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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

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Textbook ofChemical PeelsSuperficial, Medium and Deep Peelsin Cosmetic Practice

Philippe Deprez MD

Medical DirectorPoliclinica Estetica & Anti-AgingEmpuriabravaSpain

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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.

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Although every effort has been made to ensure that all owners of copyrightmaterial have been acknowledged in this publication, we would be glad toacknowledge in subsequent reprints or editions any omissions brought to ourattention.

The Author has asserted his right under the Copyright, Designs and Patents Act1988 to be identified as the Author of this Work.

Although every effort has been made to ensure that drug doses and otherinformation are presented accurately in this publication, the ultimate responsibilityrests with the prescribing physician. Neither the publishers nor the authors can beheld responsible for errors or for any consequences arising from the use ofinformation contained herein. For detailed prescribing information or instructionson the use of any product or procedure discussed herein, please consult theprescribing information or instructional material issued by the manufacturer.

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Acknowledgment vii

1 Chemical peels: definition andclassification 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

7 Alpha-hydroxy acids: histology and factors influencing penetration 53

8 Alpha-hydroxy acids: indications and results 55

9 Alpha-hydroxy acids: application ascosmetics and as peels 59

10 Alpha-hydroxy acids: side-effects of AHAs 67

11 Alpha-hydroxy acids: a new slow- release AHA complex with noneutralization required 69

12 Trichloroacetic acid: general information, toxicity, formulations and histology 79

13 Trichloroacetic acid: indications andcontraindications 95

14 Trichloroacetic acid: classic semiology 105

15 Easy TCA®: basic protocol and skin aging 109

16 Treating melasma, chloasma and post-inflammatory hyperpigmentation 121

17 Treating acne 125

18 Treating multiple keratoses on the scalp 131

19 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 papillarydermis: Unideep® 177

24 Resorcinol: Unna’s paste/Jessner’s solution 183

25 Phenol: chemistry, formulations andadjuvants 193

26 Phenol: properties and histology 203

27 Phenol: skin penetration anddetoxification 209

28 Toxicity of phenol: causes,prevention and treatment 213

29 Phenol: choice of peel and combination treatments 225

Contents

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30 Phenol: indications 233

31 Phenol: contraindications,precautions and safety 249

32 Phenol: pre-peel preparation 253

33 Full-face phenol: nerve block anesthesia and/or sedation 261

34 Full-face phenol: application 273

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

vi Contents

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The publication of this work has been assisted by an educa-tional grant from Skin Tech (www.skintech.info;www.peeling.com).

It should be noted that this textbook is comprehensiveabout all available peel products, but that there are many

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

Acknowledgment

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Definition of a chemical peelA chemical peel is a skin treatment intended to visiblyimprove the structure of treated tissue by the externalapplication of a caustic solution. It can simply acceleratethe natural processes of exfoliation, but can also com-pletely destroy the epidermis and a more or less large pro-portion of the dermis, essentially by protein coagulation orlysis. The effect of any peel reaches the dermis, directly orindirectly and to varying depths, where the processes ofregeneration are induced to a greater or lesser degree,depending on the molecule or molecules used and theapplication procedure.

Chemical peels are among the oldest forms of skin rejuve-nation and form a group of treatments in their own right.They are both flexible and effective, with a histological, chem-ical, toxicological and clinical basis. They have an ancient his-tory, have evolved rapidly and can be adapted to almost anycircumstances within the limits of their indications.

Most peels, to varying degrees, cause the same types ofhistological changes, whose clinical results lead to a moreor less rejuvenating effect on all or part of the skin.

Classification is always restrictive, as it forces highly vari-able events into a rigid framework. We will see in this bookthat so many different factors come into play that itbecomes difficult to fit all chemical peels into a simplifiedand rigid classification of ‘superficial’, ‘medium’ and ‘deep’.

Let us take the well-known glycolic acid peel as an exam-ple: its depth of action depends on the patient’s skin type, thepresence of associated disorders (e.g. seborrheic dermatitis),skin preparation in the long, medium and short term, thegalenical form (gel, liquid, mask or self-neutralizing pseudo-gel), the concentration of the product, the m/m, m/v or m+vcalculation, whether or not it is combined with other acidmolecules (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 numberof coats, how forcefully it is applied, whether it is applied onthe face or body, the exact location on the face (e.g. nostrilsor eyelids1), the contact time, how or whether it is neutral-ized or diluted at the end of the peel, the immediate post-peel care, the quality of care between peels, the number andfrequency of repeat sessions,... And the list goes on!

It is clear that it does not take much to turn a very lightglycolic acid peel into a medium-depth peel that can evenreach the deeper layers of the dermis and risk discolorationor even scarring. All it takes is for the peel not to be neu-tralized properly. The same goes for all of these causticmolecules, which is why, until recently, it was usually nec-essary to have a thorough knowledge of chemical peels andskin anatomy before undertaking this kind of treatment.Every practitioner, through personal experience and prac-tice, should aim to standardize their treatments in order toeliminate the maximum number of variables. Fortunately,new chemical peel formulas are now available that are eas-ier, safer and quicker to use, allowing young physicians toget on with the job of peeling without losing sleep and hav-ing post-peel nightmares. Sound knowledge and experi-ence are still essential for peels to the papillary dermis.

Criteria for classification

Molecular dependenceIt is very simple to understand that phenol is more aggres-sive than lactic acid.

Doctor dependenceClassification may be personal; it may be related to thepractice of one particular doctor who has standardized hismethods of treatment with a view to limiting uncontrol-lable variables. But such a classification would not allow forany scientific exchange.

What would produce a superficial peel with one practi-tioner could in fact result in a medium peel with anotherwho uses the same product with a different applicationtechnique. This is why peels are often considered to be‘doctor-dependent’.

How can we give a valid classification for a treatmentthat is doctor-dependent? We should also compare prod-ucts of the same type only, and yet the quality of the prepa-rations and excipients is highly variable and impossible tocontrol.

1Chemical peels: definition and classification

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Chemical dependenceIt is known that trichloroacetic acid (TCA) crystals, forexample, are very hydrophilic, which means that they mustbe kept in perfect conditions so that the pharmacist canprepare the solutions we prescribe properly. How can weknow how long the pharmacist’s bottle of TCA crystals hasbeen open? If the crystals have not been hydrated inadver-tently (if the pharmacist closes the bottle as soon as he hastaken out the required amount), the final concentrationwill be correct. If, on the other hand, the crystals are mostlyhydrated (if the pharmacist leaves the bottle of TCA openin order to serve another customer), the concentration ofthe solution provided by the pharmacy will be abnormallylow and not very effective. Peels are therefore also consid-ered to be ‘chemical-dependent’.

Patient dependenceEach patient has a skin type that is genotypically and phe-notypically unique. The skin has a history that the doctormust know about. Stable products that are properly pre-pared and applied with precise methodology, in the sameway, by the same doctor, on the same day, can produce dif-ferent results on different patients. Every morning, ormaybe several times a day, patients go through their ownparticular skincare routine that the doctor doing the peeldoes not necessarily know about. Let us take for examplethe application of large quantities of topical benzoyl perox-ide, which some teenagers use secretly for acne. It reducesthe thickness of the stratum corneum and makes the skinmore permeable. This of course makes it easier for the acidsused for skin peeling to penetrate the skin, and can, in

2 Textbook of Chemical Peels

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

Unna (Resorcinol) 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

TCA 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 ofcoats and preparation, or in combination (e.g. Abrasion, DryIce, Jessner)

Medium • Unideep®• Solutions of >35% m/m

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

Phenol Localized deep Lip & Eyelid® (wrinkles on lips and eyelids)

Full-face deep Lip & Eyelid®, Baker, Litton, Exoderm, etc.

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

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some cases, cause unexpected burns. A similar situationarises with patients who want to present their doctors withperfectly clean skin and use abrasive creams – the intentionis noble but the consequences are sometimes unpleasant. Apeel is therefore also ‘patient-dependent’.

If we leave aside these variables, we can fit the differenttypes of peels into their appropriate slots. This is just forthe beauty of the exercise however, as the variables stillneed to be taken into account. It is clearly possible to per-form a superficial or medium peel using phenol. But, giventhe inherent toxicity of phenol, what would be the point?What is more, 70% unbuffered glycolic acid that is left for10–15 minutes on a thin, sensitive skin that has been pre-pared with retinoic acid can result in a cosmetic disaster. Itis possible to carry out good-quality, deep peels with TCA,but the risks can be greater than if phenol is used correctly.

Summary tableTable 1.1 is intentionally incomplete. A peel is consideredas ‘very superficial’ when its action is limited to the stratumcorneum, ‘superficial’ if it does not go beyond the basal

layer of the epidermis, ‘medium’ if it reaches the papillarydermis and ‘deep’ if it reaches the reticular dermis.

In reality, it is better to determine the depth of a peel byclinically observing what is happening to the skin duringthe course of the treatment than by blindly applying setrecipes. When we say that the result of a glycolic acid peel is‘time-dependent’, this does not mean having to watch theclock but rather continuously analyzing how the skin isreacting in order to determine the best moment to startneutralization.

There is one basic principle to be respected: a peelshould not be unnecessarily deep or unnecessarily superfi-cial. There is no point completely destroying the papillarydermis when treating a purely epidermal problem, and it ispointless and ineffective to use an intraepidermal peel,even repeatedly, to treat a dermal problem.

Notes1. The nostrils can tolerate glycolic acid better than the skin

around the eyelids, and many application procedures forglycolic acid peels recommend avoiding application to theeyelids.

Chemical peels: definition and classification 3

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

Medium- and long-termpreparationAlpha-hydroxy acid (AHA) peels produce the best results ifthey are preceded by careful preparation and followed bylong-term daily cosmetic care. Easy Phytic® solution, onthe other hand, does not allow any pre-peel preparationthat is likely to accelerate penetration of the acids, as thestratum corneum must be intact for the peel to be safe.

Classic trichloroacetic acid peels, in a simple aqueous solu-tion in gel or mask form (TCA–SAS) always require around1 month’s intensive pre-peel preparation. This preparationstimulates keratinocyte regeneration and reduces the riskof post-inflammatory pigmentary changes and/or scarring.It blocks the first stages of the biochemical conversion oftyrosine into indole groups and melanin and limits thereaction of melanocytes to ultraviolet light. Easy TCA®requires no preparation under its basic protocol (untilscattered pinpoint or cloudy white frosting appears). Thepreparation required for its special deep-peel protocol orwhen combined with abrasion is discussed later in thisbook.

Resorcinol produces far better results and fewer compli-cations 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 skincarefully with tyrosinase inhibitors if there is any risk ofpost-peel pigmentary changes or to optimize results whentreating melasma. Retinoic acid and sometimes glycolicacid are used to make transepidermal penetration moreeven or to deepen the action of the acid solution.

Immediate pre-peel preparationGenerally, patients must wash their skin with soap andwater before going to the appointment. The doctor will dis-infect the skin with alcohol and degrease it with acetone orether. These degreasing products allow the peel solutions,which are usually hydrophilic and have difficulty penetrat-ing the skin’s protective oils, to penetrate more deeply andevenly. They break down some of the proteins and phos-pholipids in the cell membranes, which enhances theaction of the acids applied afterwards.

AHA peels require very careful preparation before beingapplied. The skin should be cleaned with soapy water,rinsed thoroughly, degreased with acetone and disinfectedwith alcohol. Unlike the classic AHA peels, with EasyPhytic®, the skin must be cleaned with a gentle, non-aggressive cleansing foam that only contains surfactants, sothat the acids do not penetrate the skin too quickly and sat-urate its natural buffer capacity, making it impossible for itto neutralize the sudden inflow of acids in time. Thoroughcleansing and degreasing of the skin before Easy Phytic®would oblige the doctor to neutralize it in the classic man-ner – when there is no prior preparation, there is no needto neutralize it.

With TCA–SAS, resorcinol, salicylic acid, azelaic acid orphenol peels, the skin needs to be thoroughly cleansed ofmake-up, degreased and disinfected. Easy TCA® solution,on the other hand, contains saponins that make pre-peelmake-up removal and degreasing unnecessary; the skin’snatural defenses are only very slightly diminished by thispeel, and therefore there is no need for any particular pre-peel preparation against infections.

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

2Pre-peel care

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Prevention of infectionPrevention of the herpes simplex virus is essential forpatients who have a history of the infection (a single inci-dence of herpes is enough). Herpes prevention is necessarywith a peel to the papillary dermis. It is also worthwhilewhen a more superficial peel is usually accompanied by asevere inflammatory reaction, as is the case with resorcinol,‘classic’ AHAs and TCA–SAS. It is not necessary whenusing 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 protectionIt can be beneficial to protect the skin against the sunbefore certain peels. Effective sun protection should start 2weeks before a medium or deep peel and even before aseries of superficial peels to inhibit melanocyte activity andavoid excessive stimulation of melanin production beforethe peel.

Prevention of pigmentary changesBefore any ‘classic’ peel, steps must be taken to limit therisk of pigmentary changes. Preparing the skin with tyrosi-nase inhibitors (hydroquinone, kojic acid, azelaic acid,arbutin, Morus Alba, licorice extracts, etc.) is especiallyrecommended to curb the enthusiasm that certainmelanocytes have for converting tyrosine into melanin.Preventive measures should begin 3–4 weeks before amedium 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 severaltyrosinase inhibitors, antioxidants and concentrated retinol(Blending Bleaching® cream). Some patients may develophyperpigmentation, or even ochronosis, when treated withhydroquinone. Patients with dark skin types are most at risk.Long-term use of high-concentration hydroquinone canalso cause confetti-like depigmentation (Figure 2.1).

Hydroquinone is prohibited from sale as an ingredientin cosmetic or cosmeceutical products in many countries(although it is available on medical prescription) and hasbeen successfully replaced by new formulas combiningother tyrosinase inhibitors. Creams containing azelaic acid(usually at a concentration of 20%) are considered slightlybleaching when used for at least 4–6 months. Azelaic acid isan irritant, and is used mainly when other formulationscannot be used. For oily or thick skins, tyrosinaseinhibitors can be prescribed in a gel form that penetratesthe skin more easily and allows instant and easy applicationof make-up. For more information, see the discussion ofpigmentary changes in Chapter 37.

Even penetration of acids andstimulation of skin regenerationTo perform a medium or deep TCA–SAS peel, the activemolecule in the peel solution has to penetrate more deeplyand the skin must regenerate more quickly. We have twolarge groups of molecules at our disposal: AHAs andretinoids.

AHAs (e.g. 10–15% glycolic acid) break down cor-neodesmosomes that maintain intercorneocyte cohesion;they make it easier to shed this layer of dead cells (whichare, however, essential to the skin’s defenses, as they arelargely responsible for maintaining the permeability barrierfunction in the skin as a whole). The epidermis is thinnedby the AHAs, making the stratum corneum more perme-able, and the acids can penetrate more deeply and evenly.The risk with this preparation is that the epidermis maybecome too permeable and the effect of the peel can go toodeep. A peel that is meant to reach the papillary dermiscould penetrate as far as the reticular dermis as a result oftoo ‘strong’ a preparation of AHAs. A peel that is meant toremain intraepidermal could become intradermal andresult in post-peel complications and more downtime: anintraepidermal peel removes several layers of ‘skin-color’keratinocytes in light flakes for around 3 days, whereas anintradermal peel removes the entire epidermis in the formof strips of brownish skin. The darker the skin type, themore visible is the flaking.

Retinoids form a growing range of products with ever-widening indications. The retinoid most used in pre-peelpreparation is tretinoin. Among other things, it stimulateskeratinocyte growth in the basal layer and causes an overallthickening of the epidermis but also a relative thinning ofthe stratum corneum. The pre-peel use of tretinoin


Figure 2.1Confetti-like depigmentation.

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enhances penetration of the acids at the same time as stim-ulating the regeneration processes in the keratinocytes ofthe basal layer.

The choice of one or another of these molecules dependson the condition of the patient’s skin. Tretinoin is not usedif the patient has many telangiectasias; AHAs are avoided ifthe skin is very thin. Conversely, the two products can bemixed in the same prescription, in variable concentrations,depending on the skin type and the desired effect. The con-centration of tretinoin would be increased to stimulatereepithelialization; the concentration of glycolic acidwould be increased to improve and even out transcornealpenetration.

TretinoinTretinoin (all-trans-retinoic acid, ATRA) is the carboxylicacid form of vitamin A (retinol). It is one of the first-gener-ation retinoids and has been used since the 1970s to treatacne complaints and dyskeratosis. It is important to knowall about this molecule in order to obtain benefit from itsactions.

Histological changesDuring long-term treatment with tretinoin, the results canfirst be seen through a microscope, long before they areclinically visible. These histological changes explain theindisputable clinical efficacy of continuous treatment. Theepidermis increases in thickness by 10–40%, with a thick-ening of the stratum granulosum to the detriment of thesuperficial stratum corneum (which decreases by about25%); the overall water content of the epidermis is thusincreased and the skin appears more hydrated. This epider-mal hyperplasia is observed both on the face and on the restof the body, especially on the arms or forearms. Unfortu-nately, it is not certain whether the improvement is perma-nent, as some studies show a reversibility of the action oftretinoin (a habituation phenomenon?) after 6 months’treatment on the forearms and the disappearance of histo-logical improvement altogether 1 year after the start of thetreatment, whereas clinically the improvement persists.Normal epidermal differentiation is restored and ker-atinocyte abnormalities gradually decrease. The atypicalkeratinocytes are eliminated and the tretinoin prevents ordelays keratoses from reappearing. The melanocyte clustersin the basal layer gradually disperse as a result of theincreased cell turnover. The marks on the skin thus tend tobe more diffuse, or even to disappear. The overall pigmen-tation 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 contentof the epidermis continues to decrease and causes the skinto lighten in the long term. As with chemical peels, a newlyformed collagen layer appears, in horizontal bands, just

beneath the basal membrane, in the Grenz zone. Newactive fibroblasts appear in the dermis, and new elastic andcollagen fibers are secreted. An increase in glycosaminogly-cans thickens the dermis, and elastotic tissue is pusheddeeper down.

After 26 months of daily treatment with 0.05% tretinoin,the events described above are extensive enough to pushthe elastotic tissue deep down and hide it under the newvascular, elastic, collagen and epidermal growth. It must benoted, however, that not all authors accept the existence ofthese histological changes in the dermis in the long term. Inparticular, a study by Gilchrest4 on 500 biopsies carried outduring a 5-year observation of daily topical tretinoin treat-ments (in concentrations between 0.001% and 0.1%) couldnot find any evidence of histological changes in the dermalparameters. This is surprising, and contradicts the estab-lished fact that clinically visible angiogenesis exists.

Mechanism of action Tretinoin is a synthetic (all trans) retinoic acid. Retinol andretinaldehyde are also converted into retinoic acid in thetarget cell where it participates in metabolic activity. Theretinoic acid penetrates the cell’s nucleus, where it bindswith a retinoic acid receptor (RAR). The complex formedby the retinoic acid and the RAR (RA–RAR) interferes withcertain areas of DNA by modulating the expression ofsome genes. It appears that retinoic acid alters the regula-tion of the cell cycle.4

For many years, tretinoin was considered capable ofreducing sebum production in the sebaceous glands, butserious doubt has been cast on this theory. It is generallythought that the mode of action of tretinoin is essentiallylinked to the increase in epidermal turnover and enhancedexfoliation of the stratum corneum, which makes it easierfor the pilosebaceous units to drain. A reduction inmelanin production has also been observed. Used specifi-cally as a pre-peel preparation, tretinoin evens out thethickness of the stratum corneum and reduces overall skinthickness. In these conditions, skin permeability increasessignificantly. Tretinoin also stimulates keratinocyte divi-sion and thus facilitates the regeneration phase, which cansometimes be too slow with certain peels. Topical tretinoinstimulates fibroblast production of collagen as well as othercomponents of the dermal extracellular matrix, and some-times creates a new layer of ‘repair’ collagen that is laid ontop of the photodamaged collagen.

IndicationsClinical results appear slowly and gradually, after histolog-ical improvement. The skin soon appears to be intenselyhydrated, once the erythema has disappeared or subsided.Clinically, it takes a year for the rejuvenating action oftretinoin to show. Patients, who hope to see rapid

Pre-peel care 7

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improvement, are not best pleased with these slow clinicalresults on aging skin. Progress can sometimes be seen morequickly when treating dyschromia: some results may beseen after 1 month of daily application of 0.1% tretinoincream.

Comedonal acne and acne rosacea respond well totretinoin. In fact, the anti-aging effect of tretinoin was firstobserved in patients being treated with tretinoin for come-donal acne: their skin texture and skin tone were graduallyseen to improve.

Oral isotretinoin (9-cis-retinoic acid) is often used intreating severe or stubborn acne rosacea. A 1994 study5

compared the treatment of rosacea with 10 mg/day low-dose oral isotretinoin, 0.025% low-dose topical tretinoinand a combination of the two. The results showed thatbefore the 16th week of treatment, isotretinoin was moreeffective, but that afterwards there was no differencebetween tretinoin and isotretinoin. The combination ofsystemic and topical treatment does not give any furtherimprovement in low doses.

It is generally accepted that tretinoin with a concentra-tion of 0.05% is as active as 5% benzoyl peroxide. Topicaltretinoin makes the skin smoother: the same patients whobenefited from the visible rejuvenating effect of tretinoinwhen being treated for acne noticed, among other things,that their skin had become smoother and softer after treat-ment. The improvement brought about by this topicaltreatment is therefore visual as well as tactile.

The application of topical tretinoin improves senileatrophy of the skin: a decrease in cell abnormalities anddysplasias can be seen, as well as an antitumor effect thatpersists after the end of treatment if it has been adminis-tered correctly and for a sufficiently long period.6

Topical tretinoin reduces the size and number of lentig-ines and other age-related discolorations. In some cases,however, because of its photosensitizing potential,tretinoin can aggravate certain types of dyschromia. Thiscan be problematic for Asian patients, for whom hyperpig-mentation is more of a problem than wrinkles as they age.The study by Griffiths et al3 proved (clinically, histologi-cally and by colorimetry) that 0.1% tretinoin significantlyimproved hyperpigmentation in these patients. There wasa 41% improvement with tretinoin, compared with a 37%aggravation in patients receiving the vehicle alone.

Post-inflammatory hyperpigmentation is also improvedby tretinoin, as proved clinically, histologically and by col-orimetry, in a study by Bulengo-Ransby et al2 on subjectswith black skin. A 40% improvement can be expected after40 weeks of treatment with 0.1% tretinoin. In the treatmentof melasma, topical 0.1% tretinoin was studied in compari-son with the vehicle alone in black patients.1 A 10-monthtreatment lightened the melasma by 32% (an improvementfactor established both clinically and by colorimetry).

Histological studies have shown a significant decrease inepidermal pigmentation in patients treated with tretinoin

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

How to prescribe tretinoinOne study7 showed that a tretinoin concentration of 0.01%is effective for the face, hands and forearms, whereasanother8 showed that there is no difference betweenplacebo, 0.01% tretinoin and 0.001% tretinoin. A concen-tration between 0.05% and 0.1% is, on the other hand,always considered active. The average concentration usedis 0.05%, but different skin types or sensitivities mayrequire different concentrations, and it is recommended tostart any treatment with a trial dose of 0.02% or 0.03%.

The following is one frequently used formulation(0.025%):

tretinoin 15 mgurea (carbamide) 6 gwater 4 gNeribase® cream ad 60 gor Eucerin® O/W ad 60 g

If this dose is well tolerated, it is possible to go immedi-ately or gradually to a concentration of 0.05%. This con-centration is common in proprietary medicines, but ifprescription medicines are preferred, it is possible to pre-scribe 0.05% tretinoin in the following formulation:

tretinoin 30 mgurea (carbamide) 6 g water 4 gNeribase® cream ad 60 gor Eucerin® O/W ad 60 g

Formulations in alcohol gels dry out the skin, increasethe penetration of the tretinoin and make the treatmentmore uncomfortable. Gels should only be used on thickand oily skins.

When the patient can tolerate a concentration of 0.05%without any notable side-effects, the concentration cangradually be increased to 0.07%, 0.09% and 0.1%. Concen-trations higher than this are rarely used. If, on the otherhand, the skin is very sensitive and becomes irritated inspite of a low concentration of 0.025%, the concentrationmust be decreased to 0.0125%9 or the patient should beasked to do one of the following. The skin can be sprayedwith warm water immediately before applying a small


ch02 7/11/06 8:35 am Page 8

quantity of cream. The cream will spread more easily andless of the active ingredient will be applied on the skin.Alternatively, the tretinoin cream can be mixed in the palmof the hand with an equal quantity of hydrating vitamin Ecream10 in order to halve the final concentration.

If the skin is still sensitive to the treatment, as a lastresort, the treatment can be applied every other day or onceevery 3 days for the first month. Experience shows thatdaily application of low concentrations is a better way toprepare the skin for higher doses than applying higher con-centrations two or three times a week. The ‘normal’ con-centration for daily application (0.05%) is reachedgradually over 2–3 months.

It makes little sense to combine tretinoin with a topicalcorticosteroid to limit the inflammatory reaction. It maywell be that this combination is supposed to stop inflam-mation, but inflammation is beneficial in that it stimulatesthe process of skin repair. Furthermore, the combinedeffect of corticosteroid and tretinoin could potentiallycause telangiectasia. The tretinoin would stop skin atrophyas a result of the application of topical corticosteroid,whereas it should increase the thickness of the epidermisoverall. A large part of the effect would therefore be lost.Finally, corticosteroids should not be applied to the skinfor a prolonged period, whereas long-term application oftretinoin is necessary.

If the skin is resistant from the start and does notrespond at all to the above formulation at 0.05%, a concen-tration of 0.1% can be used. This high concentration hasbeen shown to produce results rapidly, but can often haveserious side-effects. Therefore, before such a suddenincrease in concentration, there are a few ‘therapeutictricks’ that can be tried: when the skin appears not torespond to a single daily application of 0.05%, a 0.05%cream can be applied twice a day – once in the morning fol-lowed by a sunscreen and again in the evening. To increasethe effect, it is possible to prescribe an alcohol gel, startingwith a concentration of 0.05%, and increasing to 0.1% ifthe patient can tolerate this. To increase the potency of thetretinoin, the impermeability of the skin barrier can bedecreased, either by applying a 10% glycolic acid cream 20minutes before applying the tretinoin or by using a mildlyabrasive sponge (Buf-Puf®) on the skin before using thetretinoin. In some extreme cases, a light facial or bodyscrub twice a week increases skin permeability and makes iteasier for the tretinoin to penetrate. Very superficial micro-dermabrasion with corundum crystals or sandpaper canalso make the skin more permeable.

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

Various recommendationsTretinoin cream should be kept out of direct sunlight andaway from heat sources, to which it is sensitive. In spite ofthese precautions, it gradually loses its efficacy and it is rec-ommended that the prescription be renewed every 3months. Tretinoin is sensitive to oxidation, heat and ultra-violet light: the refrigerator (4°C) seems to be the best placeto store this cream. The by-products of degradation turnthe cream a yellowish color, in which case it should nolonger be used.

Tretinoin is photosensitizing, and it is therefore prefer-able to apply the cream in the evening and to use a hydrat-ing antioxidant or a cream such as Blending Bleaching®combined with a sunscreen (UVB + UVA + HSP) of factor20 or above in the morning. The tretinoin cream is appliedafter washing the skin with a mild soap (Avene® or SkinTech’s Pre-Peel Cleanser®), and is rubbed gently onto theface and neck (very gently on the neck where the skin ismore sensitive). It is striking to note that the earlobe isoften missed out in skin rejuvenation or tretinoin creamtreatments – and can be a telltale sign of a person’s real age.

When tretinoin is applied to skin with seborrheic dermati-tis (even when this is subclinical), it is common for erythemato develop, often in the middle of the face. One week’s pre-ventive treatment with topical nystatin can often prevent ery-thema, and considerably improves treatment compliance.Men whose skin tends to become irritated or infected aftershaving can use tretinoin as an aftershave cream. Shavingsoon becomes more comfortable: within 48 hours, the irrita-tion or potential acneform dermatitis has subsided or disap-peared altogether. The tretinoin cream should be appliedevery day for at least 12–18 months and two or three times aweek thereafter to maintain the results. When the treatmentends, the effect does not last indefinitely, and the skin slowlyreturns to a state close to its original condition. However, ifthe treatment is followed with one to three applications aweek afterwards, the positive effects remain visible.11 Whenthe treatment lasts 5–6 years, the elastotic material in the der-mis is gradually replaced by new collagen and elastic struc-tures.12 The results should last a long time if the skin isprotected from factors that accelerate the aging process.

Combining tretinoin and benzoyl peroxide could inacti-vate the tretinoin. If absolutely necessary, benzoyl peroxidecan be applied in the morning and tretinoin in the evening.

Side-effectsPatients should be warned of the high probability ofadverse effects, which fortunately are only temporary.Tretinoin is more irritant than glycolic acid. The irritationis usually mild, but can take the form of ‘retinoid dermati-tis’ if high concentrations are used or if the skin is delicate.

This dermatitis is in fact a positive side-effect whentretinoin is used to prepare for a TCA–SAS peel, at least to

Pre-peel care 9

ch02 7/11/06 8:35 am Page 9

the level of the papillary dermis, as it helps the TCA pene-trate more deeply and evenly. A concentration of 0.05%tretinoin should be used once or twice a day (depending onthe thickness and sensitivity of the skin) for 1 week; the fol-lowing week, the concentration is increased to 0.07% andthe third week to 0.1%. This relatively aggressive prepara-tion improves the penetration, evenness and re-epithelial-ization of the TCA–SAS peel, but will not improve thecosmetic results (or will do so only very slightly).

If the skin is not properly hydrated during treatmentwith tretinoin, it will usually flake visibly and fairly rapidlyafter a few days of treatment.

Erythema is to be expected with effective tretinoin treat-ment. This is not an adverse effect, but rather is collateraland natural. The skin of a patient properly treated withtretinoin is pinker than normal, and this provides the doc-tor with an essential means of observation: a patient show-ing no erythema is undertreated or incorrectly treated.

Erythema that appears very rapidly, 2–3 days after treat-ment begins, and that is localized in patches may be sebor-rheic dermatitis; it soon clears up with nystatin cream.Erythema that appears in the medium or long term, 1 ormore weeks later, can spread over the whole face and some-times to the neck in patients with very sensitive skin. If thisshould happen, treatment should be stopped for 1–2 weeksand started again at a lower dose, as explained above, toavoid excessive neoangiogenesis. More often than not,retinoid erythema does not last long in patients with a darkskin phototype, whereas patients with a lighter phototypecan suffer from persistent, if not permanent, retinoid ery-thema. Sometimes, the redness is more of a passing flushthan fully established erythema.

The skin becomes more sensitive to the sun, perfumesand detergents. In fact, right from the start of treatment,the skin becomes more sensitive to any irritant: beware ofchemical hair removal products, waxes, dyes, etc.

People who use tretinoin often report that their skin ismore sensitive to the sun and burns more easily. This pho-tosensitization is better explained by the thinning of thestratum corneum rather than by a photochemical reactionbetween the tretinoin and the sun’s rays. It is thereforeessential to recommend the use of a sunscreen (SPF 25–50UVA + UVB + HSP induction) to patients being treatedwith tretinoin. It should also be borne in mind that there isa potential risk of skin cancers developing as a result of thestratum corneum thinning and the enhanced penetration ofthe sun’s rays. Nevertheless, it appears that patients on long-term tretinoin treatment do not have a higher incidence ofskin cancers. Tretinoin has in fact proved to be effective inthe treatment of photoaging and actinic keratoses.

Teratogenicity of tretinoinThere is one important thing to note about the risk of ter-atogenicity: to date, and in spite of the fact that no terato-

genicity has been officially attributed to tretinoin,13 we donot have all the necessary facts at our disposal to allow itsunreserved use during pregnancy or in women who wishto become pregnant. Despite the fact that application oftretinoin under occlusion on more than 30% of the bodyhas not been found to lead to any abnormal increase inplasma levels, and despite there being no higher incidenceof fetal deformities among the children of women whohave used tretinoin during the first months of pregnancy,it is nonetheless possible for retinoic acid to penetrate thecell nucleus and alter the expression of certain genes.4

Caution dictates that one should not go ahead with treat-ment in a particular case until all the necessary facts areavailable to allow a risk-free choice to be made. Hypervit-aminosis A is theoretically possible and could be insidiousand chronic. 14 Practitioners should remain on their guardand make sure that patients are not taking extra vitamin Asupplements.

Benefits of skin preparationMajor benefitsAvoiding various side-effectsPreparing the skin before a TCA–SAS peel helps preventherpes and bacterial and mycotic infections. It also helpsreduce the risk of inadequate results (thanks to combina-tion with other treatments).

Improved penetration of the activeproductPreparation with AHAs or tretinoin reduces the thicknessof the stratum corneum, the skin’s natural barrier. As thebarrier is not as thick, it is easier for the products applied tothe skin to penetrate to the basal layer of the epidermis andmore deeply into the dermis. It should be noted that not allpeels require this kind of preparation.15

Even penetration of the peelThe skin does not have the same thickness all over, and thiscan produce differences in the level of penetration. Correctpreparation with AHAs and/or tretinoin tends to even outthe thickness of the skin and allow the active products ofthe peel to penetrate evenly.

Areas of hyperkeratosis (senile keratoses, and flat andseborrheic warts) are a perfect example of this difference inthe level of penetration. Keratoses, which are characterizedby a localized thickening of the stratum corneum, are lesspermeable to the acids. Pre-peel preparation with tretinoinevens out the thickness of the stratum corneum and hencethe overall permeability of the epidermis.


ch02 7/11/06 8:35 am Page 10

Reduced risk of pigmentary changePatients with olive and dark skin, or of Hispanic or Asianorigin, are more prone to pigmentary changes thanpatients of Caucasian origin. It should be remembered thatgenotype does not always correspond to phenotype andthat there are light skins that react in the same way as darkskins.16 Tretinoin, even more than AHAs, dispersesmelanin granules and reduces the overall quantity ofmelanin in the epidermis. This reduces the risk of post-inflammatory or post-peel pigmentary changes.

Tyrosinase inhibitors should be used in post-peel treat-ment as well as in pre-peel preparation (1 month before thepeel when there is a risk of pigmentary change, i.e. whenTCA–SAS or AHA peels are used).

Some commercial creams have interesting formulationswith AHAs (to enhance penetration of the other activeproducts), tretinoin precursors, lactic acid, extracts ofMorus Alba and kojic acid, combined with Transcutol®, anadjuvant that concentrates the active products near thebasal layer and the melanocytes.

Accelerated healing of the skin

After a peel, the skin needs to heal as quickly as possible inorder to maintain homeostasis of the whole organism.Tretinoin accelerates re-epithelialization if used before thepeeling. For this it must be used at a dose of 0.05%–0.1%,sometimes to the point of irritative dermatitis. Ideally, thetreatment should start 3–4 weeks before a TCA–SAS peel. Itis accepted scientifically that the preventive application oftretinoin promotes post-peel healing of the skin. In con-trast, applying tretinoin during the post-peel periodappears to slow down skin regeneration. Not all peelsrequire this help with re-epitheliazation.

Minor benefitsTesting patient complianceA patient who refuses to comply with instructions forpreparing the skin before a peel will not be naturallyinclined to heed advice for care during or after the peel ses-sions either. It is always preferable not to ‘peel’ a patientwho is incapable of understanding or accepting theseinstructions. Testing patient compliance is all the moreimportant since preparing the skin and keeping up cos-metic care afterwards affect the quality of the results.

Getting an idea of follow-up care

For patients who accept it, preparation gives them a fore-taste of between- and post-peel care.

Monitoring skin preparationMonitoring the preparation process can give an idea of howreactive and sensitive the skin is. Thus, a patient who cannottolerate hydroquinone during pre-peel preparation will tol-erate it even less in the days following the treatment as theskin becomes more sensitive to any irritant. Similarly, if thepatient develops an allergy to one of the products used inthe preparation, it can be isolated and avoided after the peel.

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

Notes1. Kimbrough-Green CK, Griffiths CE, Finkel LJ, et al. Topical

retinoic acid (tretinoin) for melasma in black patients. Avehicle-controlled clinical trial. Arch Dermatol 1994; 130:727–33.

2. Bulengo-Ransby SM, Griffiths CE, Kimbrough-Green CK, etal. Retinoic acid treatment for hyperpigmented lesionscaused by inflammation of the skin in black patients. N EnglJ Med 1993; 328: 1486–7.

3. Griffiths CE, Goldfarb MT, Finkel LJ, et al. Retinoic acidtreatment of hyperpigmented lesions associated withphotoaging in Chinese and Japanese persons. J Am AcadDermatol 1994; 30: 76–84

Pre-peel care 11

Figure 2.2Treatment of telangiectasias by (Ellman®) radiofrequencyimmediately before the application of Easy TCA®. Scatteredpinpoint frosting signals the penetration of the acid at eachpoint treated by radiofrequency. This combinationsignificantly reduces scabbing and includes a ‘pixillized’deeper peeling.

ch02 7/11/06 8:35 am Page 11

4. Gilchrest BA. Retinoids and photodamage. Br J Dermatol1992; 127(Suppl 41): 14–20.

5. Ertl GA, Levine N, Kligman AM. A comparison of the effi-cacy of topical tretinoin and low-dose oral isotretinoin inrosacea. 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 emollientcream: a new therapy for photodamaged skin. J Am AcadDermatol 1992; 26: 215–29.

9. By altering the formulations given above: 7.5 mg tretinoin in60 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 pharma-

cology. In: Hardman JG, Limbird LE, Molinoff PB, RuddonRW, Gilman AG, eds. Goodman & Gilman’s The Pharmaco-logical Basis of Therapeutics, 9th edn. New York: McGraw-Hill, 1996: 1600.

14. Farnes SW, Setness PA. Retinoid therapy for aging skin andacne. Postgrad Med 1992; 92: 191–6, 199–200.

15. For example: Easy TCA® and Easy Phytic® need no pre-peelpreparation.

16. Which is why it is important to question the patient.


ch02 7/11/06 8:35 am Page 12

Immediate post-peel care is described in detail in the chap-ters 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 theexfoliation phase is completely finished.

Sun protectionAny peel, even a very superficial one, reduces the thicknessof the stratum corneum that protects the skin against theeffects of radiation: the diffractive and reflective protectionusually afforded in these outermost layers is no longeravailable, and the overall quantity of rays that penetrate theskin increases. This extra radiation can cause actinic dam-age in cells that are usually physically protected by thethickness of the skin. Melanocytes are more strongly stim-ulated, and there is an increased likelihood of pigmentarychange. All peels thus allow the sun’s rays to penetratemore easily to at least the basal layer of the epidermis,where keratinocytes ensure re-epithelialization andmelanocytes can induce hyperpigmentations.

Greater irradiation increases the risk of these cells beinggenetically modified. All peels put the skin at risk of lightstress, which makes the use of sun protection creams essen-tial. A powerful, broad-spectrum sunscreen providesgreater protection. The deeper the peel, the more importantit is to use sun protection. After any medium or deep peel, itis 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 shouldbe applied immediately after washing in the morning,preferably with a cleansing lotion. Post-peel sun protectionshould be re-applied every 3 hours on average under anymake-up, even if the make-up itself is considered to be pho-toprotective. After a peel, sun protection is necessary even ifthe patient does not go outside and even in foggy or cloudyweather: windows block out most UVB but not UVA, andnot all clouds filter UV. Halogen lamps and spotlights andcathode-ray screens also appear to produce a sufficientquantity of radiation to induce post-inflammatory hyper-pigmentation (PIH) in sensitive individuals.

Effective sun protection factorThe sun protection factor should be even more ‘aggressive’when treating post-inflammatory hyperpigmentation, andshould protect against UVA as well as UVB. Protectionfrom the sun means not only avoiding lying on the beachbut also avoiding daylight. The skin is subjected to manylight shocks; it is constantly under attack from the sun anddaylight. One pitfall to be avoided is applying sunscreensthat contain tanning accelerators that could have a harmfuleffect.1 Between peels and during the first few weeks after apeel, a generous amount of Melablock HSP® 50+ suncream, for example, should be applied every 3 hours.2

Thereafter, daily sun protection can be lighter: for exampleMelablock HSP® 25+ every 3 hours. Patients should beadvised to keep their backs to the sun and to wear light pro-tective clothing. UV is not the only cause of hyperpigmen-tary 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 thatstarts within the first few hours after injury and continuesthroughout the different proliferative phases of skin repair.Viable keratinocytes (Figure 3.2) that are at the edge of thewound and have not suffered lethal or sublethal heat shock

3Post-peel care

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90

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0SPF0 SPF2 SPF10 SPF25 SPF50

1101009080706050403020100

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

ch03 7/11/06 8:36 am Page 13

migrate horizontally and centripetally in order to form aninitial single cell layer of keratinocytes, the ‘new basallayer’, before starting vertical growth that will regenerate anormal epidermal structure.

Re-epithelialization uses up a lot of proteins, both dur-ing the synthesis of the temporary matrix that acts as a pro-tein highway for the new keratinocytes and during theintense mitotic activity that creates new skin cells. Proteinsare absolutely essential to cell life; each enzyme in the bodyis a protein whose unique three-dimensional structure isresponsible for its highly specific action. They have vitalfunctions that are specific and strictly linked to their three-dimensional structure. The spatial structure of proteins isaltered by even the slightest increase in temperature;3 anythermal stress can ‘unfold’ the cell proteins, making themineffective and leading to apoptosis (programmed alldeath). In laser or flashlamp treatments, the temperature ofthe target must be raised in order to destroy it, but the nor-mal cells around the target also undergo sufficient heatstress to induce apoptosis or severely disrupt cell function.The rise in temperature thus creates a central zone oflesions that are lethal to cells, surrounded by a peripheralzone of sublethal damage in which the heat-damaged cellsmust be repaired or replaced. As a result, skin regenerationmay be slower than it should be as the cells on the edge ofthe treated area grow and migrate. Preventive protection ofthe proteins in the cells surrounding the target, increasingtheir resistance to heat, can help enhance the skin healingprocess and reduce the incidence of complications associ-ated with slow re-epithelialization.

Where there is sublethal damage, or very light damage,the cells must eliminate or repair the damaged and ineffec-tive 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 the1960s in the fruit fly in response to an increase in cell tem-perature of just a few degrees. These proteins were subse-quently found in all types of living cells; they are secreted inresponse to any kind of stress, not only in response toincreased temperatures. HSP70 and other similar stressproteins appear rapidly in the cytoplasm and mitochondr-ial matrix of cells that are subjected to stress. Essentially,their role is to ensure protein viability. HSP70 binds topolypeptide chains as soon as the latter have been synthe-sized in ribosomes (which translate RNA information intothe amino acid sequence of the polypeptide) and facilitatethe folding of these chains into the three-dimensionalstructure essential for protein activity. The HSP70 thenseparates from the folded protein. HSP70 is a member of agroup of diverse proteins (also including HSP60 and thechaperonins) that play an essential role in creating theappropriate 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 chap-erones’ and have a fivefold role: do well as providing thecorrect spatial structure for a new protein coming out ofthe ribosome, they also protect the structure of existingproteins, repair damaged proteins by refolding them cor-rectly, and act as protein transporters, carrying proteinsfrom one place to another within the cell and eliminatingproteins that are irreparable. Some HSPs are constitutionaland others are inducible. The latter are synthesized ingreater numbers after stress and give the cell increasedresistance to future stress, thus allowing the cell more timeto repair itself without having to resort immediately toapoptosis.

With age, HSP function deteriorates in human skin, andaging cells are increasingly more prone to protein destruc-tion.

Sun protection and HSPsIt is therefore beneficial to boost the synthesis of HSPs inthe cytoplasm and mitochondrial matrix of cells subjectedto heat and light stress, thus improving not only their resis-tance but also their defenses and better equipping them torepair proteins in case of stress. An interesting disaccha-ride, trehalose (Figure 3.3), was isolated from cells oforganisms that can survive in extreme conditions such asdehydration; having this disaccharide in sufficient concen-trations allows these organisms to increase their resistanceto the lack of water. It has been shown4 that trehalose canstimulate HSP70 production. An interesting experimentshowed that this disaccharide increases cell viability afterexposure to UVB. The study involved subjecting a cultureof keratinocytes to a slight increase in temperature of 3°Cfor 1 hour in order to induce slight heat stress. The ker-


Figure 3.2 Diagram of the peripheral thermal damage after ablativelaser treatment. The number of lethal lesions is proportionalto the degree of shading. The skin is repaired from peripheralkeratinocytes: some have suffered sublethal damage. Heat-shock protein (HSP) inducers help improve keratinocyteresistance to heat shock.

ch03 7/11/06 8:36 am Page 14

atinocytes were then cultured for 6 hours either in amedium containing trehalose or in a medium without thedisaccharide. After 6 hours, the culture medium wasreplaced by physiological saline solution and the ker-atinocytes were exposed to UVB radiation. Cell viabilitywas studied after 48 hours. There was a huge difference inkeratinocyte survival in the cells from the different culturemedia: only around 4% of viable keratinocytes remainwhen cultured without trehalose eter, whereas the survivalrate was nearer 40% in the group of keratinocytes culturedin the medium rich in trehalose (Figure 3.4).

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

and thus increase its permeability; they make it easier forthe active molecules to penetrate the epidermis whencreams are applied both immediately after and betweenpeeling sessions. The type of cream depends on the prob-lem being treated. The results for acne treatment can, forexample, be improved by applying a layer of anti-acnecream immediately after a ‘classic’ AHA peel has been neu-tralized and leaving it to act under an occlusive dressing5

for around 30 minutes. The patient can apply the samecream twice daily thereafter. The same applies for melasmaand aging or sagging skin, etc.6 After an AHA peel, thepatient’s daily care routine plays an essential role in deter-mining the quality of the results. Mesotherapy can be com-bined with AHA peels in a number of ways: the ‘mesolift’mixture7 can be injected before the peel or immediatelyafter the peel has been neutralized and before creams areapplied under occlusion. There is no danger of the glycolicacid penetrating beneath the skin through the perforationsmade by the mesotherapy needle. Most often, however, thetreatments are alternated every other week: in the firstweek, the peel and the cream under occlusion are applied,and in the following week, the mesolift is injected, followedby the cream under occlusion. If an AHA peel is done cor-rectly, there is usually no downtime. Nevertheless, therecan be complications, which are described in Chapter 10.

ResorcinolResorcinol in paste form9 is used in a very specific manner:the paste is usually applied three times, once a day for 3days in a row. Post-peel care is very important during thefollowing week: the skin should not be hydrated at all, as ithas to dry out completely for the peel to be effective and,above all, the patient must not pull off or pick at the flakingskin. Only the doctor can safely cut off any strips of flakingskin with sterile scissors. Cosmeceutical creams for agespots, acne, aging or sagging skin, etc. should only beapplied after the skin has flaked. Effective sun protection(UVA + UVB + HSP inducers) is absolutely essential forapproximately 6 weeks after the peel.

Downtime may be around 4–5 days. After the first appli-cation of the paste, the patient can usually have a normalsocial life, but subsequent applications dry out the skin andleave it looking papery.

TCA–SASTrichloroacetic acid in simple aqueous solution(TCA–SAS) involves pre-peel preparation, application ofthe TCA–SAS solution to the required depth (usually thepapillary dermis), flaking, natural skin regeneration andpost-peel care.

The post-peel period for TCA–SAS requires special atten-tion and, even if the peel is applied correctly, pigmentarychanges are the most common and benign complication. It

Post-peel care 15

HO

H

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H

H

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Figure 3.3 Chemical structure of trehalose.

0% 0.5% 1%

Trehalose eter concentration

4035302520151050

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

ch03 7/11/06 8:36 am Page 15

is clear from the many illustrations in books on TCA–SASpeels that there is an astonishing variety of post-TCA pig-mentary changes, with varying degrees of severity. If pre-peelprevention does not prove effective, or in cases of localizedoverpeeling, post-inflammatory hyperpigmentation (PIH)usually appears within a week after the peel in the form ofdark patches or persistent erythema that will become pig-mented under the effect of the sun’s rays. For more informa-tion, see the section on hyperpigmentation in Chapter 37.These genuine pigmentary changes should not be confusedwith the darkening of epidermal melasma appearing thenext day after the peeling, and caused by dehydration of thehydrophilic spaces between melanosomes, which makes theskin seem to have a greater concentration of melanin andhence appear darker. This darkening, which is temporary, isa positive sign and will fade at the end of the first week.

Flaking should not be helped along under any circum-stances. Peeling off any bits of skin can result in uneven skintone, infection, hyperpigmentation, scars or localizedachromia. It is also essential to take preventive measuresagainst infection after a papillary TCA–SAS peel, as the lat-ter destroys most of the skin’s defenses. An antibiotic creamis applied during the first week after the peel. The skinshould be cleaned before each application of cream, and anyoccurrence of contact allergies, which can sometimes beconfused with secondary infections, should be monitored.

The results of a TCA–SAS peel also depend on the qual-ity and consistent use of cosmeceuticals after the peel. It isclear that a melasma treatment will produce better results ifthe TCA–SAS peel is followed by the application of aretinol–anti-tyrosinase–anti-oxidant cream or a hydro-quinone-based preparation. For acne or aging or saggingskin, the same comments apply as for AHAs above. Thesecreams can be applied as soon as flaking is finished, usuallyon the 7th day.

Effective sun protection is absolutely essential and shouldbe used in the first few days after the peel, before the skin hasstopped flaking. Even a total sunblock is not enough to avoidpigmentary changes altogether, and the patient should betold to completely avoid exposure to the sun. Sun creamscontaining tanning accelerators should, of course, not beused after the peel.9 Chemical tanning with sprays contain-ing dihydroxyacetone should also be avoided, as these prod-ucts, which are non-toxic when picked up by thecorneocytes and eliminated within 1 week, are not intendedfor keratinocytes, which are the cells exposed to the externalenvironment 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 coverup any persistent erythema.

Easy TCA®

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

peel care in the medium term nor any immediate pre-peelpreparation, and pigmentary changes are very rare if the‘basic protocol’ is followed.10 Some brown discoloration ispossible after the first or second application, but thisshould fade after the following peel. Flaking skin can bepeeled off or a light cosmetic scrub can be used. Withdeeper protocols, which are not usually necessary with thispeel, there is a greater likelihood of complications.

Combining Easy TCA® with appropriate post-peel cos-meceuticals helps improve and maintain results. The cos-meceuticals should be applied the day after the first peeland continued between sessions and for at least 6 weeksafter the last application. As with any peel, effective sunprotection is necessary to make up for the temporary lossof the stratum corneum. Easy TCA® causes the skin toflake, but not so much as to disrupt the patient’s social life,although certain activities may be compromised: televisionpresenting, customer contact in the food industry, etc. EasyPhytic® is recommended in these cases as there is almost novisible flaking of the skin (see Chapter 11).

PhenolPhenol entails the most complex post-peel care: occlusivemasks, healing masks and cosmetic care during the monthsfollowing the peel. Chapters 25–36 are devoted to this tech-nique. The expected downtime is between 7 and 15 days,depending on the formula used. The patient will have towear camouflage make-up to hide any redness, which canlast for several weeks or months.

Post-peel cosmeticsChemical peels do not always treat the underlying cause ofa skin problem. For example, there can be many causes ofacne, and chemical peels do not alter the synthesis oftestosterone or the potency of the 5α-reductase that con-verts testosterone into its active derivative, dihydrotestos-terone. Acne may also be partly due to excessive cellcohesion that blocks the sebaceous glands or to an immun-odeficiency of genetic origin. Chemical peels do not alteran individual’s genetic make-up. Follow-up care shouldcome after the peel, which is only the first phase of thetreatment. Topical anti-acne treatments or cosmeticsshould be used between and after the peels to improve andprolong results. The same goes for blemishes, melasma andaging.

Peels can provide quick cosmetic results, but it is the carebetween and afterwards that improves and maintainsthem. This is why the same peel may be indicated for thetreatment of acne, which typically affects young patients, asfor aging, which affects older patients. In short, we can saythat chemical peels regenerate, restructure and stimulatethe skin, and that care between and after peels widens their


ch03 7/11/06 8:36 am Page 16

indications to problems such as acne, dyschromia andaging.11

There are cosmetic products that have been specially cre-ated for application very soon after a peel. They can be usedthe morning after the first AHA peel, Easy Phytic® or EasyTCA®. With TCA–SAS, Only Touch® or phenol peels, cos-metics usually are not applied until the 8th day after thepeel. With Unideep®, an anti-oxidant cream (RenutrivACE Lipoic Complex®) can be applied two days after thepeel.

Treatment for acneTretinoin should be avoided between and after sequentialpeels, as it would irritate the skin and increase penetrationof the acids during the next peel. Other topical productscan be used. Glycolic acid can be applied in low concentra-tions (8%); it makes the skin softer to the touch. Likeretinol, it prevents pores from clogging, helps the piloseba-ceous units to drain and stimulates skin turnover. Toco-pheryl acetate can be used as an antioxidant to combat thefree radicals generated by inflammation. Triclosan12 is anti-septic, anti-inflammatory and antimycotic. Glycyrrhetinicacid is used for its hydrating, antipruritic and anti-allergicproperties. It stops patients scratching. Tea tree oil(Melaleuca alternifomlia) is extracted from an Australianshrub and has a similar action to benzoyl peroxide butwithout its pro-oxidant effects. It is antiseptic (antibacter-ial: anti-gram-positive and -negative), anti-inflammatory(it can suppress the production of pro-inflammatory medi-ators), 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 hyperpigmentationChemical peels are one of the preferred indications forhyperpigmentation. A number of cosmetics can be usedbetween and after peels. Hydroquinone was used for a longtime, and still is in many countries. Its cosmetic use, how-ever, is forbidden in Europe. There are many depigmentingderivatives that can be used in its place. Kojic acid can beused pure or as an extract of Aspergillus, and has an anti-tyrosinase and antioxidant action. It even potentializesleukocyte phagocytosis. Glabridin (a licorice extract)inhibits the pigmentation and erythema caused by UV; it isanti-tyrosinase and anti-inflammatory. Liquiritin containsglycyrrhizin and glycyrrhetinic acid (which are anti-inflammatory as they inhibit the degradation of endoge-nous cortisol) and antioxidant flavonoids. Extracts ofMorus alba contain arbutin and mulberroside F, which areboth tyrosinase inhibitors. Mulberroside F is also an anti-oxidant. Transcutol® helps build up a reserve of activeproducts near the dermoepidermal junction and improves

the action of tyrosinase inhibitors (Figure 3.5). AHAs canbe used to enhance penetration of active products throughthe skin. Lactic acid has also been described as having atyrosinase-inhibiting action. Finally, various vitamins (A,C and E) can be used in the treatment of hyperpigmenta-tion: they are antioxidant and anti-inflammatory, protectagainst UV damage and stimulate epidermal turnover.

The well-known Kligman’s formulas combine the actionof tretinoin, a corticosteroid and hydroquinone, but aremore irritating than medical cosmetics. The cosmetics usedfor hyperpigmentation should be applied very soon after thepeels (if possible the very next day). If possible they shouldbe applied two or three times a day, before effective sun pro-tection. For more information on topical depigmentingagents, see the section on hyperpigmentation in Chapter 37.

Treatment for agingThe author’s cosmetic post-peel treatment for aging skin issimple.

Patients under 40–45 years oldThe main thrust of the treatment is daily oxidation. In themorning, an antioxidant cream with vitamin E should beapplied, and in the evening another anti-oxidant cream:Renutriv ACE Lipoic Complex®.

Vit E Antioxidant® is a cream with a relatively complexbut complete formulation. It does not contain AHAs, so

Post-peel care 17

Figure 3.5Blending bleaching cream, contains antityrosinases andantioxidants.

ch03 7/11/06 8:36 am Page 17

can be applied daily without the risk of interference withthe protective function of the corneocytes. It has been spe-cially formulated for use very soon after a chemical peel. Itsqualitative formulation is as follows:

� Biosaccharides: these are polymers of the sugar, fucose.– They have filmogenic properties that induce immedi-

ate 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 moststable derivatives of vitamin E, and forms a reservoir inthe skin after penetration

� Glycyrrhetinic acid: this is hydrating and anti-allergic; itreduces itching.

� Natural moisturizing factor (NMF): this comprisesamino acids + hexoses + urea + aspartic acid + hexyl-nicotinate

� PFPE (perfluoro polymethyl isopropyl ether): this is afilmogenic polymer that protects the skin without anyocclusive effect.

Renutriv ACE Lipoic Complex® is ideal for dry skin, andcan also be applied in the morning. With normal or oilyskin, it is better applied in the evening. It does not containany AHAs, for the reasons explained above. Its qualitativeformulation 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 Rform is active (Figure 3.6). Lipoic acid is absorbed rapidlyboth orally and topically. Enzymes in cell cytoplasm con-vert it into dihydrolipoate (DHLA). DHLA penetrates thecell and mitochondrial membranes easily. It is a mitochon-drial cofactor that boosts mitochondrial activity at the

same time as protecting against excess production of freeradicals. Lipoic acid has the major advantage of being bothfat-soluble and water-soluble, which means that it is activeat all levels in the cell. It recycles vitamin C, when it is con-verted into the ascorbyl radical after acquiring a free elec-tron, thus restoring its antioxidant activity. It also recyclesvitamin E indirectly. Lipoic acid protects the natural enzy-matic antioxidant defenses, such as catalase, coenzyme Q-10, glutathione and cysteine. It is an iron, copper, mercuryand aluminum chelator (Figure 3.7). It combats excessivesecondary cell apoptosis resulting from various stresses.

Patients over 40–45 years oldThe fight against aging should take into account not onlythe damage caused by the various sources of cell oxidationbut also the fall in hormone levels. For menopausal or post-menopausal women, a standard formula is testosteronepropionate 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 beused, or other estrogen precursors or dehydroepiandros-terone (DHEA).

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


HO

O

S

SH

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

SH S

O

O

O

SS

Fe2+

O–

Fe2+

Figure 3.7 Iron chelation by lipoic acid.

ch03 7/11/06 8:36 am Page 18

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 appli-cation to produce a ‘face-lift’ effect. Even if there is nodoubt that it produces a tightening effect on the face, thereis no definitive evidence regarding its mode of action. Wewill see below what type of skin structures respond toDMAE and why it would be difficult to explain this actionby an improvement in tension of the striated muscle massof the face.

Chemistry of DMAEDMAE (also called deanol, dimethylethanolamine andnorcholine) is a small hydrophilic molecule. Its low molec-ular 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 morereminiscent of fish long past its sell-by-date. Anchovies,sardines and salmon are important natural sources ofDMAE. It is naturally present in the body, and there aretraces of it in the brain. DMAE is a very basic molecule(pH 11) that cannot be used in its pure state without therisk of causing chemical skin burns. It must be partiallyneutralized for use at pH 7. Many derivatives have beenused in its place (e.g. DMAE bitartrate or acetamidoben-zoate), but these are more suitable for oral rather than top-ical use.

DMAE formulations tend to give only the total dosage ofthe DMAE derivative used, of which pure DMAE is only

part of the weight. For example, 100 mg of DMAE cyclo-hexylcarboxylate contains only 33 mg of pure DMAE,while 350 mg of DMAE bitartrate contains 130 mg of pureDMAE. The author prefers to use a formulation withDMAE lactate (Skin Tech’s Actilift®) in order to benefitfrom the properties of an AHA (lactic acid) combined withthe DMAE.

Side-effects and precautionsThe high pH of DMAE means that the pure compoundshould not be brought into contact with strong acids,mucous membranes or the eyes. Pure DMAE is alsoincompatible with copper and zinc. DMAE is volatile andshould be contained in sealed tubes rather than bottles, toprevent its evaporation. Some cases of allergic dermatitishave been reported after prolonged contact with very high

Post-peel care 19

Figure 3.8A 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.

A B

(CH3)2NCH2CH2OHDMAE

(CH3)3N+CH2CH2OHCholine

O ��>

(CH3)3N+CH2CH2OCCH3

Acetylcholine

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

ch03 7/11/06 8:36 am Page 19

concentrations of DMAE, and it should be applied withextreme caution around the eyelids of atopic subjects.DMAE is not considered to be carcinogenic, cocarcino-genic or immunosuppressive. Chronic exposure to con-centrated fumes of DMAE in the workplace can causevisual problems.

ToxicityDMAE has mostly been used orally. It is most widely avail-able in 100 mg tablets for the treatment of cognitive disor-ders associated with senile dementia, at a dose of600 mg/day. The LD50 for oral administration in rats is2 g/kg. The LD50 in rabbits after application to the skin is1.370 mg/kg. For subcutaneous injection in mice, the LD50is 961 mg/kg. In a human clinical study,13 oral administra-tion of 1600 mg/day showed no side-effects. The dosesused in topical applications are nowhere near the theoreti-cal toxicity limit. It takes a twice-daily application ofaround 30–50 mg of DMAE on the skin to improve skintension and achieve the ‘lifting’ effect. It is important toremember that a topical application, even if it is very effec-tive, cannot as yet compete with a surgical procedure.

DMAE and N,N-dimethylisopropanolamine (DMIPA)solutions are used in high concentrations (45–50%) inindustry, especially in the printing industry. They are usedin sprays, and a study was conducted on their role in theappearance of intermittent corneal opacity in workers incertain types of printing works.14 The corneal opacitiescaused blurry vision on the way home from work. Theseproblems were only evident from Mondays to Thursdays,but never at the end of the week. Eye tests revealed theappearance of intermittent and reversible corneal opacity,limited to the part of the cornea in contact with thedroplets of vaporized solution and lasting just a few hours.A complete study was undertaken that put the blame onDMIPA but cleared DMAE of involvement. Lowering theconcentrations of DMIPA without changing the concen-trations of DMAE solved the problem once and for all andproduced no visual sequelae.

DMAE has also been claimed to be teratogenic. Studieson this subject remain controversial: some have shown thatDMAE can be teratogenic in mouse embryos at highdoses;15,16 other studies have shown no evidence of toxicityin rodents.17 In my knowledge nothing has been publishedon teratogenic effects in humans, and no research hasshown teratogenicity in humans, despite the wide use ofDMAE in industry.

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

criticized) Gerovital H3 developed by Dr Ana Aslan ofRumania. Procaine or 2-diethylaminoethyl 4-aminoben-zoate hydrochloride (Figure 3.10) was synthesized in 1905by the German chemist Alfred Einhorn, who called it‘novocaine’ (from the Latin novus = new, with the addedsuffix of cocaine, a gold-standard product up until then).Another German, Dr Heinrich Braun, introduced the useof novocaine in medicine.

In the body, the ester link of procaine is hydrolyzed,yielding p-aminobenzoic acid (PABA) and N,N-diethyl-aminoethanol (DEAE), an analog of DMAE. It is PABA(Figure 3.11) that is responsible for the large majority ofallergic reactions to ‘procaine’; it is excreted rapidly by thekidneys. PABA is most often used as a sunscreen, but issometimes called ‘vitamin B-x’, although it is not essentialfor humans and the body cannot synthesize folate fromPABA. According to some authors, the ‘Aslan’ methodrelies solely on the combined action of PABA andDEAE/DMAE. It is assumed that the action of PABA is dueto its anti-free-radical properties.

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 musttherefore have a different basis from that of procaine.

As well as having an anti-oxidant19 and anti-inflamma-tory effect, DMAE taken orally has been claimed to havemany properties: an anti-aging effect, improvement ofmemory and intelligence, increased synthesis of acetyl-choline, amelioration of depressive states, improvement inmotor coordination, improvement in compulsive, impul-sive, hyperactive or antisocial behavior, reduction ofchronic fatigue and improvement in the quality of sleep,aid in giving up alcohol and tobacco, reduction ofheadaches, improved ability to concentrate, improvementin schizophrenia, improved muscle tone, and overallhigher energy levels.

DMAE can be incorporated into the membrane struc-ture of cells, where its anti-oxidant properties improve


NH2 CO.CH2CH2N(C2H5)2

O��

Figure 3.10 Chemical structure of procaine.

NH2 C

O

OH

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

ch03 7/11/06 8:36 am Page 20

membrane resistance to the oxidative stress resulting fromthe release of free radicals from the phospholipid bilayerand the production of eicosanoids associated with skininflammation. The degradation of cell membranes andsubsequent inactivation of the transmembrane proteinsand receptors are considered to be the main factors respon-sible for cell aging.

Carbachol (Figure 3.12), and the closely related bethane-chol, is a powerful cholinergic agent (used to induce mio-sis). Its structure is similar to that of choline and itsprecursor, DMAE. Other muscarinic agents (e.g. pilo-carpine), have a completely different chemical structure tocholine.

Topical skin application of DMAETopical application of DMAE has a visible tightening, firm-ing effect, often called the ‘lifting effect’. This tighteningeffect can already be felt 20–30 minutes after the producthas been applied to the skin, and, when only one side of theface is treated with DMAE, the difference in tensionbetween the two sides is clear. Skin tension continues toimprove during the first 6 months of twice-daily applica-tion, with individual variations, and remains stable for 4–8weeks after topical treatment is finished. This would seemto indicate that the product accumulates in the skin andforms a reservoir.

Potential mode(s) of action ofDMAEDMAE is a precursor of choline; it also inhibits the metab-olism of choline in the tissues. As there is more cholineavailable, the biochemical reactions may tip the balancetowards an increase in ACh synthesis. DMAE may stimu-late 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 musttherefore put forward several hypotheses in an attempt tounderstand this tightening effect.

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

of that of DMAE. BTX relaxes the muscles, whereas DMAEincreases muscle tone. Are these two compounds thereforeincompatible? It appears not, as they have different targets,and the muscle cells that are deactivated by BTX are not thesame as those activated by DMAE. BTX is a large moleculewith a high molecular weight, which means that it cannotpass through the skin when applied topically. To achieve acosmetic result, BTX must be injected directly into themuscle to be paralyzed. BTX has no effect on the epidermisor dermis, as it blocks cholinergic transmission in the neu-romuscular junction of the striated muscles and in this waylimits the facial expressions that cause expression lines.

BTX is picked up immediately, and there is no chance of itdiffusing up through the hypodermal fat layer. DMAE, onthe other hand, is a very small hydrophilic molecule with amolecular weight of 89.1 that can easily penetrate the epider-mis and the dermis but cannot penetrate the hypodermalfatty layer. DMAE cannot act on the striated muscle groupsthat produce voluntary facial movements, and so cannotcounter the effects of BTX. This physiological hypothesis isconfirmed clinically when the two treatments are usedtogether. The physicochemical properties of DMAE give thismolecule a great affinity for the dermis and epidermis. As theaction kinetics of DMAE lead to the hypothesis of a cuta-neous ‘reservoir’, this could only be located in the deep epi-dermal layers, as, if it was in the dermis, this small moleculewould soon be eliminated by venous or lymphatic resorp-tion because of its concentration gradient.

The way in which they are administered, their targets,their characteristics and their different modes of action donot make BTX and DMAE incompatible: administeringone will not alter the effectiveness of the other. There is noestablished link between age-related sagging skin and mus-cles and a deficiency in ACh in the muscles. Any action ofDMAE on striated facial muscles is thus not only unlikelybut also pointless. We must therefore look for other morelikely modes of action than muscle stimulation, especiallyas there have been reports of improvements in tone andyounger-looking skin around the eyes and lips after only afew days of treatment. Given that it is accepted that paraly-sis (or hypotonia) of the muscles by BTX ‘smoothes’ theskin, it would be illogical to claim that stimulating the samemuscle groups (with DMAE) can give similar results. Wemust therefore look elsewhere: in the skin structures thathave cholinergic receptors.

Epidermal actionHuman keratinocytes express cholinergic receptors in thecells of the stratum basale, the stratum spinosum and thestratum granulosum. They use ACh, among other things,to stick together. They also synthesize, store, degrade andrelease ACh.

ACh synthesis has been shown to occur in the perinu-clear regions of human keratinocytes due to the presence of

Post-peel care 21

(CH3)3N+CH2CH2CNH2

O��

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

ch03 7/11/06 8:36 am Page 21

a choline acetyltransferase (this enzyme converts acetylcoenzyme A into ACh). On the other side of the cell, insideor near the cell membranes, an acetylcholinesterase hasbeen identified. This enzyme degrades ACh in order to pre-vent a toxic build-up. Keratinocytes can move, which isessential during the second phase of healing, thanks tocytoplasmic myosin and actin: the actin moves in relationto the myosin when the two interact,19 in the same way thatan oar stroke moves a kayak or an athlete runs on a tread-mill (the athlete representing the myosin and the treadmillthe actin). It has recently been shown, by immunohisto-chemistry, that there are free nerve endings in all of the lay-ers of the epidermis, and it is now suspected thatkeratinocytes have a neurotropic function. The ACh actslocally, in the epidermis, like a hormone that can also be a‘messenger’ stimulating the dermis. We can then supposethat an epidermal reservoir of DMAE can interact with thedermis via ACh, of which it is a precursor.

DMAE is also assumed to inhibit formation and enhanceelimination of lipofuchsin, a waste product of the aging cellmetabolism of fatty acids. Experiments have shown thatlipofuchsin is eliminated from the liver by DMAE. Thisbuild-up, which occurs in all organs, has not been associ-ated with any disorder apart from lentigines. Some authorshave reported a gradual reduction in lentigines on thehands with oral DMAE treatment. To date, there have beenno studies published on the topical use of DMAE in thetreatment of lentigines.

Dermal actionDMAE is used for its antioxidant properties, membranestabilization and inhibition or repair of protein cross-linksthat clearly play a role in the aging process. It could thushelp maintain good-quality collagen and elastin and slowdown dermal aging.

Vasomotor effectThe dermal blood vessels are innervated by adrenergicfibers, which cause vasoconstriction, and cholinergicfibers, which cause vasodilation. DMAE, as a precursor ofACh, could cause vasodilation that is clinically unde-tectable but sufficient to produce temporary edema, abuild-up of water in the hydrophilic structures of the der-mis, and, as a result, a tightening of the skin. This hypothe-sis only partly explains the particular kinetics of topicalDMAE. The fact that treating one side of the face onlyshows improvement on one side only suggests that theDMAE has a purely local action and is not converted intoACh throughout the organism. Local blood flow, whichdecreases with age, is vital for the nutrition and defense ofthe dermis and epidermis. Constant slight vasodilationwould thus improve skin perfusion – especially in smokers– and by diffusion would bring in more of the elements

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

Effect on myofilaments and smoothmuscle cellsMyofilaments make up the endoskeleton of a cell (Figure3.13). They can be found in the smooth muscle cells(SMCs) and in the cytoplasm of ‘non-muscle’ cells, wherethey are capable of moving and contracting. SMCs can reg-ulate contraction far more subtly than striated muscle cells.SMCs can shorten to a greater extent than striated musclecells. Shortening of striated muscle cells is limited to move-ment within the sarcomere, whereas with SMCs, themyosin filaments can move over a far greater distance,along the network of actin filaments in the cytosol. Theforce generated by SMCs is less than that generated by stri-ated muscle cells, but can be sustained for much longer.

The arrector pili muscle is under adrenergic control anddoes not respond to a local increase in ACh concentration.The fibroblasts and myofibroblasts are very interesting cellsas far as the possibilities of the action of DMAE is con-cerned. Fibroblasts have cytoplasmic myofilaments thathelp them move in the dermis when necessary.20 There aredifferent types of fibroblast subpopulations. Some authorsmaintain that these different subpopulations expand whenthey are needed through different phenotype expressions,whereas others believe that these subpopulations coexistpermanently in the dermis. These two hypotheses are notincompatible. Myofibroblasts (MFBs) are phenotypicallymodified fibroblasts that have the secretory capacity offibroblasts, which helps them synthesize strong fibronectinfibers. They express the phenotypic characteristics of ‘non-muscle’ cells, but with the contractile capacities (of SMCs)that make them responsible for most of the phenomena offibrotic contraction in the body. The fibronectin fibers syn-


+

Nucleus

Direction of displacement

Microtubule

Dense bodies

Cellular center

+

++

++

+

+

+

+

‘Stress’ contractile fibers

Network tightened withactin microfibrils

Radial network withactin microfibrils

Loose network withactin microfibrils

in all cytosol

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

ch03 7/11/06 8:36 am Page 22

thesized by the MFBs serve as a support for them to ‘pull’on during contraction, which helps the wound to close byas much as 40%.

MFBs synthesize far more actin fibers than ‘standard’fibroblasts, and also have myosin fibers that, when inter-acting with actin, constitute the contractile motor activityof MFBs. MFBs are found in healing tissue, of which theyform 40% of the total number of fibroblasts present. Alarge number of MFBs are also found in the periprostheticcapsule of encapsulated breast implants, while there is noevidence of MFBs if no capsule has formed around theprosthesis. In pathology, abnormal quantities of MFBs arefound in diseases such as pulmonary fibrosis and Crohn’sdisease. Many SMCs respond to a kind of paracrine stimu-lation, where the mediator is released into the environmentof the target cells and diffuses towards the cell, where itinteracts with a membrane receptor.

MFBs are not linked to any synapse, which would makeit impossible for them to move, but the exposure of MFBsto certain mediators causes significant contraction, compa-rable to that in SMCs. We can imagine the contractilepotential of these SMCs when we recall that the nipples, aswell as the scrotum, have many contractile cells of this typethat are sensitive to different stimuli. The difference is thatthe contraction of MFBs during wound healing is irre-versible. Fibroblasts and MFBs, like many SMCs, havenumerous receptors on their surface for different media-tors: ACh, adrenaline (epinephrine), noradrenaline (nor-epinephrine), oxytocin, vasopressin, histamine, angio-tensin II and prostaglandins. As ACh is a small water-solu-ble molecule, its membrane receptor can be a ligand-gatedion channel receptor or can be coupled with the het-erotrimeric G proteins (RCPGs) that control the activity ofa target protein, which can be an enzyme or an ion channel.Opening and closing of the ion channels causes polariza-tion or depolarization of the myofilaments, and the SMCs(e.g. endothelial cells) contract or dilate. The G protein actsas a transducer. As ACh is a small ligand, the N-terminus ofthe G protein in the extracellular environment will besmall. The presence of a larger quantity of ACh in the peri-cellular environment of the MFBs could then stimulate cer-tain membrane receptors more strongly and increase theircontractile potential. DMAE, a precursor of ACh, mightthen stimulate the contraction of MFBs. However theremust be a reactivity threshold for MFBs to ACh, to guardagainst unnecessary contraction of these cells and the for-mation of pathological fibroses. The hypothesis put for-ward here is that a slight increase in the extracellularconcentration of ACh (by conversion from DMAE) couldslightly stimulate the contraction of the fibroblasts and doso reversibly, without fibrosis setting in, as, clinically, theeffect of a topical application of DMAE is reversible 4–8weeks after treatment has stopped. This improved tone, thereversible contraction of the fibroblasts, could explain theclinical kinetics of DMAE in a topical application.

