruritic erythema after a resorcinol peel might be a sign of contact dermatitis.

Treating erythema Erythema has a natural tendency to resolve spontaneously without treatment. The patient should be told to see the doctor if there is any abnormal, localized and persistent

Figure 37.18 Normal, localized erythema 8 days after Lip & Eyelid® on the upper lip and Unideep® on the rest of the face. Note the light erythema from the Unideep® on the 8th day.

erythema. A peel can reveal a subclinical condition of eczema or lupus. Clinical examination and close questioning of the patient is of prime importance to bring these problems to light before treatment.

Treat until complete resolution Persistent, localized erythema means that there is a risk of hyperpigmentation or scarring. Erythema can be extremely unpleasant for patients, and they might ask for a treatment to get rid of it more quickly. Localized erythema requires topical treatment, and erythema in the whole treated area requires systemic treatment.

Recommended treatments Topical cosmetics Effective sun protection is always indicated with erythema, as it tends to develop into hyperpigmentation after UV exposure. Antioxidant creams can limit the negative effects of free radicals and the damage they cause to the cells. Creams containing vitamins A, C and E and lipoic acid13 can be combined with an antioxidant cream. The Easy TCA® post-peel mask provides effective protection against erythema. Local corticosteroids Treatment consists in prescribing a cream containing steroid anti-inflammatories. The sooner treatment is started, the more effective it is with low-dose products. If treatment is delayed, higher doses of fluoro-corticosteroids have to be used, and the results are less satisfactory. A (2.5%) hydrocortisone cream or a topical clobetasone

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cream applied three or four times a day for 2 weeks should be sufficient. If treatment is started later still, fluocinolone or halcinonide must be prescribed. Some authors recommend preventive application of a cortisone cream immediately after a peel, although these creams do not help skin regeneration and penetrate far more readily and rapidly through skin that is far more permeable. Applying a corticosteroid during the first week after a peel does not pose any problems. On the other hand, excessive use of corticosteroids increases the risk of acne and bacterial, viral and fungal infections, and can cause telangiectasia. What is more, long-term use of topical corticosteroids thins the skin, causing atrophy that defeats the purpose of a peel. In cases of indurated erythema likely to lead to scarring, corticosteroids can be repeatedly injected locally into the erythema, and the lesion can be covered with a silicone sheet pressure dressing, day and night, until the lesion disappears. General treatments Corticosteroids by the systemic route will only be needed very rarely to treat erythema. They can be administered in a single and preventive injection at the start of a phenol peel. Promethazine can be recommended, at a maximum dose of six times 25 mg/day, when the erythema causes pruritus and reflex scratching that could lead to unsightly scars, infections or dyschromia.

Lasers Rubin describes using the Candela pulsed dye laser to good effect to reduce persistent erythema. Intense pulsed light can also be used to treat post-peel erythema.

A

Telangiectasias Telangiectasias result from vasodilation and a proliferation of dermal blood vessels. There are many different causes: sun aging, hormone therapy, inflammatory dermatosis, corticosteroids, alcohol, etc.

AHAs These do not usually have any effect on telangiectasias and do not cause neovascularization.

TCA In the month following a TCA peel to the papillary dermis, pre-existing telangiectasias can be seen more clearly through the relatively transparent epidermis because of the temporary loss of thickness and pigmentation. It is rare for new telangiectasias to develop, and this does not often pose a problem after a peel, even a deep one. The doctor can coagulate the telangiectasias immediately before applying an Easy TCA® peel (Figures 37.19 and 37.20). The fact that the solution will penetrate into the small holes left after coagulating the blood vessels does not cause any complications. On the contrary, this prevents the usual scabs that form after the coagulation of telangiectasias and that can last up to 2 weeks. The duration of scabbing is more than halved and there is less risk of secondary infection.

Phenol Phenol can improve the appearance of very fine, superficial telangiectasias through coagulation. Deeper telangiectasias

B

Figure 37.19 (a) In this case where there are many telangiectasias and lentigines, a combination of treatments will be used in the same session: coagulation of the telangiectasias with a Kobayashi needle mounted on the handpiece of a radiofrequency unit (Ellman), an application of Only Touch® to the lentigines and finally an application of Easy TCA® to the whole face. Coagulation and Only Touch® will be repeated just before the fourth session of Easy TCA®. (b) Results of these combined treatments. The lack of nasolabial folds in (a) comes from the patient’s position.

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A

B

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C

Figure 37.20 (a) Telangiectasia on the tip of the nose, treated by coagulation with a Kobayashi needle mounted on the handpiece of an Ellman unit (radiofrequency). Immediately after coagulation, Easy TCA® solution is applied. (b) When it is dry, the post-peel cream is applied. (c) The almost total lack of scabbing on the fourth day after the combined treatment.

may be pushed deeper into the skin by the synthesis of new collagen in the upper part of the dermis, and will be less visible. On the other hand, inflammatory vasodilation can also aggravate them. The patient should be warned that telangiectasias are not in themselves an indication for a peel and that results vary. The doctor should be wary of raised telangiectasias that are difficult to hide. There are reported cases of deep peels being performed despite the presence of telangiectasias, which remain unchanged by the peel, but a phenol peel can also cause numerous small telangiectasias to appear during the first weeks after the peel. These telangiectasias must be treated to stop them turning into hyperpigmented marks.

Scarring and dyschromia Intraepidermal peel (Figure 37.21) An intraepidermal peel is characterized by the following symptoms: erythema without frosting after an AHA peel or erythema and maybe some pinpoint frosting after a TCA peel. Phenol is not indicated for this depth of action.

Prevention The type of peel must be carefully chosen. These vascular dilations must be treated preventively as indicated above (see Figure 37.20).

Treatment This can involve electrocoagulation, Surgitron® (Ellman),15 scarification, microsclerosis, laser or flashlamp. These treatments should be carried out 1–2 weeks before the peel. The one exception is Easy TCA®, where the telangiectasias can be treated immediately (a few minutes) before the peel solution is applied.

Figure 37.21 Intraepidermal peel.

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Risk of scarring This is non-existent. Re-epithelialization after an intraepidermal peel is rapid and easy, as it comes from growth stimulation in the still intact basal layer of the epidermis. The epidermis ‘feels’ the loss of the stratum corneum as a dangerous attack and reacts by sending a clear growth message to the ‘mother’ keratinocytes in the basal layer. These keratinocytes divide16 and rebuild a normal epidermis as quickly as possible. A local increase in the concentration of tumor necrosis factor alpha (TNF-α) stimulates the keratinocytes to transform themselves into corneocytes and restore the skin’s initial state of impermeability. The stratum corneum is largely responsible for the skin’s total impermeability (maybe >70%). This relative impermeability not only affects the fluids coming in and going out, but also fungal, bacterial or viral invasion. The constant shedding of dead cells from the stratum corneum is in itself a phenomenon of great importance to homeostasis: it gets rid of epidermal garbage and a large quantity of xenobiotic microorganisms.

Risk of dyschromia Intraepidermal peels do not stimulate melanocytes and never cause achromia. There is no risk of skin discoloration. However, some sensitive skins react to any inflammation by stimulating melanogenesis. The risk of post-peel hyperpigmentation cannot therefore be ruled out completely.17

Peel to the basal layer A peel to the basal layer (Figure 37.22) is characterized by erythema and the appearance of pinpoint frosting after TCA or generalized erythema after AHAs. Phenol is not indicated for this depth of peel.

The acids destroy most of the epidermis. Histologically, the basal layer does not form the perfect sine wave that is usually shown in diagrams. On the contrary, the keratinocytes are embedded deeply and unevenly in the dermis and form the deep ‘dermal papillae’. Even if the acid reaches the papillary dermis in places, a large number of keratinocytes survive, allowing the skin to regenerate very quickly. The process of re-epithelialization is the same as for intraepidermal peels: the basal layer keratinocytes are stimulated to grow.

Risk of scarring This is non-existent. The skin can easily repair itself without having to rely on stimulation of the myofibroblast system to contract an area that is taking too long to heal.

Risk of dyschromia There is no risk of achromia. Melanocytes are stimulated more directly, and the risk of hyperpigmentation is higher. The inflammatory reaction that follows any peel to the basal layer can cause post-inflammatory hyperpigmentation, even if it is slight. A vicious circle can set in that has the potential to cause post-peel pigmented marks: the peel causes inflammation – that is, among other things, vasodilation that brings oxygen as well as pro-inflammatory substances to the treated areas. Free radicals are formed that damage the structures regenerating the skin. The structural damage maintains inflammation, and post-peel hyperpigmentation may occur on dark and reactive skins. It is important to break this vicious inflammatory circle by scavenging free radicals as soon as they are produced. Large quantities of antioxidants are therefore needed in the skin, in the very same places that the free radicals are produced.18

Peel to the Grenz zone (Figure 37.23) The Grenz zone19 is a transition area between the epidermis and the dermis. A TCA peel to the Grenz zone is characterized by the appearance of cloudy-white frosting in which spots of normal skin color can be seen where the keratinocytes of the deepest dermal papillae have not been coagulated by the acid. AHA and phenol peels are not appropriate for this depth, and TCA is ideal for a peel to the Grenz zone. The process of skin repair is slightly more complex, and relies both on the many surviving keratinocytes being stimulated to divide and the keratinocyte reserve in the pilosebaceous units.

Risk of scarring Figure 37.22 Peel to the basal layer.

The keratinocyte reserves allow rapid and easy regeneration of the epidermis. The retractile myofibroblast system is not stimulated. There is no risk of scarring.

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even, pink–white frosting and epidermal sliding sign. Reepithelialization after a peel to the papillary dermis is slower as it relies on:

Figure 37.23 Peel to the Grenz zone.

Risk of dyschromia

■ the keratinocytes on the edges of the treated area ■ the keratinocytes still present in the basal layers most deeply embedded in the dermis that have been spared by the acids ■ the keratinocytes in the pilosebaceous units ■ the keratinocytes in the excretory ducts of the sweat glands ■ the sebocytes of the sebaceous glands, which are differentiated keratinocytes that specialize in sebum production; they must first dedifferentiate before they can regenerate the epidermis

Risk of scarring

The skin becomes lighter simply because of the epidermal melanin stock being eliminated. Enough melanocytes survive for the skin not to lose its natural color permanently. There are substantial reserves of melanocytes in the pilosebaceous units. Hypochromia is therefore rare after a peel to the Grenz zone, and there is no reason why achromia should occur. On the contrary, melanocyte stimulation is relatively strong and the risk of hyperpigmentation is increased. With this kind of peel, the preventive measures described in the section on hyperpigmentation later in this chapter should be heeded.20

The papillary fibroblasts are stimulated directly.22 They will produce a layer of collagen that can differentiate histologically from the collagen that is naturally present in the papillary dermis. The fibrils of the new collagen are aligned horizontally. This more complex process of skin regeneration can give rise to more complications than more superficial peels. In principle, only the fibroblasts in the papillary dermis are stimulated, and an effective keratinocyte layer can be regenerated quickly enough to avoid activation of the myofibroblast system and scar retraction. Only overpeeling can cause localized scarring. A peel to the papillary dermis is still very safe as far as scarring is concerned.

Peel to the papillary dermis (Figure 37.24)

Risk of dyschromia

AHAs and phenol are not indicated, and TCA is again the gold-standard peel to the papillary dermis. The following signs show that the papillary dermis has been reached:

A peel to the papillary dermis causes severe inflammation and strongly stimulates melanogenesis, often irregularly, with a risk of post-inflammatory hyperpigmentation. Preventive treatment of this is one of the most important phases in a peel to the papillary dermis. Areas of achromia may also appear when the peel has penetrated too far locally. A peel to the papillary dermis therefore marks the safety limit beyond which the risks are higher, though most often controllable. How far this limit can be stretched depends – among other things – on how permeable the skin is: in local areas of increased permeability, the TCA can penetrate too deeply.

Peel to the reticular dermis (Figure 37.25) Figure 37.24 Peel to the papillary dermis.

Phenol is the ideal agent for a peel to the reticular dermis. The following signs indicate that the peel has reached the reticular dermis: even, pure white or gray–white frosting.

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A

Figure 37.25 Peel to the reticular dermis.

Occasionally, small, buff-yellow patches may appear. Epidermal sliding is soon replaced by edema. Skin repair after a peel to the reticular dermis is slower, as all the basal layer keratinocytes have been destroyed and the skin can only rely on the differentiated keratinocytes of the pilosebaceous units and the intradermal excretory ducts of the sweat glands. To repair the dermis, the sebocytes in the pilosebaceous units must dedifferentiate, and horizontal growth is required to ‘close’ the skin quickly. Next comes a phase of vertical growth whose purpose is to regenerate a physiologically sound epidermis that will maintain homeostasis and restore the vital barrier function after the keratinocytes have differentiated into corneocytes.

Risk of scarring Under ideal conditions, healing after a peel should be supple and constant, leaving skin that is rejuvenated, hydrated, even in texture and without scars. The risk of scarring is much higher after a peel to the reticular dermis than after a peel to the papillary dermis. Delayed healing, resulting from excessive local penetration or local infection, strongly stimulates all of the skin’s regeneration mechanisms; they can trigger the phenotypic conversion of simple fibroblasts into myofibroblasts and start retractile-type healing. Particular attention must be paid to scar prevention measures (see later in this chapter).

Risk of dyschromia There is a major risk. Achromia is possible.

Difference between a facial peel and a body peel It is conventionally accepted that post-peel regeneration on the body takes twice as long as on the face. With peels to the

B

Figure 37.26 (a, b) Papillary dermis on body skin: only few pilosebaceous units are able to regenerate the destroyed layers of skin. Healing is slow and risk is higher.

papillary dermis, and especially the reticular dermis, it is important to consider the number of pilosebaceous units. The more pilosebaceous units there are, the greater the chances of healing without major problems (Figure 37.26). It is easier for the skin to heal on the scalp than on the face and easier on the face, than on the neck or décolletage. Rapid skin regeneration means that there is little chance of infection and retractile scar formation. Slow and difficult regeneration sharply increases the risk of retractile scars, infection and dyschromia.

Hyperpigmentation General considerations The skin responds to any lesion, burn or abrasion with an inflammatory reaction that may be accompanied by melanocyte stimulation and excessive melanin production. This reaction is generally considered to last for 3 months at the most. Different types of pigmentation disorders can occur after a peel: ■ partial or total depigmentation (see melanocyte toxicity). ■ local or general hypopigmentation (see melanocyte toxicity). ■ local or general, absolute or relative hyperpigmentation.

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Fitzpatrick skin phototypes I to III rarely develop postinflammatory hyperpigmentation (PIH), whereas skin phototypes IV to V carry a much higher risk. PIH can be ‘absolute’ or ‘relative’ to the surrounding skin. Relative PIH occurs when some areas of skin do not lighten as much as the surrounding areas and therefore appear darker. An area of normal skin color surrounded by an area of a lighter tone can look like PIH. Absolute PIH consists of a patch of skin that is hyperpigmented in relation to the normal skin color that surrounds it. Figure 37.27 shows an absolute PIH reaction.

Risk depending on peel type On the whole, the risk of PIH is proportional to the depth of the peel.

AHAs The risk of hyperpigmentation is low, and often results from localized overpeeling or delayed neutralization that leads to excessive penetration and possibly epidermolysis. There is still a risk of PIH, however, even if the peel has been neutralized correctly (Figure 37.28).

TCA–SAS Figure 37.27 Post-inflammatory hyperpigmentation (PIH): TCA peel, aqueous solution with uneven penetration to the papillary dermis.

A

B

As the risk increases with the skin phototype, it is obvious that a patient with Fitzpatrick skin type III will have fewer pigmentary changes than a patient with Fitzpatrick type V. Skin type V most often develops hyperpigmentation. That

C

Figure 37.28 PIH after a peel with 70% unbuffered glycolic acid; neutralization with a sodium bicarbonate solution as soon as erythema appeared. There is no visible frosting. Postoperative developments were normal. On the 8th day, the patient consulted the doctor about the appearance of PIH 3 days before (a). Treatment consisted of tyrosinase inhibitors, topical antioxidants, sun avoidance and protection. (b) The patient after 5 weeks. (c) After 8 weeks. The hyperpigmentation has improved significantly. A telephone call revealed that the problem has cleared up completely after 3 months.

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tion techniques: the cotton bud should be partially squeezed out before applying the solution and only the beginnings of pinpoint frosting should be achieved. The deeper Easy TCA® is allowed to penetrate, the greater is the risk of hyperpigmentation: pinpoint frosting is far less likely to trigger PIH than even, pink frosting. Repeating the peel is an important part of the strategy of avoiding PIH. The risk of PIH is sharply increased if only one Easy TCA® is done instead of the four included in the usual protocol.

Only Touch®

Figure 37.29 Transient local PIH after the first Easy TCA® peel. The second peel will erase this pigmentation. Combine with Blending Bleaching® and Melablock HSP®.

Applying Only Touch® peel too deeply can cause prolonged punctiform erythema that has a strong tendency to cause hyperpigmentation when exposed to daylight. The contact time between the applicator and the skin must be brief – the equivalent of the contact time between the fingers and a phone keypad (Figure 37.30). If an application of Only Touch® is followed by prolonged, punctiform erythema, treatment consists in avoiding pulling off the small scabs, effective sun protection of the whole face and sun avoidance, applying a cortisone cream locally, applying an antioxidant cream and tyrosinase-inhibitors on the whole face and close monitoring. Heavy-handed application of Only Touch® triggers edematous and hard gray–white frosting that, on palpation, feels frozen, as if with dry ice. This type of reaction is a sign that scarring is likely.

Phenol in alcohol solution is why some authors maintain that TCA cannot be used to treat hyperpigmentation, whereas in fact it produces excellent results when used correctly and as part of an overall treatment program for the patient, possibly including repeated peels and the use of appropriate topical treatments between and after the TCA peels. Patients with dyschromia always require an overall treatment program, not matter which type of peel is used. TCA in aqueous solution is nevertheless a molecule that carries a higher risk of PIH (see Figure 37.27). Many publications stress the absolute necessity to prime the skin for an application of TCA in aqueous solution. Any peel of this type requires 3–4 weeks of preparation, with tretinoin (to speed up recovery and even out penetration) and hydroquinone (to induce melanocyte sedation).

Easy TCA® One of the four weekly peels sometimes causes transient and limited PIH (Figure 37.29), often on the sides of the face, and mainly occurs when the patient has not used effective sun protection from the morning after the first treatment. This PIH is easily reversible, erased by the following treatment, and can be avoided with good applica-

Manquat23 relates the following: ‘Hayem tried phenic acid as a counterirritant. A brush is dipped in a solution of 9 parts crystallized phenic acid [phenol] to 1 part 90% alcohol and is painted on evenly and without letting the solution run. After these applications, the skin often becomes pigmented and retains the burn marks indefinitely.’ As a result of the almost immediate formation of an impenetrable protein coagulum, solutions with a high concentration of phenol (88%) that are ‘untamed’, as described above, do not penetrate deeply enough to become fully toxic to melanocytes, and the skin becomes hyperpigmented in reaction to the chemical burn.

Baker–Gordon and Litton formulas Litton7 reported that 67% of practitioners who answered his questionnaire have had to deal with pigmentation disorders. It should not be concluded from this that 67% of patients have problems with dyschromia, but that 67% of practitioners have come across it at least once, which is different. What is more, it is surprising that not all the practitioners questioned have been confronted with it at one time or other. Melanocyte toxicity appears to be more frequent than PIH with these formulas.

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A

C

B

D

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Figure 37.30 (a) Lentigines before Only Touch®. (b) Only Touch® applied too deeply: frosting has turned buff yellow. The contact time between the applicator and the skin was too long. (c) Prolonged erythema (6 weeks), abnormal after Only Touch®: the contact time between the applicator and the skin was too long. (d) Three months after treatment: almost complete resolution of erythematous spots and no PIH. Lentigines have gone.

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tion above on inadequate results). PIH resulting from an application of phenol is readily treated with Easy TCA® and tyrosinase-inhibiting creams.

Prevention Proper patient selection Sensitivity test If there is a personal history of PIH, a sensitivity test could be carried out on a hidden area. It is worth bearing in mind that if the test is negative, patients will be convinced that they are safe from complications and it is far more likely that any problem that might arise will be put down to the practitioner’s presumed incompetence rather than any particular skin sensitivity. Different areas of the face do not react to peels in the same way: a patch test behind the ear does not really say anything about how the area around the mouth will react. Sensitivity tests should therefore be seen more as a means of dissuading a patient who is likely to have complications rather than a means of preparing for any potential problems. A patient with a pigmentary reaction to a test should be ruled out for treatment with medium or deep peels and be oriented towards a peel that causes less melanocyte stimulation.

Figure 37.31 Unexpected pigmentary change after a full-face phenol peel. Note also the inadequate results.

Oily formulas These formulas (e.g. Lip & Eyelid®) seem to cause hyperpigmentation disorders rather than melanocyte toxicity, which is a good thing, as it is easier to treat PIH, and depigmentation is not readily reversible. Post-peel cosmeceutical care is therefore extremely important. Hyperpigmentary reactions often go hand in hand with inadequate results (Figure 37.31) and this particular combination means that the peel solution did not penetrate far enough (see the secBox 37.1 Not counting the importance of skin preparation, the adjuvants used, technical errors and preventive postpeel care and treatment, the risk of pigmentary changes can be quantified diagrammatically as follows: Phenol < TCA > AHA > Easy TCA®

Genetic factors The capacity to develop PIH is largely dependent on genetic factors. Patients who suffer from pigmentary changes after a peel often develop hyperpigmentation from insect bites or small operative scars, and it is worth questioning patients before starting treatment. Skin phototype The risk of pigmentary changes increases with the skin phototype: as a general rule, Fitzpatrick skin types I to III develop little or no hyperpigmentation and are therefore excellent candidates for deep peels. The lighter and more even the complexion, the fewer problems there will be with pigmentary changes. The darker the skin, the greater is the risk of pigmentary changes. Phototypes IV to V rapidly develop hyperpigmentation after any inflammation, even without sun exposure. A medium-depth peel (to the papillary dermis) on a dark skin phototype should always be preceded by skin preparation. These treatments will not stop all PIH, however. It is therefore wise only to perform less aggressive peels on patients with a dark skin type. Asian skins and patients whose genotype does not correspond to phenotype24 are more susceptible to PIH.

Preparing the skin Prevention of infections If there is any history, no matter how transient, of herpes, valaciclovir should be prescribed (two times 500 mg/day before and after the peel). In principle, herpes outbreaks do

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not leave scars, but they can sometimes leave some localized pigmentation for months or even years. To avoid secondary infections, medium or deep peels should not be performed during infectious outbreaks of acne.25 Cleansing and degreasing the skin If the skin is not cleansed and degreased evenly or not properly prepared before a TCA–SAS peel, the acid can penetrate unevenly and PIH may occur. Organic matter inactivates the acids,26 and the presence of lipids or surface debris can alter the depth of penetration. Easy TCA® solution was designed not to be affected by the presence of this surface organic debris. It is a saponified solution of TCA that is applied without prior degreasing and cleansing. Over-cleansing should be avoided: the skin must not be mechanically abraded when disinfecting and degreasing; the stratum corneum must not be destroyed by overenthusiastic wiping.27 This manual abrasion would be uneven and create areas of deeper penetration, increasing the risk of scarring and pigmentation. The pressure applied when cleaning the skin should be firm and above all even.

Even application of the peel AHAs AHAs must be applied quickly, since if they are applied slowly, the areas treated first should also be the first areas to be neutralized. Partial and gradual neutralization is difficult and a source of errors. AHAs should therefore be applied as quickly as possible, starting with the most resistant areas, such as the forehead. If the acid is applied quickly, all areas can be considered to have had almost exactly the same contact time and the whole face can be neutralized at one go. The whole treatment area should be monitored extremely closely to make sure that the peel is neutralized as quickly as possible if it is about to penetrate too deeply in any specific area. TCA–SAS The more force applied on the applicator, the more deeply will the TCA penetrate. Applying TCA with a brush gives a more superficial peel than applying the same concentration with a gauze pad. The number of coats must be the same all over: the depth of the peel increases with the successive number of coats of TCA applied. At a constant concentration, three coats of TCA produce a deeper peel than two coats. The concentration of the TCA must also be taken into account: with the same number of coats, a more highly concentrated TCA will give a deeper peel. It is important to watch out for any teardrops that may dilute the TCA and its action. Tear tracks on the cheeks can leave a line of more superficial penetration. Tears can also carry TCA onto the neck, where it can produce an unwanted linear peel together with PIH.

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EasyTCA® The ease of application and weekly repetition of this peel guarantee even results and an almost complete lack of PIH, if Easy TCA® is applied to pinpoint frosting. Only Touch® For information on the application of Only Touch®, see above and Chapter 22. Phenol Phenol must be applied evenly. The depth of the peel depends on the number of coats and the type of solution used. Chapter 34 describes in detail the application methods needed to get an even result. It is extremely important to follow the application methods for each particular formula carefully. In all cases, any occlusive mask must be even and not form ‘bubbles’ or areas of pressure. Any tears could carry phenol onto the neck (linear peel and increased probability of PIH).

Sun avoidance and protection The sun is not the only cause of post-peel hyperchromia. Rubin14 describes coming across cases of hyperpigmentation where there has been no sun exposure. For more information on sun protection, see Chapter 3.

Some medicines can cause pigmentation These include estrogens, and progestins (including oral contraceptives), phenothiazines, thyroid hormones and photosensitizers, among others.