Exocrine glandsThe sweat glands have cholinergic innervation.21 Theeccrine sweat glands, which open directly onto the skin,have denser autonomous innervation than the apocrinesweat glands associated with pilosebaceous units. ACh is theactive neurotransmitter at this level, and the response of thesweat gland will depend on the dose of ACh that stimulatesit. 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. Atlower 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 ofDMAE cannot, of course, stimulate the muscarinic recep-tors, and no profuse sweating has been noted after applica-tion of DMAE. On the other hand, a slight increase in theconcentration of dermal ACh could stimulate the sweatglands’ nicotinic receptors – in a paracrine manner – andincrease hydration of the stratum corneum, making the skinmore ‘supple’ and resistant. The sweat glands themselvesare controlled by circulating hormones and are not undercholinergic control. DMAE will not alter their function.

ConclusionsDMAE is a precursor of ACh, a neuromediator that isimportant to the skin. Keratinocytes, as well as fibroblasts,myofibroblasts, sweat glands and endothelial cells, havereceptors that respond to ACh. They are not stimulatedpre- or post-synaptically but by paracrine diffusion, whichcan activate specific membrane receptors. The hypothesisis that DMAE in a topical application cannot stimulate thestriated muscle fibers, to which it has no access. Further-more, muscle sagging associated with aging is not causedby a deficiency in ACh. The tightening effect of DMAE mayresult from cholinergic stimulation of the membranereceptors of (myo)fibroblasts and stimulate the gradualcontraction of the myofilaments in their cytosol. DMAEalso has anti-free-radical and anti-lipofuchsin activitiesand repairs protein (collagen and elastin) cross-linking.The mode of action of topical DMAE could therefore stemfrom a combination of effects working together at differentlevels: tension of the ‘non-muscle’ dermal cells, ker-atinocyte cohesion and movement, hydration and supple-ness of the stratum corneum, improved skin nourishmentand defense, antioxidant, and skin tone evener. As a result,it is very effective at improving skin tone and firmness.

Summary of the maincosmeceuticals used post peelSee Table 3.1 for a list of post-peel cosmeceuticals accord-ing to skin type, together with their times of application.

Post-peel care 23

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TrolamineTrolamine (triethanolamine salicylate, TEAS) is a salicylatederivative, which is also known as ‘topical aspirin’. It is anamino alcohol that is used for its topical analgesic and anti-inflammatory properties. Like the better-known salicylatederivative, methyl salicylate – which has a rubefacientaction used to good effect in sports injuries and rheuma-tism – TEAS is rapidly absorbed through normal skin aftertopical application. It is used widely for treating sunburn.

Mode of action and absorptionVarious studies show that salicylate derivatives act as muchthrough direct local diffusion as through absorption by thedermal blood vessels and redistribution of salicylates in thewhole body. The blood level of salicylates increases indirect proportion to the quantity applied, the resorptionsurface and the number of topical applications. A largeamount of salicylates can be absorbed through the skin.

When TEAS is applied unilaterally on one limb, the concen-tration of salicylates has been found to be identical in the cor-responding tissues of the contralateral limb. This supports thetheory of action by redistribution through the blood. The useof radiolabeled TEAS also shows renal and fecal elimination.Phonophoresis helps salicylates penetrate further into the skin.

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

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


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

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 Morning and eveningcream or Actilift® body lotion (Figure 3.14)

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 Morning (all over)Purifying cream or gel Evening (only on the lesions)

Hyperpigmentation (melasma–lentigines) Blending Bleaching® cream Morning (all over)(Avoid exposure to sun: Melablock® HSP

Blending Bleaching® cream Evening (only on the lesions)50+ at 9 AM, 11 AM, 2 PM; serious cases: 3–4 times a day)

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

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PrecautionsTrolamine must not be applied in cases of infection: salicy-lates can accelerate the penetration of microbes into theskin and aggravate any pre-existing infection. It has beenshown to cause local skin irritation and scabs to form onthe areas to which it has been applied. Skin irritationincreases the more it is applied. In smaller quantities,repeated application only induces epidermal hyperplasia.Some authors consider TEAS to be a potential cytotoxicagent. It is a potential skin irritant that makes the skin sen-sitive and can cause contact allergies.

Trolamine is a salicylate derivative, and salicylic acid is akeratolytic agent that dissolves the intercorneocyte amor-phous matrix and impairs the barrier function of the stra-tum corneum.

Symptoms of salicylism can appear with chemical peelswhen large amounts of salicylate derivatives are applied onthe skin, on large surface areas or repeatedly, causing a highblood level of salicylates. In cases of toxic levels of salicylate inthe blood, an increase in oxygen consumption causes hyper-thermia by the uncoupling of oxidative phosphorylation.

Trolamine should therefore not be used during the imme-diate post peel period.

Tips for the care of sensitiveskin� Prolonged use of creams containing more than 8–10% of

AHAs can make some skins more sensitive by reducingthe thickness of the stratum corneum for long periods.

� Use cleansing milks, lotions or mineral water sprays towash.

� Do not let water dry on the skin; when it evaporates, itsoon dries the skin out. Damp skin should be dried witha soft cloth or paper tissues.

� Avoid exfoliating scrubs, repeated micropeels andcreams containing microcrystals on sensitive skins. Donot use any masks that might dry out the skin.

� Do not use aggressive soaps.� Tretinoin (vitamin A acid) makes the skin more sensi-

tive.

One Easy TCA® peel per week for 4 weeks can restructurethe skin and eliminate any abnormal sensitivity. In thisindication, the cosmeceuticals that can be combined with itare restricted to Vit E Antioxidant® cream in the morningand the more nourishing Renutriv ACE Lipoic Complex®cream in the evening.

Characteristics of ‘normal skin’Normal skin should be:

� Firm: contain a sufficient quantity of elastin and colla-gen

� Soft: compact stratum corneum protected by skin lipids� Hydrated and unwrinkled: hydrated keratinocytes and

dermis� High in color: active microcirculation; pink color visi-

ble through the skin� Resistant to external aggression: active protective func-

tion•� Unscarred: no stellate or secondary scars

Notes1. Even though this type of sunscreen can protect the skin

against free radicals some could also cause post-inflamma-tory 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 whiteas it goes from transparent to white as a result of structuralmodification 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 vitaminC + 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 treat-ment, application of the solution until scattered pinpoint orcloudy white frosting appears, application of the post-peelcream (tyrosinase inhibiting, anti-oxidant, stimulating).Repeat this process four times at weekly intervals.

11. This paragraph particularly concerns superficial peels orpeels to the ‘Grenz zone’. Papillary dermal peels are notreally 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 ofcholine uptake and metabolism cause developmentalabnormalities in neurulating mouse embryos. Teratology2001; 64: 114–24.

16. Fisher MC, Zeisel SH, Mar MH, Sadler TW. Perturbations incholine metabolism cause neural tube defects in mouseembryos in vitro. FASEB J 2002; 12: 619–21.

17. Leung HW, Tyl RW, Ballantyne B, Klonne DR. Develop-mental toxicity study in Fischer 344 rats by whole-bodyexposure to N,N-dimethylethanolamine vapor. J Appl Toxi-col 1996; 16: 533–8.

18. The antioxidant effect of DMAE has been shown by electronspin resonance (ESR) for the hydroxyl radical. It does notseem to have any anti-superoxide action.

Post-peel care 25

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19. There are different types of myosin for different types ofmovement; cell movements (myosin II) are not facilitated bythe same myosin that permits endocytosis (myosin VI) orthe movement of vesicles between cells (Myosin V).

20. For example, movement along the fibrin/fibronectin fibersduring the healing process.

21. Catecholamines, vasoactive intestinal peptide and natri-uretic peptide have also been detected near the sweat glands.

22. Intradermal injection of 0.1 mg of ACh: postganglioniccholinergic stimulation (Biology of the Skin: 58).

23. Hurley HJ. The eccrine sweat glands: structure and function.In: The Biology of the Skin, Parthenon Publishing, Lancaster2001; 47–76.


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AllergiesThese are common when using antibiotic creams or oint-ments in the post-peel period: between 5% and 10% ofallergies should be expected when using antibiotic creamscontaining neomycin after a peel. The temporary thinningof the stratum corneum allows products applied on theskin after peels to penetrate more easily, which promotesthe development of contact allergies.

InfectionsThese are more common when patients have to undertakecomplex post-peel care themselves. The basic principles ofsterility are not widely known by the public and requirespecial training in order to be effective. The more patientshave to take part in the post-peel care, the higher the risk ofinfection.

Pulling off small scabsThis often leads to infection, prolonged erythema and evenscarring. The less patients touch their skin, the better!

The sunIt should be remembered that direct exposure to the sunfor 10 minutes is enough to trigger pigmentary changes insensitive individuals during the post-peel period. See thesection on effective sun protection in Chapter 3.

Dehydration of the skin after apeelDrying and flaking skin causes an irresistible urge to scratchand therefore a risk of complications (including secondaryinfections, inflammation and scars). Applying white Vase-

line® immediately improves the pruritus and the feeling oftightness in the skin after a medium or deep peel. Sterilewhite Vaseline® is an excellent topical ointment that can beapplied to the treated areas in the first few days after amedium peel or after removing the healing mask (after the8th day) following a phenol peel. Only a thin layer need beapplied to avoid itching caused by the drying out of surfacekeratinocytes that have not yet differentiated into corneo-cytes. The Vaseline® creates an impermeable layer on thesurface of the skin and prevents the water in the epidermisfrom evaporating. The water accumulates under the layer ofVaseline® and provides instant natural hydration that soonrelieves the itching caused by the keratinocytes drying out.

Influence of age post peelOlder patientsIntraepidermal and dermal peels are performed as usualeven on patients aged 80 or over. With elderly people, thereseem to be fewer pigmentary changes, but the theoreticalrisk of infection is higher. In theory, the weakened capaci-ties of the keratinocytes to regenerate, the presence ofnumerous cell abnormalities, dormant fibroblasts andunderlying vascular sclerosis should slow down healingafter a peel in older people. In practice, the only real prob-lem is increased susceptibility to infection resulting from aweakened immune system. A more important factor seemsto be the degree of skin photoaging rather than age itself.Many phenol peels have been performed on patients whoare well into their 80s, without any particular problems.

Young patientsAt the other end of the scale, what is the minimum age forhaving a chemical peel? The answer is simple: in the major-ity of cases, a peel is only necessary for young patients if theyhave acne. Acne responds extremely well to intraepidermalpeels or peels to the basal layer of the epidermis. Deeperpeels are not recommended when the skin is infected. Veryyoung patients benefit from relatively superficial techniques

4Factors influencing chemical peels

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with a high safety level (Easy Phytic®). The presence of acnemeans that the young patient’s developing hormone systemhas created an adult skin – thick and oily and resistant toacids.

Use of corticosteroidsTopical corticosteroidsThese are only indicated in cases of serious edema or pruri-tus during the first few days after an aggressive peel. It isalways best to start with a short-acting corticosteroid(hydrocortisone or betamethasone). A cortisone-basedcream can be used during the first few days after a peel toreduce excessive edema or pruritus. The deeper the peel,the greater is the need for emollients. Hydration after a peelis vital (except after a peel with Unna’s paste); the hydrat-ing cream should contain no alcohol or perfumes.

Oral corticosteroidsThese are very rarely indicated in combination with peels,and then only in the case of very specific problems (seeChapter 37).

Intravenous corticosteroidsThese can be used before a deep peel to limit edema imme-diately after the peel and avoid any allergic or laryngealreactions.1 They reduce post-peel inflammation, which isin fact necessary to initiate the skin repair processes. If thedegree of inflammation is reduced, there is a risk of slowingdown the first stages of skin regeneration.

Understanding the healingprocessUnderstanding the skin healing process after a peel allowsevaluation of the risks of scarring, infection and dyschro-mia. For more information on how the skin heals in rela-tion to the depth of the peel and on risk evaluation, see thesection on scars in Chapter 37.

Histologically, the skin healing process follows a precisesequence of different stages. The process starts almostimmediately: neutrophils enter the treated area as soon asthe peel has been applied, and stay there for 3–5 days.Macrophages are present from the 3rd to the 10th day andlymphocytes from the 6th or 7th day. Re-epithelializationstarts just 24 hours after the peel and first manifests as acentripetal migration of keratinocytes, followed by rapidcell proliferation. After the re-epithelialization phase, der-mal 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 peeldepends on the concentration of pilosebaceous units(PSUs) in the treated area: the face has many PSUs, and thenose and forehead have more than the cheeks and temples.Statistically, the cheeks and temples prove more sensitive toscarring. The dermis of the eyelids is thinner but denserthan the rest of the face, and the dermoepidermal junctionis flatter. The skin on the back of the hand has few PSUsand little subcutaneous fat. Atrophy develops there fairlyrapidly. The skin on the back is very thick, and its dermis isdense in collagen. Nevertheless, it has fewer PSUs than theface, and the risk of developing post-peel scars there ishigher. The dermis of badly sun-damaged skin has adepleted cell population, and is thin and slower at detoxify-ing acids. The effect of the acids is therefore increased, andpeels on sun-aged skin are more dangerous than on young,well-hydrated skin. Moreover, skin with actinic damagehas fewer appendages (PSUs), and tends to regeneratemore slowly.

Healing is slower when a wound is left to heal in theopen air than when the wound is covered. This does notmatter much for intraepidermal peels, but is more impor-tant when dealing with medium or deep peels. One advan-tage that peels have over laser treatments is that they leavea layer of dead, but protective, skin in place, and thisenhances re-epithelialization. The strips of skin thatremain after a peel should be left alone, as they protect theregenerating skin. Lasers, on the other hand, graduallyvaporize the layers of skin to be removed, and the skin isleft to heal uncovered. The colloid dressings available onthe market (e.g. Convatec, Omniderm, Vigilon) allow bet-ter-quality healing, in a moist environment, after lasertreatment. The problem with occlusive dressings is thatthere is an increased risk of infection, and they need to bemonitored carefully, as bacteria are known to proliferatemuch more quickly under an occlusive dressing than in theopen air. As bacterial proliferation increases under occlu-sive dressings and as the skin’s immune defenses arereduced after a deep peel, it is often preferable for the skinto heal ‘under a scab’. To do this, a mask of bismuth sub-gallate should be used (Figure 4.1, and see Chapter 35).

Preparing the skinThis is worthwhile when the patient is willing and when itis carried out under medical supervision. Unsupervised orsecret use of aggressive products by the patient can some-times cause problems for the doctor who has not beeninformed of the patient’s self-administered treatment. Thedoctor should watch out for unacknowledged use oftretinoin or other retinoids, concentrated glycolic acid,benzoyl peroxide, or any other product that increases pen-etration of the acids, making them penetrate more quicklyand deeply than originally intended. Some patients can


ch04 7/11/06 8:37 am Page 28

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

Skin colorThis must be taken into account when choosing a peel:Fitzpatrick skin phototypes I–III can tolerate any kind ofpeel. Patients of type IV with light-colored eyes have fewerproblems with dyschromia after a peel than dark-eyedpatients of the same type. Type V and VI patients are atmost risk with peels, and it is recommended not to gobeyond the papillary dermis with these patients to avoidhypochromia. Type V patients are also quick to develophyperpigmentation. Special care should be taken withpatients who have prolonged hyperpigmentation withmosquito bites or small wounds.

Localized phenol peels should only be carried out onpatients with a skin phototype lower than IV, so that thearea treated with phenol is not left lighter than the sur-rounding skin, even if it has been treated with a mediumpeel to even out the color. The same applies to patientswith many freckles, which mostly disappear after a peel tothe papillary dermis.

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

The fact that in most cases they cannot use camouflagemake-up makes it difficult to carry out a local or full phe-nol peel. Moreover, phenol peels produce less spectacularresults on thick skins than on thin skins. Shaving does notpose a problem, as a peel to the basal layer of the epidermisdoes not rule out shaving, even with a blade. For a peel tothe papillary or reticular dermis, it is best not to shave whilethe skin is flaking. It is usually possible to shave after the8th day. Alcohol-based aftershaves should be avoided, anda hydrating, anti-oxidant or firming cream should be usedinstead, followed by effective sun protection.

Make-upPatients often ask about make-up. The general principle isthat it is possible to wear make-up, even when the skin isflaking, after an epidermal peel or a peel to the basal layer,but it is unlikely to look good. After a peel to the papillaryor reticular dermis, make-up is usually allowed, and evenrecommended, on the 8th day. Patients who do not likewearing make-up should be warned of the likelihood ofpost-peel erythema, depending on the depth of the treat-ment. Some patients are thus ruled out, as their profes-sional lives do not allow any visible erythema or theycannot stand the idea of wearing make-up. In these cases, itis recommended to repeat an Easy TCA® peel four timesrather than use Unideep®.2

Smoking and peelsIt is generally accepted that the free radicals produced eachtime smoke is inhaled contributes to the overall aging ofthe body and of the skin in particular. Publications thatshow the difference in skin quality between two twins, oneof whom is a smoker and the other not, speak for them-selves, so marked is the deterioration of the smoker’s skin.Smoking causes repeated vasoconstriction and chronicmicrovascular damage, which contribute to the overallimpoverishment and aging of the skin. There are no majorproblems, however, with heavy smokers who have peels tothe papillary dermis. Full-face phenol peels should be car-ried out with caution because of the increased risk of laryn-geal edema. A localized phenol peel does not pose this kindof problem, and phenol can, for example, be appliedaround the edges of the mouth (which is usually very dam-aged in smokers), while the rest of the face is treated with atrichloroacetic acid peel to the papillary dermis.

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

Factors influencing chemical peels 29

Figure 4.1 After a phenol peel the crust of bismuth subgallate appearsdry but actually helps healing in a moist environment.

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Nutrition and peelsThe patient’s nutritional condition at the time of a peel isan important factor in the treatment. For all the phases ofhealing to take place correctly, a perfect balance of nutri-tion and micronutrition is necessary. It is clear that poornutritional balance will have more impact on healing aftera deep peel than after a light peel – all the more so as deeppeels, rather than light peels, are usually intended for olderpeople. Many proteins are synthesized during healing afteran intraepidermal peel: many amino acids are needed toform the provisional matrix as well as to synthesize newcollagen. Catabolic patients, or patients who have recentlyhad significant, involuntary weight loss, do not have suffi-cient protein reserves for the skin to regenerate properly. Adermal peel also induces stress, which causes a hypercata-bolic state that is more or less acute depending on thedepth of the peel. Patients with insulin-dependent diabetesor patients who have recently undergone significanttrauma or surgery, who have liver or kidney deficiencies, orwho suffer from chronic inflammation are not the bestcandidates for dermal peels, as the need for proteinincreases sharply. The average daily protein requirement is1.5 g/kg per day. The amino acids considered most essen-tial include arginine and glutamine. However, to date, ithas not been proved that supplements improve the qualityof wound healing. Arginine is a precursor of proline andcollagen, and the recommended dose is between15–25 g/day. It acts as a local stimulant of lymphocytes anda general stimulant of human growth hormone (HGH) andinsulin-like growth factor I (IGF-I) production. Glutaminealso stimulates the production of HGH, and is an anti-oxi-dant and an energy source for fibroblasts, keratinocytes,lymphocytes and macrophages. A daily intake of10–30 g/day is recommended.

Carbohydrates and fatty acids are also necessary forrapid and good-quality skin regeneration. The extracellularmatrix is made up of glycosaminoglycans and proteogly-cans, which are polysaccharides linked to proteins. Omega-6 fatty acids are essential for cell membrane formation.Supplements of linoleic and linolenic acid can be recom-mended when the patient’s blood is not properly bal-anced.3

Numerous trace elements are necessary for manyenzymes to function properly: copper is needed for the for-mation of the collagen network and the anti-oxidant actionof superoxide dismutase; iron is needed for collagen synthe-sis; zinc is a cofactor for DNA and RNA polymerases, playsa part in protein synthesis and stimulates cell division.

Vitamins also play a role in the healing process. VitaminA is involved in angiogenesis and keratinocyte differentia-tion, stimulates collagen synthesis, and enhances intercel-lular adhesion and skin immunity. Vitamin E can be usedas a lipophilic antioxidant. Vitamin C is necessary for col-lagen synthesis, and for stabilizing the collagen triple helix.Between 500 and 1000 mg/day can be given before andafter an intradermal peel.

Notes1. Preventing laryngeal edema in smokers undergoing a phenol

peel.2. Unideep® (Skin Tech) TCA peel: to the papillary dermis,

with a qualitative formulation based on Easy TCA®, but witha more concentrated solution and post-peel cream.

3. The Roman Pais laboratory in Nivelles, Belgium, provides –among other nutritional and micronutritional tests – a veryprecise and scientifically annotated blood count of circulat-ing fatty acids.


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The possibilities for treatment with chemical peels aremany and varied and depend on the agent chosen as muchas on the way in which it is used. We can, of course, take thenarrow view of peels as the destruction of damaged tissuewith acid.1 From this perspective, a result can only beachieved by ‘destroying beneath the lesion’. This is, ofcourse, often the case, but we must not forget that chemicalpeels help to stimulate as much as destroy. Many of theirpositive effects are largely due to this stimulation. Let ustake glycolic acid, for example, whose action is mainlyintraepidermal2 but which is associated with activation ofthe papillary dermal fibroblasts. The destructive effect,which removes the stratum corneum and even part of theepidermis (depending on the concentration used),improves the appearance of rough skin, while the effects ofremote stimulation improve the extracellular matrix con-stituents secreted by the fibroblasts.

Choosing the right peel is often a source of stress for adoctor who is starting his career in peeling: opting for atechnique that is too superficial will satisfy neither patientnor doctor, while using a medium-strength product couldcause unexpected side-effects that can be hard to cope with,especially if the results are mediocre. Deep peels have theirown 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 meansthat they are often rejected by beginners, who will insteadattempt to push the limits of a peel and do a medium peelwith an agent that is intended to be superficial. They willoften pay for the consequences in cash.

When choosing a peel, a simple equation should betaken into account: the results expected from the peel mustbe greater than the sum of the fear of the treatment’s com-plexity, the risk of complications, and the downtime andfinancial cost for the patient. The ratio [Results/(complex-ity + complications + downtime + cost)] must always bepositive. During the preliminary consultation, the doctorshould first discuss downtime and treatment cost with thepatient, who always expects breathtaking results. It is easierto deal with these two factors first before embarking on thecomplexity of the technique and the potential risks and

complications. In this way, the treatment can quickly beoriented to what the patient is prepared to go through. Ifpatients say straight off that they cannot accept any down-time or have limited funds, it is pointless wasting theirtime, which is as precious as yours, explaining unnecessarytechnical details about deep peels.

A few logical rules make iteasier to choose� Sagging skin only responds to a phenol peel and only if

the skin is relatively thin. Peels are not indicated for sag-ging in thick skins or for nasolabial folds. Chemicalpeels cannot compete with surgical face-lifts; they can-not 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 botu-linum toxin prior to any peel; it allows the skin to regen-erate on a non-moving base.

� Photoaging and free-radical aging from smoking andpollution can be treated with a peel; the speed and qual-ity of the results depend on the depth of the treatment.

� Active acne should only be treated by a medium peelafter it has been treated medically and the infection hascleared up;3 it can, however, be treated by lighter peelseven during the active infectious phase.

� Facial acne scars are difficult to treat, sometimes evenwith phenol. Acne scars on the back, décolletage or facecan fade or improve with a combined technique ofchemical peeling and dermabrasion. It is still difficult,however, to get rid of them completely.

� Results of the treatment of hyperpigmentation disordersdepend entirely on the depth of the problem and thedepth of the treatment. They are frequently treated withpeels that reach or go beyond the Grenz zone, in con-junction with appropriate daily care. The only way totreat melasma permanently is by completely destroyingthe cells that produce melanin, by peeling ‘beneath the

5Choosing the right peel

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lesion’ with an agent that is toxic to melanocytes, whichis a fairly aggressive treatment. Another option is totreat the skin more superficially in order to reduce therisk of complications. Only a certain proportion ofmelanocytes are destroyed in order to lighten themelasma at the same time as stimulating keratinocyteturnover. The relative increase in the number of ker-atinocytes compared with the number of melanocytesdilutes the melanin produced in the epidermal cells (theblending effect). Melanogenesis is reduced with tyrosi-nase inhibitors and antioxidants, which are applied inthe long term and combined with effective sun protec-tion (bleaching effect).

� Solar or senile lentigines respond partially to peels to theGrenz zone and the papillary dermis. They sometimesrequire a peel to the reticular dermis to get rid of themcompletely. This deep peeling can be local.

� Stretch marks can only be treated definitively by apply-ing aggressive treatments that can improve the epider-mal and dermal atrophy that accompanies them.

� Peels are not indicated for hypertrophic scars. Some finefacial scars (from a face-lift, for example) improve vastlyafter local application of some phenol peels; others areimproved by a combination of abrasion and peeling.

� Body peels produce fewer results and more problemsthat facial peels.

� Peels on the backs of the hands are very easy and causefew complications with trichloroacetic acid in the formof Easy TCA®.

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

Start of photoagingThe patient shown in Figure 5.1, who is approaching 40,has a few lentigines and a thick and oily skin with dilatedpores. There are no wrinkles, but a slight sagging of the skinthat is only noticeable in a standing position.

A deep peel would not be the best way to treat thispatient, as the ratio of results to complexity + complica-tions + downtime + cost would not be favorable. The pos-sibility of a medium peel to the papillary dermis could bediscussed, if the patient wanted fairly quick results or if shedid not have enough time for a series of lighter peels. Shecould also be advised to have a series of peels, eitherintraepidermal (to remove the epidermis) or down to thebasal 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 careroutine should include DMAE4 to firm the skin, tyrosinaseinhibitors and antioxidants to limit melanin production,5

and, of course, effective sun protection. If the lentigines donot clear quickly, they should be treated locally with a sin-gle careful application of Only Touch®, immediately beforethe last of the four Easy TCA® peels.

Under-eye bagsMany patients want to get rid of or improve under-eye bags(Figure 5.2) that leave them looking permanently tired. Thisis a purely surgical problem, although it has been suggestedthat local injections of phosphatidycholine would dissolvethe fat, but this treatment can be very risky.6 Peels and cos-metic products cannot improve them. In some circum-stances, a phenol peel can improve bluish circles under theeyes if it succeeds in making the thin skin in this areathicker. The best treatment is to remove the weak veins ofthe inner and outer canthus with a Müller hook, followedby treatment with blue laser light.7


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

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

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Sagging skinApart from an improvement in overall skin quality and tone,the patient shown in Figure 5.3 will not benefit from anypeeling technique – either repeated superficial peels or a deepphenol peel. Actinic damage is light and there are not manylines or wrinkles. On the other hand, the folds of sagging skinare very marked in this patient, who is a heavy smoker.Examination and palpation show that the dermis has emp-tied of its ground substance and atrophied. The daily careroutine should combine powerful antioxidants,8 DMAE andpossibly DHEA. This patient refused to have any surgicaltreatment, and was treated with a phenol peel in an attemptto get the skin to retract. Unfortunately, on a dermal basetotally emptied of ground substance, this treatment resultedin an ‘accordion effect’.9 This patient would only benefit cos-metically from a surgical face-lift, possibly followed by peelsto the Grenz zone to improve the quality of the skin.

The patient in Figure 5.4, on the other hand, receivedmuch benefit from the stimulating and evening effect ofEasy Phytic® on the epidermis and dermis.

The skin tension is better and the yellow discolorationcaused by actinic damage has been reduced. The daily careroutine also consists here in Actilift® (DMAE cream) andDHEA-Phyto®: see Chapters 2 and 3 for more informationon these two products. When retightening is indicated, EasyPhytic® can be applied in a single layer every morning forseveral days, depending on how the skin reacts. The resultsare surprisingly quick, and the skin soon tightens visibly(see Chapter 11).

Comedonal acne Comedonal acne (Figure 5.5) can be treated with anintraepidermal peel or a peel to the basal layer. Atrichloroacetic acid (TCA) peel to the papillary or reticulardermis could be considered, but such a deep treatmentwould be pointless for this type of disorder, which can betreated with a lighter peel and, in any case, requires long-term maintenance treatment.

It is essential to ‘clean’ the skin beforehand with a come-done extractor to limit damage to the skin; the skin shouldbe cleaned in this way a week before an alpha-hydroxy acid(AHA) peel10 or immediately before each of four EasyTCA® peels. Removing the comedones helps producequicker results and prevents post-peel infections.

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

Choosing the right peel 33

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

Figure 5.3 General sagging of the skin with little actinic damage: this isnot a good indication for a peel.

Figure 5.5 Comedonal acne.

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Either the applicator provided with the product or the pointof a 30G1/2 needle should be used to limit the action pre-cisely 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 ofEasy TCA® or Easy Phytic® solution into the center of thecomedone. Post-peel care, which is very important, consistsin avoiding comedogenic cosmetics, having the skincleansed professionally once a month, and applying an anti-acne cream containing AHAs, tretinoin or precursors, dis-infectants, anti-inflammatories, tea-tree oil, etc.11 once ortwice a day. For details of this treatment, see Chapter 15.

Lentigines, acne anddyschromia The patient shown in Figure 5.6(a) has numerous treat-ments to choose from. She does, however, have an impor-tant restriction to take into account: downtime must beminimal and the overall cost low. Resorcinol, TCA to thepapillary dermis and phenol are all automatically ruled out.However, a relatively strong acid is needed to treat thelentigines that can be seen at the top of Figure 5.6(a). Forthis, Only Touch® can be used, applied locally and preciselyon the lentigines, with Easy TCA® being applied on the restof the face to treat the dyschromia, superficial lentigines,photoaging and acne and to even out the result. See Chap-ter 15 for details on applying this product. Daily post-peelcare should consist of an anti-acne cream and a blendingand bleaching cream to even skin tone. Figure 5.6(b) showsthe lentigines clearing up, an improvement in the overallappearance of the skin and the dyschromia evening out.This improvement can still be seen 1 year after treatment.

PhotoagingThe more severe the photoaging, the more important it isto consider the depth of the peel. The patient shown in Fig-ure 5.7 has a light skin type that is sensitive to the sun’srays. She has developed a number of solar lentigines andfine wrinkles caused by UV rays. The eyelids are very wrin-kled and the nasolabial folds and marionette lines are slack.

In the long term, this patient’s nasolabial folds and mar-ionette lines will only improve slightly, even with a deeppeel. Other techniques12 should be used to treat them.There are many peels to choose from. The wrinkles on thelower eyelids can be softened with a TCA peel to the Grenzzone (Easy TCA®) or to the papillary dermis (Unideep®),but only phenol can be guaranteed to get rid of them. Manylentigines respond to a TCA peel to the basal layer of theepidermis, 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 butonly 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 bedone in a single session: a full-face phenol peel that willtreat all the symptoms of photoaging at once and tightenthe skin. If the patient opts for this treatment, she mustaccept at least 8 days’ downtime and a high treatment cost.The second option is a less aggressive, more gradual andstimulating treatment that can be combined with a localphenol peel on the lower eyelids. Only Touch® is appliedlocally on the deeper lentigines and Easy TCA® on the restof the face to even out the result and improve the fine wrin-kles. A localized phenol peel on the lower eyelids14 is rec-ommended if the patient wants to get rid of her eyelidwrinkles. If this course of action is chosen, the possibility ofcombining a localized phenol peel with Unideep®, a TCA


A B

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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peel to the papillary dermis, should be discussed. Withphenol, the downtime is 8 days and it might be moreappropriate to combine the local phenol peel with a singlesession of Unideep® that has a downtime of 5–6 days,instead of having four weekly sessions of Easy TCA®. As theresults are comparable,15 the decision is often based on costor the risk of complications, which is higher with a dermalpeel. Depending on requirements, daily post-peel careshould include a vitamin E antioxidant cream, a blendingand bleaching cream, and/or a DMAE cream.16 Some solarand senile lentigines may only respond to peels to the retic-ular dermis as, histologically, the lentigines may be charac-terized by deep dermal papillae and elongated rete ridgeswith golf club-shaped extensions.

Post-inflammatoryhyperpigmentation andscarringThe patient shown in Figure 5.8(a) had had a serious roadaccident 6 years before the treatment. The surgeon did aperfect job given that the face had been completelylacerated by the car’s windscreen. Severe post-traumaticinflammation quickly turned into post-inflammatory

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


Figure 5.7 More severe photoaging.

Figure 5.8(a) Post-traumatic scars and hyperpigmentation. (b) Followingtreatment with a local phenol peel. (c) Four Easy TCA® peelsand Blending Bleaching® cream were applied to even out theskin color.

C

B

A

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phenol. The skin color was evened out by applying fourEasy TCA® peels until a cloudy white frosting wasachieved, combined with Blending Bleaching® cream thatwas applied twice a day from the day after the first peel andcontinued for at least 6 months (Figure 5.8(c)). An effectivesunscreen (see Chapters 3 and 35) must be applied everyday between the four weekly peels and until the end of themaintenance treatment.

Severe aging of the skinThe patient shown in Figure 5.9 has thin skin marked byexpression wrinkles, sagging skin and photoaging. Using apeel that does not reach the dermis is always disappointingin cases like this. Some light peels might tighten the skintemporarily as a result of the edema that occurs after-wards. It would be impossible to attempt to correct all ofthese wrinkles, even by frequent repetitions of an intraepi-dermal peel or even a peel to the Grenz zone. A peel to thepapillary dermis might improve the finer wrinkles and thequality of the skin, but only a full-face phenol peel couldtighten the skin definitively through a ‘three-dimensionalfacelift’.17 The expression wrinkles should be treated first –1 week before the phenol – with botulinum toxin, whichwill allow the skin to regenerate without the movementsthat would soon reimprint the wrinkles on a healing der-mis.

Perioral wrinklesPerioral wrinkles (around the upper lip and chin) onlyrespond to very deep peels (Figure 5.10). Many differentagents have been tried: e.g. pyruvic acid, that has a highpotential for scarring, and this particular agent, which is dif-ficult to control in concentrated solutions, is very rarely used.

Chemical cheiloplasty can only be considered underthree conditions:

� The natural skin color allows treatment without the riskof pigmentary changes.

� The skin around the area to be treated is in goodenough condition that the demarcation line will not betoo obvious.

� Other treatments (i.e. hyaluronic acid, collagen, etc.)would have no effect.

Patients with skin phototype above IV are therefore ruled outfrom this treatment, as are patients with a light skin photo-type but a lot of freckles,18 and patients whose skin is severelyphotoaged. Phototype IV patients should make a choicebetween deep wrinkles and a possible depigmentation.

Lip & Eyelid® formula was originally developed to treatonly the lips and eyelids before its indications wereextended to the full face. It can be applied locally withoutnerve blocks or any kind of anesthetic (see Chapter 36). ATCA Unideep® peel (to the papillary dermis) is applied tothe rest of the face immediately after the phenol peel hasbeen applied locally (Figure 5.11). The Unideep® must notcome into contact with the skin that has been treated withphenol.

Botulinum toxin often has to be used at the same time asa deep peel on patients with thick skins in order to limit thecontractions of the orbicular muscle of the lips and toimprove/maintain results. The horizontal fold between thelower lip and the prominence of the chin does not usuallyrespond well to peels, even deep ones. It can easily be filledin, however, together with the nasolabial folds 1–2 monthsafter the phenol peel.

Dermal atrophyThe wrinkles on the cheeks of the patient shown in Figure5.12(a) have been caused by dermal and hypodermal atro-phy. Only a deep peel could improve the cosmetic appear-ance of this patient. Dermal fillers are, however, anotherpossibility for treatment. Figure 5.12(b) shows the rejuve-nating effect of injecting 2.5 cm3 of Bioalcamid® 19 in eachcheek. The deep wrinkles have completely disappeared andthe shape of the face has been restored to look like it did ina photograph of the patient when younger. Note the persis-tent bruising in the injected areas. This bruising can largelybe avoided by using a trocar or blunt-tipped needle instead


Figure 5.9 A clear indication for a phenol peel.

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of a conventional needle. This treatment can of course becombined with a peel: Bioalcamid® can be used perfectlysafely with Easy TCA® in the same session. The peel is per-formed after the liquid implant has been injected. A deeperpeel, on the other hand, should only be applied a few weeksafter the filling to avoid interference with the necessaryprocess of encapsulation that fixes the filler material inplace.

Deep wrinklesIf the patients in Figures 5.13(a) and 5.14(a) want quickrejuvenation that will last around 15 years, a phenol peel isthe only indication (Figures 5.13(b) and 5.14(b)). Theextent of the problems would be beyond dermal fillers,and if these were used, the results would be temporary.


A

B

C

Figure 5.10 (a) Deep wrinkles on the upper lip and chin. (b) Bismuthsubgallate powder mask during the first few days after aphenol peel. (c) Results after treatment of these wrinkles withLip & Eyelid® formula (phenol peel – chemical cheiloplasty).

Figure 5.11 (a, b) Wrinkles on the upper lip treated with a singleapplication of Lip & Eyelid®, with the rest of the face beingtreated with a Unideep® peel in the same session. Note theexcellent results for facial skin tension with TCA.

A

B

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Botulinum toxin, used alone, would only partiallyimprove the areas around the eyes, lips and cheeks. A sur-gical facelift would tighten the neck and the cheeks, but itwould not treat the crow’s feet satisfactorily and wouldhave no effect at all on the wrinkles on the lips and theoverall skin quality. A light peel would only improve skinquality and even out skin tone, but would not get rid of thewrinkles. A peel to the papillary dermis would have a sim-ilar and more noticeable effect, but would not get rid ofthese deep and long-standing wrinkles. An experienced

doctor could use full-face dermabrasion. Full-face carbondioxide laser treatment used to be very popular, but isgradually being abandoned because of the serious compli-cations faced by both patients and doctors. A phenol peelwill treat the sun-damaged skin and tighten these patients’faces. An inexperienced doctor should not, of course, usethis type of peel. Treating the deep wrinkles on the upperlip often calls for a combination of techniques: phenol plusdermabrasion, phenol plus botulinum toxin, second phe-nol treatment, etc.


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 adermal filler: 2.5 cm3 of Bioalcamid® in each cheek.

A B

A

B

Figure 5.13 (a) Deep wrinkles. (b) Results after a session of full-faceExoderm®.

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MelasmaMany techniques are now available for treating melasma.Some are more aggressive, some more effective and othersmore costly or complex. Only one technique can provide adefinitive and effective treatment in one single session: aphenol peel. After a phenol peel, melanocytes can no longerproduce melanin. If we rule out this treatment, whichwould be extreme for melasma alone, then the basic princi-ple is relatively clear, if not always 100% effective. Theexisting melanin reserves must be eliminated by carryingout one or more peels, and melanin must be preventedfrom building up again by long-term topical post-peeltreatment and effective sun protection. How quickly themelanin reserves can be eliminated depends on thestrength of the peel: an intraepidermal peel will beextremely slow, a peel to the basal layer will be slow, a peelto the Grenz zone will be quicker, and a peel that destroysmost of the papillary dermis will be quicker still. This pro-gression raises the following problems: if the peel acts tooslowly, either the patient will tire of the treatment, or theskin, once exposed to the sun’s rays, will resynthesize themelanin as it is being eliminated; if the peel is deeper, to thepapillary dermis, and the inflammation is not controlled,the skin might react and develop post-inflammatory

hyperpigmentation. In any event, success depends on sunprotection/avoidance and long-term topical treatment.Patients who refuse to go through with post-peel careshould not be accepted for melasma treatment. The choiceof treatment for the patient shown in Figure 5.15(a) wasfour sessions of Easy TCA® (Figure 5.15(b)). The solutionwas first applied to the melasma spots until cloudy whitefrosting appeared; it was then applied to the whole face toeven out skin tone.20 One session was done per week. Anti-tyrosinase and antioxidant Blending Bleaching® cream wasused twice a day. The cream was first applied the morningafter the first peel, on the whole face in the morning and onthe melasma spots in the evening.

Any melasma treatment (apart from phenol) must beaccompanied by long-term care with antioxidants, tyrosi-nase inhibitors and effective sun protection for a minimumof 6 months (although 1 year would be more effective).

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


A B

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

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doctor’s choice of preparation depends on the patient andthe method of application (when pre-peel preparation isindicated). It also depends on how rigorously the actualpatients, who will only really benefit from TCA in simpleaqueous solution (TCA–SAS) when the skin has reachedthe 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 beapplied to all areas of the skin. Pigmentary changes arealways a risk with TCA–SAS, and should be prevented asmuch as treated. There is also a risk of scarring when theconcentration of TCA is higher than 35% m/m. Treatingthe neck and décolletage is dangerous, as effective treat-ment depends on relatively high concentrations ofTCA–SAS being applied to an area that is quick to scarbecause it has few appendages, because of its histologicalstructure and because of the twisting and stretching move-ments it is constantly undergoing.

For an inexperienced doctor, the choice may seemdaunting! What is the best way to deal with general skinaging of ‘average severity’? Phenol would be too aggressiveand glycolic acid not strong enough. A TCA peel would bemore appropriate, but how much preparation would thepatient accept? What concentration of TCA should be

used? 25%, 35% or 50%? m/m, m/v or m + v? How muchacid solution should be applied and how many coats?What depth should be reached? How much pressureshould be applied on the gauze pad? And is it better to usegauze or a cotton swab? Or a brush? What kind of post-peel care should be used? What are the usual develop-ments? What will the results be? What complicationscould arise? Should the peel be repeated? If so, how manytimes and how often? The questions posed to an inexperi-enced doctor are endless. Fortunately, a new concept inTCA peels came into being in the second half of the 1990s:Easy TCA®. This peel can be performed in a doctor’ssurgery, without preparation, without anesthetics, with-out close follow-up, on all skin types, on all areas of theskin and in all seasons.

Differences between Easy TCA®

(ETCA) and TCA in simpleaqueous solution (TCA–SAS)There are many differences between ETCA and TCA–SASapplied in the classic manner.


A B

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

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ETCA logic versus TCA–SAS logicThe logic behind a TCA–SAS peel is different to that forETCA. TCA–SAS is used to destroy damaged tissue(removing the papillary dermis) with the skin being left toheal naturally. It is a destructive rather than a stimulatingprocess. The indications for ‘destructive’ peels are differentto those for ‘stimulating’ peels. An ETCA peel is stimulat-ing rather than destructive: it does not destroy much skin(the Grenz zone or basal epidermis is removed: see Chapter12), but strongly stimulates the regeneration process.

All peels induce inflammation (tumor – dolor – rubor –calor), which is responsible for the redness, swelling andmost of the pain21 and heat felt in the treated skin. Theswelling and edema come from rapid permeation of thedermal blood vessels, which pour out a large quantity ofneutralizing serum, oxygen and pro-inflammatory compo-nents into the dermis and maintain vasodilation. Free rad-icals are also soon released and damage all the surroundingstructures, especially those needed for re-epithelialization.Every peel has to take the advantages and disadvantages ofinflammation into account:

� The upside is the stimulation without which regenera-tion could not take place.

� The downside is the self-maintained production of freeradicals that damage the skin and slow down re-epithe-lialization.

An ETCA peel attempts to make the most of the positiveeffects of inflammation at the same time as limiting, as faras possible, the negative effects of oxidation with the helpof the post-peel cream. TCA–SAS, on the other hand, hasto contend with the good and bad sides of inflammation.

ETCA solution versus TCA–SASsolution

TCA–SASTCA–SAS is a simple dilution of TCA in water. Its charac-teristics are described at length in Chapter 12, together withthe various approaches used to counter the difficulties aris-ing in its use. TCA–SAS is usually considered to be effectivefrom 25% m/m.

ETCAETCA consists of a base solution to which the doctor mustadd a specific quantity of TCA to make up a peel solutionthat contains 15% m/m TCA. This solution is saponified,stabilized and adjuvanted.

Saponins are natural extracts, glycosides, which havelathering and binding properties for water-soluble prod-

ucts in the skin’s lipids. They help the acids spread andpenetrate evenly, on and through the skin. Some studieshave shown that saponins have antimicrobial propertiesthat enhance skin regeneration after a peel. ETCA solutionalso contains the surfactant (Box 5.1) sodium laureth sulfate(SLES).22 SLES degreases the skin, emulsifies fats and holdsskin impurities in suspension.

Coconut fatty acid monoethanolamide (cocamide)improves the effectiveness of saponins. Citric acid is atricarboxylic AHA, an antioxidant, chelator and buffer thathelps break down corneodesmosomes and makes it easierfor the TCA to penetrate the epidermis. Ascorbic acid has a


Box 5.1 Surfactants

Emulsifiers are necessary to allow water and lipids tocombine. A surfactant is an amphiphilic molecule thathas affinities for fats as well as water and that can beincorporated into lamellar lipid structures (e.g. cellwalls). Surfactants increase the fluidity of the lipidstructures by partitioning into the lipid membranes, astheir lateral interactions with the membrane-forminglipids reduce the force of their attractive interaction.The mobility of the membrane lipids increases consid-erably in a similar manner to when a liquid crystal isconverted into a gel. Finally, lipids can be seen tomicellize or simply dissolve. Membranes lose their rel-ative impermeability. See Figure 5.16.

Normal membrane structure:active transmembrane protein

Lipid breakdown:inactive transmembrane protein

Figure 5.16 Effect of surfactants on cell membranes.

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dual role, acting as a buffer and protecting against freeradicals. It protects the solution as well as the skin fromoxidation.

Pre-peel ETCA versus pre-peelTCA–SASTCA–SAS should be preceded by several weeks of skinpreparation to even out and reduce the thickness of thestratum corneum, reduce melanocyte activity and enhancere-epithelialization. ETCA, on the other hand, is applied onunprepared skin, as the acid and the post-peel cream pene-trate evenly; the risk of pigmentary changes (basic proto-col) is extremely low and re-epithelialization takes placewithout prestimulation.

Calculating the solution mix:ETCA versus TCA–SASWe saw that preparing a TCA–SAS solution appears easy atfirst sight but that numerous factors come into play thatcan change the behavior of a solution, gel or paste consid-erably.

ETCA provides a standardized solution that always pro-duces the same results when the same protocol used.

Herpes prevention: ETCA versusTCA–SAS Herpes prevention is essential before a TCA–SAS peel, asthe dermis of the skin has to be destroyed for the peel to beeffective, and the skin’s immune defenses suffer from thisdestruction. ETCA is more stimulating than destructive; itwill not destroy the skin’s immune defenses. On the con-trary, repeated peels appear instead to stimulate it. No her-pes prevention is necessary before using ETCA in the ‘basicprotocol’ (scattered pinpoint or cloudy white frosting).

Bacteria prevention: ETCA versusTCA–SAS For the same reasons outlined above, the risk of secondarybacterial infection is considerably lower with ETCA thanwith TCA–SAS. Systematic prevention of infection is notnecessary with ETCA: no antibiotics, no disinfectants. TheLangerhans cells (LCs) in the epidermis and papillary der-mis are not destroyed, nor are the other antigen-presentingcells, and they continue to prepare the body’s defensesagainst microscopic predators. The lymphocytes,macrophages and other defense cells remain present in thedermis. The ‘post-peel cream’, applied as soon as the first

epidermal pinpoint frosting appears, contains tretinoinprecursors that boost the LCs and improve their antigen-presenting function.

Immediate pre-peel ETCA versusTCA–SASWith a TCA–SAS peel to the papillary or reticular dermisthe patient’s skin needs to be properly cleansed, cleaned ofmake-up, disinfected (with alcohol) and degreased (withacetone). The doctor must disinfect his hands properly andthe patient must be kept away from any potentially infec-tious staff. The TCA–SAS cannot penetrate the skin prop-erly through grease and make-up, and the skin must bedisinfected to limit the risk of post-peel secondary infec-tion.

ETCA is usually applied without any prior cleansing,make-up removal, degreasing or disinfection. The peelsolution can even be applied on top of make-up, as theemulsifiers in the base solution hold these molecules insuspension and allow the TCA to come into contact withthe skin. The endpoint of ETCA treatment is scattered pin-point frosting or cloudy white frosting, and there is there-fore no need to increase penetration of the peel solutionartificially.

Make-up removal, disinfection and degreasing are notforbidden before an ETCA peel, but could increase skinpermeability and cause the solution to penetrate too deeplyand destroy the dermis. A TCA to the dermis is not thesame as an ETCA peel.

Depth of peel: ETCA versusTCA–SAS TCA–SAS is applied with a view to destroying damaged(usually sun-damaged) skin structures and benefiting fromthe skin regeneration that naturally follows a peel. It isreally effective when it destroys the papillary dermis.

With ETCA, the aim is not to destroy the dermis in thehope of its rebuilding later, but rather to stimulate all thephenomena of skin repair repeatedly, in all the differentlayers of the skin. With frequently repeated ETCA sessions(every 8 days), the sum of the results is comparable to thatof a papillary peel without any of the drawbacks.

The ‘basic protocol’ for ETCA is intended to reach thebasal layer of the epidermis or the Grenz zone. There are(many) other deeper protocols but they are not as straight-forward as ETCA and the risk of complications is relativelymuch higher. ETCA is not necessarily a light peel; it can beused to reach all depths, from the basal layer of the epider-mis to the reticular dermis, depending on the protocolused. 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–SASA TCA–SAS peel to the dermis is painful and requires the useof analgesics. Some resistant patients can tolerate a peelreaching the superficial dermis, but are left with suchunpleasant memories that they might well refuse furthertreatment. A peel to the papillary dermis should not be donewithout facial nerve blocks (FNB) and/or sedation. Perform-ing FNB requires a whole series of measures, including pulseoximetry at the very least. Any painful intervention can trig-ger vagal reactions for which the doctor must be prepared.Pain after a peel can be dealt with easily by prescribing oralanalgesics (e.g. acetaminophen (paracetamol) or codeine/acetaminophen).

ETCA does not require any type of anesthetic, sedationor analgesics. Any mild pain caused by the application ofthe ETCA solution can be dealt with immediately, as soonas frosting occurs, by applying the post-peel cream.23 Nopulse oximetry monitoring is necessary and no vagal reac-tion has been described, perhaps because it is a short pro-cedure.

Length of peel: ETCA versusTCA–SASIt takes 10 minutes to apply ETCA to the basal layer or theGrenz zone, from the time patients lie down to when theyget up.

Applying a TCA–SAS peel, usually to the papillary dermis,takes a lot longer: at least an hour should be allowed for set-tling the patient in, disinfection, make-up removal, settingup the monitoring equipment, FNB or sedation, a series ofapplications and letting the patient rest after the peel.

Post-peel care day 1 to day 8:ETCA versus TCA–SASPost-ETCA care consists simply of asking patients to pro-tect their skin from the sun (Melablock®-HSP) and toapply the most suitable cosmeceutical for their particularproblem (see Chapter 3). They should start the very dayafter the first of the four peels and continue until the end ofthe 6th week after the last peel. The post-treatment careafter a TCA–SAS peel is more complex and needs muchcloser monitoring, as the risk of complications is muchhigher. Follow-up monitoring after a TCA peel to the pap-illary dermis is described in Chapter 23.

Repeating peels: ETCA versusTCA–SASA TCA–SAS peel can only be repeated after a rest period ofusually 6 weeks to allow the skin to regenerate completely.It provides a single strong stimulation that decreases withtime.

ETCA is repeated four times at weekly intervals to pro-vide ideal stimulation of the skin regeneration processes.The post-peel cream and ETCA application techniqueallows for this repetition.

If the ETCA were repeated less often (once every 2–3weeks), the effects of stimulation would not be cumulative.Weekly repetition, in contrast, ‘stimulates the stimulation’resulting from the previous peel.

Combination treatments: ETCAversus TCA–SASTCA–SAS allows hardly any concomitant combinations,and most of the treatments that one might wish to combineit with must be carried out 8–15 days before the peel. Forexample, nothing can be injected immediately before aTCA–SAS peel. It is, of course, possible to inject botulinumtoxin in the upper part of the face just before or after apply-ing a TCA–SAS peel to the area around the lips, but thetoxin should not be injected before applying a TCA–SASpeel in the same area. The immediate inflammationinduced by the peel could cause the toxin to migrate.

ETCA, on the other hand, allows all concomitant combi-nations.

Botulinum toxinThis can be injected immediately before applying ETCA inthe same area. The technique is simple: inject the toxin,wait 5 minutes, apply the ETCA until pinpoint frostingappears and then apply the post-peel cream. The cream hasan immediate and pronounced anti-inflammatory effect,which prevents edema and toxin migration.

The restructuring of the skin by the peel improves theresults of the toxin, and resting the muscles improves aneven collagen deposition.

Filling wrinklesFilling techniques can also be used immediately beforeETCA, as the ETCA post-peel cream soon stops inflamma-tion and oxidation. The cream can also absorb the free rad-icals that are released by the peel and that could damage thethree-dimensional structure of dermal fillers, such ashyaluronic acid. In fact, the instructions for most dermalfiller products specify not to apply a peel after the filler, but


ch05 7/11/06 8:37 am Page 43

this does not apply to ETCA.

FlashlampsETCA can be used after flashlamp treatment24 when treat-ing pigmentation or photoaging on the face, décolletage orhands. It is preferable to start with the lamp and to followup with the peel, for the following reasons:

� Epidermal permeability does not seem to change signif-icantly after the lamp and there is no marked change inthe penetration of the ETCA. Caution is, however,advised when applying ETCA solution to make surethat it does not penetrate the skin further than antici-pated: the cotton-tipped applicators should be squeezedout properly after the first application and the treat-ment should not go beyond scattered pinpoint frosting.

� Applying ETCA and the post-peel cream before theflashlamp would change the refractive and diffractiveproperties of the epidermis, as well as its water contentand color.

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

InfectionsAs described above, no herpes or bacteria prevention isnecessary with ETCA, unlike TCA–SAS.

Risk of exhausting the skin’s resourcesAt the level of the dermis, the fibroblast is a cell of majorinterest in understanding how peels work. Like Langerhanscells, they have dendritic morphology; they are fusiform orstellate but have no antigen-presenting activity. Fibroblastssynthesize all the constituents of the extracellular matrixand play an essential role in the formation and contractionof granulation tissue during wound repair. Peels to the der-mis destroy a large number of fibroblasts, and the survivorsmust multiply in order to reconstitute the fibroblast popu-lation. Each time they do this, their telomeres shorten,which gradually exhausts their capacity for future multipli-cation. Peels to the dermis should therefore not be repeatedtoo often. ETCA, on the other hand, does not destroy der-mal fibroblasts (and there is no shortening of telomeres),but stimulates their metabolism and obliges them to pro-duce more and more rapidly. Logically, repeating ETCA(basic protocol) cannot accelerate skin aging, which is notthe case with repeated peels to the dermis.

ScarringDuring the healing process, hybrid cells, known as myofi-broblasts, appear in the dermis. They have the morpholog-ical characteristics of both fibroblasts and smooth musclecells. They are responsible for tissue contraction–retractionduring healing. Their cytoplasm contains networks ofmyofilaments that are in contact with specialized zones ofthe plasma membrane and can interact with the adjacentcells or connective tissue. These myofibroblasts appear tobe differentiated fibroblasts that have acquired the proper-ties of smooth muscle cells. Controlled stimulation withDMAE, for example, is a good way to achieve a tighteningeffect on the skin.

Correlating this theoretical data with the clinical data onpeels is not without interest, as it allows us to anticipatewhich peels might potentially cause scarring and whichones will not. Deep peels, which go beyond the upper retic-ular dermis and practically lay the hypodermis ‘bare’, aremore dangerous as far as retractile scarring is concerned, asthey stimulate the conversion of fibroblasts into retractilemyofibroblasts that can cause scarring. Not all agents areequally potent; there are more descriptions in the literatureof problems with scarring with deep TCA peels than withphenol-based peels. There is no reason why peels that donot go beyond the Grenz zone should stimulate the con-version of fibroblasts into myofibroblasts, as there is no‘laying bare’ of the internal tissue and hence no need forretraction. Retractile scar reactions are therefore extremelyrare with the basic ETCA protocol; they can only occurwhen the peel has not been applied correctly. Peels thatreach the Grenz zone or the papillary dermis stimulatesmall fibroblasts that are parallel to the epidermis and havedendritic processes that connect with several collagen andelastin bundles. The synthesized collagen is aligned hori-zontally in the border zone (Grenz zone), and the resultingtension from the activity of any potential myofibroblastsproduces a positive cosmetic effect: improved tension inthe papillary dermis, which can be called the ‘lifting effect’.The ‘lifting effect’ achieved with medium-depth peels in noway compares with the lift achieved when sagging skin andmuscle mass are treated surgically. In some cases, doctorand patient can be sent off on the wrong track and delaytaking the often dreaded and sometimes formidable deci-sion to go ahead with surgery.

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


ch05 7/11/06 8:37 am Page 44

ing to come across many cases of post-inflammatoryhyperpigmentation (PIH).25 ETCA, in the basic protocol,causes almost no PIH.

Generally, IV, V and ‘light VI’ skin phototypes are atgreater risk of PIH.

DowntimeDuring the post-peel period after a TCA peel to the papil-lary dermis, the patient has to put up with a week of edema,scabbing, erythema, pain and other inconveniences. Anyform of social life is out of the question, and the patient canonly return to normal social activities, with the help ofmake-up, after the 8th day. It is several weeks before theskin returns to normal. With ETCA (basic protocol), onthe other hand, the patient can lead an almost perfectlynormal social life, as the flaking is no more serious thanwith sunburn and only lasts for 48–72 hours.

Notes1. 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 under-

eye bags, there is a risk – among other complications – of dis-rupting the adipocyte cell walls as well as the muscle cellsthat come into contact with this product. Moreover, it trig-gers severe and painful edematous erythema that lasts severaldays and is only really effective after several sessions. For themoment, fatty bags under the eyes can only be treated surgi-cally.

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,

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 thepapillary dermis. The latter can destroy a large number oflesions that peels to the Grenz zone do not always reach.

16. Some studies suggest that DMAE can eliminate the lipo-fuchsin 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, asthere 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 andvery 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, forexample. These machines significantly change skin perme-ability and can cause the acids to penetrate too far, with therisk of scarring.

25. See Chapter 37 for more details.


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ch05 7/11/06 8:37 am Page 46

Alpha hydroxy acids (AHAs) occur naturally in a numberof fruits (from where they get their ‘eco-friendly’ name offruit acids) and dairy products. This class of acids containsa number of molecules that have in common the presenceof a carboxylic acid group (COOH) and a hydroxy group(OH) in the alpha position relative to the acid group (Fig-ure 6.1). As early as 1946, the application of a 3% lactic acidsolution at pH 3.8 was already considered a treatment forichthyosis, although cosmetic dermatologists only reallystarted using AHAs when in 1974 Van Scott and Yudescribed how effective they were in the treatment of dry orichthyotic skin. From then on, the scope of AHAs broad-ened, and some authors reported their beneficial effects onacne, photoaging and benign hyperplastic epidermallesions. It was often suggested that AHAs should be used totreat age-related wrinkles and sagging skin. Although thedirect target of AHAs seems to be corneodesmosomes, theindirect action of topically applied AHAs affects not onlythe whole of the epidermis but also the papillary dermisand the pilosebaceous units. However, while all peels pro-duce similar1 histological effects on the different layers ofthe skin, clinical results clearly show that AHAs, used aslight peels, do not improve the skin’s appearance to thesame extent as TCA or phenol. Moreover, indications forglycolic acid peels tend to be restricted to the treatment ofsun-damaged or acneic skin, especially in patients who

cannot or do not want their skin to flake, often because oftheir professional activities, which are incompatible withvisible peeling.

A number of AHAs have been proposed for medical use:glycolic acid, lactic acid, malic acid (with two COOHgroups), tartaric acid (with two OH and two COOHgroups), citric acid (with three COOH groups) and man-delic acid (which has an aromatic (phenyl) group attachedto the alpha carbon atom) – see Table 6.1 below.

Glycolic acid Glycolic acid (hydroxyethanoic acid, hydroxyacetic acid) isthe shortest AHA, with just two carbon atoms (Figure 6.2).It was originally extracted from sugar cane, but the acidused in treatment today is synthesized chemically. AHAshave become popularized as ‘fruit acids’, and this benign-sounding name has had a great influence on the interestshown by patients. The situation is similar to that whenpatients talk of lasers, gold threads or caviar rejuvenatingcreams. These words evoke dreams of miracle cures in theimaginations of some: odorless, colorless and painless, per-manently effective and, of course, without side-effects.

Glycolic acid is extremely hydrophilic, and a pure aque-ous solution of glycolic acid, saturated at a concentration ofabout 80%, has a pH of 0.5. This pH, considerably lowerthan its pKa of 3.83, shows that the solution consists mostlyof pure acid and is effective for performing a peel. The pHof a glycolic acid solution determines its acidifying poweron the skin: a 3% glycolic acid solution at pH 3 can acidifythe first five layers of corneocytes, whereas at 10% andpH 3, it causes a deeper and more rapid acidification of the

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

Hydroxygroup

�OH

�R — Cα — C

�H

�—OH

O

Carboxylicacid group

Figure 6.1 General chemical structure of an alpha-hydroxy acid. αindicates the alpha carbon atom; R represents a generalorganic group.

H — C — C

OH

O

H

H

—— —

�

Figure 6.2 Chemical structure of glycolic acid.

ch06 7/11/06 8:38 am Page 47

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

Lactic acidLactic acid (2-hydroxypropanoic acid, α-hydroxypropi-onic acid) is the next shortest AHA after glycolic acid. Amethyl group (CH3) replaces the terminal hydrogen atomon the alpha carbon (Figure 6.3). It has a pKa of 3.86, whichis close to that of glycolic acid. Lactic acid occurs naturallyin sour milk. After penetrating the skin, lactic acid is con-verted automatically and reversibly into pyruvic acid, thealpha-keto acid derivative of lactic acid: a keto (=O) func-tion replaces the hydroxy (–OH) function on the alpha car-bon. At identical concentrations, lactic acid destroys theepidermis more slowly than glycolic acid.

Concentrations of lactic acid of 10–20% or strongerbegin to destroy the stratum corneum and stimulate skinregeneration, the renewal of epidermal cells. However,some studies have shown that cell renewal is not maintaineduniformly during long-term treatments with 3% lactic acid

at pH 3. In fact, cell renewal gradually falls off during thefirst 10 weeks of treatment with 3% glycolic or lactic acid atpH 3, decreasing to 29.3% and 28.3%, respectively.3 Whenapplied regularly, lactic and glycolic acids (at 3%, pH 3) losea significant percentage of their capacity to destroy corneo-cytes and renew the epidermis around the 12th week. Sali-cylic acid (a beta-hydroxy acid), on the other hand, retainsits ability to destroy corneocytes much longer.

At a concentration of 50–70%, lactic acid produces thesame amount of exfoliation as glycolic acid. As early as1974, it had been shown that lactic acid improved skinhydration and suppleness and that a pH of 3 was moreeffective than a pH of 5. Lactic acid is also a better hydratorthan urea or glycerol. Some studies tend to show that 3weeks of daily application of 12% lactic acid would allow asmuch collagen to be deposited in the papillary dermis as


H3C — C — C

OH

O

H

HO

—— —

�

Figure 6.3 Chemical structure of lactic acid.

Table 6.1 Hydroxy and keto acids used in cosmetic treatments

Acida pKa Chemical structure and alternative names

Tartaric acid pKa1 = 3.02 HOOC.CH(OH).CH(OH).COOHpKa2 = 4.54 (+)-2,3-dihydroxybutanedioic acid;

d-2,3-dihydroxysuccinic acid (only the dextrorotatory (+, or d) form is active)[dicarboxy dialpha-hydroxy acid]

Citric acid pKa1 = 3.06 HOOC.CH2.C(OH)(COOH).CH2COOH 2-Hydroxy-1,2,3-propanetricarboxylic MW 192.13 pKa2 = 4.74 acid

pKa3 = 5.40 [Tricarboxy alpha-hydroxy acid]

Mandelic acid pKa = 3.36 C6H5.CH(OH).COOHMW = 122.14 (+)-phenylhydroxyethanoic acid; d-α-hydroxyphenylacetic acid;

d-phenylglycolic acid; amygdalic acid [alpha-hydroxy acid]

Pyruvic acid pKa = 2.50 CH3.CO.COOHMW = 88.06 2-Oxopropanoic acid; acetylformic acid; α-ketopropionic acid; pyroracemic

acid [alpha-keto acid]

Malic acid pKa1 = 3.40 HOOC.CH2.CH(OH).COOHMW = 134.09 pKa2 = 5.5 hydroxybutanedioic acid; hydroxysuccinic acid, [dicarboxy alpha-hydroxy acid]

HOCH2.(CHOH)4.COOH2,3,4,5,6-pentahydroxyhexacetic acid

D-Gluconic acid pKa = 3.86 α,β,γ,δ,ε-pentahydroxycaproic acid; dextronic acid; glycogenic acid; glyconic MW = 196.16 acid; maltonic acid [alpha-hydroxy acid]

Salicylic acid pKa = 2.98 HO.C6H4.COOH MW = 138.12 o-Hydroxybenzoic acid, [beta-hydroxy acid]

a MW, molecular weight.

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applying 25% trichloroacetic acid (TCA) or phenol. Wemust remember, however, that histological findings, asimportant as they are, do not always translate into cosmet-ically visible clinical results and that laying down new col-lagen is only one of the changes associated with peels.

Other hydroxy and keto acidsMany other hydroxy acids (and the related keto acids) areused in cosmetic treatments (Table 6.1).

Ascorbic acid (vitamin C) is an alpha-hydroxy acidderivative. It has been shown to stimulate collagen produc-tion and reduce melanin production. Under identical con-ditions, classification of the acids described above in orderof strength would give the top three as:

1. pyruvic acid2. glycolic acid3. lactic acid

In the rest of this chapter, it is mainly the use of glycolicacid that will be discussed – and by default this is what theinformation given applies to.

It is clear, however, that, as a general rule, and even ifsome acids have specific properties, most of the hydroxyacids (alpha or beta), carboxylic acids (containing theCOOH group), dicarboxylic acids and alpha-keto acidsproduce the same positive effects on the skin, dependingon the concentration, the pH of the solution (Figure 6.4)and how they are applied.

BuffersIn low concentrations, the pH of a glycolic acid solutionvaries with the concentration of acid: an unbuffered gly-colic acid solution, at less than 1%, has a pH of approxi-mately 2.5.4 At 2%, the pH is 2.1. When the concentrationreaches 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 aggressivethan a 50% solution.

A concentrated glycolic acid solution at pH 0.5 consistsof free and active acid, and is aggressive to the skin. It is athousand times more acidic than a solution at pH 3.5.5 Asolution this strong needs to be properly neutralized by thedoctor applying it. Applying a 70% non-neutralized gly-colic acid solution to the skin can destroy the epidermis in2–7 minutes, depending on the skin type, the thickness ofthe stratum corneum, the degree of photoaging and thepre-peel preparation of the skin.

The pH values on the surface of normal skin varybetween 4.5 and 6, and up to a certain point the skin has theability to defend itself against pH variations and can main-tain a stable pH in the face of moderate acid or alkaliattacks. This is the skin’s ‘buffer’ capacity (Box 6.1).

Applying large quantities of pure acid to the skin (duringa glycolic acid peel with a non-neutralized solution) satu-rates its natural buffer capacity, and the excess acid must beneutralized to avoid burning the skin.

The contact time for a glycolic acid peel, as well as forother AHAs, is the time between applying the peel6 and

AHAs: chemistry, pH and pKa, and mechanism of action 49

ACIDIC BASIC

0 1.5 3 5.5 7 9.5 11 12.5 14Easy TCA®Unideep® Lemon

juiceRedwine

MilkSaliva

Egg whiteSeawater

70%unbufferedglycolic acid

Gastricjuices

Coca Cola®Vinegar

BeerPhenol

peel

Human bloodTears

EMLASodium

bicarbonate

Ammonia

1 M NaOH1 M HCl

pH 3 is 10 times more acidic than pH 4pH 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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neutralizing it. The contact times for partially bufferedAHAs, at pH>2.5, are far longer than for pure unbufferedAHA solutions at pH 0.5,7 which are a hundred times moreacidic.

Neutralizing an AHA peel consists in applying a basesolution (usually pH 9–10) to the treated area. Rinsing withwater only dilutes the acid without neutralizing it (Table6.2) – an acid is neutralized by a base. However, dilutiondoes have the merit of reducing the proton concentration8

and so eventually increases the pH (without changing thepKa, of course) when enough water is added. The high acid-ity of concentrated and unbuffered AHA solutions, as wellas the complications that stem from such treatments, hasbrought the pH of many glycolic acid solutions to aroundpH 4–5.5.9 Ammonium salts, sodium bicarbonate orsodium hydroxide (NaOH) are often used for this. Theresulting chemical reaction produces a salt10 and water –the pH increases and the potency of the acid solutiondecreases:

glycolic acid + NaOH ← sodium glycolate + H2O

pKa

The natural pH of an aqueous solution of 60% glycolic acidis 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 aresult of the gradual addition of the base, we know that thissolution contains exactly 50% of active free acid and 50%of salt produced by the reaction of the glycolic acid with thebase (e.g. sodium glycolate or ammonium glycolate).

A pH of 3.83 corresponds to the pKa value of a glycolicacid solution. If we keep on adding a base solution to theglycolic acid solution, the pH will gradually increase, whilethe proportion of free and active acid and the strength ofthe solution decrease. A glycolic acid solution whose pHhad been brought up to 7 would be completely neutralizedor buffered and inactive. A glycolic acid solution at pH 5 ispartially neutralized or buffered and partially inactive, as itdoes not contain much free acid. It is far less aggressive tothe skin, of course, but it is also less active.

The pKa is therefore an important notion that allows usto understand and anticipate how aggressive an AHA peelsolution will be, on condition that we also know the pH ofthe solution. Knowing the pKa alone, which is a definitiveand set parameter for each acid, does not help determinehow aggressive a peel solution is. The pKa of glycolic acidis and will always be 3.83, whereas the pH of the solutioncould vary between 0.5 and 7 or above. The greater the pHthan the pKa of an acid solution is, the less aggressive itwill be. The lower the pH than the pKa of an acid solutionis, the more aggressive it will be. It is therefore not possi-ble to choose the pKa of the solution that we want to use,as this parameter has been determined chemically, onceand for all, for each acid, and it gives the exact pH atwhich 50% of the active molecules remain. We can, on theother hand, change the pH of the solution and make itlower than the pKa to make the solution more aggressive.We can also raise the pH above the pKa to soften theeffect.

A partially neutralized solution at pH 4 still containsenough free acid to achieve a clinical effect, but is far lesseffective than a solution at a lower pH. Partial neutraliza-tion of a glycolic acid solution is therefore a compromisebetween effect and risk. It is, in fact, surprising that gly-colic acid is still partially active at pH levels of around 5. Itseems that the alpha position of the hydroxy group in asmall molecule like glycolic acid is the reason for this par-tially maintained effectiveness, even if the pH is relativelyhigh. Other AHAs do not appear to remain active at highpH levels.

Using a partially neutralized solution at pH 4.5achieves the same results in a few months that could beobtained in a few weeks with the same unbuffered con-centration. It is therefore true to say that it is possible toachieve the same results using neutralized or non-neu-tralized peel solutions. But patients would then have to beconvinced to have many more peels, which, on top of theinconvenience of repeated visits to the surgery, meansmore expense – and that is never appreciated. The doctormay think it necessary to sacrifice effectiveness to safety,


Box 6.1 Importance of buffers in the body

The body’s – and the skin’s – enzyme reactions are pH-sensitive. It is vital for the body to keep the pH of anorgan stable in order to stabilize enzyme reactions.Protection against pH variations – the buffer capacity –must be extremely active and strong, as natural meta-bolic processes permanently synthesize acids and alka-lis that are liable to modify the pH.

The blood, for example, is protected by two impor-tant buffer systems: the hemoglobin system and thebicarbonate system, which stabilize its pH between7.37 and 7.43. The bicarbonate system is the mostimportant buffer for plasma and interstitial fluids.Neutralizing the skin with sodium bicarbonate is themost ‘natural’ method.

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 volumemust be brought up to 85 ml for the pH to rise from 3to 4. See Figure 12.9.

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but the patient usually thinks that the doctor should finda quicker and more effective solution without sacrificingsafety.

An application of dansyl chloride accumulates in theepidermis and stains the skin. It is possible to measure therate of disappearance of this coloration after the applica-tion of different hydroxy acid solutions at a constant pH.The rate at which the color disappears is correlated with therate of cell replacement, and therefore provides informa-tion on the stimulation of epidermal turnover and on thecapacity of the acid to stimulate skin regeneration. TCA(which is not a hydroxy acid), at 0.5%, stimulates skinrenewal up to 50%, lactic acid (at 4%, pH 3) stimulates upto 34%, acetic acid (3%, pH 3) up to 30%, and pyruvic acid(4%, pH 3) up to 23%. Partial neutralization of these solu-tions, to pH 5, quite clearly reduces the rate of renewal, andneutralizing these same solutions to pH 7 takes away all oftheir clinical effectiveness.

The ultimate goal of treatment with AHAs is to stimulateskin regeneration at the same time as avoiding as far as pos-sible the side-effects that stem from their irritant potential.It is not easy to achieve this goal, as a very acid pH isrequired to ensure optimum clinical effectiveness. Theaggressiveness of these acid solutions usually entails ahigher risk of complications. We shall see further on that itis possible, however, to use a solution made up of differentAHAs at a concentration higher than 60% and pH 0.5, atthe same time as limiting the risk of complications: EasyPhytic® is an unbuffered solution of three AHAs, at pH 0.5.This solution uses a slow-release technology that does notneed neutralizing in spite of its very acid pH, which ismuch lower than its pKa.

Mechanism of actionAHAs do not coagulate proteins. Applying them in a peelshould not therefore produce a ‘whitening effect’. Accord-ing to Forestier, the mechanism of action of AHAs is as fol-lows. Even at low concentrations, AHAs can insertthemselves between two protein chains. Here, they build asort of bridge that reduces corneocyte cohesion. As a resultof the lytic action of AHAs on corneodesmosomes, corneo-cytes are shed more easily from the skin, and the thicknessof the stratum corneum is reduced. The skin appears morehydrated as the stratum corneum is thinned or disappearstemporarily.

AHAs, even at low concentrations, acidify the upper lay-ers of the skin. Experimentally, at pH <5, this acidificationcauses an increase in the epidermal activity of lipases, phos-phatases and transforming growth factor beta (TGF-β). Athigher concentrations, the protein chains are separatedfrom each other, and this causes epidermolysis – more orless visible exfoliation. Because of this corneocyte-sheddingactivity, AHAs have been used primarily to treat certain

hyperkeratinization disorders. Not all corneocytes react inthe same way to AHAs: the more superficial, less hydratedcorneocytes seem to be less sensitive to the action of AHAsthan the corneocytes at the base of the stratum corneum.

AHAs may also limit or prevent the cross-linking of pro-teins in the extracellular matrix. Unlike TCA or phenol,AHAs do not bind with proteins and so are not neutralizedby them. The type of action they produce depends on theirconcentration, the pH of the solution, the pKa of the acidsand the contact time with the skin before neutralizationwith a base solution. For example, a 70% glycolic acid solu-tion (pH 0.5 for pKa 3.83) in contact with the skin for 5minutes will be more aggressive than a partially buffered(pH 3.5) 50% solution left in contact with the skin for 2minutes before neutralization with a base solution (a satu-rated solution of sodium bicarbonate, for example).

The type of AHA molecule used is also of prime impor-tance. Glycolic acid is the most aggressive AHA because it isthe smallest. The type of vehicle used, the skin type and thedisorder being treated are also factors to be taken intoaccount when anticipating the action of a peel.

The accelerated shedding of corneocytes disrupts theprotective barrier function of the epidermis. From there, acascade of secondary events stimulates growth in the basallayer of the epidermis and accelerates the conversion ofkeratinocytes into corneocytes11 to restore optimum bar-rier function as soon as possible. Stimulation of the mothercells by the keratinocytes of the basal layer can unfortu-nately go hand in hand with reactional and inflammatorymelanocyte stimulation, the cause of potential pigmentarychanges.12 The stimulation of keratinocyte growth is alsoaccompanied by positive stimulation of fibroblast prolifer-ation and synthesis of proteins in the dermis (collagen,elastin and glycosaminoglycans).13

Another indirect effect of AHAs, which also comes fromthe disruption of the barrier function of the epidermis, isthat they enhance the penetration of other topical agentswith which they are mixed. AHAs are often used as agentsto enhance the penetration of other molecules, in thetreatment of acne or melasma, for example. Histologicalstudies show that the injury to the skin and the principlesof repair are similar during a peel and during dermabra-sion. The extent of repair is directly related to the depth ofinjury. In the case of glycolic acid peels, scabbing occursonly when the peel has penetrated too deeply. The scabconsists of keratin, necrotic keratinocytes and a proteinprecipitate. Glycolic acid may be an antioxidant and pro-tect against UV radiation through the same mechanism ofaction as ascorbic acid, but, given that it reduces the thick-ness of the stratum corneum, it can also enhance penetra-tion of UV radiation through the epidermis. Even if thethinning of the stratum corneum is only temporary, AHAsare therefore not used to protect the skin against the sun,but can be applied after exposure for their anti-free-radi-cal effects.

AHAs: chemistry, pH and pKa, and mechanism of action 51

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Notes1. 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. ConsejoGeneral 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 thetime of neutralizing.

7. Except for Easy Phytic®, which is not neutralized.8. An acid is, by definition, a molecule that can donate a pro-

ton.9. Lidocaine with epinephrine (adrenaline) has a similar acid

pH, but it is impossible to do a peel with lidocaine. Acidity istherefore not the only important parameter.

10. A salt is formed by the interaction of an acid and a base; anester (R–COO–R' if R' is not –H) is formed by the interac-tion of an acid and an alcohol.

11. Via tumor necrosis factor alpha (TNF-α), among othermediators.

12. Known as post-inflammatory hyperpigmentation (PIH).13. Ammonium lactate has been shown to prevent dermal atro-

phy resulting from the use of topical corticosteroids.


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Histological changesEpidermisEpidermal regeneration is histologically visible after 2–7days, and the epidermis is completely replaced 2 weeksafter a single light alpha-hydroxy acid (AHA) peel. A singleapplication of a glycolic acid peel (20–30%) reduces cor-neocyte cohesion, which accelerates the elimination of cellsin the stratum corneum and hence reduces the thickness ofthe epidermis for around 2 weeks (the time it normallytakes for the superficial layers of the epidermis to heal).Using 50% concentrations of glycolic acid ‘unglues’ thecells in the stratum granulosum. Higher concentrations(70%) or a more aggressive mode of application cause epi-dermolysis, or skin necrosis, beneath the stratum corneum.

Unlike single applications, daily use of AHAs seems tothicken the epidermis over time because of the constantstimulation it provides.1 However, other authors suggestinstead a possible thinning of the epidermis in the longterm.

DermisThe histological effects of AHAs also reach the dermis. Moyshowed that fibroblast cultures in a glycolic environmentproduced up to 10 times as much hydroxyproline (a pre-cursor of collagen) than when cultivated in a normal salineenvironment.1 A practical problem is that AHAs do notnormally reach the dermis (because, apart from EasyPhytic® solution, they are neutralized before they can pen-etrate that far) and therefore cannot directly stimulatefibroblasts as well as they did in this in vitro study.

In the papillary dermis and sometimes even in the upperreticular dermis, mild edema, an inflammatory reactionand production of new collagen and elastin are observed.Production of these dermal components does not appear tobe directly proportional to the extent of the inflammatoryreaction. Glycolic acid stimulates fibroblasts to produce col-lagen, but not in the same way as trichloroacetic acid (TCA)or phenol, which produce a thick horizontal layer of papil-lary dermal collagen proportional to the dermal injury andhence the repair caused by the acid.2 However, the layingdown of a new layer of collagen in the dermis is one of the

essential elements of cosmetic improvement and skin reju-venation. Some studies have presented biopsies showing thepresence of new collagen arranged horizontally, with a pre-dominance of fibroblasts 2–3 weeks after a peel.3 This newcollagen remains for around 1 year.2 The concentration ofglycosaminoglycans increases and gradually stabilizes. Thiseffect could be one of the mechanisms responsible for thepositive effect of glycolic acid on fine wrinkles (a fillingeffect after several peeling sessions).

‘Chronic’ use of AHAs seems to allow the dermis andepidermis to thicken gradually and regenerate after an ini-tial period of flaking that, in contrast, thins the epidermisand requires the daily use of effective sun protection.

Factors influencing AHApenetrationOther factors also influence the aggressiveness of a glycolicacid solution (Box 7.1).

Other components of the solutionSome components can slow down or accelerate the pene-tration of AHAs. Let us bear in mind the esterification reac-tion: an organic acid (R.COOH) reacts with an alcohol(R'.OH) to form an ester (R.COO.R') and water:

acid + alcohol a ester + waterR–COOH + R'–OH a R–COO–R' + H2O

7Alpha-hydroxy acids: histology and factorsinfluencing penetration

Box 7.1 Parameters determining the extent of skinnecrosis

pHThe lower the pH is in relation to the pKa, the moreaggressive the solution is

ConcentrationThe closer the glycolic acid concentration is to 80% (asaturated solution), the more aggressive the solution is

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This reaction is slow and reversible. The ester does not pro-duce a peel. An alcoholic solution of AHAs would partiallyconsist of ineffective esters that could be converted backinto acid by shifting the balance of the reaction, after theacids in the solution have been medically or naturally neu-tralized. Applying alcohol to the skin, as a pre-peel disin-fectant, does not interfere with the peel if the alcohol isgiven time to evaporate.

Preparing the skin in the weeksbefore the first peelAny treatment that thins the stratum corneum increasesthe permeability of the epidermis4 and the speed of pene-tration of AHA. Tretinoin, AHA creams and benzoyl per-oxide are all examples of products that allow AHAs topenetrate more deeply.

Preparing the skin just before thepeelBefore an AHA peel, the skin must be cleansed and degreased– but not aggressively. AHAs are actually hydrophilic, andfats in the skin reduce their clinical effectiveness. Degreasingthe skin vigorously, by using an ether swab firmly pressed onthe skin for example, would make it difficult to predict howfar the AHAs would penetrate. Immediately before an AHApeel, the skin should be cleansed and degreased with alcoholand acetone (although not aggressively), in contrast to whatcan be done before a TCA peel to the papillary dermis.

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

Neutralization versus simplerinsingRinsing with water only dilutes the acid without neutraliz-ing it. Only the application of a base solution can neutral-ize the acid.

Frequency of repeated peelsessionsRepeating peels too often gradually deepens their actionand can cause chemical burns. Repeating peels after toolong a delay does not allow gradual stimulation of the der-mis – the peel will not be able to achieve its full effects.

Force of application of a peelThe more forceful the application, the deeper is the pene-tration.

Type of applicatorA brush simply spreads the acid solution on the stratumcorneum, whereas using gauze causes some abrasion at themoment of applying the acid solution and makes it pene-trate more deeply.

Skin condition before a peelA young, healthy and hydrated skin is less permeable thanskin treated with tretinoin or skin with seborrheic dermati-tis, severe photoaging or acne.

Volume of acid applied on theskinAt the same pH and concentration, applying a greater vol-ume of acid on the skin of course induces greater necrosis;applying just a few drops of 70% unbuffered glycolic acidsolution on the face will be far less aggressive than applying5 ml of the same solution.

Other factorsThe penetration of AHAs through the skin is also increasedby prior use of:

� wax and other hair-removal products (watch out for theupper lip area)

� exfoliants or scrubs� preparatory masks and vinyl masks� tretinoin and other retinoids� benzoyl peroxide creams� hair perms (increased penetration on the hairline)

Notes1. Rubin MG. Manual of Chemical Peels, Superficial and

Medium Depth. Philadelphia: JB Lippincott, 1995.2. Moy LS, Mene R. Glycolic acid chemical peel. In: Roenigk &

Roenigk’s Dermatoligic Surgery, Principles and Practice,2nd edn. 1103–12.

3. For this reason, it pays to inject botulinum toxin beforestarting the peel: immobilizing the muscle mass will allowthe smooth synthesis of new collagen.

4. Epidermal permeability in descending order: genital organs> facial skin > skin on torso > skin on upper and lowerlimbs.


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The results following daily topical application of low con-centrations of glycolic acid in a simple aqueous solutionstart to show after 2–3 months of continuous treatment, ifthe concentration is higher than 8%. Alpha-hydroxy acids(AHAs) produce almost no results after a single applica-tion;1 they have to be repeated several times to produceclinical results. Whatever the number of AHA peels, theresults for wrinkles, dyschromia or photoaging will nevercompare with the results of a medium or deep peel (cf. theindications for phenol), except in rare cases where the der-matological problem being treated is very superficial in ori-gin. The results are not permanent, and biological analysisshows a return to the original condition 1–2 years afterAHA peels. We must accept these limitations of superficialpeels.

AHAs are not toxic to melanocytes, and can therefore beapplied on dark skins and in all seasons, on condition thateffective 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 prepa-ration, etc. At an identical pH, a 50% concentration of gly-colic acid will penetrate half as deep as a 70%concentration, and will take twice as long to do so.

AcneThe use of AHAs (especially glycolic or lactic acid) in treat-ing acne has often given good or even excellent results. EasyPhytic® solution (see Chapter 11) is especially safe, effectiveand comfortable for this indication. Keratinocyte cohesion

in the follicles is also reduced, and this stops the folliclecanals closing. AHAs are excellent comedolytics: glycolicacid eliminates the hyperkeratosis responsible for theclogged pores. After a glycolic acid peel, the top of the lesionwill sometimes whiten to a certain degree as a result of theincrease in epidermal permeability around the edge of theinflamed lesion. The whitened areas will disappear in a fewdays, allowing the sebaceous glands to open and drain.

When treating facial acne, concentrations of 50% ormore seem to be the most effective, with contact times of1–3 minutes. Higher concentrations or prolonged contacttimes cause unexpected frosting (areas of epidermolysis)and slow down post-peel healing.

When treating the back, a concentration of 50% is notenough, and concentrations of 70% should be used for4–10 minutes. If frosting occurs on the back, it is a sign ofgreater effectiveness, in contrast to facial treatment. Maxi-mum effectiveness is achieved when treating active inflam-matory acne.

Superficial scars are only rarely and very slightlyimproved by repeated AHA peels. Ice-pick acne scars arenot an indication for superficial peels, and deep scars onlyrespond to a combination of other treatments: dermabra-sion, punch elevation, deep peels, filling, dermal stimula-tion or laser. Treatment of active acne (comedonal, papularor papulopustular) involves a combination of skin prepa-ration, weekly sessions of glycolic acid peels and appropri-ate and effective daily cosmetic care (see Chapter 3). AHAsproduce only a cosmetic result and do not alter the partic-ular genetic traits that lead to acne in some patients: a peeldoes not change the blood testosterone level, the activity of5α-reductase, receptor sensitivity or the tendency of thecorneocytes to stick together and block the pilosebaceousunits. AHA peels must be accompanied by appropriatelong-term anti acne daily cosmetic care (Skin Tech’s Puri-fying® cream or gel).

Aging of the skinAHAs were first used to treat dry skin (hyperkeratinizationand xerosis) before the positive effects on photoaging skin

8Alpha-hydroxy acids: indications and results

Table 8.1 Suggested contact times for glycolicacid

Condition Glycolic acid Contact time (min)concentration (%)

Acne 50–70 1–3 Keratoses 70 4–8Fine wrinkles 50–70 4–8Back 70 4–10

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gradually came to light. Photoaging causes the stratumcorneum to thicken (the skin becomes dry and rough),local proliferation of melanocytes (lentigines and pig-mented hyperkeratosis) and dermal elastosis (wrinkles,fine lines and sagging skin). AHAs can partially help tofight these three types of involution that progressively andinexorably make the quality of the skin deteriorate.

AHAs can only provide superficial treatments, whosedirect action is limited to the epidermis. However, for thecareful observer equipped with good photographs, long-term repetition of AHA peels shows a gradual improve-ment in the quality and tone of the skin, which becomessofter and more even in tone, as well as partial correction ofthe appearance of fine lines.3

Contact times can be relatively short when AHAs arebeing used to prevent aging, but when the photodamage ismore severe, the length of contact time between the gly-colic acid peel and the skin before neutralization should beincreased to help improve penetration, as sun-damagedskin 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, butobvious clinical results can be seen more clearly after sev-eral months of treatment. Patients should never be led toexpect too much too soon.

Even though patients soon feel an improvement in the‘feel’ and quality of their skin, it is pointless to exaggerateand promise that wrinkles, folds or fine lines will disappearaltogether: a long series of 50–70% unbuffered glycolic acidpeels (for 6–12 months) only moderately improves finelines. Wrinkles and skin folds are not indications for AHAs.A histological study did not show any significant changeafter four monthly AHA peels.5 The long rest periodbetween peels could be to blame for the lack of histologicalresults, as the peels must be repeated in relatively close suc-cession to be effective and benefit from the gradual cumula-tive effect of the stimulation produced by the different peels.Once a month is too infrequent and, clinically, weekly rep-etition is far more effective. Weekly sessions should be keptup for the first 4–6 weeks of treatment, if the patient’s skincan tolerate it. Thereafter, peels should be repeated twicemonthly, and eventually once a month as maintenancetreatment. Treatment for aging skin should, of course, beaccompanied by active daily cosmetic care: DHEA-Phyto®,Actilift® or Renutriv ACE Lipoic Complex®.6

Treatment of photoaging is the second preferred indica-tion for Easy Phytic® solution, and results (tighteningeffect) appear rapidly, after the first few sessions.

Dyschromia – melasmaCombining glycolic acid in a 50% peel and daily creams of8–12% helps moderately improve dyschromia of a purelyepidermal origin.

There is relatively little risk of post-peel pigmentarychanges if the peel is applied correctly, but this risk cannotbe ruled out, even when the glycolic acid peel has been keptin technically perfect conditions (see Figure 37.28, p 331).When treating hyperpigmentation, the skin must becleansed and degreased with the utmost care before thepeel, since if the skin is handled too roughly, too much gly-colic acid could penetrate too quickly locally and causepost-inflammatory hyperpigmentation.

Use of an AHA cream aloneMore often than not, it takes 3–4 months of daily applica-tions of AHA creams alone to get a clinical result. AHAs arenot renowned for their anti-tyrosinase action; they limitmelanin synthesis mainly through their antioxidant powerand increase the turnover and renewal of cells laden withpigment. Using just AHA creams as the only form of treat-ment for melasma is disappointing.

AHA cream and peelCombining regularly applied glycolic acid peels with AHAdaily care creams increases the effectiveness of both. One ofthe mechanisms of action of AHAs is to facilitate penetra-tion of the components of cosmeceutical creams usedbetween the different peel sessions.AHA peels help rid the superficial layers of the epidermis ofan excess of melanin, and AHA creams applied dailyincrease keratinocyte turnover, with the melanin producedbeing diluted in the increased number of keratinocytes.Combined used of effective sun protection reducesmelanocyte production and improves the results.

AHA peels and non-AHA cosmeticsCombining regular peels with Blending Bleaching® creamand effective sun protection (see Chapters 2 and 3) is themost effective option for treating melasma. Tretinoin canbe combined with other cosmetics, as can hydroquinone,tyrosinase inhibitors and antioxidants. It has been provedthat applying a depigmenting cream between peeling ses-sions is more effective than applying a glycolic acid cream.It has also been proved that a treatment combining peelsand a depigmenting cream is more effective than treatmentwith depigmenting cream alone.

AHA peels are not, of course, the first choice of treat-ment for melasma.

Xerosis, ichthyosis and wartsAHAs have been prescribed for a long time in the treatmentof xerosis, ichthyosis and sometimes warts. Dry and roughskins are an excellent indication for AHA creams and peels.


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

Hyperkeratotic eczemaGlycolic or lactic acid 15–20% has been used in the treat-ment of hyperkeratotic eczema and hyperkeratosis of thepalms and soles.

Glycolic acid as a pre-peeltreatmentGlycolic acid helps to increase penetration and enhancesthe action of the active molecules in the cosmeceuticals ormedication applied between peeling sessions. It may act asan antioxidant and chelate iron ions (reducing the produc-tion of free radicals). Applying a 12% glycolic acid creamafter exposure to the sun helps reduce the duration of theerythema. Glycolic acid has also been used as a preparationfor a medium-depth peel, to enhance the penetration oftrichloroacetic acid (TCA) to the papillary dermis (i.e.before a 35% m/v TCA), for example. However, in myopinion, the uneven penetration of the glycolic acid peel isnot ideal for enhancing TCA penetration. The TCA willpenetrate more deeply where the glycolic acid penetratedmost, and the overall result could be uneven.

AHA peels have been used unsuccessfully in the treat-ment of stretch marks, both as monotherapy and in combi-nation with corundum crystal microdermabrasion beforethe peel. Treating the stretch marks with microdermabra-sion beforehand enhances AHA penetration, but does solinearly, in the form of claw marks (Figure 8.1). The resultsare poor, even on fine, white, superficial stretch marks.

Effectiveness of AHA peelsThe effectiveness, in cosmetic terms, of a glycolic acid peelcan sometimes be miraculous, sometimes non-existent.Some patients are delighted and others are deeply disap-pointed, but more often than not the result of a series ofpeels with glycolic acid in an aqueous solution is consid-ered ‘average’. However, long repetition of the peels canmaintain the appearance of the skin or even visiblyimprove it. One clear advantage of glycolic acid lies in thefact that patients can carry on with their professional andsocial lives immediately after the peel, without any visiblesigns of flaking7 in the days following the treatment. Cos-metic improvement is very gradual, and often, if there is nogood-quality pre-treatment photographic record, thepatient as well as the practitioner may wonder if the treat-ment has really been effective. Although the patient’simmediate entourage might not really notice any differ-ence, the people the patient meets less often will noticesome change and might comment on how rested or youth-ful they look. Repeating peels over a long period of timeensures the progressive effectiveness of peels with glycolicacid in an aqueous solution.

Effectiveness is doctor-dependentThe application technique used by the doctor, how care-fully he applies the peel and his experience are all factorsthat influence the outcome of treatment.

Effectiveness depends on thegalenical formNot all glycolic acid peels are the same as far as the skin isconcerned. The peels that are the most difficult to use areglycolic acid in simple aqueous solution and glycolic acidmasks (because it is difficult to monitor how the skin isreacting). The most effective peel would be one that doesnot need neutralizing, in spite of having a pH of 0.5 for asolution with a pKa between 3 and 4.

Effectiveness is doubly time-dependentThe effectiveness of a peel with glycolic acid in aqueoussolution depends on the amount of time for which the acidis contact with the skin and therefore on how soon it isneutralized.8 Neutralizing too soon only allows a small pro-portion of the acid to act.

Effectiveness also depends on the number of sessions.The greater the number of sessions, the more visible are theresults. The effectiveness of glycolic acid is thereforeentirely dependent on time in both the short and long

AHAs: indications and results 57

Figure 8.1 Alpha hydroxy acids peel after microdermabrasion.

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term. In the short term, the same concentration will reachthe deeper layers if it is left on longer before being neutral-ized. In the long term, for the results to be visible, a num-ber of repeated peels are necessary, even with 70%unbuffered glycolic acid on a well-prepared skin. A singleapplication of partially buffered 50% glycolic acid onlyallows exfoliation ‘just beneath the surface’ – plainly sub-clinical.

Effectiveness is patient-dependentPreparing the skin properly during the weeks before thepeel helps the glycolic acid penetrate more evenly anddeeply. The quality of the results will be better if the patientfollows the doctor’s recommendations to the letter. Somepatients underestimate the importance of preparation anddo not put on the creams they have been prescribed. Theupshot is inadequate and uneven penetration, which leadsto inadequate results and an increased risk of complica-tions. Some overenthusiastic patients, on the other hand,think they can get into the doctor’s good books by applyingthe pre-peel treatment more often or more liberally thanprescribed. This results in an unexpected increase in skinpermeability that deepens the effect of the glycolic acid andincreases the risk of complications, without the advantageof a better outcome. With Easy Phytic®, there should be nopre-peel preparation, as the stratum corneum must beintact to allow it to act progressively. Creams likely to facil-itate AHA penetration should be stopped 2 weeks beforethe first Easy Phytic® treatment.

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

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

Effectiveness on wrinkles, finelines and foldsA glycolic acid peel is not an effective treatment for foldsand wrinkles. Fine lines can improve gradually over thecourse of repeated glycolic acid peels. New collagen synthe-sis has been noted in the papillary dermis, but what seems tobe responsible for a large part of the results of a glycolic acidpeel on fine lines is the edema that is caused and maintainedby the repeated application of the acid. The tautening andfilling effect on the skin is sadly only temporary. Whateverthe case may be, it is interesting to note that it is possible toimprove fine lines, if only slightly, without causing skinnecrosis. The treatment plan must be rigorous, and carebetween and after peels is of vital importance.

Notes1. Except that the skin’s texture may feel smoother.2. Peyronnet B. Acide trichloracétique ou acide glycolique? J

Med Esth Chir Derm 1994; XXI (84): 257–60.3. 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 seenafter 4–6 months of daily application of 10–12% glycolicacid cream.

4. The stratum corneum is thicker and so more impermeable inphotoaged skin.

5. Piacquadio D, Grove MJ, Dobry M. Efficacy of glycolic acidpeels questioned for photodamaged skin: a pilot study. Der-matol Times 1992; May: 52.

6. Skin Tech (www.skintech.info).7. If the glycotic acid is neutralized as soon as erythema appears

and before any frosting appears.8. In other words, it depends on the ‘contact time’.


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Cosmetic application of glycolicacidSince the application of glycolic acid at first reduces thethickness of the epidermis, the skin can no longer providethe same protection against light, and it is essential to useeffective sun protection to avoid the risk of acceleratedphotoaging. A glycolic acid cream or gel can easily be pre-pared in a pharmacy dispensary, at concentrations of8–15%. There are many commercial preparations of gly-colic acid that have the combined advantage of spreadingevenly and a galenical form that allows better penetrationof the acid. These low-concentration, daily topical treat-ments are mainly indicated for preparing the skin for othertechniques, for follow-up treatment between peels or formaintenance treatment afterwards. In general, patientswho use glycolic acid as a cosmetic do not expect or will notaccept any flaking. If the skin does flake, treatment shouldbe stopped and started again a few days later at a lower con-centration (or warm water can be sprayed on the facebefore applying the glycotic acid cream to dilute it).

As monotherapy, 8–15% gels (which can be buffered tothe physiological pH to 4.55)1 are applied twice a day, afterwashing the face with a mild soap (e.g. Avene®) if the skinis ‘normal’. If the skin is dry, care should be taken not todegrease the skin, so that the gel does not penetrate toodeeply. If the skin is oily and/or acneic, it should bedegreased with a glycolic acid-based cleanser before apply-ing the gel. It is essential to use effective sun protection.

As a precaution, the initial concentration of glycolic acidshould not be more than 8% and the gel should be appliedevery other day at first. The concentration and frequency ofapplication can be increased, depending on the skin’sresponse and tolerance. When treating severe photoaging,the concentration of the glycolic acid should be graduallyincreased from 8% to 12%, 15% or possibly 20%.

Alpha-hydroxy acids (AHAs) can be applied on the faceas well as the neck, décolletage, hands, forearms and otherparts of the body. It must be remembered that the skin onthe face is far more permeable than the skin on the limbs ortorso.

Combination of AHAs andtretinoin

Shared effectsTretinoin and AHAs act on the epidermis and the dermis.When used over a long period of time, they both have thefollowing effects:

� an increase in the overall thickness of the epidermis atthe same time as a decrease in the thickness of the stra-tum corneum: the skin appears smoother and morehydrated

� increased dermal thickness and new synthesis of colla-gen and elastin fibers

Specific effectsRetinoids induce neoangiogenesis, whereas AHAs act onthe dermis without necessarily going through a phase ofinflammatory reaction. We can therefore assume that theircombined effects can produce better results at the sametime as reducing the incidence of side-effects thanks to theuse 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 penetratemore efficiently. Tretinoin and AHAs can be applied sepa-rately, but they can also be mixed in the same gel.

If, on the other hand, a patient cannot tolerate a concen-tration of tretinoin at 0.05%, applying an 8–10% glycolicacid cream in the morning will make a tretinoin cream at0.015% applied in the evening more effective, at the sametime as reducing the irritation caused by the retinoid.These combinations must always be used under close med-ical supervision, however, as in dual therapy, skin reactionscan 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

9Alpha-hydroxy acids: application as cosmetics andas peels

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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 gradu-ally thereafter. If the patient has a tendency to erythema,photosensitivity or telangiectasias, the glycolic acid shouldbe increased and the concentration of the tretinoindecreased.

If the patient has thin skin, the tretinoin should beincreased more quickly than the glycolic acid.

Combination of AHAs andhydroquinone There is no point combining hydroquinone and AHAs in apeel solution, as hydroquinone has a tyrosinase-inhibitingaction that can only establish itself gradually and act on thefirst biochemical stages of melanin synthesis.

On the other hand, it is worthwhile combining the twoin the daily treatment of melasma between or after peels.The pharmacist should be asked to add 3–8% hydro-quinone to a water-in-oil cream with an 8–10% glycolicacid concentration.

Gels are more active and better tolerated by oily skins,while the most suitable galenical form for dry skins iscream. Kojic acid (2–5%) can also be added gradually tothe combined glycolic acid plus hydroquinone formulationto enhance its action.

Combination of AHAs and othertopical pharmaceuticalsThe reduction in corneocyte cohesion caused by AHAsallows topical preparations containing cortisone, antifun-gal and antimitotic agents, etc. to penetrate more easily.

5-Fluorouracil (5-FU) has been widely combined withglycolic acid in the treatment of severe photoaging. Appli-cation should be ‘pulsed’ to limit the inflammatory reac-tion caused by daily application of 5-FU. Glycolic acid 10%should be applied once or twice a day while the 5-FU (as acream with a concentration of 1–5%) should only beapplied on two consecutive days per week, every otherweek. Actinic keratoses on the scalp can tolerate a weeklyapplication of 5-FU combined with glycolic acid. David R.Harris3 reports treating actinic cheilitis by applying a Vase-line® or silicone ointment containing 5% glycolic acid andparaffin. This treatment can be deepened by periodic appli-cations of 5-FU and/or light trichloroacetic acid (TCA)peels.

AHA peels can be used to treat patients of all skin photo-types who cannot accept any downtime. Results are, how-ever, difficult to predict: some patients show a rapid

improvement in the quality and color of the skin, whileothers do not notice any cosmetically visible change. Theunexpected, though rare, occurrence of complicationsalways poses a major problem when a treatment has beenguaranteed ‘not be noticed by a third party’.

Application of glycolic acidpeelsPre-peel preparationLong-term preparationLong-term preparation starts 4–6 weeks before a water-based AHA peel. It can be non-specific or specific. It is notessential, but noticeably improves results by ensuringdeeper and more even penetration of the glycolic acid peel.Greater vigilance is required when applying the peel, how-ever, as it must be neutralized more quickly.

Non-specific preparation to make a water-based AHApeel deeper and more evenIn the evening, a 0.05% tretinoin cream should be applied(see Chapter 2). This cream reduces the thickness of thestratum corneum and provides a deeper peel with thesame concentration. A 10% (non-photosensitizing) gly-colic acid gel could be applied on younger women in themorning.

Specific preparation: to give patients a focused careplanPreparing a patient who has acne is not the same as prepar-ing a patient with photoaging or melasma. Hyperpigmen-tation of all sorts responds extremely well to pre-peeltreatments.

Menopausal or post-menopausal women can benefitfrom a hormone cream as part of anti-aging treatment. Thefollowing formulation can be prescribed:

testosterone propionate 100 mgestrone 5 mgestradiol benzoate 5 mgeucerin® O/W 45 g or Neribase® 45 g

See Chapter 2 for more details.

Medium-term preparationThis concerns combined treatments used before the peelsas well as the cosmeceuticals or pharmaceutical productsused by the patient (see above). Medium-term preparationstarts 2–4 weeks before a peel.


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Folds, wrinkles and fine lines should be treated before-hand with dermal fillers, thread lifts, mesotherapy, stimu-lation or any other treatment chosen by the doctor. Benigntumors can be excised or treated by shave biopsy or lasers.Rosacea should be treated before the peel during this sameperiod. Botulinum toxin, ideally should be injected 8 daysbefore the first water-based glycolic acid peel.

Short-term preparationIt is preferable not to put on any cream that could perme-abilize the skin or use any technique likely to damage thestratum corneum during the few days before an AHA peel.Small retention cysts can be removed with a needle ornumber 11 scalpel blade 1 week before applying the water-based glycolic acid.

DesquamationBuffered solutions of glycolic acid, when applied correctly,only produce virtual desquamation. Water-based glycolicacid does not penetrate evenly, and the risk of localizedoverpeeling, scabbing or post-inflammatory hyperpigmen-tation is not insignificant.

The destruction of the epidermis that causes visible flak-ing depends on how the peel is applied, as well as on thetype of peel used. A short contact time with a 50% glycolicacid peel at pH 3.5 produces almost no visible flaking,while a longer contact time with 70% glycolic acid atpH 0.5 induces epidermolysis and the appearance of smallscabs and visible flaking. The correct contact time with awater-based 70% glycolic acid at pH 0.54 causes little or noflaking, but repeating it too soon could trigger visible flak-ing. Applying a water-based 70% glycolic acid peel atpH 0.5 with a flat brush will cause less flaking than if it isapplied with a gauze pad (which is slightly abrasive) afterthe skin has been disinfected with alcohol or degreasedwith acetone or ether, or after the skin has been preparedfor several weeks with tretinoin cream. All other conditionsbeing equal, applying a greater quantity of AHA causesmore of the epidermis to be destroyed and more visibleflaking.

Easy Phytic® solution, in spite of its pH of 0.5, causesalmost no flaking and penetrates more evenly than otherAHAs, because of its formulation and application proce-dure.

Treating the face or bodyAHA peels have mostly been used to treat the face, but canalso be used to treat other areas of the body. Facial skin ismore permeable to AHA peels than the skin on the rest ofthe body. The neck, décolletage, hands and forearms can betreated with a combination of AHA peels and effectivepost-peel care (see Chapter 3).

With these body treatments, we can expect an improve-ment in the quality of the structure of the skin, improvedhydration and some temporary lightening of the complex-ion.

Lentigines and keratoses should be treated by anothermethod in parallel with AHA peels. There are other, moreefficient, techniques to treat these problems: liquid nitro-gen, dry ice, Only Touch® peel, ‘intense pulsed light’ (IPL),laser, etc. Dr Robert Vergereau (France) compared the useof dry ice, Erbium laser, Q-switched laser, coagulation andOnly Touch® peel. He concluded that: ‘If all these methodsare satisfactory, in my opinion, the technique usingtrichloroacetic acid5 is the most beneficial’.

Treatment of other areas of the body with AHAs is notoften described, because of the poor penetration of theseacids through the skin of the body. A technique combiningabrasion and an application of Easy Phytic® solution (seeChapter 11) is more successful on the legs, arms and torso.

Buffered or unbuffered AHAs?The results produced by buffered AHA peels can, in away, be compared to those produced by unbuffered peels,but only when applied over a longer period of time andmore frequently. From a histological point of view, allpeels produce comparable results depending on thestrength of the peel. The action of an AHA peel with a pHhigher than its pKa and close to the skin’s physiologicalpH (4.5–6) is very slow. A buffered solution will oftenonly be applied for the first ‘reconnaissance’ peels or onsensitive skins. Thereafter, the peels will be performedwith 70% unbuffered glycolic acid solution in a gel orEasy Phytic® solution.

How many sessions should beanticipated?AHA peels should be considered a long-term treatment.No noticeably visible improvement, except for a softerskin, should be expected until after many sessions.

Sometimes, the results do not become obvious untilafter 8–10 sessions of water-based unbuffered 70% gly-colic acid peels. How frequently the sessions should berepeated depends on how the skin reacts or how sensitiveit is. Some thin and sensitive skins will not tolerate morethan one session every 2 weeks, whereas thicker or oilierskins will easily tolerate a weekly session or even more. It isclearly difficult for people who can only tolerate one ses-sion a month to achieve visible results. Even the most will-ing patients can be worn down by the boredom of repeatedsessions that can sometimes be unpleasant and have a lim-ited effect. Patients who cannot be treated more than oncea month often give up treatment long before it has fin-ished.

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Classic application technique forglycolic acidA glycolic acid peel can be applied in an aqueous solutionor in a gel, with a gauze pad, a brush, presoaked cottonswabs or pads, gloved fingers, etc. Compact and opaqueAHA masks have been used, but monitoring the skin whilethe mask is on is neither easy nor certain.

The glycolic acid solution is applied quickly (in 15–20seconds maximum), so that the contact time is the same forthe whole face. The solution should be applied to the mostresistant areas first (the forehead) and to the more sensitiveareas last (the eyelids). It is important to develop applica-tion habits and always use the same system, both for apply-ing and neutralizing the peel.

Partially squeezing out the applicator before using itguards against the product forming ‘pools’ on the skin.Massaging the skin with a gloved finger allows more evenpenetration or deeper local penetration if the doctor con-siders it necessary. By closely monitoring changes in skincolor, the AHA solution can be neutralized before anyfrosting occurs. To a certain degree, the contact time ismore important than the total quantity of AHAs applied tothe skin: a low overall quantity of glycolic acid left to act fora longer time can penetrate the skin more deeply than alarger quantity that is neutralized immediately. As well asthe choice of peel, monitoring the contact time is an essen-tial part of any glycolic acid peel. This is why the glycolicacid peel has been called ‘time-dependent’, prompting thepurchase of many completely redundant timers.

Glycolic acid can be applied up to a few millimeters fromthe eyelashes, no matter what its concentration. If any gly-colic acid comes into contact with the eyes, they should berinsed immediately with plenty of water, and drops of arti-ficial tears or physiological solution should be applied. Gly-colic 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 toavert most of the danger. The author has never come acrossany objective ocular damage, even in the extremely rarecase of contact between glycolic acid and the eyes. Some-times, a very small quantity of glycolic acid can be drawnup into the eye by capillarity if the peel is applied too closeto the conjunctivae. This immediately causes the formationof tears, which dilute the acid and reduce its aggressiveness.Patients should be asked to keep their eyes shut while wait-ing to have eye drops put in that will bring immediaterelief.

Contact timeThe contact time is the time during which the AHA is leftto act before being neutralized and stopping its effect. Itdepends more on the appearance of erythema than on the

concentration, the pH, the total volume applied, the num-ber of applications, etc. AHAs in aqueous solution do notpenetrate the epidermis evenly, and the erythema, which isthe first sign of the skin reacting to a peel (Table 9.1), doesnot appear evenly either, but rather in spots or patches. It istherefore essential for the doctor to stay beside the patientduring this phase of the peel and not to take his eyes off thetreated area. The safety limits are not very flexible whenusing 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 tofrosting, and the doctor is often faced with the followingdilemma: neutralize too soon and have limited results, ortry to neutralize a bit later and risk complications. It was toavoid this dilemma that the author developed Easy Phytic®solution.

Contact time for a glycolic acidpeelEach patient’s skin reactivity should be tested by an initialapplication of a less concentrated and/or a partially neu-tralized peel (e.g. 50% at pH 3.5). As a precaution, the ini-tial contact times should be short, in order to test the skin’sreactivity. When we say that an AHA peel is ‘time-depen-dent’, we mean that the contact time depends on examin-ing the skin directly and not on the clock. We do not reallyneed to know exactly how long the product should be leftto act: the right contact time is enough time for erythemato occur, but no frosting at all. Table 9.2 shows, as anapproximate guide, the depths reached by unbuffered 70%glycolic acid (pH 0.5) with different contact times on theface. It should always be remembered, however, that AHAsshould never be used to do anything other an epidermalpeel.

Each patient has their own particular level of sensitivityand contact time. It is therefore important to take precisenotes on the treatment given: the type of solution, the con-centration used, the contact time (except in the case of EasyPhytic® solution, which does not need neutralizing), theplaces where erythema first appears,7 the number of coats,


Table 9.1 Correlation between skin appearanceand depth of AHA peel

No erythema Virtual peeling effectSpots of erythema Very, very superficialPatches of erythema Very superficialWidespread erythema Superficial peel, suitable depth for

AHAsFrosting Too deep for an AHA peel

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the type of neutralizing solution applied, etc. These noteswill come in very useful for working out any potentialchange in contact time for subsequent peels. A cautiouscontact time of 2 minutes for a first peel with 70% glycolicacid, pH 0.5, on a patient with healthy skin of normalthickness can gradually be prolonged by 30–60 seconds insubsequent peels, if the skin can tolerate it – that is to say aslong as there is no frosting.

NeutralizationAn AHA peel should be neutralized as soon as erythemaappears and before (or, at the very latest, just as) the firstpinpoints of protein coagulation (frosting) appear. Thepeel can be neutralized with a solution saturated withsodium bicarbonate, for example. We saw above that the‘bicarbonate system’ is a natural and powerful system forneutralizing organic acids. Neutralizing an AHA peel witha bicarbonate solution immediately stops its action. Thereaction of an acid with a base produces a salt that has nopeeling activity. The question is then what proportion ofacid 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 willhave been effective: 30% or 50%?

If a solution is applied with a concentration of 70% butbuffered at exactly pH 3.83 (which is the pKa of any glycolicacid solution), it contains only 50% free and active glycolicacid; the other 50% consists of an inactive salt. In reality,this solution corresponds to only 50% of the 70%, that is35% of pure glycolic acid. Rapid neutralization of this solu-tion reduces its effectiveness even further.

The problem with AHA peels clearly lies in the neutral-ization. Easy Phytic® provides a solution to this difficultproblem, as, in spite of its pH of 0.5, this peel does not needto be neutralized and therefore benefits from the effective-ness of 100% of the molecules applied to the skin.

It should be remembered that rinsing with pure waterdilutes an acid (lowers its concentration), whereas a basesolution neutralizes it (raises its pH). The neutralizing solu-tion should be prepared before the peel so that it is instantlyavailable when neutralization is necessary (Box 9.1). Skinburns as a result of neutralizing too late because of lack ofpreliminary preparation of the neutralizer would always beconsidered as professional misconduct by an expert.


Table 9.2 Depths reached by unbuffered 70%glycotic acid (pH 0.5) as a function of contacttime

Contact time Depth of effect(min)

1–5 Gradually deepening epidermolysis,depending on contact time and skinsensitivity

5 The acid reaches the dermoepidermaljunction

10 The acid reaches the dermis – which isnot desirable, as its effect, locally, will besimilar to that of 30–35% TCA m/v

15 The depth of skin necrosis, locally, ishistologically comparable to or greaterthan that reached with 35–40% TCAm/v

Box 9.1 Preparing the neutralizing solution

The simplest neutralizing solution consists of a solu-tion saturated with sodium bicarbonate: fill a bowlwith warm water and gradually add the sodium bicar-bonate powder (Figure 9.1a), stirring all the time.When the sodium bicarbonate no longer dissolves andforms a sediment in the bottom of the bowl, the solu-tion is saturated (Figure 9.1b). There is no point tryingto get a more concentrated solution.

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

B

A

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The doctor and assistant should carefully monitor all theareas treated with acid. Surfaces that develop any local ery-thema should be neutralized there and then with the tip ofa sponge soaked in saturated bicarbonate solution (sodiumbicarbonate is readily available at pharmacies).

It is possible to apply corticosteroid cream to the local-ized erythema. When several areas have become erythema-tous and been neutralized, the whole face should beneutralized by applying strips of paper, for example,8

soaked in the neutralizing bicarbonate solution (Figure9.2). If the glycolic acid is not completely neutralized,applying a solution of sodium bicarbonate triggers a chem-ical reaction that produces a warm tingling sensation andmay contribute to the development of temporary post-neutralization erythema together with bubbles. The skin is

completely neutralized when no more ‘bubbles’ are felt.Neutralizing with a bicarbonate solution, or any othercommercial neutralizing solution, is only obligatory whenusing unbuffered solutions. When the pH is close to thephysiological limits (pH >4), thoroughly rinsing with run-ning water is enough,9 since the relatively high pH of thesepartially buffered solutions is not too aggressive for theskin, and diluting the acid is all that is needed to increase itspH sufficiently.

AHAs are the only peels where neutralization is impor-tant – TCA, resorcinol, salicylic acid and phenol do notneed neutralizing.

Glycolic acid is not a protein coagulant. It does not com-bine with proteins and is not neutralized, like TCA. Itremains aggressive until it is neutralized, diluted or pickedup by the skin’s buffer systems. After neutralization, thepatient may continue to feel the acid burning in places. Thepatient can be given a cotton pad soaked in bicarbonatesolution and asked to neutralize the more sensitive areasmore thoroughly until the burning sensation has com-pletely gone. The patient will often go back to the nostrilsand eyebrows several times. More sensitive areas can actu-ally be protected before the peel with Vaseline® applied ona cotton bud.

Neutralizing partially bufferedsolutionsA (partially) buffered solution has an artificially high pHthat makes it less aggressive. In fact, to allow doctors to dotheir job properly, the pH of glycolic acid or other AHAsolutions should be given on the bottle. When using a pre-scription solution from a pharmacy dispensary, it is vitalfor the doctor to take the trouble to check the pH of eachsolution 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 thepH is not known, it is, in any event, better to opt for neu-tralization: there is no danger in neutralizing a peel,whereas it can be disastrous not to (Table 9.3). In the inter-ests of caution, it is best to neutralize the peel in the face ofany doubt. After neutralization, spraying the skin withwarm water gets rid of any excess bicarbonate, and the facecan then be dried.


A

Figure 9.2 (a) Soaking paper strips in the bicarbonate saturated solution.(b) Application of paper strips.

B

Table 9.3 Neutralization of glycotic acid peels:appropriate guide

pH of peel Procedure

>3.5 Rinse with water0.5–3.5 Neutralize, then rinse with warm water

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Post-peel careFurther information is available in Chapter 3.

Immediate post-peel careThe appearance of uniform erythema indicates that the gly-colic acid has penetrated properly, and is the signal for neu-tralization. After neutralization, spraying with warm watercleans the skin of any residual chemicals.

Immediately after the glycolic acid peel, the skin is verypermeable, and products applied to it during this periodwill penetrate more deeply and thoroughly. This is an idealtime to apply the classic post-peel care treatments: seeTable 3.1 in Chapter 3.

Care between peelsGlycolic acid peels help cosmetic or medical treatmentsapplied between peeling sessions to penetrate more easily.

Tretinoin should be used carefully during the daysimmediately following a peel, especially when the skin isthin and dry. The choice of vehicle should be discussedwith patients: a patient with oily skin will not always likeusing creams and might prefer a gel; the same gel would beunpleasant for a patient with thin, dry skin.

Maintaining the results after peelsWhen it comes to the patient’s overall treatment plan, he orshe will often ask how best to maintain or improve theresults achieved. A monthly maintenance peel can be rec-ommended, as well as continued use of the treatmentstarted between peels. Sun protection is indicated in allcases to limit UV penetration through a temporarilythinned and hyperpermeable skin. See Chapter 3.

Notes1. See comments on buffering AHAs later in this chapter.2. Resistance to tretinoin: no visible signs and no discomfort,

even with relatively high doses; there is no erythema and nounpleasant sensation in the skin.

3. 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.

4. Effective neutralization as soon as erythema appears.5. Author’s note: The comparison was made using Only

Touch® peel combined with Easy TCA®.6. That is, too deep in relation to the peel used: a glycolic acid

peel should be superficial.7. During the next peel, the AHA should be applied last on the

areas where erythema appeared soonest.8. Cotton pads or any other means of application can also be

used.9. 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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Complications with alpha-hydroxy acid (AHA) peels arerare, easily avoided, and often spontaneously reversible ortreatable by simple topical applications. More details oncomplications, their origins, prevention and treatment canbe found in Chapter 37.

AllergiesThe author is not aware of any documented case of allergyto glycolic acid or other AHAs. In the case of an allergicreaction, the doctor should test for allergies to the solventsor additives in the AHA solution. Some allergic-type reac-tions are, in fact, caused by the AHA penetrating the der-mis, which triggers a limited and localized inflammatoryreaction whose symptoms are redness and swelling. Thisreaction disappears without treatment within 48 hours.

PainThere 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 treat-ment. The more the skin has been ‘prepared’ or the thinnerit is, the more painful it will feel when the peel is applied.The pain is proportional to the concentration of the acidand inversely proportional to the pH. A 70% peel is morepainful than a 50% peel. A 50% peel at pH 3.5 is not aspainful as a peel at pH 1.5. A 70% unbuffered solutionapplied to a thin skin prepared with tretinoin will be morepainful than a 50% solution at pH 4 applied to an oily,unprepared skin. Whatever the case, this pain – a kind oftingling or burning sensation – is quite bearable. There isno need for anesthesia, analgesia or nerve blocks. Morenervous patients might appreciate having their facesfanned (with an electric or hand-held fan) or the calmingeffect of a voice during the peel. Neutralizing the peel withsodium bicarbonate solution stops the pain.

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

pale pink; this coloring lasts between 15 and 60 minutes.Solutions that are too highly concentrated or are left on toolong and allowed to penetrate too deeply locally can causethe formation of scabs, which, if pulled off, leave persistenterythema for several weeks or months. This eventuallyresolves naturally and leaves the skin a little softer. It is bestto increase concentrations and contact times graduallywith patients whose professional lives will not allow themto spend time locked away recovering.

TelangiectasiasAlthough there is evidence of a certain degree of angiogen-esis with AHAs, telangiectasias are rare.

Dryness, desquamation,sensitizationLong-term topical use of 8–15% glycolic acid creams gradu-ally reduces corneocyte cohesion and can cause the skin toflake. This effect is not as pronounced as with tretinoin.Dampening the skin before applying the cream dilutes theproduct and reduces the risk of skin sensitization. Daily use ofprogressively higher concentrations of AHAs can, however,cause continuous lysis of the corneodesmosomes and perme-abilization – a long-term thinning of the epidermis. Patientsmay then complain that their skin is getting more and moresensitive. However, some histological studies show that theskin thickens with long-term treatment with AHAs.

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

Bacterial or viral infectionsBacterial infections result from scratch lesions or epider-molysis 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 hasbeen performed correctly is no higher than in the untreatedpopulation at large. In instances of overpeeling and epider-molysis, the probability of a secondary herpes infectionincreases with the depth of injury. There is no need for sys-tematic herpes prevention before an AHA peel, but if apatient is very prone to herpes, it would be wise to pre-scribe valaciclovir to be taken before the peel.

ScarringA correctly applied glycolic acid peel does not reach thereticular dermis, and there is therefore no reason for it tocause scarring. I have never come across any cases of scar-ring after a glycolic peel, no matter what skin preparationor concentration of acid has been used. It is obvious,though, that a combination of technical errors can result ina cosmetic disaster. Applying 70% unbuffered glycolic acidin multiple coats with a gauze pad pressed firmly onto athin and dry skin that has been irritated by a strong dose oftretinoin, without constant monitoring and diluting sim-ply in water instead of neutralizing with sodium bicarbon-

ate, could seriously damage the skin and produce unsightlyscars. Any danger of scarring can be avoided by neutraliz-ing areas of local erythema with sodium bicarbonate solu-tion and not allowing any frosting to occur. If the texture ofthe skin should become uneven as a result of particularlyuneven penetration, it can be evened out in the course oflater peels.

Shiny skinThe effect of AHAs on corneodesmosomes can cause all thepores of the skin to unblock and allow all the sebaceousglands to empty at the same time. The skin will remainshiny until it is next washed.

AchromiaIf the peel penetrates too deeply in a particular place, caus-ing scabbing and delayed healing, it could lead to total andirreversible depigmentation that, fortunately, is limited tothe surface area of the scab. It is a rare complication ofAHA peels.


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General remarksSince the 1980s, alpha-hydroxy acids (AHAs) have beenused alone or in combination with other acids with a viewto achieving good cosmetic results, locally or generally,temporarily or permanently, and without running the risksof deeper peels. The natural origins of the first AHAs – fruitor dairy extracts – account for much of their resoundingsuccess. How could anyone resist such a benign-soundingname as ‘fruit acids’? The AHA most often used is withoutdoubt glycolic acid, a small molecule with a low molecularweight that has no difficulty penetrating the stratumcorneum, where it acts as a ‘corneodesmosome chainsaw’.It was for this property that it was first indicated in thetreatment of ichthyosis and other disorders involvinghyperkeratinization. An AHA applied to a clean anddegreased skin breaks down the protein structures thatform corneodesmosomes. The superficial cell layers arethen shed from the epidermis. The skin immediately feelsmore hydrated, as the fingers no longer touch the dead anddehydrated corneocytes that have been shed but rather liv-ing and well-hydrated keratinocytes. AHAs are not toxic tomelanocytes, and can therefore be applied on all skin types.They can also be used at any time of the year, on conditionthat they are combined with a strong sunscreen. AHA peelshave other advantages as well: they are non-toxic andhypoallergenic, do not cause protein coagulation, have anexcellent safety record, are easy to use and produce satis-factory results in a variety of indications.

There is one sizeable cloud on this bright horizon, how-ever: AHAs have to be neutralized at the right moment tolimit their penetration. If they are not neutralized, AHAswill continue working until they go beyond their desiredeffect. Neutralizing too late may cause serious side-effects,while neutralizing too soon makes the peel completely inef-fective. Nor is neutralizing the peel the easiest part of theprocedure either: the action of the acids has to be stoppedwhen erythema occurs and before the first pinpoint frost-ing appears. The moment the AHAs have to be neutralizedcomes between two events that are open to subjective judg-ment, which increases the degree of risk. Many doctors will

run through the following interior monologue: ‘I shouldhave left the product to act longer for it to be effective’, orworse, ‘I should have neutralized the AHAs much earlier,because now there are going to be complications andunwanted reactions after the peel.’ With the second sce-nario comes a long period of uncertainty for the doctor,sleepless nights and early mornings filled with anxiety,because complications resulting from neutralizing AHAstoo late can only be treated slowly and gradually, some-times taking several months.

The problems raised by neutralization are well known,and various solutions have been put forward to minimizethe danger and risk involved with neutralizing conven-tional AHAs too late. Partially neutralized, less aggressiveAHAs with a pH of between 3.5 and 5 can be found on themarket. These acid solutions do not need neutralizing, butthey do need diluting with water before any frostingoccurs. Less risk, however welcome, goes hand in handwith a less effective peel.

Another drawback to having to neutralize conventionalAHAs with a very acid pH is that the effectiveness of an AHAlargely depends on how long the acid is left in contact withthe skin. The longer the contact time, the more active the peelwill be. Hence, there is a temptation to leave an AHA peel toact as long as possible, in spite of the risk of facing complica-tions. The aim of neutralizing is to stop the effect of the acid.A contact time of just a few minutes before neutralizing thepeel gives it just a few minutes to be effective. I thereforeaimed to develop a low-pH formulation – between 0 and 1for maximum effectiveness – that does not need neutralizing.Easy Phytic® solution (EPS: Figure 11.1) was the first of thisnew class of low-pH AHAs that are active with no need forneutralization. Its pH of 0.5–1 (Figure 11.2) is much lowerthan 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 isonly a minor risk of side-effects, even when each molecule isleft to achieve its full effect, undisturbed by external neutral-ization. It is the skin itself that neutralizes the acids in the EPS.

EPS can therefore be defined as a slow-release AHA solu-tion for patients who do not want any visible flaking (it is a

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non-flaking peel) or for doctors who want to minimize therisk of the sometimes serious complications of conven-tional AHAs. The solution is saponified3 and adjuvanted,and consists of glycolic, lactic, mandelic (phenylglycolic)and phytic acids. The peel solution – which does not needneutralizing – allows the acids to work gradually and to fulleffect. This particular property allows a ‘bipolar’ action: thesolution starts working on the superficial layers of the epi-dermis, shedding corneocytes in the same way as conven-tional AHAs. It then continues working its way through theskin to reach the deeper layers, slowly and not too aggres-sively. The acid molecules gradually lose their effectivenessas they are neutralized by the natural buffer capacity of theepidermis. The skin can in fact defend itself perfectly wellagainst acid or base attacks thanks to its buffer capacity,which is its ability to maintain the homeostasis of its pH aslong as the attack is not disproportionate to its defenses.

When its defenses are overwhelmed by a massive acid orbase attack,4 the skin cannot defend itself, and its proteinsare destroyed, denatured or coagulated; the skin is ‘chemi-cally burned’. With EPS, the acid molecules in the peelsolution are stabilized on the surface of the skin and con-centrate in the stratum corneum.5 They are released slowlyand therefore reach the epidermis gradually. This ‘slowrelease’ allows the epidermis to use its full buffer capacity toneutralize the acid molecules that are slowly attacking it.

Unfortunately, there is another significant problem withwater-based AHAs: they do not penetrate evenly.6 Theypenetrate more quickly in areas where the stratumcorneum is thinner – and therefore more permeable – andmore slowly where the stratum corneum is thicker. Theypenetrate more slowly on the oilier6 parts of the face andmore quickly where the skin is dry, infected or irritated. Itis therefore essential to prepare the skin for 2–3 weeksbefore the first water-based AHA peel to even out thethickness of the stratum corneum. The melanocytes alsoneed to be ‘stabilized’ to avoid any potential pigmentarychanges.

With EPS, the AHAs penetrate far more evenly becauseof the type of vehicle used and the slow-release mechanism,which eliminates the need for pre-peel preparation. Thedifferent types of AHAs used in EPS are important: thethree AHAs in the solution actually penetrate at differentspeeds. Small molecules penetrate the skin more rapidlythan larger molecules: the glycolic acid is therefore the firstto penetrate, followed by the lactic acid and finally themandelic acid, the largest molecule, which relies on thelytic action of the other acids on the corneodesmosomes tohelp 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 hexaphos-phoric acid or cyclohexanehexyl hexaphosphate (Figure11.3). Because of its high molecular weight, 660.08, it doesnot pass easily through the epidermis. The action of thethree AHAs combined with the phytic acid in the solution,however, makes the stratum corneum more permeable and


Figure 11.1 Bottle of Easy Phytic®.

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

HO OH

P

O O

HO

HOP

O

OO

O

P OH

OH

OHOH

O

PO

O

OP

OHHO

O

PHO

HOO

Figure 11.3 Phytic acid.

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therefore easier for the phytic acid to penetrate. Phytic acidis well known for its anti-tyrosinase and antioxidant action.It is also an iron chelator. This molecule is therefore a goodindication for skin-lightening and anti-aging treatments.Finally, phytic acid scavenges the free radicals produced bythe inflammation that follows any peel and breaks theusual vicious cycle of post-peel inflammation:

peel → inflammation7 → vasodilation → O2 intake + pro-inflammatory components → free-radical production → cell damage → self-perpetuating inflammation → more freeradicals ⇒ vicious cycle established

There are two sides to inflammation. The first is positive,as it is an essential trigger for post-peel regeneration andthe synthesis of new dermal components – no inflamma-tion, no repair. The other side is negative, as the combina-tion of vasodilation (which, among other things, helpsimprove tissue oxygenation) and pro-inflammatory com-ponents increases the generation of free radicals that dam-age the cell structures upon which the body relies to repairthe skin. The presence of phytic acid, an excellent antioxi-dant thanks to its 12 hydroxy groups, could reduce theincidence of post-peel inflammatory reactions.

IndicationsAHAs thicken the epidermis and papillary dermis, increasethe production of mucopolysaccharides, improve the qual-ity of the elastin produced and increase collagen density.8

Patients treated with EPS also describe an appreciabletightening effect. Although EPS can be used for the sameindications as other AHAs, its two areas of choice are agingand acne. EPS can be used as a combined treatment or as amaintenance peel with other deeper treatments; it can alsobe used alongside other techniques such as mesotherapyand pulsed light.9 EPS is more of a stimulating and regen-erating treatment than an actual peel, as there is almost novisible flaking. The epidermis flakes almost cell by cell andnot in ‘cell plates’. Patients who are put off having a ‘peel’for fear of downtime seem to prefer EPS being presented asa ‘stimulating solution’. The term ‘superficial peel’ con-jures up images of something relatively ineffective thatcauses unsightly flaking. EPS can be combined with ‘meso-lift’ mesotherapy to particularly good effect: alternating amesolift and EPS every other week would seem to be thebest way to proceed.

Aging skinAging skin is an excellent indication for EPS. Note, how-ever, that it is still a relatively superficial peel and cannotclaim to eliminate folds or wrinkles, which have to be

treated by surgery and deep peels or laser treatments. EPScould be called a ‘lunchtime peel’, as it can be performedduring the lunch hour and the patient can go back to workimmediately.

EPS as a classic anti-agingtreatmentThe classic treatment consists of weekly applications of EPStogether with use of a suitable cosmeceutical cream (seeChapters 2 and 3,10 and also the section later in this chapterapplication protocol). The total number of peels will varybetween 6 to 10, depending on the skin and how it reacts.At the end of the active phase of the treatment, a mainte-nance peel can be applied once every 2 weeks and eventu-ally once every month.

EPS combined with mesotherapyA mesolift is a mesotherapy technique that involves inject-ing stimulating, relaxing or tensing or filling agents such ashyaluronic acid, polymerized DNA, vitamins, trace ele-ments, dimethylaminoethanol (DMAE), eligopeptides, etc.into the dermis. Facial mesotherapy can be rather painful,however, and may require the use of topical anestheticssuch as EMLA. The side-effects are not always invisibleeither: redness, swelling and minor bruising may occur.

EPS is therefore ideal for use with a mesolift: mesoliftone week, EPS the week after. It is wiser not to apply EPSimmediately after a mesolift, because the multiple needleperforations in the dermis and epidermis would enhancelocal penetration of the peel solution. Similarly, a mesoliftperformed immediately after an EPS peel would beextremely painful for the patient and the acids in the EPSsolution would penetrate through to the deep dermis. Nev-ertheless, many European, American and Asian doctorshave reported using a combination of ‘EPS + mesolift’ or‘mesolift + EPS’ at the same time, and have achieved excel-lent results.

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

AHAs: a new slow-release AHA complex with no neutralization required 71

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quarter of an hour before the EPS. Another potential prob-lem is that the post-peel inflammatory reaction – even ifminor – could move the toxin. Leaving a few days betweenEPS and the botulinum toxin would seem to be a wisechoice.

Handling the skin during the peels and post-peel vasodi-lation11 does not seem to have much effect on the outcomeof the botulinum toxin injection. In 10 years of experienceinjecting botulinum toxin immediately before applying thetrichloroacetic acid peel Easy TCA®, I have seen no evi-dence of any direct interaction between these two proce-dures.

Combining EPS and ‘flashlamp’ inanti-aging treatmentsThe use of ‘intense pulsed light’ (IPL) for treating agingskin (Figure 11.5) is a widely used technique nowadays.However, many doctors are disappointed with the resultsobtained with pulsed light as a monotherapy and are look-

ing for a combination of treatments that will benefit theirpatients. Phototherapy should not be used immediatelyafter EPS, as the light rays will have a much greater depth ofaction, and may cause photochemical reactions. The pres-ence of EPS on the skin could also refract the pulsed light.EPS can be used after flashlamp treatment, but it is best tobe cautious, as the energy from the lamp might breach thestratum corneum and the acids in the EPS might penetratemore quickly.

The doctor should be ready to neutralize the peel at theleast sign of protein coagulation (frosting). It is a good ideato alternate flashlamp treatment and EPS, as with themesolift: EPS one week and flashlamp the following week.

Anti-aging treatment for the bodyEPS does not penetrate body skin as easily as it does facialskin. Several coats are needed to trigger erythema and largeamounts of solution have to be used. Treating the bodywith EPS takes a long time and large quantities of the prod-uct. A combination of sandpaper abrasion and EPS (Figure11.6) can be used to treat photoaging on the back, upper orlower limbs. Light abrasion12 can thin the stratum corneumenough to allow the EPS solution to penetrate the skin


A B

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

Figure 11.5 Sun aging, thinning skin, yellowish color.

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

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more easily and more quickly. The sandpaper should beused gently and evenly, without causing any unpleasantsensation, pain or bleeding.

Only the most superficial layer of the stratum corneumshould be removed. Any deeper abrasion that destroys thestratum corneum completely is to be avoided, as the activecomponents of the EPS would penetrate the skin tooquickly and soon saturate its defenses, its buffer capacity.When using this abrasive technique, it is essential to havethe necessary equipment at hand to neutralize the peel (seethe section on neutralizing glycolic acid in Chapter 9) incase it penetrates more deeply than desired. This techniquecan be repeated at a minimum of 2-weekly intervals only.

More frequent applicationAnother application technique for EPS can be considered,especially for patients with resistant skin who would bene-fit from a more intense tightening effect. EPS is applied fol-lowing the usual protocol as described later on in thischapter, but it is repeated more frequently. Applying thesolution more frequently requires great care and experi-ence. Daily applications of EPS allow the peel to graduallypenetrate more deeply. After a few days, small scabs willstart to appear, signaling that the maximum depth has beenreached and must not be passed. Within about 2 weeks, thescabs will have healed, and daily applications can be startedagain. Appropriate cosmeceuticals should be used betweenthe two series of daily peels. For quicker results, the EPScan also be applied two or three times a week (e.g. on Sat-urday, Monday and Wednesday), especially on thick andoily male skin or in cases of acne.

Used as an anti-agingmaintenance treatmentEPS can be used to maintain the results of other peels whenthe patient wants a maintenance treatment without visibleflaking. It should then be applied once a month.

AcneEPS is an excellent treatment for mild comedonal, papularor papulopustular acne. Peels are obviously not indicatedin more severe cases of acne, for which only dermatologicaltreatments will do. Comedones, microcysts and ‘white-heads’ should be removed13 during the week before the firstEPS to avoid handling the skin immediately before the peelat the risk of the EPS penetrating too deeply. Some doctorsreport removal of comedones or microcysts immediatelybefore EPS, with good results.

EPS can improve the appearance of acneic skin in just afew sessions when it is combined with Skin Tech’s Purifying®cream, which consists of glycolic acid, retinol, vitamin E, tri-

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


A

B

C

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

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inactive. The oldest post-acne pigmentation persisted, how-ever, 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) totreat the persistent pigmentation. After eight sessions of EPS,of which the first four were combined with Purifying® creamand the last four with Blending Bleaching® cream, thepatient’s skin started to look healthier (Figure 11.7c).

Pigmentation disorders and otherindicationsEPS acts similarly to other AHAs.

Unwanted effects – precautionsEPS is a very particular peel and has its own particular side-effect. The day after application, an average of 2% ofpatients develop an allergic-type reaction consisting ofsmall, slightly pruritic pinkish nodules (Figure 11.9). Thisreaction is only seen with this peel. It can often result fromusing products before a peel that enhance penetration ofthe acids or from post-peel treatments that are unnecessar-ily aggressive or incompatible. Questioning patients closelyabout their cosmetic routine may provide an answer. Inmost cases, however, it seems to be for the following rea-son: in classic AHA peels,14 the AHAs have to be neutral-ized, but with EPS they are not; as they are not neutralized,the acids may penetrate as far as the dermis and cause alocal inflammatory reaction (a source of fibroblast stimula-tion and new collagen production as well) in the ‘highest’dermal papillae. This inflammatory reaction subsides by


A

B

C

Figure 11.8(a,b) Papulopustular acne before treatment. (c) After foursessions of EPS and Purifying® cream, the acne is no longeractive. After cleaning active acne, the Purifying® cream shouldbe replaced by Blending Bleaching® cream to get rid of thepigmentation. Figure 11.9

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

ch11 7/11/06 8:40 am Page 74

itself within 1–2 days at most. An allergic reaction is alsotheoretically possible, and should be treated accordingly.That will also disappear within a few days.

This type of reaction should be seen as purely inflamma-tory – a positive reaction if the inflammation is controlledby antioxidants and does not last more than 2 days. If itdoes go on any longer, it could be considered an allergy.

Contact of EPS with the eyes should be avoided: in thecase of contact, the eyes should be rinsed with artificialtears or physiological saline solution.

EPS may also, in some cases, penetrate too deeply or tooquickly if the patient has been using skincare products thatthin or remove the stratum corneum. Patients using topicalretinoids, AHA creams or benzoyl peroxide should stopusing them 2 weeks before EPS to ensure that the stratumcorneum regains its normal thickness and function.

Figure 11.10 shows the results of overpeeling in a youngpatient who had been using a benzoyl peroxide cream. Ben-zoyl peroxide is a powerful pro-oxidant used in the antibac-terial treatment of acne, and it reduces the stratum corneum’simpermeability properties. The EPS can then penetrate moredeeply into the skin. In this case, a fluorocortisone cream wasapplied immediately. Between the second and sixth day, the

patient was showing areas of local erythema that were treatedwith topical cortisone. On the 10th day, there were no visiblesequelae.

Other complications caused by AHAs are extremely rarewith EPS. Infection or pigmentation problems are oftencaused by errors made when neutralizing AHA peels. EPS isautomatically neutralized by the skin’s buffer capacity, andpost-peel complications are far rarer than with conven-tional AHA peels.

Application protocol

Pre-peel preparation This is likely to increase the penetration of the acids unnec-essarily. EPS was designed to avoid any pre-peel treatment.Application of EPS should be delayed for 2 weeks if therehas been any pre-peel preparation: EPS uses the stratumcorneum as a reservoir for the slow release of the acids, andif it has been damaged, it can no longer fulfil this role andthe acids will penetrate too rapidly through the thinnedlayer of skin. Body skin is much less permeable than faceskin. This is why an abrasive technique has been describedearlier in this chapter.


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

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

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Cleaning the skinAny make-up should be removed and the skin cleansedtwice 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 acetoneshould not be used before EPS: these products remove sur-face lipids and increase skin permeability (which is not nec-essary with EPS).

ApplicationSmall cotton wool balls seem to be the best method ofapplication. A syringe is used to draw out 2–2.5 cm3 of theEPS. The cotton wool ball is soaked (not too much), andthe solution is applied evenly and quickly over the wholeface. Two coats are usually enough to produce a tinglingsensation on the skin. When the patient can feel some tin-gling, one last coat is applied with the same applicator.There should be no frosting. In the case of inadvertentfrosting,15 a neutralizing solution of sodium bicarbonateshould be applied immediately.

If there is no frosting, a neutralizing solution should notbe applied – the skin neutralizes EPS automatically. Patientswith very permeable skin may feel some tingling as soon asthe first coat is applied. They should be given a total of twocoats only: the first triggers the tingling and the second fin-ishes off the peel. Patients with thick skin may not feel any-thing before the third coat. They should be given a total offour coats (Box 11.1).

The treated area should be massaged with a gloved handto ensure even penetration until the tingling sensation


Figure 11.12Skin Tech cleanser has a neutral pH.

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

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

Box 11.1 Average number of EPS Coats

Thin skin: 2Normal skin: 2–3Thick skins: 3–4

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

Immediate post-peel periodAs soon as the patient says that the tingling has subsided,the skincare cream best suited to the patient’s skin shouldbe rubbed in: Purifying® cream in the case of acne, Blend-ing Bleaching® cream in the case of pigmented marks,DHEA cream for anti-aging in the over-40s and RenutrivACE® with lipoic acid to prevent aging in the under-40s.Actilift® cream with DMAE can be used to increase skinfirmness. These creams penetrate much more easily imme-diately after the AHAs have been applied, but using a plas-tic occlusive film (Figure 11.14) for 20–30 minutes furtherenhances penetration of the skincare creams.

In vivo, the natural water content of the stratumcorneum is relatively low. When the surface of the skin isoccluded with an impermeable plastic film, the water thatnormally evaporates through the epidermis (TEWL16) canno longer do so, and water of endogenous origin graduallysoaks the stratum corneum, which can absorb up to 5–6times its dry weight. The thickness of the stratum corneumincreases in proportion to the amount of endogenouswater absorbed and can become up to four times thicker.17

It is then far more permeable to the water-soluble ingredi-ents, and this improved permeability lasts for several hoursafter the occlusive film has been removed. Occlusion raisesthe temperature of the hyperhydrated epidermis andmakes the various hydrophilic ingredients in the creamsmore soluble. Finally, occlusion prevents the active com-ponents in the creams from evaporating too quickly. Theplastic film is then removed and any excess cream is rubbedin to enhance penetration one last time. All of the products– EPS and cream – are left on the skin until the followingmorning, when the patient can wash his or her face.

Post-peel period (3–4 days)The skin flakes only very slightly, usually unseen by thenaked eye, because it practically flakes ‘cell by cell’. Theskin should be kept fully hydrated with a cream containing

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

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

Repeating the peelWhen EPS is the main treatment, it can be repeated once orseveral times a week (see above).

When EPS is used as a maintenance treatment withother peels, it can be repeated once or twice a month.

In standard treatment, EPS can be applied once a weekfor 6–8 weeks. Thereafter, it is applied as a maintenancetreatment: four extra EPS peels, once every 2 weeks.Finally, in the long term, EPS can be applied once every 4–6weeks (Figure 11.15).

Contraindications� Women who are pregnant or breast-feeding (as a pre-

caution)� Presence of herpes or other active lesions� Lesions of unknown origin� Allergy to one of the components� Unrealistic hopes

ConclusionsEPS is the first slow-release AHA peel not to need neutral-izing, in spite of its pH of 0.5–1. This makes it extremelysafe to use. It combines the known superficial peeling


8 days

7

8 days

7

8 days

7

8 days

7

15 days

7

4–6 weeks

7

Time line

1st EPS 2nd 3rd 4th 5th 6th 7th

Figure 11.15 Diagram of repeated EPS peels.

ch11 7/11/06 8:40 am Page 77

effects of three AHAs with the antioxidant, chelating andtyrosinase-inhibiting action of phytic acid. It is a new typeof peel that overcomes all the problems associated withneutralizing conventional AHAs. It allows each of themolecules in the solution to act to full effect, withoutbeing neutralized. The best indications for EPS are thetreatment of adolescent acne and aging skin, on which ithas a tightening effect.

Notes1. 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 com-

plete when using EPS. If any preliminary treatments reduceits thickness, the solution may penetrate too quickly and sat-urate 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 ofalpha-hydroxy acids on photoaged skin: a pilot clinical, his-tologic, and ultrastructural study. J Am Acad Dermatol1996; 34(2 pt 1): 187–95.

9. EPS can be applied after pulsed light treatment, unless theskin has been made excessively permeable. See later in thischapter.

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-peelinflammatory reaction. This is not the case with the majorityof other peels. My experience is only based on the combina-tion of botulinum toxin and EPS or Easy TCA®. Combina-tions 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 cor-

neocyte cohesion related to the unusual hyperhydration ofthe stratum corneum.


ch11 7/11/06 8:40 am Page 78

Haloacetic acidsHaloacetic acids are derivatives of acetic acid in which oneor more hydrogen atoms on the alpha carbon1 are replacedby halogens (fluorine, chlorine, bromine or iodine) (Figure12.1). The haloacetic acid most commonly used in peels istrichloroacetic acid, and we will therefore look at the chlo-rine derivatives of acetic acid.

Acetic acidAcetic acid (Figure 12.2), also known as echanoic acid, hasa low molecular weight of 60.05 and a pKa of 4.76.2 It isobtained by distilling vinegar (the acetic acid which comesfrom the action of certain aerobic bacteria on dilute alco-hol) or through the Monsanto process by the reaction ofcarbon monoxide with methanol at high temperature andpressure. It is a strong irritant to the eyes, mucous mem-

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 dermati-tis can trigger temporary frosting through protein coagula-tion. This disorder is in fact often improved by dailyapplication of white vinegar (which contains 4–8% aceticacid), used as an aftershave before the morning shower (toavoid smelling of vinegar!). Acetic acid has disinfectant andfungicidal properties. It is not carcinogenic, mutagenic orteratogenic to animals or humans. The oral LD50 in rats is3.310 mg/kg.

Monochloroacetic acid (MCA)Monochloroacetic acid (Figure 12.3), also known aschloroacetic acid and chloroethanoic acid, which has amolecular weight of 94.5, can be obtained from the reac-tion 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 skeletalmuscles, the renal system and cardiovascular system and israpidly absorbed through the skin and mucous membranes.

MCA poisoning by ingestion, inhalation or exposure ofmore than 5% of the body surface area is frequently lethal.The symptoms of poisoning are not immediate: they canappear between 1 and 4 hours after exposure. The non-cor-rosive sodium salt does not penetrate the skin and is nottoxic by skin contact (unlike MCA, which passes throughthe skin very easily). It is, on the other hand, highly toxic bythe oral route. There are no data available on the parenteraladministration of MCA in humans. In laboratory animals,

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

X�

Y — Cα — C�Z

�—OH

O

Carboxylicacid group

Figure 12.1 General chemical structure of a haloacetic acid. α indicatesthe alpha carbon atom. X, Y and Z represent hydrogen (H) ora halogen (F, Cl, Br or I) – at least one of these must be ahalogen.

H — C — C

——

H

HO

OH—

�

Figure 12.2 Chemical structure of acetic acid.

H — C — C

——

H

CIO

OH—

�

Figure 12.3 Chemical structure of monochloroacetic acid (MCA).

ch12 7/11/06 8:40 am Page 79

however, an injection is rapidly lethal. MCA accumulatesin the liver and kidneys before it accumulates in the brain.Elimination of MCA is renal in humans: most of it is elim-inated in its free form, with a small part being eliminated inconjugated form with glutathione.

The mechanism of MCA toxicity seems to be via inhibi-tion of the enzyme pyruvate dehydrogenase; this inhibitionblocks the Krebs (tricarboxylic acid) cycle and disrupts thecell’s energy supply. Almost immediately, the cell findsitself without energy. Ketoglutarate dehydrogenase activityis also reduced, which causes lactic acidosis. The MCA alsodamages the blood–brain barrier, probably through theformation of vascular endothelial microlesions.