Close monitoring Pigmentation disorders (as well as scars) are often preceded by persistent localized erythema that must be treated as quickly as possible (see above). Once again, the patient should have an overall treatment program. The patient

Figure 37.32 Pseudo-hyperpigmentation of the forehead: photograph taken on the 4th day after a Unideep® peel to the papillary dermis. The skin has started to flake above the left eyebrow.

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does not come just for a peel but to improve their skin. The practitioner is not being asked for a treatment but for a result, especially one that does not damage the skin. Patients should be seen as often as required. Generally, the deeper the peel, the more frequent the checkups should be. A phenol peel, for example, requires daily monitoring for the first 8–10 days after treatment. Over the first few days after a TCA peel to the basal layer of the epidermis or the Grenz zone, a pseudo-pigmentary change can be seen to appear (Figure 37.32) that actually results from dehydration of the epidermal layers where melanin is found. Acids bind readily with water molecules and dehydrate the skin. The melanin granules are brought closer together and the skin appears darker in places.28 It is not possible for a genuine pigmentary change to set in within 2 or 3 days.

Prevention through re-peeling TCA–SAS Fouque and Seban29 limit pigmentary changes by automatically applying an AHA peel after a TCA in aqueous solution. Although AHAs are not toxic to melanocytes, these superficial peels can – partially or completely – put a stop to any pigmentary changes that are common between the 2nd and 4th week following a TCA peel in aqueous solution, especially in countries with very sunny climates. The protocol includes three phases: ■ First phase: the patient applies a depigmenting cream for the first 2 weeks after the peel with TCA–SAS. ■ Second phase: 3 weeks after the aqueous TCA: a 50% buffered glycolic acid peel is done to test the skin’s sensitivity. ■ Third phase: the following week a 70% unbuffered peel is applied for 1 minute, then neutralized. As soon as the condition of the skin permits, a peel to the basal layer of the epidermis can be envisaged to reduce the quantity of intraepidermal melanin and improve the penetration and action of depigmenting agents. Any additional inflammation must, of course, be avoided, as this would create a second wave of hyperpigmentation. I use only Easy TCA® to treat pigmentary changes: application of the peel solution to the start of pinpoint frosting and application of the post-peel mask cream, whose main properties are antioxidant, tyrosinase-inhibiting and anti-inflammatory.

occur. Pregnancy is contraindicated in the months following a deep peel, especially in patients with a high risk of pigmentary changes.

Treatment If prevention fails, treatment must follow. The more superficial the pigmentation, the better will it respond to treatment. If the hyperpigmentation originates in the dermis, it will not respond as well to treatment. It is often necessary to treat the actual inflammation that is maintaining the pigmentation. Examining the skin under a Wood’s lamp (354 nm) – also called ‘black light’ – can help determine the depth of the lesions. The more pigmented the skin appears in the Wood’s light, the more superficial is the pigmentation. The angle of the light should be varied to improve the visual accuracy of the diagnosis. Skin that looks washed out by the Wood’s light will not respond well to depigmenting treatment.31 Whatever the case may be, my first choice of treatment for epidermal or dermal post-peel PIH is always four sessions of Easy TCA® to the basal layer (pinpoint frosting) in combination with Blending Bleaching® cream. Results can often be seen after the first re-peel.

Topical depigmenting agents Monobenzone Monobenzone (Figure 37.33), also known as monobenzyl hydroquinone, benoquin and hydroquinone monobenzyl ether, has a molecular weight of 200.27 and is a stable chemical compound under normal conditions. It is not a new depigmenting molecule: the Journal of the American Medical Association published an article about it in 1956. Monobenzone is used to completely inhibit the production of melanin from tyrosine, mainly in certain severe cases of vitiligo. However, it is rare to resort to this rather extreme treatment. Doctors are, in fact, more willing to use techniques for repigmenting areas of vitiligo than techniques for complete depigmentation of normally pigmented areas.33 HO

Easy TCA® If there should be a pigmentary change after one session of Easy TCA®, the next session will ‘stop it in its tracks’ and treat it.

O

Pregnancy Cortez30 relates that if a patient falls pregnant in the first few months after a phenol peel, dyschromia disorders may

Figure 37.33 Monobenzone.

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Monobenzone34 should only be applied after attempts at repigmentation have failed and when the vitiligo makes social life difficult. Patients with severe vitiligo are happy to be one color again. However, the cosmetic risks are high: the skin becomes completely white, burns in the sun, and any hope of normal repigmentation, if for example a cure for vitiligo were discovered, vanishes as soon as monobenzone is applied. This product should never be used a simple whitening agent, at any concentration. In any event, complete depigmentation usually only develops after 6 months to 4 years, with three daily applications, and the depigmentation protocol, which is very precise, is full of pitfalls.35 The patient must also be aware that there can be permanent and complete depigmentation in areas other than those being treated; the hair can go gray, but the eyes do not change color. Nevertheless, 11 out of 15 vitiligo patients treated with monobenzone developed conjunctival melanosis; and one patient had a line of corneal pigment deposit in each eye after one year of monobenzone.36 Monobenzone can cause contact allergies37 that, oddly enough, occur mainly on areas of normal color skin and very rarely on the vitiligo patches. Fifteen per cent of patients develop skin rashes. Sun protection must be worn permanently, as the skin loses all its melanin protection. Depigmentation does not occur systematically, and some patients who respond well at first do less well later on. Others regain pigmentation in patches over the summer months. A few rare vitiligo patients repigment, sometimes fairly evenly, without the underlying mechanism being understood, when monobenzone is stopped and they no longer need to depigment. Nevertheless, there are still some monobenzone depigmenting creams on the market: they have low concentrations of monobenzone (around 1.5%). Nevertheless, some highly concentrated means at 20% can be found on the market. When applied to the hands, there have been cases of permanent, confetti-like depigmentation that has spread to the forearms.38 Monobenzone is therefore not indicated in the treatment of freckles, melasma, age spots, PIH and other dyschromias, apart from cases of severe vitiligo that resists attempts at repigmentation. Other topical depigmenting agents Conventional topical depigmenting agents (hydroquinone, kojic acid, Morus alba, arbutin, azelaic acid, lactic acid, etc.) do not destroy the melanin in the skin, but inhibit tyrosinase and the oxidative stages of the chemical reactions that turn tyrosine (Figure 37.34) into indole groups during the first stages of melanogenesis. AHAs, retinoic acid, salicylic acid, etc. increase flaking and eliminate the intraepidermal melanin stock more quickly. Corticosteroids and nonsteroidal anti-inflammatory agents combat inflammation. Topical depigmenting agents cannot be expected to produce rapid results: the active products have to penetrate the

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OH

NH2

COOH

Figure 37.34 Tyrosine. Note the resemblance to the usual tyrosinase inhibitors.

skin and change the metabolism of the melanocytes, reducing melanogenesis or changing the quality of the melanin.29 A completely new epidermis then has to be built from cell growth in the basal layer, which takes 4–6 weeks. Depigmentation is therefore gradual, and topical depigmenting agents are often combined with products that accelerate epidermal flaking. Hydroquinone Hydroquinone is closely related to phenol and can reduce melanin production. It appears that it can also degrade melanosomes. It has a tyrosinase-inhibiting activity and can change the membrane structure of the intracellular organelles of melanocytes. Hydroquinone acts mostly on the first stages of melanin synthesis. Its action is therefore gradual, like any tyrosinase inhibitor. Is it worth using preventively? Applying hydroquinone creams during the weeks before a peel reduces melanin synthesis, and the patient will slowly see a certain improvement in the hyperpigmentation, depending on how long and how potent the treatment is. However, it is not certain that the preventive application of hydroquinone before a peel can reduce the reactive potential of melanocytes during inflammation. I never apply hydroquinone before a peel for two main reasons: firstly because of the problems associated with hydroquinone itself, which we shall consider below, and secondly because of its low anti-inflammatory potential. On the other hand, it can be advantageous using hydroquinone after a peel to inhibit melanin synthesis. It should be applied as soon as possible after the peel: during the reepithelialization stage. It can therefore be applied immediately after a glycolic acid peel or Easy Phytic® solution,40 5–7 days after a peel to the papillary dermis41 and 8–10 days after a peel to the reticular dermis. The concentration normally used is between 2% and 6%. It should be noted that European legislation limited hydroquinone to 2% in cosmetic products for many years and finally banned it altogether. Concentrations of less than 4% hydroquinone are less effective. Concentrations higher than 4% are more effective but also more irritating.

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It takes several months to achieve an acceptable clinical result when hydroquinone is used as monotherapy, but abnormal epidermal and dermal pigmentation can eventually be reduced. There are reports in the literature that hydroquinone has been prescribed in high doses (up to 10–15%) to counter dramatic pigmentary changes; at these doses, it must not be applied for more than 8 days and a more conventional concentration of 3–5% should be used for the rest of the treatment. The effect is dosedependent, and it might be concluded that a high concentration is always required to get a rapid and clinically satisfactory result. However, it is important to bear in mind the problems that have been associated with the use of this agent: ■ Its action is due to its cytotoxic effect. ■ Hydroquinone is irritating to the skin. ■ It can cause ochronosis:42 the patient soon develops a blue–black patch that is not easy to treat. Ochronosis can appear even if the patient has not had a peel beforehand. Ochronosis usually appears after concentrations higher than 4% have been applied, but lower concentrations can cause it in patients with Fitzpatrick skin type V or VI. ■ It can cause confetti-like depigmentation. ■ It is potentially mutagenic. Hydroquinone has also been combined with other molecules to increase its penetration and effectiveness, as in the Kligman formulas: ■ Kligman’s original triple-combination formula:43 hydroquinone powder 5% dexamethasone powder 0.1% tretinoin powder 0.1% hydrophilic ung qs ad 60 g ■ Kligman’s four-ingredient formula: hydroquinone 2.5 g tretinoin 0.05% ascorbic acid 0.1 g dexamethasone acetate 0.05 g eucerin O/W ad 50 g (or natural unguent La Roche–Posay ad 50 g) in an opaque tube

glycolic acid hydroquinone

10% 4%

Substituting 0.1% tretinoin with 10% glycolic acid removes an irritant and potentially photosensitizing factor at the same time as enhancing penetration and therefore the effectiveness of hydroquinone. Lower concentrations have been tested successfully. Their synergy means that the concentrations of each active product can be reduced and hence their side effects are also reduced. The formula is as follows:14 citric acid lactic acid hydroquinone kojic acid

3% 3% 2% 2%

Many prescription formulas have been developed, combining, for example, vitamin C and indomethacin: hydroquinone tretinoin vitamin C dexamethasone acetate indomethacin cream O/W

All of these hydroquinone creams are still fairly irritating to the skin, and many commercial formulations have been developed with new cosmeceutical technologies that are not available in pharmacies.44 Finally, it should be noted that hydroquinone poses a serious galenical problem, as it tends to oxidize quickly: preparations containing hydroquinone have to be mixed and packaged in an oxygen-free atmosphere (in nitrogen). Preparations packaged in jars oxidize too quickly and lose most of their effectiveness within a few days. The ideal packaging for hydroquinone cream is a hermetically sealed, double-layer, aluminum tube. Kojic acid Kojic acid (Figure 37.35, also known as 5-hydroxy-2(hydroxymethyl)-4H-pyran-4-one and 5-hydroxy-2(hydroxymethyl)-1,4-pyrone, is a tyrosinase inhibitor

Other depigmenting formulas can be prescribed:

OH O

tretinoin 0.1% hydroquinone 4% ana (+ triamcinolone acetonide to combat inflammation if desired) twice daily until the local problem is resolved.30 Rubin,14 quite rightly, highly recommends the following, less irritating formulation:

5% 0.025% 0.2% 0.01% 2% ad 30 g

O

OH

Figure 37.35 Kojic acid.

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(through copper chelation and caseinase inhibition). It has been isolated from Aspergillus, Acetobacter and Pencillium species. It has antibacterial properties and reduces the production of free radicals (iron chelation). It has been used since 1988 (Japan) as a bleaching agent, for both the skin and teeth and in the food industry. It also has antiseptic and antioxidant properties. Kojic acid is more stable and better tolerated than hydroquinone, but prolonged use has caused contact dermatitis, especially on Asian skin types. It is usually used in doses 2–4%. It can be combined with glycolic acid, and enhances the penetration and action of the latter. The toxicity of kojic acid has been tested in mice: oral administration produced thyroid follicular adenomas. Kojic acid is a strong goitrogen in rodents, lowering blood concentrations in thyroid hormones and stimulating thyroid-stimulating hormone (TSH). As a result, the thyroid gland increases in volume and weight and there is diffuse thyroid follicular hypertrophy/hyperplasia. Azelaic acid Azelaic acid (Figure 37.36), also known as nonanedioic acid, 1-7-heptanedicarboxylic acid, anchoic acid, lepargylic acid and azelainic acid, has a molecular weight of 188.22, which limits its penetration through the skin. Azelaic acid is therefore more effective when it is combined with other molecules that can enhance its penetration (AHA, retinoids, etc.). It has antibacterial45 properties used in the treatment of acne or rosacea. At doses of 20% (Skinoren®), azelaic acid has tyrosinase-inhibiting properties46 through competition. Even though its tyrosinase-inhibiting activity is not as strong as that of hydroquinone, it is useful for treating melasma or PIH. It reduces DNA synthesis in hyperproliferating melanocytes in hyperpigmentation. Unfortunately, it is slow-acting (several months) and has little effect on old PIH and on deep, dermal pigmentation. Azelaic acid does not act on normal melanocytes or fibroblasts and does not cause leukodermia or ochronosis. Tests on animals show that azelaic acid is not cytotoxic, mutagenic or teratogenic.47,48

O

O H

HO

OH

Figure 37.37 Glabridin.

on melanogenesis, without affecting melanocyte DNA or RNA synthesis. It is therefore not cytotoxic. Glabridin 0.5% inhibits erythema and UVB-induced pigmentation. It also has anti-inflammatory properties through the inhibition of superoxide anion production and through cyclooxygenase activity.49 It is therefore a good indication in the treatment of PIH. Arbutin The arbutin molecule (Figure 37.38) consists of hydroquinone labeled to glucose, and is also known as hydroquinone-β-D-glucopyranoside. It mainly works by inhibiting tyrosinase activity rather than suppressing the synthesis or expression of this enzyme. Apparently, arbutin does not hydrolyze to release hydroquinone, which is not therefore directly responsible for the inhibition of melanin synthesis.50 Nevertheless, it has not been officially proved to have a strong depigmenting effect, and one study even shows that applying arbutin can increase pigmentation.51

OH

O

O

OH

O

O

OH

OH

HO

Figure 37.36 Azelaic acid. HO

Glabridin, licorice extract Glabridin (Figure 37.37) is the most active depigmenting component of licorice extract. It has an inhibiting action

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Figure 37.38 Arbutin.

OH

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4-Hydroxyanisole (4-HA) 4-HA is a cytotoxic molecule that inhibits melanogenesis (at 2%), but only seems to be effective when combined with tretinoin (at 0.01%). Used alone, it appears not to be active. α-tocopherol) Vitamin E (α Vitamin E (α-tocopherol: Figure 37.39) is one of the best antioxidants for cell and organelle membranes. It stabilizes and prevents the destruction of the lipids that make up these membranes, which are very susceptible to oxidation. It blocks the chain reactions that cause intracellular lipoperoxides to form, thus protecting the nucleic acids and proteins. It also inhibits the peroxidation of membrane arachidonic acid, which prevents the subsequent formation of pro-inflammatory prostaglandins.

HO

O

Figure 37.39 Vitamin E (α-tocopherol)

Vitamin E has a beneficial antioxidant effect during the post-peel period. One single molecule of vitamin E protects 3000 membrane phospholipids: stabilization of the lysosome membranes prevents the release of histamine, which reduces the duration of solar erythema. Vitamin E has other actions: ■ protection of the superoxide dismutase (SOD) enzyme that neutralizes superoxide radicals ■ limitation of the formation of links that make the collagen protein chains rigid ■ limitation of the production of malonedialdehyde, whose action on the glycation of proteins is linked to the aging process ■ acceleration of the healing of burns Japanese publications report that vitamin E can be used effectively in the treatment of facial pigmentation. It inhibits tyrosinase indirectly by inhibiting its hydroxylase activity. It also acts by limiting the oxidative phases required in the first stages of the transformation of tyrosine into indole derivatives. Vitamin E oxidizes easily, and more stable derivatives than pure α-tocopherol have to be used in cosmetic preparations. Tocopheryl acetate is one of the more stable derivatives of vitamin E. Tocopheryl ferulate is also frequently used.

OH

Figure 37.40 Vitamin A (retinol).

Vitamin A (retinol) It has been proved that vitamin A (retinol: Figure 37.40) and its analogs,52 used in topical applications, enhance skin regeneration by increasing the rate of keratinocyte division. Retinol induces cell differentiation in the basal layer of the epidermis and enhances apoptosis of old cells, which in turn facilitates the regeneration of healthy keratinocytes. Retinol controls cell migration in the skin epithelium; this migration is an essential stage in skin regeneration. Many different mechanisms of action have been suggested: one is that the retinol acts as a signal that facilitates the interaction of epidermal growth factor (EGF) with the cells of the skin epithelium. Retinol also modulates the transcription of certain genes. Many other effects have been attributed to retinol in topical application: it is a hydrating molecule that increases the thickness of the epidermis through selective multiplication of living keratinocytes at the expense of the keratinocytes that make up the stratum corneum. Because the stratum corneum is thinner, the skin appears softer and more hydrated. Retinol also prevents the formation of comedonal acne by preventing corneocytes from building up in the outlets of the pilosebaceous units and forming plugs. Retinol counters post-inflammatory hyperpigmentation by accelerating keratinocyte turnover, which helps eliminate epidermal melanin more quickly. Topical retinoic acid (tretinoin) has a well-known irritant effect, due to the fact that it builds up in places where it does not exist naturally in these concentrations. Pure, encapsulated retinol in cyclodextrins can be an effective replacement. In fact, pure retinol penetrates more readily than its palmitate or acetate esters. Pure, encapsulated retinol in cyclodextrin reaches the deep layers of the skin in a few hours and arrives at its target without being oxidized. Bearing in mind the stages of retinoic acid synthesis in the skin, it is clearly worthwhile to use retinol. Retinoic acid is synthesized inside keratinocytes. The retinol is first converted into retinal (retinaldehyde), which is in turn converted into retinoic acid. Both of these stages are enzyme-dependent. Retinoic acid regulates the transcription of genes that code for the synthesis of important intracellular proteins. Retinol also induces the expression of the protein that transports retinoic acid. Retinol encapsulated in cyclodextrins (Renutriv ACE Lipoic Complex®–SkinTech) has greater bioavailability and its antioxidant action is of better quality.

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OH

HO P O

O O O HO HO

OH

Figure 37.41 Vitamin C (L-ascorbic acid), in the form of ascorbyl phsophate.

Vitamin C (L-ascorbic acid) Vitamin C (L-ascorbic acid: Figure 37.41) can limit melanin production, as it has a tyrosinase-inhibiting and antioxidant activity. Skin cells naturally use ascorbic acid in energy metabolism and when synthesizing collagen. A deficiency in vitamin C is a well-known cause of many disorders, including hyperkeratotic folliculitis and delayed wound healing. Ascorbic acid is unstable in aqueous solution and is not liposoluble. It oxidizes rapidly, losing its protective properties, and more stable derivatives are generally used. Magnesium ascorbyl phosphate is one of the most stable and hydrophilic vitamin C derivatives. On the surface and inside the skin, it is rapidly converted into vitamin C by a phosphatase enzyme found in abundance both on and inside the skin. Magnesium ascorbyl phosphate is a more effective antioxidant and longer lasting than the derivative ascorbyl palmitate, often used in topical preparations. This is because the enediol function53 of the second carbon atom of ascorbyl phosphate is protected, while the palmitate derivative has no protection for this area of the molecule, which is responsible for the acid and antioxidant properties of vitamin C. Magnesium ascorbyl phosphate can be used on the most sensitive skins, such as skin that has just benefited from a peel. It is readily absorbed by the topical route and lasts for a long time inside the skin, which gives it a sustained tyrosinase-inhibiting action and therefore a lightening and depigmenting effect. Topical vitamin C (Purascorbol aesthetic dermal) also has an antiaging effect that works in different ways: ■ It modulates the three genes responsible for the synthesis of procollagen leading to an increase in type III collagen synthesis. This action is very important for post-peel healing and maintaining normal skin structure. ■ It is a cofactor of prolyl and lysyl hydroxylase enzymes in the first stages of collagen synthesis; these are necessary for the inclusion of proline in collagen. ■ It takes part in elastin synthesis. ■ The antioxidant effect of vitamin C provides protection against the harmful effects of UV rays.

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■ It protects vitamin A from oxidation and prevents protein chains from breaking. ■ It has a protective action on other antioxidant systems, which is beneficial in situations where free-radical production is increased (e.g. during post peel oxidative stress). This is also the case with infected or uninfected wounds and areas exfoliated by peels or other abrasive or resurfacing techniques. ■ It enhances re-epithelialization. Morus alba (mulberry or white mulberry) extracts Mulberroside F (also known as 3′-di-O-β-D-glucopyranoside and moracin M-6), extracted from mulberry leaves, inhibits tyrosinase activity, in the conversion of dopa (3,4dihydroxy-β-phenylalanine) into dopachrome (dopa oxidase activity). This tyrosinase-inhibiting activity has been measured as 4.5 times more powerful than that of kojic acid.45 Mulberroside F also has an antioxidant activity on the superoxide anion. AHAs The melanogenesis-inhibiting properties of lactic acid and glycolic acid have been shown55,56 in the treatment of melasma as well as solar lentigines and PIH. The mechanism of action not only lies in the faster dispersion of pigments in a more rapidly renewed epidermis, but also in the inhibition of tyrosinase activity. This inhibition has no relation to the acidity of these products, as studies show that tyrosinaseinhibiting activity is constant, even below pH 5.6. Important observations on the use of topical depigmenting agents One of the explanations for the failure of depigmenting treatments is that they are often applied extremely locally, to the hyperpigmentation itself, whereas they should be applied evenly to the whole face in the morning, for example, and again in the evening on the hyperpigmentation alone.

Sun avoidance Complete sun avoidance can by itself resolve many hyperpigmentation problems within 6–18 months. See also Chapter 3.

Local corticosteroids When a peel causes localized inflammation that visibly develops into hyperpigmentation, even with sun protection and avoidance, a corticosteroid (preferably a fluorocorticosteroid) should be applied. It should be applied twice a day locally to the erythema before it develops into hyperpigmentation and should not be used long term (1 week at the most), to avoid the side-effects associated with corticosteroids. This treatment should of course be combined with sun protection/avoidance measures and a topical depigmenting agent.

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Scarring Unlike pigmentation problems that are common after many peels, scarring is fortunately a rare complication. Some areas of the face are more sensitive. Scars can arise directly from excessively deep, chemical destruction of the dermis57 or can be the ‘logical’ result of neglecting a sign – for example, ignoring and not treating persistent erythema properly. Treatment needs to start as soon as possible: as soon as scarring seems likely, as a stabilized scar is unfortunately a permanent scar. The deeper the peel, the more effective it is, but also the more dangerous. A deep peel, when performed correctly, produces exceptional results in the majority of cases. I have never come across any report of complete facial necrosis after a peel. Fortunately therefore, the problem remains localized. Scarring can be atrophic, hypertrophic or retractile, depending on the depth of the burn and the area treated. To have a better understanding of the risk of post-peel scarring, we must take another look at the physiology of skin healing.

Brief chronology of healing Initial phenomena The process starts almost immediately: neutrophils enter the treated area during the peel and stay there for 3–5 days. Macrophages are present from day 3 to day 10 and lymphocytes from day 6 or 7.

Re-epithelialization This starts 24 hours after the peel and begins with centripetal keratinocyte migration followed by accelerated cell proliferation. It should be effective within a week – that is, protect (partially, as there is only one layer of cells) the dermis.

Collagen regeneration After re-epithelialization, dermal collagen is regenerated over a 2- to 3-month period.

Various facts about post-peel healing Open healing is slower than when the re-epithelializing wound is covered. This does not matter for intraepidermal peels, as the dermis is still covered by several layers of living and protective keratinocytes. On the other hand, when it comes to medium or deep peels,58 this is of major importance. Peels have an advantage over laser or mechanical abrasive treatments in that they leave a layer of skin in place. This layer of skin is of course dead, but it offers pro-

tection against external aggressions and enhances reepithelialization. The strips of skin that survive after a medium or deep peel should therefore be left in place, as they protect the regenerating skin. Lasers gradually vaporize the layers of skin to be eliminated, and if it were not for colloid dressings, the skin would have to heal in the open. The colloid dressings on the market (Convatec®, Omniderm®, Vigilon®, etc.) allow better-quality healing in a moist environment after laser treatment. Totally occlusive dressings (including Vaseline®) carry an increased risk of infection and have to be monitored actively, as bacteria proliferate far more rapidly under occlusion than in the open air. Because of the increased bacterial proliferation and the skin’s lowered immune defenses after a medium or deep peel,59 it is preferable to use a moist healing method after a phenol peel. A mask of bismuth subgallate or thymol iodide is used for this after a phenol peel (see Chapter 35). Post-peel hydration is also important. The skin should not be allowed to dry out while it is re-epithelializing after a medium or superficial peel; it needs to be hydrated. Proper hydration prevents pruritus and delayed healing.60 Hydration after a deep peel is essential after the first week. Sterile white Vaseline® is an excellent topical that can be applied to treated areas: ■ during the first few days after a peel to the papillary dermis ■ after the healing mask has been removed (from the 7th–8th day) after a phenol peel. Only a thin layer of Vaseline® need be applied to stop any pruritus triggered by surface keratinocytes (that have not yet differentiated into corneocytes) drying out. Vaseline® creates an impermeable layer on the surface of the skin and prevents water evaporating from the epidermis (TEWL: transepidermal water loss). Water accumulates under the layer of Vaseline® and provides immediate natural hydration that soon relieves the pruritus caused by the keratinocytes drying out. Patients on whom Vaseline® is applied should be monitored particularly closely, because of the increased risk of secondary infection under occlusion. Aloe vera extracts appear to accelerate healing after dermabrasion, but have the disadvantage of potentially causing contact allergies. The use of antioxidant creams may also be indicated during the first few weeks after a peel (Renutriv ACE Lipoic Complex®–SkinTech).