Symptoms of poisoning begin with nausea and vomiting,diarrhea, and central nervous system (CNS) excitation withdisorientation. The effects observed later on or with higherdoses include CNS depression, cerebral edema, severemyocardial depression, coma and cardiogenic shock result-ing from non-specific myocardial lesions and significantarrhythmias. Within the first few hours, severe metabolicacidosis4 with hypokalemia occurs. The severity of the rhab-domolysis causes myoglobinuria severe enough to causekidney failure5 in those who survive it. One treatmentinvolves administering dichloroacetate by slow (in 10 min-utes) intravenous injection (50 mg/kg), if possible beforemetabolic acidosis begins. The dichloroacetate is only activeas long as all the pyruvate and ketoglutarate dehydrogenasemolecules have not been deactivated by the MCA.

The severity of poisoning due to skin contact depends onthe surface area of skin exposed: applying an 80% MCAsolution on less than 5% of the body surface area can causesevere poisoning, while exposing 6–10% of the body sur-face to MCA is often lethal.

MCA has nevertheless been suggested as a dermatologicaltreatment for mosaic warts or periungual warts at a concen-tration of 80% or 60 g of MCA + 10 ml of water. Treatingwarts involves MCA coming into contact with a very limitedarea of skin, which explains the absence of poisoning whenthe treatment is carried out carefully. MCA has also beencombined with salicylic acid and is considered more effectivethan dichloro- or trichloroacetic acid in the treatment ofwarts. Because of this product’s very high and potentially fataltoxicity, 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 isfatal after doses of 50 mg/kg.6

Dichloroacetic acid (DCA)Chemistry and toxicity of DCADichloroacetic acid (Figure 12.4), also known asbichloroacetic acid and dichloroethanoic acid, has a mole-cular weight of 128.94 and a pKa of 1.3. It is soluble inwater, alcohol and ether.

DCA has been used in the treatment of severe lactic acido-sis. No clinical side-effects have been observed after par-enteral administration. On the contrary, intravenousadministration of DCA during experimental poisoning ofrodents with MCA increased the survival rate, bringing itfrom 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 pro-tocols for the injection of DCA in the case of MCA poisoning.

When ingested, DCA is rapidly absorbed by the digestivetract. In animals, only 1–2% of the quantity ingested isfound in the feces, which means that the acid is almostcompletely absorbed. Only 1% is found, in free form, in theurine. In humans, up to 5% of DCA can be found in theurine, very soon after DCA has been absorbed. Peak plasmalevels are reached within 15–20 minutes in humans. Intox-ication by inhalation is rare, as DCA is not a very volatilesubstance.

DCA causes the liver to increase in volume as a result ofa build-up of glycogen. Increases in aminotransferase(transaminase) levels have been observed during treatmentwith high doses of DCA, in both rodents and humans.DCA can cause focal, or even widespread, hepatocellularnecrosis 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 andpotential peripheral neuropathy that is reversible.

DCA undergoes oxidative dechlorination that convertsit into glyoxylate,7 which is in turn oxidized into oxalate,8

reduced into glycolate9 and eventually transaminated intoglycine.10 However, in certain individuals, the DCA can bepartially converted into MCA. This has been described in achild suffering from congenital lactic acidosis. It appearsthat the DCA may enhance the development of hepatocel-lular carcinoma in animals, although not in humans.11

DCA is genotoxic in vitro and in vivo and induces DNAhypomethylation in vivo. The oral LD50 in rats is2.820 mg/kg. The human toxicity of DCA is mainly local,through chemical burns, but DCA could be considered tobe potentially carcinogenic in humans. To date, there is noconvincing data on this subject.

Application protocol for DCADCA has been shown to stimulate keratinocyte growth anddifferentiation in vitro.12 It has been used in the treatmentof human papillomas, without much success,13 as well as inthe treatment of epistaxis.


CI — C — C

——

H

CIO

OH—

�

Figure 12.4 Chemical structure of dichloroacetic acid (DCA).

ch12 7/11/06 8:40 am Page 80

DCA is used as a cauterizing agent in the treatment of alltypes of warts, calluses, corns, xanthelasma, seborrheic ker-atoses, ingrown toenails, etc. It is just as effective as othermethods such as electrodessication or dry ice.

DCA is a powerful keratolytic and it is important toapply it only to the lesion being treated. Before any treat-ment, Vaseline® should be applied around the lesion toprevent any contact with healthy skin. The doctor shouldalso have some water at hand to wash the skin in case ofinadvertent contact. A neutralizing solution of sodiumbicarbonate can also be used immediately in case of acci-dental contact with the skin.

The quantity of DCA required largely depends on thetype of lesion being treated. Very thick and horny lesionsare treated using a cotton bud. A wooden toothpick soakedin DCA solution can also be used; it should be pushedinside the callus or wart. Three to five applications are nec-essary to get results on very thick lesions, whereas only oneor sometimes two applications are enough on relatively flatlesions. The depth of application is monitored by watchingout for the appearance of protein coagulation, which turnsthe skin a whitish-grey color. A combination of shave exci-sion and chemical coagulation can also be used. The top ofthe wart is first removed with an electrosurgical orradiofrequency knife. The DCA is applied after the edges ofthe wart have been protected with a thin layer of Vaseline®.Foot calluses should be pared surgically before the acid isapplied. Post-treatment care consists of covering the skinwith Vaseline® to help it flake more quickly. Large callusesoften have to be treated several times. Treating xanthe-lasma with DCA is fairly common.14 The skin around thexanthelasma must be protected with Vaseline® and theDCA applied carefully and not to excess. The scars aremostly invisible. Treating xanthelasma with phenol, how-ever, leaves no scarring (see Chapter 36). The potential tox-icity of DCA means that it cannot be used on a largeabsorbent surface area. The author has found no signifi-cant references to the use of DCA in full-face or body peels.

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

concerned, industrial accidents have been reported inwhich individuals were subjected to high doses of TCA,either by being splashed with the solution over large areasof the body or by accidental ingestion or inhalation of con-centrated vapors. However, such toxicity has never beendescribed when TCA has been used as a chemical peel. It isnevertheless worthwhile becoming acquainted with thepotential symptoms of industrial poisoning.

TCA is readily absorbed through the respiratory and diges-tive tracts. Acute accidental exposure to TCA has caused skinnecrosis. Contact with the eyes causes burns or irritation,depending on the concentration of the acid. Exposure of theeye to small amounts of solution with a concentration equalto or lower than 15% m/m does not appear to cause any irre-versible damage to the cornea. Immediate dilution withphysiological saline solution instantly stops the burning andany risk of damage to the eye. However, the proteins in thecornea could coagulate with larger amounts of low-concen-tration TCA or smaller amounts of high-concentration TCA.

Inhaling concentrated vapors of TCA can irritate the res-piratory tract. Poisoning through inhaling high doses ofTCA can cause headache accompanied by nausea, vomitingand coughing. Higher concentrations cause weakness,dizziness, bronchitis and/or pneumonia. Acute poisoningwith TCA vapor can lead to chest pains, breathing difficul-ties, low blood pressure, edema of the respiratory tract, suf-focation and death.

Accidental ingestion of TCA causes irritation and burnsin the digestive tract, vomiting, diarrhea, and low bloodpressure. Accidental ingestion of high concentrations canerode the teeth and cause necrosis of the jaw.

Controlled ingestion of 3 mg/kg of TCA in three male vol-unteers showed a half-life of 50 hours. Liver toxicity has beenstudied in mice: hepatomegaly (30% enlargement) wasobserved in male mice given water containing 1 g/l of TCAfor 52 weeks. In a group given water with a concentration of2 g/l of TCA, the liver enlarged by 63%. The incidence ofliver carcinoma did not increase, irrespective of the adminis-tered dose. In another study, it was proved that TCA doesnot cause adenomas or liver cell carcinoma, even in rodentspretreated with ethylnitrosourea, conventionally used toinduce carcinomas. No in vitro studies using human cellshave shown any chromosomal abnormalities after contactwith TCA. To the best of my knowledge, no studies haveshown any link between even chronic exposure to TCA15 andcancer in humans. When TCA is applied to the skin, it is notabsorbed, and is therefore not toxic in this application.

Aqueous solutions of TCAHydrophilicity of TCA crystalsTCA crystals are very hydrophilic and therefore unstable inthe presence of water: they readily dissolve on exposure to

TCA: general information, toxicity, formulations and histology 81

CI — C — C

——

CI

CIO

OH—

�

Figure 12.5 Chemical structure of trichloroacetic acid.

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atmospheric humidity. This extreme hydrophilicity cancause problems when TCA solutions are made up in apharmacy. In fact, the packaging of pure TCA crystals usu-ally allows for the preparation of far more peel solutionthan the doctor actually needs. The pharmacist does notusually dissolve all the crystals at one time, as this wouldproduce a large quantity of solution that is difficult tostore. He will usually measure out the quantity of crystalsneeded for each order of peel solution. Every time the bot-tle is opened and every time the pure TCA crystals aretaken out, they come into contact with atmospheric water,which gradually hydrates them. The larger the bottle, themore likely it is that the remaining crystals will be hydratedevery time the bottle is opened. The longer it takes to weighthe crystals, the more hydrated they will become.

Peel solutions are therefore prepared by diluting crystalsthat are gradually becoming more and more hydrated: atthe same weight, the pharmacist is in fact weighing TCAcrystals that are slowly swelling with water. The solutionsthat he prepares are more and more diluted and thereforeless and less effective. The doctor, for his part, gets into thehabit of applying increasingly weaker TCA peels withincreasing firmness, in spite of the fact that the same labelsshow the same concentration. The doctor therefore getsused to applying ever increasing volumes of peel solutionto achieve the same results – until the day when the phar-macist starts using a new bottle of pure TCA crystals andmakes up a peel solution with fresh, anhydrous crystals thatare more aggressive than the ‘old’ hydrated crystals. Apply-ing this new and more concentrated solution of courseresults in a peel that is deeper than the doctor expected, andthe risk of complications is increased, even though there isno apparent difference in the application procedure.

Unlike pure crystals, TCA solutions do not hydrate bythemselves. It is therefore safer not to keep TCA in crystalform and instead to use reconstituted solutions whose con-centration is more stable than crystals.

Inhomogeneity of TCA solutionsA solution is said to be homogeneous when the different ele-ments of which it is made up are evenly distributed in thecontainer that holds it. The homogeneity of peel solutionsis one of the essential elements of their safety.

Simple aqueous solutions of TCA(TCA–SAS)Unfortunately, TCA–SAS16 solutions are neither homoge-neous nor stable. The TCA molecule is very mobile in thesolution and its motion has both a random element and acomponent determined by its chemical structure.

When an aqueous solution of TCA is left in an unmov-ing container, the concentration of the solution does notremain uniform. The TCA temporarily becomes more

concentrated in some parts of the container and moredilute in others. For example, if a TCA solution of 33%m/m is prepared and left at room temperature, someregions of the solution will have a concentration of 35% fora certain length of time while neighboring regions will haveconcentrations of 30% or 40% (Figure 12.6). As thisprocess continues, the region that just had a concentrationof 35% will now have a concentration of 37%, while otherareas of the solution will have different concentrationsagain, for example 25% and 29%, and so on and so forth.17

Depending on the position of the tip of the needle usedfor taking the acid out of the bottle, the solution will bemore concentrated or more dilute. A solution that is toodilute or too concentrated could be applied to differentparts of the face. Simple aqueous solutions of TCA have tobe mixed continuously, both when they are being taken outof the bottle and while they are being used. Certain compli-cations that arise unexpectedly after a TCA–SAS peel canbe explained – at least partially – by this phenomenon ofinhomogeneity.

Awareness of this problem led to the rapid developmentof new TCA peel formulas between 1990 and 2000. One ofthe first solutions put forward was the New Peel® combi-nation of TCA and Mikuda® complex. The soft Peel® for-mulation used asiaticosides and ginsenoids, glycerol, urea(carbamide), sorbitan monolaurate and methyldibromo-glutaronitrile, among other ingredients. Easy TCA®,Unideep® and Only Touch Peel® (OTP) provided anotheranswer to the problem: these stabilized solutions consist ofa base solution to which a determined quantity of 50%m/m TCA is added. There are no complicated calculationsto be performed, the directions for use state precisely whatvolume of 50% m/m TCA solution should be added to thebase solution to make up the Easy TCA®, Unideep® andOTP solutions, which provide peels to the basal layer, thepapillary dermis and the reticular dermis, respectively.

Calculating the concentration ofTCASince TCA peels first came into use, practitioners have suf-fered from a lack of standardization regarding how a solu-tion’s concentration is to be calculated. The calculation canbe done in different ways: by mass per mass (m/m), massper volume (m/v) or mass plus volume (m + v, e.g. m +100 ml). There are also different formulas for diluting thesesolutions using approximate curves. Therefore, ‘50%’ TCAdoes not really mean very much if we do not know whetherthe calculation is m/m, m/v or m + 100 ml. In 1995 and1996, Trauchessec and Pissot18,19 suggested standardizingthe calculation of the concentration of a TCA solution byexpressing it in mass per mass (m/m), which is the onlylogical way of calculating a percentage. It should be possi-ble to make a strict comparison of the terms of a percent-


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age. For example, the carbohydrate content of a meal isgiven in %: a content of 20% carbohydrate means that100 g contains 20 g of carbohydrate and 80 g of somethingelse. Unless it is clearly indicated on the packaging, there isno way of knowing that a volume of 100 ml of this mealwould contain 20 g of carbohydrate. It would be impossi-ble to understand exactly how much carbohydrate is in thefood. Unfortunately, it is this very type of calculation(weight by volume, w/v) that is widely used in somecountries: a volume of 100 ml of TCA solution contains xgrams of TCA. If we know the concentration in w + v only,it is difficult to calculate the exact amount of TCA in thesolution. To get the correct answer, one has to calculatemass with mass, volume with volume, and not volume withmass.20 Examples of calculations of concentration using thew/w, m/v and w + v methods are given in Boxes 12.1–12.3.

Methods of calculation based on volume lead to valuesof 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. Ide-ally, therefore, these methods should not be employed forthe calculation of concentrations – only the m/m methodshould be used.

Nevertheless, for the sake of simplicity, pharmacistsoften 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 add100 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


29%

40%25%

37%

30%

15%

Figure 12.6 Inhomogeneity of simpleaqueous solutions of TCA. (a)A solution with a presumedconcentration of 33%contains mobile regions ofdifferent concentrations. (b)At a later time, same TCAsolution with a presumedconcentration of 33%contains mobile areas ofconcentrations that aredifferent.

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 ofpure, unhydrated TCA crystals and 50 g of water. 100 gof this solution is not, however, 100 ml, but only79 ml. In fact, 1 g of TCA displaces 0.6 ml and not 1 mlof water.b Scientifically, this is the most rigorousmethod of calculation, as 100 ml of a solution at 50%m/m would contain (50/79) × 100 = 63.3 g of TCA.

% Mass of Volume of Final Final TCA (g) water (ml) mass (g) volume (ml)

10 10 90 100 9620 20 80 100 9230 30 70 100 8840 40 60 100 8350 50 50 100 7960 60 40 100 7570 70 30 100 71

a Taken from Trauchessec JM, Pissot F. Solutionsd’acide trichloroacétique masse pour masse pour peel-ings 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 anacceptable approximation. It means that 1 g of TCAdisplaces 0.6 ml of pure water, whatver the concentra-tion of the solution.

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much TCA these solutions contain! Examples of calcula-tions of dilutions using the m/m, m/v and m + v methodsare given in Boxes 12.4–12.6 and Tables 12.1 and 12.2.

Publications can be misleadingA major problem arises when reading publications fromdifferent sources. Suppose that an American doctor wantsto use a peeling technique described by a European authorwho gives concentrations in m/m but does not mention thisin the publication, as is too often the case. The American


Box 12.2 TCA solution at 50% mass per volume (m/v)a

This solution is prepared in the following manner: 50 gof TCA is diluted in a small amount of distilled water toget a small amount of solution, then the volume ismade up by adding distilled water until the final vol-ume reaches 100 ml. To get 100 ml of solution and anend mass of 121 g, 50 g of TCA will be dissolved in71 ml of water. This method of calculation is easy forthe pharmacist, as 100 ml of solution contains 50 g ofTCA (100 g of this solution would contain 41.32 g ofTCA).


10 10 94 104 10020 20 88 108 10030 30 82 112 10040 40 77 117 10050 50 71 121 10060 60 65 125 10070 70 59 129 100

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

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

This method of preparation involves adding 100 ml of water to 50 g of pure TCA crystals. The final volumeof 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 ofthis solution m + 100 ml contains 33.33 g of TCA. Thisis the easiest but also the worst method of calculation,as it is extremely difficult to work out the exactamount of TCA.


10 10 100 110 10620 20 100 120 11230 30 100 130 11740 40 100 140 12350 50 100 150 12960 60 100 160 13570 70 100 170 141

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

Box 12.4 Dilution of a base solution at 50% mass permass (m/m)

100 g of a solution of TCA at 50% m/m contains 50 g ofTCA and 50 g of water (50 g of water is in fact equiva-lent to 50 ml of water) and has a volume of 79 ml. If79 ml of solution contains 50 g of TCA, then 1 ml con-tains 0.633 g of TCA and so 100 ml of TCA solution at50% m/m contains 63.3 g of TCA. If this solution isdiluted with the same volume of water (i.e. 100 ml), itproduces 200 ml (but not 200 g) of TCA solution, inwhich there is still 63.3 g of TCA. Therefore, 100 ml ofthe new diluted solution contains 31.65 g of pure TCA.

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

100 ml of TCA solution at 50% m/v contains 50 g of TCAdiluted in 71 ml of water, to give a solution with a vol-ume of 100 ml for a mass of 121 g. If 100 ml of purewater is added to 100 ml of solution at 50% m/v, it pro-duces 200 ml of solution, which weighs 221 g andcontains 50 g of TCA. 100 g of this solution contains22.6 g of TCA, while 100 ml of the same solution con-tains 25 g.

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 contains38.75 g of pure TCA for a mass of 116.27 g. Adding100 ml of water with the aim of converting the theo-retical concentration into 25% therefore gives a solu-tion of volume 200 ml, whose mass is 226.27 g andwhich still contains the same 38.75 g of TCA. 100 g ofthe new solution therefore contains 17.12 g of TCA.100 ml of the new solution contains half of the38.75 g, which is 19.38 g of TCA.

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doctor gets his pharmacist to make up the solution asdescribed by the European doctor. The American pharma-cist, however, prepares a solution in m/v or m+v, or evendilutes it as described above. The European technique maywell be based on an aggressive TCA, with a concentration of45% m/m. The American doctor orders a solution at 45%from his pharmacy, but is in fact using a concentration of38.1% m/m when the calculation has been made at 45% inm + 100 ml. A solution with a concentration of 31% m/mwill clearly not produce the same results as a concentrationof 45% m/m. The American doctor cannot achieve the sameresults as the European author, whose results might there-fore easily be considered exaggerated or even rigged.

The situation is more serious when a European doctorwants to use an American application technique with aTCA solution at 50% m + 100 ml. This solution contains50 g of pure TCA to which 100 g of water is added. Thefinal volume of the solution will be 129 ml for a mass of150 g, and 100 g of this solution is actually equivalent to33% m/m. The American author who applies a TCA solu-tion at 50% m/v – which is in fact a European 33% m/msolution – to a patient’s face can achieve excellent results.The European doctor, who wants to achieve the sameresults by applying a solution at 50% m/m provided by thepharmacist, is running a huge risk of burning the patient’sskin and causing hypo- or hyperpigmentation, scarring,21

etc. It is therefore essential to stipulate the type of concen-tration to use, and this is one of the first pitfalls awaitingany doctor who is new to peeling.

The technique for applying TCA, which is actually veryeasy, has for a long time been made difficult because of thedifferent methods for calculating concentrations (seeabove) and the approximate explanations given in many

publications.22 There are many inconsistencies: some pub-lications consider a TCA peel at 50% to be a ‘superficialpeel’. Yet we know that a peel at 50% reaches the reticulardermis easily and quickly, and can sometimes even gobeyond it: this is a deep peel – in most cases too deep. Thissolution penetrates the whole of the papillary dermisimmediately, achieving a ‘medium’ or ‘deep’ peel, but cer-tainly not a superficial one. The same solution at 50%, butcalculated in m + 100 ml, would be equivalent to a 33.3%m/m solution, and the first coat of TCA at 33% m/m wouldsoon reach the papillary dermis. It is then difficult tounderstand how anyone can say that a ‘TCA peel at 50%produces a superficial peel’: in whatever way the calcula-tion is made, it is wrong and a TCA solution at 50% willproduce, at the very least, a medium-depth peel even if it iscalibrated in m + 100 ml. The type of applicator used, thenumber of coats and the total quantity of TCA applied tothe skin, as well as any pre-peel preparation, etc. must alsobe taken into account.

There have been histological studies comparing thedepths reached by different concentrations of TCA used inconjunction with different techniques such as dry ice orprior application of Jessner’s solution. A histological studyby Brody and Stegman, at 3, 30 and 90 days,23 showed thatthe deeper the injury, the more necrosis and regenerationare histologically visible. It has thus been shown that threesuccessive applications of TCA cause deeper necrosis thanone application.24 The technique used in this studyinvolved the application of TCA at a concentration of 35%– presumably calculated in mass per volume, although itwas not stated whether this was a w/v calculation, m +100 ml calculation or a dilution of TCA solution. The Jess-ner’s solution in the study was supposed to be preparedfrom lactic acid crystals rather than from an 80% (w/w,w/v?) lactic acid solution. This solution was applied with acotton bud: the volume, form and texture of the cottonbud has an influence on the quantity of solution that comesinto contact with the skin. The dry ice was applied firmly(how firmly was not stated) in acetone (exactly how muchand at exactly what temperature were also not stated) for15 seconds. The importance of studies such as this shouldnot be underestimated, but it is necessary to draw attentionto the number and importance of the variables that have tobe taken into account when evaluating results.

A good method of calculationA consistent method of calculating concentrations must beadopted. It would of course be preferable to use pharmaco-logical concepts such as molar mass, but practitioners arenot used to handling such data. From a practical point ofview, there are two units of measurement that are easilyaccessible: mass and volume. As we have just seen, the onlyacceptable values are calculations in m/m (if we are refer-ring to mass) or in m/v (if we are referring to volume).


Table 12.1 Calculation of a TCA solution at50% in mass or in volume

Method of calculation

m/m m/v m + 100 ml

Grams of TCA in 100 ml 63.3 50 38.75Grams of TCA in 100 g 50 41.32 33.33

Table 12.2 Obtaining a solution at ‘25%’ byadding 100 ml of water to a solution at ‘50%’

Method of calculation

m/m m/v m + 100 ml

Grams of TCA in 100 ml 31.65 25 19.38Grams of TCA in 100 g 25 22.6 17.12

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Measurements in m + 100 ml are too approximate, as isusing dilutions of pre-existing solutions. Anyone is capableof measuring an approximate volume, although not anexact one, and this introduces another margin of error.With the help of precision scales, it is possible to measure amass precisely – more precisely, in any case, than by judg-ing gradients on a measuring glass with the naked eye. Thisconfusion over concentrations is extremely dangerous, anda standardized concentration should be used to avoid dis-appointment as well as complications. McCullough25 hasdrawn attention to the discrepancies between calculationsof TCA concentrations, but prefers to use the m/v method.We have chosen to calculate the concentration in m/m forthe following reasons, as expressed by Trauchessec:19

1. Measuring mass is more precise than measuring vol-ume.

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 vol-ume concentrations: m/v in QS, adding 100 ml of waterto a mass of TCA or diluting pre-existing TCA solu-tions.

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 massof crystals is and the temperature of the solution are allelements that have to be taken into account when mak-ing m/v or m + v calculations. The m/m calculationdoes not depend on these parameters.

Easy TCA®, Unideep® and OnlyTouch® solutionsEasy TCA® is a stabilized,26 homogeneous and adjuvantedsolution 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 onthe same principles as Easy TCA® and reaches the papillarydermis readily and evenly; it has a TCA concentration of23% m/m. The application protocols for these two peelsallow all depths to be reached. There is no point usinghigher concentrations that could cause complications (seeChapter 37).

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

above. TCA-SAS solutions are the cheapest a doctor canbuy. They are also the most dangerous.27,28 It is clear fromthe literature on chemical peels how dangerous thesesolutions are – most photographs of serious complica-tions show patients treated with TCA–SAS. It is clear thatan experienced doctor can avoid most of the serious com-plications, but an inexperienced one can easily fall intoeach and every trap that these cheap solutions set. Toparaphrase: it is definitely cheaper to spend the night on apark bench in a big city than to rent a room in a decenthotel, but it is nonetheless true that you would get a muchbetter and safer night’s sleep in a hotel room than youwould in the park or subway! Even though some of theworld’s best peelers can use TCA–SAS with completesafety, it is still true that the vast majority of all complica-tions occur after the application of these cheap solutions.Some ill-informed doctors have ended up claiming thatTCA simply cannot be used to treat melasma, for exam-ple.

Reading the textbooks on chemical peels is very instruc-tive, and the pictures of complications often reflect thecomplexity of using TCA–SAS correctly. Today’s newTCA peel solutions have been developed with a view toconvenience and safety. I can already hear reproachesfrom those who claim the contrary and are perfectly ableto use TCA–SAS safely, but I can also hear the sobs andregrets of those who listened to them and whose patientshave suffered for it. The simple aqueous solution of TCAwas born in the 19th century: it has had its day – let usmove on!

‘Adjuvanted’ TCAApplying TCA–SAS to the skin causes frosting that israrely even,28 especially when using intermediate concen-trations. Applying TCA–SAS at 10% m/m does not usu-ally cause any frosting at all and is almost risk-free;applying TCA–SAS at 50% m/m causes very rapid frost-ing whose depth is difficult to evaluate and control.29

Intermediate aqueous concentrations (e.g. at 25% or30% m/m) do not penetrate evenly and produceintraepidermal peel zones next to peel zones to the papil-lary or reticular dermis. It is difficult to get even frosting,and the results of the peel are not homogeneous: under-treated areas are next to overtreated areas that could eas-ily create problems with post-inflammatory hyper-pigmentation (PIH), hypopigmentation, or even scarring(Figure 12.7).

Various adjuvants have been added to TCA to even outits effect. The term ‘adjuvanted’ is used to describe a TCAsolution to which something has been added to enhance oreven out its action. Many different products have beenadded to TCA.


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GlycerolGlycerol (Figure 12.8), also known as glycerine, glycerin,1,2,3-propanetriol or 1,2,3-trihydroxypropane, has a mol-ecular weight of 92.09. It is often used as an antimicrobialpreservative (in concentrations >20%), a humectant (≤30%), an emollient (≤ 30%) or a solvent. It is used in cos-metic products, as well as in parenteral or oral prepara-tions. Adding glycerol to a solution increases its viscosity.Glycerol does not oxidize easily on contact with air. It is nottoxic: after absorption by the digestive tract, it is metabo-lized into carbon dioxide and glycogen or is used for lipidsynthesis. High doses of glycerol taken orally have a laxa-tive effect and can cause headaches, hyperglycemia, thirstand nausea. Glycerol is also used in the laboratory as a pro-

tein stabilizer (which seems a little paradoxical, consider-ing that the effect sought by applying TCA is the destruc-tion of proteins).

Soft Peel® was presented as a solution for improving thetolerance and effectiveness of TCA. Nevertheless, addingglycerol did not remove the need to prepare the skinbeforehand, 3 weeks before the peel:30

� with a depigmenting formula to prevent pigmentarychanges in patients with a high skin phototype (overFitzpatrick IV); it was also necessary to wear a total sun-block before this peel – this suggests that pigmentarychanges are common after this type of peel

� with retinoids or benzoyl peroxide in cases of acne:treatment with isotretinoin was not given as a strictcontraindication to Soft Peel® on condition that thedaily prescribed dose 2 or 3 weeks earlier did not exceed0.3 mg/kg per day

� with tretinoin at 0.05% once a day in the evening com-bined or not with glycolic acid to increase and even outpenetration of the TCA and accelerate regeneration ofthe epidermis after the peel, which suggests that thesolution did not penetrate evenly and readily and thathealing was slow

The total number of ‘soft peels’ required was 5–10, with aninterval of 8–21 days in between, depending on the depthreached by each peel. The peel solution had to be ‘neutral-ized’ with water as soon as frosting occurred.31 It should beremembered, however, that adding water to an acid solu-tion does not neutralize it but simply dilutes it.

The pH increases very slowly when the solution isdiluted, and large quantities of water are needed (Figure12.9). Rinsing with water was necessary, however, toremove the excess solution that was no longer needed afterthe appearance of frosting on the skin. It would be morecorrect to say ‘remove any surplus solution with water assoon as frosting appears’ instead of ‘neutralize the acid’.Without rinsing, the TCA in the TCA–glycerol solutionwould continue to destroy the skin proteins and deepen theeffect of the peel. Choosing the right moment to rinse istherefore essential and has to be timed very carefully, whichis not easy for an inexperienced doctor. Some formulations


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

H|C| C | C | H

H —

H —

H —

— OH

— OH

— OH

Figure 12.8 Chemical structure of glycerol.

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(called ‘composite’ or ‘compositum’) still use solutionswith glycerol and the post-peel rinsing technique, which isboth restrictive and the source of errors. It is also impor-tant to make sure that the water does not carry the TCAinto the eyes or onto the neck and décolletage, where it willcause an accidental peel.

Glyceryl monooleateSome glycerol derivatives can be used as adjuvants. Glyc-eryl monooleate (Figure 12.10), for example, is a nonionicsurfactant and polar lipid with a molecular weight of356.55. It is a monoester of glycerol in which one of thehydroxy groups is replaced by a long side-chain derivedfrom oleic acid (CH3(CH2)7CH=CH(CH2)7COOH).32

Propylene glycolPropylene glycol (Figure 12.11), also known as 1,2-propanediol and 1,2-dihydroxypropane, has a molecularweight of 76.1. It is used as an antimicrobial preservative(at 15–30%), a disinfectant, a humectant (at 15%), a sol-vent 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 prob-lems, especially in patients with renal insufficiency. Its dis-infecting power is slightly lower than that of ethanol.Propylene glycol is stable at low temperatures. At high tem-peratures, it tends to oxidize and form lactic acid, aceticacid, pyruvic acid and propionaldehyde. Locally, propyleneglycol is more of an irritant than glycerol, especially if itcomes into contact with the mucous membranes or is usedunder occlusion. It is neither mutagenic nor teratogenic.

Stability of TCA solutions withglycerol or propylene glycolAttempts to stabilize TCA solutions by adding glycerol(‘soft peeling’31) or propylene glycol improved the safety ofTCA peels, although they did not necessarily make themcompletely stable. Moreover, the addition of glycerol or itsderivatives was still empirical and varied from one doctor toanother – more of a do-it-yourself approach than a profes-sional one. It is difficult to compare the different solutions,since the exact concentrations of these adjuvants were nei-ther uniform nor even known for certain. Soft Peel®involved the ad hoc combination of TCA at variable con-centrations with the same quantity (volume) of glycerol.

Other adjuvantsOther attempts to stabilize and even out TCA were made inthe 1990s.

‘Enzymatic’ TCAAn enzyme is, by definition, a protein. TCA coagulates pro-teins. It is therefore difficult to include active proteins andTCA in the same solution, since, even if some enzymes areacid resistant (e.g. in the stomach), the conditions for acidresistance are strict and not reproducible in a TCA solu-tion. To my knowledge, there is no preparative approachthat would allow proteins to be encapsulated innanosomes, liposomes, cyclodextrins, etc. to protect themfrom the coagulating action of concentrated TCA.


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

H|C| C | C | H

H —

H —

H —

— O — C —C17H33

— OH

— OH

||O

Figure 12.10 Chemical structure of glyceryl monooleate.

H|C| C | C | H

H —

H —

H —

— H

— OH

— OH

Figure 12.11 Chemical structure of propylene glycol.

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Sorbitan monolaurate Sorbitan monoesters are partial esters of sorbitol with fattyacids (monolaurate in this case). They have a molecularweight of between 346 and 964. Sorbitan monolaurate iswidely used in cosmetics, the food industry and pharma-ceutical preparations. Sorbitan monoesters are non-ionicsurfactants, dissolving and dispersing agents. One of theproblems of using sorbitan monoesters is that in the pres-ence of strong acids (like TCA) they tend to form soaps thathave no power to attack the skin. This is partly why TCA‘adjuvanted’ with sorbitan monolaurate is less aggressivefor the skin.

Phenoxyethanol Phenoxyethanol, C6H5OCH2CH2OH, also known as ethyl-ene glycol monophenyl ether, 2-hydroxyethyl phenyl ether,1-hydroxy-2-phenoxyethane, β-phenoxy-ethyl alcoholand 2-phenoxyethanol, has a molecular weight of 138.16. Itis a simple disinfectant in the adjuvant solution, an antimi-crobial agent that seems not to have a real adjuvant effecton the peel.

Chelation of TCASome TCA masks33 have been presented as ‘chelated’ TCA.Chelation34 is a medical therapy that aims to detoxify thebody of harmful minerals and metals. Chemically, chela-tion is the process by which an organic substance (thechelator) binds metal ions (iron, copper, lead, calcium,etc.) into inactive, non-toxic and water-soluble complexesthat are easily eliminated in the urine. Intravenous chela-tion 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’ thereforeseems inappropriate as far as TCA is concerned, and has nochemical basis since TCA is not a metal. The little informa-tion available states that chelation reduces the speed ofpenetration of TCA and therefore its depth of action.35

Might what we call chelation be partial inactivation of theTCA? The directions of use for Accu Peel® state that a‘process called chelation allows the TCA to reach an evendepth at the same time as using lower concentrations ofTCA’. Might chelation, on the contrary, be a process thatactivates 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 con-centrations (the stakes are being raised) and so there is lesspain and stinging and healing is faster. Is chelation the ulti-mate answer for TCA? The Holy Grail of the peeler?

The Plastic Surgery Group states that ‘chelation’ of AccuPeel®, on the contrary, provides a superficial peel that healsmore quickly – which at least seems logical. Chelation is

therefore presented as the ultimate solution to all the prob-lems posed by TCA. The most scientific-sounding explana-tion seems to be of a specific technique where, and I quote,‘the TCA binds to metallic ions in bentonite clay’. It is nottherefore strictly chelation, which would imply the bindingof metallic poisons and their elimination through urine.But it is partly true insofar as an organic substance (theTCA) binds with silicon and metal ions (aluminum andmagnesium). Even if the process is the exact opposite ofchelation – since in this case it is the TCA itself that is thechelating agent – this explanation merits closer examina-tion to understand the possible interactions between theTCA and the structure of the clay.

TCA in clay masksTCA sometimes comes in the form of a clay paste. Gener-ally, clays consist of two types of compounds: aluminumsilicates (bentonites) and magnesium silicates (hectorites).Clays36 are made up of stacked three-layer platelets (Figure12.12): a middle layer of magnesium oxide (in the case ofhectorites) or aluminum oxide (in the case of bentonites),surrounded by two layers of silicon dioxide (silica). Thelateral surfaces of each platelet are positively charged37 andthe lower and upper surfaces are negatively charged.38 Theclay platelet therefore reacts like a dipole, and the differentparticles rearrange themselves depending on the electricalcharges that encourage contact between the lateral surfaceand the upper surface. Clay has a ‘house of cards’ structure,and macroscopically forms a coarse gel with a grainy tex-ture in the aqueous phase.

The TCA molecule is itself electrically neutral. When it isin an unbuffered solution, it more or less completely breaksup, releasing its proton (H+) into the solution, which thenbecomes acidic. The TCA, without its proton (i.e.trichloroacetate anion), has an overall negative charge thatcan therefore combine electrically with the positivelycharged lateral surfaces of the clay, while the positivelycharged protons will combine more readily with the lowerand upper surfaces of the negatively charged clay particles(Figure 12.13). The protons therefore combine with the


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

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oxygen atoms of the silica molecules on the lower andupper surfaces, whereas the negatively charged trichloro-acetate anion will combine with the metallic cations on theother surfaces of the clay particles. This then explains howthe TCA binds with metallic ions. It is easy to understandhow this might stabilize the TCA, as once it has broken up,it binds electrically with the different parts of the clay par-ticles. It is, however, difficult to understand the real clinicaladvantage of this combination, as the protons that producethe peeling effect are still attached to the part of the TCAthat has not broken up or else they have to break away fromthe clay in order to be effective. It could then be argued thatthe protons (and the trichloroacetate) and the clay are rel-atively united and that the TCA in a clay mask will act moreslowly and be less aggressive. It is difficult to reconcile thiswith the statement that a low-concentration TCA claymask produces the same effect as a more concentratedwater-based TCA in which all the molecules exert theirpeeling 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 liq-uid at 45–50%. Even then, it would be necessary to knowwhether the concentration is m/m, m/v or m + v. It cannotpossibly be m/m, as a TCA at 50% m/m is extremelyaggressive and causes more complications than effectiveresults. Besides, 20% TCA masks are marketed as superfi-cial peels, which is incompatible with the gratuitous claimthat ‘20% in mask form is equivalent to 50% in liquidform’, but completely compatible with the scientific expla-nation given above. Another major problem comes fromthe fact that the clay mask forms a coarse and opaque layer:it is impossible to observe the effect of the TCA directly andcontinuously through the clay mask (Figure 12.14). Onecommon method of monitoring the peel consists in using atongue depressor to remove the clay from a small area to

see if, or how much, frosting has occurred. If there is nofrosting, the acidified clay is replaced. This examination isrepeated after a few minutes or if the patient makes anycomment. It should be noted that removing the clay with aspatula creates an abrasion on the skin where the acid canpenetrate more deeply. The next time, therefore, the samearea must be checked again as well as a different area.

When a TCA paste is called ‘homogeneous’, it shouldnot automatically be assumed that the TCA is distributedevenly, although it may well be. It should be assumed thatthe paste itself has a homogeneous consistency and is notgrainy. It is possible – though not easy – to spread TCAhomogeneously in a clay paste. However, the even distrib-ution of TCA in a paste does not in itself guarantee that theacid will penetrate the skin evenly.

Another argument that counters the claim that lowerconcentrations are more effective is that the applicationtechnique for a TCA mask involves degreasing the skin andapplying glycolic acid or tretinoin beforehand.35 Thismakes the skin far more permeable and enhances the pen-etration of the TCA,39 which means being very carefulabout how long the paste remains in contact with the skin.

Some TCA clay pastes are presented as causing simpleerythema with no protein coagulation, but they neverthe-less have a downtime of 6–8 days.35

The absence of frosting is compatible with a superficialpeel – but not with an improvement in the appearance ofdeep wrinkles, which can only be treated with a deep peel.Then again, a downtime of 6–8 days is not compatible witha superficial peel, as it is the same as the downtime follow-ing a ‘medium’ TCA peel to the papillary dermis.

The TCA mask is not the easiest40 or safest of peels, as itis not possible to check in real time whether the TCA ispenetrating too deeply under the mask. It does, however,make application a little easier for doctors who doubt theirability to apply a superficial TCA peel evenly. We cantherefore conclude by saying that TCA masks are easy toapply but difficult to monitor. Even if ‘chelation’ makes theclay mask less aggressive, it is on the whole not as safe as an‘open’ TCA peel, which can be monitored at all times. Myexperience with a TCA mask preceded by a glycolic acidmask is in the context of a regular medium-depth TCA peelto the papillary dermis.


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

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

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HistologyEven though histological sections taken 30 minutes afterthe application of a medium-depth TCA peel on the skinhave not revealed any skin necrosis, and even though histo-logically everything appears normal, it is certain thatnecrosis is taking place both clinically and chemically. Theepidermis is functionally dead, although it appears to behistologically normal. Maybe this can be explained by theprotein-coagulating action of the TCA: with conventionalhistology, it is not possible to see membrane proteins(essential to cell life) coagulating. It is only later on thatnecrosis can be detected histologically when the normal cellstructure has radically changed as a result of its proteinmembranes becoming devitalized. The overall histologicaleffect of a TCA peel consists in the destruction of the livingcells of the epidermis and possibly the dermis (the depth ofdestruction depends on the concentration used). Abnor-mal keratinocytes are replaced by healthy cells from deepsurviving islets of keratinocytes, the pilosebaceous unitsand the sweat glands.41 As the skin re-epithelializes, newcollagen is formed.

The depth of skin necrosis is directly proportional to theconcentration of the TCA. Necrosis should not be the onlyendpoint of a TCA peel – stimulation also plays an impor-tant role. Repeated application of less concentrated TCAhelps rebuild the papillary dermis directly and/or indirectlyas a result of the repeated dermal irritation of the peel-induced inflammation. It is possible to reach the dermisusing a low-concentration solution applied to an epidermisthat has been made temporarily more permeable by a priorpeel or ‘robust’ preparation.

TCA peels allow different depths of penetration to bereached (Table 12.3).

A study by Roenigk41 shows that regeneration of dermalcollagen starts within 2–3 weeks. The increase in papillarydermal collagen and the production of elastic fibers contin-ues for 6 months. Another study42 on mice artificially pho-toaged by exposure to UV rays compared the histological

effects of four different types of peels against a controlgroup:

� 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 collagenincreased from the 3rd day, fell around the 7th day andreached a positive peak around the 28th day. There wasmore of an increase with the TCA and phenol peels thanwith the glycolic acid. There was a significant increase inthe concentration of glycosaminoglycans with the 50%TCA and phenol at 14 and 28 days. On the 60th day, thedermal concentrations both of collagen and glycosamino-glycans had returned to their original values in all of thegroups.

These findings cannot be considered as proof that thesepeels are not clinically effective, as the structure of the epi-dermis and dermis improved histologically, the collagenfibers were significantly rearranged in the papillary andreticular dermis and elastotic material disappeared in thedeep TCA and phenol groups. At the same time, it wasnoticed that the elastic fibers rearranged themselves. Thesepositive histological changes are more marked in the deepTCA and phenol groups than in the other peel groups. Asfor the global effect, the study shows an overall increase indermal thickness with the deeper peels.

In the long term, the histological changes brought aboutby TCA are temporary when the TCA penetrates superfi-cially and long lasting when the TCA penetrates to the pap-illary dermis at least.

Dermal fibroplasia causes hypertrophic scarring, scaradhesions and keloids. Black or dark skins are more likelyto develop this type of reaction. The shoulder girdle andthe lower thorax are both high-risk areas, as is the jaw areaon the face. This type of scarring does not occur whennecrosis 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–Danlossyndrome), the destruction of the papillary dermis doesnot cause hypertrophic scarring.

There is a risk of skin atrophy when all of the appendagesof a treated area undergo necrosis. The skin does not haveany source of supply to regenerate cells quickly. The ker-atinocyte clones can only come from the (distant) edges ofthe necrotic areas; they cannot be produced in sufficientnumbers for rapid skin regeneration if the lesion is morethan a few centimeters in diameter. Lesions smaller than1 cm in diameter, even in the deep reticular dermis, do notpose a high risk of scarring unless there is a secondaryinfection or the patient scratches the scabs.

When all of the appendages have undergone necrosis,the melanocyte reserve as well as the keratinocyte reservesuffers, and scarring will be hypopigmented or unpig-mented.

Occlusion of TCAFollowing the example of phenol, it was suggested in thepast that occluding TCA could potentially enhance pene-tration. A histological study by Stegman43 in 1980 throwssome light on this question. Occlusion does in fact increasethe depth of action of phenol, but actually reduces that ofTCA.

An occlusive dressing applied quickly after phenol helpsit macerate and deepens its action. An occlusive dressingapplied immediately after TCA creates a barrier to epider-mal water evaporation and to the water in the solutionitself. Under occlusion, this water accumulates in theuppermost layers of the skin, where it dilutes the TCA fairlyrapidly. With phenol, this slight dilution enhances its pen-etration. An occlusive dressing applied 30 minutes afterTCA does not dilute the acid, as it has had enough time tocoagulate the proteins in the skin and neutralize itself bycombining with the proteins before occlusion can dilute it.

Applying a greasy substance, such as Vaseline® or anantibiotic ointment, immediately after a TCA peel is equiv-alent to occlusion, and can reduce the depth of necrosiscaused by the TCA.

Increasing the permeability of thestratum corneumThe thicker the stratum corneum, the less the TCA pene-trates, and any method used to make the stratum corneumthinner before applying TCA deepens its action. Applyingtretinoin for 2 weeks before a TCA peel thins the skin andcauses the keratinocytes and corneocytes to dedifferentiate.

Acetone degreases the skin and causes chemical changesin the membrane lipids, which increase the skin’s perme-ability 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 applicationto a thick and impermeable skin.

Another way of increasing the depth of skin necrosiswould be to use higher concentrations of TCA, but thismethod produces variable results because of the wide vari-ation in penetration of TCA in an aqueous solution. Therisk of scarring increases with the concentration of theTCA.

Notes1. 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 therenal tubules.

6. Bismuth Ch. Toxicologie clinique, 5° ed. Paris: EditionsMédecine–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 Chap-

ter 6). Glyoxylate is converted into glycolate by glyoxylatereductase.

10. Glycine (aminoacetic acid, aminoethanoic acid) is H2N.CH2.COOH, with pKa = 2.4. It is transaminated by an ala-nine–glyoxylate aminotransferase. The glycine can then beincorporated into proteins and used for serine synthesis orsimply be degraded.

11. DCA was administered orally in the drinking water ofrodents. No specific data have been reported in humans.

12. Kitamura N, Ota Y, Mimura K. Effects of diisopropylaminedichloroacetate on proliferation and differentiation of nor-mal keratinocytes in vitro. Skin Pharmacol Appl Skin Phys-iol 1999; 12: 317–325.

13. Johnson K, with the Canadian Task Force on the PeriodicHealth Examination. Periodic Health Examination, 1995update: 1. Screening for human papillomavirus infection inasymptotic 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 dis-infection.

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, nécessitéd’une formulation explicite pour les solutions d’acidetrichloracétique. 18° réunion du GRCD, Perpignan, 9 Sep-tembre 1995: 28–38.

19. Trauchessec JM, Pissot F. Solutions d’acide trichloracétique


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masse par masse pour peelings dermatologique. Nouv Der-matol 1996; 15: 252–5.

20. One apple plus one apple equals two apples, whereas oneapple plus one pineapple equals two pieces of fruit!

21. According to Roenigk, applying TCA at 70% m/v on the faceusually causes scarring, while in gynecology, treating vaginalor cervical condylomas does not produce any scarring.McCollough EG, Langsdon PR, Maloney BP. Chemical Peelwith Phenol. Roenigk RK, Roenigk HH (eds.), DermatologicSurgery, Principles and Practice, 2nd edn. 1147–60. 1996UK, Oxford, Marcel Decker Ltd.

22. Rereading the textbooks that I used at the beginning of mycareer as a ‘peeler’ now makes me realize why it was so diffi-cult to get an overall grasp of the field and to understand theconsistency of the technique.

23. Brody H, Stegman S. Histological study by Harold Brodyand Samuel Stegman, at 3, 30 and 90 days.

24. TCA therefore does not have an ‘all or nothing’ action.25. McCollough EG, Langsdon PR, Maloney BP. Chemical Peel

with Phenol. In: Roenigk RK, Roenigk HH (eds.), Dermato-logic Surgery, Principles and Practice, 2nd edn. 1147–60.1996, UK, Oxford, Marcel Decker Ltd.

26. Easy TCA® and Unideep® consist of peel solutions as well asa post-peel cream whose ingredients help achieve betterresults and avoid complications. Only Touch® consists of asolution alone, but has to be combined with Easy TCA® orUnideep®, and thus benefits from the application of thepost-peel cream of these peels as well.

27. Chiarello SE, Resnik BI, Resnik SS. The TCA masque. A newcream formulation used alone and in combination with Jess-ner’s solution. Dermatol Surg 1996; 22: 687–90.

28. Vergereau R, Trauchessec JM, Peyronnet B. Le new peel. JMed Esth Chir Derm 1990; XXII (68): 243–55.

29. See the many previously published works on the semiologyof 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 ofwhich 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 whensoaked 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 diffi-

cult monitoring of the contact time and downtime are nec-essary.

41. McCollough EG, Langsdon PR, Maloney BP. Chemical Peelwith Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermato-logic Surgery, Principles and Practice, 2nd edn. 1147–60.1996, UK, Oxford, Marcel Decker Ltd.

42. Butler P, Gonzales S, Randolp M et al. Quantitative andqualitative effects of chemical peeling on photo aged skin: anexperimental study. Plast Reconstr Surg 2001; 107: 222–8.

43. Stegman SJ. A study of dermabrasion and chemical peels inan animal model. J Dermatol Surg Oncol 1980; 6(6): 490–7.


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Main indications fortrichloroacetic acid Trichloroacetic acid (TCA) is an extremely versatile peelthat can reach all depths, and can be applied to all skintypes, on all parts of the body and in a great many indica-tions. Using solutions that are properly prepared and fol-lowing strict protocols ensures a safe and effective peel.Repeating several easy peels, such as Easy TCA®, can boostcollagen and elastin production to the same degree as adeeper peel; repetition may even be preferable to using amore aggressive peel when the aim is to stimulate the skinand renew the epidermis, as is the case in the treatment ofphotoaging.

On the other hand, when the desired effect is destructionof deeper layers of the dermis and epidermis to eliminatecertain lesions, a single deeper peel may be a better indica-tion than repeating several peels to the Grenz zone, as is thecase when treating lentigines and mixed or dermalmelasma.

Folds and wrinklesDeep wrinkles and folds are not a good indication for TCApeels:

� Folds cannot be treated by peels, and require surgery,dermal fillers or thread lifts. Deep nasolabial folds andmarionette lines do not always respond to phenol.

� Dynamic wrinkles respond well to a combination ofbotulinum toxin and peels: the peels restructure the epi-dermis and the dermis on an unmoving base and theclinical results are better when these two treatments arecombined than when used alone.

� Fine sun-related wrinkles respond well to TCA, butdeeper ones respond better to phenol.

� Wrinkles around the mouth and eyes are very poorindications for TCA, even in high concentrations; phe-nol is far more effective (see Chapter 36).

PhotoagingEarly photoaging (Figure 13.1) is one of the best indica-tions for a TCA peel. In short, it improves and evens outthe complexion, reduces or gets rid of lentigines, improveselastosis and fine lines, improves skin tone, and generallybrightens the skin. TCA peels have often been combinedwith tretinoin in this indication (see Chapter 2). Photoag-ing on the hands is an excellent and easy indication forTCA (see below and Figure 13.3).

Solar elastosisThe papillary dermis is sometimes so atrophic that the epi-dermis appears to be lying directly on the middle dermis,

13Trichloroacetic acid: indications andcontraindications

Figure 13.1 Early photoaging: a good indication for TCA.

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without the intervening Grenz zone. The epidermis thenbecomes ‘too big’ for the underlying dermis, and wrinklesappear – like baggy clothes that crease on a body that hasgrown too thin. In theory, only a very deep peel can treatsolar elastosis, by producing enough good-quality collagenand elastin in the papillary dermis to fill the atrophied der-mis and bury the sun-damaged fibers deep down (seeChapter 26). Repeating certain types of peel to the Grenzzone1 once a week may be effective enough to improve theappearance of the skin without the downtime thatinevitably follows medium or deep peels. Of course, thedeeper peels will be more effective: there is no comparisonbetween 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 facialskin. Body skin only benefits from other agents. Solar elas-tosis appears in several forms. It starts with the appearanceof limited areas of elastosis that as yet have no or little clin-ical expression. Its maximum expression is seen when theskin has a cobblestone appearance (Figure 13.2). The typeof treatment depends on whether the elastosis is in its veryearly stages or if it is more advanced (Figure 13.2). Earlyelastosis, which is characterized by very fine lines and anuneven complexion, can be treated successfully with fourEasy TCA® peels or one Unideep® peel, while advancedelastosis can only benefit from a deep reticular peel (full-face Lip & Eyelid® formula) and a major restructuring ofthe skin. TCA would have no effect on the deep wrinkles inFigure 13.2, no matter which concentration, adjuvants orother combined treatments were used.

Solar elastosis often affects the legs if they are frequentlyexposed to the sun, which is the case with women who wearskirts. The skin between the knee and the malleolus issometimes affected by visible elastosis that can beimproved by combining abrasion and Easy Phytic® solu-


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

Figure 13.4Lentiginosis and photoaging. (a) Before treatment, there areabout 40 lentigines and/or actinic keratoses. (b) After foursessions of Easy TCA® peels to the Grenz zone, there are onlyabout 10 lentigines/keratoses left. The signs of photoaging arevisibly reduced: fine lines, quality of the skin, improvedeyelid tension, etc.

Figure 13.2 Solar elastosis (skin with a cobblestone appearance): this isnot the best indication for TCA.

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tion (see Chapter 11). The hands and forearms respondextremely well to Easy TCA®, with no side-effects (Figure13.3).

Lentiginosis2

TCA is effective in treating solar lentigines: the concentra-tion of the TCA is chosen depending on the assumed depthof the lentigo. Relatively superficial lentigines are easilytreated with Easy TCA® (Figure 13.4). Lentigines ofmedium depth respond to Unideep®. Lentigines originat-ing from the deepest dermal papillae and embedded deepin the dermis only respond to very concentrated TCA(Only Touch®), or even phenol (Lip & Eyelid® formula),applied locally and combined with Easy TCA® (orUnideep®) to even out the results and treat the smaller sub-clinical lesions (Figure 13.5). It should be noted that a TCApeel, even to the papillary dermis, does not always treatlentigines definitively and that several peels to the papillarydermis may be necessary for long-term results.

Perioral wrinklesVery fine lines around the mouth can be improved by acombination of filling techniques (e.g. hyaluronic acid)and one or more TCA peels to the papillary dermis, but theresults achieved with TCA never equal or even come any-where near those achieved with phenol, which is preferredin chemical labioplasty or cheiloplasty (see Chapter 36) incombination with botulinum toxin, if possible.

Prevention of skin agingThe wisest patients go to see their doctor before the clinicalsigns of aging appear and seek advice on how to preventskin aging. The preventive treatments that might be sug-gested to these patients are straightforward and superficialprocedures that do not disrupt their social lives too much.They may simply be prescribed cosmeceuticals: DHEA-Phyto®, Actilift® (dimethylaminoethanol (DMAE) cream),Renutriv ACE Lipoic Complex® (an antioxidant) or Vit E

Trichloroacetic acid: indications and contraindications 97

Figure 13.5Photoaging, actinic keratosesand lentigines. (a) Before and(b) after a peel to the papillarydermis with TCA (Unideep®)and phenol (Lip & Eyelid®formula) around the mouthand on the large lentigo on theleft temple only. (c) Before and(d) on the 6th day after thepeel. For more details, seeChapter 23.

A

C

B

D

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Antioxidant® (a hydrating antioxidant). These cosmeceu-ticals should be combined with sun protection againstUVA, UVB.

A series of AHA peels or TCA peels to the basal layer ofthe epidermis can be repeated on a yearly basis. If the signsof aging are beginning to show clinically, Easy Phytic®solution can be extremely beneficial. When the signs aremore obvious, Easy TCA® is the best choice of peel (Figure13.6). Very obvious photoaging can benefit fromUnideep®, a papillary intraepidermal peel. An excellenttreatment for preventing photoaging is a combination of amesolift3 and a peel, sometimes called a ‘mesopeel’: a peeland a mesolift are used alternatively every other week orsometimes even in the same session when mesotherapy iscombined with Easy TCA®. The need for a surgical faceliftor a deep phenol peel can be put off for several years.

Melasma and chloasmaMelasma (Figure 13.7) is a common acquired hyperpig-mentation disorder of the face, neck and forearms. It isusually symmetrical. The density of color in the hyperpig-mented area can vary, but is clearly delimited. Patients witha dark skin phototype are more prone and can get melasmaearlier in life than light skin phototypes.4

Melasma appears almost exclusively on areas of skin thathave been exposed to the sun. It can be of the followingtypes:

� Purely epidermal: there is a lot of melanin in the basaland suprabasal layers of the epidermis. It is occasionallyfound throughout the epidermis. A Wood’s light5

increases the contrast between the melasma and normalskin. This is the most common type of melasma.

� Dermal: the melanin accumulates in the macrophagesof the papillary and/or reticular dermis. A Wood’s lightdoes not increase the contrast.

� Mixed epidermal–dermal: a Wood’s light accentuatesthe contrast in some areas and not in others, but an ‘epi-dermal’ area can hide an ‘underlying dermal’ area.

The cause of melasma is still widely debated, and potentialpathogenic factors include the influence of UVs, the hyper-pigmenting effect of some cosmetics,6 genetic predisposi-tion, hormone therapy and pregnancy.7 Estrogens andpossibly progestogens can trigger melasma.

Topical treatments for melasma usually include tyrosi-nase inhibitors, with or without tretinoin or one of its pre-cursors. Azelaic acid is also a viable treatment option. Acorticosteroid can be combined with it to counter anypotential active inflammation. Lasers, intense pulsed light(IPL), dermabrasion and microdermabrasion have alsobeen suggested, but often cause post-inflammatory hyper-pigmentation. TCA can be an excellent treatment formelasma: it eliminates the melanin stored in the papillarydermis and epidermis (Figure 13.8). Mesotherapy has beenrecently reputed as an effective treatment of melasma.8


Figure 13.6Early photoaging: treatment ofrosacea on the cheeks with aradiofrequency device (Ellman) andfour applications of Easy TCA® (basicprotocol). Daily care: Vit EAntioxidant® cream.

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

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If the melanin responsible for the melasma is too deep,TCA will only be effective after many repeated sessions. Inany event, the TCA peel must be combined with effectivesun protection and appropriate post-peel care in the longterm. Simple aqueous solutions of TCA also require theskin to be prepared, in order to even out penetration andprevent common pigmentary changes.

See Chapter 16 for the exact protocol for treatingmelasma.

Post-inflammatoryhyperpigmentation and berloquedermatitisPost-inflammatory hyperpigmentation (PIH) (Figure13.9) and berloque dermatitis9 usually respond well toTCA; they can be treated in the same way as melasma, buthave a better prognosis as the original trauma disappears

after treatment, unlike melasma, which often persists orrecurs.

FrecklesFreckles (Figure 13.10) are small, clearly delimited, benignpigmented macules that appear on areas of sun-exposedskin in patients with a light skin phototype. They are neverpresent at birth, but can start to appear from the age of 3years, and there is an autosomal dominant pattern ofgenetic transmission. They result from melanocyte hyper-trophy, although not from an increase in melanocyte num-bers. In the basal and suprabasal layers, more melanin issynthesized and transferred between the melanocytes andkeratinocytes. This increased melanin synthesis couldresult from melanocyte clones that have mutated followingUV exposure. The structure of the epidermis remains nor-mal, apart from the parabasal keratinocytes, which containmore melanin in relation to the neighboring unpigmentedcells.


A B

C D

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

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A peel to the basal layer lightens the freckles, sometimesonly temporarily. A peel to the Grenz zone removes manyfreckles and lightens others. A peel to the papillary or retic-ular dermis gets rid of freckles altogether (Figure 13.11).

Easy TCA®, Unideep® (TCA) and Lip & Eyelid® (phe-nol) can all be used as treatments for freckles, althoughphenol will generally not be used as the TCA can get rid ofthem by itself. Other treatments have been suggested. Asfreckles grow darker on exposure to UV rays, using a sun-screen helps to lighten them. Tyrosinase inhibitors, antiox-idants, and tretinoin and its precursors can be used inconjunction with the peels to improve or prolong results.

Post-acne scarringTCA has some effect on shallow scars, but can onlyimprove the general condition of the skin and cannot getrid of scars altogether. TCA can be combined with sandpa-per abrasion (see the discussion of abrasive peels in Chap-ter 15) or scar subcision before the acid is applied. Even aphenol peel cannot always guarantee to heal acne scars.High concentrations of TCA can be directly applied onacne scars, levelly, with good results.

Dilated poresAlthough it has been claimed that TCA has a ‘circular con-traction’ effect that ‘narrows the follicle opening’, itappears that it has a limited effect on dilated pores, or, atbest, the results are difficult to predict. Patients shouldnever be promised visible results for dilated pores. Anyresults should be considered a bonus and not taken forgranted. Using an abrasive technique before applying EasyTCA® may give promising results, but this remains to beconfirmed with more experience. High concentration TCAcan be successfully used for treating dilated pores or pikeacne scars.

Seborrheic dermatitisSeborrheic dermatitis, resulting from an excess produc-tion of sebum and overgrowth of the commensal yeastPityrosporum ovale,10 improves rapidly but only tem-porarily after the application of TCA peels. Follow-uptreatment after the peels consists simply of applying vine-gar every morning before showering (for the antisepticqualities of the acetic acid) and the use of antimycoticcreams. In some cases, the reaction of the yeast andmetabolites causes eczema, which can be treated with top-ical corticosteroids. It should be noted that Easy Phytic®


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

Figure 13.10Freckles.

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

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solution rapidly improves the inflammation associatedwith seborrheic dermatitis, without having to resort tocorticosteroids.11

Widespread flat wartsFlat warts are localized skin-colored papules that mostlyappear on the back of the hands, the forearms and the face.Clinically visible flat warts do not respond to moderateconcentrations of TCA (10–30%), and higher concentra-tions (40–50% m/m) often produce only temporary orincomplete results. Figure 13.12 shows how flat warts onthe back of the hand reacted to a combined treatment ofOnly Touch® and Easy TCA®. Smaller flat warts can disap-pear completely, as can subclinical flat warts. Medium-sizewarts will come back, and they will sometimes need shav-ing with a radiofrequency scalpel (Ellman), for example.Not only are larger warts impermeable to TCA, but alsotheir very size prevents the TCA from getting round themto ‘undermine’ and treat them from underneath (Figure13.13). They should be treated by shave excision at thesame time as the others are being treated with a peel.

Sensitive skinAbnormal skin sensitivity is a clear sign of dysfunction ofthe skin’s protective properties against a hostile environ-ment. Sensitive skin should be treated until its tolerance toexternal aggression returns to normal. Many productscause skin allergies that are not always easy to identify sincethey may manifest as ‘over-reactive’ or ‘oversensitive skin’.


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

Figure 13.13 (a) Multiple flat warts. (b) Localized frosting of the flat warts after multiple applications of Only Touch®. Note that the thickerdome 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.

A B

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

Actinic keratosesThe treatment of actinic keratoses, like photoaging, is acommon indication for chemical peels (Figure 13.14). Thechemical elimination of actinic keratoses reduces the inci-dence 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 visiblelesions and leave clinically undetectable microlesions todevelop. A chemical peel, on the other hand, will treat alllesions, both visible and subclinical ones, and will improvelong-term prognosis. In comparisons between TCA peelsto the papillary dermis and the application of a 5-fluo-rouracil (5-FU) cream, the peels fare better, as applying 5-FU gradually causes severe and rather nasty-lookingdermatitis (Figure 13.15). Patients and friends can find thelong-drawn-out treatment difficult to bear. A medium-depth TCA peel, on the other hand, is generally a one-offtreatment (few sessions at most).

Oncological indicationsAs Vergereau et al12 reminds us, after a biopsy to confirmthe diagnosis and depth of a lesion, TCA is indicated in thetreatment of primitive malignant intraepidermal and intra-dermal tumors (depending on the depth of action of theTCA). Keratoses that have developed into microinvasivespinocellular or basocellular carcinomas can be treated

with TCA without leaving any scars: Only Touch® easilyreaches the reticular dermis. Non-degenerated lentigomaligna (Hutchinson’s freckle or Dubreuilh’s melanosis) isalso given as a potential indication for TCA, although phe-nol is no doubt more effective.

AcneAll common types of acne can be treated with TCA. Severeacne, such as ‘acne necrotica’, ‘acne conglobata’ or ‘acnefulminans’, should first be treated medically and theinflammation eliminated before the cosmetic use of peels.Oral isotretinoin (13-cis-retinoic acid) is the gold-standardtreatment for severe acne (Box 13.1), but new retinoidscome to light regularly.

Here too a combination of techniques proves worthwhile.Acne responds well to a TCA peel to the basal layer or theGrenz zone, whether it is comedonal, microcystic (Figure13.16), papular or papulopustular. Deeper peels, to the pap-illary 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 expectedto decrease after several TCA peels. We shall see how theEasy TCA® technique allows comedones and microcysts tobe opened immediately before the peel, which gives fasterand better results. Seborrhea is often reduced after TCA


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

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

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peels and seborrheic dermatitis improves significantly(although only temporarily). Acne in fact improves morequickly when treated with easy TCA than it does whentreated with tretinoin, benzoyl peroxide13 creams, glycolic orazelaic acid creams, or ‘purifying’ creams used alone. Thesecreams do, however, play an important part in the post-peeltreatment of acne. Pigmented acne scars usually respondwell to TCA. Shallow scars gradually soften. Ice-pick scars donot respond at all to TCA. A combination of sandpaperabrasion followed by Easy TCA® – a technique similar to theone described below for the treatment of stretch marks – cansignificantly improve post-acne scarring, even on the back.

XanthelasmaEyelid xanthelasma has been presented as a good indica-tion for TCA and dichloroacetic acid. Nevertheless, the

high concentrations required make it relatively dangerouscompared with the ‘chemical blepharoplasty’ techniqueusing phenol, which is more effective and easier to controlthan highly concentrated TCA.

It must be remembered that xanthelasma is associatedwith dyslipidemia in 50% of cases. It can also be sympto-matic of hepatobiliary disorders (biliary atresia and biliarycirrhosis) when associated with cholesterol deposits thatstart to build up in the hands and feet before spreading.Monoclonal gammapathies have also been described inassociation with xanthelasma.

Stretch marksCountless suggestions have been made for the treatment ofstretch marks, but none of them have really been effective.Some techniques are not deep enough and others notextensive enough. Superficial, intraepidermal, basal, Grenzzone and papillary techniques can only improve theappearance of stretch marks temporarily, but cannotreduce their size or depth. Some peels have been developedto give the atrophic base of the stretch marks a similar colorto that of the surrounding skin; they contain resorcinol,which is oxidized to match the normal skin color. Theresults of these peels are good, but only temporary. Deeptechniques, limited to the deepest part of the stretch marks,can do no more than tighten the little collagen that is leftand slightly stimulate the few surviving fibroblasts: in spiteof the fact that these localized treatments reach the deepestpart of the stretch marks, the results are always disappoint-ing. That is why I developed a technique for treating stretchmarks consisting of sandpaper abrasion followed by EasyTCA® peel solution and post-peel cream. The excellentresults achieved with this method are due to the fact thatthe atrophic base of the stretch marks contracts at the sametime that the cells on the edge of the stretch marks beingstimulated. The results seem to be permanent. See the sec-tion describing this technique in Chapter 15.

Other indicationsThese include alopecia areata, liposuction scars, neuro-genic excoriations and rosacea. TCA has often been triedon vitiligo, but without success.

General contraindications forTCA–SAS� General run-down condition� Epidermolysis or dermolysis bullosa� Active bacterial, mycotic or viral skin infections� Depression or personality disorders


Figure 13.16TCA will reduce the number of lesions and the inflammationof this type of microcystic acne. Opening the microcysts witha No. 11 scalpel blade or a needle and removing theblackheads with a comedone extractor immediately beforeapplying Easy TCA® will produce faster and better results.

Box 13.1 Isotretinoin for acne

Tablets dosed at 10 mg or 20 mgTotal cumulative dose 120 mg/kgDaily dose 0.3–0.5 mg/kgFor 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

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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 nota contraindication for peels. Patients with stableinsulin-dependent diabetes can be given a peel to theGrenz zone

� Prior treatment with isotretinoin, if the peel is to theGrenz zone

� Ehlers–Danlos syndrome, keloid scars, if the peel is tothe papillary dermis

� Extensive telangiectasias: these should be treated beforepeeling

Notes1. 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 Easternpatients, melasma can appear before the age of 10, while it israrely seen in Caucasian patients before puberty.

5. It is not possible to do a Wood’s light examination on verydark skin types.

6. To date, however, it has not been possible to reproduce themelasma by applying these cosmetics intentionally.

7. The mask of pregnancy tends to lighten naturally and evendisappear in patients with a light phototype unless they aretaking estrogens and progestogens, which can cause themask of pregnancy to persist.

8. www.astheticdermal.com9. Berloque dermatitis is an acquired hypermelanosis resulting

from contact photodermatitis caused by a sensitizing agent(perfume or metal in jewelry). Berloque, or berlock, der-matitis gets its (misspelled) name from the French word‘breloque’ meaning a trinket or charm that is attached to abracelet. These charms are often of poor quality and causecontact allergies in the shape of the trinket itself.

10. It should be noted that the precise pathogenic relationshipsbetween hyperseborrhea and yeast colonization are still con-troversial, even though ketoconazole can (temporarily)eradicate seborrheic dermatitis. It is suspected that it iscaused 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 morningand leave it to act during the time it takes to brush the teeth.Take a shower. Repeat the application every day for 3 con-secutive days.

12. McCollough EG, Langsdon PR, Maloney BP. Chemical Peelwith Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermato-logic Surgery, Principles and Practice, 2nd edn. 1147–60.1996, UK, Oxford, Marcel Decker Ltd.

13. Vergereau R, Trauchessec JM, Peyronnet B. Le new peel. JMed Esth Chir Derm 1990, XXII (68): 243–55.

14. Recall that benzoyl peroxide, alpha-hydroxy acids andtretinoin thin the stratum corneum and enhance penetra-tion of the acids.


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Preparing the skinPre-peel care is discussed in Chapter 2. Further informa-tion can be found in Chapter 12. The safety of peelsemploying trichloroacetic acid in simple aqueous solution(TCA-SAS) has been greatly improved by systematicpreparation of the skin before peeling. Preparing the skinhelps improve microcirculation, increase glycosaminogly-can synthesis, increase the number of mitoses in the basallayer keratinocytes, stimulate production of epidermalgrowth factors, deactivate melanocytes and even out anddeepen the effect of the TCA.

One month before a peel with TCA-SAS (Soft Peel®), thepatient should apply a cream consisting of hydroquinone(4 g), micronized hydrocortisone acetate (0.5 g), paraffinoil (16 g), or emulsifier based on polyglycol stearate(21.5 g) and excipient qs 100 g, twice a day. Tretinoin isthen mixed into this cream in gradually increasing quanti-ties. The concentration of tretinoin is increased every weekto reach a final concentration of 0.3%.1 Dermatitis devel-ops due to the tretinoin: irritation with flaking and rednesssignals that the skin has been properly prepared, and guar-antees a successful peel. However, the need to use a tech-nique to enhance and even out penetration of theTCA–SAS proves that the action of TCA–SAS is unevenand inadequate. The need to apply hydroquinone twice aday at a concentration of 4% as a preventive shows howaggressive the peel is to the skin and how it triggers post-inflammatory pigmentary changes. In short, the introduc-tion of skin preparation before a TCA–SAS peel and addingadjuvants greatly improved safety, and is still essential tocompensate for the inadequate and uneven penetration ofthis type of peel, as well as to reduce the risk of complica-tions, especially pigmentary changes.

For the record, it is interesting to note that the first timeI presented Easy TCA® at a congress of the Belgian Societyof Cosmetic Medicine in Brussels in 1997, there was anoutcry. The peel was shouted down, demonized and criti-cized even before it was presented, as it flew in the face ofthe all too recent dogma of aggressive skin preparation thatthen held sway. Anyone tempted to use it was told thattheir worst nightmares would come true if they did notprepare the skin beforehand. It was soon proved that theEasy TCA®2 technique is perfectly valid and that, apart

from certain specific cases such as the treatment of stretchmarks or resistant melasma, this peel does not require anyskin preparation. The doom-mongers, partisans of thedogma of preparation, gradually fell silent, and the swornenemies of Easy TCA® started to talk about the relativemerits of preparation and eventually the pointlessness ofpreparing the skin in many cases. Everything has finallyfallen into place, and preparing the skin is now consideredas an additional tool for many peels, a weapon that isoptional in some cases, but that still remains essential whenusing TCA–SAS.

Treatment with oral isotretinoin is sometimes essentialin cases of severe acne, but is contraindicated before a peelto the papillary dermis. An Easy TCA® peel to the basallayer,3 on the other hand, can be performed without anyrisk of complications, and can produce excellent results forsevere acne that has been treated beforehand with oralisotretinoin.

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

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

� deactivation of melanocytes� thinning and evening out of the stratum corneum� stimulation of keratinocyte regeneration� botulinum toxin, coagulation of telangiectasias, exci-

sion of benign tumors, cleaning the skin, etc.� obtaining photographs, informed consent and other

legal documents.

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

14Trichloroacetic acid: classic semiology

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

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

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

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

Effect of pressure of applicationThe pressure of application also plays a role in determiningthe depth of action of the TCA. The harder the solution isapplied, the more deeply will the TCA penetrate. A swabheld in the hand has less abrasive force than a swab heldwith Kocher forceps.

A smooth applicator does not abrade the skin whiledepositing the acid and the action of the TCA remainsmore superficial.

Using a brush to apply the same number of coats of thesame TCA solution with the same concentration producesa more superficial peel than using a swab.

The depth of action of the same peel solution can there-fore be varied simply by changing the applicator or thepressure of application.

Effect of speed of applicationThe 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.

The speed of application depends on:

� The patient’s sensitivity: a very sensitive patient will findit difficult to stand the burning sensation of the TCA onthe whole face, and will be better off if the TCA isapplied zone by zone.

� The surface area being treated: Only Touch® can beapplied quickly on lentigines, as only small areas areaffected by the burning from the acid. Large areas (e.g.the back) should be treated by TCA zone by zone for thepatient’s comfort.

� The depth of the peel: applying TCA is painful, but anintradermal peel is far more painful than an intraepi-dermal peel. An intradermal peel should be appliedzone by zone for the patient’s comfort, while anintraepidermal peel can be done in one go.

Symptomatology of TCAapplicationApplying TCA causes protein coagulation more or lessrapidly, depending on the formulation of the peel, its con-centration, 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. Even pink-white frosting (Figure 14.5) and ‘epidermal sliding’ (Figure Flaking: more or less brownish skin, depending 4. 14.6): the TCA is in the papillary dermis. The sliding (wrinkling) can be on phototype and photodamage (Figures 14.7 4. seen when the skin is pinched, and corresponds to the coagulation of and 14.8)4. 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 thedeep reticular dermis

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application, the skin type, etc. A 35% m/m TCA coagulatesproteins.

Different symptoms appear gradually: see Table 14.1 andFigures 14.1–14.9.

A low-concentration formula is applied in several coats;the doctor can progressively see each of the symptomsdescribed 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 isimpossible to see them clearly. The technique is muchquicker but the doctor cannot choose when to stop.

TCA: classic semiology 107

Figure 14.1 Scattered pinpoint frosting.

Figure 14.2 Flaking after scattered pinpoint frosting.

Figure 14.3 Cloudy-white frosting.

Figure 14.4 Flaking after cloudy-white frosting.

Figure 14.5 Even pink-white frosting (the differences in color come fromthe presence of melasma). The contours of the eyes havebeen chemically resurfaced locally.

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Two endpoints are worthy of more attention:

� Scattered pinpoint and cloudy-white frosting signal themost superficial peel to the dermis: this is the limit ofeffectiveness (see Chapter 15).

� Even pink–white frosting signals a peel to the papillarydermis: this is the safety limit (see Chapter 23).

Post-peel carePost-peel care is also discussed in Chapter 3.

In short, post-peel care is extremely important anddepends on the skin type, the depth of the peel and thedermatological problem being treated. It is more impor-tant than preparation when using Easy TCA® orUnideep®. Any ‘peeler’ very soon learns that applying a

peel solution is extremely easy – you do not need a uni-versity degree to take a cotton bud and get skin to frostgradually! The choice of indications and managing post-peel care are different matters entirely, and a thoroughknowledge of medicine is essential to do these properly.

Notes1. Preparing the skin with tretinoin before the peel accelerates

post-peel healing.2. Easy TCA® was called ‘Easy Peel’ at the time. The name was

changed when Easy Phytic® peel came out, in order to avoidany confusion between the two ‘Easy’ peels: Easy TCA®, acombination of a TCA peel and Easy Phytic®, uses AHAs andphytic acid. See Chapter 11 for more information on this peel.

3. The peel produces scattered pinpoint frosting only.


Figure 14.6The skin wrinkles when pinched between the fingers.

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

Figure 14.8 Flaking after a papillary peel on a light skin phototype thathas been badly damaged by the sun.

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

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In 1968, Paul Langerhans discovered the presence of a par-ticular type of epidermal cell in humans, which is nownamed after him. The Langerhans cell (LC) is a mobiledendritic cell that has no desmosomes and is found in mostmultilayered malpighian epithelia. LCs make up 2–5% ofepidermal cells. They come from the medulla and migratetowards and within the skin and stay within the epidermisfor 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 oneimagines the impressive number of potential antigen con-tacts over the entire epithelial surface of the body. Whenthe entire epidermis is destroyed by certain peels, this notonly affects the keratinocytes and the LCs but also otherdermal dendritic cells (DDCs) that are potentially antigen-presenting cells. New generations of sentinel cells migraterapidly from the bone marrow to the epidermis, which isbeing rebuilt after the peel, but this process is not effectiveimmediately. What is more, the first LCs to arrive as rein-forcements on the battlefield of the skin are ‘overwhelmed’as soon as they reach the dermis by the different types ofantigen stimulation that they have to face on skin that haslost its impermeability and physical defenses. The stratumcorneum can be compared to the ramparts of a medievalcity and the Langerhans cells to the soldiers who have todefend it.

The likelihood of unexpected bacterial and viral compli-cations occurring will be even higher, as there are fewercells in the skin capable of an immune response. It isimportant to consider these basic notions of biology to geta better understanding of what happens and anticipatewhich type of peel might be associated with a higher inci-dence of complications in the form of bacterial or viralinfections. It then seems obvious why applying peel solu-tions capable of destroying the epidermis and part of the

dermis on a skin with active herpes, acne or other infec-tious disorders is strongly contraindicated. Any medicalstaff suffering from respiratory or nose-and-throat infec-tions should be kept well away from the patient, and thedoctor’s hands should always be surgically disinfectedbefore applying medium or deep peel solutions.

Superficial peels with alpha-hydroxy acids (AHAs), onthe other hand, are known to cause very few bacterial orviral complications after peeling, as their direct action islimited to breaking up the spaces between corneocytes.1

Even if the peel penetrates too deeply in places, it is, quitelogically, exceedingly rare for an AHA peel to cause com-plications in the form of infection, when the endpoint isfocal or localized frosting.

With AHAs, the stratum disjunctum (SD), the outer-most 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 mediumor deep peels could lead doctors to think that, in order toavoid these problems, only superficial peels should be per-formed and patients with active acne or herpes should notbe treated at all. With a medium or deep peel, herpes pre-vention – as far as it goes – consists in a sandwich treatmentwith aciclovir, which is not well tolerated by patients withsensitive stomachs. With acne, caution limits the range oftreatment choice to careful superficial peels (which havelimited effectiveness even after repeated sessions). We areforced to put off, sometimes indefinitely, performing‘medium-depth’ peels on patients with acne or herpes thathave not responded to preliminary medical treatment.

With the development of Easy TCA® (ETCA), anotherpossibility for treatment has opened up, however. In manyindications, ETCA can produce the results of a mediumpeel with only the complication risks – usually non-exis-tent – of a superficial peel. ETCA can be applied quite suc-cessfully to active acne lesions, and the presence of herpeslesions on the lips is only a formal contraindication to thepeel applied following the basic protocol. It is still advisableto 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 for-tuitous and not directly related to the treatment. To date,there has been no reported incidence of herpes spreadingafter the application of ETCA (basic protocol).

With regard to acne, in 80% of cases, the first applicationof ETCA to active papulopustular facial lesions improvestheir number and severity by 50%, and the lesions seem toheal without scarring. ETCA is applied on the basis of onepeel per week for 4 weeks that clear the lesions almost com-pletely without having to resort to antibiotics. Deep wrin-kles and acne scars do not disappear: they lie deep underthe skin and even phenol or carbon dioxide laser resurfac-ing cannot always treat them. A combination of several dif-ferent techniques is clearly needed in these indications.

Although the face can be treated separately, the neckshould always be treated at the same time – to at least theseventh cervical vertebra – to ensure a better ‘tighteningeffect’. Ideally, all ‘visible areas’ should be treated: face,neck, décolletage, forearms and hands.

General remarksPresentationA growing number of doctors consider ETCA to be thesafest and easiest TCA peel, and it is used in over 50 coun-tries worldwide. ETCA now comes in two different kits.

The first kit (Figure 15.1) consists of 12 phials of basesolution and three tubes of post-peel cream for 12 facialpeels – enough to treat three patients on the basis of fourpeels per patient. The second kit (Figure 15.2) consists oftwo bottles of base solution for 24 peels – enough to treatsix patients on the basis of four peels per patient, and alarge tube of post-peel cream.

The phials, introduced more recently, are safer for thepatient and prevent any cross-contamination.

With both kits, the doctor adds TCA to the base solutionto activate the peel: the quantity of TCA to be added to thebase solution may vary from country to country and fromkit to kit. To avoid any confusion, it is best to refer to thevolumes that are clearly indicated on the inside cover ofeach kit.

Post-peel mask creamThe post-peel mask cream, which is highly antioxidant,contains vitamins, trace elements, growth factor, fatty acidsand tyrosinase inhibitors. The doctor applies it only once,immediately after the required level of frosting has beenachieved.

Its formulation is responsible for a significant propor-tion2 of the beneficial results of ETCA. It stops the burningsensation almost immediately and greatly reduces the riskof post-peel complications (see Chapter 5, p41). Its com-ponents are as follows.

Vitamin CMagnesium ascorbyl phosphate (MAP) is more effectivethan ascorbyl palmitate (AP), as the protection of its activefunction by esterification protects the MAP against oxida-tion and provides an antioxidant effect that is of betterquality and longer lasting than that of ascorbyl palmitate, amolecule in which the enediol function of the ‘2’ carbonatom is not protected by esterification.

Vitamin C is a powerful antioxidant, effective in aqueoussolutions, that scavenges free radicals and prevents thebreakdown of protein chains. It protects other antioxi-dants, which is an advantage in situations involving oxida-tive stress, such as infected or uninfected wounds and inthe post-peel healing period.


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

Figure 15.2Easy TCA® kit for 24 peels.

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

Silicion (trimethylsilanolmonomannuronate)This is strongly linked to proteoglycans and mucopolysac-charides, hyaluronic acid, and chondroitin sulfate. Silicionplays an important role in skin healing and is essential inanti-aging treatments.

Citric acidA tricarboxylic AHA, this is an antioxidant, chelator andbuffer.

Phytic acidAn antioxidant and tyrosinase inhibitor, this protectsagainst the risk of hyperpigmentation and post-peelinflammation.

Vitamin AThe post-peel mask cream contains retinol microencapsu-lated in a cyclodextrin. Vitamin A is involved in theprocesses of cell division and differentiation that help theepidermis regenerate after the peel from the cells of thebasal layer.

Retinol induces the expression of retinoic acid-bindingprotein (RABP) and regulates cell migration in the skinepithelium, which is vital for skin regeneration after a peel.Encapsulating retinol provides better bioavailability of thevitamin and protects the skin against oxidation. Ker-atinocytes have the enzyme tools required to convertretinol into retinoic acid (the corresponding carboxylicacid), which is the molecule ultimately responsible for theeffect of vitamin A.

SeleniumThis is a trace element that accelerates skin healing; it hasbeen proved to penetrate more easily when combined withmethionine. The post-peel mask contains a combination ofselenium and methionine, which improves healing afterlaser resurfacing or a peel, and prevents seborrheic der-matitis. Selenium is a component of glutathione peroxi-dase (GPX), an antioxidant enzyme that helps fight againstperoxidation. Selenium helps reduce inflammation by low-ering the number of hydroperoxide intermediates incyclooxygenase and lipoxygenase reactions. It prevents theproduction of inflammatory and immunosuppressivecytokines and stimulates cellular immunity as well ashumoral immunity. Combining it with vitamin E rein-

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

Vitamin ETocopheryl acetate is the most stable ester of vitamin E. Itis readily hydrolyzed by esterases into pure vitamin E afterit has been absorbed by the skin. The advantage of theacetate form is that it forms a reservoir that graduallyreleases the vitamin E inside the skin. Vitamin E scavengesfree radicals that could damage neighboring tissue. Itblocks oxidative chain reactions by inhibiting the forma-tion of lipoperoxides inside the cell, and in this way pro-tects the nucleic acids and proteins.

Propylene glycolA disinfectant, moisturizer and vitamin stabilizer, thisreduces corneocyte cohesion, enhancing penetration of theother active ingredients in the post-peel mask.

PhenoxyethanolAn antibacterial agent, this is used to disinfect wounds andburns.

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

Note The fact that the peel solution has been applied on the skinbeforehand has a significant effect on the rate of penetra-tion of the cream’s ingredients. The cream penetratesmuch more deeply after a peel than on untreated skin: theskin is far more permeable immediately after a peel; sebumand corneocytes no longer function as a barrier and thepurely water-soluble ingredients can penetrate the alteredepidermis rapidly. In this way, large quantities of stimu-lants and antioxidants can reach the dermis.

The post-peel mask has a pH of 6.5: it is not a neutralizingcream.

Base solutionETCA solution, reconstituted by the addition of acid, has apH <1, which is much lower than the solution’s pKa: it ismostly made up of free and potentially active acids.3 ItsTCA concentration is 15% m/m and also contains the fol-lowing ingredients:

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Ascorbic acidThis has an anti-free radical action and protects the solu-tion itself as well as the skin it is applied on. It is an acidify-ing agent and a buffer.

Citric acidThis evens out penetration of the ETCA. It is also an acidi-fier and a buffer with anti-free-radical properties.

Cocamide (coconut fatty acidmonoethanolamide)This protects the skin and improves the effectiveness of thesaponins.

Sodium laureth sulfateA surfactant, emulsifier and wetting agent, sodium laurethsulfate 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 excipientsSaponins are natural extracts known as glycosides that havespecial foaming and soapy properties. As a glycoside, asaponin may have binding properties for water in the skin.Some studies show that saponins have an antimicrobialeffect. They are also used to even out penetration of theacids through the skin and enhance skin healing.

IndicationsETCA has a very wide range of indications and depths ofaction, both for the face and the body.

Indications for basic protocolThese include comedonal, microcystic, papular and papu-lopustular acne, melasma, chloasma, post-inflammatoryhyperpigmentation, photoaging, smoker’s skin, fine lines,keratoses, and superficial solar lentigines.

ETCA can be applied to the face, hands, neck, décol-letage and body.

Indications for abrasive protocolThese include stretch marks, acne scars on the face andbody, keratosis pilaris, and badly damaged décolletage.

Indications for combinedprotocolsETCA 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 & Eye-

lid® formula� electric hair removal, skin cleaning, botulinum toxin,

wrinkle filling, minor surgery, coagulation of telangiec-tasias, mesotherapy, slimming diets (to stop the facesagging), etc.

� combinations with laser and flashlamps are not con-traindicated but should be judged case by case, depend-ing on the type of equipment used

Other protocols ETCA can be applied as a peel to the papillary dermis, whena sufficient number of coats are gradually applied to pro-duce even pink–white frosting and ‘epidermal sliding’. Theprotocol developed to treat stretch marks has sometimesalso been used successfully for facial rejuvenation.

Preparing the ETCA solutionThe base solution has to be activated by adding TCA at50% m/m. If the distributor cannot supply the 50% m/mTCA solution ready for use, the pharmacist should beasked to prepare the following TCA–SAS solution at 50%m/m.

TCA crystals 10 gdistilled water 10 gpf 20 g of TCA aqueous solution

In order to activate the peel,4 a precise quantity of this solu-tion 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 inadvance, should be kept in the fridge.

Details for preparing the 12-phialkit for 12 peelsThe procedure is illustrated in Figures 15.3–15.6. The solu-tion once made up cannot be kept, as it has been contami-nated by the cotton buds used to apply it on the patient’sskin. One phial therefore corresponds to one peel perpatient. This is the most hygienic method and avoids anyrisk of cross-contamination.


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

Figure 15.4 The contents of a phial of base solution are transferred into aglass container.

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

Figure 15.6 The TCA is added at 50% m/m to the base solution in theglass container.

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Preparing the peel solution in the24-peel kit In those countries where the solution comes in 2 bottles fortwo sets of 12 peels (Figure 15.7), the TCA must be injectedinto each bottle through the cap designed to this effect.Opening the bottle completely would accelerate oxidationof the solution.

After the TCA has been added, the doctor takes out thequantity of peel solution needed for each procedure (Table15.1), the mixture having been made for a total of 12 peels.

Preparing the patientAs a general rule, no skin preparation is necessary duringthe weeks preceding the peel or even immediately beforethe procedure itself. It is not necessary to clean or degreasethe skin, or to remove any make-up5 (except for imperme-able make-up with a silicone base). If the doctor wants, theskin can of course be cleaned carefully, without irritating itor increasing its permeability. Skin Tech’s pre-peel cleans-ing mousse is recommended, as it is not acidic and does notincrease skin permeability.

ApplicatorDifferent types of applicator can be used, but experienceshows that the best results are achieved using a double cot-ton bud (Figure 15.8). A single cotton bud cannot with-


Figure 15.7 Bottle of base solution. The 24-peel kit contains two identicalbottles: each bottle contains enough solution for 12 facialpeels.

Table 15.1 Volume of ETCA solution for onepeel (as a rough guide – see the differentprotocols for details)

Procedure Approximate volumes (ml)

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

Figure 15.8 A single cotton bud cannot withstand sufficient pressure.

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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 thecotton budsTwo cotton buds should be soaked in the ETCA solutionthat has been made up in the glass container (Figure 15.9).Any excess solution should be removed by squeezing out

the cotton buds on the rim of the glass container (Figure15.10).

Application sequence for eachcoatThe first coat of ETCA is applied in sequence on the face(Figure 15.11). This coat should be left to dry. If the appli-cation is even, following the recommendations describedabove, this first coat should not cause any problems. Itmust be allowed to dry completely before the second coat isapplied. The doctor applies the number of coats needed toproduce the first pinpoint frosting or, at the most, cloudy-white frosting. The number of coats necessary to producethe first pinpoint frosting depends on the skin type (Table15.2).7


Figure 15.9 Soaking the cotton buds.

Figure 15.10 Squeezing out the cotton buds.

Figure 15.11 (a–h) Application ofone coat of ETCA. Thepeel solution is appliedin sequence on theface following thenumbers shown in theimages. For eachdifferent number, thedouble cotton budsmust be soaked againin the peel solution.The eyelids are treated1 mm away from thelashes.

A B C D

E F G H

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Thin skin versus normal or thickskin

Easy way to determine the thickness ofthe skinIt is possible to determine the thickness of the skin by sim-ply ‘pinching’ the cheek, where the cheekbone is mostprominent (Table 15.3).

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


Table 15.2 Number of coats needed to achievepinpoint frosting (a rough guide )

Skin type Numberof coats

Thin skin 1 onlySkin treated with AHA, benzoyl peroxide, etc. 1 onlySkin treated with retinoic acid 1 onlyNormal skin 1–2 Thick and oily skin 2–4

Table 15.3 Thickness of pinched skin

Thickness (cm) Skin type

<1 Thin1 Normal>1 Thick

Figures 15.12 Pinpoint frosting.

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 Pinpoint frosting 4 peels: 1 per week peel reaches the basal layer

Basic protocol: removal of the Grenz zone. The Cloudy-white frosting 4 peels: 1 per week peel reaches the Grenz zone

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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If the pinpoint frosting occurs quickly (with very perme-able skin), the post-peel mask can be applied even if theacid has not completely dried.

If the pinpoint frosting appears slowly (with not verypermeable skin), the post-peel mask should be appliedafter the skin has completely dried out.

Potential depths of actionThe potential depths of action of ETCA are summarized inTable 15.4.

Applying the post-peel maskThe post-peel mask cream is not a neutralizing cream,9 andshould be used in specific quantities according to the indi-cations on the dosage card provided in the kit (Figure15.14). The kit for 12 peels contains three 10 g tubes of post-

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

Basic protocol: end ofapplicationThe peeling session is over after the post-peel mask creamhas been applied. The inflammatory reaction is beginning:therefore the production of oxidants must be stoppedquickly and the free radicals must be scavenged in order tobreak the vicious circle of self-perpetuating inflammation(see Chapter 5, p41). The post-peel mask cream reducesthe risk of complications. The ETCA solution has perme-abilized the skin: the components of the post-peel creamare rapidly absorbed and ready to act precisely where thefree radicals have been produced. It scavenges the free rad-icals in order to reap the benefits of inflammation (stimu-lation of the regeneration processes) but not thedisadvantages (uncontrolled and self-perpetuating inflam-


A

B

Figure 15.14 Dosage card from the ETCA kit. (a)One side of this card shows icons,beside each one of which thequantities of cream needed for eachzone are indicated: to treat the face,2 g are needed, while to treat theface and neck, 3 g are needed. (b)The lines on the other side of thecard help to dose the post-peelcream correctly: 1 line is equivalentto 0.5 g of post-peel cream (therefore2 lines = 1 g and 4 lines = 2 g).

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mation), which are the cause of most post-peel complica-tions. The patient should be warned not to wash the treatedarea until the next morning and to leave the post-peel maskto work for at least 12 hours. The next morning, the treatedarea should be washed with a mild soap or cleansing lotionand rinsed with water. No metal jewelry should be wornnext to the skin on the treated areas for 48 hours.

Post-peel tipsSun protectionMelablock HSP® 50+10 should be applied before the patientleaves the surgery, as the skin is very sensitive after the peel.

The day after the first peel, the patient must applyMelablock HSP® 50+ after putting on the prescribed dailycare cream and before putting on any make-up. For sunprotection to be effective, the cream must be reappliedevery 3 hours between peels and for the first few weeks afterthe last peel. Thereafter, the patient should use MelablockHSP® 25+ spray.

The patient should avoid exposure to direct sunlightboth in the course of treatment and for 6 weeks after thelast session.

If the skin is highly photoreactive or if the patient lives ina very sunny climate, Blending Bleaching® cream should beapplied twice a day from the day after the first peel. ETCAcan be applied in all seasons and on all skin phototypes.

Daily care routineThere is no need to know how to use many different cos-meceutical creams – fewer than 10 products are required to

cover the vast majority of cases treated in cosmetic medi-cine: aging, dyschromia, acne and sagging skin. Daily carecreams should be used from the day after the first ETCApeel. See Table 3.1 in Chapter 3 for details of the creamsrequired. These care creams have been specially formulatedfor 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 beenstudied during the inter- and post-peel periods. Applyingcosmetics that are not adapted for the post-peel period cancause fairly serious complications.

Obvious precautionsThe patient should avoid aggressive scratching or pickingat the flaking areas of skin, and should call the doctor withany questions or if they are in the least doubt.

Weekly repetition of ETCAThe basic ETCA protocol (basic protocol to achieve scat-tered pinpoint frosting) is repeated four times,11 at weeklyintervals for a facial peel and at 2-weekly intervals for abody peel. This repetition is in fact one of the peel’s built-in safety features; applying just one ETCA peel may not beenough and may cause complications.

Repetition of facial peelsA schematic illustration of the repetition of ETCA treat-ment for facial peels is shown in Figure 15.16. Eight days isthe average frequency: the outside limits are a minimum of5 days (if the condition of the skin allows) and a maximumof 15 days.

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

Repetition of abrasive protocolsAbrasive protocols are repeated once a month.

After four sessions,11 a rest period of 4– 6 weeks allows theskin to regenerate fully and the results to be improved ormaintained through the use of appropriate cosmeceuticals.

Abrasive protocols alter the reticular dermis and there-fore cause a definitive and irreversible skin reaction. Theresults achieved in each session can therefore be considereddefinitive, and the rest period of 4–6 weeks is a minimum.


Figure 15.15 A 10 g tube from the ETCA kit for 12 facial peels.

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

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

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

Maintaining results in the longtermETCA is more of a stimulating peel than a destructive one,and there is no risk of repeated peels making the skin lesscapable of regenerating in the future. One ‘regenerationcycle’ a year (four peels plus 6 weeks of post-peel care),combined with daily care creams, helps the skin stayhealthy in the long term. This is the technique pompouslyknown as ‘SYFE’ or ‘Stay Young For Ever’.

Treating photoaging andsmokers’ skin

Applying the peelThe ETCA basic protocol can be used to treat the visiblesigns of aging: dull, dry, wrinkled skin and uneven skintone. To combat the signs of photoaging, the basic protocolshould be followed, as described above.

Four (sometimes five) peels should be applied in all, atweekly intervals.


8 days 8 days8 days 6 weeks of regeneration

1stETCA

2ndETCA

3rdETCA

4thETCA

1stETCA

2ndETCA

3rdETCA

4thETCA

2 weeks 2 weeks 2 weeks 6 weeks of regeneration

Figure 15.16 Repetition of ETCA on the face.

Figure 15.17 Repetition of ETCA on body skin.

Daily care

Daily care

Daily care

8 days 8 days 8 days

1stETCA

2ndETCA

3rdETCA

4thETCA

1stETCA

1stETCA

2ndETCA

2ndETCA

3rdETCA

3rdETCA

4thETCA

4thETCA

8 days 8 days 8 days 8 days 8 days 8 days

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

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

Notes1. The breakdown of the corneodesmosomes has deeper reper-

cussions 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 aredifferent types of presentation kits (Classic kit for 12 peels,

Classic kit for 24 peels and Starter’s kit for 4 peels), and it ispreferable to refer to the information contained in each kit.

5. See the discussion at the start of Chapter 14 regarding differ-ences between ETCA and TCA–SAS peels.

6. Recall that the penetration depth of TCA also depends on thepressure with which it is applied: it is recommended to applythe same amount of pressure as when scratching.

7. This is why there is usually a lot of solution left when pin-point frosting appears. The volume of solution allowed for isto treat oily, thick and resistant skin.

8. With some protocols, it is recommended to produce cloudy-white frosting locally (see Chapters 16 and 22 on the treat-ment of melasma and entigines).

9. Some attempts to copy ETCA have been made, where aproduct illegally called ‘Easy Peel’ was brought out consist-ing of a TCA–SAS solution with a neutralizing base post-peelcream. The many complications that occurred after use ofthese copies led to them being dropped.

10. 50+ sun protection (EU standards) with induction of heat-shock protein synthesis. See Chapter 3.

11. Four times is, of course, an average. If the results are obvious,the treatment can be stopped after three sessions. If resultsare slow to appear and the skin is thick, up to six peels mightbe necessary.


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

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The histological features of melasma and chloasma are dis-cussed elsewhere in this book. The standard recommenda-tions for treatment often only mention topical applicationsof tretinoin, hydroquinone and other tyrosinase inhibitors;corticosteroids and peels are considered as a last resortbecause of their potential to turn melasma into post-inflam-matory hyperpigmentation (PIH). Conventional peelsrequire conscientious pre-peel preparation to avoid thisdanger. Easy TCA® (ETCA), in combination with appropri-ate post-peel care, can be used to treat melasma without theconstraints of pre-peel preparation (Figures 16.1–16.5).

Preparing the skinIt is not usually necessary to prepare the skin, but withlong-standing or resistant melasma or with a skin photo-type higher than Fitzpatrick IV, preparing the skin can beworthwhile and can improve results:

� Blending Bleaching® cream (see Chapter 3): appliedtwice a day on the melasma itself and once a day on therest of the face

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

16Treating melasma, chloasma and post-inflammatory hyperpigmentation

Figure 16.1 Melasma on the neck. The position might suggestpoikiloderma of Civatte, but there are neither telangiectasiasnor any atrophy of the skin around the follicle.

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

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

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Applying the peel solutionA first coat of ETCA solution is applied to the melasma andleft to dry completely (Figure 16.6). The desired endpointis cloudy pink–white frosting that is exactly the same shapeas the melasma plus 1 cm. If there is no frosting after thefirst coat, more coats of ETCA solution must be applieduntil cloudy pink–white frosting occurs. There is no setnumber of coats required, and there is no way of knowingin advance; each coat of ETCA solution must be left to drycompletely before applying the next coat if the skin has notfrosted sufficiently. More resistant skins only show cloudypink-white frosting after three or four coats.

Once localized cloudy frosting has been achieved on themelasma, the ETCA solution is applied to the whole facefollowing the instructions for the basic protocol: see above.

It is up to the doctor whether this last coat should goover the frosting on the melasma as well:

� If the frosting on the melasma is pink and even, withsome epidermal sliding,1 the ETCA solution should notbe applied there again.

� If the frosting is uneven, the ETCA solution can beapplied there again at the same time as it is beingapplied to the whole face.

The previous coat must be completely dry before anothercoat can be applied.

Applying the post-peel maskThe ETCA post-peel mask cream is applied to the wholeface, starting from the melasma. A little more of the post-peel mask is applied to the melasma itself.2 The compo-nents of the ETCA post-peel mask cream work directly andspecifically on pigmentation. If possible, the face shouldnot be washed until the following morning.

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

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

Daily post-peel carePost-peel care is essential to achieve optimum results andavoid complications.

Lightening creams (Blending Bleaching® cream: Box16.1) and sun protection (SPF 50+) should be applied fromthe morning after the first ETCA peel.

To boost the resultsBlending 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)


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

Figure 16.4

Figure 16.5

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Long-term maintenance (6months–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 edgeof the melasmaIn this case the pink-white frosting has not gone beyondthe edge of the melasma – it should go 1 cm beyond. Thepeel could not work on the melanin around the edges (Fig-ure 6.7).

Treating melasma, chloasma and PIH 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.

A B

C D

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 syn-thesis:vitamin E (tocopheryl acetate)

• Natural anti-inflammatory effect:Glycyrrhetinic acid: slows down degradation ofendogenous cortisol

Transcutol™• Concentrates the active ingredients near the

melanocytes

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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 melasmaimmediately after the post-peel mask cream, after everypeel, to reduce any inflammation.

� The use of 5% hydroquinone (and 0.05% tretinoin) incombination with the Blending Bleaching® creamshould be evaluated.

Slightly disappointing results� Another cycle of four ETCA peels should be started

after 6 weeks of Blending Bleaching® cream andMelablock HSP® 50+.

� Post-peel care: the doses and frequency of BlendingBleaching®cream and Melablock HSP® 50+ should beincreased.

Extremely disappointing results� Unideep® (pure white frosting) could be applied locally

on the melasma.

� ETCA should be applied to the rest of the face also.� Application of the following may be considered:

– a strong corticosteroid immediately after the post-peel mask cream– tretinoin 0.05–0.1%

Appearance of pigmentarychange after a few sessions� ETCA sessions should be continued until there is pin-

point frosting only� Blending Bleaching® cream should be applied every 3

hours, before sun protection and before the eveningmeal

� 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

ResistanceThe method of treatment should be changed.

Post-inflammatoryhyperpigmentation With a topical treatment alone, PIH usually has a goodprognosis. Blending Bleaching® cream or a prescriptioncream with hydroquinone and effective sun protectionshould be used. PIH tends to improve gradually and natu-rally, and disappears completely if it is not too severe andas long as the melanocytes are not stimulated by UV pho-tons.

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 ses-sions of ETCA following the same guidelines as formelasma treatment.

Notes1. Fine wrinkling of the skin when pinched: the acid coagulates

proteins that ensure cohesion between the dermis and epi-dermis, and the epidermis slides on the dermis to which it isno longer firmly attached.

2. The quantities of post-peel mask cream have been overesti-mated to allow for more cream to be applied in certain areas:each small tube contains 10 g of post-peel mask, and 8 g isenough to do four basic facial protocols.


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

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Treatment of comedonal acne1

Extraction of comedones (Figure17.1)After disinfecting the skin, the comedones are extractedusing a comedone extractor. The doctor will judge whetherhe prefers to extract all the comedones before the first ofthe four Easy TCA® (ETCA) peels or to extract only someof the comedones before each peel – patients usually preferthe second option as it is less aggressive.

Applying the peel solutionAs soon as the comedones have been removed, the ETCAsolution is applied following the basic protocol (Chapter15). The solution penetrates and disinfects the openingsleft by the comedones. This localized penetration has notbeen reported to have any negative effect.

The irritation caused by extracting the comedones can,however, cause the ETCA solution to penetrate moredeeply and produce ‘cloudy’ rather than ‘pinpoint’ frost-ing. To reduce the risk of cloudy frosting developing, thecotton buds should be squeezed out properly before apply-ing the ETCA solution.

17 Treating acne

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

A B

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Maintenance treatmentThe skin is cleansed once a month. The four ETCA peelsare repeated once a year. For daily care, see below.

Treating microcystic acne

Opening cysts and applying thepeel (Figure 17.2)The microcysts are opened and drained using the tip of aNo. 11 scalpel blade. The doctor can choose whether toopen all the microcysts before the first of the four ETCApeels or to extract some of them before each peel. Only theuppermost layers of the epidermis are cut; there is nobleeding, no pain and no scarring.

Applying the peel solutionAs soon as the microcysts have been opened, the ETCAsolution is applied to the whole face. The peel solution dis-infects the openings left by the microcysts, and may pene-trate inside them, causing more intense frosting locally.There is no danger, and the doctor can limit the penetra-tion 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 skinThe comedones and the cysts and whiteheads are opened(comedone extractor, No. 11 scalpel blade; see above). Thepapules should not be touched. The open pustules aredrained.

Applying the peel solutionThe basic ETCA protocol is used once again. More of theETCA solution will penetrate into the inflamed lesions,where the distension caused by the edema makes the stra-tum corneum more permeable.

To limit this penetration, the cotton buds should besqueezed out properly before applying the ETCA solution.

Each coat of ETCA solution should be left to dry outcompletely before applying another coat.

Care between and after peelsfor all types of acneCare creams (Box 17.1) should be used from the morningafter the first peel. The skin should be cleaned in the morn-ing 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 17.2 Micro cystic acne.

Figure 17.3 (a, b) Detail of the temple area of a young patient withpapulopustular acne treated with ETCA and Purifying® cream.

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Long-term maintenance treatmentThe oil-free gel Purigel® should be applied once or twice aday according to medical advice. The four ETCA peelingsessions are repeated once or twice a year.

Combined antibiotic treatment:The doctor decides if it is necessary to have combined med-ical treatment. For example, if the papular acne does notimprove after the first two sessions, they should be com-bined with 100 mg/day of minocycline.

Treating the side-effects ofacne� Post-acne pigmentation (Figure 17.5), on the face can

be treated in the same way as melasma, combiningETCA (basic protocol), Blending Bleaching® cream andsun protection (Melablock HSP® 25+ is sufficient).

� Post-acne pigmentation, on the décolletage can betreated in the same way, but there is also an abrasiveprotocol especially for the décolletage: abrasion plusocclusion of the post-peel mask without the applicationof acid (see Chapters 20 and 21).

� Post-acne pigmentation on the back does not respondreadily to ETCA alone. The protocol developed fortreating stretch marks produces excellent results, how-ever – not only on the residual pigmentation but also onthe depth of the acne scars.

� Facial acne scars can be treated by dermabrasion fol-lowed by peeling (see Chapter 21).

Potential problems during acnetreatment These are listed in Table 17.1, together with methods ofdealing with them.

General remarks on treatingacne with peels

Speed of resultsWhen treating acne, as with melasma, getting early results fastis a positive sign that could indicate excellent end-results. If

Treating acne 127

Box 17.1 Care creams during and after peels foracne

Purifying cream® (Skin Tech)

Glycolic acid (8%): softens the skin, prevents pores clog-ging up, stimulates epidermal turnover (pH 4)

Retinol: tretinoin precursor, helps drain the piloseba-ceous units

Vitamin E: tocopheryl acetate: anti-free-radical, breaksthe vicious circle of oxidation–inflammation

Triclosan: antiseptic, anti-inflammatory, antimycotic

Glycyrrhetinic acid: hydrates, antipruritic, anti-allergic

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

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

A

B

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the acne or melasma improves after the first session, thepatient can usually be guaranteed satisfactory and rapidresults. If, on the other hand, the situation has not started tochange after the second ETCA session, it is likely that resultswill be slow and only partial, and other treatments should becombined with the peels (antibiotics with acne and hydro-quinone with melasma). It is best to warn the patient, who willunderstand that the doctor is in full control of the treatment.

Treatment of acne must remainmultifocal� Normalize the rate of exfoliation/hyperkeratinization

by enhancing elimination of dead cells and hydratingthe skin properly: retinyl palmitate, glycolic acid andglycyrrhetinic acid.


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. 11scalpel blade

Too many comedones Extract them gradually – a few before each ETCA peel, instead of trying to removethem 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 theskin with Blending Bleaching® cream

Folliculitis barbae Unless it requires treatment with oral antibiotics, folliculitis of the beard can betreated in the following manner: Open the ‘whiteheads’ with the tip of the No. 11scalpel. Drain the infection by squeezing gently and disinfect the skin. Apply ETCA tothe 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. Theycan use the non-oily Purigel®

Figure 17.5Active 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 andazelaic acid.

� Help the pilosebaceous units drain: glycolic acid, lacticacid, retinyl palmitate, glycyrrhetinic acid and azelaicacid.

� Eliminate or reduce inflammation: tea tree oil, tri-closan, glycyrrhetinic acid and azelaic acid.

� Reduce sebum production: thiosome.

The protocols established for treating acne with ETCA inno way take away the doctor’s freedom to choose the treat-ment that is best for his patient based on his own knowl-edge and personal experience.

ETCA helps combat acne lesions by exfoliating the skinchemically and through use of the post-peel mask cream.Daily care helps maintain the results of dermatological orsystemic acne treatments. No peel can change the genetic

make-up of a particular skin or individual: applying an aciddoes not reduce androgen production or change the sensi-tivity of sebocyte membrane receptors or the strength of5α-reductase. The peel works on other parameters, such asintercorneocyte cohesion or unclogging the openings ofthe pilosebaceous units. Maintaining the results in the longterm depends on prolonged treatment with Purifying®cream, which should be applied twice a day, starting fromthe day after the first peel and continuing up to at least 6weeks after the last peel. Long-term maintenance of theresults sometimes requires continued use of Purifying®cream or Purigel®, for several months.

Note1. There are of course other treatments for acne. This book

only describes the use of peels in this indication.

Treating acne 129

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

Preparing the patient andscalpThirty minutes before the peel, the patient is given a para-cetamol (acetaminophen) plus codeine tablet or any otherrelatively strong analgesic. The skin is cleaned (Skin TechPre-peel cleanser®), rinsed and dried. It is then disinfectedwith alcohol and degreased with acetone, which are left toevaporate.1

Applying the peel solutionThe whole area should be treated, and not only the locallesions. A first coat of ETCA solution is applied to the

whole scalp and left to dry. The necessary number of coatsare then applied to achieve an even frosting of the skin. Thekeratoses are relatively impermeable to acids and, gener-ally, frosting is not strictly even (Figure 18.1). As soon asthere are signs of epidermal sliding, the frosting is sufficient(Figure 18.2) (see Chapter 14). The acid works by ‘under-mining’ – going underneath the keratosis. Each coat is leftto dry before applying the next one. Up to five coats aresometimes required.

Other peels can be used, depending on the case beingtreated. Unideep® is also indicated for the treatment of ker-atoses on the scalp: the Unideep® solution produces evenfrosting more rapidly. Only Touch® can be used in combi-nation with a more superficial ETCA peel (cloudy-whitefrosting instead of even white frosting) on isolated ker-atoses on the scalp.

Local anesthesia of the scalpIf the doctor thinks that more than three coats will be nec-essary, nerve blocks should be applied to the front and backof the scalp.

18Treating multiple keratoses on the scalp

Figure 18.1 Frosting – considered to be even because of the large numberof keratoses.

Figure 18.2 Epidermal sliding: this appears when the skin is pinched aftera peel to the papillary dermis.

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Anterior and lateral regions ofthe scalpThe anterior half of the scalp is innervated by the frontalnerve. In its intraorbital journey, this nerve divides into theinternal and external frontal nerves. The nerve branchesemerge from the supraorbital foramen and innervate thefront of the skull after traveling vertically upwards. Block-ing these nerve branches anesthetizes the forehead as wellas 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 thefrontal nerve, but by branches of the lesser cervical plexusor the auriculotemporal nerve.

Posterior and vertex of thescalpThe posterior region of the scalp that concerns us is inner-vated by the occipital nerve of Arnold, which is easilyblocked by an injection of 2% lidocaine with adrenaline(epinephrine).

The vertex of the scalp is innervated by all the nerve end-ings that sensitize the skull. This region is therefore some-times difficult to anesthetize completely without doing afull circular nerve block of the scalp.

If the doctor does not want to perform nerve blocks, or ifthey are inadequate for more sensitive patients, he can also doa tracer injection, 1 cm beyond the outside edge of the zoneto be treated and a ring block on the whole area to be peeled.

Ventilation or cooling (3M Cold Pack®) can help easethe pain of the acid.

Post-peel developments andcare (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 appliedto help the flaking as soon as it starts. Effective sun protec-tion is essential, as well as keeping out of the sun.

The treatment is repeated four times at 2-weekly inter-vals, if flaking has finished.

Results can be maintained in the long term with a com-bination 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 ofthe acid solutionGentle abrasion with sandpaper or intraepidermal erbiumlaser treatment help accelerate penetration of the ETCAsolution considerably. When sandpaper abrasion is used, atopical anesthetic should be applied (a swab with 2% lido-caine with adrenaline (epinephrine)) after the abrasion,before applying the acid. With an erbium laser, a nerveblock or ring block is necessary.

Relative impermeability ofkeratosesKeratoses are relatively impermeable, and the acid needsmore time to get through them: patience is required, andfrosting is (much) slower to appear. Enough ETCA solu-tion has been applied when the skin immediately sur-rounding the keratosis has frosted.

How to determine the totalnumber of coats requiredWhen the skin around the keratosis turns pink–white, itmeans that a sufficient number of coats has been applied.When the skin on the scalp is pinched between two fingersand 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 Blending Bleaching® cream every 3 hourshyperpigmentation during treatment; then twice a day for 3 months

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

Post-peel painThe pain felt after a peel is bearable, but the patient can bemade more comfortable if prescribed a medium-strength

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

ExampleFigure 18.3 shows an example of a scalp treated with ETCApeels.

Treating multiple keratoses on the scalp 133

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) Ayear after treatment: maintenance with topical 0.05% tretinoin.

A

B

C

D

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Note1. This is an exception to the normal procedure in the use of

ETCA: the skin on the scalp has to be disinfected anddegreased because it is much thicker and oilier than the skinon the face; the treatment has to reach the papillary dermis.


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The forearms and hands are treated in the same way.

Aging of the handsOver the last decade or so, facial rejuvenation treatmentshave been developed and refined. Major technical advanceshave changed the face of surgery as well as peeling and der-mal filling techniques. The results of these treatments lookmore and more natural. Surgical scars, less visible nowthan they were in the past, can be softened even more byusing peels or laser treatment after surgery. The blade hasmore respect for the architecture of the face, peels canmaintain it perfectly well, and dermal filling techniques caneven improve it. Cosmetic medicine helps to hide imper-fections that cannot be put right by other means. The use ofgentler or less aggressive techniques has drastically reducedthe risk of permanent complications. In short, nowadays, aperson’s age is not written on their face, and patients whoare properly treated can easily claim to be 15 years youngerthan they really are. The risk of this little white lie beingfound out is minimal – on condition that the person doingthe guessing only looks at the face. The quality of the skinon the neck and décolletage is often still a sure sign of timespent in the sun or on a tanning bed. Surgery can of courseimprove the tension of the skin on the neck, but only cer-tain peels can improve the quality of the skin or make a tell-tale décolletage look younger. Even if the rightcombination of the most appropriate techniques has beenused to excellent effect and a patient’s face, neck and décol-letage do not show their real age, there is still one impor-tant area that can give the game away: the hands. They areoften the weakest link in the treatment chain, a telltale signof a patient’s real age and the fact that she or her has hadother treatments. There are always mittens, of course, butwho wears those nowadays?

If you look at a patient’s hands, you notice that they startaging 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 skindehydrates and starts to wither. Between the ages of 40 and50, the patches of hyperpigmentation grow and solar ker-atoses may start appearing. Between 50 and 70, in parallelwith a decline in sex hormone production (more gradual inmen 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 outthrough the thinned epidermis.

Very old hands are typically arthritic, atrophic (espe-cially in women), dehydrated and covered in hyperchromicpatches and hyperkeratoses. The often fragile capillarieseasily cause bruising. Friction wounds are more frequentand more spectacular, as the dermal papillae are no longeras deep and the epidermis is not held as tightly to the der-mis. Our calendar age is not the only thing responsible forthe aging process, and we are ourselves directly responsiblefor several contributing factors: smoking, for example,either through vasoconstriction immediately after smokehas been inhaled or through excessive production of freeradicals in the body, is one of the major causes of aging thatmight well be termed autogenous as it is directly linked tothe behavior of the individual.

Avoiding repeated traumas, a balanced diet of vitamins,antioxidants and fatty acids, keeping out of the sun, andgood hormone levels all play an important preventive role inkeeping the hands looking young. But what can we do whenthe damage is done, when the signs of aging are obvious anda patient wants to have younger-looking hands? What can bedone to slow down the aging process once it has started?There is a 10-year age difference between the hands of thepatients shown in Figure 19.1: the patient in (a) started themenopause and estrogen–progesterone hormone replace-ment 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 muscleatrophy are clearly visible, and 10 years of (southern) sun ontop have also left their mark on the skin.

19Treating aging of the hands and forearms

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Treatment of photoagingwithout lentiginesSometimes, all that is needed for the skin on the hands is torebuild the dermis and epidermis. This type of skin regener-ation is perfectly suited to Easy TCA® (ETCA): two exam-ples of this treatment are shown in Figures 19.2 and 19.3.

Applying the peelAll jewelry should be removed. Without disinfection ordegreasing of the skin, three successive coats of ETCA solu-

tion are applied to the hands. Do not try to achieve frost-ing. Each coat should be left to dry completely beforeapplying the next. If cloudy frosting appears after the firstor 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-peelmask cream is applied using the quantities indicated on thedosage card, and is left to work until the following morn-ing.

Flaking often occurs after at least 1 week and lastsaround 4–5 days. The treatment is repeated four times, at2-week intervals, unless the skin has not finished flaking.


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

A

B

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

A B

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

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

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

Treating aging of the hands and forearms 137

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

A

B

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

C

A

B

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Combined aging of the handsThe hands have aged completely when superficial photoag-ing and solar lentigines are combined with atrophy of theinteguments, subcutaneous tissue, muscles and bones.Peels do not correct hormone-induced atrophy, and oftenthe only option is fat transfer combined with chemicalpeels (Figures 19.6 and 19.7).


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 scabshave gone.

A

B

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

A

C

B

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Flat wartsThe hands of pre-menopausal patients do not show anysigns of atrophic aging, but too much sun produces awhole range of spots, sessile tumors, flat warts andsolar keratoses. Small flat warts can be treated success-

fully with Only Touch® combined with ETCA (Figure19.8).

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-fre-quency shaving.

Treating aging of the hands and forearms 139

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

A B

C

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Maintaining the results in thelong termResults can be maintained in the long term by using appro-priate daily care and repeating the peels once a year.

Notes1. I shall make no comment on the validity of this type of

replacement therapy.2. See Chapter 3. DHEA-Phyto® cream (in the morning) and

Renutriv ACE Lipoic Complex® (in the evening) are partic-ularly effective on the hands.


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

A B

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

Slightly sun-damaged neckand/or décolletage (Figure20.1)The décolletage is usually treated at the same time as theface and neck. It does not really matter which order theseareas are treated in, other than out of consideration for thepatient’s comfort, as treating the décolletage is usually lesspainful than the face. The basic protocol for Easy TCA®(ETCA) should be used.1 The peel should be repeated fourtimes at weekly intervals on the face and at 2-weekly inter-vals on the neck and décolletage, which take twice as longto flake as the face.

Moderately sun-damaged neckand/or décolletage (Figure20.2)A moderately damaged décolletage should be treated moreaggressively than a slightly damaged décolletage. TheETCA is applied to the décolletage and neck until cloudy-white frosting appears and is followed by the post-peelmask. 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® andETCA (see Chapter 22). Regular maintenance treatment aswell as sun protection are essential to avoid recurrence orthe appearance of new lentigines.

20Treating the neck and décolletage

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.

A B

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

protocol, to avoid acid penetrating too deeply and poten-tially causing scars.

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


Figure 20.2 Only the top part of the décolletage has been treated withtwo sessions of four ETCA peels: there is a noticeableimprovement in the texture of the skin in the treated area.

Figure 20.3 Treatment of lentigines on the hands and décolletage withOnly Touch® plus ETCA.

A B

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

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Treating the neck and décolletage 143

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 ofdécolletage photo aging with Unideep® (TCA peel to the papillary dermis). Endpoint of the treatment and application of the postpeel mask; (e) skin desquamation of décolletage at day 3 after papillary dermis peeling Unideep®.

A

C

D

B E

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Repeating peels on thedécolletageETCA (pinpoint or cloudy-white frosting) can be repeatedevery 2 weeks on the décolletage. Unideep® can be repeatedafter approximately 4 weeks. For Only Touch®, see Figure15.18 in Chapter 15.

The abrasive protocol can be repeated after about 4weeks.

Care between and after peelsOn the day after the first peel, patients should start usingsun protection SPF 50+ and a care cream appropriate fortheir condition: see Table 3.1 in Chapter 3. Post-peel care isessential to maintain results in the long term.

A follow-up peeling session should be planned for oncea year.

Note1. Treatment should be stopped when pinpoint frosting has

been achieved (see Chapter 15).


Figure 20.6 Daily care is as follows: on days 1-6, Renutriv ACE LipoicComplex®; on days 6 and 7, sterile white Vaseline®. Thephotograph shows the results after 8 days.

Figure 20.7 Unideep®: results after 12 days. Sun protection SPF 50+ anddaily care are essential to maintain the results in the longterm.

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General remarksStretch marks, acne scars on the back and severe photoag-ing on the décolletage are three common problems, andtreatment results were disappointing in the past. The doc-tor would be disappointed at having to refuse treatmentand admit to being powerless to help. In some cases wheretreatment was not refused, the doctor might end up regret-ting having used inappropriate techniques and having todeal with the resulting complications. Patients, for theirpart, would suffer from their doctor’s refusal to treat them,which meant having to put off indefinitely the blessed daywhen their problems might improve.

Origins of the treatmentThe high level of safety and effectiveness met with whenfirst using the Easy TCA® (ETCA) peel led me to developsome effective application protocols for the treatment ofstretch marks and scars. ETCA had proved effective in var-ious areas, including acne, hyperchromia and skin aging,both on the face and on other parts of the body. ETCA con-sists of an acid solution and an active post-peel cream thatthe doctor applies to the treated area immediately after theacid solution has produced pinpoint or cloudy-white frost-ing and that is then left to work until the following morn-ing. The active ingredients in the acid solution are citricacid, ascorbic acid, trichloroacetic acid (TCA), saponinsand excipients. The basic protocol provides a peel to thebasal layer of the epidermis or the Grenz zone. The post-peel cream is not a neutralizing cream, but, on the con-trary, an active cream with a high concentration ofvitamins C, E and H, tretinoin precursors, phytic acid,anti-free-radical agents, selenium, methionine, tyrosinaseinhibitors, trace elements, fatty acids, and various plantextracts. This cream is used to provide a strong stimulus tothe dermis, epidermis and regeneration processes and toprotect against complications. Unlike a conventional TCApeel, the ETCA basic protocol does not use the acid solu-

tion to destroy the skin, but rather to make it more perme-able for the post-peel cream to penetrate and take effect.

The cosmetic problems dealt with in this chapter, how-ever, do not respond well to chemical peels, even whenthey reach the papillary dermis. In an attempt to achievebetter results, deeper peel procedures were tried that wentas far as the reticular dermis. The peels were in fact dan-gerous at this depth; the reasons for this are discussed inChapter 37.

Other authors have suggested using a combined tech-nique of chemical peeling and dermabrasion, but always inthe order of a peel followed by dermabrasion. This tech-nique is known as ‘chemabrasion’. We could use the term‘post-chemabrasion’ for a peel followed by dermabrasion,and ‘pre-chemabrasion’, the technique described in thischapter, for dermabrasion followed by a peel, in order todistinguish between the two techniques.

The treatment that I developed consists in using evensuperficial dermabrasion followed, in some cases, by ETCAacid solution and post-peel cream. Applying the creamunder occlusion deepens the treatment, and the longer theocclusion is left, the deeper the treatment will be. Repeatingthe peels allows the epidermis to renew itself gradually (achemical resurfacing effect) at the same time as ‘filling’ thedermis with fibroblast products, the fibroblasts havingbeen stimulated by the treatment. Internal and gradualretraction reduces the width of the stretch marks (a fill-ing–shrinking effect).

The combination of sandpaper abrasion, with or with-out the application of the acid solution and occlusion of theETCA post-peel cream,1 allows a whole range of differentdepths of action.

Classification of stretch marksThe Deprez–Adato classification2 is based on the clinicalappearance of the stretch marks (Table 21.1). Stretchmarks in stages 2B to 4 seem to respond best to this treat-ment.

21Stretch marks and scars: dermabrasion andpeeling

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Equipment needed for theabrasive protocolThe sandpaper abrasion kit consists of 10 sheets of single-use sandpaper (3M Wet-or-Dry® P220) sterilized3 withgamma rays and a yellow disinfecting and healing powder:bismuth subgallate.

Mechanism of action of thetechniqueThe mechanism of action could be as follows: the sand-paper abrasion and acid have a synergistic effect of physi-cal and chemical resurfacing that improves the quality ofthe entire epidermis (Figure 21.1). When the post-peelcream penetrates the atrophic base of the stretch marks, itcauses inflammation (controlled by the antioxidants) thatstimulates fibroblast proliferation and metabolic produc-tion of the non-cellular components of the dermis (Figure21.2).

At the same time, the depth of injury to the skin couldstimulate deep myofibroblast contraction and improveskin tension, as has been observed clinically after treat-ment.

AbrasionThe whole area – not only the atrophic base of the stretchmarks – must be abraded. Other techniques (laser andmicrodermabrasion) have failed because they tend only tostimulate the atrophic base of the stretch marks, wherethere are very few keratinocytes capable of proliferatingand very few fibroblasts available to fill the dermis. Sand-paper abrasion produces even, physical resurfacing, level-ing the skin and stimulating the healthy skin between thestretch marks to regenerate. The inflammatory reactioncaused by the treatment stimulates the growth of healthykeratinocytes on the edge of the stretch marks. As thesekeratinocytes are stimulated, the epidermis can graduallyrebuild in a clinically visible way.


Table 21.1 Deprez-Adato classification of stretch marks

Stage 1 Inflammatory New, developing stretch marksStage 2A Ladder rungs (–) Non-palpable depression Superficial, white stretch marksStage 2B Palpable depressionStage 3A Ladder rungs (+) <1 cm wide Atrophic stretch marksStage 3B <1 cm wide Atrophic pearly white stretch marksStage 4 Ladder rungs (++) >1 cm wide Atrophic pearly white stretch marks

Figure 21.1 The abrasion and acid resurface the normal skin surroundingthe atrophic base of the stretch marks both physically andchemically.

Figure 21.2 Occlusion of the post-peel mask cream, on the other hand,causes severe inflammation of the dermis at the atrophicbase of the stretch marks.

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Peel solutionWith the help of pre-peel abrasion, the ETCA solutionrapidly penetrates to the papillary dermis and provideschemical resurfacing on top of the physical resurfacing ofthe abrasion itself. The combined physical and chemicaleffect accelerates stimulation of keratinocyte growth on theedges of the stretch marks. The subsequent occlusion doesnot deepen the action of the ETCA. We have seen else-where in this book that occluding TCA tends instead tosoften the effect of the TCA.

Post-peel cream under occlusionThe mechanism of action of the post-peel mask cream,under occlusion, is less easy to understand. This antioxi-dant and anti-inflammatory cream4 immediately stops theburning sensation and the inflammation caused by the acidduring an ETCA peel (standard use as a peel to the basallayer or Grenz zone5), but when it is used under occlusionin the treatment of stretch marks, it appears to be responsi-ble for the depth of the treatment. Clinically, it is plain tosee that the longer the occlusion is left in place,6 the deeperis the treatment.2 We have also already seen that the post-peel mask cream can be applied without the acid solutionafter sandpaper abrasion and can deepen the treatment sig-nificantly, liquefying the skin under occlusion in the sameway as phenol does (see the section later in this chapter ontreating the décolletage).

Sequenced photographs of the treatment show that thepost-peel mask cream penetrates more readily through theatrophic base of the stretch marks after abrasion and appli-cation of the ETCA acid solution. Here, it causes inflam-mation, which triggers regeneration, and it appears to belimited to this area. The large majority of signs of activeinflammation disappear very quickly, in around 2–3 days,but a non-irritative edema can persist for around 15 days atthe base of the stretch marks.

Bismuth subgallateBismuth subgallate (BSG) is a yellow powder that makespost-peel care easier and spares patients having to applycomplicated localized treatments themselves, which couldcause infection (see also Chapter 34). A generous amountof BSG is sprinkled directly onto the moist areas of skinwhere the epidermis has been destroyed. It can also bespread on with a gloved hand or sterile swab.

Post-peel care has become much easier of late. The BSGis covered with a silicone sheet, such as Mepitel®, which isin turn coated in a thin layer of neutral, sterile Vaseline®and protected by a thick absorbent dressing that is held inplace in a way that is comfortable for the patient. On thethird day, the silicone sheet is carefully cleaned and putback in place. It is again coated in a thin layer of Vaseline®

to prevent it sticking to the outer, absorbent dressing. Thedressing is removed for the last time around 6 days after thetreatment (see below for details).

The abrasion procedure is summarized in Box 21.1.

Three treatment possibilitiesafter abrasionThere 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 isused in rejuvenation treatments and in the treatment ofacne scars on the décolletage.

� In the deepest protocol, after abrasion and applicationof the ETCA solution, the post-peel mask cream isapplied under occlusion. This is the protocol used totreat stretch marks and surgical scars, when the skinneeds tightening.

Origin of stretch marksStretch marks may result from the following, among otherfactors:

� 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.

Stretch marks and scars: dermabrasion and peeling 147

Box 21.1 Summary of abrasion

The abrasion is carried out with 3M Wet-or-Dry® sand-paper, P220, sterilized with gamma rays. It should begentle, steady, careful and even (intersect each pass)and be stopped as soon as the patient feels pain.

The ‘keratinocyte touch’ should be positive: a glovedfinger slides easily over the corneocytes (dead cells)that are still present in the area surrounding theabraded zone, but ‘brakes’ on the hydrated ker-atinocytes (stratum spinosum) that have been laidbare by the sandpaper. The first appearance of pin-point bleeding signals that the sandpaper has reachedthe basal layer. Abrasion that goes any deeper cancause permanent complications.

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Position of stretch marksFigure 21.3 is a schematic illustration of the locations ofstretch marks and the areas treated with ETCA/abrasion.

Summary of stretch-marktreatmentsTable 21.1 provides a summary of treatments for stretchmarks (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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Preparing the patientThe patient is prepared psychologically: they are informedin detail about the treatment, developments and possiblerisks. Preparing the skin for 3–4 weeks before treatmenttends to limit the risk of pigmentary changes, which arecommon after this treatment. The stretch-mark treatmentcauses severe inflammation and tends to stimulatemelanocytes, albeit only temporarily. Phototypes I–III canbe treated without preparation, but patients with a higherskin phototype must apply effective sun protection andBlending Bleaching® cream twice a day, especially if theylive in a country with a very sunny climate (see Chapter 2).Applying products that stimulate synthesis of heat-shockproteins (HSP) helps all cells to resist this type of stress (seeChapter 2). Preparing patients also involves getting themto sign an informed consent form, explaining how thetreatment and post-peel care will proceed, and giving thema paracetamol (acetaminophen) plus codeine tablet 30minutes before treatment and 2 hours after treatment.

Disinfection and degreasingThe doctor’s hands must be washed surgically or sterilegloves should be worn.

The patient’s skin is disinfected with alcohol (75° alcoholand sterile gauze – firm pressure should be applied on thegauze) and degreased with acetone (pure acetone and ster-ile gauze – firm pressure should be applied on the gauze).

The acetone starts to break down the membrane phos-pholipids. It makes no difference clinically which order thealcohol and acetone are applied in, but both products needto be applied several times.

Sandpaper must be sterilized, ideally with gamma rays.7

Determining the ideal depth ofabrasionWearing gloves, the doctor rolls a sheet of sandpaperaround a round object (e.g. a bottle of pre-peel cleanser).The skin is held taut with one hand, and intersecting, care-ful, gentle and repeated passes are made with the sandpa-per. Pressure must be firm and even. If the pressure is toolight,8 the skin will not be abraded properly. On the otherhand, if the pressure is too firm, it will take off more skinand make it too permeable.

When done correctly, the sandpaper abrasion graduallypermeabilizes the skin, is not painful at first and is there-fore done without anesthetic. The depth can be classified infour different grades (Figure 21.4).

Grade 0 sandpaper abrasion� Subjectively: the patient feels almost nothing.� Objectively: the fingers slide easily over the superficial

layers of corneocytes: the ‘keratinocyte touch’ is nega-tive.


Figure 21.3 Picture used to take note of the general position of stretchmarks and the areas treated with ETCA/abrasion.

0IIIIII

Figure 21.4Sandpaper abrasion: grades 0–III.

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Table 21.1 Summary of stretch-mark treatments

Pre-peel • Phototype I-III: Blending Bleaching® 1 week before30–60 mins before • Phototype IV-V: Blending Bleaching® 3 weeks beforeabrasion • Give the patient a paracetamol (acetaminophen) + codeine tablet

• Disinfect and degrease the skin

Abrasion (depth?) • Too superficial: no pinpoint bleeding – no pain The sandpaper can be found • Right depth: first pinpoint bleeding – first pain – K touch in Skin Tech’s Abrasion Kit• Too deep: a lot of bleeding – very painful

Abrasion depth check: pain + pinpoint bleeding + keratinocyte touch (K touch)

Anesthetic 2% lidocaine with adrenaline (epinephrine) on gauze pad+ No EMLA creamplastic film 15 min

ETCA solution • Right depth: even pink–white frosting Acid or no acid?(how many coats?) • Too deep: pure white frosting (décolletage, breast, ... )

Post-peel mask 0.5 g/10 cm × 10 cm area

Occlusion duration • Superficial treatment: 6–8 hours Occlusion or no occlusion?• Medium treatment: 8–16 hours (back, breast ... )• Deep treatment: 16–24 hours

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 • Take paracetamol if painful• Gently cleanse with a dry gauze • No showers, no baths, no scratching• Apply BSG: thick coat to dry the skin • No sports, no swimming• (BSG powder can be found in Skin Tech’s • Keep out of the sun (be careful, the sun can filter • Abrasion Kit) • through clothes)• Apply a silicone sheet coated in Vaseline® to cover • the BSG (see Figure 37.45)• Protect with a thick gauze

Between days 1 and 2: take paracetamol(acetaminophen) if painful

Day 3: • Change dressing • No showers, no baths, no scratching• Clean the silicone sheet and reapply the dressing • No sports, no swimming• as on day 1, without adding any more BSG • Keep out of the sun (be careful, the sun can filter • Avoid infection; administer antibiotics if necessary • through clothes)

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: • Moisturize, protect, prevent PIH • 08.00: Blending Bleaching® cream followed by • Prevent prolonged erythema: if erythema + 2 • Melablock HSP® (even if no sun exposure)• weeks, treatment with 1 week fluorinated corticosteroid • 12.00: Blending Bleaching® cream followed by • Prevent PIH: Blending Bleaching® cream should be • Melablock HSP® (even if no sun exposure)• used before PIH begins, from day 8 Melablock HSP® • 17:00: Renutriv ACE Lipoic Complex®• SPF50+ (sun protection cream)•• Prevent infection: administer antibiotics if necessary • 20:00: Renutriv ACE Lipoic Complex® + DHEA • Prevent scratching: • Phyto® cream• – if skin is very dry: Vaseline® • Call the doctor with any questions or problems • – If skin is dry: Vit E Antioxidant® cream • such as pain, temperature, itching, redness• Check patient every week: • Baths/showers are not allowed until the skin is • – If PIH begins, even out with Blending Bleaching® and • completely healed (average day 7–8)• Melablock® HSP • Sports allowed from day 10–15

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This depth of abrasion provides only low-quality topicalanesthesia and the peel itself will be painful and too super-ficial.

Grade I abrasion� Subjectively: the abrasion feels unpleasant, but still pain-

less to the patient, as the sandpaper is still a long wayfrom the free nerve endings that are in the lower part ofthe epidermis.

� Objectively: the ‘keratinocyte touch’ is still negative –although the fingers can be felt to brake slightly as theyslide from the healthy zone to the abraded zone, theystill slide easily over the skin. Grade 1 sandpaper abra-sion does not provide adequate topical anesthesia, andthe peel is still painful and too superficial.

Grade II abrasionThis is the correct level for effective abrasion combinedwith this peel.

� Subjectively: the patient starts to feel pain from thesandpaper abrasion. Usually the abrasion should bestopped here, but the pain thresholds vary from patientto patient. It is therefore essential to look out for theobjective signs.

� Objectively: The ‘keratinocyte touch’ is positive – thefinger feels a marked braking sensation as it passes fromthe slippery dehydrated corneocytes of the non-abradedsurrounding skin to the living, well-hydrated ker-atinocytes exposed by the abrasion. The first pinpointbleeding appears on the skin as the ‘highest’ dermalpapillae, where the blood vessels of the papillary dermisare located, are abraded (Figure 21.5).

Topical anesthesia will be of good quality, and the peel willreach the required depth.

Grade III abrasion� Subjectively: the patient usually finds the abrasion very

painful, even unbearable, and will let the doctor knowthis – the abrasion is going into the papillary dermis,and care must be taken!

� Objectively: there is a lot of pinpoint bleeding as theloops of blood vessels in the dermal papillae are nowbeing abraded (Figure 21.6). Abrasion must be stopped.If it were to continue, the pinpoint bleeding wouldincrease rapidly and appear as extensive surface bleed-ing.

Topical anesthesia under these conditions would be rapidand of good quality, but the peel would be too deep andtrigger permanent side-effects such as achromia and/orhyperpigmentation and/or scarring.


Table 21.1 continued

– If necessary add hydroquinone 4–5% to the • Sun not allowed for 3 months: sun protection for Blending Bleaching® • 3 months (Melablock HSP® 50 or 25)

– Maybe do ETCA peel on area with PIH

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® andMelablock HSP®

For updates go to http://www.estetik.com-Treatment Tips.

Figure 21.5Pinpoint bleeding – grade II abrasion. The arrows indicatethe first pinpoint bleeding. This depth of abrasion is ideal forthis treatment: it gives the right anesthesia and depth ofaction.

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Other abrasion techniquesOther abrasion techniques have been tried, depending onthe doctor’s experience and the equipment available:

� microdermabrasion: it is impossible to get the microscop-ically even abrasion obtained with sandpaper; the corun-dum crystals also have to be cleaned after abrasion.

� erbium laser: it is also possible to use laser abrasion aftera local anesthetic, but this technique takes much longer,and is more difficult and more expensive; it has noadditional advantages.

The sandpaper abrasion technique has the advantage ofbeing even over the whole area, and is cheap, fast and inex-pensive.

Three signs that guide abrasion1. PainIf the abrasion is completely painless, it has only reachedthe stratum corneum. When it goes deeper and the sandpa-per comes into contact with the keratinocytes, it is uncom-fortable but not yet painful, as the upper layers ofkeratinocytes are not directly innervated.

When the patient says that the abrasion feels uncomfort-able but not painful, the doctor must pay very carefulattention, as it will become painful at any moment whenthe sandpaper gets closer to the free sensitive nerve endingsin the deeper layers of the epidermis. Abrasion usuallybecomes painful when it reaches the keratinocytes next to

the basal layer of the epidermis. Sensitivity varies frompatient to patient, and other objective signs, discussedbelow, must be taken into account.

The doctor should nevertheless ask patients to describethe pain they feel:

� No feeling: the depth is assumed to have reached thestratum corneum.

� Uncomfortable but not really painful: the depth isassumed to have reached the keratinocytes.

� First pain felt: the depth is assumed to be close to thebasal layer – stop abrasion!

� Very painful: abrasion is definitely too deep or thepatient is squeamish.

With a squeamish patient, before applying the acid, thedoctor must check the anesthetic for effectiveness. Whenthe abrasion is too deep (grade III), the doctor must moni-tor carefully how much acid is applied to the skin so as notto go beyond even pink–white frosting (see below).

2. Keratinocyte touch When sliding the fingers (even with gloves on) from a non-abraded area to an area that has been abraded, there shouldbe a braking sensation if the abrasion has reached the rightdepth.

3. BleedingIf there is no pinpoint bleeding (grade I abrasion), thetreatment is not deep enough. If there is too much pinpointbleeding (grade III abrasion) or surface bleeding, there is arisk that the peel will be too deep and cause permanentcomplications.

Topical surface anesthesiaApplying ETCA solution immediately after abrasion wouldbe extremely painful without an anesthetic. There are sev-eral different types of anesthesia to be considered:

� EMLA cream or other topical anesthetic cream: as pointedout in Chapter 33, EMLA cream should not be appliedbefore a peel. For the same reasons, topical anestheticcreams should not be used before applying ETCA forstretch marks.

� Anesthesia with lidocaine spray: lidocaine spray containsalcohol and is very painful on abraded skin.

� Klein solution: injections of Klein solution have beentested, but the results are unsatisfactory: it anesthetizesthe deeper layers not reached by the acid, but the sur-face anesthetic effect remains largely inadequate.

� Topical application of 2% lidocaine solution with adrena-line (epinephrine), poured directly onto sterile gauze


Figure 21.6Pinpoint bleeding – grade III abrasion. Contact anesthesia willbe just right, but there is a risk that the peel will be toodeep. Care must be taken over how much acid is applied tothe skin, in order to avoid complications such as scarringand/or pigmentary changes.

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pads on the skin, provides an excellent anesthetic (Fig-ure 21.7a). One percent lidocaine is not effectiveenough. Lidocaine without adrenaline is rapidly reab-sorbed, and its effect is too short-lived after epidermalabrasion. Two percent lidocaine with adrenaline shouldbe covered with an impermeable plastic film for 10–15minutes to stop it evaporating too quickly and toenhance its effect (Figure 21.7b).

Checking the effectiveness of thetopical anestheticAfter 10–15 minutes’ occlusion, the lidocaine–adrenalinesolution has penetrated the skin and reached the epider-mis: the adrenaline induces vasoconstriction. Uniformvasoconstriction is a sign that the local anesthetic hasworked. Applying a single 5 cm ‘line’ of ETCA peel solu-tion with a cotton bud is enough to test the patient’s sensi-tivity. If the patient feels no pain at all where the acid hasbeen applied, the ETCA solution can be applied to thewhole area to be treated.

If the patient still feels some pain, the doctor shouldreplace the occlusion for another 5 minutes.

Applying the ETCA solutionThe plastic film from the anesthesia is gradually lifted, theskin is dried and the ETCA solution is applied with a dou-ble cotton bud until pink-white frosting, never pure whitefrosting, occurs (Figure 21.8).

The first coat of ETCA solution may cause linear anduneven frosting, as can be seen in Figure 21.9. This applica-tion is not perfect, and more ETCA solution should beapplied between the lines of frosting to even it out. In somecases, the first coat of ETCA solution does not trigger anyfrosting, so another coat must be applied perpendicular tothe first.

Epidermal sliding is easy to recognize, as the dermal andepidermal proteins have been coagulated by the TCA. TheETCA solution should not be neutralized or removed. Itstays where it is, and will be covered with the post-peelmask cream.


A B

Figure 21.7(a) Topical application of 2% lidocaine with adrenaline (epinephrine): the lidocaine is poured over the gauze. (b) Occlusion of thelidocaine for 10–15 minutes.

Figure 21.8Starting application of the ETCA solution

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Applying the post-peel maskcream and occlusionAs soon as frosting occurs, 0.5 g of post-peel mask creamshould be applied per 10 cm × 10 cm surface area (Figure21.10). The dosage card in the ETCA kit can be used todetermine the right quantity. After applying the post-peelmask cream over the whole area that has been abraded andcoated in ETCA solution, it should be covered with animpermeable, occlusive plastic film (Figure 21.11). Theplastic film is secured with a hypoallergenic dressing andheld in place for 24 hours. The actual depth of the peel and

the amount of ‘phenol-like’ skin liquefaction depend onhow long the post-peel cream is occluded. From 8 to 12hours’ occlusion does not liquefy the skin, and the resultsare often inadequate. More than 24 hours’ occlusion car-ries a higher risk of infection.

Removal of the occlusionHow long the occlusion is left in place depends on thedepth of action desired. Twenty-four hours seems to be agood compromise between effectiveness and the risk ofcomplications. The occlusive plastic film is removed and


Figure 21.9(a) Linear and uneven frosting following application of a first coat of ETCA solution; (b) uniformization of the frosting after passinga second careful coat of Easy TCA solution between the lines of frosting.

A B

Figure 21.10Application of the post-peel mask cream on the first quadrantto be treated.

Figure 21.11Occlusion with impermeable plastic film.

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reveals skin that is extremely inflamed and covered in a liq-uid that can be thick, runny and have an unpleasant smell(Figure 21.12). This liquid consists of the remains of thecream, inflammatory serous fluids and dead cells. Thesmell, which can even be unpleasant for people standingclose by, is the same for all patients. It is the same as thesmell that follows occlusion of a full-face phenol peel.

Close-up of the skin afterocclusionThe treated area is severely inflamed. The atrophic base ofthe stretch marks stands out and signals the extent of thedermal reaction (Figure 21.13). The controlled inflamma-tion caused by the treatment is essential, as it triggers theskin regeneration processes.

In short, abrasion and the application of acid appear tostimulate the regeneration of normal keratinocytes on theedge of the stretch marks, and occlusion of the post-peelmask cream strongly stimulates the fibroblasts.


Figure 21.12(a) The occlusive plastic film is left in place for 24 hours. Afterit has been removed, the skin can be seen to be inflamed (b)and covered in a thick runny, foul-smelling liquid. Softlyremove this liquid before applying the bismuth subgallatepowder (c).

C

A

B

Figure 21.13Severe inflammatory edema at the base of the stretch marksand in the surrounding skin.

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Applying bismuth subgallateAny excess liquid is mopped up with sterile gauze, althoughthe skin is not dried completely. Some liquid is needed forthe bismuth subgallate (BSG) powder to stick.

Skin Tech’s Stretch Mark Kit contains P220 sandpaper aswell as a sprinkler of BSG.9 A generous amount of the pow-der should be sprinkled directly onto the skin, leaving athick layer (Figure 21.14). Gently passing a sterile gauzepad over the powder evens it out and makes it stick to theliquid left on the skin.

Different types of dressing have been tried in order toprotect the BSG.

Melolin® (Smith & Nephew) (Figure 21.15) is an excel-lent sterile dressing that has one ‘normal’ side and one sidecovered in a transparent plastic film that does not stick towounds. The plastic is applied on top of the powder andthe Melolin® is secured on the healthy surrounding skin. Iused this method for many years until I could no longer geta supply of Melolin®. I then used Mölnlicke’s silicone orabsorbent dressings (Mepilex®, Mepitel®, etc.) to goodeffect (Figure 21.16).

Mepilex® and Melolin® are not always easy to find, and Itherefore had to look for another type of cheap and readilyavailable protective dressing. I then went back to using ster-ile white Vaseline®. Applying a thin coat of sterile whiteVaseline® to the BSG turns it into a paste that is easily spreadwith a tongue depressor and sticks to the skin (Figure 21.17).


Figure 21.14Application of bismuth subgallate to the left half of theabdomen.

Figure 21.15Smith & Nephew’s Melolin®.

Figure 21.16Mölnicke’s Mepilex®.

Figure 21.17The BSG is covered with sterile white Vaseline® and protectivegauze.

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The Vaseline® and BSG paste is then covered with a thickand absorbent sterile gauze that is secured on the healthysurrounding skin, as can be seen in Figure 21.18. In somepatients, the BSG and Vaseline® can act as an occlusion andunexpectedly deepen the action of the peel. Any overpeelingcan lead to complications with scarring or dyschromia.

Checking the dressing after 72hoursThe sterile gauze does not stick to the skin too much, andcan usually be removed easily by drawing it back smoothlyand carefully. If the dressing sticks in places, it should notbe pulled off: instead, the doctor should cut around thepart that is stuck to the skin and leave it in place (Figure21.19). Vaseline® can be applied to this area to help the

dressing come away naturally and quickly. The skin canlook rather gruesome, as can be seen in Figure 21.20. Theuse of a silicone sheet coated in a thin layer of Vaseline® tocover the BSG, as described above, drastically reduces therisk of the dressing sticking to the skin and causing lesions.

On the third day, the skin will be dry and flaking (Figure21.21). To help the flaking proceed, a thick layer of sterile


Figure 21.18Wide, thick gauze secured on the surrounding healthy skin.

Figure 21.19The dressing is sticking slightly: it should not be pulled off –rather, the doctor should cut around the part that is sticking.

Figure 21.20Appearance of the skin after 72 hours, following removal ofthe dressing.

Figure 21.21 Dryness and flaking on the third day.

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white Vaseline® can be applied (Figure 21.22) and the skinprotected with a new gauze dressing (similar to that shownin Figure 21.18).

Care on the 5th or 6th dayThe doctor sees the patient one last time to evaluate thecondition of the skin and apply another thick layer of Vase-line® (Figure 21.23) and one last dry dressing (as in Figure21.18).

It is common to see lines of depigmentation on patientswith a phototype higher than IV (Figure 21.24). Thisdepigmentation tends to return naturally to the original

skin color within a few weeks, even without BlendingBleaching® cream (Figure 21.25), which reduces the risk ofpost-inflammatory hyperpigmentation.