Risk of scarring depending on the molecule used AHAs When an AHA peel is strictly intraepidermal,61 the risk of scarring is non-existent, as there is no phenotypic conver-

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sion of fibroblasts into myofibroblasts (see above). During the 1990s, when the use of AHAs in cosmetic medicine first took off, women’s magazines carried reports of real disasters with gruesome photographs. At the time, a patient gave me a copy of a popular German magazine62 (Brigitte – 19/95: 62–8) that told the story of a journalist who, out of professional conscientiousness (or curiosity?), decided to test a peel of 70% glycolic acid in simple aqueous solution in a reputable cosmetic surgery clinic. After a few months of preparation with tretinoin,63 the doctor quickly applied several coats of 70% glycolic acid and left his nurse to take charge of the immediate follow-up. According to the journalist, the peel was not neutralized, but simply rinsed with water64 several times, even though the patient complained of persistent burning. The eyes also had to be rinsed, as the copious amounts of water used on the face had carried the acid into the conjunctival cul-de-sacs. The patient went home and the doctor left on vacation the very same day. The next day, alarmed by the condition of her skin, the patient wanted to see the doctor and, as her surgeon was away, saw one of his colleagues, who was of course horrified to see that a product as strong as an AHA at 70% had been applied on such lovely skin. The danger was so great that he had to prescribe manual lymphatic drainage! Other colleagues told the patient that ‘it would last for years’. The article goes on to say that three months later not all the after-effects had gone, but it omits to describe the state of the skin, and the results of a single AHA peel obviously is little. The journalist concluded that she would never again let herself be treated with any acid whatsoever, given the ‘daily horror’ she had to live through after trying the lightest one. This is confirmation once again that a thorough knowledge of the techniques, together with a high degree of professional conscientiousness, is essential to avoid problems and that any peel, even a superficial one, can cause complications.

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A

TCA Publications often present this molecule as being the most likely to penetrate too deeply and cause scars. Books and journals about peels are full of photographs of complications and scars resulting from peels with TCA–SAS (Figures 37.42 and 37.43).7 According to Litton7 and Stone,65 ‘deep’ TCA has a natural tendency to cause hypertrophic scars. In reality, it must be used in accordance with precise rules, and practitioners must be aware of and respect its symptomatology and TCA should never leave any scars. The risk of scarring after a TCA peel is linked to the acid penetrating too deeply. The total quantity of TCA applied to the skin during a peel determines the depth of the peel. This quantity depends (among other things) on the concentration of the solution and the number of coats applied. Applying a highly concentrated TCA peel means that a lot of acid goes

B

Figure 37.42 (a,b) A scar probably due to uneven application of TCA–SAS, 50% m/m.

into the skin in one go and it is impossible to control the depth. The more concentrated the TCA is, the more deeply it penetrates. One of the major problems stems from the fact that the concentration is calculated in different ways in different parts of the world: although percentages are

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Figure 37.43 Scarring after TCA in aqueous solution of unknown concentration: probably 50% m/m.

always given, a concentration in mass per mass (m/m) is not the same as in mass per volume (m/v) or mass plus volume (m+v).66 The m/m concentration is the strongest. At equal concentrations, the more coats that are applied, the deeper the peel, as each coat that is applied soaks the skin in a little more TCA, which will combine with more proteins and destroy other cells. The risk of scarring is also linked to the thickness of the skin. The thinner the skin, the more deeply will the TCA penetrate; the thicker the skin, the less it will penetrate. Nevertheless, scars do not only form where the skin is thinnest. On the contrary, they can also form in areas where the skin is thicker, with areas of thin skin remaining scar-free. These ‘paradoxical’ scars can often be explained by an intentionally ‘forceful’ application on an area that is mistakenly believed to be more resistant and in an attempt to get better results. Dry skin allows TCA to penetrate more rapidly and more deeply than hydrated or oily skin, which is usually thicker than dry skin. Skin lipids deactivate TCA and wellhydrated skin dilutes it. TCA that penetrates well-hydrated skin encounters more water than it does when it penetrates dry skin. The more aggressively the skin is prepared, the more permeable will it be and the TCA will penetrate more rapidly: caution must be observed with regard to pre-peel

degreasing and disinfecting, which abrade the skin and which are not recommended for all peels. Patients should be questioned before a peel to find out if they regularly use products on their skin that reduce the thickness or impermeability of the stratum corneum (AHAs, tretinoin, benzoyl peroxide, salicylic acid, etc.) The type of applicator also plays a role in determining the depth of penetration of the acid: gauze abrades the skin as the acid is applied and promotes quicker and deeper penetration, while a brush spreads the TCA on the stratum corneum without enhancing penetration and therefore produces a more superficial peel. TCA penetrates more readily where the skin has been damaged. TCA–SAS should therefore not be applied immediately after hair removal, coagulation of telangiectasias, a session of mesotherapy, filling wrinkles, etc. Easy TCA® is not a simple aqueous solution of TCA, but rather a ‘tamed’ solution that can be applied safely after the treatments listed above. An aqueous solution of TCA is unstable; a tamed solution67 is far more stable and penetrates more evenly. The risk of scarring after a TCA peel is also linked to the quality of the care surrounding it. Apart from some serious cases, scars do not form immediately, but are preceded by prolonged local erythema and/or infection that should be diagnosed and treated appropriately. Many problems (see below) can be avoided by proper patient selection, and post-peel monitoring can limit others. Scars usually – but not always – occur in patients with dry and thin skins that have been treated with too much TCA–SAS with an inappropriate concentration or quality and when monitoring and post-peel care have been neglected or inadequate. They can also occur in patients with thicker skin, with a history of hypertrophic scars.

Phenol It is reported that, at the same depth of injury, phenol causes fewer problems with scarring than TCA.68 According to Fintsi,69 the Exoderm® formulation is ‘self-blocking’: it somehow recognizes the reticular dermis and stops its action there. Other new formulations (e.g. Lip & Eyelid®) have this advantage. Although some phenol peels with rather exotic or inappropriate protocols have produced scar reactions, certain current phenol peel formulations are less aggressive, kinder to the skin and just as effective. The fact that the phenol automatically stops acting at the reticular dermis should be treated with caution: it cannot be safely assumed that a phenol formula will stop in every case right at the most superficial part of the reticular dermis, even if technically phenol is self-blocking, as it neutralizes itself by combining with proteins. We still do not know at which depth it is completely neutralized! Our ‘self-blocking’ also depends on the total amount that was applied in the skin.

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General prevention of scarring Patient selection Special care should be taken with patients who have extremely thin, dry or sun-damaged skin, as the acids penetrate this very permeable skin more quickly and more deeply and the skin can sometimes overreact. Careful anamnesis will reveal any personal or family history of keloids or any tendency to scar hypertrophy. Insulindependent diabetics should be ruled out from a peel to the reticular dermis (because of the increased risk of scarring and infection), whereas diabetic patients (type 2, noninsulin-dependent) who are stabilized on oral antidiabetic drugs can have a deep peel on condition that they are monitored more closely than usual.

Ehlers–Danlos syndrome It would be more appropriate to talk of Ehlers–Danlos syndromes,70 as this is a heterogeneous group of connective tissue disorders, a ‘diffuse hereditary’71 disease, of which to date ten groups and different subgroups have been identified. Paganini is suspected to have suffered from it.72 Types I to IV and type VIII can be diagnosed clinically, while types VI, VII, IX and X require laboratory diagnosis.73 The different subgroups are characterized by deficiencies at different levels: there are mutations of genes coding for type I or III collagen or for certain enzymes.70,74 In certain subgroups (VIIC), electron microscopy shows that the collagen is laid down in sheets rather than fibrils and takes on a hieroglyphic pattern.75 The incomplete or light forms of the syndrome are certainly more common than reported in the literature71 and some authors suggest a worldwide incidence of 9% of the population.68 It typically manifests as fragility and hyperelasticity of the skin and joint hypermobility. The skin can be stretched further than normal skin and returns to its original state when let go. Minor traumas cause disproportionate loss of substance and atrophic, parchment-thin scarring. The skin eventually loses its elasticity, and its appearance resembles ‘cutis laxa’ – loose, hanging and wrinkled. From a clinical point of view, the coexistence of at least two of the following symptoms should arouse suspicion:76 ■ ■ ■ ■ ■ ■

skin hyperelasticity joint hyperlaxity frequent bruising atrophic scars or pseudotumors calcified subcutaneous cysts family history of the syndrome.

A depressed nasal pyramid and prominent paranasal folds change facial morphology; the skin is hyperelastic and can sometimes hang on the face.77 It is especially important to be aware of this syndrome and try to detect borderline

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cases in patients wanting rejuvenating techniques. Surgeons should be particularly wary because of the possibly fatal vascular complications.78,79

Treatment with isotretinoin Patients who have used isotretinoin (13-cis-retinoic acid, Roaccutane®) or other more recent retinoids during the previous year or are going to use it within the next 12 months should be ruled out from medium or deep peels. Some authors even suggest leaving a gap of 2–3 years between isotretinoin and a peel, as this product: ■ ■ ■ ■

destroys the sebaceous appendages inhibits the expression of collagenase inhibits procollagen production inhibits cell growth and delays wound healing

Delayed re-epithelialization exposes the damaged skin to mechanical injury as much as physical injury and infection, and there is a risk of hypertrophic, star-shaped scars on the cheeks that can form months after a peel has been carried out too soon after isotretinoin. Patients whose skin has been significantly changed by isotretinoin and who still complain of dry or fragile skin should not be given any type of peel.80 It is absolutely vital to wait for the skin to heal completely with restitutio ad integrum before performing any kind of peel, even if it takes years. Common sense dictates that it is better to live a few more years with wrinkles than live the rest of one’s life with scars. Intraepidermal peels or peels to the basal layer theoretically do not pose such a serious risk, as regeneration does not rely on the fibroblasts or skin appendages. The problem in this case lies in increased skin permeability, which could deepen the action of the acids. AHAs and TCA in aqueous solution should be considered likely to cause scarring in combination with isotretinoin.

Skin preparation Skin preparation must be even, suitable to the skin type and not excessive. Some peels are only really effective after several weeks’ of skin preparation (TCA–SAS), whereas for other products (Exoderm®, Easy TCA® and Lip & Eyelid®) pre-peel preparation is pointless, and in some cases any pre-peel preparation is contraindicated (Easy Phytic®82). If preparation is too rough, the skin will be too permeable to the acids – overall and locally. Results might sometimes be better, of course, but if preparation is too aggressive, the safety factor is reduced. It is essential to follow the instructions provided with each formulation and each technique. They are based on the experience and errors of their authors and help avoid pitfalls and accidents.

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Avoiding injuries ■ Except in cases where the doctor wishes to increase the depth of peel penetration intentionally,83 patients must be warned not to use ‘exfoliating scrubs’ on their skin during the days before a peel. If the patient uses an exfoliating scrub, or a ‘home-peel’, as it is known for marketing purposes, it may be uneven and enhance penetration of the acid locally. ■ Secondary infections must be avoided: close post-peel monitoring is necessary. ■ Premature re-peeling should be avoided: a re-peel should not be done if re-epithelialization is not complete. ■ A full face deep peel should not be done at the same time as a face-lift; however, it is possible to do a chemical cheiloplasty84 or a chemical blepharoplasty at the same time as a surgical face-lift, for example. ■ Scratch lesions should be avoided.

Persistent localized erythema As we have seen earlier in this chapter, persistent localized erythema (especially in high-risk areas) is more often than not a sign of dyschromia rather than scarring. Indurated erythema poses a risk of scarring more than PIH.

Specific prevention depending on peel type AHAs AHA peels are superficial peels that do not have a natural tendency to cause scarring. If the doctor himself monitors the peel and the neutralization stage as usual, in principle there is no chance of scars forming. If the peel is neutralized as soon as erythema appears, there is no risk of scarring. A peel that is neutralized too late, however, can cause scarring. Neutralization (acid + base) should not be confused with dilution (acid + water). Dilution is not always enough: the recommendations given in the protocol for each particular product must be followed.

Easy Phytic® solution Easy Phytic® solution (see Chapter 11) is a slow-release and self-neutralizing mixture of fruit acids and phytic acid (pH <1). The peel solution can only be applied on an intact stratum corneum, where it will concentrate and gradually be released. The gradual penetration of the acids does not overwhelm the skin’s buffer capacity.85 Any prior treatment likely to accelerate or increase penetration of the acids could overwhelm the skin’s buffer capacity and cause problems. There have been no reports of scarring to date, and

Easy Phytic® can be considered extremely safe as far as scarring is concerned.

TCA–SAS TCA penetrates very rapidly through the skin. If it penetrates too deeply, it is often too late before it is noticed, and surface neutralization is not enough to reverse the caustic, scarring processes triggered deep down. In reality, TCA is only partially neutralized, even if base solutions are applied immediately: only the excess TCA on the skin surface can be neutralized. In high-risk areas or on thin and permeable skin, it is therefore recommended to use lower concentrations of TCA and to apply the product less vigorously (cf. choice of applicator). Care should be take to avoid any inadvertent drips of TCA86 or the acid stagnating in the base of deep wrinkles: there is a risk of linear overpeeling, traces of which can remain visible for many months or even be permanent in cases of large excesses. Scars can be avoided by not using TCA to reach the reticular dermis, apart from focal treatments (Only Touch®).

Easy TCA® Easy TCA® consists of a base solution and a post-peel cream. A specific quantity of TCA in aqueous solution at 50% m/m must be added to the base solution to activate it. Using the basic protocol (i.e. to pinpoint frosting only), prevents any risk of scarring, as the peel only reaches the basal layer of the epidermis. Moreover, applying the postpeel cream limits or stops the immediate post-peel inflammatory reaction. If the application procedure is followed correctly, there is no risk of overpeeling and no risk of scarring. Care should be taken not to use the aqueous solution of TCA 50% m/m as it is, without mixing it with the adjuvant, base solution. There is no doubt that applying an aqueous solution of TCA 50% m/m directly to the skin carries a high risk of scarring. This error has been made several times,87 but if the doctor follows the recommended application technique, he will notice that with 50% m/m TCA, an unusually intense and rapid frosting appear on the forehead and the patient will feel an intense pain; the doctor will stop the application before starting to treat the more sensitive areas of skin, where the risk of scarring is greater. As we have already seen, the skin on the forehead is more resistant to chemical injury. If this wrong concentration is used, applying plenty of Easy TCA® post-peel cream immediately after washing the skin with copious amounts of water will limit the injury and prevent serious complications in the majority of cases.

Only Touch® Only Touch® consists of a base solution whose qualitative formula is based on that of Easy TCA® and to which

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a specific quantity of TCA in aqueous solution at 80% m/m must be added. The 80% aqueous solution, which is very aggressive, cannot of course be applied directly to the skin at the risk of penetrating too deeply and causing permanent scarring. Following the application procedure is absolutely essential: Only Touch® is dabbed quickly88 on lentigines and keratoses of less than 1 cm in diameter. Treating larger areas rapidly increases the risk of scarring. It is easy to avoid scarring if the following rules are observed: ■ Be careful not to apply 80% m/m TCA directly to the skin. ■ Touch the area to be treated quickly and precisely. ■ Achieve pure white frosting and not gray–white. ■ Avoid any excess solution (drips, runs). ■ Monitor any persistent erythema and treat it.

Phenol Phenol solutions must be made up rigorously; any small variations in preparation causes unwanted local or systemic effects. Baker–Gordon solution is unstable. Applying phases of different concentrations to different areas of the face can be avoided by shaking the solution constantly throughout the whole peel procedure and keeping the solution homogeneous. If the solution is not shaken, it can produce an uneven peel: undertreated areas will be next to overpeeled areas, where scars might form. For this reason, it is preferable to use formulas that remain homogeneous (Lip & Eyelid®). When an occlusive mask is used, it should be applied evenly, without air bubbles or excessive pressure: ■ If there are air bubbles in the occlusive dressing, the phenol cannot macerate evenly, and some areas will be undertreated, whereas if the occlusive mask is too tight, scars can form where the severe edema that develops in the first few hours after a phenol peel causes too much local pressure. ■ The occlusive mask does not usually go under the jaw, as the movements and traction to which the dressing will be subjected will cause the same phenomenon as described above. ■ The patient must be closely monitored, as bacterial, viral or fungal infections can develop unnoticed over the days after a phenol peel. ■ Any pruritus should be treated to avoid scratch lesions, a source of scarring. ■ The application protocol recommended with one type of peel formula cannot necessarily be used with another. Nevertheless, although phenol is a deep peel, it

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does not cause scarring as readily as TCA at the same depth. ■ Applying Vaseline® as occlusion after phenol is just as effective as a dressing, and does not carry the risk of air bubbles or areas of pressure. However, Vaseline® increases the risk of infection and rules out any touchup the day after the peel.

Treating scars ■ It is better to prevent scars than treat them. ■ The results will be better if treatment is started quickly. ■ It is a mistake not to aggressively treat developing scars.

Ectropion The first case of ectropion after a peel was described in 1984,89 and surgical correction was successful. No doubt there are other previous cases that have not been published or that I have not heard of. Severe cases have also been reported90 after eyelid peels; however, ectropion is not a specific complication of deep eyelid peels. Ectropion can also be a complication of: ■ Surgical treatment: it is in fact the most common complication after surgical blepharoplasty. Particular care should be taken when doing a peel if the patient has a history of blepharoplasty and even more so in cases of multiple blepharoplasties. Patients with lagophthalmia should in principle be ruled out from deep peels, although some cases can be treated cautiously. ■ Various cosmetic treatments: ectropion can occur after deep peels with TCA or phenol and after laser treatment or mechanical abrasion. ■ Systemic medication: 5-fluorouracil (5-FU) by the systemic route can cause ectropion. A case of ectropion that occurred after topical application of 5% 5-FU has been described.91 The complication was bilateral and resolved when treatment was stopped. ■ Topical treatments: the appearance of ectropion after long-term treatment with tretinoin has been described. In this case, it is reversible when treatment stops. Prevention of ectropion If ectropion seems to be developing: ■ A flexible silicone dressing that will resist the pull of the scar should be applied (Figure 37.44). ■ A strong corticosteroid should be rubbed gently and slowly into the affected area. ■ Corticosteroid injections in situ may prove effective.

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Figure 37.44 Silicone sheets: (a) Mepiform®. (b) Mepitel®.

Prevention and treatment of scars Strong, topical corticosteroids should be applied, twice daily, very locally. A self-adherent silicone dressing (Silastic® or Mepiform®/Mepitel®92: Figure 37.44) should be worn 24 hours a day that adapts to the curves of the skin and does not pull away growing cells when the dressing is changed. Corticosteroids (e.g. Celestone®–Depomedrol®) can be infiltrated. The injection technique is important: ■ Location: the corticosteroids must be injected into the scar tissue itself and not in the tissue surrounding the scar. Not only is an injection underneath or beside the scar ineffective, it can also cause fat atrophy underneath or beside the scar that would make it more obvious. ■ Frequency: two injections should be given per month, with gradually increasing doses until the scar goes. The scar should become soft and non-adherent. Scars often respond well to this treatment within 1 month. If no treatment seems to be working and the scar is permanent, there are a few solutions: ■ surgical excision combined with a preventive silicone pressure dressing to avoid local recurrences – as for ectropion, Litton and Trinidad7 recommend simply waiting for a few months instead of rapid surgical excision ■ laser treatment ■ concealing with special camouflage make-up (e.g. Cover Mark®)

The prognosis is much better if the scar results from overpeeling (technical error) rather than the nature of the skin itself (e.g. with Ehlers–Danlos syndrome). A technical error can be put down to experience, and there is no reason why it should happen again during a repeat peel. If the scarring results from the patient’s genetic make-up, she or he should not be given another peel.

Secondary infections Skin that has just been treated with a peel93 is more prone to all types of infection, as it can no longer rely on its different defense mechanisms being intact. The risk mainly depends on the depth of the peel and how carefully it is applied. However, other factors come into play. Secondary infections rarely cause major problems, and do not really leave scars if treatment is started in time. Infections are most often local, but can become generalized in some serious cases or after a peel to the reticular dermis.

Risk of infection depending on peel type Peel to the epidermis and basal layer:94 very low risk One of the skin’s defenses against infection is ‘neutralized’ by all peels: the destruction of the stratum corneum makes the skin more permeable to microorganisms. The cells of the stratum disjunctum – the outermost cells in normal

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skin – are shed regularly and take with them a large amount of microbial fauna. This desquamation, which is a natural drainage route for the skin, cannot take place immediately after a peel, as the epidermis tends to keep its cells in order to regain its normal thickness and form a physical barrier to microorganisms. Without regular desquamation microorganisms that have managed to penetrate through the skin’s first line of defense cannot be physically eliminated. The majority of the skin’s immune defenses are found in the deep layers of the epidermis and dermis. An intraepidermal peel lets in many xenobiotic microorganisms, but all of the skin’s defenses remain viable and usually stop any local infection from developing. After an intraepidermal peel, skin regeneration is very rapid and there is not really enough time for infection to set it. Intraepidermal peels are usually repeated once a week or every 2 weeks. Each intraepidermal peel stimulates the skin’s regenerative capacities, and the skin finds it more and more easy to resist infection. Therefore, these peels do not increase the risk of infection (or only very little). The risk of herpes is not increased.

Peel to the Grenz zone:95 fairly low risk The risk of infection increases with the depth of action of the acids: the absence of the stratum corneum explains the increased penetration of microorganisms; the destruction of many of the skin’s immune defenses gives more freedom to microorganisms to grow. However, the epidermal barrier is still partially effective;96 the dermal barrier is completely active and even stimulated. Apart from scratch lesions that can develop into very localized infections, a peel to the Grenz zone is not particularly dangerous as far as infection is concerned. If an infection should develop after a peel to this depth, a topical antibiotic is usually enough to control it. Easy TCA® applied to pinpoint or cloudy white frosting causes virtually no infections, apart from a few potential transient infections of scratch lesions (the frequency is around 1 in a 1000).

essential to take all necessary precautions to avoid, prevent and/or treat any infection.

Peel to the reticular dermis:98 very significant risk The skin no longer has any physical or immune defenses, and is at the mercy of any microbe attack. The patient’s health depends entirely on the hygiene measures taken during the peel and on the quality of post-peel care. Secondary infections can be local, loco-regional or general. They can be bacterial, fungal or viral.

Secondary bacterial infections Local and loco-regional bacterial infections Local and loco-regional infections occur in cases of local overpeeling99 above all or after scratch lesions (Figure 37.45). Although peels to the papillary or reticular dermis are more likely to become infected, infections can nevertheless develop after a more superficial peel. Fortunately, serious local infections are rare, as the peeling agents, especially phenol, are germicidal.100 Moreover, the skin on the face is rich in blood vessels and has effective defenses against infections. With age, however, there are fewer blood vessels in the face and the skin becomes more susceptible to external aggression. Infections seem to develop more readily and are more serious when peels are performed in a hospital setting, because of the presence of multiresistant strains. I am fortunate enough not to have any dramatic photos of post-peel infections to show, but many cases of secondary infection and scratch lesions from streptococci, staphylococci and Pseudomonas have been

Peel to the papillary dermis:97 significant risk The acid puts the majority of the skin’s immune defenses out of action. The doors are wide open to microorganisms (there is no stratum corneum or epidermis): they are no longer eliminated by the continual shedding of dead cells, and the immune system cannot fight against them. The acids have burned the Langerhans cells and other defenses in the papillary dermis, and the skin is waiting for its immune defenses to be renewed. The risk of infection is significantly higher than with a peel to the Grenz zone. It is

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Figure 37.45 Secondary infection: scratch lesions after Easy TCA®.

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described in the literature.68 The result of following rules will allow you to perform secure peelings with a very low infection rate. Pruritus must be treated rapidly to prevent infections. Deep peels, to the reticular dermis, obviously pose a particular risk of secondary infection during the first week after treatment. Conventional care often includes the application of an antibiotic cream or ointment. This local antibiotic cannot be applied in superimposed layers, and patients should wash their skin before applying a new layer of antibiotic. Cleaning the skin is a problem in itself, as it may injure the extremely sensitive skin and is often painful. As a result, patients do not always clean their skin before each new application, and put one layer of ointment on top of another. After a few days of maceration, it is almost inevitable that a secondary infection will develop. Other patients clean the skin too vigorously before each application of antibiotic: the regenerating skin gets damaged, severe inflammation is maintained and secondary infections develop more readily. The antibiotic ointment should therefore be cleaned off carefully and evenly, using a showerhead to gently spray tepid water directly onto the skin. The skin can be degreased with a gentle cleansing lotion before showering. Using a ‘powder mask’ (bismuth subgallate or thymol iodide) during the first week after a peel to the reticular dermis (Lip & Eyelid®) limits or even prevents secondary infections – not only because of the properties of the powder itself, but also because the patients have absolutely nothing to do themselves: they will not have to touch the skin directly and therefore cannot import any infectious agents (Figure 37.46). The powder protects the skin from external aggression and from microorganisms in particular long enough (6–7 days) for the skin’s defenses to be suffi-

ciently restored by the time the powder mask is removed. I have never come across any infection when using this ‘dry’ technique, while I have often met with small infections when using antibiotic creams.