Protecting the skinAt the end of the first week after the peel, the skin is thinand delicate, quick to hyperpigment, slightly itchy, andswollen. The edema can persist for more than 2 weeks atthe base of the stretch marks.

It is essential to apply appropriate care creams to the skin.

� Hydration: Vit E Antioxidant® cream (see Chapters 2and 3) or a thin layer of sterile white Vaseline® shouldbe applied.

� Prevention of pigmentary changes: Blending Bleaching®cream and Melablock HSP® 50 or 25 should be applieduntil the following treatment or for at least 6 weeks.

� Prevention of infections: the patient should check forinfection and prescribe antibiotics as necessary (the firstweek is the most dangerous).

� Prevention of oxidation: the patient can apply an antiox-idant cream if the extent of the inflammatory reactionappears to make this necessary.

� Stimulation of the skin’s metabolism: the patient canapply a dehydroepiandrosterone (DHEA) cream if theextent of atrophy appears to makes this necessary.

Results of treatmentThe results appear gradually after stretch-mark treatment,but they are permanent (Figures 21.26–21.28).


Figure 21.22Application of Vaseline® on the third day.

Figure 21.23A thick layer of Vaseline® is applied.

Figure 21.24On the sixth day, areas of depigmentation are common inpatients with dark skin phototypes.

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Progression of results

Stretch marks are the result of severe dermal and epider-mal atrophy, lack of appendages and an extreme paucity

of cells. It would be impossible to get rid of them in a sin-gle treatment session. With each treatment, the quality ofthe skin improves visibly, and patients themselves can seethis. Photographs do not do justice to the improvement


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.

A B

Figure 21.26Before (a) and after (b) two treatments on day 30 in a patient with phototype V.

A B

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in skin quality, and in order to understand how thistreatment works, detailed studies are necessary in thefuture.

The first treatment usually brings great satisfaction tothe patient in terms of how the stretch marks feel: they donot feel as deep, and the depressed atrophic base starts tofill out. Gradually, the atrophic base comes level with thesurrounding skin, and in places its structure returns com-pletely to normal. Regeneration continues throughout thefollowing treatments.

In one published study,2 69 patients of all phototypesand aged between 14 and 63 were treated for stretch marksin different places: abdomen, breasts, back, hips, etc. Thepatients were followed up for an average of 18 months, andthe stretch marks treated were between light/recent andvery deep/old. An average improvement of 70% in theappearance of the stretch marks was observed after an aver-age of four treatments (4.2 exactly) and the results havebeen published.

Duration of resultsIt is commonly acknowledged that the histological changesthat take place in the deep dermis should be consideredpermanent. We can therefore assume that the resultsachieved are also permanent, and this corresponds to cur-rent clinical experience. The first treatments were carriedout in 1996, and the results achieved then were still com-pletely stable in 2005.

Post-peel details� This peeling technique is one of the most difficult: it

requires sound experience in post-peel care and shouldnot be the first peel that a doctor performs.

� Post-peel monitoring is of vital importance, and the fol-low-up care during the first week after the peel must berigorous: the doctor should see the patient several timesduring these first 8 days.


Figure 21.27Before (a) and after (b) two ETCA abrasive protocols.

A B

Figure 21.28Two treatment sessions on aphototype V patient: anteriorchemabrasion as described in thischapter.

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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 verypainful and increases the risk of infection. The patientobviously cannot have a bath during the first week untilthe skin has completely restructured and is impermeableagain. The patient can have a quick shower if an imperme-able plastic covering is placed over the protective dressing.

� Oral painkillers make both the patient and the doctorfeel more at ease: a 500 mg tablet of paracetamol (aceta-minophen) or paracetamol plus codeine taken half anhour before the peel and 2 hours after allows the patientto carry on as normal. The patient can take anotherpainkiller before going to bed if need be. There shouldbe no pain the following morning – only a feeling ofslight discomfort.

� The patient should keep out of the sun for 3 monthsafter the treatment. Effective sun protection is essential,even under clothing.

� There is a risk of an isomorphic response, especially inpatients with progressive vitiligo or psoriasis and inpatients where a minor trauma such as friction fromclothing has induced the Köbner phenomenon in thepast. The Köbner phenomenon can be induced by otherdisorders: reactive perforating collagenosis (transepi-dermal elimination of collagen), eruptive xanthoma(seen, e.g., in cases of secondary hypertriglyceridemia),erythema multiforme, macular or maculopapular exan-thema associated with juvenile arthritis, and varioustypes of lichen (e.g. planus or sclerosus). Cautionshould be exercised in all cases.

ComplicationsComplications from this deep peel are relatively common,but can be prevented or treated. Caution and adherence tostrict methodology should ensure safe treatment. Thedeeper the peel, the higher is the risk of complications.

Complications include hyperpigmentation (Figures21.29-21.31), depigmentation or scarring, depending onhow serious the cause is:

� Uneven abrasion: if abrasion is too deep, the acid pene-trates too deeply and there is a risk of scarring. Evenabrasion produces even results.

� Uneven application of the peel solution: the solution mustbe applied evenly to achieve even results. It is especiallyimportant that the cotton buds be squeezed out prop-erly, as the ETCA solution penetrates very quicklythrough the abraded skin.

� Pulling off a dressing: if a dressing is stuck to the skin, itmust not be pulled off; this would pull off the regener-ating epidermis, and the skin would have to start thehealing process again, leaving a hyperpigmented area.The dressing should be cut off around the area that is

sticking to the skin, and a coat of Vaseline® should beapplied to help the dressing come away without causinginjury to the skin.

� Pruritus: this causes scratch lesions.� Infections: these can result from not cleaning hands and

equipment properly, inadequate pre-peel disinfectionor overlong occlusion (more than 24 hours’ occlusionusually causes infection). A pre-existing skin infectioncan also be the cause: treating acne scars when there arelesions that are still active.

� Technical error.

See Chapter 37 for more information.


Figure 21.29

Figure 21.30

Figures 21.29 and 21.30Two cases of post inflammatory hyperpigmentation linked tothe lack of post peel use of antityrosinase/antioxidant creamand sun protection. Treatment applied used BlendingBleaching® cream and 2 Easy TCA peels without sandabrasion,using the ‘base protocol’.

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Treating scars Treating surgical scars and acne scars is never easy. A scar isthe tip of a fibrotic iceberg buried deep under the skin:effective treatment is therefore by definition a deep treat-ment.

Post-acne pigmentation scars are easy to treat (Figure21.32).

Facial scarsPhenolAlong with laser and abrasion treatment, a full-face phenolpeel is certainly one of the best options for treating facialscars. It is not completely effective, however, and it is oftennecessary to use chemabrasion – that is, a combination of aphenol peel followed (immediately or the next day) byabrasion with a diamond fraise or sandpaper. See Chapter30 for more information on the treatment of acne scars andphenol peel face lifts.

Dermabrasion plus ETCA (Figure 21.33)A ‘pre-chemabrasion’ technique has been developed forthe treatment of facial acne scars. The results are very good,and are similar to those achieved with phenol. The tech-nique is the same as for stretch marks, apart from the fol-lowing points:

� The sandpaper abrasion must be taken a step further(grade III) on the face: confluent pinpoint bleedingappears on the abraded area of the scars. This physicalresurfacing makes the skin appear smoother after abra-sion.

� The topical anesthetic (the same as used for stretch-mark treatment) dries up the blood and anesthetizes thewhole area before the acid is applied. The anesthetic isapplied after abrasion and before application of theETCA solution.

� Application of the ETCA solution triggers pure white oreven gray–white frosting. The solution penetrates to thereticular dermis.


Figure 21.31Scarring after anterior chemabrasion, resulting from anirregular abrasion and supposed poor follow-up. Treatmentapplied used topical and injected corticosteroids,antityrosinase and antioxidant cream, silicone sheetcompression.

A B

Figure 21.32(a, b) Post-inflammatoryhyperpigmentation (acne) treatedwith ETCA (non-abrasive, basicprotocol) combined with dailydepigmenting treatment andsunblock.

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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 scarsThe treatment of body scars is more complex than that offacial scars. The same technique described for stretch marksis used: abrasion plus ETCA peel plus post-peel mask creamplus occlusion. The results, although not exceptional, arequite good, as can be seen in Figures 21.34 and 21.35.

Scars that are in the same area treated for stretch marksby abrasion and ETCA respond well to this technique ifthey are stable and permanent. It is out of the question touse this deep peel on recent scars, as there is a risk that thescars will open.

Acne scars on the back (Figure21.36)TechniqueAn intraepidermal abrasion is performed with positive‘keratinocyte touch’. Applying an acid solution immedi-ately after abrasion would be very painful, and a surfaceanesthetic must be applied with gauze pads soaked in 2%lidocaine with adrenaline (epinephrine) (with 10–15 min-utes under plastic film to prevent evaporation). The anes-thetic can be seen to be working as the adrenalinepenetrates and causes vasoconstriction. The ETCA solu-tion is applied carefully, and cloudy-white frosting mayappear with the first coat of acid solution. As soon ascloudy-white frosting occurs, 0.5 g of post-peel maskcream should be applied per 10 cm × 10 cm of surface areatreated10 and the skin massaged.

The doctor decides if he wants to deepen the action ofthe peel with 24 hours’ occlusion, as with stretch marks, orif he prefers to end the peel here, without occlusion.

Post-peel carePost-peel care is exactly the same as for the stretch-marktreatment.

The peel should be repeated several times at 3- to 5-weekintervals if necessary. Repeated epidermal repair and der-mal stimulation gradually improve acne scars on the back.

Scars or aging of the décolletage:easy protocol, without applicationof acid (Figure 21.37)Abrasion is applied to the skin until the first pinpointbleeding appears. Local anesthetic is not necessary after


Figure 21.33(a) Facial abrasion with 3M Wet-or-Dry® sandpaper, P220. (b)End of abrasion: confluent bleeding. (c) After application ofETCA solution, there is pure white or gray–white frosting. Thepost-peel mask cream is applied as soon as frosting occurs.

A

B

C

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Figure 21.34(a) Abdominal scar before the first stretch-mark treatment. (b) Appearance of the scar 30 days after the first stretch-marktreatment: the quality of the skin has improved significantly; the small scars left on the sides by the stitches havedisappeared/diminished, and the scar is flatter. (c) Improvement in the appearance of the scar and skin tension after the secondstretch-mark treatment (abrasive–occlusive ETCA).

A B C

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 theabdomen as well as in the stretch marks.

A B

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abrasion, as this protocol does not involve the applicationof acid. Immediately after the abrasion, the doctor applies0.5 g of post-peel mask cream per 10 cm × 10 cm of surfacearea. An impermeable plastic film is then used as occlusionfor 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 fol-licles, 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. Ared, inflamed ring may surround the cone formed by thekeratosis.

After disinfection, light abrasion (grade I) with sand-paper should be applied.

After abrasion, a topical anesthetic is applied asdescribed in the protocol for stretch marks, followed byETCA solution: pinpoint or cloudy white frosting appears,especially on the keratoses that take the brunt of the abra-sion. The post-peel cream is applied and left to act until thenext day. This procedure is repeated four or five times, at 2-week intervals.

To maintain results, the peels are repeated, and fromtime to time a simple, superficial abrasion is performed.


Figure 21.36(a, b) Treatment of pigmentary changes from acne scars on the back (without occlusion).

A B

Figure 21.37(a, b) Improvement in acne scars onthe décolletage in a young patientwith vitiligo. There is no Köbnerphenomenon on the treated area.

A B

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Notes1. 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 containing15% trichloracetic acid followed by 6–24 hrs of a patentcream under plastic occlusion. J Cosmet Dermatol 2004; 2:61–70.

3. Sterilizing sandpaper for dermabrasion poses certain prob-lems 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 occlu-sion.

7. Dry heat burns the sandpaper, damp heat twists it and inboth cases the sandpaper’s silicone grains might come awayfrom the paper and be ‘grafted onto’ the patient’s skin. Withchemical disinfection, there is a risk of toxic molecules beingimported 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. Therisk 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’.


Figure 21.38Treatment of pilar keratosis: aspect of the skin aftersandpaper abrasion and application of Easy TCA solution.Points of frosting can be seen.

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Keratoses and lentigines need relatively deep treatment,but it is not essential to give the whole face a deep treat-ment when there are only a limited number of lesions: alocal application of Only Touch® is enough in this case.

DescriptionOnly Touch® (OT) (Figure 22.1) consists of a saponifiedand stabilized solution, adjuvanted with alpha hydroxyacids (AHAs), vitamins and antioxidants. Once the doctorhas reconstituted OT by adding trichloroacetic acid (TCA),it provides a solution that can be used to treat the skinlocally to the reticular dermis in the treatment of smallbenign lesions less than 1 cm in diameter. Its pH is lowerthan 1 and the solution’s final concentration in TCA isapproximately 45% m/m. It is therefore a very strong peel,to be used only for limited indications.

IndicationsOT is used to treat localized and benign solar lentigines(SLs) and/or actinic keratoses (AKs) in patients with skinphototypes I to III, or sometimes IV1 (Figures 22.2–22.4).

Lesions should not be more than 1 cm in diameter at themost. OT must not be used on larger surface areas – noteven partially. Nor should it be used on lesions unless it iscertain that they are benign. Nevi are not an indication forOT. Some doctors, by pushing the diameter limits, havetried to use OT to treat melasma. The melasma was partiallytreated in this way by gradually applying OT to small areas.However, this technique has proved ineffective, and there isa high risk of stimulating melanogenesis in the melasma,breaking the basal membrane and encouraging the develop-ment of dermal melasma. Under no circumstances shouldOT be considered as a treatment for standard or resistantmelasma.

Preparing the skinOT is a deep TCA peel, and because of this tends to causepigmentary changes. The patient must apply BlendingBleaching® cream (see Chapter 2) twice a day2 for 2–3weeks before treatment in order to reduce melanocyteactivity. After the Blending Bleaching® cream, sun protec-tion 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 preparationreduces the risk of pigmentary changes after OT.

Preparing the solutionUsing a 1 cm3 syringe, the required quantity of 80% m/mTCA3 is drawn up and injected into the bottle of OT basesolution. It should be remembered that 80% m/m means80 g of TCA crystals with an added 20 g of distilled water.

After making up the OT solution, between 0.2 and0.5 cm3 (the amount depends on the number of lesions tobe treated) are drawn up. This solution is put in a smallglass or ceramic bowl (under no circumstances should ametal container be used).4 A cotton bud is then soaked inthis solution and partly squeezed out to make sure that

22Actinic keratoses and lentigines

Figure 22.1Only Touch®.

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there is no excess solution. Any ‘drips’ of OT on the facecan lead to cosmetically disastrous results (Figure 22.14).

Applying the solutionThe product should be tested on a small area of skin beforethe first application. OT is applied with a cotton bud or, forvery small lesions, with a wooden pick soaked in the solu-tion.5 Great care should be taken to avoid any runs or dripsof excess solution. Half a millimeter is usually enough foran application on both hands and forearms.

With the chosen applicator the lesion that needs to betreated should be touched quickly, precisely and once onlyalways combined with ETCA.

QuicklyThe contact time between the cotton bud soaked in OTsolution and the skin should be as brief as a finger touch ona keyboard, a fraction of a second. Any longer (≥1 seconds),and too much acid will be left on the skin. The frosting thenturns a gray or even a yellow color and signals prolongedsequelae (see Chapter 37). Prolonged contact or possiblyrepeated applications make the skin appear ‘frozen’ andmeans prolonged consequences. The scabbing can last formore than 3 weeks in this case, and hypochromic, achromic

or even hypertrophic scars may develop (see the section onhyperpigmentation in Chapter 37).

PreciselyAKs are less permeable to acid solutions than the normalskin surrounding them, and the frosting on the hyperkera-


Figure 22.2Solar lentigines (a) before and (b) after treatment with acombination of OT and Easy TCA®.

Figure 22.3Solar lentigines on the hands (a) before and (b) aftercombined OT and Easy TCA® treatment. Daily care consistedof DHEA Phyto® and Blending Bleaching® cream.

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tinized area appears (much) more slowly. OT should there-fore be applied first only to the hyperkeratinized area andshould not be allowed to run over onto the neighboringskin. If too much OT is applied in an attempt to achievefrosting more quickly, the neighboring skin may be dam-aged by the acid solution. Clinical experience shows that itis preferable to have uneven frosting on the AK during thefirst OT session, as a second application can be made a fewweeks later, just before the fourth application of EasyTCA® that always accompanies the OT (see below).

Once only (on face)The application of OT should ‘moisten’ the lesion. If it stilllooks dry immediately after the one dab of OT, more solu-tion should be applied. The OT should be allowed to drycompletely; frosting should now be clearly visible. Frostingon the face appears far more quickly than on the body (e.g.hands and forearms), and with a smaller amount of theproduct! One single dab of OT is enough most of the timeto treat SL on the face. However, three or four dabs may benecessary to treat AK on the body. Excess solution and anyunnecessary drips or runs should be avoided.

Combined with Easy TCA®

Concentrated TCA has a strong potential to stimulatemelanocytes, and post-inflammatory hyperpigmentation(PIH) is common when OT is used as monotherapy with-out the blocking action of Easy TCA® (ETCA) and withoutreducing melanocyte activity beforehand. PIH can alsooccur when the contact time between the cotton budsoaked in OT solution and the skin is too long – althoughnot long enough to trigger scarring. Unlike ETCA solution,OT does not protect the patient’s skin against inflamma-tory and free-radical attacks after the peel.

Applying OT correctly and combining it with ETCAhelps to avoid almost all pigmentary changes, whereasapplying OT on its own causes them in over 60% of cases.

The method for combined application is simple: OT isapplied as described above; ETCA is applied to the wholearea, including the lesions that have just been treated with

OT, as soon as there is sufficient frosting from the OT. Theprotein coagulation caused by the OT does not allow theless concentrated ETCA to penetrate.

It is unadvisable to apply ETCA before OT, as ETCA per-meabilizes the epidermis and the OT would penetrate toodeeply.

The two peels are repeated at different intervals: ETCA isrepeated once a week on the face and once every 2 weeks onthe body; OT is repeated once every 3 weeks on the face andonce every 6 weeks on the body.

Figures 22.5 and 22.6 show how the two peels worktogether and how often they should be repeated.

Treatment of solar lentiginesSLs are brown macules 1–3 cm in diameter that tend toconverge and are found on 90% of Caucasians over 60years old (Figure 22.7). They are often seen on people of

Actinic keratoses and lentigines 169

Figure 22.4(a, b) An excellent indication for OT:the patient has a few scatteredlentigines that do not justify a peelto the papillary dermis: acombination of OT and Easy TCA® isideal.

A B

1 week 1 week 1 week

6 weeks’ care

1st OTbefore

1stETCA

2ndETCA

3rdETCA

2nd OTbefore

4thETCA

Figure 22.5OT peel combined with ETCA on the face.

Figure 22.6OT peel combined with ETCA on the body.

6 weeks’ care

1st OTbefore

1stETCA

2ndETCA

3rdETCA

2nd OTbefore

4thETCA

2 weeks 2 weeks 2 weeks

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Asian origin as well. They can, however, appear on the skinof much younger subjects after acute or chronic UV expo-sure. They can disappear partially or appear more diffusewhen UV exposure stops. Melanocyte proliferation varies,but sometimes the melanocytes in the basal layer of the epi-dermis can increase to such an extent that the keratinocytesin the same layer seem to be replaced by melanocytes. Thestructure of the epidermis is hyperplastic and less perme-able to the acids. Melanocyte abnormalities have beendetected, and this suggests a potential relationship betweenSLs and lentigo maligna, but no clear link has been estab-lished to date between the two disorders. They are difficultto treat unless all the melanocytes involved are destroyed.Theoretically, this is an epidermal problem, but the treat-ment has to go deeper, as the basal layer does not form theclassic, perfect sine wave that we see in the books. The basallayer 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, SLare treated with cryotherapy or laser (Q-switched rubylaser), but it is preferable to treat them with deep and verylocalized6 peels, which give excellent long-term results.Effective daily sun protection is essential.

Before any treatment, a differential diagnosis should bemade between SLs and freckles, certain types of flat sebor-rheic keratoses, early pigmented AKs, lentigo maligna,junctional nevus and some acanthomas. There are differentways to treat solar lentigines on the face, hands, neck anddécolletage, from laser to pulsed light, cryotherapy, der-mabrasion and peels.

Applying a combination of OT and ETCA to solarlentigines on the face is a simple, inexpensive and effectiveoption (Figure 22.8).

On the face, just a single dab of OT is enough to coagu-late the skin locally to the reticular dermis. ETCA is appliedimmediately after OT, over the whole face, following thebasic protocol (pinpoint frosting).

The epidermis is more impermeable on the décolletage,and sometimes two dabs of OT are needed to obtain frost-ing. ETCA is applied over all of the neck and décolletageimmediately after OT until pinpoint or cloudy white frost-ing occurs.

Sometimes, SLs on the hands and forearms do not frostuntil after three or four applications of OT. When the frost-ing from the OT is satisfactory, three successive coats ofETCA are applied on the hands and forearms; there shouldbe no further frosting from the ETCA, however. If anyfrosting starts with the second coat of ETCA, a third coatshould not be applied.

Treatment of actinic keratosesActinic keratosesAKs can be an early stage in the development of squamouscell epithelioma (SCE) or basal cell epithelioma (BCE).These are the most common types of skin cancer inhumans, mainly caused by exposure to UV radiation. AKare usually 1–3 mm in diameter, but can sometimes reach2 cm (Figure 22.9). Most AKs remain asymptomatic, butsome can become pruritic or inflammatory. Growing AKsreach up to 3 cm in diameter and it is hard to distinguishthem from Bowen’s disease.7 Pigmented AKs should be ana-lyzed histologically to distinguish them from SL ormelanoma in situ (lentigo maligna). Moreover, any recentchange in the appearance of the AKs could indicate thatthey are becoming malignant. Until recently, AKs have beenconsidered as potentially premalignant lesions, but someauthors suggest they should be considered as an intraepi-dermal cancer, an early SCE. This classification8 has notbeen widely retained, as many SCE lesions appear without a‘preclinical’ AK stage.9 Histologically, AKs are defined bythe presence of abnormal keratinocytes in the basal layer ofthe epidermis; the thickness of the epidermis varies, and itcan be anything between atrophic and extremely hyper-trophic. On the lateral edges, there is often a clear borderbetween the abnormal areas and the neighboring normal


Figure 22.7Solar lentigines.

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A B

C

Figure 22.8(a) Solar lentigines before treatment. (b) Localized frostingfrom OT. (c) Results after one OT treatment and four ETCApeels.

Figure 22.9Actinic keratoses of different diameters.

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areas. In the large majority of cases, the keratinocyte abnor-malities do not spread to the appendages (whereas they doin Bowen’s disease), except in the case of proliferating AKs.

When treating AKs, the risk of them turning into malig-nant SCE must be taken into account, although fortunatelythis rarely happens; effective treatment of AKs reduces therisk of developing SCE in the long term. Cryotherapy,curettage, surgery, electrodessication, 5-fluorouracil (5-FU), carbon dioxide laser, photodynamic therapy (PDT),dermabrasion and chemical resurfacing with peels are allrecognized as valid options in the treatment of AK .9

Given that a more aggressive treatment gives the patientbetter protection from recurrences, applying a peel such as

OT seems to be a good option for the treatment of AKs andSLs (Figures 22.10 and 22.11). Keratin is relatively imper-meable to acids, and the frosting on the AK usually appearsslowly and unevenly (Figure 22.12). The doctor has a nat-ural tendency to apply more coats of OT too quickly, butthere is then a risk of overpeeling and burning the skindeep down. Once through the keratotic layer, the acid canpenetrate the dermis very rapidly, like a river in spatebreaking the flood barriers that held it back. The acid mustbe given time to penetrate before being applied to thelesion again. The acid spreads once it has passed throughthe keratosis and reached the dermis, and can then workfrom underneath, undermining the keratosis. It is not nec-essary, therefore, to apply too much of the product.Besides, if the results are inadequate after the first treat-ment, 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 andthe body after OT to reduce the risk of pigmentary changes.

Post-peel careAt the end of treatment, the doctor can apply a corticosteroidcream to the lesions treated with OT to limit the inflamma-tory reaction. This application should not be repeated untilafter more than 72 hours. Between peels and for at least 6weeks after the last peel, the patient should apply effective sunprotection10 3 times a day after Blending Bleaching® cream.The patient should be warned not to touch or pull off thescabs: 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 shoulduse daily care products that are suited to his or her skin.


Figure 22.10Precise application of OT solution to the lower limb.

Figure 22.11OT can be used to treat numerous lesions, as long as thehealthy skin between them is not touched.

Figure 22.12The speed with which OT penetrates gives an idea of howkeratinized the lesion is. If there is a lot of keratinization, thesolution penetrates more quickly on the edges of the lesion.

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ComplicationsProlonged erythemaThe erythema that always follows the application of OTusually lasts for 2–3 weeks. There may be prolonged ery-thema if too much OT has been applied as a result of too

much solution, too much pressure on the cotton bud ortoo long a contact time with the skin. Treatment consists incareful use of corticosteroids, tyrosinase inhibitors andeffective sun protection (see Chapter 37).

Pigmented ringA full or partial pigmented ring is sometimes seen to persistwhen the solution has been applied between lesions. Treat-ment consists in applying OT to the ring during the nextpeel session. This can be avoided by letting the OT goslightly beyond the visibly pigmented zone at the end of theapplication.

Persistence or recurrence of thelesionAn SL or AK will persist without any change unless the acidgoes deeper than the epidermis and penetrates the deepdermis.

The lesion will recur if it has not been completelydestroyed by the acid as a result of a technical error or becausethe lesion is unexpectedly deep. A differential diagnosis isnecessary 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 (seeChapter 30).

Depigmentation or scarringHypertrophic scars can be treated in the classic manner bycorticosteroid injection and long-term use of a silicone sheetdressing (see Chapter 37). If OT has penetrated too deeplyand has destroyed all the melanocytes in the area, it can causehypochromic or achromic scarring. The situation depicted inFigure 22.14 may result from different causes: either becausea pure TCA solution at 80% m/m was applied,11 or becausethe OT-type solution was applied too liberally and left toolong on the skin. From the appearance of the patient’s skin inFigure 22.14, it seems likely that undiluted 80% TCA hasbeen used or a low-grade copy of OT solution has beenapplied too liberally to areas larger than 1 cm2. Even if thelong-term prognosis is good with the right treatment, surgeryis sometimes the only solution when the damage is extensive.

Post-inflammatoryhyperpigmentationPost-inflammatory hyperpigmentation (PIH) is relativelyeasy to treat and tends to fade naturally without sun expo-sure. For its treatment, see Chapter 37. It should beremembered that nevi, melasma and patients with photo-type V or VI are not indications for OT (Figure 22.15).


Figure 22.13(a, b) Normal scabbing 8 days after the application of OT.

A

B

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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 followedby a single application of ETCA.

� OT should not be used on lesions more than 1 cm indiameter. Larger lesions should not be treated, evenpartially, with OT.

� Concentrated 80% m/m TCA must not be applied tothe skin before it has been mixed with the base solution.

� The contact time between the skin and the cotton budmust be brief.

� OT should always be used in combination with ETCA,as well as Blending Bleaching® cream and sun protec-tion (50+ then 25+) after the peel.

� Phototypes V and VI should not be treated – applica-tion 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 pig-

mentation problems. Intense application of OT cancause patches of erythema that can persist for up to 3months. This prolonged erythema can be treated by theapplication of topical corticosteroids and total sun-block.

Treatment of AKs and SLs withETCAOT may sometimes be too strong for the treatment of smallAKs or SLs. Superficial lesions can also be treated withETCA (Figure 22.16).

Phase 1With a cotton bud, ETCA is applied only to the lesions tobe treated. The peel solution is left to dry, following whichadditional coats are applied until pure white frosting isachieved. Each coat should be left to dry completely beforethe next coat is applied.


Figure 22.14A combination of post-inflammatory hyperpigmentationaround depigmented areas, which are in turn centeredaround a scar, is common when a large excess of TCA isapplied to skin of phototype IV or V.

Figure 22.15PIH after application of OT to nevi. Nevi are not an indicationfor OT.

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Phase 2After pure white frosting has appeared on the lesions,ETCA is applied to the rest of the face following the basicprotocol. The protocol to the Grenz zone reduces the num-ber of small superficial AKs or SLs, as well as lesions thatare too small to be seen by the naked eye.

Treatment of AKs and SLs witha full-face peel to the papillaryor reticular dermisAKs and SLs have been improved – sometimes temporar-ily – by peels to the papillary dermis (see Chapter 23). Afull-face phenol peel is the most effective and long-lastingtreatment for keratoses and solar lentigines (see Chapter30).

Notes1. Using OT on patients with phototype IV or dark Asiatic skin

should be discussed with the patient, because of the risks ofpigmentary changes.

2. Three times a day for patients with phototype IV.


Figure 22.16(a–c) Solar lentigines and photoaging treated with ETCA. Theareas with lentigines are treated more deeply (pink–white oreven pure white frosting) than other areas (pinpoint frosting).Daily care comprised Blending Bleaching® and DHEA Phyto®.

A B

C

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3. Presentation boxes vary from country to country; it is best toread the instructions that come with the box.

4. It is also possible to inject the peel solution directly onto thetip of the cotton bud. They usually take a volume of0.12–0.14 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 intraepider-mal invasion by abnormal keratinocytes is classified as (I)slight, (II) moderate or (III) severe.

9. Miller SJ, Moresi M. Actinic keratosis, basal cell carcinoma andsquamous 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 1week after the last peel. Thereafter, Melablock HSP® 25+ isenough for the 6 weeks of skin regeneration.

11. Which can happen if the doctor does not prepare the solu-tion himself and an inexperienced assistant is given thisessential task.


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IntroductionTrichloroacetic acid (TCA) in a simple aqueous solution(TCA–SAS) is the peel most widely used to partially orcompletely remove the papillary dermis. Strict pre-peelpreparation is required to even out penetration, reducemelanocyte activity and accelerate post-peel re-epithelial-ization. The main purpose of post-peel care is to countercomplications (see Chapter 14).

Unideep® was designed to make pre-peel preparation aseasy as possible, at the same time as maintaining rapid re-epithelialization and limiting the risks of post-peel compli-cations. Unideep® is a by-product of Easy TCA® (ETCA)‘technology’ and is a medium-depth peel that reaches thepapillary dermis.

DescriptionThe Unideep® kit contains a bottle of base solution (whichhas to be activated by mixing it with 50% m/m TCA), twotubes of post-peel mask cream, two applicators, a glassbowl and an instruction leaflet (Figure 23.1).

Unideep® is a saponified and stabilized TCA peel thatcontains 23% m/m TCA. It is a good peel for patients who

want quick results with a lower risk of side-effects thanTCA–SAS. The Unideep® solution coagulates proteins inthe epidermis and the papillary dermis, but not the proteinsof the vessel walls: the resulting frosting is an evenpink–white rather than pure white. The skin is regeneratedby the keratinocytes that have remained intact in the deeperdermal papillae, the pilosebaceous units and the sweatglands. These keratinocytes regenerate a new epidermis,while the dermal action of Unideep® stimulates fibroblastproduction: collagen, elastin and glycosaminoglycans.

The post-peel mask cream should be applied twice: 50%immediately after the peel and the remaining 50% themorning of the first day after the peel. It stimulates the skinand breaks the vicious oxidative circle: ‘inflammation ↔free radicals’, and accelerates healing time. It also helps tolimit the vicious inflammatory circle that follows anymedium-depth peel and counters post-peel pigmentarychanges.

IndicationsThe main indications for a TCA to the papillary dermis arethe following: photoaging, non-active acne, hyperpigmen-tation, melasma, chloasma, keratoses and fine lines.Unideep® can also get rid of most freckles (Figure 23.2). Asingle peel is usually enough to achieve deep regenerationof the skin, but it may sometimes be necessary to repeat thepeel 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 roundthe mouth or eyes (see Chapter 36). The downtime withlips and eyelid (1 week) is the same as for a peel to thepapillary dermis.

� as a local application (e.g. on the forehead only) in com-bination with a more superficial peel (ETCA) on the

23Trichloroacetic acid to the papillary dermis:Unideep®

Figure 23.1Unideep® kit for two patients: a bottle of base solution, twotubs of post-peel mask and two applicators.

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rest of the face so that the patient can keep up his or hersocial life more easily (Figure 23.3).

It is sometimes difficult to choose between doing a singleUnideep® peel and four ETCA peels. Overall, the two peelsoffer patients the same results. However, one Unideep® issometimes more effective than ETCA when treating pig-mentation problems originating in the dermis, whereas theopposite is true in the treatment of photoaging, whenstrong stimulation is needed to regenerate a healthier-


Figure 23.2(a) Natural darkening of freckles 24 hours after theapplication of Unideep®: they will disappear 5–6 days afterthe peel. (b) Freckles 1 month after a Unideep® peel.

A

B

Figure 23.3(a–c) Combination of peels: Unideep® has been applied to theforehead only, and ETCA has been used to treat the rest ofthe face that is not so badly damaged by the post-acnepigmentation. (d–e) Forehead view of a full face Unideep®.

A

B

C

D

E

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looking skin. The best indication for Unideep® is inpatients with skin phototypes I to III. The risk of PIH mustbe discussed with patients with darker skin phototypes.

Method of application

Preparing the skinThe skin is cleaned with Skin Tech’s cleanser, disinfectedwith alcohol and degreased with acetone. To degrease theskin properly, it needs to be wiped with acetone severaltimes. It is wise to reduce melanocyte activity in patientswith a skin phototype higher than Fitzpatrick III. Patientswho are prone to labial herpes should be given preventivetreatment.

Preparing the applicatorThe ideal applicator is a cotton dental swab held in a clamp(Figure 23.4): this makes it easier to handle and to apply theright amount of pressure. The cotton swab in the kit is toolong, needs to be cut in two equal halves for use as an appli-cator.

Preparing the peel solutionFollowing the instructions in the kit, the doctor adds therequired amount of TCA.

AnesthesiaMost patients can easily tolerate this treatment withoutnerve block anesthesia if the peel is done slowly, cosmeticunit by cosmetic unit. More squeamish patients may preferto have intravenous sedation, along with nerve blocks.

Analgesic medicationThe patient can take a paracetamol (acetaminophen) pluscodeine tablet half an hour before going to the doctor. Thepatient may also benefit from taking a second tablet 1 or 2hours after the peel, at the peak of the discomfort.

CryoanesthesiaAny pain can be eased considerably by simply chilling theskin before the first application and between the differentcoats. Cold packs (e.g. 3M’s products: Figure 23.5) or aventilator can be used for this. If neither is available, a bagof ice or simply contact with a cold surface (e.g. an emptybottle) soon eases the burning sensation. Cold packs can beapplied directly on the acid if they have been dried before-hand.

Nerve blocksA local anesthetic (nerve blocks) may be necessary for sen-sitive patients. Application is completely painless withnerve blocks. There are more details on how to performblocks in Chapter 33.

TCA to the papillary dermis: Unideep® 179

Figure 23.4Unideep® applicator held in a clamp.

Figure 23.5Cryoanesthesia with 3M’s cold pack.

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Vocal anesthesiaVocal anesthesia or medical hypnosis is enough in manycases to alleviate the burning sensation of the acid inUnideep®.

Topical anesthesiaFor reasons outlined in Chapter 33, anesthesia with a topi-cal cream should not be used before a peel to the papillarydermis.

Applying the solutionPeel applied with nerve blocks andsedationThe solution is applied to the whole face and left to dry.Additional coats are applied to achieve an even pink–whitefrosting and signs of epidermal sliding. The post-peel maskcream after the peel,1 is applied to the whole face.

Peel applied with nerve blocksWith nerve blocks, application is painless and quicker.After nerve blocks have been applied to the area undertreatment, the peel solution is applied to the face: it isapplied on the forehead and temples first, until an evenpink–white frosting is obtained; the post-peel mask cream

is applied on the area that has just been treated before mov-ing 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 theburning sensation.


Figure 23.6The first coat of Unideep® often produces uneven frostingthat will even out with the second coat.

Figure 23.7(a, b) Sequenced application.

B

A

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Peel applied without nerve blocks orsedation

Ideally, the patient has taken an analgesic (paracetamolplus codeine). The peel solution is applied to each cosmetichalf-unit (e.g. half of the forehead) until even pink–whitefrosting and epidermal sliding2 occur (Figure 23.8), all thetime making the best use of cryoanesthesia and vocal anes-thesia. The post-peel cream soon alleviates the pain causedby the acid, and it is possible to do a peel to the papillarydermis without anesthesia.

Post peel mask applicationAfter frosting occurs, the solution should not be neutral-ized – rather, 5 g, or half a tube, of post-peel cream shouldbe applied to the face (Figure 23.9). It should be rubbed in,and the solution and cream left to work until the nextmorning.

The patient then applies the rest of the post-peel creamto the face, after washing with neutral soap or cleansinglotion.

Follow-up and post-peel careDays 1–4Renutriv ACE Lipoic Complex® is applied three times aday. The skin dries and starts to peel on the second or thirdday. The patient is seen on the third day to check the con-dition of the skin and to make sure that there is no sec-ondary infection.

Days 4–6 Pure Vaseline® is applied to facilitate flaking. The patient isseen on the seventh day.

From day 7 and for at least 6weeks� Phototypes I to III: hydrating and antioxidant cream,

combined with effective sun protection.

TCA to the papillary dermis: Unideep® 181

Figure 23.8Epidermal sliding.

Figure 23.9(a, b) Two different types of flaking (on the sixth day).

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� Darker skin phototypes: to be treated very carefully:Blending Bleaching® morning, midday and evening,combined with effective sun protection and completesun avoidance. The skin should be washed with purewater between the two applications of creams.

From the sixth week, for all allowed phototypes and for atleast 6 months, the patient should use a care cream bestsuited to his or her skin (see Chapter 3).

Results can be maintained in the long term by repeatingthe peel as and when the doctor thinks it necessary (once ayear, once every 2 years, once every 3 years, ...).

Precautions and complicationsPotential complications from this type of peel are describedin detail in Chapter 37.

General precautionsUnideep® is a peel to the papillary dermis: it is essential tofollow the indications and method of application. Misuseof Unideep® could produce the classic side-effects ofmedium-depth peels.

The patient should be warned not to scratch. Concen-trated TCA should not be applied to the skin without mix-ing it with the base solution.

Specific precautions for darkphototypesThe techniques described are for patients with phototype Ito III. To treat patients with a higher phototype (IV to VI),extra precautions are needed: the skin should be preparedby application of Blending Bleaching® cream twice a dayfor 2–3 weeks before the peel; sun protection cream(Melablock HSP® 50+) should be used, and exposure ofthe skin to daylight should be avoided. The peel should beapplied carefully, and great care should be taken not tohave any excess solution.

After the peel, Blending Bleaching® cream should beapplied as soon as possible, when flaking has finished, andcontinued for 6 weeks after the peel.

Pigmentary changesPigmentary changes can be treated with three or fourETCA sessions and Blending Bleaching® cream. Total sunprotection is essential.

Notes1. 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 addi-tional application on the evening of the peel and the morn-ing after.

2. The sliding occurs as the TCA coagulates the anchor proteinsin the dermis and epidermis. Pinching the skin makes theepidermis slide over the dermis.


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ChemistryResorcinol (Figure 24.1), also known as resorcin, meta-dihydroxybenzene, 1,3-dihydroxybenzene, and 1,3-ben-zenediol, has a molecular weight of 110.11 and a relativedensity of 1.272. It is slightly more acidic than phenol, witha pKa of 9.15. It is soluble in water, alcohol, ether and glyc-erol. It comes in the form of white needle-shaped crystals.Resorcinol crystals oxidize easily, and turn pink on contactwith light, air or iron.

Properties of Resorcinol1

AntisepticResorcinol has antiseptic properties similar to those of phe-nol, and was used to dress minor wounds before the era ofantibiotics. It has antifungal properties, and was alsoapplied on chancroids and syphilitic ulcers. Its bactericidaleffect is 30% of that of phenol.

Proteolytic and protein coagulantResorcinol is a phenol derivative and its proteolytic power isabout 1/40 of that of phenol. It breaks the weak hydrogen linksof keratin and acts as a proteolytic agent, even at concentra-tions as low as 5%.2 At higher concentrations, it can also pre-cipitate skin proteins and become a protein coagulant.

AntipruriticResorcinol is used in many antipruritic formulations, espe-cially in chronic kidney dialysis. It is mainly used in paste

form, usually called Unna’s paste, or in solution form, asJessner’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 respondto this treatment.

� Photoaging: solar keratoses, pigmentary lesions, epi-dermal atrophy and solar elastosis are indications for resorcinol if their histological origins are not toodeep.

� Dyschromias: resorcinol has been used with varyingsuccess to treat melasma, chloasma, post-inflammatoryhyperpigmentation (PIH) and post-acne pigmentation.It can get rid of some freckles. Resorcinol is contraindi-cated in patients with phototypes IV to VI because ofthe risk of pigmentary changes.

Obsolete indicationsManquat’s ‘Elementary Treatise on Therapeutics’ (1903)describes the heroic experiments of colleagues who tested,on their own persons, the effects of medication taken inever-increasing doses until convulsions ensued (ingestionof 10 g of resorcinol in 15 minutes). The indications offi-cially retained in 1903 were the following:

� Antipyretic: resorcinol was considered a dangerous andrather ineffective antipyretic.

� Antiseptic: the antiseptic use of resorcinol was recom-mended for surgery in place of phenol, as it is less toxicand 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 ‘pityri-asis capitis’ and seborrheic eczema.

24Resorcinol: Unna’s paste/Jessner’s solution

Figure 24.1Chemical structure of resorcinol.

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Histological changesEpidermalAfter a resorcinol peel, the superficial stratum corneumcomes away from the germinative layer in the stratumgranulosum.3,4 The basal layer shows increased mitosis andaccelerated turnover. The total thickness of the epidermistherefore increases, to the detriment of the stratumcorneum, and the skin appears more hydrated.

DermalThe fibroblasts in the papillary dermis are stimulated andproliferate: they synthesize a large quantity of new collagen,which is deposited in bands beneath the epidermis (in theGrenz zone). The intercellular matrix is enriched in gly-cosaminoglycans. Further down, short-lived but rapidvasodilation occurs, that signaling the presence of dermalinflammation.

Four months after the peel, the histological changes inthe dermis, apart from vasodilation, are still visible. Theintercellular space has a higher concentration of gly-cosaminoglycans, and there are more collagen and elasticfibers in the dermis.

Ingredients of resorcinol peelsMany classic formulas use resorcinol combined with old-fashioned ingredients that may now sound somewhatstrange and mysterious.

Wool fat (lanolin)Wool fat is obtained from extracts of soapy water in whichsheep’s wool has been washed or extracted with solventsfrom grease wool. Lanolin is obtained by purifying thegrease (or suint). This emollient is a yellow and viscoussubstance, consisting of fatty acids and fatty acid esters.

Petrolatum (Vaseline®)This neutral, semisolid unctuous substance, tasteless andodorless, is derived by distilling or purifying petroleum.Thin layers are transparent. Petrolatum is the officialgeneric name; Vaseline® is a (genericized) trademark.

Benzoin axungeAxunge is a greasy excipient used to reduce erythema. It is,in fact, simply lard – i.e. grease extracted from pig’s epi-ploon. Benzoin axunge is prepared by adding 5 g of tinc-ture of benzoin per kilogram of melted axunge and stirringuntil the mixture has cooled.

BenzoinBenzoin, or gum benzoin, is a resinous secretion obtainedfrom cuts made in the trunk or branches of the Styrax ben-zoin tree. It contains coniferyl benzoate, benzoic acid, ben-zyl cinnamate, vanillin (a phenol aldehyde) and a numberof triterpenes.5

Benzoin resin is a local irritant. A hundred years ago, itwas considered to be an aphrodisiac when ingested. At thebeginning of the 20th century, benzoin was mostly admin-istered as an antiseptic in fumigation to treat chronic respi-ratory diseases: it was thrown in small pieces onto a heatedmetal plate.6 Tincture of benzoin is obtained from dissolv-ing (1/5) benzoin in alcohol.

Ceyssatite and zinc oxideCeyssatite is a white clay (from Ceyssat in France) whoseabsorbent properties, similar to those of kaolin, have beenwidely used in cases of hyperhidrosis and eczema.Ceyssatite and zinc oxide have an exfoliating and desiccantaction that is absolutely essential for resorcinol to actevenly.

KaolinKaolin is a white clay mostly made up of silicon dioxide,aluminum oxide, iron oxide, titanium dioxide, magnesiumoxide and sodium oxide. It was first found in China, in Kao-Ling. European kaolin is formed by the decomposition offeldspath in granite rock in Brittany or Limousin. Kaolinhas good absorbent properties and is gentle on the skin; it isvery well tolerated by very sensitive or reactive skins. It isused for its healing, antiseptic7 and anti-inflammatory qual-ities and its excellent coverage in Unna’s paste formula.

Benzoic acidBenzoic acid is a weak carboxylic acid.8 It is not very solu-ble in water (3 g/l at 25°C) and has a molecular weight of


Box 24.1 Benzyl and phenyl

Benzene is a molecule

Benzyl is a group that has to be attached tosomething else. It is methyl benzene whose methylgroup (CH3-) has lost a (H-)

Phenol is a molecule; the suffix -ol means that it hasa (-OH) radical.

Phenyl is a group that has to be attached tosomething else. It is a benzene minus a (-H) or aphenol without its (-OH) group.

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122. It comes in the form of a white silky-looking solid andis used as an antiseptic and antifungal agent or as a preser-vative in some fizzy drinks.

Resorcinol pastesFormulations of different pastesThe formulations for resorcinol paste most often used inthe past are shown in Table 24.1. The preparation of thispaste involves a lot of work for the pharmacist, who has touse centrifugation and/or ultrasound. The resorcinol crys-tals have to be thoroughly ground in a mortar before mak-ing up the paste to make sure no big crystals remain in it.9

The resulting mixture will be more homogenous and eas-ier to spread. Unna’s paste does not remain active verylong, as it oxidizes rapidly. The doctor should thereforealways use a freshly made paste. Another formulation con-tains resorcinol, olive oil, kaolin, zinc oxide, petrolatumand wool fat.

Preparing the peelPreparing the skinThe best results are achieved when the skin has been pre-pared for 15 days beforehand; see Chapter 2. If the skin hasbeen prepared with tretinoin or alpha-hydroxy acids(AHAs), if the patient has used products (benzoyl perox-ide) or techniques (scrub, or abrasion with a massageglove) that increase the permeability of the stratumcorneum, the resorcinol paste should not be left on toolong.

Allergy testAn allergy test should be done before each resorcinol peel, byapplying a small bit of paste on the skin behind the ear for20 minutes: this provides a minipeel to evaluate the risk ofallergy. This allergy test should be carried out like a localizedpeel: the skin must be allowed to dry and flake: the normalaction of resorcinol on this thinner and more sensitive skinshould not be confused with an allergy. Any hint of an aller-gic reaction (e.g. swelling, redness, itching, blistering orweeping skin) should rule out this peel immediately.

There is one significant cloud on the horizon: the allergytest itself can make a patient who was not previously allergicto resorcinol allergic. It is therefore not wholly predictive.

Clean and degreaseThe skin should be disinfected (with alcohol) anddegreased (with ether or acetone) before applying thepaste.

Hydrating the patientThe patient must be well hydrated to facilitate diuresis andelimination of the metabolites of the resorcinol. An intra-venous drip of saline solution should be set up, but if this isnot possible, the patient should be asked to drink severalglasses of water before the resorcinol is applied.

Preparing the pasteResorcinol paste is compact and difficult to apply. It is eas-ily softened by putting it in a bain-marie at 45° for around10 minutes. If that is not possible, small blocks of pasteshould be applied to the patient’s skin. Heat from the skinwill slowly ‘melt’ the paste and make it easier to spread,although the resorcinol may penetrate too deeply wherecontact time has been longer.

Analgesia and anesthesiaNo analgesia or anesthesia is necessary. A resorcinol peel isneither painful nor stressful – besides which, resorcinol hasa mild local anesthetic effect.

Settling the patient inThe patient lies down during the peel and for half an hourafterwards.

Applying resorcinol pasteApplicationThe eyelids are protected with Vaseline® or damp cotton(make-up remover) pads. A thick coat of paste is applied

Resorcinol: Unna’s paste/Jessner’s solution 185

Table 24.1 Formulations of resorcinol paste

50%a,b 50%c 30%c

Resorcinol 40 g 60 g 30 gZinc oxide 10 g 15 g 15 gCeyssatite 2 g 3 g 5 gBenzoin axunge 28 g 50 gBenzoic acid 2 gDermagor® cold cream 40 g

aTrauchessec JM, Vergereau R. Les peelings. In: Bartoletti CA,Legrand JJ (Eds.), Manuel pratique de médecine esthétique, 2ndedn. 159–67. Paris, France, Société Française de MédecineEsthétique.bRusciani L, Rossi G, Bono R. Les peelings chimiques. J MedEsth et Chir derm 1993; XIX (78) 78–80.cCohen, Letessier, Préparations magistrales en Dermatologie. In:Arnette (Ed.), Collection des Manuels pratiques de médecineesthétique, 1989, Paris.

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with a tongue depressor – enough to make a mask of eventhickness. The paste should not be applied to the eyelids ormucous membranes. The paste has to be applied a littleway into the hair, and should just touch the eyebrows.

On the jaw area, as with phenol, the paste is applied upto 2 cm below the upper jaw. The paste should be rubbedgently to make it more homogenous. Resorcinol paste isoften applied on the décolletage and back. Great care mustbe taken in these areas, however, as the extent of the sur-face area treated can induce toxicity. Large surface areasshould be treated in several stages, and a rest periodbetween two applications will help the body eliminate themetabolites from the detoxification of this phenol com-pound.

Contact time for a facial peelThe contact times given and commented on below are arough guide only, and should be modified to suit thepatient’s skin type, the disorder being treated, the resultsdesired, etc.

First application (first day): contact time 10–25 minutes.A few minutes after the first application, the patient feelssome heat and then a tolerable burning sensation. This sen-sation starts where the resorcinol has penetrated mostrapidly. The cheeks are usually more permeable than theforehead. The areas where the patient first feels burning arethe first to be cleaned of the resorcinol paste at the end ofthe peel. The sensation of acid ‘burning’ can sometimesbecome intense, and a yellow serous fluid may be seen toweep through the partially lysed epidermis. In this case, thepatient 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 20–30minutes. The resorcinol is left to work for longer: 10 min-utes more than the first session, or even 15 minutes moreon areas that did not react as well on the first application,mainly on the forehead.

After the second application, the skin becomes brown-ish, and the patient’s social life is disrupted.

Third application (third day): contact time 30–35 min-utes. The third application must be carried out withextreme caution: if the ‘resorcinol membrane’ that isforming has modified the permeability of the skin, epider-molysis is present and the skin has been badly injured:rough handling (or paste that is too compact) could pullaway the skin and sharply increase the risk of post-peelcomplications in the form of erythema and pigmentarychanges.

After the third application, a ‘resorcinol membrane’ hasformed. It is made up of lysed and dried out corneocytesand keratinocytes, stuck together by any serous fluid seep-ing through the epidermis.

Contact time for a body peelThe skin on the body is less permeable than the skin on theface, and the contact times will therefore be longer.

On the first day, the contact time should be 30–50 min-utes, on the second day 40–60 minutes, and on the thirdday 50–70 minutes. Once again, extreme caution is recom-mended in peels on non-facial skin because of its limitedcapacity to regenerate and because the extent of the area tobe treated increases the risk of general toxicity.

End of the peelAt the end of contact time, the paste is removed with atongue depressor and a dry gauze pad. A small amount ofpaste can be left on the skin at the end of the peel so that athin layer of resorcinol remains to give full results. It is notstrictly necessary to take the paste off in the same order itwas applied. It can be left to work longer in certain places toincrease the strength of the peel locally – for example onthe more resistant skin on the forehead.

If the doctor wishes to remove all of the paste, the fol-lowing solution can be used:

tincture of Benzoin 50 mltincture of Quillaja10 50 mlrose water 100 ml

Immediate post-peel careThe patient remains lying down for around half an hourafter the peel. The back of the table is raised to take thepatient gradually from a lying position to a sitting position,and he or she continues to be hydrated. The patient thengoes home, with an analgesic or an anti-inflammatory todeal with any pain or unpleasant burning. 3M cold packscan help ease the sensation of heat. Resorcinol peels owesome of their effectiveness to the presence of siccativeagents.11 Any topical hydration of the skin must thereforebe strictly avoided until flaking has begun. Actual down-time will start after the second application of the resorcinolpaste, and will last for 8 days. It is important to warn thepatient about the downtime and explain clearly how theface will look during the week it is flaking. The ‘resorcinolmembrane’ flakes from the fourth day. The more mobileareas of the face will flake first: around the mouth and eyes.The resorcinol membrane slowly cracks, making the skinlook around 100 years old! It grips the skin in a straitjacket,making it difficult to speak and eat sometimes. The patientshould 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, withoutpulling the skin at all. The skin is pink and sensitive under-neath the resorcinol membrane. As soon as flaking starts,


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the skin needs hydrating (vitamin E hydrating and antioxi-dant cream, or even Vaseline® if necessary). Effective sunprotection (see Chapters 2 and 3) must be used perma-nently for 1–3 months. How long sun protection is useddepends on the risk of hyperpigmentation (skin phototypeIV, sunny climate, working outside, etc.).

Repeating the peelAccording to Unna, the resorcinol paste can be appliedagain as soon as flaking has finished. We are rarely calledupon to repeat an application of resorcinol paste nowa-days. The results of an Unna’s paste peel remain modest inrelation to the complexity of the treatment and the down-time involved, and patients are not prepared to acceptthese conditions.

Jessner-type resorcinolsolutions

Formulations of differentsolutionsSome authors use m/m instead of m/v, which changes theactual concentration of the active ingredients. It is alsoimportant to stress the need for the pharmacist to use thecrystal form of the lactic acid and not the solution form.Lactic acid in fact comes in liquid form with a concentra-tion of 85%. The pharmacist should use lactic acid crystalsand not solution to prepare the Jessner solution. Moreover,different molecules, many of them unknown, are used todenature alcohol, to make it unfit for drinking, and there isa risk of potential chemical interactions with the acids. Thealcohol used by the pharmacist must be pure, not dena-tured. Resorcinol solutions have been used at concentra-tions of 10–50% in alcohol or ether to treat keratoses.

Resorcinol solutions have the distinct advantage of nothaving to be neutralized.

Eller and Wolf’s solution (1941)12

resorcinol (crystals) 17 gsalicylic acid13 (crystals) 8.5 glactic acid14 (crystals) 8.05 cm3

rose oil 0.05 cm3

alcohol 95° ad 100 ml

Five to eight coats are applied one after the other with cot-ton, depending on the depth of peel desired and the skintype. Three coats produce frosting and six coats produceedema. Eller and Wolf recommended constant hydrationof the patient before and after treatment.

Urkov’s solution (1946)resorcinol 38 gsalicylic acid 6.6 glactic acid (solution) 13 cm3

alcohol 95° ad 100 cm3

After leaving the solution to rest for 24 hours and filteringit, UV exposure was what made it effective! Solutions notexposed to UV did not appear to work. The skin was alsoprepared by UV exposure, and the solution was applied fivetimes, leaving each coat to dry before the next application.Urkov then applied an occlusive mask. This mask allowedthe superficial layers to hyperhydrate by blocking transepi-dermal water loss (TEWL). The hyperhydration dissolvedthe salicylic acid that would have precipitated on the skinwithout occlusion and could not have penetrated, as onlythe acids in solution can readily penetrate the skin barrier.He then applied zinc stearate powder (which is antisepticand anti-inflammatory). The erythema subsided in 5–6days and exfoliation was superficial. The solution can bekept in the fridge for 10 days.

Jessner’s15 solution or Combes’16

solution (1950s)resorcinol (crystals) 14 gsalicylic acid (crystals) 14 glactic acid (crystals) 14 gethanol 95° (not denatured) ad 100 ml

Jessner’s solution must be kept in a glass, light-protected,hermetically sealed bottle. It can be kept in the fridge formore than 2 years like this. When the solution oxidizes, itturns pink. Contact with the fingernails can turn themorange–yellow.

Other combinationsResorcinol solutions have been used in combination withglycolic acid, trichloroacetic acid (TCA) and 5-fluorouracil(5-FU). Many modified versions of Jessner’s solution havebeen presented, containing kojic acid, hydroquinone, etc.The effectiveness of these resorcinol solutions depends onskin preparation, skin sensitivity and thickness, the type ofapplicator and the force of application, the number of coatsapplied, the type of solution used, the quality of the solu-tion’s preparation, etc. Moreover, products with a tyrosi-nase-inhibiting action (kojic acid, hydroquinone, etc.) onlyproduce their effect in the long term. Single application ofthese products cannot treat melasma in any way. Onlyrepeated applications, allowing the gradual absorption ofproducts that inhibit melanocyte metabolism, can be con-sidered as an effective treatment.


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Jessner’s formulaIndicationsJessner’s solution provides an exfoliating peel, effective inthe treatment of acne and dyschromias of superficial ori-gin.

SafetyIt is a relatively safe peel. Overpeeling is rare with this treat-ment, but phototypes IV to VI are still contraindicatedbecause of the risk of pigmentary changes. Unlike resorci-nol paste, Jessner’s solution does not cause dizziness, tinni-tus or faintness. When applying the solution on largesurface areas, however, it must be taken into account thatthe potentially toxic agents that it contains may beabsorbed and are likely to be eliminated via the liver andkidneys. According to Rubin, applying Jessner’s solutionon the face, neck and décolletage in a single session remainswithout danger of salicylism. Salicylism was described,however, again by Rubin, when doing Jessner peelstogether on the face, neck, arms and lower limbs.17

Standard application of Jessner’ssolution (original formula)Preparing the skinStandard skin preparation increases the depth of penetra-tion of Jessner’s solution and improves the results – at thesame time as increasing the risk of complications. Anallergy test is essential, especially because of the resorcinolin the formula.

Cleaning and degreasingThe skin is cleaned and degreased with alcohol and ace-tone. Care should be taken not to abrade the skin manuallywith the gauze pad while degreasing.

Applying the solutionApplying Jessner’s solution is about as painful as a TCApeel at 15%. It is applied gradually, leaving each coat to drycompletely before applying the next coat. The strength ofthe peel depends on the number of coats applied; it istherefore possible to penetrate the skin gradually. Care-lessly applying one coat immediately after the other wouldtake the peel beyond the desired effect and increase the riskof complications. It takes time to do a peel with Jessner’ssolution. The depth of action also depends on the force ofapplication: the greater it is, the deeper will the acids pene-trate. Patients with thin skin should be treated with lighterhand 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 touse disposable applicators to avoid any risk of transmit-ting infection. The first coat usually causes erythema andoccasionally some pinpoint frosting. Some ‘pseudo-frost-ing’ can usually be seen after the ethanol has evaporated:this is caused by the ingredients of the solution, especiallythe salicylic acid, precipitating on the skin. Unlike genuinefrosting, which is protein coagulation, ‘pseudo-frosting’can be brushed off easily. The patient should be fannedwith a hand-held or portable fan, to alleviate the ‘burning’sensation and get rid of any unpleasant fumes. If theapplication remains at level 1, only a very slight drying ofthe skin will be observed afterwards.

� Level 2: The skin is left to dry for 4–5 minutes betweentwo successive coats. The second and third coats triggermore pronounced erythema and cloudy white frosting,as well as some pain and discomfort. The discomfortwill last around quarter of an hour. Trauchessec19

applies the solution once a week until results areachieved. The first treatment consists of only one coat,the second of two, and the third of three coats of solu-tion. After level 2, the patient’s skin feels dry and tight.The top layers of the epidermis, dried out by the solu-tion, appear transparent but still stick to the underlyingcells. Flaking occurs within 4–5 days. Locally, someareas may turn a brownish color where Jessner’s solu-tion has penetrated more deeply than anticipated. Afterthree coats, the stratum corneum separates from theskin, there is no blistering or epidermal necrosis, andthe dermis is not directly affected.

� Level 3: applying further coats deepens the effect of Jess-ner’s solution. The erythema becomes established and thefrosting tends to spread over a wide area, sometimes overthe whole of the treated area. Flaking is more pro-nounced, and the skin is brownish and comes away inlong strips. This can last around 10 days. Downtime iscommon at this depth, even if there is rarely any scabbing.

Post-peel careThe skin still feels tight and dry, but it should not behydrated. When flaking has finished, the patient can wearmake-up and should use effective sun protection. Thepatient must not help the flaking along at the risk of caus-ing erythema and pigmentary changes.

Jessner’s as a preparation for a TCApeelJessner’s solution can be used as a preparation for a deeperpeel.

Monheit techniqueThe skin is prepared and cleaned in the usual manner. TheJessner’s solution is applied to level 1: erythema occurs,


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along with some localized pinpoint frosting at most. Fiveminutes should be left between each coat. The last coat isleft to dry, and then TCA is applied – this will penetratemore quickly and more evenly20 because of the breakdownin the epidermal barrier function. It will also be morepainful. This technique could be used on patients withthick and oily skin when better TCA penetration isneeded.

Jessner’s as a preparation for an AHApeelA Jessner’s peel would improve and even out AHA pene-tration through the skin.

Moy techniqueThe skin is prepared and cleaned in the usual manner. Jess-ner’s solution is applied to level 1. The last coat is left to dryfor 5 minutes, and then glycolic acid is applied until theerythema spreads. This is followed by neutralization.Because of the erythema already caused by Jessner’s solu-tion, it is difficult to judge the progress of the AHA peel,and it is common for it to penetrate too deeply causingunexpected frosting. This more delicate technique shouldonly be used for treating very thick and oily skins that cantolerate high concentrations of AHAs being left on the skinfor long periods before neutralization.

Jessner’s for the neck and décolletageJessner’s solution is applied in the usual manner, but at arate of one peel every 2–4 weeks. Under no circumstancesshould the patient help the skin to flake, which could leavedepigmented or hyperpigmented patches.

Jessner’s for keratosesTo treat actinic keratoses with Jessner’s solution, the skin isfirst degreased carefully with acetone. Jessner’s solution isthen applied once a week for around 8 weeks. This treat-ment is not very effective, however, as no more than 15% ofthe actinic lesions disappear.

Toxicity and side-effectsJ Andeer tested the toxicity of resorcinol at the end of the19th century.6 He consumed gradually increasing doses ofresorcinol and made objective and careful notes of the sen-sations he felt and the symptoms he developed. In this way,he tested a daily intake of 1 g of resorcinol, and graduallyincreased the doses until he was taking 10 g of resorcinol in15 minutes. This triggered auditory, visual, muscular andproprioceptive symptoms, then convulsions with breath-ing difficulties and muscle contractions. He was fortunate

enough to be able to report that all these phenomena dis-appeared after 5 hours of ‘resorcinol agony’. History doesnot tell us if he tried the experiment again to evaluate itsreproducibility, but we know that other colleagues havetried the same kind of experiment on themselves withresorcinol and many other toxic agents as well.

Although it belongs to the phenol group of chemicals,resorcinol has very different exfoliating properties and it isfar less toxic than phenol itself. The routes of metabolicdetoxification are mainly via the liver and kidneys. As aprecaution, patients with liver or kidney deficienciesshould be ruled out, as well as patients with arrhythmia andwomen who are pregnant or breast-feeding.

ToxicityResorcinol is toxic by ingestion of an average dose of 6 g.Serious accidents have been described after ingestion of3.5 g, however.6 It irritates the mucous membranes and theskin, and ingestion can cause methemoglobinemia,cyanosis, convulsions or even death. Cases of methemoglo-binemia have been described after application on legulcers, but not after a peel on normal skin.

The problem raised with the use of Jessner’s solution ismore the fear of salicylism than the toxicity of the resorci-nol itself. Cases of salicylism have been described afterapplication of Jessner’s solution together to the face, chest,arms and legs.17

The size of the surface area treated, body weight and howwell hydrated the patient is are all key factors: the risk oftoxicity increases with the surface area treated. There is agreater risk in patients with low body weight and patientswho are not well hydrated.

Secondary hypothyroidismThyroid injury after chronic skin application of resorcinolhas been reported several times. In 1977, Katin and col-leagues21 published a case of hypothyroidism following reg-ular application of a 2% resorcinol cream in a chronicdialysis patient suffering from pruritus. The mechanism ofaction seems to be as follows: the presence of a hydroxygroup in the meta position in the resorcinol would blockthe metabolism of iodine by inhibiting the peroxidaseneeded to oxidize iodide into iodine, the only form that canbe assimilated by the body.

AllergiesUnna’s pasteAllergies to resorcinol have been widely described. It istherefore wise to do a skin sensitivity test behind the ear 8days before a resorcinol peel. Any contact with resorcinolcan 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 firstpeel does not trigger an allergic reaction is no guaranteethat the next peel will not trigger one. Allergy to resorcinolis permanent – there is no point trying again.

In the allergy test, a small quantity of Unna’s paste isapplied to a patch of skin 2 cm × 2 cm behind the ear andleft for 15 minutes. The test is read immediately and thenagain 48 hours and 5 days later – although Letessier3 rec-ommends just one reading, after 4 days.

It is important not to confuse an allergy with the skin’snatural response to the chemical peel applied behind theear. A highly localized and normal skin reaction to the peelwill occur: erythema followed by flaking. The appearanceof any blistering or pruritus contraindicates any furthercontact with resorcinol completely and definitively. If apatient is allergic, Unna’s paste causes reversible facialeczema, with no cosmetic benefit.

Jessner’s solutionThe allergy rate to resorcinol is less than 0.1%.17

HyperpigmentationPigmentation disorders are relatively common after aresorcinol 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 thosewho had pigmentation problems before the peel, thosewho take oral contraceptives or are on hormone therapy,and those who have a record of post-traumatic or post-inflammatory hyperpigmentation or have a high density ofmelanosomes (phototypes IV to VI).

Potential problems with pigmentary changes are treatedin the usual manner, as described in Chapter 37. Pigmenta-tion problems such as ochronosis after a resorcinol peel,also described in the literature, are more complicated totreat.

Prolonged erythemaA few areas of mild erythema, which changes color with thecold, alcohol or emotion, can very occasionally last for sev-eral weeks. Erythema after a resorcinol peel is usuallyreversible without treatment, but requires preventive treat-ment against pigmentary changes, especially in high-riskpatients (see the preceding paragraph and Chapter 37).

Dizziness and nauseaDizziness and nausea can occur during or after applicationof the paste.

Some authors attribute these symptoms to peripheralvasodilation and the resulting low blood pressure. Thisexplanation is not very satisfactory, however, as facial

vasodilation is in no way correlated with low blood pres-sure. Other facial peels produce at least the same degreeof vasodilation without causing low blood pressure orfaintness. What is more, there would have to be a greatdeal of peripheral vasodilation to make blood pressure solow that a patient in the lying position can feel it. Bloodpressure readings taken after a peel are not low enough toexplain this ‘dizziness’. It would appear instead that weare witnessing the actual symptoms of the beginnings ofresorcinol poisoning, which fortunately soon resolve. Weshould not forget that resorcinol is a phenol compound.Using Unna’s paste and Jessner’s solution on large areascan theoretically lead to the usual phenol complications.If we consider that resorcinol is usually 40 times less toxicthan phenol itself, we must also take into account that100 g of Unna’s paste contains 40 g of resorcinol. That isthe toxic equivalent of 1 g of phenol. The precautions ofslow application (in 1 hour) that are taken with phenolare not observed for resorcinol and, with resorcinol, thearea treated is often larger. Resorcinol is a small moleculethat, like phenol, is easily absorbed by the capillaries.Rapid application of a thick and warm layer of resorcinolcan introduce a relatively large quantity of the substanceinto the bloodstream and trigger the start of neurologicaltoxicity typical of phenol compounds. As a result, theface can be treated in perfect safety, but when large areasare being treated, as is the case with a peel on the back, itis essential that the treatment consist of several separatepeels.9 Arouette9 reports an unpublished clinical case ofan extensive application of Unna’s paste bringing oncoma in a few hours with full recovery.

Secondary infectionsA recurrence of herpes lesions should be anticipated, andpreventive treatment should be taken if necessary. Scratchlesions22 can trigger impetigo on the face. Scratching is theonly explanation for signs of infection after a peel withUnna’s paste or Jessner’s solution.

ScarringAs with any superficial peel, and under normal conditions,the risk of developing scars is very low. Nevertheless, scabsand dry skin should not be pulled off.

Inadequate resultsIf the results are considered inadequate, the patient mightbenefit from further peels. A maintenance resorcinol peelcan be done every year, if indicated. According to Unna(quoted by Arouette9), ‘under some circumstances, it isnecessary to do several successive exfoliations that can beperformed without interruption’.


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Notes1. 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 andPractice, 2nd edn. 1115-19. 1996, UK, Oxford, MarcelDecker Ltd.

4. Collins PS. Chemical face peelings. In: Evaluation and Treat-ment of the Aging Face. 34–67.

5. Terpenes are are a class of compounds whose chemicalstructures are based on a number of ‘isoprene units’, derivedfrom the hydrocarbon CH2=C(CH3)–CH=CH2; they maythemselves be hydrocarbons, but may also contain alcohol(OH), aldehyde/ketone (CO) and carboxylic acid (COOH)groups. Monoterpenes are C10 compounds derived from twoisoprene units, sesquiterpenes (C15) are derived from threeisoprene units, diterpenes (C20) from four and tritepenes(C30) from six. Terpenes are widespread in plants, where theyare largely responsible for the odor, and they are the majorconstituents of plant-derived ‘essential oils’. Among the bestknown terpenes are β-pinene (turpentine), camphor, men-thol and citronellal (all monoterpenes) and farnesol (asesquiterpene that is a constituent of the essential oils ofmany plants). Certain terpenes have important biologicalroles: vitamin A, for example, is a diterpene, and steroid hor-mones have a structure related to triterpenes (and arebiosynthesized by a similar route).

6. Manquat A. Traité élementaire de thérapeutique de matièremédicale et de pharmacologie, 5° ed, tome 1. 1903: 240-60.

7. Kaolin (like ceyssatite) has absorbent properties that allow itto trap microorganisms.

8. Note the distinction between benzoic acid (C6H5COOH), inwhich a carboxylic acid group is attached to the benzenerign, and phenol (C6H5OH), in which the substituent on thebenzene ring is a hydroxy group.

9. Arouette J. Dermabrasion, relèvements, peelings. In: Black-well A. (Ed.), Collection des Manuels pratiques de médecineesthétique. 1989, Paris.

10. Quillaja bark is a natural soap containing 9–10% saponins,

and is used in phytotherapy for dandruff, athlete’s foot, andirritated or sensitive skins.

11. Used alone, a resorcinol peel at 5% triggers light exfoliation.The real peeling effect starts at 25% and becomes more obvi-ous at 40%.

12. Dr Eller and his assistant Shirley Wolf described this formulain New York in 1941.

13. Salicylic acid (3–5%) triggers light exfoliation. A concentra-tion of 15% is needed for a superficial peel. A concentrationof 50% (beware of salicylism) produces a dermal peel.

14. Such weak concentrations of lactic acid are ineffective inthemselves, but may enhance penetration of the other ingre-dients.

15. Max Jessner qualified as a dermatologist in Germany in1922. He developed the solution that bears his name for thetreatment of acne in the 1950s at New York University Hos-pital. Dr Jessner’s aim was to improve the performance ofpeels at the same time as reducing the risk of side-effects, byexploiting the synergy between the different ingredients.

16. Dr FC Combes made wide use of Jessner’s formula in the1960s, and is better known in the USA.

17. Rubin MG. Manual of Chemical Peels, Superficial andMedium Depth. Philadelphia: JB Lippincott, 1995.

18. Frosting is reached more quickly with a brush than with adouble cotton bud, unless greater pressure is applied.Brushes should be used once only or disinfected with povi-done–iodine. Single-use brushes are preferable: would youlike to treat your skin with a brush that has already been usedon acres of unknown skin?

19. Trauchessec JM. Teoria y practica de los peelings. Med Estet1996; 40: 11–21.

20. This would not be the case with AHAs before a TCA peel(Coleman technique). AHAs do not penetrate evenly, andmight cause the TCA to penetrate still more unevenly.

21. Katin MJ, Teehan BP, Sigler MH, Schleifer CR, Gilgore GS.Resorcinol induced hypothyroidism in a patient on chronichemodialysis. Annals of Internal Medicine 1977; 86(4): 447–9.

22. As well as over-enthusiastic personal hygiene (e.g. using asponge such as a Buf Puf®, non-prescribed cosmetic scrubs, aface cloth – which is a breeding ground for microbes – etc.).


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Chemistry of phenolAs a class, phenols are compounds in which a hydroxygroup is attached to a benzene ring. The name ‘phenol’ isalso used to refer specifically to the simplest compound inthis group, which is also known as hydroxybenzene, ben-zenol and carbolic acid (Figure 25.1). Phenol has a molec-ular weight of 94.11, a specific gravity of 1.071 and a boilingpoint of 182°C. It can react vigorously or even violentlywith other compounds, including formaldehyde, acetalde-hyde and trifluroacetic acid, as well as aluminum chloride,nitrobenzene, some nitrates and nitrites, and other oxidiz-ing agents. Phenol crystals are white or pink, and melt at41°C. Most commercial phenol has a purity of 98%, but100% pure phenol is obtainable.2

Phenol was formerly obtained from coal tar, but is nowmade by hydrolyzing chlorobenzene at 350°C or, most fre-quently, by air oxidation of cumene3 and treatment of theresulting cumene hydroperoxide to yield, phenol and ace-tone (Figure 25.2). Estimates of the amount of phenol pro-duced worldwide vary, but since 1980 have usually beenover 5 000 000 tons.

Phenols may have more than one hydroxy groupattached to the same benzene ring – for example, the threeisomeric4 dihydroxybenzenes catechol (ortho-dihydroxy-benzene or 1,2-benzenediol), resorcinol (meta-dihydroxy-benzene or 1,3-benzenediol) and hydroquinone (para-dihydroxybenzene or 1,4-benzenediol): see Figure 25.3.

Molecules that have a single benzene ring with one ormore hydroxy substituents are known as ‘simple phenols’ –examples are phenol itself and the three dihydroxybenzenesmentioned above, as well as the cresols (see below). Thereare also ‘diphenols’ (Figure 25.4) and polyphenols. Polyphe-nols are complex molecules containing several benzene ringswith one or more hydroxy substituents. They are widespreadin nature, often lending plants their color. Polyphenols(flavonoids and anthocyanins) constitute an importantgroup of antioxidants used in anti-aging medications;flavonoids (Figure 25.5) are a distinctive group of polyphe-nols with a specific structure, containing two benzene rings,one of which is fused to an oxygen-containing ring.