General bacterial infections: toxic infections A few cases of toxic shock were reported after facial peels with Baker’s solution in 1982, 1983 and 1987 and after rhinoplasty in 1983. Todd and colleagues described the first cases of toxic shock syndrome in 1978 as a result of the use of certain tampons. It appears to be caused by an enterotoxin F and/or exotoxin C with the same molecular weight (22 000), secreted by Staphylococcus aureus. Other authors suspect that the two toxins are really one and the same.101 Symptoms The following symptoms should alert the practitioner: ■ a temperature over 39°C in the first 2–4 days after a medium or deep facial peel; the patient’s temperature may, however, rise slightly and innocuously (37–38°C maximum) in the first 12 hours after the peel In cases of toxic shock, other symptoms follow the rise in temperature: ■ ■ ■ ■ ■ ■ ■ ■

skin rash low blood pressure (systolic <90 mmHg) vomiting and diarrhea muscle pain mucous membrane infection kidney damage liver damage hematological problems (anemia or thrombocytopenia) ■ damage to the central nervous system Treatment Treatment is aggressive and requires hospitalization. Patients should be taken to hospital as soon as there is any suspicion of toxic shock (raised temperature) and before any other symptoms appear. The symptoms of infection are often hard to spot: there was no visible sign of infection beneath the thymol iodide powder before the start of toxic shock described in the 1980s after a phenol peel (Baker’s solution). Toxic shock syndrome can come like a bolt from the blue. In the cases described, the skin recovered normally and no scars were left after recovery.

Figure 37.46 Protective mask of bismuth subgallate powder after treatment of wrinkles on the upper lip with Lip & Eyelid® formula.

Prevention of bacterial infections Intraepidermal peels to the basal layer or the Grenz zone do not require such stringent precautions as deep peels, and

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treatment can be monitored as normal. There should be no particular problem with infection with this type of peel. Deeper peels require more attention.

General precautions for deep peels ■ A basic precaution is surgical sterilization of everything that comes into contact with the patient. ■ Any staff with a microbial infection should be kept out of direct contact with the patient and, in cases of ear, nose and throat (ENT) infections, should wear a mask. ■ Patients should be ruled out from treatment if: – they have an active infection in the area to be treated with a deep or medium peel102 – they have an ENT infection – they have insulin-dependent diabetes – they are immunodeficient The peel solution is usually applied with a swab or cotton buds. The skin should never be touched with the bare hands during or after the peel.

Special precautions for phenol peels The phenol solution is ‘rolled’103 onto the skin with a cotton bud soaked in the product. If the doctor makes the applicator himself, he should check that his hands are sterile beforehand. It is difficult to make this rolling movement with gloved hands, as the glove can wind around the applicator and make application awkward, or even dangerous. Only the left hand should be gloved, and the right hand should be surgically disinfected and not come into contact unnecessarily with the skin. Infections are more common with the ‘moist’104 healing technique than with the ‘dry’105 technique. The drawback to using creams when the epidermis is regenerating is that skin debris builds up and forms a base for the infection underneath the occlusive layer. The

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advantage, however, is that it is possible to see how the epidermis is progressing during the first week, which is not possible with an occlusive mask of thymol or bismuth. If practitioners prefer the ‘moist’ technique, they should prescribe an antibiotic cream, preferably without corticosteroids, and bear in mind the possibility of contact allergies. Patients have to wash their skin under a showerhead four times a day to get rid of the skin debris and then apply a new layer of antibiotic cream (e.g. bacitracin). Special care must be taken not to damage the growing epithelium. Not cleaning the skin properly has led to alarming secondary infections from Pseudomonas,106 in the form of pyoderma. Proper debridement and cleaning together with appropriate antibiotic treatment stop this infection.

Treating bacterial infections It is enough to proceed logically: topical or systemic antibiotic treatment should be used. A bacteriological sample should be taken before any treatment in order to make a culture and an antibiogram. Treatment should start before the results of the culture arrive.

Small, localized infection If the patient does not have a temperature, they should be treated with local antibiotics. In the particular case of phenol used in combination with a ‘dry’ healing technique, topical antibiotics can be applied directly onto the powder mask. The powder will come away (not a serious consequence) and the epidermis will be laid bare. A ‘moist’ technique should then be used locally.

Loco-regional bacterial infection Figure 37.47 shows a case of loco-regional infection beginning at the end of the occlusive regeneration phase of a fullface phenol peel. The patient did not have a temperature, but

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Figure 37.47 (a) Acneiform dermatitis on the neck, 7 days after a full-face phenol peel: a sign of skin infection. (b) After 13 days, the acneiform dermatitis has been cured with oral antibiotics.

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had numerous painless, papular lesions on the neck. Oral antibiotic treatment cleared the problem up in a few days.

Post-peel acneiform dermatitis Post-peel acneiform dermatitis occurs readily under a greasy ‘dressing’ (e.g. Vaseline®), and should be treated with oral antibiotics. It clears up in 6–8 days.

Suspected toxic shock The patient should be hospitalized immediately.

Secondary herpes infections Secondary herpes infections are very widespread107 and the risk of ‘waking up’ the virus is very real, especially for peels to the papillary dermis.

Risk depending on peel type Peel to the epidermis or basal layer The risk of herpes activation is minimal.108 The skin is not badly injured and its defenses are still strong enough. AHA, Easy Phytic® or Easy TCA® peels can therefore be carried out – no further than the basal layer – without any fear of a herpes outbreak. Peel to the Grenz zone Depending on how prone the patient is to herpes, valaciclovir can be used to prevent it. Patients who say they have only had one outbreak of herpes, ‘20 years ago’, can quite reasonably be treated without any herpes prevention if the peel does not go beyond the Grenz zone (Easy TCA – cloudy frosting), but they should still be closely monitored. Patients who say they suffer from herpes ‘all the time and at the drop of a hat’ should, of course, automatically receive Herpes prevention. Peel to the papillary or reticular dermis A person who has had even just one outbreak of labial herpes in their life is at serious risk of a recurrence in the days following a peel to the papillary or reticular dermis. This cannot be considered as just a potential complication. On the contrary, it should be considered as an almost certain side-effect of peels to these depths. Herpes prevention is therefore obligatory. Only Touch® is a deep peel that reaches the reticular dermis, but because its use is limited to areas of 1 cm in diameter at most, the immune defenses are not damaged enough to trigger herpes, and there have been no cases of herpes described after this peel. No prevention is necessary.

Specific herpes symptoms after a peel Diagnosing a herpes outbreak is relatively complex in the days following a peel, because the superficial layers of the

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Figure 37.48 (a) Secondary herpes infection 5 days after a TCA peel to the papillary dermis. No herpes prevention treatment was used. (b) Close-up of the upper lip: only painful erythema can be seen; treatment with valaciclovir brings rapid remission without hyperpigmentation or scarring.

epidermis have been removed and this is where the blisters that allow easy diagnosis form. Sometimes herpes will manifest only as painful erythema (Figure 37.48b), but sometimes also in a clearly necrotic form. The herpes outbreak may be delayed and occur after the 8th day. In general, the sudden onset of pain accompanied by erythema between the 4th and 7th days is a sure sign of herpes. The herpes can spread over the whole face within a few hours, but fortu-

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nately does not usually leave any scars109 and it appears that there have been no cases of herpes spreading to the eyes after a medium or deep facial peel.106 Severe local outbreaks can, however, leave local hyper/hypopigmentation.

Differential diagnosis: herpes/bacterial infection An infection can be assumed to be herpes if the patient has a personal history of herpes. If pain is felt on the upper lip first, this also suggests herpes, while pain felt on the cheek would rather suggest a bacterial infection, especially if there are scratch lesions and pus. Given that the epidermis has been exfoliated by the medium or deep peel, the doctor should not expect to see herpes blisters. Pain is an important clinical sign: herpes is painful even before it is visible, whereas a bacterial infection is usually painless or only becomes painful after it has developed clinically for a certain amount of time.

Differential diagnosis: herpes/overpeeling In addition to the signs and symptoms described above, overpeeling does not usually cause much pain at first, whereas herpes does.

Prevention of herpes outbreaks Herpes prevention is sometimes advisable with a peel to the Grenz zone, and is essential with peels to the papillary or reticular dermis (except for Only Touch®; see above). Questioning the patient and clinical examination In the majority of cases, patients forget that they once had a ‘cold sore’ when they had ’flu several years ago, and the doctor should of course look very carefully for any dyschromia in places where herpes is usually located, and should not forget that herpes may develop in other areas apart from the upper lip, as can be seen in Figure 37.49, which shows herpes located in the ear. Preventive treatment This comprises: ■ aciclovir: two times two tablets a day, 3 days before and 5 days after a medium or deep peel ■ valacyclovir: two times 500 mg/day, 2 days before and 5 days after a medium or deep peel

Treating post-peel herpes outbreaks Oral antiviral treatment This comprises aciclovir by mouth from four times 400 mg/day to 800 mg five times a day or valaciclovir by

Figure 37.49 Unusual location of herpes blisters in the helix above the tragus.

mouth: three times 500 mg to three times 1 g per day. The higher doses are for treatment of herpes outbreaks that have occurred in spite of proper preventive treatment. Topical treatment Topical aciclovir is not well tolerated by patients after a deep peel because of the burning sensation it triggers.109 If pain is very local, EMLA cream can be used cautiously, as it is absorbed more readily through skin that has no stratum corneum and is damaged by herpes. Local corticosteroids should not be used. Treating pain and/or pruritus Nerve blocks can be given in cases of very painful outbreaks. A mixture of lidocaine with adrenaline (epinephrine) and ropivacaine or bupivacaine110 can be used. In some cases, the doctor will have to prescribe opioids to relieve severe pain. However, treatment with opioids might well get rid of the pain but will not affect the itching. It could even aggravate the pruritus. The itching sometimes resists hydroxyzine and diphenhydramine. Asken109 reported that he once had to inject propanolol intravenously to relieve unbearable pruritus. Benzodiazepines111 and strong analgesics112 sedate patients and prevent scratching, secondary infections, pigmentation problems and permanent scars. Daily doctor–patient contact is essential to reassure the patient that the herpes lesions are healing properly.

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Special case of herpes under post-phenol occlusive mask It is difficult to diagnose and impossible to monitor herpes outbreaks, large or small, beneath an opaque occlusive mask of bismuth subgallate or thymol iodide. If there is any hint of herpes, any acute pain between the 4th and 7th day after the phenol, the powder mask113 should be removed immediately in order to examine the skin thoroughly. If the doctor’s suspicions are confirmed, the herpes should be treated as described above. Once the diagnosis has been made, the powder mask should not be replaced, and the ‘moist’ technique should be used instead, with regular application of an antibiotic cream (e.g. bacitracin) to avoid secondary bacterial infection.

Pruritus All peels destroy at least part of the epidermis and stimulate keratinocyte growth. The rapid dehydration of the noncornified keratinocytes can cause pruritus, which, however, is easily controlled.

Superficial peels Intraepidermal peels or peels to the basal layer rarely cause pruritus, except in overpeeled areas, where it may be temporary. Peels to the Grenz zone do not cause much pruritus. There have been no reports of severe pruritus with Easy TCA®, except for two cases of allergy to the post-peel cream.114

Dermal peels Pruritus is a logical result of a dermal peel. It sometimes starts very quickly, towards the 3rd day, or later, between the 8th and 30th days. It gradually becomes less severe, and eventually disappears on its own. Medication is sometimes necessary for patients who tend to scratch and are at risk of causing lesions, secondary infections or scars. Sublingual lorazepam (2.5 mg) or promethazine (25 mg/tablet, 2–6 tablets a day) usually stops post-peel pruritus. A calm or sleepy patient tends not to scratch! Cool compresses can also be applied. Cold compresses help the patient cope with the pruritus, but frozen compresses are not advised immediately after a dermal peel. Following a phenol peel, pruritus usually starts gradually underneath the bismuth subgallate powder mask. The patient must be told not to scratch, since if the powder mask is pulled off accidentally when scratching, it may create bleeding lesions that could become infected (Figure 37.50). Fortunately, these lesions heal rapidly and only leave a few areas of dyschromia. Instead of scratching, the patient should gently tap any area that is itching.

Facial edema All peels cause edema in the treated area. In fact, all peels trigger an inflammatory reaction whose cardinal signs are ‘rubor, dolor, tumor, calor’.115 The redness (rubor) and heat (calor) come from vasodilation that enhances the passage of liquids through the vascular endothelium and causes swelling (tumor), whose rapid onset can be painful (dolor). The pain can of course be superficial and be no more than a feeling of tightness when the inflammation is limited. The inflammation is also due to the presence of pro-inflammatory components in the dermis, which, together with the increased oxygen supply (because of the vasodilation), promotes the formation of free radicals. The free radicals damage the neighboring structures and maintain the inflammation. The result is a ‘vicious circle’ in which vasodilation promotes inflammation that causes vasodilation. From a physiological point of view, the movement of fluids follows Starling’s hypothesis (1896):116 movement of fluid = K [(CP + IO) – (IP + PO)] where CP and IP are the capillary and interstitial hydrostatic pressure, IO and PO are the interstitial and plasma osmotic pressures, and K is the filtration constant for the capillary membrane. If the resultant is positive, there is plasma filtration into the interstitial space. If the resultant is negative, there is absorption into the capillary lumen. The edema creates an additional barrier to capillary absorption by increasing the physical distance between the capillary wall and the molecules to be absorbed.116 If the edema resolves rapidly by itself, it does not need treatment. The rapid onset of edema dilutes the acids that arrive in the immediate surroundings of the blood vessels and prevents protein coagulation in the vessel walls: blood continues to circulate. When there is too much acid, extravascular plasma filtration can no longer make up for the fall in pH, and the vessel walls coagulate. Blood no longer circulates, and the skin changes color from pink–white to pure white or even gray.

Severity of edema depending on peel type Peels to the epidermis or basal layer Edema comes from dermal inflammation, and peels that do not cause inflammation in the papillary dermis do not cause much edema. If the patient has an allergic reaction to one of the components used (e.g. resorcinol), then severe edema can set in rapidly, however. Any severe edema after a peel that does not go beyond the basal layer is most likely associated with an allergy or infection.

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Figure 37.50 (a) Scratch lesion after a phenol peel – treated with bismuth subgallate. Note the intense and uneven erythema 10 days after the peel. (b) The scratch lesion has completely healed. This photograph was taken about 5 years after (a), during the course of other treatment.

Peel to the Grenz zone Mild and short-lived edema (48 hours) might develop.117 It does not require treatment. Edema that lasts any longer could be an allergy, and, if so, should be treated accordingly.

Peels to the papillary or reticular dermis A peel to the papillary dermis always causes edema, whose severity depends on the inflammatory reaction following the peel (Figures 37.51–37.53). An inflammatory reaction is desirable insofar as it sets in train the skin regeneration process; it is therefore responsible for the rejuvenating effect of a peel. But, at the same time, it generates free radicals that have well-known negative effects. Inflammation therefore has its downside and must be controlled by antioxidants in order to limit the negative side and make the most of the restructuring effect. This is why Easy TCA®, Unideep® and Easy Phytic® are rich in antioxidants, both in the peel solution and in the cream ‘mask’ that the doctor

applies immediately after the peel. These antioxidants reduce post-peel inflammation, allowing patients to resume their social activities more quickly and allowing more frequent repetition of the peels. In general, the deeper the peel, the more severe is the edema, as the edema translates the severity of the dermal inflammation into visible signs. It is therefore logical that edema is more severe after a phenol peel. The extent of the ‘lifting effect’ of a peel depends on the depth of the peel and the severity of the edema. It can therefore be concluded that the overall lifting effect of a peel will be proportional to the edema it triggers. Edema is sometimes so severe as to cause the lips to protrude118 or prevent patients from opening their eyes. Deep peels therefore give rise to dramatic edema that can sometimes be very worrying for patients and their immediate friends and family. A case has been reported of a patient who was rushed to the nearest hospital by the family, who were worried by what appeared to be severe burns. It is essential to warn patients of the severity of the edema and to show them photographs of the post-peel period so that they do not worry. If a detailed explanation is not given beforehand, anything the doctor might say

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Figure 37.51 (a) Edema beneath the occlusive mask, 24 hours after a phenol peel. (b) Facial edema after the occlusive mask has been removed, 24 hours after the peel. A bismuth subgallate powder mask has just been applied.

Figure 37.52 (a) Before a TCA peel to the papillary dermis. (b) facial edema 24 hours after TCA to the papillary dermis (Unideep®).

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Figure 37.53 (a) Before the peel. (b) Facial edema the day after a TCA peel to the papillary dermis (Unideep®): note that the edema on the first day not only gets rid of the cheek wrinkles but also the facial sagging. The erythema is reduced by antioxidants in the post-peel cream.

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after treatment will ring hollow to patient, friends and family! It is extremely important for the doctor to have regular contact with the patient during the first week after the peel, as the doctor can check on progress every day and reassure the patient that everything is normal.

Edema and local phenol peel

Fortunately for the patient, there is no linear relation between the pain felt and the severity of the edema. It is not painful even when it is so severe that patients cannot open their eyes for anything from a few hours to several days, depending on the formula used. If after the 3rd day the edema is painful, there might be a secondary infection.

A local phenol peel on the eyelids or lips (Lip & Eyelid®) also gives rise to severe edema (Figure 37.54) that can make it difficult for patients to eat or open their eyes, which can make some patients extremely anxious. This edema reaches its peak, locally, during the first 2 days and then subsides according to the laws of gravity. During the 3rd and 4th days, edema of the eyelids migrates downwards to the cheeks and then the jaw, reaches the neck on the 5th day, and disappears on the 6th or 7th day. The edema that follows a localized phenol peel on the lips subsides more quickly, as it has less distance to cover before it reaches the neck.

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Link between pain and edema

Figure 37.54 (a) Appearance of the upper lip before a phenol peel (Lip & Eyelid® formula). (b) Appearance of the upper lip 24 hours after Lip & Eyelid®.

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ate the discomfort of eyelid edema. The patient should sleep in a half-sitting position to help the edema go down. The doctor should wait for some months before judging the permanent effect of the peel. As the swelling goes down, wrinkles that have not responded to the medium or deep peel reappear on the patient’s skin. It is not necessary to prescribe diuretics in the large majority of cases. Edema associated with an infection or an allergy should be treated accordingly. Steroids and non-steroidal anti-inflammatories should be avoided so as not to interfere with collagen generation. Oral Varidase®119 can be used to help the swelling subside.

Milia

Figure 37.55 Frosting of the skin after application of Lip & Eyelid® formula: note that the skin of the upper eyelid tarsus has not been treated, to limit the post-peel edema.

Prevention of edema Peels to the papillary dermis and especially to the reticular dermis trigger the most dramatic edema, and it is only in these cases that prevention should be considered. The severity of the edema is hard to predict; some patients have (relatively) little swelling, whereas others have severe edema even before the whole face has been treated. Preventive, intravenous injections of corticosteroids before the peel do not appear to make much difference, and the edema develops in spite of the corticosteroids. With phenol peels, it is often possible to limit edema in the upper eyelids by not treating the skin of the upper eyelid tarsus (Figure 37.55). The eyelid edema is then less uncomfortable for the patient. When the impermeable dressing (occlusive phenol) is being applied, it should not be placed too close to the eyes, to avoid excessive swelling on the part of the eyelids not covered by the occlusive dressing.

Treating edema Small, paper or textile bags containing China tea, after they have been boiled and cooled in the refrigerator, make excellent, refreshing compresses that can be used to allevi-

These small epidermal inclusion cysts120 are a relatively common and fortunately benign complication of medium or deep peels, and occur mainly when the peels have been followed by greasy occlusion or occlusive make-up. They can vary in number from a single cyst to several hundred, and usually appear in the midface region or on the cheeks. A latency period of several weeks (3–6) is necessary before they become visible, and it takes 6–12 weeks of patience for them to disappear, unless patients run out of patience and remove them themselves or ask the doctor to do it.

Prevention of milia Topical tretinoin Applying topical tretinoin (all-trans-retinoic acid) before a peel can often reduce the incidence of milia. However, the undesirable effects of retinoic acid in combination with a deep or medium peel must be taken into account. Retinoic acid increases the depth of penetration of caustic agents, could increase the risk of hyperpigmentation68 and, if it is applied too soon after a medium or deep peel, slows down the rate of re-epithelialization.

Dry technique for phenol During the phase of skin regeneration that follows a phenol peel, the ‘dry’ technique121 should be used instead of the ‘moist’ technique that most often causes milia to form. Inclusion cysts rarely occur when the ‘dry’ technique is used, and if they do, they are small, few in number and leave no marks after excision.

Treating milia Patients should not try to remove these small, white, subcutaneous cysts themselves. If they are handled unnecessarily or too roughly, sometimes with the help of unorthodox instruments, secondary infections and/or scars can follow,

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and the milia can remain deeply embedded in the skin. At the most, patients can use a Buf-Puf® (3M) sponge to gently scrub the skin if it is not too sensitive. One of the easiest ways to treat milia is simply to wait. Milia should be given time to clear up by themselves: a period of 1 month is left for them to clear, by which time re-epithelialization is complete. The doctor should carefully make an incision in the top of each cyst with the tip of a No. 11 scalpel or an 18G needle, which will make it easier to extract them with a blackhead remover without leaving any marks, as the cut is strictly intraepidermal. This treatment is carried out with sterile equipment after disinfection, and there is no need for local anesthetic.

Acne Acne can be either treated or triggered by a peel. An intraepidermal peel (Easy Phytic®) or a peel to the basal layer (Easy TCA®) is usually a good treatment for comedonal, papular or even papulopustular acne. Intraepidermal peels or peels to the basal layer do not usually trigger post-peel acne, unlike peels to the papillary dermis, which can promote secondary infections. Active acne must be treated in the weeks before a peel to the papillary or reticular dermis, and the medium or deep peel can only be started once the infection has completely cleared. The increased epidermal permeability resulting from prescription treatments must be taken into account. Doing a papillary or reticular dermal peel during the active phase of pustular acne would trigger a potentially serious infection of the whole treated area that could even develop into toxic shock. A fortiori, peels should not be performed on patients suffering from active acne conglobata, necrotica, etc. Some comedones may occur in certain patients during the post-peel period: they should be extracted with a blackhead remover. It is common for acneiform dermatitis to develop under greasy dressings (see also the section above on microbial infections) after deep peels treated with the ‘moist’ technique. Vaseline® in fact creates an impermeable layer that acts as total occlusion. It is known that bacterial proliferation is much more rapid under occlusion than in the open air. Antibiotics and standard local treatments are used to treat post-peel acne.

Pain The pain threshold is virtually the same for all human beings, who perceive the stimulation of their nociceptors from the same intensity threshold. Pain tolerance, however, varies considerably from one patient to another. It is very important to consider patient psychology, especially

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during the first peel session. Patients have absolutely no idea what they are about to go through, and words like ‘chemical’ or ‘burn’ evoke images that contribute to the general anxiety generated by the first sensation of pain. Peels that do not go beyond the Grenz zone have to be repeated several times in order to be effective. The first session is the most painful, as the patient feels the pain ‘blindly’, not knowing what is going to happen next, and becomes increasingly anxious, which amplifies the sensation of pain. Patients find the following sessions less painful, as they can anticipate when the pain will stop. In general, pain tolerance seems to increase with age. Contrary to rumor, men have a slightly higher pain sensitivity threshold than women, but women, who are more used to pain, tolerate it (much) better. It is personality more than race or gender that influences how a person experiences pain, and it is often difficult to draw the line between pain and suffering, sensation and emotion, pain experienced and pain felt, as regardless of a person’s pain threshold, in the end the pain always feels real.

Pain during application of the peel The pain caused by a peel is largely proportional to its depth. The type of pain, its intensity and its duration vary depending on the peel used. It is recommended to give patients details about the pain they will feel, how intense it will be, how it will develop, and how long it will last. It is essential to tell them about any change in technique, as patients may become anxious if the pain they feel is different to what has been described.

AHAs Partially buffered glycolic acid at 50% or 70% is not painful. Unbuffered 70% glycolic acid (with pH <1) causes a burning sensation that is as bearable as it is shortlived. Neutralization with a solution saturated in sodium bicarbonate immediately stops any burning sensation. Other AHAs are less aggressive on the skin and less painful. The pain decreases as the molecular weight of the molecules increases, as larger molecules have more difficulty penetrating the skin. Lactic acid is sometimes used to test skin sensitivity (the STINGING test): applying a 10% solution triggers a burning sensation in patients with sensitive skin. Easy Phytic® solution (glycolic, lactic, mandelic and phytic acids in a self-neutralizing solution) produces a specific type of pain that starts with rapid burning from the glycolic acid, quickly followed by a relatively painless tingling sensation that soon decreases in intensity. These sensations arise from the successive and gradual penetration of the different acids and their natural neutralization by the skin.