25Phenol: chemistry, formulations and adjuvants

OH

Figure 25.1Chemical structure of phenol.

CHCH3CH3

CH3CH3OOH

A B

Figure 25.2Chemical structure of cumene (a) and cumene hydroperoxide(b).

OH

OH

OH

OH

OH

OH

A B C

Figure 25.3Chemical structures of catechol (a), resorcinol (b) andhydroquinone (c).

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Phenol derivativesMedicine has made wide use of phenols in many indica-tions, as we shall see later in this book. Medical publica-tions on peels abound in terms that are no longer in useand names of outdated molecules, which makes some textsdifficult to read. It is therefore worthwhile taking a quicklook at what these terms and compounds correspond to.

Cresols – Lysol®

Cresols are simple phenols in which the benzene ring hasone methyl and one hydroxy substituent. There are threeisomers: ortho-, meta- and para-cresol5 (Figure 25.6). Coaltar cresol or cresylol is a mixture of the three isomers and isalso called cresylic acid, hydroxytoluene and methylphe-nol. Coal tar and cade oil are mixtures of cresol and guaia-col (see below). Lysol® is the trade name of a solution ofcresols in saponified vegetable oil, developed to counter thedifficulties of putting cresol in solution form. It was analkaline detergent containing 47–50% crysylol (= cresol =cresylic acid = cresylic phenol) as well as a little guaiacol,xylol, etc. Chemically, therefore, it was a poorly definedsolution that nevertheless had the advantage of providing aclear solution when mixed with distilled water. Crudecresol comes from coal tar and consists of the three iso-mers: ortho-cresol 35–40%, meta-cresol 35–40% and para-cresol about 25%. Cresol mixtures are used as

preservatives, deodorants and disinfectants. Ortho-cresol isa solvent and disinfectant. Meta-cresol is mainly used ininsecticide chemistry or to produce antioxidants. Para-cresol is mostly used in perfumery. Many foods containcresols: butter, wine, tomatoes, asparagus, cheeses, baconand smoked foods. Cresol is four times as toxic as phenol.

Cresol mixtures are irritating to the respiratory tract andthe skin. Although only anecdotal information is availableon the potentially carcinogenic effects of cresols inhumans, the US Environmental Protection Agency hasclassified these molecules as ‘possible human carcinogens’.Signs of intoxication include abdominal pain and vomit-ing. Other symptoms have also been described, such asheart, liver and kidney problems. Facial paralysis, comaand death are also possible with higher concentrations,even through simple skin contact.

GuaiacolGuaiacol (Figure 25.7) is also called o-methoxyphenol, 1-hydroxy-2-methoxybenzene and catechol methyl ether. Itis found in Valda® pastilles and expectorants, and is alsoused to make vanillin. It was originally extracted from atree (Acacia catechu Willd), and then distilled from guaiacresin. Nowadays, pure guaiacol is synthesized from cate-chol, of which it is the methyl ether. Guaiacol salicylate hasanalgesic and anti-inflammatory properties. Its analgesicproperties are due to the inhibition of cyclooxygenase andprostaglandin synthesis and the release of bradykinin. Gua-iacol salicylate is anti-inflammatory as it stabilizes the lyso-


Figure 25.5An example of a polyphenol: the flavonoid catechin.

OH

OH

OH

OH

HO O

OH

OH

Figure 25.4An example of a diphenol: 2,3'-dihydroxybiphenyl.

OH

CH3

OH

CH3

OH

CH3

A B C

Figure 25.6Chemical structures of ortho-cresol (a), meta-cresol (b) andpara-cresol (c).

OH

OCH3

Figure 25.7Chemical structure of guaiacol.

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somal membrane and inhibits the action of the chemicalmediators of inflammation.

Halogenated phenolsHalogenated phenols are more powerful disinfectants thansimple phenols, as they are more lipophilic. They are alsomore toxic to the central nervous system. The chlorinatedphenols are the most active. Toxicity is specific to eachcompound.

Phenolic acidsPhenol acids are phenols in which there is also a carboxylicacid group attached to the benzene ring. They include sali-cylic acid (ortho-hydroxybenzoic acid) and para-hydroxy-benzoic acid (Figure 25.8). Acetylsalicylic acid (aspirin)and sodium salicylate are derivatives of salicylic acid. Likephenol, they have antipyretic and analgesic properties. Themethyl, ethyl and propyl esters of para-hydroxybenzoicacid (parabens) are used as preservatives in pharmaceuti-cals, cosmetics and foodstuffs.

BisphenolsBisphenols (not to be confused with the diphenols), areformed by two phenols linked with a bridge (–CH2–, –O–or –S–) in the ortho position, which makes the product eas-ier to tolerate. Bisphenols are often chlorinated to increasetheir disinfectant power. Dichlorophene, tetrachlorophene

and hexachlorophene (Figure 25.9) are members of thisgroup of compounds. Septisol is a hexachlorophene soapused widely as a wetting agent in old phenol peel formula-tions.

Picric acidPicric acid (Figure 25.10) is 2,4,6-trinitrophenol. It is usedin the treatment of burns in a 1% solution because of itsstimulating effect on keratogenesis. The dry crystals areextremely sensitive to friction or shock6 and were widelyused as an explosive before the discovery of TNT (trinitro-toluene). Picric acid can be synthesized from phenol, ben-zene or aspirin. It is soluble in water and alcohol. It turnsthe skin yellow. Applying swabs with 1.2% is not irritatingbut produces light flaking within 2–4 days. Using picricacid on open wounds and ulcers appears to stimulate epi-dermal regeneration.

Paracetamol (acetaminophen)Paracetamol (known as acetaminophen in the USA) is N-acetyl-para-aminophenol (Figure 25.11). It has the samedetoxification pathways as phenol and also carries the riskof inducing methemoglobinemia. To be on the safe side, itshould not be used as an intravenous analgesic during afull-face phenol peel, so as not to saturate the detoxifica-tion pathways. Paracetamol is also an intermediate in thepathway for detoxification of aniline derivatives, beforehepatic glucuronide and sulfate conjugation allow them to

Phenol: chemistry, formulations and adjuvants 195

C

OH

O OH CO OH

OH

Figure 25.8Chemical structures of salicylic acid (a) and para-hydroxybenzoic acid (b).

A B

CH2

CI CI CI

CICICI OH

HO

Figure 25.9Chemical structure of hexachlorophene.

OH

NO2

NO2

O2N

Figure 25.10Chemical structure of picric acid.

OH

HN.CO.CH3

Figure 25.11Chemical structure of paracetamol (acetaminophen).

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be eliminated in urine. The aniline derivatives acetanilideand phenacetin were once used as analgesics andantipyretic agents, but turned out to be excessively toxic,and were replaced by paracetamol, which had been shownin 1949 to be their major metabolite.

Different formulations ofphenol peelsPeels of the pastReviewing publications on phenol peels reveals a greatmany different formulations. The first surgical operationwhere phenol was used as a disinfectant took place inMarch 1865 (Lord Lister 1827–1912: Figure 25.12). At thevery beginning of the 20th century, Manquat’s treatise onpharmacology7 described in detail the use of phenol as ananesthetic and disinfectant, at concentrations of around5% in aqueous, oil or alcohol solutions. Preparationinvolved the use of various ingenious tricks to prevent thesolutions from separating into multiple layers and to pre-vent the formation of isolated caustic droplets. After a rela-tive lull, other formulations started to appear in medicalpublications. They reflect the constant search for the idealsolution and the increasingly clear understanding of themechanisms that lie behind the excellent results achievedwith today’s phenol peels. From this mass of publications. Ihave selected 13 major authors or groups of authors whoseformulas will be surveyed in alphabetical order.

Ahronson presented a glycerinated phenol formulation:88% liquid phenol is solubilized in anhydrous glycerol(glycerin) and a few drops of alcohol. This highly concen-trated formula, used without occlusion, produces a peelthat is not as deep as a peel with Baker–Gordon solution.

Ayres achieved a medium-depth peel by combining phe-nol and trichloroacetic acid (TCA). These two formulas areno longer used today, as there are many other modern peelsolutions that provide effective medium-depth peels usingother molecules, such as TCA, that are not potentiallytoxic.

Two Baker solutions are described. The first containsliquid phenol USP 5 cm3, distilled water 4 cm3, croton oil 3drops and septisol 5 drops. The second contains liquid phe-nol USP 3 cm3, distilled water 2 cm3, croton oil 3 drops andseptisol 8 drops. The water determines the concentration,which is variable. Baker’s solution has to be stirred con-stantly, as it is not stable and separates into layers if left to rest.

Brown and Kaplan presented a more complex solution ofphenol (at varying concentrations between 60% and 95%)mixed with saponified cresol in oil at concentrations of upto 10%. The application technique included a patch testbehind the ear. This test made it possible to assess thenecrotic effect of the solution on the patient. If the necrosiswas too severe, the test was repeated with increasing con-centrations of oil until the right solution for the patient wasfound. They recommended applying the solution area byarea, leaving 2 hours between applications. The peel took 2days to complete.

Combes, Sperber and Reisch used an aqueous solutionwith a high concentration of phenol, combined with citricacid and sodium salicylate.

Eller and Wolff, on the other hand, advocated an alcoholsolution 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 applica-tion depending on how sensitive the skin was.

Grade’s three formulas (aqueous phenol with crotonoil), which had widely varying amounts of phenol andwater, had to be left to rest for 6 weeks before use. This rest-ing time was needed for ‘peroxides’ to form and buffer thesolution.

Klein presented a solution that was largely based onBaker’s, but with different concentrations.

Karp’s three formulas are well known: the first wasalmost 80% glycerinated phenol, the second combinedphenol with acetic acid, boric acid, salicylic acid and citricacid, but could only be applied locally, as it was too strong.Karp called his third formula ‘the phoenix’: it was an aque-ous solution of glycerinated phenol combined with aceticacid and sodium salicylate.

Litton proposed using a detergent other than septisoland recommended using glycerol. He was one of the first todescribe an increase in the thickness of the Grenz zone aftera phenol peel.


Figure 25.12Lord Lister.

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Litton’s solution, as well as that of Truppman andMaschek, had the dual advantage over Baker’s of being sta-ble in space and time. These aqueous and glycerinatedsolutions with concentrations of around 50% in phenolcontained croton oil. Once prepared, they could be kept forseveral years when stored away from light and heat sources.Litton’s solution contains more croton oil than that ofTruppman and Mascheck.

Urkov used a simple alcohol solution of phenol, andtreated deep wrinkles with electrocoagulation after thepeel.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 phe-nol: Lysol® (an oil solution of cresol) and phenol with var-ious oils, including croton oil. The water has to be distilled,as Lysol® forms calcium cresate when mixed with tapwater. The solution then becomes opalescent instead ofclear.

Peels of todayExoderm®My late friend, Yoram Fintsi, deserves special mention inthis book, because, as well as being a close friend, he wasone of the main catalysts for the current success of phenolpeels, thanks to the formula he developed, Exoderm®.According to Fintsi, the Exoderm® formula was made in1986 and then refined in 1990. Thereafter, Fintsi in Israeland Benhamou in France improved the formulation. Sev-eral formulations were put forward, one after the other, asshown in Table 25.1. The elements in common are listedabove the dashed line. The first two formulas used septisol,a disinfectant soap with hexachlorophene, while the thirdformula – the one used today – simply contains saponins.The first formula contains TCA, the second salicylic acidand the third citric acid. The second two formulas arebuffered to stabilize the pH. Fintsi commented on his owncurrent Exoderm® formula in his article ‘Exoderm®, anovel, phenol-based peeling method resulting in improvedsafety’.9

Hetter formulasIn 1996, Hetter put forward a series of formulations based onthe principle that by simply changing the concentration ofcroton oil, the depth of the peel could be varied (Table 25.2).

Changing the concentration of croton oil is, indeed, oneway of changing the strength of a phenol peel. It is not,however, the only way, and it is perfectly possible to do aphenol peel without croton oil. It is also possible to vary thedepth of action of phenol without changing the concentra-tion in croton oil. It is not, of course, a matter of question-ing the intense cytotoxic effect of croton oil (see the sectionon adjuvants below), as Hetter10 stresses in 2000. Nor is it amatter of questioning Hetter’s legitimate refutation of thedogmas that claim, on the one hand, that lower concentra-tions of phenol wound more deeply (a lower concentrationof phenol can penetrate more rapidly11 through an epider-mis that is made more permeable by protein lysis and cantherefore be more toxic) and, on the other hand, that phe-nol has an ‘all-or-nothing’ action, which is clearly untrue asalso said by Dr Hetter. Attempts are currently being made


Table 25.1 Exoderm® formulas

Formula 1a Formula 2 Formula 311

Liquid phenol Liquid phenol Liquid phenolPhenol crystals Phenol crystals Phenol crystalsDistilled water Distilled water Distilled waterAlcohol Alcohol AlcoholOlive oil Olive oil Olive oilSesame oil Sesame oil Sesame oilGlycerol Glycerol GlycerolCroton oil Croton oil Croton oilResorcinol Resorcinol ResorcinolSeptisol Septisol SaponinsTCA 30% Salicylic acid Citric acid

Buffers Buffers

aFormulation certificate with bottles of Exoderm®, September1995. The solution’s pH is 4.8.

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 abovemixture 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® formulaLip & Eyelid® formula is a phenol peel that I first developedto increase dermatological safety and to achieve resultswithout any occlusion on the sensitive skin of the eyelids.The same solution was then applied to the wrinkles aroundthe mouth and then to the whole face, but with 24 hours’occlusion in these two indications. It is an oil solution ofphenol at over 60%. Four different oils are used in the var-ious stages of the product’s preparation. The aim of the oilyformulation is to slow down the penetration of the phenolthrough the skin and to improve dermal and epidermalmaceration. It limits the toxicity of phenol by saturatingthe biochemical hepatic detoxification pathways moreslowly.

Split face treatment, comparing exoderm and lip & eyelidformula showed a higher efficacy of the last formula.

Storing phenol peel solutionsPure phenol is resistant to light, but the presence of impu-rities, even in small traces, turns it red due to oxygen fixa-tion. This coloring does not change the properties of theproduct. Exoderm® solution must be stored away fromlight12 and humidity, however. It can be stored for 3 yearsin its original, unopened bottle. The contents of an openedbottle must be used within 1 year. Baker’s solution must beprepared for immediate use, unlike Litton’s solution,which can be kept for 3 years in the refrigerator. Medicalpublications report using the same solution successfullyduring a great many years. Lip & Eyelid® formula alsoremains stable for at least 3 years if kept in the refrigeratorin the original, closed bottle.

Adjuvants of phenol peelsGeneral remarksSolutions with a high concentration of phenol cause rapidprotein coagulation, which translates clinically into imme-diate frosting of the skin. This opaque coagulation acts as ashield that increases the skin’s impermeability, stops thesurface phenol penetrating and prevents it from passingrapidly into the reticular dermis. A solution with a concen-tration higher than 80% therefore produces a more super-ficial peel than might be logically expected. Solutions withlower concentrations, of around 15–20% for example, arekeratolytic 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. Asmall quantity of free phenol, which can only act on thedermis for a short space of time, does not make for excel-lent results. If larger quantities of these low concentrationsolutions are applied to the skin in an attempt to getaround this problem, the increased rate of reabsorption ofphenol could saturate the detoxification pathways and therisk of intoxication is higher. At both higher and lowerconcentrations, effectiveness is blocked and adjuvants areneeded to make it more effective.

Everything that surrounds the phenol molecule, frompre-peel treatments to formulation methods, can be con-sidered an ‘adjuvant’. Unlike superficial or medium peels,preparing the skin before a phenol peel is not intended toenhance or even out the penetration of the phenol, as itdoes not need help to penetrate the skin. Tretinoin or fruitacids are not necessary in pre-peel preparation, and perfectresults are achievable without using them. Small, benigntumors can be treated with electrocoagulation immediatelybefore the peel. Urkov, for his part, treated deep wrinkleswith electrocoagulation after applying phenol and beforeapplying the occlusive dressing. The skin must be cleansedand degreased thoroughly to get rid of any epidermal lipidsand debris that can interact with or partially inactivate thephenol. Pre-peel and post-peel care, which are discussed indetail in Chapters 32 and 35, help to prevent or treat poten-tial complications. Adjuvants can, for example, enhancethe spread of the phenol within the epidermis, reduce skinsurface tension, enhance liquefaction necrosis of the epi-dermis, help the phenol reach the dermis (where it causes asevere inflammatory reaction that generates collagen andelastin and blocks its action in the upper reticular dermis)and slow down and/or reduce the capillary absorption ofthe phenol (thus allowing time for sulfate and glucuronideconjugation of the toxin before its elimination).

Different chemical adjuvantsThe peel solutions should never be prepared simply by dis-solving phenol in one of its potential solvents. Since phenolwas introduced into treatment, doctors who use it havetried to:

� Moderate (tame) its systemic toxicity. Different sub-stances have been combined with phenol to reduce itsadverse effects. It should be noted that the only demon-strated way to avoid cardiac toxicity lies in the applica-tion technique for a full-face phenol peel.

� Improve its effectiveness. Different chemical adjuvantshave been combined to modify the action of phenol.

The application technique and pre-peel and post-peel carehave very important roles. The latest formulations aretherefore tamed and adjuvanted.


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The qualitative formulas of recent products are known,but the percentages and preparation methods are notrevealed. Fintsi explained that adjuvanted and tamed phenolpeels must be prepared according to a precise method andthat he was afraid that if he revealed the exact proportions ofthe ingredients, doctors would try to make up the formulathemselves without keeping to the necessarily strict order ofpreparation, and that this could lead to disastrous results.

Logic must prevail in the attempt to understand howadjuvants work: it should be remembered that phenol hasan anesthetizing action on sensitive nerve endings throughprotein coagulation; this anesthetizing effect developswithin 10–15 seconds after application. This means that 15seconds after application, the phenol is already in the der-mis: it is therefore doubtful that combining it with productsthat penetrate more slowly, such as salicylic acid or citricacid, can improve the already rapid penetration of phenol.On the other hand, there is no doubt that phenol improvesthe penetration of these adjuvants, if they can survive with-out reacting chemically with the phenol solution itself.

ResorcinolSee Chapter 24 for more details. Although resorcinol isknown to have allergenic properties, there have been noallergies reported when it has been used in small quantitieswith phenol. However, the combined use of these two sub-stances in the same peel solution does not appear to haveany clinical value, as the phenol will have finished workingbefore the resorcinol has started. Resorcinol cannot there-fore modify the effect of phenol. No data are available onthe potential clinical effect of resorcinol on skin that hasjust been coagulated by phenol.

Trichloroacetic acid TCA is an acid whose strength of action is proportional tothe concentration used. However, it also depends onnumerous other factors that are described in detail in thechapters on TCA.

Salicylic acidSalicylic acid is a keratolytic agent that dissolves the amor-phous intercorneocyte matrix and thus diminishes the bar-rier function of the stratum corneum. It is sometimescombined with phenol, but does not improve its action.See also the comments on resorcinol and TCA above.

Croton oilCroton oil is extracted from the seeds of the shrub Crotontiglium (Figure 25.13), of the family Euphorbiaceae. In thepast, these seeds were also called Moluccas seeds, Tillyseeds or small Indian pine nuts.

Rubbing 2–10 drops of pure croton oil or croton oil witholive oil on the skin causes an intense burning sensationwithin 5 minutes that lasts for several hours and is followedby erythema. Clusters of small blisters then form and turninto pustules that dry, scab and drop off within a few dayswithout leaving any scars. If, however, the croton is appliedtoo vigorously, keloid scars may result.7

The crotonic acid (Figure 25.14)13 that it contains is anirritant that accelerates epidermal lysis and enhances thecutaneous penetration of the phenol. Some authors main-tain that a phenol peel will only produce good results if cro-ton oil is present. The croton oil enhances dermalpenetration and epidermal protein coagulation, and thuslower concentrations of phenol can be used. We have seen,however, that many phenol peel formulations do not con-tain croton oil.


Figure 25.13The shrub Croton tiglium – the source of croton oil.

C � C

CH3 H

CH �OH

O

Figure 25.14Chemical structure of crotonic acid.

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The irritant action of croton oil is used to advantage incancer research to enhance the penetration of carcinogensthrough the skin barrier. Croton oil is therefore a co-car-cinogen. In 1994, Wilmer et al14 showed that keratinocytescan produce interleukin (IL)-type substances, growth fac-tors and tumor necrosis factor (TNF). Phenol and crotonoil induce keratinocyte production of IL-8 (at non-cyto-toxic concentrations), TNF-α and also a growth factor.TNF-α is a cytokine synthesized (among others) by thekeratinocytes in the stratum spinosum and the stratumgranulosum. It stimulates the differentiation of ker-atinocytes into corneocytes and thus accelerates the fullregeneration 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 mechanismof action is probably due to the chemotaxy of the fibroblastsbeing stimulated, which improves the efficiency of the firststages of healing, without affecting the following stages.16

At the beginning of the 20th century, the vesicant prop-erties of croton oil were used to good effect on people withedema. Rubbing croton oil on large areas created numer-ous vesicles, the combined serous fluids from which pro-duced enough liquid to relieve edema in the lower limbs ofheart patients. Experiments were carried out involving theingestion of croton oil: this produced intestinal inflamma-tion with diarrhea and weight loss.17

Croton oil is a powerful toxin that taken orally in smallquantities of around 20 drops can cause fatal hemorrhagicgastroenteritis.18

SeptisolSeptisol is a liquid soap with hexachlorophene, a bisphenolused as a disinfectant. It is also a surfactant. At low concen-trations, hexachlorophene uncouples the oxidative phos-phorylation of cells and causes morphological changes inmembranes.19 It might be keratolytic.20 Intoxication ofinfants from hexachlorophene preparations (in France, in1972) resulted in neurological (encephalitis) and cuta-neous symptoms. These products have turned out to bedangerous after chronic use if not rinsed off or if applied todamaged skin or to large areas of the body with an occlu-sive dressing.

SaponinsLiquid soap helps to reduce surface tension (Box 25.1) andtherefore improves the penetration of active agents. It alsoimproves maceration under an occlusive dressing. Anionicand cationic soaps, like alcohol, enhance the action of phe-nol.19 Formulation requirements are strict. If there is toomuch surfactant, the phenol ends up within a micelle andits action is reduced. If there is not enough, the solutionsare not stable.

Cresol – Lysol®In the past, saponified cresol as well as Lysol® was used as awetting agent to increase the penetration and therefore thestrength of phenol. See the discussion of cresols earlier inthis chapter.

Acetic acidFor a description of acetic acid, see the beginning of Chap-ter 12.

Oil formulations21 versus aqueousformulationsA cell membrane is a ‘fluid mosaic’ of phospholipids in twolayers. The hydrophilic poles face outwards and thehydrophobic poles form the inside of the membrane. Thelipid cell surface is strewn with proteins. If we compare acell membrane to a chocolate cream sandwich cookie, thehydrophilic poles would be the cookies on the outside andthe hydrophobic poles would be the chocolate cream in themiddle. The surface proteins would be found in the smallholes on the surface of the cookies. If we compared a cellmembrane to a jam sandwich, the hydrophilic poles wouldbe the slices of bread and the lipophilic, hydrophobic poleswould be the jam. The surface proteins would be set in theair bubbles in the bread.

At the beginning of the 20th century, the relative imper-meability of cell membranes to many water-soluble com-ponents had already been attributed to the lipid nature ofthe membranes. Molecules that are soluble in non-polarsolvents (e.g. olive oil, sesame oil and ether) enter cellsmore rapidly than water-soluble molecules with the samemolecular weight.22 Fat-soluble molecules ‘dissolve’ in thelipophilic layers and readily penetrate the interior of the


Box 25.1 Surface tension

The forces of attraction and repulsion are more or lessevenly distributed within a liquid. The surface mole-cules, however, are unable to balance the lateral inter-molecular forces of attraction. The tension on thesurface of a liquid acts like an elastic membrane,opposing penetration in the liquid. Agents called sur-factants, wetting agents or detergents reduce this elasticsurface tension and enhance penetration in the liquid.Wetting agents also have antiseptic properties. Thereare two large groups:

• Cationic surfactants (cetrimide, lauralkonium, etc.):powerful bactericides and fungicides

• Anionic surfactants (e.g. sodium lauryl sulfate): usedto sterilize the skin before surgical operations

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cell. The ratio of the solubility of a substance in olive oil inrelation to its solubility in water provides the oil/water par-tition coefficient.

Phenol has a good oil/water partition coefficient.19 Theability of a molecule to penetrate the cell membrane is pro-portional to its partition coefficient. Adding oils to phenolenhances its action in the epidermis and papillary dermisand slows down the penetration of the oil-bound phenolthrough the skin so that it reaches the deeper dermal layersmore slowly. Phenol is also soluble in water and has a lowmolecular weight (94.11). Very small molecules that arewater-soluble and non-polar pass through cell membranesmuch more quickly than one might expect given the mole-cular structure of the actual membrane and the partitioncoefficient. These small molecules appear simply to passbetween two adjacent molecules in the membrane, withoutreally dissolving in the pole taken up by the fatty acid. It isalso possible that the proteins set in the membrane arehighly permeable to these tiny water-soluble molecules.With increasing molecular weight, membrane permeabilitydecreases and stops molecules with a molecular weightgreater than 200 from getting through. Phenol’s low mole-cular weight and its high partition coefficient would allowit to pass through the membrane rapidly if it were notbound to oily components. Moreover, phenol coagulatesmembrane 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 outabove also apply to the capillaries.

The antiseptic derivatives of phenol have structuralmodifications (halogenation and alkylation) that, byincreasing their liposolubility, improve their antisepticaction.

Brown and Kaplan made use of the ‘buffering’ propertyof oils in phenol solutions. Their formulation contained upto 95% phenol combined with oils. A patch test behind theear had to be carried out before the facial peel. If there wasskin necrosis, they reduced the strength of the phenol bygradually adding oil in small quantities until the right dosewas found for the patient’s skin. To increase the strength ofthe mixture, on the other hand, soap (saponified cresol)was added or the concentration of phenol was increased.

GlycerolAdding glycerin to phenol makes it less irritating. Glyceri-nated phenol at 10% is no longer an irritant.

BuffersBuffers keep the pH of a solution stable. Phenol is moreaggressive in an acid environment. The presence of bufferskeeps the solution at an appropriate pH. The pH of today’s

phenol solutions is usually close to the skin’s physiologicalpH.

Alcohol and waterAlcohol is used at different points during preparation tohelp products solubilize more efficiently in the aqueoussolution. Phenol, for example, is more soluble in alcoholthan in water. The purer the phenol crystals, the more sol-uble they are in water. Alcohol also enhances the action ofphenol.21 Water is also used as a solvent for certain prod-ucts or to modify the concentration of the phenol.

Notes1. In this book, ‘phenol’ is used in this sense; the plural, ‘phe-

nols’ 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 strongdepressant effect on the central nervous system.

4. Isomeric compounds (isomers) have the same empirical for-mulas but different chemical structures.

5. Also known as ortho-methylphenol and ortho-hydroxy-toluene, 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 for-

mulation?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 effec-tiveness.

12. To limit the risks of photochemical reactions. Storing thesolution at low temperatures slows down the chemical reac-tions, and is the best way to store any chemical.

13. Crotonic acid is also known as 2-butenoic acid and has amolecular weight of 86.09.

14. Wilmer JL, Burleson FG, Kayama F, Kanno J, Luster MI.Cytokine induction in human epidermal keratinocytesexposed to contact irritants and its relation to chemical-induced inflammation in mouse skin. J Invest Dermatol1994; 102: 915-22.

15. Vulnerary – promoting the healing of wounds.16. Porras-Reyes BH, Lewis WH, Roman J, Simchouritz L, Mus-

toe TA. Enhancement of wound healing by the alkaloidtaspine defining mechanism of action. Proc Soc Exp BiolMed 1993; 203: 18–25.

17. Pol O, Ferrer I, Puty MM. Diarrhea associated with intestinalinflammation increases the potency of mu and delta opioidsand the inhibition of gastrointestinal transit in mice. J Phar-macol Exp Ther 1994; 270: 386–91.

18. Klein DR, Little JH. Laryngeal edema as a consequence ofchemical peel. Annual Meeting of the American Society forEsthetic 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 – reviewand 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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Miscibility with waterPhenol is not completely miscible with water; to obtain ahomogeneous solution, an excess of water is required.1

Neurolysis and local anesthesiaPhenol has been widely used in a large number of disor-ders, including spasticity and chronic pain, because of itsneurolytic and local anesthetic properties (5% solution).Topically applied phenol has a lasting local anestheticaction that can affect all the layers of the skin and occurs atthe same time as frosting (Figure 26.1). Phenol has beenused as a surface anesthetic to perform small operations. Itis neurolytic;2 it coagulates the sensitive nerve endings atthe base of the epidermis and in the superficial papillarydermis. During a phenol peel, the first application of acidcauses an intense burning pain that can be alleviated byprior or immediate application of something cold. After

frosting, the anesthetic effect takes hold and spreadsbeyond the frosted area by up to a centimeter. During aphenol peel, after an initial period of analgesia, patientscomplain of renewed pain that they all describe differently,however. The second wave of pain is more likely to comefrom the rapid onset of inflammatory edema; this distendsthe tissues and stimulates the deeper nerve endings. Thispain wears off during the first night, when the edema is atits height and is no longer actively distending the tissues.

CarcinogenicityPhenol is not considered to be carcinogenic.3 On the con-trary, long-term histological studies show that phenol(even when the formula contains croton oil) has a protec-tive effect against skin cancers. A logical explanation of thisprotective effect may lie in the fact that the cells that takethe brunt of UV rays are the keratinocytes closest to thestratum corneum, the ones that form, for example, the topof the dermal papillae. On the other hand, the ker-atinocytes that are in the lower regions of the dermal papil-lae are relatively protected compared with those higher up:the UV photons have been partially absorbed or diffractedby the epidermal layers above them. In addition, the sebo-cytes4 or keratinocytes that make up the shaft of the hair areanchored more deeply in the skin, at a depth where theharmful effects of the sun are not as severe.

The cells that are most active in skin regeneration after adeep peel are those that are least damaged by the sun’s rays,the cells that have undergone the least UV-induced geneticmutation. After a phenol peel, the skin is much healthierthan the skin that the acid coagulated, and statistically willdevelop fewer cancers. Moreover, phenol may well coagu-late and get rid of any intraepidermal cancer in situ.

Protein coagulationPhenol coagulates proteins simply by combining withthem, and this produces frosting similar to that occurringwhen the normally transparent proteins of an egg whitebecome cloudy on cooking, as a result of their three-

26Phenol: properties and histology

Figure 26.1Immediately after application of phenol to the upper lip, theanesthetic effect is enough to be able to pinch the skin anddraw blood without any feeling of pain (note the red spots inthe photograph, taken during a chemical cheiloplasty).

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dimensional structure being modified. The coagulatedproteins and phenol can be separated by the action of alco-hol.5 For the phenol and proteins to form a stable bond, thetemperature must be raised. When phenol comes into con-tact with the skin or mucous membranes, it causes imme-diate proteolysis if the concentrations are high enough,with protein coagulation occurring at higher concentra-tions .

DisinfectionPhenol is a powerful disinfectant that is more active in vivothan in vitro, because it coagulates the proteins of livingorganisms. It is bacteriostatic (at a concentration of 2 g/l)and bactericidal (at a higher concentration of 10 g/l). From13 g/l (about 1.3%), it is tuberculostatic and fungistatic. Itis not considered to be virucidal,6 although one commer-cial formulation containing 0.13% of glutaraldehyde andsodium phenate has a virucidal activity (according toAFNOR Norm T727). Some more lipophilic phenol deriva-tives have been declared virucidal against HIV and thehepatitis B virus.1 The fragility of the HIV envelope wouldexplain this action, though the action against the hepatitisB virus is not so clear. Many patients report that labial her-pes outbreaks are less frequent or even disappear altogetherafter a phenol peel. Phenol is found in bactericidal, tuber-culostatic and fungistatic concentrations in all phenol peelformulas. Even after 24 hours’ contact, no phenol deriva-tive has shown any sporicidal action.

Histology of phenolA study8 on guinea pigs showed that the reticular dermisreacts to injury as if it were made up of two distinct layers,whereas histologically there is no evidence that these twolayers exist, and the reticular dermis appears to be homoge-nous (Figure 26.2 is a schematic illustration of the layers ofthe skin). When the uppermost part of the reticular dermisis attacked, it reacts by reorganizing the tissues, while thedeeper part forms scars. It must be remembered that thedeeper dermis contains fibroblasts that can react pheno-typically as ‘conventional’ fibroblasts as well as myofibro-blasts. Myofibroblasts are differentiated (in response tocytokines) fibroblasts that can both synthesize a strong col-lagen bundle and activate a cytoplasmic motor running onactin. This transforms them into ‘non-muscular’ motorcells that can activate a contractile capacity comparable tothat of a smooth muscle cell.

The myofibroblasts interact between themselves – as ifthey were holding hands across their thick and resistant col-lagen bundles; as if, after taking each other’s hands, theywere bending their arms to draw closer to each other andthus contract the skin. Myofibroblasts (Box 26.1) are theskin’s final bulwark, the last defense against physical, chemi-cal and biological attack: when a peel injures the dermis to adepth where there are fibroblasts capable of turning intomyofibroblasts, it means that there are many keratinocytes(that have been destroyed) upon which the body can nolonger count, to regenerate the skin and that skin regenera-tion will be slow and therefore dangerous for homeostasis.


Stratum corneum disjunctumStratum corneum compactum

Keratinocytes

Epidermal basal layer

Grenz zone GZ

Papillary dermis

Reticular dermis

Hypodermis

GZ GZ GZ GZ

K K KK

Figure 26.2Schematic diagram of the layers of the skin adapted to peelings.

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The activation of the myofibroblast actin-based contractilemotor, 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 entrenchedguard that has nothing to lose and prefers to produce a scarrather than undergo extensive necrosis. When a peel injuresthe reticular dermis, the safety margin is therefore narrowerand the risk of scarring is greatly increased. In 1985, Kligmanstudied and documented the long-term after-effects of aphenol peel in his remarkable study ‘Long-term histologicfollow-up of phenol face peels’.9 Fintsi also studied the histo-logical effects of phenol peels.

It is still very difficult, however, to tally the clinicalresults and the histological changes of the different types ofpeels: the formulations, adjuvants and concentrations aredifferent, as are the methods of preparation and applica-tion of the various active agents used. Each patient has dif-ferent cell characteristics, either in the quality or thequantity of phospholipids, sterols and proteins embeddedin the cell membranes. Doctors are guided by their ownexperiences and follow the application protocol they havegradually developed in the course of their practice. Thisdisparity makes it difficult to compare the results of differ-ent studies. Some general principles can, however, bedrawn: we can consider that all peels produce comparablehistological effects. The differences arise from the extent ofthe inflammation caused and how this inflammation iscontrolled, as well as the relative depth reached. As far as

Phenol: properties and histology 205

Box 26.1 Myofibroblasts

Normally, fibroblasts do not exert much tension on thematrix of non-inflammatory tissue, but when all thelayers of the skin are affected by an injury, localgrowth factors send fibroblasts to colonize the fibrinplug closing the wound and forming the temporarymatrix. The fibroblast invasion and neoangiogenesisform the granulation tissue. The fibroblasts that haveinvaded the temporary matrix already exert a certainamount of traction on this tissue. The mechanicalstress then stimulates the fibroblasts to produce morecollagen and to turn themselves into ‘protomyofibro-blasts’. The persistent stress induces the phenotypictransformation of the protomyofibroblasts into differ-entiated fibroblasts, the myofibroblasts, which secreteactin fibers and increase their contractile force at thesame time as producing collagen and releasing pro-teases. Usually, the myofibroblasts disappear via apop-tosis (programmed cell death) as soon as the scar issolid, but where stress persists, they do not disappearand 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 undergoneliquefaction. This makes no difference to the overall result, as can be seen in (b), which shows the same patient 12 days after thefull-face phenol peel with Lip & Eyelid® formula. The skin tone is completely even, even in the non-liquefied areas.

A B

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medium and deep peels are concerned, effectivenessincreases when the injury is close to the deep reticular der-mis. The risk of retractile scars developing is greatlyincreased at this depth. There is therefore a fine linebetween achieving excellent results and the incidence ofscarring. At the same peel depth, however, phenol peelsproduce the most significant changes and the most spectac-ular results (Figure 26.3).

Epidermal changesA phenol peel usually produces complete epidermolysis inkeratinocytes and all other living cells in the epidermis. TheLangerhans cells, which play an important role in the skin’simmune defenses, are also affected. There is a certainamount of dermolysis accompanying the destruction of theepidermis.

Superficial epidermal layersThe epidermal layers are dissolved down to the basal layerin 24–36 hours under an occlusive mask. Thereafter, thearchitecture of the cells returns to normal and the histolog-ical coloring evens out. After a peel, the palisade structureof the keratinocytes is more even.

Basal layerPhenol restructures the architecture of the basal layer. Itdoes not completely destroy the melanocytes: they are stillfound in the basal layer after peeling. In some histologicalstudies, the density of melanocytes is sometimes higheroverall. The melanocytes have, however, become incapaci-tated or partially incapacitated: melanin synthesis isreduced, as is the ability to transmit melanosomes to theneighboring keratinocytes. This histological observationexplains any hypopigmentation or depigmentation follow-ing a phenol peel. How much the phenol damages themelanocytes largely depends on the formulation of thesolution used and the application technique, whichexplains why total achromia occurs more often with someformulations than others. For example, with Baker’s for-mula, the risk of developing a ‘porcelain skin’ is higherthan with Lip & Eyelid® formula. PIH is more frequent thanachromia when using today’s phenol formula

Dermal changesOn contact with the papillary dermis, phenol destroys theentire elastotic layer within it. Thereafter, the architectureof the dermis is spectacularly restored. Immediately under-neath the basal membrane, in the Grenz zone, a dense newlayer of collagen fibers is formed, arranged parallel to the

basal membrane and interspersed with good-quality elasticfibers in an effective network.10 Brown described this histo-logical reaction as early as 1960. The new collagen andelastin that is formed covers the sun-damaged structuresthat have not been destroyed by the phenol and pushesthem deeper down. The fibroblasts are strongly stimulatedand secrete all the components of the extracellular matrix:ground substance, collagen, elastin, etc.

The morphology of the fibroblasts varies widely depend-ing on their location:

� Papillary dermis: here the fibroblasts are small and havehorizontal dendritic processes; each fibroblast is in con-tact with several collagen fibers. These observationsexplain the dense horizontal arrangement of the newcollagen in the papillary dermis after a phenol peel.

� Mid and deep dermis: the fibroblasts are larger and are incontact with just one bundle of collagen fibers.

� Deep dermis and hypodermis: the fibroblasts are evenlarger here (four times bigger than in the papillary der-mis), and the dendritic processes are long and form acontinuous network. Collagen synthesis by the fibro-blasts causes scars to contract. Myofibroblasts (see Box26.1) are cells produced by fibroblast differentiation.They contain myofilaments that make them look likesmooth muscle cells and are involved in the phenomenaof scar retraction. Depending on the depth reached by apeel, different types of fibroblasts are stimulated andwill react in a specific way because of their differentgenetic programming. All of these histological changesexplain how the skin becomes thicker and the some-times dramatic face-lift effect of deep peels.

The blood vessels that are newly formed after a phenol peelprovide an effective and lasting supply of nutrients to thenew skin.

After a deep peel, the body takes 4–6 weeks11 to regener-ate a structurally normal skin. During these 6 weeks, theskin appears very red, as the many newly formed blood ves-sels are showing through an incomplete, thinned and paleepidermis. Six weeks is usually the minimum time that ery-thema lasts after a phenol peel. After this time, inflamma-tion may persist and the skin can still appear red for severalmore months.

Dermal lymphocyte infiltration associated with pho-toaging is reduced after a phenol peel. On the other hand,there is significant lymphocyte infiltration in the reticulardermis 2–5 days after a phenol peel.

Overall, the wrinkled superficial layers are liquefied andreplaced by structurally young and homogenous tissue.The inefficient elastotic dermal layers are renewed and/orpushed deep down by the synthesis of new fibers. The qual-ity of the new collagen is not quite as good as the collagenthat had been present since birth. However, it is producedin sufficient quantities, along with new elastin, to provide


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better support to the newly rebuilt epidermis.12 The newlyformed blood vessels supply the dermis with the nutrientsit had slowly been deprived of because of the gradual vas-cular degeneration caused by photoaging.

Long-term histological follow-up after a phenol peelThe changes described above last a long time. In histologi-cal sections taken 15 years after a phenol peel (Baker’s for-mula) the difference between the treated and non-treatedskin is incredible, and this explains why, most of the time,only one phenol peel is necessary for long-lasting rejuvena-tion of the face.

Other authors13 have confirmed these histological resultsafter 15-20 years and even talk about permanent results insome patients. In 1985, Kligman10 showed that dermalreconstruction lasts for 20 years at least and that the risk ofcancer is reduced. Clinically, the rejuvenated appearance ofthe skin can be maintained for a great many years (Figure26.4).

Notes1. 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 trans-mitting the sensation of pain.

3. Material Safety Data Sheet. Fisher Scientific, USA.4. Sebocytes are in fact keratinocytes that have been differenti-

ated phenotypically into cells capable of producing sebum.When under attack, they can quickly dedifferentiate andturn back into keratinocytes and regenerate the skin.

5. By separating the phenol from the protein that it has coagu-lated, alcohol can enhance the action of the acid on anotherprotein.

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. HealthQuest Publications, 1997: 75-81.

8. Hayes DK, Berkland ME, Stombaugh KI. Viability of skinflaps subjected to simultaneous chemical peel with occlusivetaping. Laryngoscope 1989; 99: 1016–19.

9. Kilgman AM, Baker TJ, Gordon HL. Long-term histologicfollow-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 lift-ing. In: 44° Congrezzo Nazionale della Società Italiana diChirurgia Plastica Ricostructiva ed Estetica, Bologna, Nov1995.

12. Asken S. Unoccluded Baker–Gordon phenol peels – reviewand update. J Dermatol Surg Oncol 1989; 15: 998–1008.

13. Matarasso SL. Glogan RG. Chemical face peels. DermatolClin 1991; 9: 131–50.

Phenol: properties and histology 207

Figure 26.4The skin of a 78-year-old patient 10 years after a full-facephenol peel (Exoderm®) and 1 year after a medium-depthtrichloroacetic acid maintenance peel (Unideep®).

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Skin penetration of chemicalsThe skin has many different functions: it can be the site ofaction of a product or the reservoir for a product; it cansimply be a transit site or it can be an impermeable barrier.The skin’s main role is to form a barrier limiting the trans-fer of molecules in and out. It is especially adapted for thisthanks to the multiple external layers of corneocytes. Forthe stratum corneum to be impermeable to both chemicaland physical agents,1 it is essential for it to be intact. It isthis layer that forms the main barrier to the penetration ofactive products through the skin. Corneocytes are made upof α-keratin filaments, buried in an amorphous matrix richin disulfide bonds. There is a thick protein envelope ofinvolucrin round each corneocyte, and the intercellularspaces are full of extremely hydrophobic lipids. The outerlayer of the plasma membrane is hydrophilic. The outerlayer of skin can be described as a hydrophilic ‘brick wall’sealed with hydrophobic ‘mortar’.2 The whole forms anefficient barrier against both hydrophilic and hydrophobicmolecules. This barrier is so efficient that chemicals canpenetrate living or dead skin to the same degree, just asthere is the same degree of penetration through the wholeskin or the stratum corneum alone!2

Consequently, eliminating all or part of the stratumcorneum drastically enhances the absorption of physicaland chemical agents that could not have penetrated anintact protective stratum corneum. The ability of a productto penetrate the skin also depends on how it interacts withthe corneocytes and the intercellular matrix. At the samemolecular weight, a proteolytic product will penetrate theskin more readily than a product that is not proteolytic.The more liposoluble a molecule is, the greater its partitionbetween the vehicle and the skin barrier and as a result itsability to penetrate is improved. Another factor to be takeninto account is how solvents interact: ethanol diffuses bet-ter in the stratum corneum when it is mixed with oil ratherthan water.2 How well hydrated3 the stratum corneum isalso plays an essential role in the skin’s absorption capacity.When the stratum corneum is hydrated, products can beabsorbed up to 10 times more efficiently.2 Hydration swells

the corneocytes and makes them less dense and less resis-tant to diffusion. The fact that on facial skin the stratumcorneum is not very thick means that molecules areabsorbed more quickly. The skin on the face is more per-meable than the skin on the limbs and the torso, but lesspermeable than the skin on the genital organs.

What happens to phenol afterpenetration (Figure 27.1)Lymphatic absorptionThe lymphatic system, which is highly permeable even to largeprotein molecules, slowly collects some of the phenol in theinterstitial fluid. The total daily volume carried by the lym-phatic system is approximately equal to the volume of bloodof the same individual. This absorption route is very slow andtherefore negligible from a toxicological point of view.

Capillary absorptionPhenol penetrates rapidly through the skin and is immedi-ately absorbed by the dermal blood vessels. The metabo-lization and/or excretion sites immediately pick up thephenol that has penetrated into the bloodstream.

Metabolization and eliminationTwenty-five percent of phenol is metabolized into water andcarbon dioxide and eliminated directly through the lungs.The remaining 75% is eliminated in free and conjugatedform or undergoes oxidation. Phenol is oxidized to hydro-quinone in the liver. Still in the liver, it is esterified by thetransfer of the sulfuryl group of 3'-phosphoadenosine 5'-phosphosulfuric acid to the hydroxy group of the phenoland produces phenylsulfuric acid: this is sulfate conjugation.Phenol also undergoes glucuronide conjugation throughexchanges with glucuronic acid. The conjugated phenol isno longer toxic to the organism, and can be eliminated by

27Phenol: skin penetration and detoxification

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the kidneys. Other detoxification enzymes have been identi-fied, such as phenol 2-monooxygenase, phenol O-methyl-transferase and phenol β-glucosyltransferase.4

Active transport processes excrete organic acids such asglucuronide and phenol sulfate conjugates in the proximaltubule. All forms of free or detoxified phenol are thereforefound in urine.

Hepatic and renal integrityBecause of the way in which phenol is metabolized, hepaticand renal integrity is a prerequisite for a phenol peel.Applying phenol more quickly than it can be detoxifiedand eliminated by a deficient liver or kidneys could resultin severe intoxication.

An interesting study in 1953 by Ruedmann and Deich-mann5 concluded that hepatic and renal integrity wereabsolutely vital when using phenol. They wanted to draw theattention of practitioners to the potential dangers of applyingphenol to large surface areas of the body, even though this typeof treatment had previously presented only minor drawbacks.

A patient did die, however,6 after a phenol solution witha concentration of 2.3%7 was applied under an occlusivedressing8 on one-third of the body surface area and on fleshburnt by kerosene.9 This death led the authors to study themetabolism of phenol by applying 1 g of phenol to 75% ofthe body surface area in a first group of human ‘guineapigs’. Three other groups were given total doses of up to 4 gon the same body surface area (75%). A rest period of 90minutes was left between successive applications of 1 g.


100 - E

100 - (E+D)

100 - (E+D+L)=T

100% phenol

Renal elimination of conjugatesActive transport of detoxifiedphenol in the proximal tubule

Pulmonary metabolismElimination of H2O and CO2

About 20–25% (T)

Elimination of non-conjugated free phenolDiuresis, hydration

Phenol + 3′-phosphoadenosine 5′-phosphosulfuric acid→ phenylsulfuric acid (sulfate conjugation)

Phenol + glucuronic acid → phenyl glucuronide(alucuronide conjugation)

Quinone and catechol subsequently undergorenal elimination�

Hepatic detoxification

About 70–75% (T)

Capillary resorption sloweddown by oils, edema, etc.

Epidermis

Dermis

Oily? Dry? Thick? Thin? Prepared? etc.

Thick? Hydrated?Rich in proteins?

Rich vascularization?Occlusion?

Slow lymphatic elimination

Concentration? Adjuvants?Formulation, phenol

Sequestered in applicator, etc.

E = quantity of phenolsequestered in the epidermis

D = quantity of phenolsequestered in the dermis

L = quantity of phenoleliminated by the lymphatic system

T = quantity of potentiallytoxic phenol

Figure 27.1Metabolization of phenol.

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Toxic phenolemiaDoses of free and conjugated phenol show the followingresults: the levels of free circulating phenol do not varymuch whether 1, 2, 3 or 4 g of phenol is applied on the skinor if a rest period of 90 minutes is left between each gramapplied. The peak values in free phenol recorded werearound 0.60–0.80 mg/100 ml. Benatar10 describes a reas-suring 1962 study by Litton in which he recorded the fol-lowing blood concentrations after applying 3 ml of 50%phenol on the face: after 1 hour, 0.68 mg/100 ml; after 2hours, 0.19 mg/100 ml and after 3 hours, 0.10 mg/100 ml.According to the same author, phenol only becomes sys-temically 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 theblood at any given moment. Detoxification by conjugationis initiated immediately after applying phenol on the skin.

Aqueous or oil vehiclePhenol in aqueous solution is absorbed very differently tophenol in oil solution. Maximum blood levels reached0.9 mg/100 ml when phenol was applied in an oil solutionand 1.1 mg/100 ml in an aqueous solution. In 1950, Deich-mann11 published a study on the reabsorption of phenol inan aqueous and an oil vehicle: 71 mg of phenol was absorbedby the skin of a rat in 1 hour’s contact with an aqueous solu-tion of phenol at 4.7%, whereas only 15 mg was absorbedwhen the same concentration was present in (mineral) oilsolution. Phenol penetrates the skin more slowly from an oilsolution than from an aqueous solution. In this way, it alsobecomes less toxic. Applying 4 g of phenol to the skin doesnot make the blood concentration of the free form or conju-gated form of phenol any higher than if 3 g were applied.Deichmann did not offer any explanation of this phenome-non, but the rest period of 90 minutes between each 1 gapplication most probably allowed enough time for the phe-nol to be detoxified. After 3 g, the phenol levels returned tonormal within 48 hours. A little longer was needed to elimi-nate 4 g. On the third day, the blood levels of phenol reacheddoses lower than that of any normal individual, that is,around 0.15 mg. No sign of systemic intoxication wasdetected in the course of this study. It must be noted, how-ever, that control mechanisms were not as sophisticated asthey are today and continuous Holter-ECG recording mon-itors were, for example, not yet available then.

Effects of occlusionIn the past, it was thought that applying a dressing was thecause of local necrosis. In fact, the necrosis occurred whenvery tight, thick dressings soaked in phenol were applied tothe wounds. According to studies by Ruedemann andDeichmann,5 applying a dressing (unsoaked) after applying

phenol actually reduces the speed with which the phenol isabsorbed – although not the total quantity. There are twoadvantages to a dressing: it allows surface maceration andincreases the contact time with the epidermis. In this way,it can improve the cosmetic results. Impermeable occlu-sion reduces the rate at which phenol is absorbed throughthe skin and increases the chances of hepatic metaboliza-tion, as the organism is not overloaded or saturated by amassive influx of phenol. Peaks of free phenol are lowerunder occlusion.

The literature is unclear on whether occlusion improvesthe results of phenol. In 1980, McCollough and Hillman12

reported that the results of phenol (Baker’s solution) with-out occlusion were comparable to those of phenol underocclusion. They went on to say that not using occlusionimproves patient comfort and lowers the risk of complica-tions. What is true for Baker’s solution is not necessarilytrue for other formulas, however. In 1989, Baker publisheda study showing that occlusion with Vaseline® producesthe same results as occlusion with impermeable tape.Stegman,13 Alt and Brody published studies that show thatphenol is more active under occlusion.

Occlusion can therefore be used to increase the depth ofaction of a peel when the practitioner wants the penetra-tion to be deeper. This is the case with Lip & Eyelid®: occlu-sion is recommended when treating wrinkles around thelips and chin, but not for the treatment of eyelid wrinkles.Occlusion with Vaseline® appears to be as effective as animpermeable occlusive dressing. There is one small practi-cal problem with using Vaseline®: heat from the skinmakes it more liquid, and as it liquefies it tends to drip ontothe eyes and neck, getting on to the clothes, hands and any-thing 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 greatlength, with Baker recommending 48 hours’ occlusion.When I use occlusion, I leave it on for 24 hours. I have notnoticed any difference with longer occlusion times – whichseems logical, as after 24 hours all the phenol applied hashad plenty of time to be reabsorbed by the skin; leaving itfor more than 24 hours merely increases the risk of sec-ondary infections. The importance of the question of occlu-sion becomes clear when it is considered that manysurgeons take the occlusion off under anesthetic or seda-tion, which increases the cost and the risk for the patient.On the first day, there are very few nerve endings left thathave survived the phenol, and taking the whole occlusivemask off in one go, pulling it downwards, is only very brieflypainful. Another question is whether the occlusion shouldbe applied immediately after the phenol or not. Phenol is avolatile compound, and applying occlusion immediatelyafter it has been applied will stop it from partially evaporat-ing and will therefore allow for longer maceration of agreater quantity of phenol. The sooner occlusion is appliedafter phenol, the deeper the effect will be.

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Urinary eliminationThe by-products of phenol are rapidly eliminated in theurine. After intoxication with phenol, these by-productsmake the urine a dark color – anything from light olivegreen to dark brown. The intensity of the color has nodirect relation to the severity of intoxication.

Specific phenol sensitivitiesVery young children are particularly sensitive to phenol,and incidents of intoxication were recorded at the begin-ning of the 20th century after simply applying phenol dress-ings on the intact skin of infants and after ingestion of 0.25 gof phenol.14 In the early 1900s, Nothnagel and Rossbachdescribed alcoholism as a situation that improves resistanceto phenol. A logical explanation can be found in the ways inwhich alcohol and phenol are metabolized. Alcohol is oxi-dized to acetic acid in the body. Certain conjugation mech-anisms bring acetic acid into play through acetylation of thephenol function. The detoxifying conjugation could bebetween the phenol and the acetic acid. Deichmann studiedbasal blood phenol levels before and after application ofphenol to the skin. Basal blood phenol levels were lowerthan before treatment, showing that the body adapts to thedetoxification process. Wine is known to contain numerousaromatic molecules, including polyphenols. Winedrinkers15 develop a more effective polyphenol detoxifica-tion metabolism than non-drinkers, which could explaintheir relative resistance to intoxication with phenol.

Notes1. All peels remove the stratum corneum, at least partially, and

make the skin permeable to chemical, physical and environ-mental attacks. Total sun block is essential after any kind ofpeel.

2. Guzzo CA, Lazarus GS, Werth VP. Dermatological pharma-cology. In: Hardman JG, Limbird LE, Molinoff PB, RuddonRW, Gilman AG, Chren MM, Bickers DR. Dermatologicalpharmacology. In: Hardman JG, Limbird LE, Eds., Good-man & 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 peelthan 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 top-ical application of phenol-containing preparations. JAMA1953; 152: 506–9.

6. Deichmann WB. Local and systemic effects following skincontact with phenol: a review of literature. Ind Hyg Toxicol.1949; 31:146–54.

7. This proteolytic concentration means the solution pene-trates rapidly.

8. Occlusion stops phenol evaporating and enhances macera-tion in the flesh exposed by the burns.

9. Loss of skin impermeability means that the solution pene-trates rapidly.

10. Benetar D. Lee peeling au phenol. J Med Esth Chir Derm1988; XV(60): 319–23.

11. Deichmann WB, Miller T, Roberts JB. Local and systemiceffects following application of dilute solutions of phenol inwater and in camphor-liquid petrolatum on the skin of ani-mals. Arch Ind Hyg Occup Med, 1950; 2: 454–61.

12. McCollough EG, Hillman RA. Chemical face peel [Sympo-sium on the Aging Face]. Ontolaryngology Clinics of NorthAmerica, 1980; 13: 353–65.

13. Stegman SJ. A comparative histologic study of the effects ofthree peeling agents and dermabrasion on normal and sun-damaged skin. Aesthetic Plastic Surgery, 1982; 6: 123–35.

14. Manquet A. Traité élémentaire de thérapeutique de matièremédicale et de pharmacologie, 5° ed, tome 1. 1903: 240-60.

15. It should be noted that when this observation was made inFrance, at the beginning of the 20th century, the majority ofcases of alcoholism were due to wine.


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When phenol is dumped into river water, it is very toxic toaquatic fauna and lethal at a concentration of 1 ppm. Thegenuine toxicity of phenol and the almost apocalypticdescriptions of its side-effects, which can even lead to deathby cardiovascular collapse, severely limited its cosmetic useuntil 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 usedtechniques in the treatment of photoaging’.1

As we have seen in Chapter 27, phenol is rapidlyabsorbed by the skin and mucous membranes. It is alsorapidly eliminated by the lungs in the form of water andcarbon dioxide and by the kidneys in free form and in sul-fate- and glucuronide-conjugated form. Detoxificationstarts immediately after phenol has been applied.2

Phenol vapor enters the pulmonary circulation veryrapidly, and because of this respiratory absorption, doctorswho use it (regularly) have to wear a mask. The treatmentroom must also be properly aired and ventilated to preventthe patient, who is already absorbing phenol through theskin, from absorbing any significant amount through therespiratory route. Keeping the patient well hydrated (with asaline drip) promotes diuresis and therefore renal elimina-tion of free phenol as well as conjugated or oxidized phe-nol. Some authors recommend intravenoushyperhydration before and during the peel and sometimesforced diuresis with an intravenous injection offurosemide. This hyperhydration is not necessary whenphenol is applied carefully.

Data obtained from laboratoryanimalsIn rats, the oral LD50 is 530 mg/kg.3 In rabbits, 70% of thephenol applied to the skin is absorbed in 30 minutes and99% within 24 hours.4 In 1944, Deichmann and Witherup5

published the results of their experiments on the toxicity ofphenol in laboratory animals.

Their conclusions were as follows: ‘the rate of absorptionof phenol/skin surface unit is not closely dependent on the

concentration of the phenol, but is largely dependent onthe total surface area of skin exposed to the product.’

Medications containing phenolThere are many pharmaceutical products widely used inmedicine and dentistry that contain phenol, sometimes infairly high concentrations. Bonain’s local anesthetic mix-ture, combining menthol, cocaine and phenol, is wellknown, and is used, for example, as an intranasal analgesictreatment for certain facial pains. Other products contain-ing phenol include hemorrhoid creams, chilblain solu-tions, ear drops or wax remover drops, psoriasistreatments, and mouth sprays with phenol in concentra-tions ranging from 3 mg/ml to 50 mg/g. Applying theseproducts locally introduces only a small quantity of phenolinto the organism at well-spaced intervals, and does notappear to cause intoxication.

Phenol soapPhenol soap with a concentration of 5 g/100 g introduces asmall amount of the active product into the organism witheach wash. Even if resorption, and therefore phenol toxic-ity, depends more on the surface area covered than on theconcentration of the product,6 each wash only delivers asmall quantity of phenol, which is soon rinsed off.

GarglesTercinol® is a phenol solution with a concentration of15 g/100 g. It is recommended to dilute a teaspoon of con-centrated solution in a glass of water and to gargle three orfour times a day. One teaspoon is generally equivalent to5 ml and therefore contains about 0.75 g of phenol. It isapplied to irritated mucous membranes, and a smallamount of the product will be swallowed every time it isused unless the user is an expert at gargling. Some 2–3 gcould come into contact with the irritated mucous mem-branes every day. The package notice warns patients of thepotential side-effects of phenol.

28Toxicity of phenol: causes, prevention andtreatment

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Dental wickThere are dental wicks that can contain up to 375 mg/g ofphenol. They are introduced into the dental cavity beingtreated and are reapplied every 10 minutes. The explana-tory notice simply recommends not touching the mucousmembranes. Nevertheless, it is possible for the patient toaccidentally ingest a total of 1 g, although the time lapseallows any phenol that might have been ingested to beeliminated without toxicity. The products with the highestconcentrations of phenol benefit from its antiseptic andlocal anesthetic properties.

MouthwashArgentofenol® is a disinfectant mouthwash recommendedto be dabbed on the mucous membranes every other day. Itcontains up to 35% phenol. Phenol is still used in medicineand dentistry, sometimes at high concentrations. Side-effects remain rare, as the product is relatively diluted,applied in small quantities or little surfaces and thereforereadily eliminated, even when applied repeatedly duringthe day. There is plenty of time for the liver to detoxify andthe kidneys to eliminate the phenol.

Phenol peelDuring a full-face phenol peel, 2.5–5 ml of phenol solutionis 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 ofphenol on the skin. It is important to be aware of the factthat the toxicity of phenol solutions appears to be paradox-ical, as, up to a certain point, diluted solutions can be moretoxic than concentrated ones. Publications report that sim-ple aqueous dilutions of 2 parts phenol to 1 part water (i.e.solutions with a concentration of around 33%7) are usuallythe most dangerous. Some phenol peel formulations stilluse this concentration, however, confusing speed of pene-tration with cosmetic effectiveness.

Paradoxical toxicityAt a concentration higher than 80%, phenol is a keratoco-agulant. The first applications of phenol precipitate theskin proteins and thus create a biological barrier that pre-vents further applications of phenol from penetrating toorapidly. Concentrations lower than 80% are keratolytic,8 asthey break the disulfide bonds between the keratin mole-cules and allow more of the solution to penetrate morerapidly. Reducing the concentration of a phenol solutioncan therefore make it more dangerous, both locally andsystemically. Lowering the concentration of phenol in apeel solution is therefore not enough to make it non-toxic,

and quicker penetration should not be confused withimproved results. Solutions with lower concentrationspenetrate more rapidly through the skin and are morerapidly absorbed: they are therefore more toxic at the sametime as being less effective from a cosmetic point of view.

The distinction between keratolytic and keratocoagulantmust be given careful consideration. It is clinically obviousthat solutions that are assumed to be keratolytic cause pro-tein precipitation, or coagulation. Roenigk9 published aninteresting article on this subject: in spite of the concentra-tion of approximately 50% (48.5% to be precise), phenolacts as a keratocoagulant in Baker’s solution because –according to him – of the combination with croton oil andseptisol. Other protein coagulating peels do not use septisolor croton oil, however.

Stone8 performed a histological study of the depth ofpenetration of various phenol formulas: the Gordon–Bakerformula at 48.5% phenol, the Verner–Dickinson formulaat 67% and liquid phenol at 88%. The results, in keepingwith the principles set out above, show that Baker’s for-mula penetrates twice as deeply as Verner’s and four timesas deeply as liquid phenol at 88%. Although phenol isabsorbed rapidly by skin tissue, only a part of it will gradu-ally reach the innermost regions, as the skin proteins floc-culate almost immediately, and this creates a physicalcatchment area for the phenol as well as a natural dam thatstops it penetrating the deeper layers too quickly.

Lessons from medical history General remarksThe average fatal dose (death within 24 hours) in humansis 8–15 g by ingestion (according to Nothnagel and Ross-bach in Manquat10). Individual predisposition largelyexplains the variations in the toxic dose. In 1903, Man-quat10 reported two extreme cases: his colleague, Bouchard,had ‘by mistake injected’ (sic) two patients with enemascontaining 48 g of phenol. Their temperatures fell to 35°C,went up to 41.8°C in the evening, returned to normal thenext day and remained stable the following days. There isno information available on the long-term outcome of thisaccident: chemical intestinal necrosis, fistulization, sec-ondary infection, survival, death, or liver and kidney toxic-ity?

Ingesting just 0.5 g of phenol can lead to symptoms oftoxicity, and sometimes an oral dose of 5 g is enough tocause death. The patient shows signs of corrosive esophagi-tis and gastritis, then signs of kidney damage, cardiac col-lapse, breathing difficulties and a feeling of inebriationfollowed by coma. Medical history tells us that the ‘Lister’technique took the life of many patients. Lord Lister, bornin England in 1827 (Figure 25.12 in Chapter 25), was thefirst 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 dis-infect wounds or when catgut was disinfected with phenoloil. Phenol proved toxic when applied directly in too greata quantity to skin that was unprotected by the stratumcorneum. Lysol®, used as a household disinfectant for toi-lets and bathrooms, is an oil mixture of cresols and otherill-defined phenols dating from before the First WorldWar. Even if Lysol® is less toxic and less irritating than phe-nol, it was the method of choice for suicide11 and abortion12

at the beginning of the 20th century.

Phenol administration routes inthe pastEvery possible route (apart from perhaps intra-arterialinjection) was used to administer phenol:

� Oral or rectal routes (0.5–1 g of phenol in enemas, 6–12times a day in the case of typhoid fever); the rectal routewas 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 aboutthe toxic effects of phenol and described the symptoms indetail. It is obvious that the doses used caused frequent andserious accidents. Doctors then became more cautious, andwould use a maximum concentration of 0.5 g of phenol inenemas, to be repeated every 3 hours, so as not to reach atotal daily dose of 4 g. Doses of 4–20 g/day were considereddangerous or lethal. Manquat10 reported: ‘inside the body,we have nearly always administered phenol in enemas (0.5to 1 gram of phenol to 200 to 500 grams of vehicle) thathave sometimes been repeated every three hours (Desplats).A dose of 4 grams has brought the patient’s temperaturedown as low as 34° (Van Oye). Caution dictates that weshould not go beyond 0.5 g per enema,’ and that ‘We some-times prescribe a dose of 1 to 4 grams in a potion; patientshave difficulty tolerating this preparation.’

Desplats recommended the following ‘lemonade’:

‘Phenic acid 2 to 4 gramsLemon water 100 gramsSimple syrup 100 to 150 gramsWater q.s. for one literTake 100 grams of this solution every 3 hours.’

A simple calculation shows that patients at the beginning ofthe 20th century were supposed to ingest 800 g of this

‘lemonade’ every 24 hours, that is 1.6–3.6 g of phenol perday. Toxic accidents, however, were mostly described whena dressing soaked in phenol left some of the product in acavity that was having difficulty draining and the majorityof serious cases was reported when phenol was injectedinto perirectal cell tissue.10 Reading these old texts providesaccess to a whole theory of symptoms that today are onlyseen in cases of industrial poisoning.

All this – and even the fact that phenol was consideredhighly toxic by inhalation – did not stop Bethene andCourt13 suggesting inhalation of liquid phenol fumes totreat whooping cough in 1954. The plasma concentrationsreached were far higher than those described by Litton dur-ing full-face peels.

Symptoms of phenolintoxicationGastrointestinal symptomsIngesting more than 0.5 g of phenol triggers anorexia, nau-sea and belching. Symptoms of gastroenteritis (colic, vomit-ing and diarrhea) occurs with slightly higher concentrations.Massive ingestion destroys the mucous membranes in theupper digestive tract. It has been reported that gastric prob-lems can occur after applying phenol dressings externally.

Experience of conventional14 phenol peels also showsthat a small percentage of patients complain of nausea oreven vomiting shortly after a deep peel. This nausea andvomiting occur within a few hours after the application ofan occlusive mask.15 The cause-and-effect relationshipbetween these symptoms and excessive phenolemia has notbeen officially established.

Neurological symptomsGenerally, there are no neurological symptoms when dosesof less than 1–2 g have been ingested. The neurologicalsymptoms are headaches, tinnitus, hypoacusis, paresthesia,muscular hypotonia and stupor. If the dose is fatal, thepatient falls into a coma after a feeling of inebriation anddies without convulsions. Phenol stimulates the motorneurons of the anterior horn.16

Cardiovascular symptomsCardiovascular complications have been known aboutsince the 19th century: the pulse was described as becomingirregular and weak, slowing down to become extremelyweak or imperceptible. Hemoglobinuria and methemoglo-binemia were also described.

Details of these complications are considered later in thischapter, as well as techniques for avoiding and treating them.

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Lessons from toxicology centersIn 1993, a retrospective study was conducted over 5 years atthe Poison Center Philadelphia.17 It involved 96 cases ofpoisoning with Creolin®, a disinfectant containing 26%phenol. This concentration is known to be potentiallytoxic, as it enhances penetration through keratolysis. Expo-sure was oral in 60 cases, dermal in 2 cases, and both oraland dermal in 12 cases. Only 1 case of inhalation wasrecorded.

� Oral exposure. Eleven patients (14%) experienced rapidCNS depression that was rapidly reversible. Fourteenpatients experienced vomiting, coughing and stridor.

� Dermal exposure. Seven patients (100%) also had respi-ratory symptoms. On contact with the skin, phenol pre-cipitates keratin and forms a white film, followed byredness and then necrosis. A 5% solution causes a burn-ing sensation and then local anesthesia.18

� Antidotes to phenol. Isopropanol (isopropyl alcohol)and polyethylene glycol seem to be the most effectivelocal antidotes, both histologically and because theyslow down blood penetration.19 Immediately rinsing thearea of skin that has come into contact with the phenolwith plenty of water gets rid of some of the toxin andprevents precipitation of some of the epidermal pro-teins.

� Mixed exposure (oral plus dermal). Four people experi-enced vomiting, coughing and stridor. Skin andmucous membrane burns were recorded in approxi-mately 25% of the poisonings.

It is remarkable that no cardiovascular complications wererecorded in this study. Medical publications report thatwhen a person is exposed rapidly to a sufficient quantity ofphenol (in general, 3–4 g of phenol applied quickly to theface), abnormal heart rhythms may occur. These abnor-malities appear 15–20 minutes after the beginning of thepeel and are often rapidly reversible. If any arrhythmia haddeveloped during these cases of poisoning, it would nodoubt have occurred rapidly and disappeared again by thetime the patient arrived at the hospital. This argues in favorof the autonomous reversibility of arrhythmias with phe-nol. The authors cautiously conclude: ‘The absence of seri-ous toxicity and major chemical burns in this series doesnot eliminate concern with the corrosive and systemic risksof phenol poisoning’.

It should also be noted that phenol was widely used for112 years between 1867 (Lister) and 1979 (in a study byTruppmann and Ellenby20) without any cardiovascularmonitoring and with relatively few serious or fatal compli-cations considering that very often it was applied in non-medical circumstances (by lay peelers). Baker6 himselfasserted 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 tophenol. McCollough and Maloney21 pointed out that in 25years of using phenol, they came across a certain number ofarrhythmias of toxic origin, but that none of these casesneeded any specific treatment apart from waiting for thesinus rhythm to return and adding on 15 minutes to be onthe safe side. Asken22 confided that in 15 years of perform-ing phenol peels using the Baker–Gordon method, henever came across a case of arrhythmia that needed treat-ment. I personally, however, was faced in 1997 with a rela-tively severe arrhythmia when applying a full-face phenolpeel. How this arrhythmia developed is described later inthis chapter.

The fear of arrhythmic complications is the main brakeon the use of phenol peels today. It is therefore worthwhilestudying this problem in detail. The conclusions that canbe drawn from reading about these complications in med-ical literature help us to understand how to apply phenolwith greater safety, though the possibility of arrhythmiasoccurring cannot be avoided.

Cardiovascular complications(Figures 28.1–28.7)


Figure 28.1Sinus rhythm.

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For more than 50 years, lay peelers used phenol in full-facepeels for cosmetic purposes without any medical monitor-ing. Cases of deaths related to phenol peels date from thisera and up until the 1960s.

In 1973, Litton, Fournier and Capinpin23 published theresults of a survey covering cardiovascular complicationsduring phenol facial peels. In the 493 questionnaires

returned by plastic surgeons, only 3 cases of cardiacarrhythmias were reported. It should be noted, however,that heart monitoring was only (very) rarely used in this eraand in this indication. Reading all the works on the cardiactoxicity of phenol clearly shows that arrhythmias (easilytriggered by the rapid application of large quantities ofphenol) were only rarely diagnosed or published, and thefact that they tend to resolve spontaneously allowed practi-tioners to sleep peacefully.

Truppmann and Ellenby routinely used cardiac moni-toring when doing phenol peels, and detected manyarrhythmias. In 1979, they published the results of a studyon 48 patients treated with phenol peels.20 Saponified andnon-saponified Baker or Litton formulas were studied.They report that 23% of patients treated with phenolshowed arrhythmia, on average 17.5 minutes after the phe-nol was first applied. These arrhythmias were often prema-ture ventricular (Figure 28.3) or supraventricularcontractions, bigeminy, or supraventricular (Figure 28.2)or ventricular tachycardias (Figure 28.7). Tachycardia,which in extreme cases can sometimes reach 220–230 beatsper minute, can turn into ventricular fibrillation and leadto cardiac arrest.

These seem to be the first documented reports of cardiacarrhythmias that can definitely be attributed to phenol in


Figure 28.2Supraventricular tachycardia.

Figure 28.3Premature ventricular contraction.

Figure 28.4Bigeminy.

Figure 28.5Trigeminy.

Figure 28.6Quadrigeminy

Figure 28.7Ventricular tachycardia.

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humans. The authors also state that when they appliedphenol slowly, taking more than 1 hour, no incidence ofarrhythmia was detected.

The types of arrhythmia encountered were the following:

� 10 patients out of the 48 treated with facial peels showedarrhythmia

� 4 patients showed premature ventricular contraction;aged 30, 36, 59 and 71

� 2 patients showed bigeminy; aged 24 and 43 (Figure28.4)

� 2 patients showed paroxysmal tachycardia; aged 55 and67

� 2 patients showed ventricular tachycardia; aged 36 and 73

In order to refine their conclusions, the authors studied thepotential influence of different parameters:

� products used in anesthesia: no correlation could befound

� oxygenation before and during the peel: no correlationcould be found

� saponified or non-saponified formula: no correlationcould be found

� preexisting arrhythmia: no correlation could be found(other authors24 have confirmed this lack of correla-tion).

� 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 arrhyth-mia, with the average time for arrhythmia to occurbeing approximately 17.5 minutes; no patient devel-oped arrhythmia when the peel was applied over a min-imum period of 60 minutes

� surface area treated: No arrhythmia occurred beforephenol was applied on at least half of the face

Lotter in 1980 and Litton in 1981 published the results oftwo counter-surveys. Lotter25 highlighted the fact that only23% of doctors performing phenol peels use cardiac moni-toring to check the progress of the application. Littonrecorded in his study26 that after reading Truppmann andEllenby’s article,20 13% of plastic surgeons who hadanswered his questionnaire now reported arrhythmiasunder phenol and that 51% of practitioners now moni-tored phenol peels with a cardioscope.

The question asked of the plastic surgeons was: ‘Haveyou seen any cardiac complications during a phenol peel?’The answers were as follows:

yes: 5%no: 87%tachycardia: 6%arrhythmia: 1%premature ventricular contraction 1%

Of the doctors questioned, 51% said they used monitoring,while 42% never used it and 7% only sometimes moni-tored 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 incase of cardiovascular complication. On the other hand,not monitoring the patient does not necessarily make theprognosis for complications any worse, and most of thetime they seem to resolve spontaneously.

In response to these studies, Baker27,28 claimed that, inthe course of 5000 phenol peels, he never came across acase of arrhythmia. His observation was based on the fol-lowing evidence:

� Complications can take practitioners by surprise duringany cosmetic procedure – and facial peels are no excep-tion to this rule.