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TCA Peels to the papillary or reticular dermis The pain caused by TCA is directly proportional to the concentration of the acid in the solution applied: a solution at 20% m/m burns less than a solution at 30% m/m. Pain is one of the signs that alerts the doctor immediately to any error in the formulation used. If the patient complains of a very intense burning sensation when a solution that is not supposed to be too aggressive has been applied, it is important to stop the application and check whether the solution has been properly prepared. A peel to the papillary dermis is always painful, but the intensity of the pain does not always warrant local anesthesia; it is often enough to talk to the patient, explain the pain, and the different phases of the treatment and anticipate when the pain will stop. Patients are grateful, however, when the doctor administers nerve blocks before applying the acid. It is not necessary to block the whole face, and supraorbital, suborbital and mental blocks significantly reduce the intensity of the pain. With these nerve blocks, application to the forehead and midface region is completely painless. To avoid overreactions, more squeamish patients could be given mild premedication or sometimes, although rare, deep sedation before a peel to the papillary dermis. When TCA is applied to the reticular dermis, premedication, deep sedation and/or nerve blocks will be necessary, as peels of this depth are very painful. The anti-prostaglandin action of aspirin reduces the burning sensation and provides relief to many patients: 500–1000 mg of aspirin taken 45–60 minutes before the peel can therefore be recommended if the peel is to reach the papillary dermis. There is a greater risk of bruising, however. The Unideep® peel (TCA to the papillary dermis combined with an antioxidant, stimulating and analgesic postpeel mask) has the advantage in that it can be applied region by region and the patient benefits from the almost immediate analgesic effect of the post-peel cream mask that is applied as soon as frosting is achieved. The forehead is treated first until even pink–white frosting appears, and the post-peel cream is applied on this area before starting treatment on the next area. Patients soon experience the rapid relief brought by the post-peel cream, which makes them less anxious about the rest of the treatment. Using cold packs (ColdHot Pack® by 3M) before applying the Unideep® solution can be effective: cooling the skin before applying the solution alleviates most of the pain. It seems that most of the pain comes from the sudden warming of the papillary dermis after vasodilation; the heat-sensitive nociceptors in the papillary dermis cannot, of course, react as strongly when they are cooled beforehand with cold packs. Using cold packs is therefore effective both before applying the peel solution and immediately afterwards – the plastic of the cold packs can come into direct contact with the acid in Unideep® (Figure 37.56). Some

Figure 37.56 Cryoanesthesia with a cold pack during combined chemical blepharoplasty (Lip & Eyelid®) and TCA to the papillary dermis (Unideep®).

patients, however, find the cold almost as unpleasant as the bite of the acids, and prefer simply to have their skin fanned with a hand-held or electric fan. Squeamish patients will appreciate a frontal nerve block. The Unideep® solution is applied to the forehead first and taken beyond the anesthetized region towards the temples. The post-peel cream immediately stops the sensation of pain, and the rest of the face can be treated easily, without

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Figure 37.57 Use of a cold pack during treatment of lentigines on the hands with Only Touch®.

nerve blocks, as patients can accept pain that they know to be short-lived and bearable, having felt it on the temples and expecting it to be ‘blocked’ by the post-peel cream. Only Touch® is an adjuvanted and saponified solution with a concentration of 45% m/m of TCA. Localized application to small, benign lesions with a maximum diameter of 1 cm triggers intense burning that is not too unpleasant, as it is limited in extent. Only Touch® does not require any type of anesthesia. When treating a large number of lesions, as is often the case with lentigines on the hands or décolletage, the patient may appreciate the use of cold packs to reduce the burning sensation (Figure 37.57). The cold pack can be used in two ways: either the doctor waits for the acid to dry before applying the cold pack on the skin with a sheet of paper in between or applies the plastic of the cold pack directly on the acid as it is taking effect. The acids used do not damage the plastic of the cold pack, and this type of immediate and direct application seems to be the most effective at reducing the pain. Peels to the basal layer or Grenz zone Easy TCA®, an adjuvanted and saponified solution with 15% m/m TCA,112 only produces a sensation of heat or mild burning that the vast majority of patients find easy to bear. More squeamish patients will complain of feeling some pain, but it is short-lived, as the post-peel cream alleviates it immediately.123 After the post-peel cream has been applied, there is only a feeling of tightness.

Phenol Phenol is used to regenerate the skin down to the reticular dermis. It has useful neurolytic and anesthetic properties. The pain is therefore short-lived (around 15 seconds), as the phenol produces local numbness that lasts from 20–30 minutes. After this time, the inflammatory phenomena in

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the dermis become powerful enough to trigger a painful and intense sensation of heat that will slowly subside over the next few hours and days. Recently, some phenol formulas have been presented as allowing a full-face peel without any anesthetic. A phenol peel that can be applied to the whole face without any type of anesthetic is a more superficial phenol peel that does not induce regeneration of the reticular dermis of the same quality as the ‘classic’ phenol peels. Less pain goes hand in hand with inadequate results: the results of this type of phenol peel are the same as for a TCA peel to the papillary dermis and may not have much effect on wrinkles. The pain caused by these peels is also the same as for a TCA peel to the papillary dermis. It is pointless to put a patient through the risks of phenol toxicity only to get the results that a simple, non-toxic molecule (TCA) can achieve. An effective, full-face phenol peel should therefore be used with an anesthetic (see Chapter 33). A localized Litton or Baker–Gordon peel can be carried out with short-acting nerve blocks with 2% lidocaine without adrenaline (epinephrine). The pain is also short-lived. Phenol provides anesthesia that extends about 1 cm beyond the frosting, and the phenol can be applied slowly, step by step. Chemical blepharoplasty and cheiloplasty124 are ideally carried out with Lip & Eyelid® formula: its action is more gradual than that of Baker–Gordon or Litton phenol, and it can be applied locally without any anesthetic since the pain only lasts 12–15 seconds. Phenol is neurolytic; it makes the skin less sensitive for several days, and it is possible to touch up certain areas without causing any real pain after the nerve block anesthesia has worn off, even the day after the peel. Even if deep inflammatory phenomena make the dermis painful, the epidermis remains insensitive.

Post-peel pain AHAs Neutralization, which relieves the pain, can sometimes be unpleasant, as the process of AHA neutralization is slightly exothermic. The pain subsides very quickly after any intraepidermal peel.

Easy TCA® and Unideep® The Easy TCA® (to the basal layer or Grenz zone) and Unideep® (to the papillary dermis) post-peel mask cream has the major advantage of relieving the burning sensation caused by the acids almost immediately. Using cold packs as soon as the peel is over usually provides relief to the patient. No specific treatment is necessary for the pain that comes immediately after peels to the papillary dermis.

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Only Touch® There is almost no residual pain after Only Touch®.

Peel to the reticular dermis The fact that patients look as if they have third-degree burns after a peel to the reticular dermis has no relation to the pain they actually feel (Figure 37.58). After a phenol peel, the type of pain experienced varies enormously, and descriptions given by different patients of the intensity of the pain go from ‘completely painless’ to ‘extremely painful’. Opioids are sometimes necessary to relieve severe pain. A combination of paracetamol (acetaminophen) plus codeine is especially well suited to post-peel pain, but should not be used in the hours following a phenol peel, as paracetamol (a phenol derivative) goes through the same detoxification pathways as phenol, which could create metabolic competition and the risks of toxicity associated with phenol might be increased. Preventive administration of benzodiazepines (lorazepam 2.5 mg before the peel and on the night of the peel before going to bed) relieves the anxiety caused by these unpleasant sensations and reduces the need for analgesics after the peel. In case of very severe, localized pain (extremely rare), a nerve block could be used. Often, the pain described by the patient is an unpleasant sensation of heat, due to extensive vasodilation that imme-

Figure 37.58 After a phenol peel, patients look as if they have third-degree burns, but in fact feel no pain at all.

diately follows a deep peel. A cold pack can help the patient get through this phase. The pain that occurs after a phenol peel can be summarized as follows: ■ Application of phenol: followed by 15 seconds of pain. ■ Phase of anesthesia: 30–60 minutes. ■ Phase of burning and painful edema: sets in within 1–2 hours and lasts until the following morning. ■ Phase of simple tightening of the skin: up to the 3rd day. ■ Pulsing type pain: usually during the 3rd night, with an average duration of 8 hours. ■ Any feeling of pain then stops definitively, and pruritus sets in from the 4th or 5th day.

Sun sensitivity All peels, even if they do not cause any visible flaking, damage the skin’s protective stratum corneum and make it more sensitive to all types of aggression. Light consists of high-energy particles called photons. Photons are absorbed by the ozone layer and oxygen in the atmosphere and only 7.1% of solar energy reaches the Earth. Photons move in waves and have a characteristic wavelength and frequency. They are absorbed in the skin, where they cease to exist and are converted into energy. UV rays have wavelengths between 100 and 400 nm, but only UVA (320–400 nm) and UVB (290–320 nm) reach the Earth, as the ozone layer blocks UVC.125 High frequencies have the most energy (gamma rays have the most energy and UV rays have more energy than infrared). Different variables affect the intensity of solar radiation. As the emission of solar radiation is considered constant, the summer sun is ‘stronger’ than the winter sun, the sun on the equator stronger than the sun in Lapland, and the midday sun burns more than the afternoon sun. Fog does not slow down UV penetration, but urban pollution is, on the contrary, a powerful sunblock because of the presence of aromatic hydrocarbons, which make excellent UV blocks. Altitude in itself has less influence than the angle of incidence, but snow, on the other hand, reflects 85% of UV rays, whereas dry sand only reflects 17%, water 5% and grass 2%. Therefore, places lying between snow-covered mountains on a very sunny day are particularly dangerous. After penetrating the skin, photons are absorbed by specific molecules called chromophores. Each chromophore absorbs a set wavelength. Photons that penetrate the skin are converted into energy, and this produces biochemical changes that make certain molecules unstable by putting them in a higher-energy state. Some molecules can convert this energy into heat and/or vibrations and thus regain their original stable state (eumelanins behave in this way, for example). The energy absorbed can also break certain intramolecular bonds and convert some molecules into

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free radicals. These free radicals are very reactive and will bind rapidly with other chemical species. Free radicals can also attack the DNA molecule and block its replication locally. They can sometimes break the DNA molecule during the replication phase of the cell cycle, before the mitosis phase, or if photosensitizing molecules are used. Fortunately, human cells contain mechanisms for the repair of damaged DNA, involving DNA polymerase and other enzymes. The polyunsaturated fatty acids that make up cell membranes are very sensitive to free-radical attacks. The CH2 group that is located between the double bonds of arachidonic acid degrades as a result of free-radical attacks; it forms unstable peroxides, and at the end of these chain reactions a malonedialdehyde molecule is released at the same time as two new free radicals, and these spread the reactions to the rest of the membranes. Once the free-radical reaction has started, the damage spreads quickly. Some amino acids, either free or as components of proteins, can absorb UV rays, leading to photoionization and releasing electrons that initiate reactions that damage proteins. Moreover, in the presence of oxygen, oxygen free-radicals are formed that then react with organic molecules to produce hydroperoxides. These can then damage proteins both by breaking polypeptide chains and by forming bridges between them. In short, sunlight damages the genetic code, cell membranes, intracellular organelles, proteins, enzymes, etc. What is more, only 25% of the erythema dose is needed to cause potential damage to the genetic code of human cells. We have numerous defense mechanisms to protect us, and complex physiological reactions can repair most of the damage caused by photons. Some of the light from the sun is reflected off the fatty layer covering the corneocytes. The outermost layers of the stratum corneum also reflect light, and the photons that manage to penetrate this layer are diffused as they reflect off the different layers of cells. The UV photons that have not been reflected or absorbed reach the basal layer of the epidermis, the papillary dermis and the reticular dermis. UVA rays that are emitted perpendicular to the skin penetrate deeply: 66% get through the stratum corneum and 44% reach the basal layer. They have relatively little effect on the epidermis, but do severe damage to the dermis. Some 17% of UVB rays get through the stratum corneum and 3% reach the basal layer. They cause more damage to the epidermis than to the dermis. The thickness of the stratum corneum is therefore an important part of the skin’s defenses, and treatments that damage it (dermabrasion, laser, AHA creams, peels, etc.) allow photons in and promote the free-radical damage described above. The angle of incidence of solar rays is important: at vertical incidence, the photons only have to cover 15 µm through the corneocytes, while, at oblique incidence, they have to cover up to 35 µm to reach keratinocytes. The morning or late afternoon sun is therefore less dangerous than the midday sun.

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Skin color is in itself a defense mechanism: white skin lets in up to 64% of rays that touch it and black skin is only permeable to 18% of these rays. White skin suffers from photoaging much more quickly than black skin. Yellow skin has fewer pigments than black skin, but the stratum corneum is thicker than Caucasian skin and is better at reflecting and diffusing photons. Beta-carotene, superoxide dismutase (SOD) and catalase (CAT) are vital free-radical defenses. Epidermal betacarotene diffuses from the dermis and can scavenge free radicals. SOD and CAT block the oxidative action of UV photons. SOD blocks the first stage of oxidation, the formation of the superoxide anion. The level of SOD in the body has been directly correlated with life expectancy. Organisms with the most SOD live the longest. Some cosmetic preparations use SOD. This unstable molecule has to be protected, ideally in liposomes, to prevent it from being oxidized. These facts give us a better appreciation of the need for effective sun protection. Just one peel, of whatever kind, makes the skin more sensitive to the sun: patients soon feel the difference just hours after treatment, and complain that they can no longer expose their skin to direct sunlight because of the burning sensation this causes. The deeper the peel, the more sensitive the skin is to the sun. The thinned or absent stratum corneum cannot provide protection against the sun’s rays until the epidermis has completely recovered. After a deep peel, the skin is like that of a newborn baby, and remains sensitive to the sun for a long time. It is therefore recommended to keep using total sunblock126 and avoid the sun for a duration that is directly proportional to the depth of the peel.

Demarcation line A deep peel restructures the skin permanently and changes the quality and structure of the skin irreversibly. Treated skin is cleared of actinic lesions and there is a visible line between the treated and untreated skin. This is called a ‘demarcation line’ and can result from a difference in the quality or color of the skin (Figure 37.59). A difference in color is more obvious than a difference in the texture of the skin. It is easy to predict the risk of a visible demarcation line (Figure 37.62). Not counting the hypopigmenting (with phenol) or hyperpigmenting (with TCA) properties of different peeling agents, the parameters that should be taken into account are the depth of the peel and the patient’s skin type.

Depth of peel Intraepidermal peels or peels to the basal layer of the epidermis do not create a demarcation line. TCA peels to the papillary dermis can change the texture and color of the

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Figure 37.59 Neck demarcation line after a full face phenol peel.

skin, but there is often no visible demarcation line after TCA to the papillary dermis. TCA is not toxic to melanocytes. It can, however, get rid of the majority of freckles if it reaches the papillary dermis, and there will be a visible demarcation line between the skin with and the skin without freckles. A phenol peel is deep127 and toxic to melanocytes, and it is with this type of peel that there is a greater risk of a demarcation line.

Skin type High skin phototypes (IV to VI), dark or Asian skins, tanned or very sun-damaged skins are the most at risk of a demarcation line after a medium or deep peel. Skin phototypes I to III only very rarely suffer from permanent postpeel pigmentation problems: the only possible visible difference would be in the texture of the skin. Figure 37.60 shows the absence of a color demarcation line in a patient with a light skin type who has had a combination of a localized deep phenol peel on the eyelids (Lip & Eyelid®) and a TCA peel to the papillary dermis on the rest of the face (Unideep®). The results shown are after 1 year. The phenol has clearly made the skin firm again, and the mediumdepth TCA has significantly improved the sun damage. Nevertheless, there is still a slight visible difference in the structure of the skin between the areas treated with phenol and those treated with TCA to the papillary dermis. There is a particular risk with very sun-damaged skin, as the medium or deep peel restructures the skin to such an

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Figure 37.60 (a) Eyelid aging before treatment. (b) Results 1 year after application of Lip & Eyelid® formula (upper and lower eyelids) and Unideep® to the rest of the face to even out the results.

extent that it leaves a very visible difference in the quality of the treated and untreated areas. Loss of tanning is proportional to the depth of the peel: intraepidermal peels lighten a tan and deeper peels get rid of it altogether. A deep and localized treatment on tanned skin will always take away the color in the treated area that will appear all the lighter against the surrounding, tanned skin. Tanned, sun-damaged skins with a high phototype and dark or Asian skins should always be treated in such a way that the inevitable demarcation lines will not be visible. This is where the finer details of peel application count, as certain areas are more likely to develop demarcation lines than others.

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Figure 37.61 (a) Demarcation line 1 month after a full face phenol peel (lip and eyelids) formula; (b) same patient 4 months after the peel: the demarcation line is fading.

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High-risk areas The forehead

Go to 1 cm beyond the hairline Treat the eyebrows against the lie of the hair

Prevention consists in applying the peel in the hair, about 1 cm beyond the hairline. Neither phenol nor TCA are toxic to the hair bulb. There is no danger of localized alopecia. The eyebrows should be treated against the lie of the hair so that the peel comes into contact with the skin underneath the eyebrows.

Do not forget the nostrils

White lip–red lip, nostrils Prevention consists in taking the peel slightly over onto the oral mucous membrane and treating the skin on the edges of the nostrils, up to the junction of the mucous membrane. Contact between phenol and the first millimeter of the lip mucous membrane does not pose any problem, and allows the doctor to treat fine lines at the same time as avoiding a visible and unsightly demarcation line around the lips. Aged lips might take advantage of carefully applied phenol on the red lip.

Treat the trages and earlobe

The ear

Figure 37.62

Go to 1 cm into the red lip

Phenol: set the lower limit with patient upright

Areas at risk of a demarcation line.

Prevention consists in feathering the tragus and the earlobe.

The neck Prevention consists in clearly setting the lower limit of the peel before treatment, with the patient in the sitting position. If an occlusive phenol peel is used, the occlusive dressing should not be put under the lower jaw. The absence of occlusion under the jaw, between the face and the neck, reduces local maceration and therefore the depth reached; this creates a transition zone in the area of shadow beneath the jaw (Figure 37.61).

Dilated pores Benatar128 describes this complication when doing deeppeel treatments on patients with thick, oily skins and dilated pores. The results of deep peels – and especially medium peels – are mediocre compared with the dramatic results seen when treating drier and thinner skins. Thick, oily skin with dilated pores benefits more from ablative laser resurfacing than a peel, even a deep one. Epidermal peels and peels to the dermoepidermal junction and the papillary dermis do not usually cause the pores

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A

B

Figure 37.63 (a) Localized phenol on the upper eyelid, on day 11. Normal healing. (b) Appearance of petechiae on the morning of day 15.

A

B

C

D

Figure 37.64 (a) Before a full-face Lip & Eyelid® peel. (b) Thirty days after full-face Lip & Eyelid®: the nevi have become depigmented. (c) Four months after full-face Lip & Eyelid®: the nevi have become hyperpigmented. (d) Six months after full-face Lip & Eyelid®: the nevi are still hyperpigmented.

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to dilate. On the contrary, more often than not, they tighten the pores.

Purpura, petechiae Petechiae are small skin hemorrhages characterized by tiny bright red, purple or bluish spots that range in size from a pinpoint to several millimeters in diameter. They are caused by the rupture of small, dermal blood vessels and the extravasation of red blood cells. Purpura, unlike a telangiectasia, does not blanch when pressed with glass. Vitamin C and K deficiencies promote petechiae. Purpura usually tends to fade slowly and gradually, but recurrent purpura can leave spots of iron deposit on the skin. It is a rare complication, but petechiae can appear rapidly after a phenol peel if the patient has bouts of severe coughing or vomiting that trigger a sudden increase of pressure in the dermal blood vessels that have been damaged and temporarily dilated by the inflammatory reaction to the phenol peel (Figure 37.63). Once again, treatment is essentially preventive and consists in avoiding movements or maneuvers that might increase capillary pressure in the facial blood vessels: coughing, vomiting and even, as I was told recently, washing the hair with the head bent forwards or nighttime scratching. There are some herbal medicinal plants that may be fairly effective and that are mainly used to treat venous stasis: witch hazel, horse chestnut and red vine can increase resistance in the vessel walls and reduce their permeability, and have an anti-inflammatory and anti-edema action. These plant extracts can be taken by mouth, and vitamins C and K can be prescribed at the same time.

4. 5. 6. 7.

8.

9. 10.

11. 12. 13. 14. 15. 16. 17.

18.

19. 20.

Benign nevoid hyperpigmentation Although phenol peels have been described as a possible treatment for nevi,129 benign nevoid hyperpigmentation can develop after a phenol peel (Figure 37.64). After a period of depigmentation of approximately 6 to 8 weeks, some nevi might become hyperpigmented. This hyperpigmentation is benign. No skin cancer potentially induced by peelings has been reported in medical publications.

21.

22. 23. 24.

Notes 1. Heart, liver, kidney, larynx, neurological, digestive complications, etc. 2. TCA in aqueous solution and standard phenol formulations, for example. 3. Preparation is usually unnecessary before Easy TCA® and not advised before Easy Phytic® solution.

25. 26. 27.

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Easy TCA® to cloudy white frosting. Although this ‘rest’ time varies considerably. Schmitt D. Biologie de la peau. Les éditions INSERM, 1995. Litton C, Trinidad G. Complications of chemical face peeling as evaluated by a questionnaire. Plast Reconstr Surg 1981; 67: 738–43. Easy Phytic® solution is a slow-release and self-neutralizing mixture of AHAs that work gradually and is not therefore compatible with any preparation technique that might increase the permeability of the stratum corneum. Beware of young patients who overuse aggressive anti-acne preparations. Except for skin that is badly sun-damaged, as the area treated with phenol will have completely regenerated and will be of far better quality than the untreated, neighboring skin, which will still look old. With less than a week in between for Easy TCA®. See the photographs in the section on hyperpigmentation later in this chapter. Renutriv ACE Lipoic Complex® (see Chapter 3). Rubin MG. Manual of Chemical Peels, Superficial and Medium Depth. Philadelphia: JB Lippincott, 1995. It is preferable to use partially insulated needles, such as Kobayashi. There is an overall increase in the quantity of newly synthesized DNA in the epidermis. It should be remembered that any peel removes at least the stratum corneum, the first UV barrier. Effective sun protection should be used to make up for the loss of the stratum corneum. This is partly what Easy TCA® post-peel cream is for: it penetrates more easily when it is applied immediately after the peel solution and scavenges the free radicals as soon as they are produced. In Easy Phytic® solution, phytic acid, with its 12 free-electron-binding sites, plays this role. Grenz is the German word for ‘border’: the border between the dermis and the epidermis. Easy TCA® does not cause hyperpigmentation when it is applied to the Grenz zone, because of the anti-free-radical, anti-inflammatory and tyrosinase-inhibiting action of the post-peel cream, applied immediately after the acid solution. Weekly repetition of Easy TCA® is also a contributing factor to avoiding post-inflammatory hyperpigmentation. Epidermal sliding: the acids coagulate the proteins that bind the epidermis to the dermis and the epidermis slides over the dermis. Sliding is the pathognomonic sign of a peel to the papillary dermis. Whereas with a superficial peel, they are stimulated indirectly. Manquat A. Traité élémentaire de thérapeutique de matière médicale et de pharmacologie, 5° ed, tome 2. 1903: 193. For example, a patient with light skin with a dark-skinned parent or grandparent. Their skin appears not to react much to inflammation, but they can soon develop pigmentary changes. Easy TCA® or AHAs can, on the other hand, be applied in cases of standard papulopustular acne. Girond JP, Mathé G, Meyniel G. Pharmacologie clinique. 1590–1. Expansion Scientific Français, 2003. Some formulations do require this kind of manual abrasion in immediate preparation for peeling.

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28. It is not uncommon for the patient to phone the doctor complaining that their melasma has gone from brown to almost black during the first 3 days after Easy TCA®. This is not a pigmentary change, but normal local dehydration of the epidermis, a sign of a positive effect on the pigmentation problem being treated. 29. Fouque L, Seban D. Peelings associé TCA et acide glycolique. 18° réunion du GRCD, Perpignan, 25–27 Septembre 1995. 30. Cortez E. Chemical face peeling. Otolaryngol Clin North Am 1990; 23: 947–60. 31. The Wood’s lamp (350–390 nm) can, however, reveal intraepidermal pigmentation that is lying over another dermal pigmentation. In this case, it gives a false sense of safety, and there is a risk of promising the patient rapid results when only the epidermal pigmentation can be readily eliminated. 32. JAMA 1956; 162(10): 974–5. 33. Kenney JA, Grimes PG. How we treat vitiligo. Cutis 1983; 32: 347–8. 34. A cream with a concentration of 20% is used. (ICN pharmaceuticals, Costa Messa, CA, USA). In the case of resistance, the dermatology department at Yale University School of Medicine uses concentrations of up to 40%. 35. For example, if the product is applied at night, there is a risk of depigmenting other parts of the body through involuntary movements when asleep or by rubbing the eyes with the hand while applying the treatment, etc. 36. Hedges TR, Kenyon KR, Hanninen LA, Mosher DB. Corneal and conjunctival effects of monobenzone in patients with vitiligo. Arch Ophthalmol 1983; 101: 64–8. 37. Nordlund JJ, Forget B, Kirkwood J, Lerner AB. Dermatitis produced by application of monobenzone in patients with active vitiligo. Arch Dermatol 1985; 121: 1141–4. 38. Catona A, Lanzer D. Monobenzone, superfade, vitiligo and confetti-like depigmentation. Med J Aust 1987; 146: 320–1. 39. Pheomelanin is lighter than eumelanin. 40. Glycolic acid + lactic acid + mandelic acid + phytic acid in a slow-release solution that does not need neutralizing. 41. Five days after Unideep®; 7 days after TCA in aqueous solution. 42. Inhibition of homogentisic acid oxidase, leading to local accumulation of homogentisic acid followed by polymerization that forms the ‘ochronotic’ blue–black pigment. 43. Mills OH, Kligman AM. J Soc Cosmet Chem 1978; 29: 147. 44. For example, the possibility of including products in liposomes, cyclodextrins, nanosomes or multilayers and using specific molecules such as arbutin, magnesium ascorbyl phosphate, etc. 45. The chemical composition of the base cream can alter the antibacterial effectiveness of azelaic acid: Charnock C, Brudeli B, Klaveness J. Evaluation of the antibacterial efficacy of diesters of azelaic acid. Eur J Pharm Sci 2004; 21(5): 589-96. 46. Breathnach AS, Robins EJ, Nazzaro-Porro M, Passi S, Picardo M. Hyperpigmentary disorders–mechanisms of action. Effect of azelaic acid on melanoma and other tumoral cells in culture. Acta Derm Venerol Suppl (Stockh), 1989; 143: 62–6. 47. Nazzaro-Porro M. Azelaic acid. J Am Acad Dermatol 1987; 17(16): 1033–41. Review.

48. Mingrone G, Greco AV, Nazzaro-Porro M, Passi S. Toxicity of azelaic acid. Drugs under experimental and clinical research [Drugs Exp Clin Res] 1983; 9(6): 447–55. 49. Yokota T, Nishio H, Kubota Y, Mizoguchi M. The inhibitory effect of glabridin from licorice extracts on melanogenesis and inflammation. Pigment Cell Res 1998; 11: 355-61. 50. About 39% inhibition at a concentration of 5 × 10–5 mol/l. The minimum active concentration in a topical application seems to be 1–2%. 51. Nakajima M, Shinoda I, Fukuwatari Y, Hayasawa H. Arbutin increases the pigmentation of cultured human melanocytes through mechanisms other than the induction of tyrosinase activity. Pigment Cell Res 1998; 11: 12. 52. At the same doses, tretinoin is more effective than retinol, but it is also more irritating to the skin. Appropriate doses of retinol or retinaldehyde can be just as effective as tretinoin, without being irritating. Keratinocytes have the necessary enzyme arsenal to convert these precursors into retinoic acid, the active molecule. 53. That is, the –C(OH)=C(OH)– part of the molecule. 54. Lee SH, Choi SY, Kim H et al. Mulberroside F isolated from the leaves of Morus alba inhibits melanin biosynthesis. Biol Pharm Bull 2002; 25: 1045–8. 55. Ando S, Ando O, Suemoto Y, Mishima Y. Tyrosinase gene transcription and its control by melanogenic inhibitors. J Invest Dermatol 1993; 100: 1505–55. 56. Usuki A, Ohashi A, Sato H et al. The inhibitory effect of glycolic acid and lactic acid on melanin synthesis in melanoma cells. Exp Dermatol 2003; 12(Suppl 2): 43–50. 57. Excessive application on the doctor’s part, too high a concentration of acid, especially high permeability of the skin, etc. 58. To the papillary or reticular dermis. 59. The cells responsible for immune defense are sensitive to acids and are destroyed by them. 60. Apart from a peel with Unna’s paste, after which hydration is not advised. 61. Even and rapid application, neutralization before the first pinpoint frosting, except for Easy Phytic® solution, which is neutralized naturally by the buffer potential of the skin itself. 62. Brigitte 1995; 19: 62–8. 63. Which thins the stratum corneum, significantly increases epidermal permeability and makes the AHAs penetrate more rapidly and more deeply. 64. Water does not neutralize acids, but dilutes them, which is not enough in this case. An acid is neutralized by combining it with a base to produce a salt. 65. Stone PhA. Peelings au phénol Baker/Gordon et modifiés. J Med Esth Chir Derm 1996; XXII(90): 93–7. 66. 50% m/m = 50 g TCA crystals + 50 g water, whereas 50% m+v = 50 g TCA crystals + 100 ml water. In both cases, it is ‘50%’, but it is clear that the first solution is far stronger than the second. See Chapter 12 for more information. 67. In addition to TCA and water, a tamed solution contains other ingredients that change or regulate its activity. Results are therefore more predictable. 68. Collins PS. Chemical face peelings. In: Elson ML (Ed.), Evaluation and Treatment of the Aging Face, 34–67. 1995, Germany, Springer-Verlag.

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69. Fintsi Y. SEMCC Conference, Sitges, Spain, April 1997. 70. Yeowell HN, Pinnell SR. The Ehlers–Danlos syndromes. Semin Dermatol 1993; 12: 229–40. 71. Drockop DJ, Kuivanieni H, Tromp G, Ala-Kokko L. Inherited disorders of connective tissue. In: Braunwald E, Fauci AS, Kasper DL et al. Harrison’s Principles of Internal Medicine, 15th edn. New York, McGraw-Hill, 2001: 2290–300 (specifically 2295–7). 72. Yusel D. Was Paganini born with Ehlers–Danlos syndrome phenotype 4 or 3? Clin Chem 1995; 41: 124–5. 73. Byers PH. Ehlers–Danlos syndrome: recent advances and current understanding of the clinical and genetic heterogeneity. J Invest Dermatol 1994; 103(5 Suppl): 475–525. 74. Lloyd J, Narcisi P, Richards A, Pope FM. A T+6 to C+6 mutation in the donor splice site of COL31A IVS7 causes exon skipping and results in Ehlers–Danlos syndrome type IV. J Med genet 1993; 30: 376–80. 75. Wertelecki W, Smith LT, Byers P. Initial observation of human dermatosparaxis: Ehlers–Danlos syndrome type VIIC. J Pediatr 1992; 124: 558–64. 76. Clayton E, Wheeler JR. Ehlers–Danlos syndrome. In: Cecil–Loeb Textbook of Medicine, 30th edn, 1712–13. 77. Carr AJ, Chiodo AA, Hilton JM, Chow CW et al. The clinical features of Ehlers–Danlos syndrome type VIIB resulting from a base substitution at the splice acceptor site of tiatron 5 of the Col1A2 genes. J Med Genet 1994; 31: 306–11. 78. Mattar SG, Kumar AG, Lumsden AB. Vascular complications in Ehlers–Danlos syndrome. Am Surg 1994; 60: 827–31. 79. Berney T, La Scala G, Vetterel D et al. Surgical pitfalls in a patient with type IV Ehlers–Danlos syndrome. Dis Colon Rectum 1994; 37: 1038–42. 80. AHAs or TCA in aqueous solution could penetrate too deeply; phenol would certainly cause scarring. Easy TCA® could possibly be used, on the strict condition that it does not go beyond the basal layer of the epidermis (pinpoint frosting). 81. Although some doctors like to prepare the skin. 82. As this peel is slow-release, anything that accelerates penetration must be avoided. The AHAs in this peel build up in the stratum corneum before being slowly released into the epidermis. 83. This type of dangerous procedure consists in reaching the limits of a peel’s possibilities; the safety factor gets lower as the peel gets closer to this limit. 84. A deep peel of the radial folds of the lips (Lip & Eyelid®); see Chapter 36. 85. The skin’s buffer capacity is its physiological capacity to resist variations in pH and keep the pH stable. 86. These can form when too much product is applied at one time. 87. It mainly occurs when the doctor does not prepare the solutions himself. The nurse ‘forgets’ to mix the TCA in aqueous solution with the base solution and actually prepares only TCA 50% m/m for the doctor, who applies it directly to the patient’s skin. 88. The surface to be treated should be touched in the same way as when touching a keyboard: quickly and precisely. There is no delete key with Only Touch®! 89. Wojno T, Tenzel RR. Lower eyelid ectropion following chemical face peel. Ophthalmic Surg 1984; 14: 9–12.

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90. McKinney P, Zukowski ML, Mossie R. The fourth option: a novel approach to lower lid blepharoplasty. Aesth Plast Surg 1991; 15: 293–6. 91. Hecker D, Hacker SM, Ramos-Caro FA, Flowers FP. Temporary ectropion due to topical fluorouracil. Cutis 1994; 53: 137–8. 92. Ideally, of course, this dressing should be worn as a preventive measure rather than a cure. 93. Whether it is a chemical or physical peel. 94. See Figures 37.21 and 37.22. 95. See Figure 37.23. 96. Many of the deep dermal papillae actually survive the acid injury when it starts to affect the Grenz zone. 97. See Figure 37.24. 98. See Figure 37.25. 99. Locally, the peel is (much) deeper and the local immune defenses are destroyed. 100. Let us not forget, however, that some microbes are alcoholand acid-resistant (mycobacteria, for example). 101. LaVerme WE, Drapkin MS, Courtiss EH, Wilson RM. Toxic shock syndrome after chemical face peel. Plast Reconstr Surg 1987; 80: 115–19. 102. Patients with herpes, active acne or active seborrheic dermatitis, for example. These disorders should be treated before the peel. 103. The rolling movement is similar to that used when rolling a cigarette. 104. Using antibiotic creams or ointments. 105. Using a bismuth subgallate or thymol iodide powder mask. 106. McCulloch EG, Langsdon RR, Maloney BP. Chemical Peel with Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermatologic Surgery, Principles and Practice, 2nd edn. 1147–60. 1996, UK, Oxford, Marcel Dekker Ltd. 107. In France, studies have revealed the presence of HSV-1 antibodies in 70% of the population and HSV-2 antibodies in 17% of subjects. Overall, 20% of subjects test positive for anti-HSV-2 antibodies in developed countries, and this rate can reach 60% in developing countries. In France, labial herpes, or cold sores, affect around 12 million people. 108. Only 2 cases of post-peel herpes were counted in 5280 Easy TCA® peels to the basal layer, performed in Spain, on 1320 patients, each treated for 1 month, at all times of the year. 109. Asken S. Unoccluded Baker–Gordon phenol peels – review and update. J Dermatol Surg Oncol 1989; 15: 998–1008. 110. Bupivacaine and ropivacaine have a much longer duration of action than lidocaine. Ropivacaine poses a far lower risk of cardiac arrhythmias. 111. For example, sublingual lorazepam (Temesta®) 2.5 mg of 1/2 to 3 tablets a day. 112. For example, paracetamol (acetaminophen) plus codeine. 113. Sterile Vaseline® should be applied several times a day on the powder mask (see Chapter 35). 114. Two cases of allergy out of 5280 peels: facial edema, mild erythema and pruritus, responsive to the topical application of hydrocortisone for 2 days. 115. From Latin: redness, pain, swelling, heat. 116. Berne MB, Levy NL. Physiology, 3rd edn. Mosby Yearbook, Inc. 1993. 117. This might happen, for example, when Easy Phytic® solution is applied to thin and dry skin. The mixture of AHAs reaches

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the Grenz zone in places and can trigger a local edematous reaction that looks like an allergy, but disappears by itself in 48 hours. This is a rare, but reported, side-effect. Varidase® = 10 000 IU streptokinase and 2500 IU streptodornase. Streptokinase is a protein, an enzyme produced by beta-hemolytic streptococci. It has indirect fibrinolytic properties by binding with plasminogen. It is a fibrin non-specific thrombolytic. Small, whitish and firm formations that form epidermal cysts. They are formed from an accumulation of keratin in the pilosebaceous units. Bismuth subgallate or thymol iodide powder mask (see Chapter 35). Easy TCA® solution contains AHAs, antioxidants, vitamins and saponins, and can be applied on all skin types, without preparation and prior cleaning of the skin. The cream does not contain any local anesthetic, however, and its pH is slightly acidic. It therefore does not neutralize the solution.

124. Chemical blepharoplasty is treatment of the eyelids with a localized deep peel. Chemical cheiloplasty is treatment of the lips with a localized deep peel (see Chapter 36). 125. The nucleic acids in the thymus have the same absorption curve as the ozone layer. If there were no ozone layer, these nucleic acids would absorb UVC, and the free-radical damage caused by this absorption would destroy the body’s immune defenses. 126. Melablock HSP®: physical and chemical protection, SPF 50+ and HSP inducers. 127. The possibility of using phenol as a more superficial peel has been broached elsewhere in this book. Because of the relatively high risk of toxicity and complications, this agent should only be used for deep peels carried out under strict control. 128. Benatar D. Le peeling au phénol. J Med Esth Chir Derm 1988; XV(60): 319–23. 129. Hopkins JD, Smith AW, Jackson IT. Adjunctive treatment of congenital pigmented nevi with phenol chemical peel. Plast Reconstr Surg 2000; 105: 1–11.

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38 Combination of techniques

A trichloroacetic acid (TCA) peel, even if it reaches the papillary dermis, is not always enough to correct the patient’s cosmetic problem, and experienced doctors are often led to combining several techniques to achieve the results they want. Peels can be combined to work together or with other surgical or non-surgical techniques. Using another technique or another peel before a TCA peel is often intended to remove part of the epidermis to enhance penetration of a lower-concentration TCA. The first technique provides the equivalent of a superficial peel that will enhance the action of the TCA applied afterwards. Some authors maintain that using a combination of peels lowers the frequency of complications compared with using more concentrated TCA, in aqueous solution. Not all combinations are safe, however, and a combination of different peels on the same surface often tends to make the symptoms more complex and increase the risk of complications compared with the safer formulations of today. Post-peel care is also more complex when peels are combined, as the injury is deeper: 6–7 days of post-peel care are usually required, when the patient will use Vaseline®, antioxidant creams or antiseptic washes (e.g. povidone–iodine solution). Post-peel care should include a depigmenting cream (Blending Bleaching®) and effective sun protection (Melablock HSP®). Prolonged erythema lasting more than 15 days is common. If it is focal – and therefore suspicious – it can be treated with a strong corticosteroid cream two or three times a week. The risk of scarring and pigmentary changes is greater when peels are combined (on the same surface), because of the increased penetration of TCA. Cosmetics that are suitable for the post-peel period should be used as soon as the skin can tolerate them. Tretinoin, alpha-hydroxy acid (AHA) creams or benzoyl peroxide must not be used again for 6 weeks.

Alpha-hydroxy acids plus trichloroacetic acid AHA peels make the skin more permeable because they reduce corneocyte cohesion and induce partial epider-

molysis. The depth of action of a TCA peel is increased by the prior application of an AHA peel. Glycolic acid 70% in aqueous solution has been tried before TCA. After the usual application, the glycolic acid is quickly diluted with plenty of water. It cannot be neutralized, as if there is any bicarbonate – for example – on the skin before the TCA is applied, it will ‘pre-neutralize’ the TCA. After the glycolic acid has been diluted, the skin is wiped with a paper tissue or gauze swab and 25% m/m TCA is applied. The uneven penetration of glycolic acid in aqueous solution poses a significant problem, as it affects the penetration of the TCA that is applied afterwards. Where the glycolic acid has penetrated more deeply, the TCA will penetrate even more deeply. Where the glycolic acid has not penetrated far, the depth of action of the TCA is barely improved. A combination of AHAs and TCA cannot treat wrinkles or scars, and the indications are much the same as those for TCA in simple aqueous solution (TCA–SAS) used alone. There is no clear advantage to using this combination.

Resorcinol plus trichloroacetic acid This combination has been described in the treatment of photoaging, fine lines, actinic keratoses and on skin phototypes lower than V. It can be used to treat some hyperpigmentations, although there is a high risk of post-inflammatory pigmentary changes. Pre-peel preparation and post-peel care must be rigorous in the latter indication. Jessner’s (or Combes’) solution, described in Chapter 24, is a mixture in equal parts (14 g) of resorcinol, salicylic acid and lactic acid, mixed in ethanol to give 100 ml of solution. It is therefore a mass per volume (m/v) calculation. Jessner’s solution can be used to deepen TCA penetration. After degreasing and disinfecting the skin, a coat of Jessner’s solution is applied and left to dry. A second coat can be applied if the skin is oily and thick. Next, 25% m/m TCA is applied until even frosting is achieved. A cold pack can be applied to the skin at the end of the peel to alleviate the burning sensation that the patient feels.

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Dry ice plus trichloroacetic acid A ‘reasonable’ application of dry ice on its own usually provides a superficial peel; if the dry ice is followed immediately by an application of 25% m/m TCA, the papillary dermis is easily reached, as the prior application of dry ice deepens the lesions created by the TCA. This technique (also called the Coleman technique) can be used on skin phototypes I to III, possibly IV, but never on V or VI. The risk of developing hypertrophic, atrophic or depigmented scars is high if more than 30% m/m TCA is applied after dry ice, especially on the cheeks or around the eyes. Given the inherent risks of this combination, its indications are restricted to the treatment of keratoses or depressed scars, in which the dry ice, applied locally and combined with TCA, produces very good results, comparable to those of a phenol or Only Touch® peel. The technique is as follows: a block of dry ice is held in the hand, protected by several gauze pads to stop it from freezing. The block of dry ice is dipped in a solution of acetone (2/3) and alcohol (1/3) so that it will slide easily over the skin without sticking. The skin is then rubbed vigorously. The depth reached depends on the contact time: the longer the dry ice is left in contact with the skin, the deeper is the lesion caused (Figure 38.1). The action of the dry ice is considered ‘superficial’ if the contact time is 3–5 seconds, ‘medium’ after 5–8 seconds and ‘deep’ after 8–15 seconds.1 An experienced doctor will induce different depths of injury, depending on the type of disorder being treated, by allowing longer contact time between the dry ice and the skin and/or by following the dry ice treatment with a TCA peel of varying concentrations. For example, contact time on keratoses2 will be longer to enhance penetration of the acid afterwards, or a more concentrated acid will be used after an even application of dry ice. This technique requires very thorough preparation: the doctor must examine the problem before the peel and, using a photograph of the patient’s face, draw up a precise chart clearly showing the contact times with the dry ice and the different concentrations of TCA that may be applied after the dry ice. When dry ice that is

soaked in acetone is applied on the skin, fumes are let off that are unpleasant for the patient, who should be properly ventilated to avoid inhalation. It soon becomes clear that it is difficult to control the depth of injury caused by dry ice, and therefore the depth of treatment overall, which is a significant risk factor.

Combination of different concentrations of trichloroacetic acid It is common to combine different concentrations of TCA during the same peel session: a TCA peel to the papillary dermis (Unideep®) can be applied locally for dermal melasma on the forehead, for example, while a TCA to the Grenz zone (Easy TCA®) is applied to the rest of the face (to even out the results) after focal treatment of keratoses or lentigines with a TCA to the reticular dermis (Only Touch®).

Phenol plus trichloroacetic acid Using peels to different depths on the same patient is indicated when disorders of different depths coexist. Consider a patient who presents with early elastosis, a few lentigines and deep wrinkles on the upper lip: only phenol can get rid of the wrinkles on the upper lip, but it would be unnecessarily deep to treat the early elastosis on the rest of the face. The phenol would of course get rid of the few senile lentigines, but a deep and very localized treatment with Only Touch® can also get rid of them and with less risk. This patient would therefore benefit from the following combination (Figure 38.2): •

•

•

•

Figure 38.1 Depth of injury caused by the application of dry ice.

First session: combined peels: application of Lip & Eyelid® formula (occlusive protocol) on the upper lip, immediately followed by an application of Only Touch® peel on the lentigines. Next, Easy TCA® is applied to the whole face, except for the area treated with phenol. 8 days later: a second Easy TCA® application to the Grenz zone (cloudy-white frosting) to the whole face, except for the area treated with phenol. 8 days later: a third Easy TCA® application to the Grenz zone (cloudy-white frosting) to the whole face, except for the area treated with phenol. Last peel session: if the lentigines have not completely disappeared, Only Touch® is reapplied locally. A fourth Easy TCA® is then applied to the Grenz zone (cloudywhite frosting), except for the area treated with phenol.

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8 days

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Easy TCA® 8 days

Only Touch® peel

Full-face Easy TCA®, one per week

Easy TCA®

Only Touch® peel, senile lentigines

Easy TCA®

3

Only Touch® peel

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1 Possibly second Only Touch® before fourth East TCA®

Lip & Eyelid® upper lip Figure 38.2

Graph representing the way to associate different types of peelings and the period for repeating these peelings. A local phenol is first applied (on the upper lid for example). Immediately after, Only Touch® treats lentigines. When local frosting due to the deep TCA (Only Touch®) is perfect, Easy TCA® is applied on the whole face, but not on the phenol treated area.

Repetition of combined peels Combined peels usually reach the dermis. We have just seen that the papillary dermis is easily reached, but it is also possible to reach the reticular dermis using more aggressive combinations locally. This type of peel cannot be repeated until the skin has completely recovered, and not before 3 months. Any persistent erythema, a sign of even the slightest inflammation, rules out another peel.

Face-lift plus peel The high risk of focal or widespread facial necrosis contraindicates a phenol peel immediately after a face-lift. If a face-lift and a deep peel have to be combined, the surgical face-lift must be done first and the chemical peel afterwards to avoid the demarcation line being surgically lifted to the cheek. Caution usually dictates a gap of 6 months between a surgical face-lift and a deep peel. It is of course possible to perform a face-lift without blepharoplasty and a phenol peel around the mouth and eyelids at the same time

of operation. There is no particular risk of necrosis3 in these areas, as they have not been treated surgically. TCA, on the other hand, has been applied successfully by different authors to the whole face at the end of a surgical face-lift. The depth of peel determines the risk of necrosis.

Trichloroacetic acid plus botulinum toxin Can botulinum toxin be injected in the same session as a peel?

Thoughts on the possibility of injecting toxin before a peel Speed of absorption Symptoms of botulism have been reported as soon as 2 hours after ingestion of contaminated food, which means

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that intoxication is very rapid considering the time taken for digestion and intestinal absorption. Uptake of the toxin by the synapse is a rapid phenomenon that takes place in several stages, the first of which is the binding of the toxin with an ectoreceptor/acceptor. Next comes internalization in the presynaptic membrane, the formation of endosomes and the intracytoplasmic interactions that eventually block the release of acetylcholine in response to a nerve impulse. The internalization and ‘internal actions’ are slower and more complex phenomena than simple binding at the receptor/acceptor site. Vesicles that mediate internalization can be seen after 30 minutes through an electron microscope. Uptake of toxin at the receptor site is therefore very rapid and starts within the first few minutes (or seconds?) after the toxin has been injected into their immediate environment.

Different depths of action Botulinum toxin (discovered in 1895 by Ermengem from Belgium) is injected deep down in the facial muscles, whereas peels do not injure the skin beyond the reticular dermis at the most.

Influence of inflammation The inflammatory reaction and edema that follow TCA peels (especially in simple aqueous solution) seem to be the determining risk factor of this combination. There is a risk of the toxin traveling or diluting in the post-peel edema. Therefore, under no circumstances should botulinum toxin be injected after any peel whatsoever, as long as the inflammatory reaction and edema are still active.

tion or depth of action, nor has the toxin moved during this combined procedure. To my knowledge, injection of botulinum toxin immediately before other peels has not been tested, and it is advisable to leave a rest period of 1 week after injection of the toxin if a peel other than Easy TCA® is applied.

Trichloroacetic acid and fillers Hyaluronates and papillary peels clash on the battlefield of the dermis, and it is generally recommended not to inject sensitive polymers before applying a peel. Hyaluronic acid is a large carbohydrate polymer that is sensitive to external aggressions such as free-radical attacks. Peels that produce a severe inflammatory reaction generate a large number of free radicals that can break the hyaluronate polymers, shorten their lifespan in the dermis and introduce a great many macrophage cells into the dermis that can phagocytose the hyaluronates. Under these conditions, the lifespan of the hyaluronic acid is shortened and filler injections with sensitive polymers should be given some time after a peel. This technique also means an extra journey and more lost time for the patient. I have therefore also used Easy TCA® at the same time as injections of collagen and different reticulated hyaluronic acids (Restylane®, Juvederm®, Esthélis®, etc.) and have not seen any difference in the behavior of wrinkles, whether or not these injections are combined with Easy TCA®. The filler injection is given first and Easy TCA® (solution plus post-peel mask) is applied immediately afterwards. The antioxidant qualities of the postpeel mask seem to explain the fact that there is no interaction.

Injecting the toxin before a peel It is generally accepted (but not officially specified) that botulinum toxin should be injected at least 1 week before a peel. The obvious advantage of this prior injection is that the toxin blocks muscle movements and allows the dermis and epidermis to regenerate on a ‘smooth base’. Eight days after the toxin has been injected, its effect is complete and the peel can be applied without any risk of the toxin being moved or diluted. However, this technique means an extra journey and more lost time for the patient. After 10 years of clinical experience in the simultaneous use of botulinum toxin and Easy TCA®, I can safely say that there is no risk in combining these two procedures during the same session. The botulinum toxin is injected first, and a rest period of 10 minutes is left to give time for the uptake of the toxin at the presynaptic acceptor site. The Easy TCA® peel is then applied according to the basic protocol (see Chapter 15). There has never been any change in dura-

Trichloroacetic acid and abrasion We saw in Chapter 21 that it is possible to combine sandpaper abrasion with Easy TCA®.

Microdermabrasion with corundum crystals In reality, the advantage of preceding a peel with microdermabrasion is far from clear, as microdermabrasion does not provide abrasion as even as that produced by simple sandpaper. The handpiece of the microdermabrasion unit is comparable to a pencil, and its action can be likened to drawing a criss-cross of lines with clear spaces in between. The TCA solution penetrates more deeply in the base of the abrasion lines, giving a linear and uneven peel.

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Combination of techniques

Laser

Notes

Laser treatment is not a simple alternative to sandpaper abrasion. Unlike sandpaper, it is painful and requires prior anesthesia. Besides, it is most likely that gentle and gradual abrasion with sandpaper has a clear advantage over laser abrasion in that it does not put any heat stress on the skin.

1. 2. 3.

375

Here, 3–5 seconds means in practice: 3 seconds on thin skin and 5 seconds on thick skin. Or around the edges of scars to attenuate the difference in height. Asken S, Unoccluded Baker–Gordon phenol peels – review and update. J Dermatol Surg Oncol 1989; 15: 998–1008.

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Index

Page numbers in italics refer to illustrations or tables abrasion 152 erbium laser 152 keratosis pilaris treatment 165, 166 microdermabrasion 152 scar treatment 162–3, 163 body scars 163–5 uneven 161 with phenol peel 279, 280 with TCA peels 374 see also sandpaper abrasion accordion effect 33 acetaminophen 195–6, 195 acetic acid 79, 79 acetone, skin preparation 54, 92, 149, 259 acetylcholine (ACh) 21–3 esterase 22 achromia, following AHA peels 68 aciclovir 353 acne 16, 27–8, 34, 34, 73, 359 comedonal 8, 33–4, 33, 125–6, 125 macrocomedones 33–4 conglobata 102 fulminans 102 microcystic 126, 126 necrotica 102 papulopostular 73, 74, 126, 126 rosacea 8 scars 31, 127, 162 back 145, 163, 165 décolletage 142 ECTA treatment 163, 165 ice-pick scars 55 phenol treatment 241–3, 242, 243 TCA treatment 100, 103 see also scars treatment 15, 31, 359 AHAs 17, 55 combined treatment 127 Easy Phytic® 73–4 ETCA 125–9, 125–8 isotretinoin 102, 103 Jessner’s formula 188 maintenance treatment 127 multifocal treatment 128–9 phenol peels 240–3, 242, 243

post-peel care 126–7, 127 problems 127, 128 side-effects of acne 127 TCA 102–3, 103, 109–10 actinic keratoses see keratoses adrenaline phenol peels and 249 with lidocaine 152–3, 153, 264 aging skin 36, 36 AHA peels and 55–6 Easy Phytic® 71–3 free radical aging 31 hands 135–8, 136–9 prevention 97–8, 120 treatment 17–18 over 40–45 years old 18 sagging skin 18–23 under 40–45 years old 17–18 see also photoaging Ahronson formula 196 alcohol phenol resistance and 212 skin preparation 54 with phenol peels 201 all-trans-retinoic acid (ATRA) 7 see also tretinoin allergies to AHAs 67 to antibiotic cream 27 to local anesthetics 262 to resorcinol test for 185 Unna’s paste 189–90 alpha-hydroxy acids (AHAs) 47, 48, 69 application of 54 number of sessions 61 buffers 49–50, 61, 63 classification of peels 2 combination treatment 59–60 hydroquinone 60 TCA 371 tretinoin 56, 59–60 contact time 49–50, 54, 62–3 depth of peel 2 skin appearance and 62

378

Index

alpha-hydroxy acids (AHAs) (cont.) effectiveness 57–8 factors influencing penetration 53–4, 70 histological effects 53 dermis 53 epidermis 53 hyperpigmentation treatment 341 indications for use acne 55 aging 55–6 hyperkeratotic eczema 57 ichthyosis 56–7 melasma 56 warts 56–7 xerosis 56–7 mechanism of action 51 neutralization 50, 54, 63–4, 69 partially buffered solutions 64 preparation of neutralizing solution 63 pKa 50–1 post-peel care 15, 65 pre-peel preparation 5–6, 11, 54 Jessner’s formula as 189 repeat peels 54, 61 side-effects 67–8 achromia 68 allergies 67 dryness, desquamation, sensitization 67 erythema 67, 319, 324 hyperpigmentation 67, 331, 335 infections 67–8 melanocyte toxicity 317 pain 67, 359, 361 scarring 68, 342–3, 346 shiny skin 68 telangiectasias 67 slow-release complex see Easy Phytic® solution (EPS) see also glycolic acid; lactic acid alpha-tocopherol see vitamin E aluminium oxide 89, 184 amino acids, dietary 30 analgesics following stretch mark treatment 161 phenol peels and 253, 256, 292, 362 TCA peels and 43 Unideep® 179 see also pain anaphylactic shock 262 anesthesia abrasion and 151 with ETCA 152–3 allergy to local anesthetics 262 checking effectiveness of 153 chemical blepharoplasty 296 phenol anesthetic effect 203, 203, 261 phenol peels 262–5, 361 bupivacaine 263 combination with adrenaline 264 EMLA 264–5 general anesthesia 262

lidocaine 263–4 mepivacaine 263 prilocaine 263 repivacaine 263 scalp 131–2 scar treatment 162 TCA peels 43, 106, 360 Unideep® 179–80, 179 toxicity of local anesthetics 262–3 see also nerve blocks angina 249 angiogenesis 7, 8 retinoid effects 59 antibiotic treatment 350, 351–2 acne 127 allergies to antibiotic cream 27 phenol peels and 258, 284, 288–9 post-peel care 16 apoptosis 18 heat stress and 14 Aptos® threads 231, 231 arbutin 6, 17, 339, 339 Argentofenol® 214 arginine 30 arrhythmias anesthesia and 262, 263 phenol and 216–20, 217, 258 bradycardia 220 premature ventricular contraction 217, 217 tachyarrhythmias 217, 217, 220 ascorbic acid 41–2, 49 in ETCA 112 see also vitamin C ascorbyl palmitate (AP) 110, 341 ascorbyl phosphate 341 asepsis 259 Asian skin, melanocyte toxicity 318 asiaticosides 82 aspirin 360 atropine 220, 258, 271 Ayres formula 196 azelaic acid 6, 339 acne treatment 17 hyperpigmentation treatment 339 melasma treatment 98, 339 back acne treatment 55 scars 145 anti-aging treatment 72 bacterial infections see infection Baker–Gordon solution 273, 332 Baker’s formulas 196, 206 toxic shock and 350 basal layer peel 328, 328, 348–9, 354 bentonites 89 benzene 184 benzodiazepine herpes infection and 353 pain management 362

Index

phenol peels and 253 advantages of 256–7 benzoic acid, in resorcinol peels 184–5 benzoin in resorcinol peels 184 tincture of 186 benzoyl peroxide 8, 9 AHA peel preparation 54 Easy Phytic® 75 TCA peel preparation 87 beta-blockers 219, 264 betamethasone 28 bigeminy 217 biosaccharides 18 biotin, in ETCA post-peel mask 111 bismuth gallate 289 bismuth subgallate (BSG) 147, 156–7, 156, 288–90, 342 chemical blepharoplasty and 298–9, 298–300 making a mask 289–90, 289–91 bismuth subnitrate 289 bisphenols 195 black skin hyperpigmentation treatment 8 melanocyte toxicity and 318 TCA sensitivity 91 bleeding, abrasion and 151, 152, 152 Blenderm® occlusive mask 257, 257, 285 Blending Bleaching® cream 17, 123, 167 chemical blepharoplasty and 302 melasma treatment 121, 122 post-inflammatory hyperpigmentation treatment 124 stretch mark treatment 158 Unideep® treatment and 182 blepharoplasty surgical 295, 295 see also chemical blepharoplasty blood pressure, phenol and 220 body peels 32, 330 AHA peels 61 Easy Phytic® 72–3, 72 resorcinol peel 186 see also specific areas of the body botulinum toxin (BTX) 11, 21 combination treatment 43 Easy Phytic® 71–2 phenol 233–4, 233 TCA 43, 373–4 expression wrinkles and 31, 36 prevention 315 perioral wrinkles and 36 pre-peel preparation 61, 253, 274 chemical cheiloplasty 304 botulism 373–4 Bowen’s disease 170, 172 bradycardia 220, 262 Brown and Kaplan solution 196 buffering AHAs 49–50, 61, 63 importance in the body 50 phenol peels 201

bupivacaine 263 burns 24 calluses 81 carbachol 21, 21 carbamide see urea carbolic acid see phenol carbon dioxide laser resurfacing 232 carboxylic acids 49 carcinoma 240 TCA treatment 102 cardiac arrest, phenol and 220–1 cardiorespiratory monitoring, phenol peels 258 cardiovascular complications, phenol 215, 216–21 blood pressure 220 bradycardia 220 cardiac arrest 220–1 prevention 219–20 tachyarrhythmias 217, 217, 220 treating arrhythmia during peel 220 catechin 194 catechol 193, 193 ceramides 18 ceyssatite, in resorcinol peels 184 chaperonins 14 cheilitis, actinic 60 cheiloplasty see chemical cheiloplasty chelation 89 chelated TCA 89 iron chelation by lipoic acid 18 chemabrasion 145, 162, 279, 280 chemical blepharoplasty 235, 235, 295–304, 361 anesthesia 296 application 296–7, 296, 297 complications 302–3 delayed healing 302, 302 demarcation line 302 pain 302 pigmentation changes 302 effectiveness 301, 301, 303, 304 eye protection 296 indications 301 occlusion 297–8, 297–9 phenol solution 296 post-peel care 298–9, 300, 310–11 post-peel developments 300 edema 300, 300 erythema 300, 301 pre-peel care 309–10 chemical cheiloplasty 36, 235, 304–11, 305–9, 361 post-peel care 310–11 pre-peel care 309–10 results 309 chemical peels classification criteria 1–3 chemical dependence 2 doctor dependence 1 patient dependence 2–3 definition 1 depth of 2

379

380

Index

chemical peels (cont.) deep 3 medium 3 skin appearance and 62 superficial 3 very superficial 3 see also specific peels chemical sympathectomies 245–6 chemical tanning 16 chloasma 98–9 see also melasma choline acetyltransferase 22 cholinergic receptors 21 cimetidine 264 citric acid 41, 47, 48 in ETCA 112 in ETCA post-peel mask 111 clay 89, 89 clay masks, TCA in 89–90, 90 coal tar 194 coconut fatty acid monoethanolamide (cocamide) 41 in ETCA 112 coenzyme Q-10 18 coenzyme R, in ETCA post-peel mask 111 cold anesthetic properties 261 cold packs 251, 261, 292, 360 cooling mask 271, 271 collagen AHA effects 71 production by fibroblasts 7, 53 vitamin C effect 341 regeneration 342 TCA effects 91, 95 colloid dressings 28, 342 Combes’ solution 187 Combes, Sperber and Reisch solution 196 comedonal acne 8, 33–4, 33 macrocomedones 33–4 treatment comedone extraction 125 ETCA 125–6 see also acne confetti-like depigmentation 6, 6, 338 conjunctivitis, phenol and 221 contact time 49–50 AHA peels 54, 62–3 glycolic acid 55, 56, 62–3, 63 resorcinol 186 cooling mask 271, 271 corneal opacity 20 corneocytes 209 corneodesmosomes 6, 51 AHA effects 67 corticosteroids intravenous 28, 258, 348 oral 28 topical 9, 28 erythema treatment 325–6 following AHA peel 64

hyperpigmentation treatment 341 scar treatment 348 cortisone 60 erythema and 319 corundum crystal microdermabrasion 374 cosmetics see post-peel cosmetics cresols 194, 194, 200 croton oil 199–200, 317 Croton tiglium 199, 199 crow’s feet 38 cryoanesthesia 360 Unideep® and 179, 179, 360 cumene 193, 193 cyclohexanehexyl hexaphosphate 70 cysteine 18

dansyl chloride 51 dark skin melanocyte toxicity and 318 pigmentary changes 8, 11 TCA sensitivity 91 deanol see DMAE décolletage AHA peels 61 ETCA treatment 142–4, 142–4 Jessner’s formula use 189 lentiginosis 141, 142 photoaging 141, 142–4, 142–4, 145 scars 163–5, 165 acne scars 142 dehydration 27 demarcation line 275, 278, 279, 280, 292, 318, 363–5, 364 chemical blepharoplasty 302 depth of peel and 363–4 high-risk areas 365, 365 prevention 365 skin type and 364 depigmenting agents 336–41 dermabrasion see abrasion; sandpaper abrasion Dermacool® 261 dermal atrophy 36–7, 38 dermal filling 11 combination treatment 43–4 dermatitis acneiform 9, 351, 352, 359 berloque 99 retinoid 8, 9–10 seborrheic 9, 10, 54 TCA treatment 100–1, 103 dermis AHA effects 53 phenol effects 206–7 desquamation, AHA peels and 67 glycolic acid 61 diabetes 30 as contraindication for phenol peels 249 as contraindication for TCA peels 104 scarring and 345 dicarboxylic acids 49

Index

dichloroacetic acid (DCA) 80–1, 80 application protocol 80–1 chemistry 80 toxicity 80 dichlorophene 195 N,N-diethylaminoethanol (DEAE) 20 dihydrolipoate (DHLA) 18 dihydrotestosterone 16 dilated pores 32, 365–7 phenol treatment 245 TCA treatment 100 N,N-dimethylaminoethanol see DMAE dimethylethanolamine see DMAE N,N-dimethylisopropanolamine (DMIPA) 20 Dioscorea (Mexican wild yam) 18 diphenol 193, 194 discoloration see pigmentary changes disinfection, phenol 204 diuresis, phenol peels and 258 dizziness, resorcinol peels and 190 DMAE (N,N-dimethylaminoethanol) 18–23 chemistry of 19 historical use of 20 modes of action 21–3 action on striated facial muscles 21 dermal action 22 effect on myofilaments and smooth muscle cells 22–3 epidermal action 21–2 exocrine glands 23 vasomotor effect 22 sagging skin treatment 19, 21–3, 33 topical skin application 21 side-effects 19–20 toxicity 20 DMIPA (N,N-dimethylisopropanolamine) 20 dry ice treatment 372 dry skin 55 following AHA peels 67 Dubreuilh’s melanosis 102 dyschromias 34, 34, 56, 327–30 phenol treatment 237–9, 237 resorcinol application 183 Jessner’s formula 188 risk of 328, 329, 330 see also specific dyschromias Easy Phytic® solution (EPS) 69–78, 70 application 76–7, 76 body treatments 72–3, 72 combination treatment 71–2 botulinum toxin 71–2 flashlamp therapy 72 mesotherapy 71 contraindications 77 erythema and 319 indications 71–4 acne 73–4 aging skin 71–3 post-peel care 77 pre-peel preparation 75–6

cleansing 75, 76, 76 precautions 74–5, 75 repeat peels 77 scar prevention 346 see also alpha-hydroxy acids (AHAs) Easy TCA® (ETCA) 40–5, 86, 109–20, 110 acne treatment 125–9, 125–8 combined treatment 127 comedonal acne 125–6 microcystic acne 126 papulopustular acne 126 scars 145 side-effects of acne 127 actinic keratosis treatment 174–5 application 115–18, 115–17, 122 applicator 114–15 base solution 111–12 complications erythema 321, 321–2, 325 hyperpigmentation 332, 332, 335, 336 pain 361 scar prevention 346 décolletage treatment 141, 142–4, 142–4 depths of action 116, 117 hand treatment 136–40 photoaging 136–8, 136–7 solar lentigines 137, 137, 138, 168 warts 139, 140 indications 112 keratosis pilaris treatment 165, 166 lentigine treatment 137, 137–8, 170, 171, 174–5, 175 lip treatment 304, 305–6 maintenance of results 119, 123 melasma treatment 121–4, 121–2, 123 problems 123–4 neck treatment 141, 141 photoaging treatment 119 post-inflammatory hyperpigmentation treatment 124 post-peel care 117–18, 122–3, 137, 144 post-peel mask 110–11, 117, 122, 154, 154 sun protection 118 pre-peel preparation 114 repeat peels 118–19, 122, 144 scalp keratoses treatment 131–3, 131, 133 scar treatment 162–3, 162, 163 body scars 163–5, 164 smokers’ skin and 119 solution preparation 112–14, 113, 114 stretch mark treatment 145, 152–61, 321, 321 anesthesia 152–3, 153 complications 161 post-peel care 160–1 protocol 153–8, 153–9 results 158–60, 159–60 with Only Touch® 169 with sandpaper abrasion 146–7, 146 anesthesia 152–3 see also trichloroacetic acid (TCA) ectropion 347 prevention 347

381

382

Index

eczema 183 hyperkeratotic 57 edema 28, 319, 354–8, 356 eyelid, following chemical blepharoplasty 300, 300 pain and 357 phenol peel and 203, 277, 277, 357, 357–8 prevention 358 severity 354–7 stretch mark treatment and 155, 155 TCA peel and 356, 357 treatment 358 Ehlers–Danlos syndrome 345 elastin 95 elastosis 56 phenol treatment 236 elderly patients 27 see also aging skin electrocardiography (ECG) 258 electrocoagulation 11, 327 Eller and Wolf’s solutions phenol 196 resorcinol 187 EMLA cream 152 herpes treatment 353 phenol peels and 264–5 enzymatic TCA 88 epidermal sliding 153, 181 epidermis AHA effects 53 phenol effects 206 regeneration 53 epidermolysis 53, 206 epinephrine see adrenaline epistaxis 80 epithelioma basal cell (BCE) 170 squamous cell (SCE) 170 Epstein mask 285 erbium laser abrasion 152 erythema 319–26 AHA peels and 62, 67, 319, 324 following chemical blepharoplasty 300, 301 phenol peels and 319, 323–4, 323–4, 325 prevention 324–5 resorcinol peels and 190 TCA peels and 320–3, 320, 325 Easy TCA® 321, 321–2 Only Touch® 173, 322, 323 Unideep® 322, 322 treatment 325–6 corticosteroids 325–6 cosmetics 325 laser treatment 326 tretinoin treatment and 10 esterification reaction 53–4 estradiol benzoate 60 estrone 60 ether, skin preparation 54 excipients, in ETCA 112 Exoderm® 197, 197

acne scar treatment 242, 243 wrinkle treatment 234 expression wrinkles 31, 36, 315, 315 phenol treatment 234 eye contact Easy Phytic® solution 75 TCA 81 eyebrows, phenol application 278 eyelids, phenol application 278, 278, 279, 296–7, 296–7 see also chemical blepharoplasty face-lift combined with peel 373 phenol peel 230–1, 230 scars 243–4, 244 versus phenol peel 228–30, 228–9 facial nerve blocks (FNB) 265–9 frontal and upper eyelid block 265, 266–8 lateral regions 267–8, 269 mid-face and outer eyelid block 266–7, 267 fentanyl 271 fibroblasts 22, 44, 206 abrasion effects 146 AHA effects 51 collagen production 7, 53 resorcinol effects 184 fibronectin 22–3 fillers 43–4, 374 fine lines 56 AHA effectiveness 58 phenol treatment 233 flaking skin, post-peel care 15, 16 flashlamp treatments 14 combination treatment 44 Easy Phytic® 72 flavonoids 193, 194 flumazenil 271 fluocinolone 326 5-fluorouracil (5-FU) 60, 347 keratosis treatment 102, 102 folds AHA effectiveness 58 nasolabial 34 phenol treatment 233–4 TCA effectiveness 95 folliculitis 183 folliculitis barbae 128 forced diuresis 219 forearms aging 135 AHA peels 61 tretinoin treatment 8 freckles 29, 36, 99, 100, 318 removal 177, 178, 238 TCA treatment 99–100, 100 frontal nerve 132 frosting AHA peels 62 Jessner’s formula 188 phenol peels 276–7, 276–7

Index

TCA peels 107, 108, 320 ETCA 115, 116, 123, 137, 153, 154, 163, 321 scalp treatment 131, 131 Unideep® 180, 181 fruit acids see alpha-hydroxy acids (AHAs) furosemide 219, 220 gallic acid 289 gastrointestinal symptoms, phenol intoxication 215 giant hairy nevus 245 ginsenoids 82 glabridin 17, 339, 339 gluconic acid 48 glutamine 30 glutathione 18 glycerol 48, 82, 87 adjuvanted to phenol 201 adjuvanted to TCA 87–8 glyceryl monooleate 88, 88 glycolic acid 31, 47–8, 55, 69 acne treatment 17, 55 application technique 62 as pre-peel treatment 57 classification of peels 1, 2 contact time 49–50, 55, 56, 62–3, 63 cosmetic application 59 desquamation 61 effectiveness 58 factors influencing penetration 53–4 histological effects 53 hyperpigmentation treatment 341 neutralization 64, 64 pH 49 post-inflammatory hyperpigmentation 331 post-peel care 65 pre-peel preparation 60–1 see also alpha-hydroxy acids (AHAs) glycosaminoglycans 7, 30 AHA effects 53 TCA effects 91 glycyrrhetinic acid 17, 18 Grade’s formulas 196 Grenz zone 206, 328–9, 329, 355 infection risk 349 guaiacol 194–5, 194 hairline, phenol application 278 halcinonide 326 haloacetic acids 79, 79 see also specific acids hands 32 aging 135–8, 136–9 AHA peels 61 solar lentigines 137, 137–8, 168 TCA treatment 95, 96 ETCA 136–40, 136–9, 168 warts 101, 101 tretinoin treatment 8 healing process 28, 342 chronology 342

383

delayed healing 302, 302 heat stress 13–14 sublethal damage 14 heat-shock proteins (HSPs) 13–14 sun protection and 14–15 hectorites 89 hemorrhoids 247 hepatic toxicity, phenol 222 herpes Easy Phytic® and 77 following AHA peels 68 phenol peels and 249 pigmentary changes and 334–5 prevention 6, 10, 109 ETCA versus TCA–SAS 42 resorcinol peels and 190 secondary 352–4, 352, 353 differential diagnosis 353 prevention 353 risk of 352 symptoms 352–3 under occlusive mask 354 Hetter formulas 197–8, 197 hexachlorophene 195, 195 hormone replacement therapy (HRT), phenol peels and 250 Hutchinson’s freckle 102 hydrocortisone 28, 105 erythema treatment 325–6 hydroquinone 6, 56, 187, 193, 193 combination treatment with AHAs 60 hyperpigmentation treatment 17, 337–8 phenol oxidization to 209 TCA peel preparation 105 tolerance 11 4-hydroxyanisole (4-HA) 340 hydroxybenzene 193 hydroxyproline 53 hydroxyzine 271 hyperkeratinization 55 hyperkeratosis 10, 55 hand 139 pigmented 56 treatment 57 hyperpigmentation 8, 330–41 following chemical blepharoplasty 302 following keratosis treatment 173, 174 following resorcinol peels 190 following stretch mark treatment 87, 161 monitoring 335–6 post-inflammatory (PIH) 13, 16, 35–6, 35, 39, 100, 331 AHA peels 67, 331 phenol peels 237–8, 332–4, 334 sensitivity test 334 TCA peels 44–5, 173, 174, 331–2, 331–2 pregnancy and 336 prevention 334–6 even application of peel 335 re-peeling 336 skin preparation 334–5 sun protection and avoidance 335

384

Index

hyperpigmentation (cont.) treatment 17, 31–2, 336–41 corticosteroids 341 pre-peel treatments 60 sun avoidance 341 TCA treatment 99, 124 topical depigmenting agents 336–41 hypertrophic scars 32 hypervitaminosis A 10 hypothyroidism, secondary 189 ichthyosis 47 treatment 56–7 inadequate results 314–16 facial expressions 315, 315 histological regions 315–16 inadequate preparation and 314–15 poor product knowledge 314 prevention of 316 treatment 316 repeat peels 316 wrong indication 314, 314, 315 infection 27, 348–54 bacterial 67–8, 349–52 treatment 351–2 following AHA peels 67–8 following resorcinol peels 190 following stretch mark treatment 161 pigmentary changes and 334–5 prevention 6, 10, 350–1 post-peel care 16 TCA peels 42, 44 risk of 348–9 see also herpes inflammation 30 stretch mark treatment and 149, 155, 155 tretinoin treatment reaction 9 with Easy Phytic® treatment 74–5 with phenol treatment 203 informed consent form 253, 255 inositol hexaphosphoric acid 70 insulin-dependent diabetes see diabetes intense pulsed light (IPL) 72 intraepidermal peel 327, 327 involucrin 209 iodoform 289 iron oxide 184 isotretinoin 8, 87 acne treatment 102, 103, 128 phenol peels and 250 scarring and 345 TCA peel preparation 105 jaundice, phenol and 221 Jessner’s solution 183, 187–9 application 188 as preparation for a TCA peel 188–9 as preparation for an AHA peel 189 classification of peels 2 formulations 187

indications for use 188 keratosis treatment 189 post-peel care 187 safety 188 see also resorcinol kaolin, in resorcinol peels 184 Karp’s formulas 196 keloids 241 phenol peels and 250 keratinocyte touch, abrasion and 152 keratolytic effect, phenol 214 keratoses 7, 10, 102, 167 actinic 60, 170–2, 171 ETCT treatment 174–5 Only Touch® treatment 167, 172, 172, 173 phenol treatment 240 post-peel care 172 precautions 174 TCA treatment 96, 97, 102 treatment complications 173 tretinoin preparation and 10 impermeability of 132 scalp 131, 131 ETCA treatment 131–3, 131, 133 local anesthesia 131 post-peel care 132, 132 preparation for treatment 131 seborrheic 174, 239, 239 senile 10 treatment 61, 81, 102 Jessner’s formula 189 phenol peels 239–40, 239 keratosis pilaris 154, 166 kidney disease, phenol peels and 249 kidney insufficiency 30 Klein solution 152, 196 Kligman’s formulas 17, 338 Köbner phenomenon 161 kojic acid 6, 11, 60, 187, 338 hyperpigmentation treatment 17, 338–9 lactic acid 11, 48–9, 187 hyperpigmentation treatment 341 skin sensitivity testing 359 see also alpha-hydroxy acids (AHAs) lactic acidosis 80 Langerhans cells (LC) 42, 109, 206 Langerhans, Paul 109 lanolin, in resorcinol peels 184 laser treatments 14, 28, 375 erythema 326 versus phenol peel 232 lentigines 8, 22, 34, 34, 56, 167, 169–70, 170 hands 137, 137–8, 168 histology effect on results 315, 315 treatment 32, 61, 169 ETCA 137, 137–8, 170, 171, 174–5, 175 Only Touch® 137, 138, 167, 168, 170, 171 resorcinol 183

Index

lentiginosis décolletage 141, 142 TCA effectiveness 96, 97, 97 see also lentigines lentigo maligna 102, 170 phenol treatment 238–9, 239 Leukoflex® occlusive mask 257, 257, 285 licorice extracts 6, 339 hyperpigmentation treatment 17, 339 lidocaine 20, 152, 262, 263–4 arrhythmia prevention 220 phenol peels and 262, 263–4 nerve blocks 265–70 tachyarrhythmia treatment 220 with adrenaline 152–3, 153, 264 linoleic acid 30 linolenic acid 30 Lip & Eyelid® formula 198, 228, 235, 273, 296 application 276–9, 296–7, 296–7 dyschromia treatment 237 edema and 357, 357–8 photoaging treatment 227 post-peel care 293 use with Unideep® 228 wrinkle treatment 233, 235 upper lip 304, 305–9 see also chemical blepharoplasty; phenol peels lipofuchsin 22 lipoic acid 18 iron chelation 18 lips see chemical cheiloplasty liquiritin 17 Lister, Lord 196, 214–15 Litton’s solution 197, 273, 332 liver disease, phenol peels and 249 lorazepam phenol peels and 253, 256, 271 pruritis and 354 lunchtime peel 71 Lysol® 194, 200, 215 macrocomedones 33–4 magnesium ascorbyl phosphate (MAP) 110, 341 magnesium oxide 89, 184 make-up 29 phenol peels and 227, 250 malic acid 48 mandelic acid 47, 48 marionette lines 34 medizolam 271 melanocyte toxicity 316–19 AHAs 317 phenol 317–18 prevention 318 skin phototype and 318–19 TCA 317 treatment 319 melanocytes 206 exocytosis 317 membrane fusion 317

385

phagocytosis 317 see also melanocyte toxicity melasma 8, 98, 98, 121 post-peel care 15, 16 skin preparation 121–2 treatment 31–2, 39, 40 AHA peels 56 persistent dark ring 123, 124 phenol peel 237–8 recurrence 124 TCA 98–9, 99, 121–4, 121–2, 123 Melonin® 156, 156 men, phenol peels 29, 226, 226 mental block 270, 270 mental retardation 29 Mepiform® 348, 348 Mepilex® 156, 156 Mepitel® 348, 348 mepivacaine 263 mesolift see mesotherapy mesotherapy 11 post-peel care 15 with Easy Phytic® treatment 71 methemoglobinemia 189, 263 microdermabrasion 152 corundum crystals 374 Micropore® occlusive mask 257, 257, 285 milia 358–9 prevention 358 treatment 358–9 moist technique 288 molecular chaperones 14 Monheit technique 188–9 monoamine oxidase (MAO) inhibitors, phenol peels and 250, 253, 264 monobenzone 336–7, 336 monochloroacetic acid (MCA) 79–80, 79 poisoning 79–80 monofluoroacetic acid 80 Morus alba 6, 11 hyperpigmentation treatment 17, 341 Moy technique 189 mucopolysaccharides 71 mulberroside F 17, 341 myofibroblasts (MFBs) 22–3, 204–5, 205 abrasion effects 146 myofilaments DMAE effects 22–3 nasolabial folds 34 natural moisturizing factor (NMF) 18 nausea phenol peels and 215 resorcinol peels and 190 neck 31, 141 AHA peels 61 demarcation line prevention 365 ETCA treatment 141, 141 Jessner’s formula use 189 phenol peels 250–1, 280–1

386

Index

neck (cont.) photoaging 141, 141 neoangiogenesis see angiogenesis neomycin allergies 27 nerve blocks herpes infection treatment 353 phenol peels and 262, 265–70, 361 facial nerve block application 265–9, 266–9 mental block 270, 270 TCA peels 360–1 Unideep® 179, 180 neuroablation 246–7 neurological symptoms, phenol intoxication 215 neurolysis 245–6 neutralization, AHAs 50, 54, 63–4, 69 partially buffered solutions 64 preparation of neutralizing solution 63 nevi 245, 366, 367 norcholine see DMAE normal skin characteristics 25 nutrition 30 occipital nerve of Arnold 132 occlusive dressing 15, 342 chemical blepharoplasty 297–8, 297–9 EMLA cream and 264 herpes infection under 354 phenol application and 211, 282, 282, 283–6, 285, 286 bismuth subgallate mask 288–90, 288–91 removal 287, 386–7 TCA application and 92 ETCA 147, 154–5, 154, 155 ochronosis 338 oily skins, tretinoin treatment 8 older patients 27 see also aging skin oliganuria, phenol and 221 olive skin, pigmentary changes 11 Only Touch® 167, 167 application 168–9 combination treatment with ETCA 169 complications erythema 173, 322, 323, 325 hyperpigmentation 332, 333, 335 scar prevention 346–7 indications for use 167 keratosis treatment 139, 167, 172, 172, 173 complications 173 post-peel care 172 precautions 174 lentigine treatment 137, 138, 167, 168, 170, 171 pre-peel preparation 167 solution preparation 167–8 wart treatment 139, 140 see also trichloroacetic acid (TCA) ophthalmic toxicity, phenol 221 p-aminobenzoic acid (PABA) 20, 20 pain 359–62 abrasion and 152

AHA peels 67, 359, 361 edema and 357 herpes infection 353 phenol peels 203, 292, 361, 362 evolution of 270–1 stretch mark treatment 161 TCA peels 43, 360–1 scalp treatment 133 see also anesthesia painkillers see analgesics papillary dermis peel 329, 329, 349, 355–7 papillomas 80 paracetamol 195–6, 195, 362 partition coefficient 201 perioral wrinkles 36, 37 petechiae 366, 367 petrolatum, in resorcinol peels 184 PFPE 18 pH 49, 49 effect of dilution of solution 50 phenol 184 administration routes in the past 215 anesthetic effect 203, 203, 261 aqueous versus oil vehicle 211 capillary absorption 209 carcinogenicity 203 chemical neuroablation 246–7 chemical sympathectomies 245–6 chemistry of 193, 193–4 derivatives 194–6 disinfection 204 halogenated phenols 195 hemorrhoids and 247 lymphatic absorption 209 medications containing 213–14 dental wick 214 gargles 213 mouthwash 214 soap 213 metabolization 209–10, 210 urinary elimination 212 neurolysis 203, 245–6 peels see phenol peels protein coagulation 203–4 sensitivities 212 spasticity and 246–7 toxicity 211, 213–22 animal studies 213 antidotes 216 by inhalation 221 hepatic toxicity 222 lessons from medical history 214–15 lessons from toxicology centers 216 melanocyte toxicity 317–18 ophthalmic toxicity 221 paradoxical toxicity 214 renal toxicity 222 symptoms of intoxication 215 urinary incontinence and 246 see also chemical blepharoplasty; chemical cheiloplasty

Index

phenol peels 233 adjuvants 198–201 cresol (Lysol®) 200 croton oil 199–200 glycerol 201 resorcinol 199 salicylic acid 199 saponins 200 septisol 200 TCA 199 age of patient 225–6, 225 aging and 36, 36 photoaging 34–5 anesthesia 262–70 general 262 local 262–4 nerve blocks 265–70 topical 264–5 antibiotics and 258 application 273–82, 278–82 applicator preparation 273–4, 274 clinical signs of 276–7, 276–7 demarcation line 275, 278, 279, 280, 292 Aptos® threads and 231, 231 asepsis 259 atropine and 258 buffers 201 cardiorespiratory monitoring 258 cardiovascular complications 216–21 arrhythmias 217, 220 blood pressure 220 cardiac arrest 220–1 prevention 219–20 treatment during peel 220 classification of 2 cleansing and disinfection 258–9 combination treatment botulinum toxin 233–4, 233 face-lift 230–1, 230, 373 TCA 372, 373 Unideep® 228 complications edema 203, 277, 277, 357, 357–8 erythema 319, 323–4, 323–4, 325 hyperpigmentation 332–4, 334, 335 infection prevention 351 milia prevention 358 pain 203, 270–1, 292, 362 pruritis 354 scarring 204, 344, 347 contraindications 249–51 cost 251 heart condition 249 herpes 249 insulin-dependent diabetes 249 isolated patients 250 kidney disease 249 liver disease 249 mental or behavioral risks 250 patient history 249–50

sun exposure 251 corticosteroid injection 258 diuresis 258 formulations 196–8 Exoderm® 197, 197 Hetter formulas 197–8, 197 historical 196–7 Lip & Eyelid® formula 198 oil versus aqueous formulations 200–1 frosting 276–7, 276–7 hepatic and renal integrity requirement 210 histological effects 204–6 dermal changes 206–7 epidermal changes 206 long-term 207 hospitalization 283 indications for 233–47 acne 240–3, 242, 243 dilated pores 245 dyschromias 237–9, 237 keratoses 239–40, 239 laxity and skin elastosis 236, 237 nevus 245 scars 162, 243–5, 244, 245 superficial cancers 240 telangiectasias 240 wrinkles 233–6 xanthelasma 240, 240, 241 male skin 29, 226, 226 shaving and 226–7 neck 250–1, 280–1 occlusive mask 282, 282, 283–6, 285, 286 advantages and disadvantages 283–4 bismuth subgallate mask 288–90, 288–91 occlusion effects 211 precautions 284–5 preparation of 257, 257, 285–6 removal 286–7, 287 patient selection 251 phototype influence 227–8, 228 post-peel care 16, 283–94, 292–4 antibiotic cream 288–9 bismuth subgallate mask 288–90, 288–91 medical treatment 286 sun avoidance 292–4 touch-ups 287, 294 pre-peel preparation 253–7, 274 benzodiazepine 256–7 botulinum toxin 253, 274 clinical examination 253–6 eye protection 257 legal documents 253, 255 medication 253 photographs 253 precautions 250–1 safety factors 251 sagging skin and 31, 228, 230, 236, 237 sedation 265, 271 skin regeneration 251 skin thickness and 226

387

388

Index

phenol peels (cont.) smoking and 29 solution preparation 273 storage of solution 198 ventilation 257–8, 258 versus face-lift 228–30, 228–9 versus laser resurfacing 232 see also chemical blepharoplasty; chemical cheiloplasty; phenol phenolic acids 195 phenoxyethanol 89 in ETCA post-peel mask 111 phosphatidylcholine 32 photoaging 31, 32, 32, 34–5, 35, 56, 95 AHA peels and 55–6 décolletage 141, 142–4, 142–4, 145 hands 136–8, 136, 139 neck 141, 141 phenol peel treatment 225, 227, 237 resorcinol application 183 TCA application 95–8, 96, 97, 98 ETCA 119–20, 136–8, 136–9, 142–4, 142–4 lentiginosis 96, 97, 97 perioral wrinkles 97 prevention 97–8 solar elastosis 95–7, 96 tretinoin treatment and 10 see also aging skin; sun-protection phototherapy 72 see also flashlamp treatments phytic acid 70–1, 70 in ETCA post-peel mask 111 picric acid 195, 195 pigmentary changes confetti-like depigmentation 6, 6 following chemical blepharoplasty 302 following keratosis treatment 173, 174 pigmented ring 173 following stretch mark treatment 158, 158, 159, 161, 161 monitoring 335–6 post-acne pigmentation 127, 128 pregnancy and 336 prevention 6, 11, 334–6 even application of peel 335 skin preparation 334–5 sun avoidance and protection 335 treatment 8, 17, 182, 336–41 corticosteroids 341 sun avoidance 341 topical depigmenting agents 336–41 see also hyperpigmentation; melanocyte toxicity pinpoint bleeding, abrasion and 151, 152, 152 pKa 50–1 poikiloderma of Civatte 121 poisoning MCA 79–80 TCA 81 polyphenols 193, 194 polyunsaturated fatty acids 363 porcelain skin 206

post-inflammatory hyperpigmentation see hyperpigmentation post-peel care AHA peels 15, 65 Easy Phytic® 77 cosmeceuticals used 23–5, 24 phenol peels 16, 283–94 medical treatment 286 resorcinol peels 15, 186–7 Jessner’s formula 188 sensitive skin 25 sun protection 13–15 TCA peels 15–16, 43, 108 see also occlusive dressing post-peel cosmetics 16–18 acne treatment 17 aging treatment 17–18 sagging skin 18–23 erythema treatment 325 hyperpigmentation treatment 17 postoperative wounds, phenol peels and 249 pre-peel preparation see preparation pregnancy Easy Phytic® and 77 pigmentary changes and 336 tretinoin treatment and 10 premature ventricular contraction 217, 217 preparation 28–9 AHA peels 5–6, 11, 54 Easy Phytic® 75–6 glycolic acid 60–1 avoidance of side-effects 10 benefits of 10–11 combination treatment 11 for even penetration 6, 10 immediate pre-peel preparation 5 inadequate 314–15 infection prevention 6, 10 Jessner’s formula as preparation 188–9 medium- and long-term preparation 5 melasma treatment 121–2 monitoring 11 phenol peels 253–7, 274 pigmentary change prevention 6, 11, 334–5 pre-peel sun protection 6 resorcinol peels 185 Jessner’s formula 188 scar prevention 345 stimulation of skin regeneration 6–7, 11 stretch mark treatment 149 TCA peels 5, 6, 42, 92, 106 ETCA 114 Only Touch® 167 Unideep® 179 testing patient compliance 11 tretinoin 7–10 prilocaine 263 procaine 20, 20, 262 promethazine 271, 326, 354 propylene glycol 88, 88 in ETCA post-peel mask 111

Index

proteoglycans 30 protomyofibroblasts 205 pruritis 28, 161, 347, 354 herpes infection and 353 phenol peels and 354 treatment 350, 353 with Easy Phytic® peel 74 psoriasis 183 ptosis 230 nasal tip 279 pulse oximetry 258 Purifying cream® 127 intolerance 128 purpura 367 pyruvic acid 36, 48, 48 quadrigeminy 217 Quillaja, tincture of 186 radiotherapy, phenol peels and 249 re-epithelialization 7, 11, 13–14, 28, 342 red-headed patients, melanocyte toxicity 318–19 renal toxicity, phenol 222 resorcinol 183, 183, 193, 193 allergies to 185, 189–90 application 185–6 as adjuvant of phenol peels 199 classification of peels 2 combination treatment with TCA 371 contact time 186 histological effects 184 indications for use 183 ingredients of peels 184–5 pastes 185, 185 post-peel care 15, 186–7 pre-peel preparation 185 properties of 183 repeat peels 187 side-effects 189–90 toxicity 189 reticular dermis peel 329–30, 330, 349, 355–7 retinaldehyde 7 retinoids 6–7, 87 retinol 7 in ETCA post-peel mask 111 see also vitamin A rinsing AHAs 50, 54, 63 TCA 87–8 ropivacaine 263 safety factors 313–14 sagging skin 15, 33, 33 choice of peel and 31 DMAE treatment 18–23, 19, 33 phenol peels and 228, 230, 236, 237 salicylate derivatives 24–5 salicylic acid 48, 48, 187, 195, 195 as adjuvant of phenol peel 199 salicylism 189

sandpaper abrasion 145, 146, 147 acne scars 100 acne treatment 132 equipment 146 grade 0 abrasion 149–51, 149 grade I abrasion 149, 151 grade II abrasion 149, 151, 151 grade III abrasion 149, 151, 152 guiding signs 152 bleeding 152 keratinocyte touch 152 pain 152 scar treatment 162–3, 163 stretch mark treatment 146 depth of abrasion 149 with ETCA 146–7, 146 anesthesia 152–3 saponins 41 as adjuvants of phenol peels 200 in ETCA 112 scabbing 51 scalp 131 keratoses, ETCA treatment 131–3, 131, 133 local anesthesia 131–2 see also keratoses scars 145, 328–30, 342–8 acne 31, 55, 162 back 145, 163, 165 treatment 100, 103, 241–3, 242, 243 AHA peels 68, 342–3, 346 body scars 163–5, 164 back 145, 163, 165 décolletage 163–5, 165 dermabrasion 245, 246 face-lift 243–4, 244 facial 162 hypertrophic 32 keratosis treatment 173, 174 phenol peels 204, 344, 347 post-traumatic 35–6, 36, 244, 245 prevention 345–7, 348 Ehlers–Danlos syndrome 345 injury avoidance 346 isotretinoin and 345 patient selection 345 skin preparation 345 resorcinol peels 190 risk of 328, 329, 330, 342–4 TCA peels 44, 91–2, 317, 321, 343–4, 343–4, 346–7 treatment 162–6, 347–8 corticosteroids 348 dermabrasion 162–5, 163 ETCA 162–3, 162, 163 phenol peels 162, 243–5, 244, 245, 246 resorcinol 183 scratch lesions 349, 349, 355 sebaceous glands acne and 55 AHA effects 68 seborrheic dermatitis see dermatitis

389

390

Index

seborrheic keratoses see keratoses sebum production, reduction of 7 biotin effect 111 sedation phenol peels 265, 271 fentanyl 271 medizolam 271 premedication 271 TCA peels 360 selenium, in ETCA post-peel mask 111 senile atrophy 8 sensitive skins combined AHA/tretinoin treatment 59–60 TCA treatment 101–2 sensitization, AHA peels 67 septisol 195 as adjuvant of phenol peel 200 serborrheic dermatitis 9, 10, 54 shaving 226–7 shiny skin, following AHA peels 68 silicion, in ETCA post-peel mask 111 silicon dioxide 89, 184 silicone dressing 348, 348 silicone ointment 60 sinus rhythm 216 skin cancers tretinoin treatment and 10 see also carcinoma skin color 29 see also pigmentary changes skin necrosis 53, 53 TCA and 81, 91, 92 skin permeability 7 penetration of chemicals 209 tretinoin treatment and 9 skin phototype melanocyte toxicity and 318–19 phenol peels and 227–8, 228 pigmentary changes and 334 skin regeneration cycle 119, 119 skin thickness 116, 116 Sleek® occlusive mask 257, 257, 285 smokers’ skin 119 smoking 29 aging and 135 expression lines and 315 smooth muscle cells (SMCs), DMAE effects 22–3 sodium bicarbonate 63 neutralization of AHAs 63–4 sodium glycolate 50 sodium laureth sulfate (SLES) 41 in ETCA 112 sodium oxide 184 Soft Peel® 87 solar elastosis 95–7, 96 solar lentigines see lentigines solumedrol 258 sorbitan monolaurate 89 spasticity 246–7 Starling’s hypothesis 354

stratum corneum 209 hydration 23, 209 increasing permeability of 92 thinning 10, 13 AHA effects 51 for body anti-aging treatment 72–3 stratum disjunctum (SD) 109 stretch marks 32, 57, 145, 316 abrasion treatment 146 depth of abrasion 149 depth of abrasion, grade 0 sandpaper abrasion 149–51, 149 depth of abrasion, grade I sandpaper abrasion 149, 151 depth of abrasion, grade II sandpaper abrasion 149, 151, 151 depth of abrasion, grade III sandpaper abrasion 149, 151, 152 classification 145, 146 ETCA treatment 145, 152–61, 321, 321 anesthesia 152–3, 153 complications 161 post-peel care 160–1 protocol 153–8, 153–9 results 158–60, 159–60 hyperpigmentation following treatment 87 origin of 147 position of 148, 149 preparation for treatment 149 TCA treatment 103 treatments summary 148, 150–1 Styrax benzoin tree 184 sun sensitivity 362–3 sun-protection 6 heat-shock proteins and 14–15 phenol peels and 251, 292–4 pigmentary change prevention 335, 341 post-peel care 13–15 effective sun protection factor 13 glycolic acid peels 59 TCA peels 16, 43, 118, 122 tretinoin treatment and 9, 10 surface tension 200, 200 surfactants 5, 41 surgical scars see scars sweat glands 23 tachyarrhythmias, phenol and 217, 217, 220 tartaric acid 47, 48 taspine 200 tea tree oil 17 TEAS see trolamine telangiectasias 7, 240, 326–7, 326 AHA peels and 67, 326 phenol peels and 326–7 prevention 327 TCA peels and 326, 326 treatment 11, 327, 327 teratogenicity DMAE 20 tretinoin 10 Tercinol® 213

Index

testosterone 16, 60 tetrachlorophene 195 thiosome 129 thymol 289, 317 titanium dioxide 184 tocopheryl acetate 17 see also vitamin E topical corticosteroids 28 following AHA peels 64 tretinoin treatment and 9 touch-ups 316 phenol peels 287, 294 toxic shock 350 Transcutol® 11, 17 trehalose 14–15, 15 tretinoin 6–10, 17 age for starting treatment 9 AHA peel preparation 54 combination treatment 56, 59–60 histological effects 7 indications for use 7–8 mechanism of action 7 milia prevention 358 post-peel care 13 precursors 11 prescription of 8–9 recommendations 9 side-effects 9–10 TCA peel preparation 87, 92, 105 teratogenicity 10 trichloroacetic acid (TCA) 81–92, 177 adjuvanted TCA 86–90 chelated TCA 89 enzymatic TCA 88 glycerol 87–8 glyceryl monooleate 88 phenoxyethanol 89 propylene glycol 88 sorbitan monolaurate 89 TCA in clay masks 89–90, 90 anesthesia 43, 106 aqueous solutions 81–6 calculating the concentration of 82–6, 83–5 hydrophilicity of TCA crystals 81–2 inhomogeneity of 82, 83 see also TCA–SAS (below) as adjuvant of phenol peel 199 bacterial infection prevention 42 chemistry 81 choice of 39–40 classification of peels 2 combination treatments 43–4 abrasion 374 AHAs 371 botulinum toxin 43, 373–4 different TCA concentrations 372 dry ice 372 fillers 43–4, 374 flashlamps 44 phenol 372, 373

391

resorcinol 371 complications 44–5 downtime 45 edema 356, 357 erythema 320–3, 320–2, 325 exhausting the skin’s resources 44 hyperpigmentation 44–5, 173, 174, 331–2, 331–3, 335, 336 infections 44 melanocyte toxicity 317 pain 43, 133, 360–1 scarring 44, 91–2, 317, 343–4, 343–4, 346–7 telangiectasias 326, 326 contraindications 103–4 depth of penetration 42–3, 91, 91 Easy TCA see Easy TCA® (ETCA) herpes prevention 42 histological effects 91–2 indications for use 96–103 acne 102–3, 103 actinic keratoses 102 berloque dermatitis 99 dilated pores 100 folds and wrinkles 95 freckles 99–100, 100 melasma/chloasma 98–9, 99 oncological indications 102 photoaging 34–5, 95–8, 96, 97, 98 post-acne scarring 100 post-inflammatory hyperpigmentation 99 seborrheic dermatitis 100–1 sensitive skin 101–2 stretch marks 103 warts 101, 101 xanthelasma 103 length of peel 43 occlusion of 92 post-peel care 15–16, 43, 108 pre-peel preparation 5, 6, 42, 92, 106 Jessner’s formula as 188–9 repeat peels 43 solution mix 42 symptomatology of application 106–8, 106, 107–8 TCA–SAS (TCA in simple aqueous solution) 5, 15–16, 40–5, 86, 320, 346 application 105–6 toxicity 81 see also Only Touch®; Unideep® trigeminy 217 trimethylsilanol monomannuronate 111 trolamine (triethanolamine salicylate, TEAS) 24–5 application 24 mode of action 24 precautions 25 Truppman and Maschek solution 197 tumor necrosis factor (TNF) 200 tyrosinase inhibitors 11 tyrosine 337, 337 under-eye bags 32, 32

392

Index

Unideep® 177, 177, 360 application 179–81, 180 anesthesia 179–80, 179 complications erythema 322, 322, 325 pain 361 indications for use 177–9 lip treatment 304, 307–9 post-peel care 181–2 post-peel mask application 181 preparation 179 removal of freckles 177, 178 with phenol peel 228 see also trichloroacetic acid (TCA) Unna paste 183 allergies to 189–90 classification of peels 2 see also resorcinol urea 48 in ETCA post-peel mask 111 urinary incontinence 246 Urkov’s solution phenol 197 resorcinol 187 vagal reaction 258 valacyclovir 353 vascular endothelium 201 Vaseline® 27, 60, 342 chemical blepharoplasty and 296 in resorcinol peels 184 phenol peels and 211, 253, 284, 292, 347 eye protection 257 stretch mark treatment 156–8, 156, 158 Verner Kellson’s solution 197 Vit E Antioxidant ® 17–18 vitamin A 30, 340, 340 hyperpigmentation treatment 340 in ETCA post-peel mask 111 see also retinol vitamin C 30, 49, 341, 341 hyperpigmentation treatment 341 in ETCA post-peel mask 110

recycling 18 see also ascorbic acid vitamin E 18, 39, 158, 340, 340 hyperpigmentation treatment 340 in ETCA post-peel mask 111 vitamin H, in ETCA post-peel mask 111 vomiting, local anesthetic toxicity 263 warts 174 hands 139, 140 seborrheic 10 treatment 139, 140 AHAs 56–7 DCA 81 MCA 80 TCA 101, 101 Wood’s light 98, 238, 238, 336 wool fat, in resorcinol peels 184 wrinkles 56 AHA effectiveness 58 deep 37–8, 38, 39 expression 31, 36 filling 43–4 perioral 36, 37, 97 phenol treatment 225, 233–6 around mouth and eyes 235, 235, 236 deep wrinkles 233, 233, 234, 235 expression lines 234 folds and furrows 233–4 radial wrinkles 236, 236 TCA effectiveness 95 upper lip 304 see also chemical cheiloplasty xanthelasma 81, 240 phenol treatment 240, 241 TCA treatment 103 xanthoma 161 xerosis 55 treatment 56–7 zinc oxide, in resorcinol peels 184 zinc stearate powder 187, 289