� The most common complications involve pigmenta-tion, and through careful patient selection these com-plications can be avoided.

� Hypertrophic scars are extremely rare after a chemicalpeel.

� Systemic toxicity is also ‘extremely’ rare.

Nevertheless, Baker recommended that all patients shouldbe monitored during full-face phenol peels – which seemsobvious to us nowadays. Baker stated that he only observed‘normal’ irregularities during his phenol peels and never hada patient die. He considered the cases of prematuresupraventricular contractions and the two cases of paroxys-mal tachycardia reported by Truppmann and Ellenby20 to beepiphenomena, not very serious and fairly frequent duringminor procedures, especially if an anesthetic containingadrenaline (epinephrine) is used. The two cases of bigeminyreported by Truppmann and Ellenby did not bother himeither, as he often came across bigeminy during routine pro-cedures and drew the logical conclusion that phenol shouldnot be blamed automatically for everything. He was, how-ever, alarmed by the two cases of ventricular tachycardia inthe patients who received a ‘rapid’ application of phenol inless than 1 hour, and stressed the importance of taking timeover the peel. Baker also recommended taking at least 1 hourto apply any phenol peel. Finally, he concluded that phenolpeels produce results that no other surgical technique canrival and that an experienced practitioner, aware of the com-plications and risks, can, by carefully selecting his patients,apply phenol peels without any fear of dire consequences. In20 years of using phenol, he did not observe any cardiaccomplication that could be directly attributed to phenol withcertainty.28 Nevertheless, all of these opinions, even whenthey come from such well-known medical experts, cannotaspire to the status of scientific facts.

Gross29 decided to reproduce the study by Truppmannand Ellenby, using the same non-saponified formula in 100


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consecutive peels on the face and neck (up to the claviclesin the anterior region and up to the 7th cervical vertebra inthe posterior region). Given the number of arrhythmiasthat occurred after the 54th patient, the method of applica-tion had to be changed. Out of 54 patients, 31 (57%) devel-oped cardiac arrhythmia (supraventricular and/orventricular). Unfortunately, Gross did not reveal the quan-tities of phenol used. Logically, it was used in large quanti-ties, since the surface area treated included the face andneck up to the 7th cervical vertebra. Moreover, the pre-medication contained substances that change the heart-beat, such as beta-blockers.

The rest of the patients were therefore treated in two ses-sions with a 24-hour interval in between: the face wastreated in the first session and the neck in the second. In thisseries, ‘only’ 22% of the patients developed arrhythmia. Nocorrelation was found between the age of the patients, theirgender, the preexistence of cardiovascular diseases and theincidence of arrhythmias. On the other hand, the bloodconcentrations reached in this study seem to be very high,up to 33.29 mg/100 ml. These figures differ enormouslyfrom those in Deichmann’s or Litton’s studies (see below).We know that the systemic toxicity of phenol can manifestfrom 23 mg/100 ml.30 The arrhythmias seem to occur in thefollowing order: tachycardia and premature supraventricu-lar contractions that develop into atrial fibrillation (pulsusirregularis perpetuus). Arrhythmias lasts on average 2–19minutes and are spontaneously reversible, depending onthe clearance of the phenol and the gradual lowering ofblood concentrations after hepatic detoxification and renalelimination. This study did not show any relation betweenblood levels and the occurrence or severity of arrhythmias.Each patient appears to have his or her own particular sen-sitivity to phenol. In conclusion, Gross recommendeddividing the face into different sections and leaving a restperiod of 20 minutes between each zone (cf Chapter 33).

Baker’s point of view is fully shared by Cortez,31 who, ina retrospective study of hundreds of phenol peels that hecarried out between 1983 and 1990, did not observe anycardiac toxicity when the precautions for use were fol-lowed.

A study by Wexler et al4 on rabbits found a correlationbetween the rapid onset of arrhythmia and the speed withwhich phenol is absorbed through the skin: 70% of phenolis absorbed in 30 minutes in rabbits. Forced diuresis (intra-venous furosemide) while the peel is being applied pre-vents cardiac arrhythmia by increasing renal elimination offree phenol, even before the conjugation and oxidationprocesses of detoxification could protect the organism. Inaddition, slow application of the solution in at least 1 hourmeant that no arrhythmia was observed, as this leavesenough time for the phenol to be detoxified.

A study on humans, limited to 10 patients, was pub-lished in 1990.32 Continuous electrocardiogram (ECG)recordings (halters) were taken before, during and after the

peels. Many ectopic beats were recorded, but no direct rela-tion with the application of phenol was established,although one case of arrhythmia was found to be suspi-cious. With the documents in my possession, however, Iam unable to analyze the different factors that might haveinfluenced this study with any precision.

In 1985, Warner and Harper33 published an articlereporting a suspect case of multifocal premature ventricu-lar contractions and bigeminy in a child34 weighing 36 kgwho received a dose of 2.4 g of 40% phenol in 0.8% of cro-ton oil, hexachlorophene and water.35 This large quantity36

was applied to 1.9% of the body surface area (we know thatthe absorption surface is at least as important if not morethan the total quantity of phenol applied) and under gen-eral anesthetic. Arrhythmias from phenol usually occurrapidly, in approximately quarter of an hour, and in thiscase they occurred after 55 minutes. Phenolemia was notmeasured and, according to the authors, there was nothingin the case history that could have attributed the arrhyth-mia to phenol. The child had already had several phenolpeels in the past for dermatological problems and hadnever experienced any problems, but because of Trupp-man’s and Ellenby’s descriptions, the authors assumed thatphenol was the culprit.

Another study37 compared the toxicity of trichloroaceticacid (TCA) and phenol (Baker’s solution); the conclusionwas that ‘it would appear advisable’ to set up a cardiacmonitor 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 isan essential prerequisite when doing a phenol peel on theface, even if serious arrhythmia can be avoided by applyingthe product in at least 1 hour. Applying phenol without anycardiac monitoring is not good medical practice, and anysubsequent complications could be considered profes-sional malpractice based on negligence. It should beremembered that vagal reactions are not uncommon dur-ing any treatment that is stressful for the patient and thatthey need to be detected in order to be treated correctly.

Prevention of cardiacarrhythmiasBy observing the following seven points, the risks of car-diovascular complications can be significantly reduced:4,38

1. Pre-peel checkup: ECG, liver and kidney (blood analy-sis)

2. Application over more than 1 hour3. Monitoring (ECG and pulse oximetry)39

4. Good general health5. Good patient selection6. Good hydration40


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7. Lidocaine as a preventive (?):41 this point is highlydebatable, since arrhythmia can be avoided simply bytaking more than 1 hour to apply the phenol. Simplelidocaine used to do nerve blocks before the phenol peelshould be considered a cautious technique.

Treating arrhythmia during apeelThere are several articles describing the appropriate treat-ment for heart arrhythmias occurring in the course of aphenol peel.20,24,26,33

At the first signs of arrhythmiaIf the ECG shows the least sign of arrhythmia – even slight,seemingly insignificant and supraventricular – the applica-tion of phenol should be stopped immediately and theintravenous drip speeded up to hydrate the patient moreand force diuresis to eliminate not only the conjugatedphenol but also free phenol. Under these conditions, thearrhythmia should show rapid signs of improvement andnot get any worse. Fifteen minutes after the last arrhyth-mia, the phenol can be reapplied again carefully. It is essen-tial for the anesthetist, the doctor doing the peel and/or anassistant to read the ECG constantly. A certain amount ofcompetence in ECG reading is therefore recommendedbefore doing a full-face phenol peel. There would be nopoint plugging in an ECG monitor and being unable todetect basic heart rhythm abnormalities!

Some authors4 recommend the use of furosemide toincrease diuresis, but furosemide can cause abnormal ionicplasma levels, which can, in turn, cause arrhythmias or makethem more likely. Be that as it may, furosemide rapidlyincreases the elimination of free phenol in urine, even beforethe processes of hepatic conjugation, which come into playvery rapidly all the same, have been able to detoxify it.

Experiments undertaken by Wexler et al4 show the fol-lowing results in animals.

When 2 ml of Baker’s solution is applied quickly on theskin of rabbits weighing 3 kg and sedated with pentobarbi-tal, on a surface area proportionally 5–8 times larger thanthe human face, numerous heart arrhythmias are observed.It is interesting to note that the doses required to inducearrhythmias in rabbits are high. Forced diuresis withfurosemide significantly reduces the arrhythmias. Byapplying the product slowly, arrhythmia is avoided alto-gether, in spite of the extremely high doses and the extentof the surface area treated.

‘Benign’ arrhythmiasSimple, isolated supraventricular extrasystoles can occurfrequently during any type of procedure, simply because

the patient is under stress. The right reaction to thesebenign arrhythmias is to stop applying the phenol and waitfor the sinus rhythm to return ‘naturally’. These seeminglybenign extrasystoles can in fact be a sign of becoming moreserious arrhythmias. It is best to be prepared and have allthe necessary equipment ready to hand and to keep a veryclose eye on the ECG in order to pick up any more signifi-cant changes in rhythm. It is a bit late at this stage to bewondering whether the lidocaine is at hand or if the batteryin the laryngoscope is charged!

More serious arrhythmiasBradycardiaIn the case of bradycardia, intravenous atropine is indi-cated. In cases of severe phenol poisoning, it has beenreported that the pulse rate can at first increase and thendrop off afterwards.

TachyarrhythmiasArrhythmia can evolve rapidly: within a few seconds,benign supraventricular arrhythmias can turn into othertypes of rhythm disorders, such as nodal tachycardia, atrialfibrillation and multiple ventricular extrasystoles, in dou-blets or triplets. It is important to act quickly – which iseasy as everything that is needed to deal with these arrhyth-mias (fortunately very rare) is ready to hand and thepatient is on a drip.

The patient should be put on oxygen to maintain goodblood oxygen levels. Treatment consists in the slow intra-venous injection of 50 mg of lidocaine without adrenaline(epinephrine). Usually, the arrhythmia rights itself in lessthan 10–15 minutes. A total maximum dose of 100 mg, intwo slow intravenous injections of 50 mg (in 1 minute),provides a strong and rapid antiarrhythmic effect (50 mg oflidocaine may be sufficient to get the patient back into aregular sinus rhythm). If lidocaine does not bring therhythm back to normal, bretylium tosylate may be indi-cated42 (if in an area equipped for resuscitation).33 Otherantiarrhythmics are now available and can of course beused, depending on the type of arrhythmia and the compe-tence of the doctor injecting them.

Blood pressureIn cases of severe phenol poisoning, blood pressure can riseslightly and then drop significantly afterwards.43

Collapse and cardiac arrestTo the best of my knowledge, collapse, ventricular fibrilla-tion or flutter, torsade de pointes, and other extremely seri-ous arrhythmias have not been described during peels, but


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could occur with severe phenol poisoning, usually causedby accidental intravascular injections of phenol. In Trupp-mann’s and Ellenby’s study, none of these serious arrhyth-mias were described, and cardioversion and defibrillationwere not necessary if more than 1 hour was taken to per-form the peel. If medication proved insufficient and thearrhythmia led to collapse, external heart massage and/oran electric shock of 200 J would resuscitate the patient.Once again, however, there is no risk of this level ofarrhythmia when a phenol peel is applied correctly, and aswe have seen already, a full-face phenol peel performed inmore than 1 hour does not trigger any arrhythmia. Theonly case of arrhythmia that I have come across44 occurredwhen, for once, I allowed myself to be influenced by a col-league who is highly respected in the world of phenol peelsand who claimed that he performed all his full-face peels in30 minutes, without any ECG monitoring, as he had neverhad any patients feel unwell. The absence of an ECG obvi-ously meant that he could not pick up on any arrhythmias.His experience could lead us to the conclusion that thearrhythmias potentially caused by a full-face phenol peelremain benign and resolve without treatment. However,this conclusion would be hasty and irresponsible.

In 1994, Lalanne et al24 described two cases of cardiacarrest after the injection, in 3 minutes, of 1.4 and 1.8 g ofphenol in an aqueous solution with a concentration of 6%(2 × 15 ml). The injections were strictly extravascular, butwere near the aorta. The injections were made into thesemilunar ganglia and were given as painkillers to patientswith inoperable pancreatic cancer. These patients were in apoor state of health generally, on numerous drugs andunder general anesthesia.45 There is an accumulation ofnumerous risk factors here, and the phenol peels wereapplied under completely different conditions. The com-plications occurred almost immediately, 2–3 minutes afterthe injection, and started with a drop in arterial oxygen sat-uration to 92%. The arrhythmia began with polymorphousventricular extrasystoles that rapidly turned into ventricu-lar tachycardia, ventricular fibrillation and cardiac arrest.The treatments described above got the patients back tonormal rhythms.

In 1993, Gaudy et al46 described the same type of acci-dent, in which 30 ml of 6.6% phenol solution (around 2 g)was injected for palliative splanchnic neurolysis in a patientwith cancer of the pancreas. It seems obvious that, in spiteof the fact that the injection was extravascular and given bya competent practitioner, there was massive vascularabsorption, which can cause accidents that are fortunatelyreversible after treatment. It is most likely that the injec-tions were made in edematous tissue that had been dam-aged by surgery beforehand and that this enhancedpenetration.

When intoxication has been severe and death narrowlyavoided, jaundice and oliganuria43 follow – a sign of thehepatic and renal toxicity of phenol. These cases do not fall

within the strict framework of a phenol peel carried outcorrectly: hepatic and renal toxicity are complicationslinked to acute poisoning.

Other types of toxicityToxicity by inhalationPhenol vapors are heavier than air (vapor density 1.2). Thebest way to ventilate a room where a phenol peel is beingperformed is therefore at ground level and not higher up.This is important, as phenol vapors can travel considerabledistances at ground level. Care should be taken with elec-tric heaters, as there is a risk of the vapors coming into con-tact with a source of heat that can start a fire: the mixture ofphenol vapors and air has a flashpoint of 79°C (174°F).43

The olfactory sensitivity threshold is 0.047 ppm: phenolvapors are hard to eliminate from a surgery – it can takehours. The presence of 250 ppm in inhaled air poses animmediate danger to health and life. Acute poisoning fromphenol vapors can produce the same symptoms as oral poi-soning. Chronic exposure47 to phenol vapors produces thefollowing symptoms: vomiting, difficulty swallowing,excessive salivation, diarrhea, anorexia, headaches, dizzi-ness, weakness and myalgia, mental disturbances, darkurine, and sometimes skin eruptions. Postmortem exami-nations of animals given fatal doses of phenol vapors showthe presence of myocardial necrosis and acute pneumonia,as well as vascular, liver and kidney damage.43

Ophthalmic toxicity Direct contact with phenol crystals, concentrated solutionsor vapors (45 ppm) causes serious damage to the eyes:hyperalgesic chemical conjunctivitis, severe iritis, and pos-sibly corneal opacification with loss of vision and edema ofthe eyelids. In some cases of poisoning through direct acci-dental eyelid contact, the seriousness of the injury to theeyelids has required surgery.48

The results of phenol coming into direct contact with theeye can vary from complete recovery of vision to loss of theeye, depending on the severity of the lesions. Chronic,repeated or prolonged exposure to phenol vapors can causeconjunctivitis. A gray discoloration of the sclera along withbrown patches of pigmentation at the insertion of the rec-tus muscle tendons of the eye have been described afterchronic exposure.43 Any direct contact between phenol andthe eyes requires raising the eyelids and rinsing immedi-ately with copious amounts of water or saline solution. Theeye should be flushed with saline solution for 30–60 min-utes, while waiting for the opinion of an ophthalmologist.Ophthalmic Vaseline® or a Vaseline®-based antibiotic eyeointment should always be put in the eyes before applyingphenol, as Vaseline® largely deactivates phenol.


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Hepatic and renal toxicitySome cases of hepatic and renal toxicity after severe poi-soning with phenol derivatives have been reported in theliterature, but I have not been able to find any such recordin medical publications dealing with phenol peels.

Notes1. 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 averagehuman weight of 65 kg, would give a figure of 34.45 g of phe-nol.

4. Wexler MR, Halon DA, Teitelbaum A, Tadjer G, Peled IJ.The prevention of cardiac arrhythmias produced in an ani-mal model by the topical application of a phenol preparationin common use for facial peeling. Plast Reconstr Surg 1984;73: 595–8.

5. Deichmann WB, Witherup S. The acute and comparativetoxicity of phenol and o-, m-, and p-cresols for experimentalanimals. J Pharmacol Exp Ther, 1944; 80, 233–40.

6. Baker TJ. Chemical Rejuvenation of the Skin.7. Arouette J. Dermabrasion, relèvements, peelings. In: Black-

well A (Ed.), Collection des Manuels pratiques de médecineesthétique. 1989, Paris.

8. Stone PhA. Peelings au phénol Baker–Gordon et modifies. JMed Esth Chir Derm 1996; XXII(90): 93–7.

9. McCulloch EG, Langsdon PR, Maloney BP. Chemical Peelwith Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermato-logic Surgery, Principles and Practice, 2nd edn. 1147–60.1996, UK. Oxford, Marcel Decker Ltd.

10. Manquat A. Traité élémentaire de thérapeutique de matiéremédicale et de pharmacologie, 5° ed, tome 1. 1903: 240–60.

11. After voluntary ingestion of Lysol®, death occurs within 3–4hours; at autopsy, corrosive esophagitis and gastritis were ofcourse noted.

12. Back-street abortionists readily used irritant solutions, phe-nol and Lysol® solutions among them, as uterine enemas toinduce abortions. It is likely that this method was just as dan-gerous for the mother as for the fetus, because of the richvascularization of the uterus. Autopsy would show a highconcentration of phenol in the right side of the heart, whichdrains all the veins of the body and therefore the phenol-laden 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-yearevaluation of acute exposure to phenol disinfectant (26%). JToxicol Clin Toxicol 1993; 31: 307–13.

18. Giroud JP, Mathé G, Meyniel G. Pharmacologie clinique:

bases de la théapeutique. 2nd Edn. 1978, France, Paris,Expansion Scientific Français.

19. Hunter DM, Timerdery BL, Leonard RB, McCalmont T,Schwartz E. Effects of isopropyl alcohol, ethanol and poly-ethylene glycol/industrial methylated spirits in the treatmentof acute phenol burns. Ann Emerg Med 1992; 21: 1303–7.

20. Truppman E, Ellenby JD. Major electrocardiographicchange during chemical face peeling. Plast Reconstr Surg1979; 63: 44–8.

21. McCulloch EG, Langsdon PR, Maloney BP. Chemical Peelwith Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermato-logic Surgery, Principles and Practice, 2nd edn. 1147–60.1996, UK, Oxford, Marcel Decker Ltd.


23. Litton C, Fournier P, Capinpin A. A survey of chemical peel-ing of the face. Plast Reconstr Surg. 1973; 51(6): 645–7.

24. Lalanne B, Baubion O, Sezeur A, Tricot C, Gaudy JH. Circu-latory arrest after splanchnic neurolysis with phenol in unre-spectable cancer of the pancreas. Ann Chir. 1994; 48(11):1025–8.

25. Lotter cited in Botta SA, Straith RE, Goodwin HH. Cardiacarrythmias in phenol face peeling: a suggested protocol forprevention. Aesthetic Plastic Surgery. 1988; 12(2): 115–17.

26. Litton C, Trinidad G. Complications of chemical face peel-ing as evaluated by a questionnaire. Plast Reconstr Surg1981; 67: 738–43.

27. Discussions following Litton and Trinidad.28. Baker TJ. The voice of polite dissent. Plast Reconstr Surg.

1979.29. Gross BG. Cardiac arrhythmias during phenol face peeling.

Plast Reconstr Surg 1984; 73: 590–4.30. Benatar D. Le peeling au phénol. J Med Esth Chir Derm

1988; XV(60): 319–23.31. Cortez E. Chemical face peeling. Otolarynyol Clin North Am

1990; 23: 947–60.32. 1990 study.33. Warner MA, Harper JV. Cardiac dysrhythmias associated

with chemical peeling with phenol. Anesthesiology 1985; 62:366–7.

34. We have already seen that infants are more sensitive to phe-nol than adults.

35. This keratolytic concentration makes for rapid penetration,and blood vessel uptake of the phenol is quicker in a formulathat does not contain any oils other than croton.

36. More than is usually applied during a facial peel.37. Stagnone GJ, Orgel MG, Stagnone JJ. Cardiovascular effects

of topical TCS 50% and Baker’s phenol solution. J DermatolSurg Oncol 1987; 13: 999–1002.

38. Botto SA et al. Cardiac arrhythmias in phenol face peeling: asuggested protocol for prevention. Aesthet Plast Surg 1988;12: 115–17.

39. Both are essential, as the onset of arrhythmia is often pre-ceded by a significant drop in oxygen saturation. Besides,arrhythmia cannot be detected by a pulse oximeter.

40. 500 ml of saline solution before the peel to trigger diuresis.41. The lidocaine used to carry out any facial nerve blocks

should be taken into account.42. 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 is30 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 addi-

tional risk factor during phenol peels.

46. Gaudy JH, Tricot C, Sezeur A. Troubles du rythme car-diaque graves après phènolisation splanchnique peopèra-toire. Can J Anaesth 1993; 40: 357–9.

47. This has no relation to what a doctor performing phenolpeels, 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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Influence of the age andgender of the patient

Age of the patientA phenol peel is mainly indicated to treat facial skin forsevere photoaging. It is the only type of peel that can get ridof deep wrinkles1 and regenerate elasticity and firmness in

the treated skin in one single treatment. Phenol peels aretherefore usually aimed at people who are (well) past their40s. There is no real age limit, and phenol has been used onpatients of advanced years (Figure 29.1), as well as on othermuch younger patients. Old age is not in itself a con-traindication to phenol,2 and it is remarkable to note thatthe skin regenerates perfectly well at any age: the oldestpatient that I have ever treated was 82 when she had a phe-nol peel – and I know for a fact that I do not hold the record

29Phenol: choice of peel and combinationtreatments

Figure 29.1An 82-year-old patient (a) before and (b) after a full-face phenol peel.

A B

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for the oldest patient. Phenol has also been used on chil-dren to treat specific disorders. Young adults have alsobeen treated with phenol for acne scars or scars of otherorigins. However, because of its toxicity and the profoundchanges it makes to the skin, phenol should not be usedwithout a good reason. Phenol should not be used to treatsomething that alpha-hydroxy acids (AHA) or trichloro-acetic acid (TCA) can treat just as well. The strength of apeel should always be adapted to the problem beingtreated: there is no point applying a peel that is too superfi-cial or too deep.

Male skin and female skinThickness of the skinA man’s skin is often more resistant, thicker and oilier (Fig-ure 29.2) than a woman’s skin. Sagging skin is more com-mon than photoaging in men, and men are often bettercandidates for a face-lift than a peel. It is the type of skinmore than the gender that determines the results of a phe-nol peel. If aging has resulted in a thick skin sagging, with-out dyschromia (see also Figure 29.7), and if the folds are

more pronounced than the wrinkles and fine lines, a peel isnot at all indicated either in a man or a woman, as, even ifphenol produces a ‘three-dimensional face-lift’ effect, theextent of the retraction is no substitute for surgery (Figures29.2 and 29.3).

When aging has resulted in sun-damaged thinning skinwith wrinkles and age spots, a peel is an excellent indicationand produces surprising results, in both men and women(Figure 29.4). Men with light skin phototypes and thin andsun-damaged skin respond very well to phenol. The gen-der-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 treat-ing a man’s skin is post-peel erythema (Figure 29.5):women can easily use make-up to hide it, but this is diffi-cult for men. Men can, however, wear a tinted sunblock tohide the redness.

ShavingThe question of shaving often comes up, and it is true thatstubble can pose a technical problem for a patient who wantsto shave at all costs. This is a minor concern, however, as thepatient only has to wait for 10 days before shaving after aphenol peel. On the 11th day, the doctor might allow the


Figure 29.2A patient 8 years after a full-face phenol peel: the quality ofthe skin has remained much improved, but the wrinkles andsagging did not really benefit from the peel. A face-lift wouldbe indicated for this patient.

Figure 29.3Two years after a full-face phenol peel on a patient with thickand oily skin, the quality of the skin has improved but thefolds and sagging remain unchanged. A face-lift would havebeen a better indication for this patient.

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patient to shave carefully, after evaluating the condition ofthe patient’s skin. Wearing a beard can even be an advantageand make the demarcation line less visible (Figure 29.5).

Make-upPatients regularly ask about make-up. Patients who usuallywear foundation can go back to using it when the skin hasfinished flaking, around the 8th day and with the doctor’spermission. The first time make-up is used signals thelong-awaited return to a normal social life.

There are some patients who do not usually wear make-up, and it is important to tell them that it will probably beessential for them to wear foundation after the peel to hide

the erythema, which can last up to several months. Thereddest areas should be covered with a green (to counteractthe redness) make-up stick before foundation is put on.

If the patient refuses to use make-up, she should beadvised to use a tinted sunblock, and this should be dis-cussed with her before the peel.

Influence of the patient’sphototypeAlthough phenol has been used successfully on patientswith a ‘Mediterranean’ skin type or on Asian patients with

Phenol: choice of peel and combination treatments 227

Figure 29.4(a) Photoaging before a phenol peel. (b) Three weeks after Lip & Eyelid® formula (full-face phenol peel).

A B

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a fair skin, it is nevertheless aimed at patients with a lightskin phototype. Patients with Fitzpatrick skin type I to IIIare excellent candidates. Patients with Fitzpatrick skin typeIV and patients with severely sun-damaged skin will haveto accept the possibility of a visible demarcation line3 onthe neck.

This demarcation line (Figure 29.6) can be made lessobvious both by a good peeling technique and by combi-nation with other peels on the neck.4 Darker skin types arenot such a good indication, because of the change in skintone after the peel. Most patients with a lot of wrinkles,however, prefer to exchange their wrinkles for a differ-ence in skin color that can easily be disguised with make-up.

Skin phototype is even more important when usingphenol locally; a local5 phenol peel can only really beapplied on light skin phototypes that will not show anysignificant and visible difference in color on the eyelidsand around the mouth. The same applies to patients witha lot of freckles, keratoses or lentigines, which only disap-pear from the areas treated with phenol but still remain inthe surrounding areas. The difference in skin quality isalso very visible. These patients should only be treatedwith a full-face peel.

It is nevertheless possible for these patients to have alocal phenol peel combined with a full peel to the papillarydermis. Combining Lip & Eyelid® with Unideep® providesa phenol peel and a peel to even out skin with lentigines,keratoses or freckles.6 The two peels should be done in thesame session: the phenol first, followed immediately after-wards by Unideep® on the rest of the face, around the areatreated with phenol.

Phenol peel versus othermedical or surgical techniquesPeel versus face-liftThere is not much point asking this question, as a full-facepeel is no substitute for a full face-lift, and vice versa (Fig-ures 29.7 and 29.8). The indications are different; peels and


Figure 29.5A patient 15 days after a full-face peel: wearing a beard canlimit the effect of the demarcation line caused by theerythema.

Figure 29.6Ten days after a Lip & Eyelid® peel around the mouth on atanned patient: the phenol has taken away the tan. Easy TCA®(four sessions) or Unideep® (one session) will even out theskin tone.

Figure 29.7The sagging – more pronounced than the photoaging –contraindicate a phenol peel, which would have no effect onthis patient.

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face-lifts complement rather than compete with eachother.7

When the damage is localized, the doctor alone canadvise his or her patient on which treatment or combina-tion of techniques to use. A face-lift cannot treat wrinkleson the upper lip, but laser treatment, dermabrasion orLip & Eyelid® formula can get rid of them. These treat-ments 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 com-bination of dermabrasion and phenol: Lip & Eyelid® for-mula is locally applied on the day of the face-lift and leftunder occlusion for 24 hours; the following day, the sur-geon evaluates the results of the peel on the upper lip; ifsome wrinkles still persist, they can be touched up withthe peel solution.8 It is also possible, on the first day, to


Figure 29.8Excellent three-dimensionaltightening effect from a phenol peel:(a) before treatment and (b) 3months afterwards.

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-liftis indicated before the phenol peel. (b) Results of a full-face phenol peel (Lip & Eyelid®), 14 days after the peel. There isspectacular improvement in the skin. Oddly enough, some of the lentigines have been replaced by telangiectasias. They must betreated quickly, to avoid extravasation of iron pigments and potential multiple localized tattoo marks.

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perform dermabrasion9 after a focal application of phe-nol on the lip.

If surgical blepharoplasty is not combined with a face-lift, Lip & Eyelid® formula can be applied on the eyelids atthe same time as the face-lift.

The patient in Figure 29.9 is a typical case where thefacial photoaging10 would benefit far more from a full-facephenol 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 tothe papillary dermis or several peels to the Grenz zone(with ETCA) to improve the quality and the color of theskin after the surgical face-lift.

When the wrinkles are on the eyelids and around themouth, the problem is therefore easily solved. In the case ofsagging and wrinkled skin, it is clear that the best resultscan be achieved with a combination of treatments thatshould be carried out at different times (see below). Thelarge majority of patients are in this situation, and thedegree of facial ptosis will be the deciding factor in whetherto suggest a face-lift or a phenol peel.

A face-lift gives better results for facial ptosis (Figure29.10); a peel gives better results for wrinkles and dyschro-mias. A surgical face-lift can only tighten damaged skinthat will not have enough elasticity to remain tight defini-tively.

Phenol peel combined with asurgical face-liftWe have seen above that there is no problem with per-forming a localized phenol peel at the same time as a surgi-cal face-lift if the two treatments are aimed at differentareas. When both treatments are indicated for the wholeface,12 the face-lift should be done first, followed by a restperiod of around 6 months before the deep peel (Figure29.11). The peel will have the additional advantage of soft-ening the scars from the face-lift at the same time as


Figure 29.10This is the same patient as in Figure 29.8. Two years afterfull-face Exoderm®, the improvement on the cheeks is stillwell maintained. However, sagging has partially recurred, theresults on the upper lip are inadequate and the color of theskin is slightly uneven. The patient, who is keen on boatingin sunny climates, has not kept out of the sun asrecommended.

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 toeven out the skin tone. Daily care comprises BlendingBleaching® cream and Melablock HSP® 50+.11

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 dermisand removing the marks and fine lines that did not respondto the face-lift.

With a phenol peel, a demarcation line is left under thejaw13 that is partially hidden by shadow. A face-lift after aphenol 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 deepTCA peel14) at the same time of operation on an area thathas just been treated with a surgical lift can potentiallycause extensive facial necrosis. The general principle is notto undermine the skin’s inner vitality with surgery at thesame time as injuring the outer layers of the skin with apeel. In other words: a face-lift should not be done on thesame day as a full-face deep phenol peel.

A study15 from 1989 looked at the viability of dorsal skinflaps (on guinea pigs) subjected in vivo to transpositionand suture immediately followed by a single application ofphenol (Baker’s solution) and 24-hour occlusive tapedressing. Thirty-six skin flaps were raised and sutured backinto place, and only 18 were treated with phenol. Analysisof the results clearly shows that combining a surgical liftand phenol at the same time of operation is not a wisechoice, as the average necrosed surface area without phenolwas 3.1 cm2, compared with 6.3 cm2 for the peeled flaps.

Another study16 on animals came to the conclusion thatraising a skin flap causes changes in the tissue of the reticu-lar dermis and the underlying tissue, which makes it moresensitive to any subsequent injury. The risk of compromis-ing the viability of a raised skin flap is therefore too high toopt for a simultaneous face-lift and deep peel.

On the eyelids, however, the fat hernia around the orbitwas removed through the transconjunctival approach andcombined – in expert hands – successfully and safely with alocal phenol peel.17 McCollough and Maloney18 combinedsurgical blepharoplasty with a phenol peel, but left the skinto rest for 3 months before doing the eyelid peel.

Phenol peel and Aptos® threadsThere is a new technique that involves inserting barbed orspiral threads under the skin to tighten sagging tissue (Fig-ures 29.12 and 29.13). These are known as Aptos® threadsor Russian threads, as in their current form they weredesigned by a Dr M Sulamanidze from Moscow.19 TheAptos® threads are inserted deeper than the phenol pene-trates: there is therefore no risk of interaction between thephenol, and the thread that would, in any case, resist itchemically.

There are, however, three problems:

� The entry points of the threads must not come into con-tact with the phenol, as there is a risk that the inflam-mation will push them out.

� The inflammation caused by the phenol peel affects allthe layers of the skin: this reaction, combined with theinflammation caused by the thread itself, could makethe tissue in which the threads have to anchor them-selves more fragile and cause them to rapidly unhook.

� Phenol is, of course, a disinfectant, but a phenol peelcoagulates all of the skin’s immune structures, and theskin becomes very prone to infection. The risk of sec-ondary infection from the thread is increased.

It is therefore preferable not to insert Aptos® threads at thesame time as performing a phenol peel.

Moreover, phenol partially tightens the skin, and it maywell be more worthwhile using Aptos® threads as a secondline of treatment, when the phenol has taken full effect,after at least three months. The presence of threads insertedin the skin several months previously is not a contraindica-tion for a phenol peel, and it is possible to decide on theopposite course of action if the doctor thinks this is a betteroption for the patient: Aptos® threads can be inserted firstand a phenol peel can be done afterwards.


Figure 29.12Aptos® thread.

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Figure 29.13(a) Aptos® springs. (b) Springs.

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Phenol peel versus carbon dioxidelaser resurfacingSeveral studies have been carried out comparing the resultsof a full-face phenol peel and resurfacing with a carbondioxide (CO2) laser, sometimes known as a carbon dioxidelaser peel. A study by Langsdon, Milburn and Yarber20

looked at four women volunteers with sun-damaged facialskin and wrinkles. A phenol peel was applied to the left halfof the face and a Sharplan Silktouch Flashscanner CO2 laserwas used to treat the right half. The clinical results weresimilar in both cases, although the laser appears to give bet-ter results in areas where the skin is very thick (e.g. thechin). The laser, however, causes more hypopigmentationand complications, and the post-peel period is more com-fortable for the patient with phenol than with laser. Histo-logically, the depth of action of phenol is deeper than thatof the laser and reaches the reticular dermis. The authorsconcluded that both ablative laser and phenol peels remainuseful clinical tools. The records show that the battle hasbeen won by phenol because of the high number and theseverity 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 theface. The results were clinically obvious, and it was clearthat they were better on the half of the face treated withphenol – so much so that the patient asked for anotherphenol treatment to even out the two sides.

We could perhaps conclude, however, that the CO2 lasermight be a better indication for very thick and oily skins,especially on the chin and nose.

Notes1. 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 thepapillary dermis) or four sessions of Easy TCA® (less aggres-sive). These peels should be combined with a depigmentingcream 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 sec-

ond 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, wrin-kles and fine lines, and wrinkles around the mouth and eyes.

11. HSP sunblock: heat-shock proteins – sunblock containingstimulants to produce these proteins that protect againstheat damage.

12. For example, when the patient presents with severe photoag-ing 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 thecontrary, applied immediately after a surgical lift.

15. Hayes DK Stambaugh KI. Viability of skin flaps subjected tosimultaneous chemical peel with occlusive taping. Laryngo-scope 1989; 99: 1016–19.

16. Hayes DK, Berkland ME, Stambaugh KI. Dermal healingafter local skin flaps and chemical peels. Arch OtolaryngolHead Neck Surg 1990; 116: 794–7.

17. McKinney P, Zukowski ML, Mossie R. The fourth option: anovel approach to low lip blepharoplasty. Aesth Plast Surg1991; 15: 293–6.


19. Some attempts at copies can be found on the market: someof these copies are extremely crude, others tend to break eas-ily and others are too thick and can be felt through the skin.

20. Langsdon PR, Milburn M, Yarber R. Comparison of the laserand phenol chemical peels produce similar results in facialskin resurfacing. Arch Otolaryngol Head Neck Surg 2000;126: 1195–9.


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A phenol peel is the deepest type of peel, the one that givesthe most dramatic results but that is also the most danger-ous. Its indications are precise and limited to cases thatcannot be treated by other peels. If an alpha-hydroxy acid(AHA) or trichloroacetic acid (TCA) peel can solve a skinproblem, it will be chosen over a phenol peel without hesi-tation. The main indication for a phenol peel is severephotoaging.

Treating wrinkles: phenol plusbotulinum toxinFine lines, wrinkles, furrows and folds do not respond tophenol in the same way. Wrinkles and fine lines caused bysun damage are far more responsive (Figure 30.1) thanexpression lines or, above all, skin folds due to excess skin.

Deep wrinklesThese can respond very well to a phenol peel (Figure 30.2).Deep cheek wrinkles (Figure 30.3) caused purely by sundamage are one of the best indications for a phenol peel.

Expression wrinkles are also an excellent indication, oncondition that movement is blocked by botulinum toxinapproximately 8 days before the peel. Without this highlyeffective synergetic combination, kinetic wrinkles will ofcourse disappear during the first few weeks after the phenolpeel, but will come back afterwards, much to the annoy-ance of patients.1 ‘Compression’ wrinkles that form duringsleep are particularly problematic and difficult to get rid of:they come from an excess of skin combined with loss ofelasticity, and form during the night as a result of continu-ous pressure from the head on the pillow that ‘chisels’ theskin. Filling techniques can be tried, can be disappointingin this indication in the long term. The only real solution isto change unconscious sleeping habits, which is almostimpossible. Special pillows have been designed specificallyto combat this problem.

Folds and furrowsThese usually result from excessive skin laxity. Deep folds andfurrows are not a good indication for phenol. They resultfrom intrinsic aging and can sometimes be filled before aphenol peel. There is no need for a long time interval between

30Phenol: indications

Figure 30.1Full-face phenol (Lip & Eyelid®formula): (a) before and (b) 30 daysafter the peel. The combination ofbotulinum toxin and phenol worktogether on the forehead, crow’sfeet, frown lines and sometimeswrinkles on the upper lip.

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filling and peeling; the two treatments can even be done at thesame time if the filler is resorbable:2 furrows and folds can befilled immediately before the phenol peel. It is easy to under-stand how the severity of the inflammatory reaction after thephenol peel does not help the implant in the long term, butthe clinical results of this combination speak in its favor.Folds and furrows can also be filled after a phenol peel, afterthe inflammatory erythema has subsided. An injection giventoo soon after the peel, during the erythematous phase, caneasily cause bruising.

Expression linesExpression lines on the forehead and between the eyebrowsand crow’s feet have a natural tendency to recur partiallyand rapidly, even after a phenol peel. A botulinum toxininjection before the peel stops expression lines imprintingthemselves on the skin as it renews itself, and this combi-nation is very satisfactory, improving results significantly.The botulinum toxin should be injected 1 week before thepeel so that new collagen can be synthesized on an immo-bile dermis.

The injection can also be given 8 days after the phenolpeel, if not done beforehand. Injecting botulinum toxinduring the post-peel period of erythema and edemaincreases the risk of the toxin moving as well as the risk oftemporary cosmetic complications caused by the toxin.The duration of the toxin’s effect does not seem to changemuch, however.


Figure 30.2(a) Before full-face phenol. (b) 15 days after full-face phenol(Exoderm®). Kinetic wrinkles are starting to come back. (c) 30days after full-face phenol: the phenol has solved all the skinproblems apart from the expression lines, which have comeback.

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Wrinkles around the mouth andeyesWe will look at the chemical blepharoplasty and/or cheilo-plasty (labioplasty) technique in detail in Chapter 36.

Wrinkles on the lower eyelids, drooping upper eyelids andloss of elasticity are excellent indications for a local applica-tion of phenol (Figures 30.4 and 30.5). Wrinkles aroundthe upper and lower lips respond very well to a local appli-cation of Lip & Eyelid® formula (Figure 30.6).

Phenol: indications 235

Figure 30.3(a) Sun-damaged cheek skin. (b)Complete restructuring, 30 daysafter a full-face phenol peel (Lip &Eyelid® formula).

Figure 30.4Rejuvenation of the eyes: (a) before; (b) 30 days after a full-face phenol peel (Lip & Eyelid® formula).

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Figure 30.5Chemical blepharoplasty (Lip & Eyelid®): (a) before; (b) after.

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Radial wrinkles on the uppereyelids‘Radial’ wrinkles on the outer canthus of the upper eyelidrespond well to localized treatment with phenol using theocclusive technique (Figure 30.7).

Other wrinklesOther wrinkles, such as cheek wrinkles (see Figure 30.9) orforehead wrinkles, are excellent indications for a full-facephenol peel, but are usually not treated locally, as not onlyare the results less obvious than after a full-face peel butalso the difference between the treated area and the sur-rounding skin can be too obvious. This type of local treat-ment is reserved for very particular cases, when there is norisk of tone and structure differences between the locallytreated area and the surrounding skin.

Laxity and skin elastosisThin, elastotic and distended skin is ideal for a phenol peel(Figure 30.8). Results are better than with a surgical face-lift. On the other hand, a phenol peel, even under the bestconditions, cannot completely lift jowls. Although phenol isindicated in many cases of facial sagging, large amounts ofexcess skin still have to be resected surgically. Surgery doesnot, however, change the texture of the skin, and applying aphenol peel after surgery rejuvenates skin texture, removingall the wrinkles and marks that surgery has no effect on.When the skin is thin, a full-face phenol peel can often pro-duce sufficient retraction to make a surgical face-lift unnec-essary. The same applies for upper blepharochalasis: asurgical blepharoplasty is still the best choice in this indica-tion, but excellent results can be achieved with a singleapplication of Lip & Eyelid® formula, and drooping skincan be retracted satisfactorily, as described in Chapter 36.Oddly enough, eyelid retraction is automatically restrictedto ‘normal’ tension, and I have never had any cases of ectro-pion, entropion or lagophthalmia.


A

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C

Figure 30.6Long-term removal of wrinkles around the lips after a phenolpeel: (a) before; (b) after 1 year; (c) after 3 years. The contourof the lips has been plumped with an injection of a slowresorbable filler, 1 year after the phenol peel.

Figure 30.7(a) Occlusion of localized phenol to treat the radial wrinklesof the outer canthus of the upper eyelids in a 75-year-oldCaucasian patient. This treatment should be combined with abotulinum toxin injection (8 days before the peel) and a TCApeel to the papillary dermis (Unideep®) in the same session toeven out the skin tone of the rest of the face. (b) Three weeksafter this combination of treatments, the radial wrinkles havedisappeared. There is no visible demarcation line.

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DyschromiasWe have seen that phenol has a marked effect on dyschro-mias, and it incapacitates melanocytes, even if it does notdestroy them histologically (Figure 30.9). Even if manymelanocytes are still physically present in the basal layer,3

they can no longer produce melanin (partially or com-pletely).

Melasma and post-inflammatoryhyperpigmentationPhenol is a good indication for all types of hyperpigmentedlesions: lentigines, pigmented keratoses, chloasma,melasma, freckles and post-inflammatory hyperpigmenta-tion (PIH).4 All the same, phenol is not the first choice of


Figure 30.8(a, b) Pronounced photoaging,combined with slight sagging, is anexcellent indication for a full-facephenol peel.

A B

A B

Figure 30.9Before (a) and after (b) a full-facephenol peel (Lip & Eyelid® formula):a combination of yellow skin,wrinkles, fine lines and lentigines ina patient who smokes. Thirty daysafter the peel the erythema isnormal. The patient is not wearingany make-up. Botulinum toxin wasinjected 8 days before the peel(forehead, frown lines and crow’sfeet).

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treatment, as other, less aggressive, peels will do most of thetime. Hyperpigmentation problems have to be treated dif-ferently, depending on how deep they are: epidermalhyperpigmentation can be treated with a more superficialpeel than dermal hyperpigmentation, which will onlyrespond to a deeper peel. Phenol may be indicated to treatsevere and resistant melasma definitively. Some patchesmay recur after a period of lightening. Patients must bewarned of this possibility. The problem can largely beavoided by recommending that the patient uses BlendingBleaching® cream5 for several months after the phenol peel.

Asken6 has drawn attention to the following fact: the dis-tribution of melanosomes is particularly uneven inmelasma – a phenol peel may accentuate this uneven pig-mentation even more.

Wood’s lampIt is useful to evaluate the depth of pigmentation: a Wood’slamp can be used to do this, as shown in Figure 30.10. Theworse the pigmentation appears when exposed to theWood’s light (i.e. the more patchy the skin appears), themore superficial the melanin is and the treatment will soontake effect. Superficial pigmentation does not need to betreated with phenol, and can be treated effectively with lessaggressive peels.

Asian skinLight Asian skin is not a contraindication to phenol.Between 1986 and 1992, phenol was applied to 710 light-complexioned Asian patients and proved to be highly effec-tive and very safe to use.7

FrecklesHistologically, freckles are characterized by a normal num-ber of melanocytes in the basal layer. The melanocytes are,however, larger and more ‘dendritic’, and give up theirmelanosomes more readily to the keratinocytes. Frecklesdisappear completely and definitively with phenol. A TCApeel to the papillary dermis8 will also get rid of freckles. Alocal phenol peel is contraindicated on light skin photo-types – which in principle are a good indication for phenol– with freckles, as they will disappear where the phenol hasbeen applied and will persist in the surrounding areas. Acombination of local Lip & Eyelid® and Unideep® (TCA tothe papillary dermis) is suitable to avoid this freckle demar-cation line.

Lentigo malignaLentigo maligna9 is a flat, multicolored, pigmented lesionwith an irregular shape that may be precancerous. It has aslow radial growth phase and its diameter can vary from a

few millimeters to several centimeters. It is usually foundon the face, temples or cheekbones, in patients over 50years old. The average age of onset is 65 and the incidenceincreases with age. Lentigo maligna is formed bymelanocyte proliferation that is purely intraepidermal.Histologically, there is an increase in the number of atypi-cal melanocytes in the basal layer of the epidermis. Some ofthe melanocytes may have multiple nuclei. These atypicalmelanocytes are found at a distance from the clinical bor-der of the lesion. The epidermis is atrophic and the dermiselastotic. This lesion is, in fact, associated with chronic sunexposure over many years, mainly in patients with a lightskin phototype. Adnexal spread is not uncommon, andnumerous melanophages are found in the dermis. Thislesion can, however, degenerate into a superficialmelanoma, whose prognosis is good, as, more often thannot, it does not produce metastases. When lentigo maligna


Figure 30.10(a) Wood’s lamp and (b) patient with melasma seen under thislight.

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is diagnosed at the age of 45, the statistical risk of it devel-oping into melanoma is 47% over the lifetime of thepatient. When it is diagnosed at the age of 67, the risk of itturning into a malignant melanoma is 22%. In both cases,the 5-year survival rate is 90%. That is why dermatologicalmonitoring and sun protection are usually all that is rec-ommended. If the lesion is extensive, surgical excision andmaybe a skin graft are sometimes necessary. The excisionmust be wide and the excision margin at least 1 cm beyondthe clinical border of the lesion: the cure rate is then 91%with a 9% recurrence rate in 4 months. Mohs microsurgeryis also widely used. Many other treatments have been stud-

ied. Cryotherapy should theoretically produce good resultsbecause melanocytes are particularly sensitive to cold, butthis treatment has a 50% recurrence rate. 5-Fluorouracil(5-FU), used alone, gives poor results. With carbon dioxideand argon lasers, radiotherapy and electron-beam therapy,there have been many recurrences. Curettage, dermabra-sion and electrodessication have produced few positiveresults and a high rate of recurrence. Topical hydro-quinone and tretinoin have no effect on the lesion. It is notmy intention to suggest that a phenol peel is the ideal treat-ment for lentigo maligna, but only to say that, unlike themajority of other treatments suggested, I have never seen arecurrence of flat lentigo maligna after a phenol peel, be itfull-face or local (Figure 30.11).

KeratosesExtensive multiple keratoses (solar or senile) on the entireface should be treated with a full-face peel, whereas isolatedkeratoses can be treated by other methods (see Chapter22). According to McCollough and Maloney,10 laser treat-ment has no advantage over chemical treatment. Verg-ereau, for his part, published a study confirming theadvantage of applying Only Touch® TCA over laser, dry iceor coagulation.

Several forms of keratoses can coexist.

Seborrheic keratosesSeborrheic keratoses (Figure 30.12) are very common andare found on areas of skin that have been exposed to thesun as well as unexposed areas. The lesions are alwaysbenign, but can sometimes be difficult to distinguish frommalign melanomas. Beyond a certain thickness, the kera-totic layer makes them unresponsive to peels, even to phe-nol. They can be treated by shave excision with a snare andradiofrequency (Ellman unit) immediately before applying


Figure 30.11Lentigo maligna combined with severe photoaging: (a) beforeand (b) after a full-face phenol peel.

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Figure 30.12Seborrheic keratoses

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the phenol. When treating seborrheic keratoses by shaveexcision without combining it with phenol, a TCA peel tothe basal layer or to the papillary dermis can be applied toeven out the structure of the skin once it has completelyhealed.

Actinic keratosesActinic (or solar) keratoses11 form mainly on areas of skinthat have been exposed to the sun: the face, the pinna of theear and the hands, for example. They are tumors that areoften precancerous: 10–20% (25% according to someauthors) develop into skin cancer, often of the spinocellularcarcinoma variety. Many patients with actinic keratoses oreven subclinical epithelioma in situ could benefit from aphenol peel on the face,12 possibly preceded by curettage ofthe largest lesions. Patients who have been treated with 5-FU are often reluctant to put up with the necrotic appear-ance of their skin after each treatment. A phenol peel getsrid of the actinic keratoses at the same time as making theskin look younger overall. Many authors describe very long-term results, if the patient is prepared to change his or herattitude to sun exposure after the peel and, as well as keep-ing out the sun, is prepared to use SPF 50+ sunblock everyday thereafter. In case of recurrence, inadequate results orthe appearance of new lesions, the patient can be treatedagain 4–6 weeks after the first peel. Patients treated withphenol are at far less risk of developing cancer later on.4

Superficial cancersPhenol necroses the epidermis and part of the dermis andeliminates intraepidermal skin cancers in situ. Carcinomasform from cells in the epidermis. To my knowledge, no sci-entific article has ever reported skin cancers being causedby the application of peeling agents. If the literature is to bebelieved, a phenol peel treatment has the added advantageof lowering the frequency of other precancerous lesionsforming and probably other cancers in situ in sun-dam-aged skin. From a toxicological point of view, topicallyapplied phenol13 is not recognized as a carcinogenic or ter-atogenic agent. It is still necessary, however, to make a def-inite diagnosis before applying chemical agents to suspectpigmented lesions.

Superficial telangiectasiasA phenol peel is not used to treat telangiectasias, eventhough the more superficial ones usually disappearthrough protein coagulation along with the superficial lay-ers of the skin. Deeper telangiectasias can become evenmore deeply embedded in the dermis as the new layer ofdermal collagen and elastin form. Therefore, a phenol peel

usually brings about an improvement in the appearance oftelangiectasias. However, in some cases, the extent of post-peel neovascularization can make them worse or cause newvasodilations to appear.

‘Raised’ telangiectasias may become more visible inpatients with thin and transparent skin. Facial telangiec-tasias can be electrocoagulated immediately before thephenol is applied, while the patient is under nerve-blockanesthesia for the peel. An Ellman radiofrequency unit iscompletely satisfactory in this indication.

XanthelasmaXanthelasmas are permanent and often symmetrical yel-lowish plaques that appear on the inner canthus of the eyes(Figure 30.13). All four eyelids can be affected by this non-premalignant dermatitis. They can be soft or hard. In 50%of cases, they are associated with hyperlipidemia. Womenare affected twice as often as men.

Xanthelasmas are formed by a build-up of xanthomacells: macrophages swollen with free or esterified choles-terol and mainly located in the superficial layers of thereticular dermis. Phenol can therefore reach them (Figure30.14). Other treatment options include surgical excision,carbon dioxide laser, argon laser, electrocoagulation andcryotherapy. Dichloroacetic acid has also been used in thisindication, dissolving the xanthelasma and healing withminimal scarring.

Acne and acne scarsActive acne is not an indication for phenol, because of therisk of secondary infection among other things and because


Figure 30.13Xanthelasma. (Courtesy of Dr Munelly, UK.)

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there are other less aggressive and highly effective treat-ments.14

Acne scars15 that are deep, adherent, crater-like, some-times atrophic, sometimes hypertrophic and keloid16 are acomplex problem, and it is clear that no easy treatmentexists to date that can claim to get rid of them completelyand definitively. Applying a phenol solution will of coursebring about a cosmetic improvement, but may well be dis-appointing to both doctor and patient in some severe cases.

The patient in Figure 30.15 is an interesting case frommany points of view. A phenol solution (Exoderm®) wasapplied correctly and deeply enough to treat the many acnescars (Figure 30.16).

An occlusive dressing was then applied for 24 hours. Onexamining the skin at the end of occlusion, the scars hadonly improved very slightly, and an extra coat of phenolwas applied to the cheeks after 24 hours, without occlusionthis time. On examination after seven days, the resultsappeared inadequate (Figure 30.15) and another spotapplication was made without much success.

When discussing treatment possibilities for acne scarswith a would-be patient, the doctor should be extremelycautious. Skin that is very scarred can, however, be com-pletely renewed, evened out and smoothed using a combi-nation of treatments such as subcision,17 dermal filling,18

dermabrasion, punch excision, punch elevation, possiblymicro skin grafts or even injections of cultured stem cells orfibroblasts (Isolagen).


A B

B

Figure 30.14(a) Eyelid xanthelasma before a local phenol peel (b) Five daysafter the peel: normal erythema. (c) Nine days after the peel:the xanthelasma has gone

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Figure 30.15Acne scars treated with a full-facephenol peel (Exoderm®). On the 8thday, there is a distinct improvementin the structure of the skin: wrinkleshave disappeared, along with smallactive acne lesions. However, theimprovement in the acne scarsremains limited.

A B

A B

Figure 30.16(a) The application of phenol on this patient produced normal skin frosting, but did not reach the deeper acne scars, which arestill the same color. (b) An extra coat of phenol causes ‘buff-colored’ patches to appear – a sign that the product has reached themaximum depth of penetration.

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Treating severe acne scars therefore requires specifictechnical ‘preparation’ before applying phenol to allowcomplete and definitive renewal of the architecture of theskin, as well as to even out the tone of skin that has beendamaged by the acne itself and by the treatments givenbefore the phenol peel. It is therefore imperative to cure theacne before treating the consequences and not to forgetthat taking isotretinoin (Roaccutane®) in the year before orafter 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 skinand overall normalization of skin tone.

Some authors19 prefer to treat acne scars with dermabra-sion, on condition that the hand guiding the wheel is expertenough to be able to control the depth of skin abrasion pre-cisely and to vary the depth depending on the area and thesize of the scars being treated. Dermabrasion may be pre-scribed as monotherapy or in combination with other

techniques (Figure 30.17). The results of microdermabra-sion as monotherapy for treating severe acne scars are dis-appointing.

Other scars

Atrophic scars resulting from aface-liftA surgical face-lift always leaves scars. If there are no seri-ous complications, these scars are not really visible andpatients do not complain. Secondary infections are notcommon but they are not rare either, and in some patientsthe skin surrounding the scar behind the ear becomesnecrotic.

The scar shown in Figure 30.18 is the result of a secondaryinfection after a surgical face-lift. Note the central atrophy


Figure 30.17(a, b) A patient treated with an Exoderm® peel (full-face phenol occlusive peel), followed by mechanical dermabrasion (post-chemabrasion). (Courtesy of Dr Y Fintsi.)

A B

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and depigmentation surrounded by a hyperpigmented ring.There is a telangiectasia in the middle of the scar. The patientwanted to have a phenol peel, but was refused because of therisk of the face-lift scar not healing properly. The telangiec-tasia can be treated separately, however, and the peripheralpost-inflammatory hyperpigmentation, which shows up thecentral atrophic hypopigmentation, could be treated with amore superficial peel (Easy TCA®) combined with a topicaldepigmenting treatment (Blending Bleaching® cream). Thevisual impact of the scar would be reduced if the skin tonewere evened out.

Normal face-lift scars are not usually too unsightly, butsome patients want a treatment to soften them or get rid ofthem completely. A full-face phenol peel is the best option(Figure 30.19), but a local application of phenol preciselyon the scar is also a possibility, in combination withanother more superficial peel (to the papillary dermis, theGrenz zone or the basal layer). Standard scars from anupper blepharoplasty do not seem to respond as well to a

phenol peel. Scars on the body are not an indication forphenol.

Traumatic scarsThese can be treated with localized application of phenoland a series of Easy TCA® peels (Figure 30.20).


Figure 30.18Atrophic scar after a face-lift, resulting from a local secondaryinfection.

Figure 30.19(a) A face-lift scar that is not too unsightly. However, the skintension lines converging on the scar emphasize it. (b) Thirtydays after a full-face phenol peel (Lip & Eyelid® formula),without any make-up, the tension lines have gone and theface-lift scar is less visible.

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Dermabrasion scarsThese too can be treated with a local phenol peel combinedwith Easy TCA® (Figure 30.21).

NevusAnother less well-known indication for a phenol peel is thetreatment of generalized verrucous epidermal nevi, a disor-der that can be associated with a certain number of bone,ophthalmic or neurological malformations. Treatmentconsists in shave excision of the lesions followed by anapplication of phenol to the hyperpigmented areas of theface.20

Giant hairy nevi have been treated with phenol: 40%solution, combined with croton oil (0.8%) and hexa-chlorophene soap.

It should be remembered that some nevi fade after aphenol peel and that others, after a period of fading,become hyperpigmented.

Other indicationsDilated poresDilated pores are not the best indication for phenol, andthe abrasive technique21 combined with Easy TCA® seemsmore effective.

Neurolysis and chemicalsympathectomiesPhenol is sometimes used in paraaortic injections in thesemilunar ganglions to achieve neurolysis as an analgesic


Figure 30.20(a, b) Post-traumatic scar and post-inflammatory hyperpigmentation, 6 years after a road accident. (c) Local application of phenolto the scar. Frosting occurs immediately. An impermeable occlusion will be applied for 24 hours and followed in the standardmanner with an application of bismuth subgallate powder. The patient will also have four sessions of Easy TCA® peels, at a rate ofone 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. Theedges of the scar are less marked, the base of the scar appears less atrophic and the skin tone has evened out.

A B

C D

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technique in cases of inoperable cancers (30 ml of a 6%phenol solution can be injected in this indication) (see alsoChapter 28).

There are descriptions in the literature of the use of phe-nol in chemical sympathectomies in the treatment of pal-mar hyperhidrosis, Raynaud’s syndrome and obliterativearteriopathy.

Urinary incontinencePhenol has been used in injections beneath the bladdertrigone in the treatment of urinary incontinence due to spinabifida (30 ml of 6% phenol). Aqueous solutions of phenolhave been injected as a sclerosant in cases of hydrocele.22

Spasticity and chemicalneuroablationPublications indicate 5% phenol injections to treat spastic-ity in pediatrics. The use of chemical neuroablative tech-niques dropped off rapidly with the arrival of more specifictreatments. Injecting neurolytic solutions (e.g. phenol23 oralcohol solutions) causes non-specific damage to all thestructures that come into contact with these products,namely both motor nerves and sensory nerves, muscles,aponeuroses, and subcutaneous tissue. The effects ofchemical neurolysis last several months, and subsequentinjections often do not produce the same results. It is now


Figure 30.21(a, b) A scar resulting from lip dermabrasion: the upper left half of the lip is still wrinkled because the mechanical dermabrasionwas too superficial, whereas the upper right half of the lip is scarred as a result of the dermabrasion being too deep. The patientis seen in an attempt to correct this unsightly scar and a local phenol peel is suggested. Lip & Eyelid® solution will be used locallyand 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, thewrinkles on the upper left half of the lip have disappeared. The scar on the upper right half of the lip has softened and evenedout, and the color is similar to that of the surrounding skin.

A B

C D

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acknowledged that the risk of complications linked withthese injections is too high, considering that there are othertechniques that are less dangerous, more specific and moreeffective. Injecting phenol for the purpose of chemical neu-rolysis is now only indicated for patients suffering frompain that is unresponsive to any other treatment and whoselife expectancy is not longer than 3 months. Recently, therehave been reports of phenol being used to produce chemi-cal neurolysis and a ‘botulinum toxin-like’ effect.

Hemorrhoids Martindale23 reports the use of injections of an oil solutionof phenol as a sclerosant for hemorrhoids. The phenol isinjected into the tissue surrounding the internal hemor-rhoids as a hardening agent and painkiller.

VariousPhenol has been injected into the soft tissue of the lowerback to relieve chronic pain. Phenol ablation is sometimespreferred to surgery to treat ingrown toenails or ony-chogryphosis.

Notes1. See the section on inadequate results in Chapter 37.2. It is possible, for example, to inject hyaluronic acid immedi-

ately 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 restrictedto the production of melanin – it is interesting to note thatthey are still where they should be: in the basal layer of theepidermis.

4. Cortez E. Chemical face peeling. Otolaryngol Clin North Am1990; 23: 947–50.

5. Blending Bleaching® cream should be applied twice a dayfrom the 10th day after Lip & Eyelid®, if the skin is ready.

6. Asken S. Unoccluded Baker–Gordon phenol peels – reviewand update. J Dermatol Surg Onol 1989; 15: 998–1008.

7. Zhao QM. Clinical observation of face peeling for ephelidesand 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 asa malignant melanoma in situ or as a premalignantmelanocytic dysplasia.


11. See also treatment with localized TCA (Only Touch®) –Chapter 22.

12. Usually, phenol peels are not recommended for non-facialskin.

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. DermatolSurg 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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Contraindications andprecautionsInsulin-dependent diabetesInsulin-dependent diabetes is an absolute contraindicationto a phenol peel. Diabetes significantly increases the risk ofsecondary infection; the vascular and/or immune disordersassociated with this illness mean that complications aremore of a probability than a possibility. Stabilized, non-insulin-dependent type 2 diabetes is not an absolute con-traindication to a phenol peel. The doctor must takeparticular care with these patients to avoid secondary infec-tions.

Florid herpesActive herpes is an absolute contraindication to a phenolpeel. A history of herpes is not a contraindication to phe-nol, but requires treatment to prevent herpes recurring.For more details, see Chapters 32 and 37.

Other obvious, absolutecontraindicationsWho would dream of doing a phenol peel on a woman whois pregnant or breastfeeding? Or on a patient with an obvi-ous malign lesion? Or a patient recovering from a seriousillness? A patient with immunodeficiency?1 On a patientwith Ehlers–Danlos syndrome?2 On one with sclerodermaor collagen disease? The doctor must use his professionalskill and experience to rule out any patient who poses anincreased risk.

Local anesthesia with adrenaline(epinephrine)Adrenaline (epinephrine) is a cardiac irritant that increasesthe risk of arrhythmias. For more details, see Chapter 37.

Pre-existing heart conditionA phenol peel should of course not be performed aftermyocardial infarction or cardiac decompensation. Unsta-ble angina also rules out a phenol peel, as the stress associ-ated with a peel could trigger an angina attack. No clearlink has ever been established between a personal medicalhistory of a heart condition, if currently stabilized, and theincidence of cardiovascular complications during a phenolpeel. Apart from arrhythmias, to the best of my knowledgethere is no mention in the literature of any serious heartproblems occurring as a complication of a phenol peel.3

Of course, we cannot know for certain that such compli-cations are always reported in scientific journals, eventhough any serious complications following cosmeticinterventions always make headline news in the popularpress and on TV. As far as I know, however, recently therehave been no serious health problems resulting from a phe-nol peel.

Pre-existing kidney or liver diseaseLiver or kidney deficiency increases the risk of toxicity, asthe normal detoxification and elimination processes willnot be functioning properly (see Chapter 28).

Patient historyRecent postoperative woundsWe saw in Chapter 30 that it can improve the appearance ofstabilized surgical scars on the face. Phenol should not beused to treat recent postoperative wounds that have not yetstabilized, however, as there is a significant risk of necrosis.

History of local radiotherapyIn addition to all the structural changes that can followexposure to ionizing radiation, there is a possibility that thepilosebaceous units might atrophy. This would delay epi-dermal regeneration and promote the formation of nastyscars.

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History of keloid formationIt is better to select a peel whose depth of action does not gobeyond the papillary dermis.

Use of isotretinoinRecent use of isotretinoin (Roaccutane®) is an absolutecontraindication to phenol. For more information, see thesection on scarring in Chapter 37.

Use of MAO inhibitorsMonoamine oxidase (MAO) inhibitors are contraindica-tions to the use of the majority of analgesics and psy-chotropic drugs required for patient comfort. This wouldmake a phenol peel almost unbearable for a patient on MAOinhibitors, who is, by definition, psychologically unstable.

Refusal or inability to wear make-up Patients who absolutely refuse to wear make-up during thepost-peel period are not the best candidates for a phenolpeel, as the erythema and potential dyschromias, even iftemporary, are best covered up with make-up.

Patients at risk of dyschromiaPatients with dark skin should be warned about the demar-cation line between the treated and untreated areas, bothwith a full-face peel and a localized phenol peel.

Patients on estrogen–progesterone hormone-replace-ment therapy (HRT) will need close monitoring for pig-mentary changes. McCollough and Maloney4 ask theirpatients to try to stop HRT or the contraceptive pill for atleast the first 6 months after a peel. If they cannot stop HRTduring this time, they are warned of the risk of pigmentarychanges.

Patients who work outside most of the time should alsobe warned of the high risk of hyperpigmentation and of theabsolute necessity not only to wear an effective sunblockbut also to change their general attitude to the sun.

Patients with mental orbehavioral risksThe patient has to understand the peel procedure and thelimits of a deep peel. He or she must agree to comply withstrict rules of procedure before, during and after the peel.Any cosmetic procedure, in which the patient is required totake an active part, and especially a deep peel, is strictlycontraindicated for patients who do not have a minimumlevel of intelligence. The patient has to be capable of under-standing and accepting the necessity to wear sunblock and

make-up after the peel and be aware of the time needed forthe skin to regenerate completely.

Squeamish patients will overwhelm the doctor withcomplaints, worries, questions and reproaches. It is betterto test a patient’s mental and physical resistance by firstsuggesting a painless peel without complications and thenprogressing onto a medium-depth peel before consideringa phenol peel. Individual tolerance can be tested in thisway, and the patients themselves gradually learn what apeel is and what it can do for them.

Patients should be shown a series of photographs show-ing what the face looks like day by day during the first weekafter a peel. Ideally, the patient’s immediate family shouldalso see these photographs. Without this precaution, para-noid patients, friends and family may not believe it whenthe doctor tells them that everything is proceeding asnormal.

Isolated patientsBeing alone is of course not in itself a contraindication to aphenol peel. The dramatic results of a peel could bringcouples back together,5 but a few rules are necessary for thepatient’s safety. The phenol formulas of today allowpatients to remain on their feet: the patient can go homealmost immediately after a phenol peel. However, it doescauses significant edema that can sometimes make it diffi-cult for patients to open their eyes. It is therefore out of thequestion for a patient who lives alone to go home after thepeel. The patient needs help to go about his or her daily lifeduring the first 3 days after the peel. Clinics with hospitalbeds can keep patients in during the first few days or eventhe first week after a peel.

Neck peelA phenol peel is better intended for facial skin, and thereare other treatments for the rest of the body.6

Specific precautionsIf a phenol peel on the neck proves necessary, the followingprecautions must be taken:

� No impermeable dressing should be applied: no occlu-sion.

� The solution should be applied sparingly on the skin ofthe neck.

� Any movement or friction likely to cause scarringshould be avoided after the peel.

� The phenol must not be allowed to macerate in the foldsof the neck. This maceration is equivalent to occlusion.

� After treating the face, the solution should be appliedextremely slowly on the neck, or, preferably, should bepostponed until the following day so as not to overload


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the body’s metabolization and elimination pathways. Itis especially important in this case to avoid the toxiccomplications associated with phenol being applied toorapidly on too large an area.

Skin regenerationAfter an intraepidermal peel, to the basal layer or the Grenzzone, the skin regenerates from leftover islets of ker-atinocytes. In the case of a deep peel, the skin regeneratesfrom its appendages.7 The face has more pilosebaceousunits than the neck, and facial skin regenerates morequickly, with less risk of scarring.

Solution to the problem of neck peelsThe answer is to do a peel to the papillary dermis on theneck and décolletage. This peel can be carried out at thesame time as the phenol face peel or in the weeks followingthe face peel.

Sun exposureComplete sun avoidance and effective sun protection is amust for 2 or even 3 months (see Chapters 2 and 3). Post-inflammatory hyperpigmentation (PIH) is not at alluncommon, even after a phenol peel. After the immediatepost-peel period, which requires close and almost dailymonitoring, it is advisable to see patients again after 15days, 30 days and 2 months and to warn them of the needto treat any early signs of hyperpigmentation immediately.It should be noted that PIH frequently resolves itself with-out treatment after a phenol peel.

CostOne of the drawbacks of a deep peel is the high cost, whichmeans that this technique is not within everyone’s reach.The results that can be achieved offer excellent value formoney, however, and no patient who has benefited fromthis treatment has ever complained about the cost.

Disorders that may be aggravatedTelangiectasias, seborrheic dermatitis, eczema, acne rosacea,lupus and other autoimmune disorders are among the formsof dermatitis that may be aggravated by a phenol peel.

Safety factorsPatient selectionChoosing the right patient is a key safety factor. The few,but strict, indications and contraindications should be

taken into account, as well as the results of the essentialpreliminary clinical check-ups.

Local and systemic safetyThe following is a summary of some of the safety rules:

� The product should only be applied to the face. There isa large number of pilosebaceous units here that help theepidermis regenerate properly.

� It is better not to treat the neck with phenol, both forlocal, dermatological reasons and so as not to increasethe absorption area.

� Using the right formulation and the proper applicationtechnique ensures perfect results every time. A ‘number1’ phenol formula should not be applied using the appli-cation procedure for a ‘number 2’ formula. In somecases, this precaution is not essential, but in others it is.

� All contact between phenol and the eyes should beavoided.

� No phenol should be applied in cases of liver or kidneydeficiencies or serious heart disease.

� Phenol is contraindicated for patients with Ehlers–Dan-los syndrome, collagen disease, insulin-dependent dia-betes and active infections (acne, herpes, etc.).

� Phenol should be applied extremely carefully and inaccordance with all the safety rules (equipment, skill).

� Doctors should inform their professional insurers thatthey perform this type of peel.

� The toxicity of phenol is paradoxical, and low-concen-tration solutions are potentially more toxic than high-concentration solutions.

� A phenol solution should contain oil to slow downabsorption and allow enough time for the liver todetoxify it and the kidney to eliminate it. The solutionmust be stable, tamed and adjuvanted.

� As well as improving the cosmetic results, using occlu-sion also slows down the absorption rate of phenol andreduces its toxicity. Occlusive masks must be appliedcarefully to avoid air bubbles or pools or phenol forming.

� The doctor must be aware of all the potential complica-tions, watch out for any signs and be ready to treat themshould they occur.

� Phenol should be applied slowly, in a minimum of 1hour, on healthy patients with normal liver and kidneyfunction who can be expected to achieve good cosmeticresults.

� The patient should be hydrated, ventilated and moni-tored (pulse oximeter and electrocardiogram). Avenous drip should be set up beforehand, and if neces-sary glucose serum can be administered to avoid hypo-glycemia.

� The risks of general anesthesia and products that couldirritate the myocardium can be avoided by using localnerve blocks or deep sedation.

Phenol: contraindications, precautions and safety 251

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Notes1. Because of the risk of secondary infection, patients with

immunodeficiency (e.g. HIV) should be ruled out from afull-face phenol peel, as well as patients with hypogamma-globulinemia.

2. See the section on scarring in Chapter 373. Fiatsi Y. Exoderm®, a novel, phenol based peeling method

resulting in improved safety. Am J Cosmet Surg 1997; 14:49–54.

4. McCulloch EG, Langsdon PR, Maloney BP. Chemical Peelwith Phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermato-logic Surgery, Principles and Practice, 2nd edn. 1147–60.1996, UK, Oxford, marcel Dekker Ltd.

5. Doctors should not suggest a peel as the answer to a patient’spersonal problems. A peel repairs the skin, not the soul.

6. Vigneron JL. Les peelings en dehors du visage. J Med EsthChir Derm 1993; XX(75): 53–6.

7. Rusciani L, Rossi G, Bono R. Les peelings cliniques. J MedEsth Chir Derm 1993; XIX(78): 75–80.


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The preparation procedure for a local phenol peel has someaspects in common with those for a full-face phenol peel –however, a local application of phenol is far easier.

Eight days before the peel

PhotographsBefore any treatment, top-quality photographs (Tiff for-mat) should be taken of the face, profile and three-quarterprofile (Figure 32.1), with and without flash. A flashchanges the appearance and color of the skin: dyschromiasare less apparent and reliefs are flattened. Pigmentationand relief is more clearly visible on photos taken withoutflash, especially in natural low-angled light (Figure 32.2).

Any pre-existing abnormalities will be recorded to avoidany potential medical and legal problems later. In this way,a ‘round eye’ appearance after surgery, lagophthalmia orectropion should be photographed and this noted in thefile. Nevi and other lesions should be photographed in par-ticular. The whole peel procedure could also be filmed. Thepatient, preferably accompanied by a member of his or herfamily, will have seen sequenced photos showing the after-effects of a phenol peel, day by day.

Preparing the skinMany phenol peel techniques require skin preparationbefore the peel to ensure that penetration is even and toreduce complications (see Chapter 2). No specific prepara-tion is necessary before Lip & Eyelid® formula.

Botulinum toxinBotulinum toxin should be injected 1 week before the peelinto forehead or glabellar wrinkles, crow’s feet, lip wrinklesor radial wrinkles around the outer canthus of the uppereyelid. Blocking the muscles allows the skin to regeneratemore evenly. The results will be of better quality and longerlasting. This is also the ideal moment to shave off any

benign skin tumors, remove small sebaceous cysts and fillany deep furrows.

MedicationThe patient should be given a prescription for:

� a strong analgesic to be taken before the peel to test fortolerance. Paracetamol (acetaminophen) plus codeineis usually strong enough and well tolerated

� a benzodiazepine (e.g. 2 mg lorazepam)� aciclovir (or, better, valaciclovir) if the patient has a his-

tory 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: Couv-

rance® or Covermark® are both well tolerated bypatients from the 8th day

� beware of patients on monoamine oxidase (MAO)inhibitors: they are contraindicated in combinationwith many other drugs, including some analgesics orsedatives that have to be used for the patient’s comfortduring and after the peel

� some single-dose carmellose sodium eye drops to beused freely after the phenol peel to alleviate any eye irri-tation, which is common during the hours following afull-face phenol peel.

Legal documentsThe patient should be given the following documents toread and sign: informed consent (Box 32.1), authorizationto take and use photographs (Box 32.2) and a general ques-tionnaire on health and coagulation (Box 32.3).

Clinical examinationThe patient should be given a full clinical examination andquestioned closely; the results should be noted down in the

32Phenol: pre-peel preparation

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A B C

D E

Figure 32.1(a) Right profile. (b) Three-quarters right.(c) Full face. (d) Three-quarters left. (e)Left profile.

A B

Figure 32.2The same patient taken during thesame consultation: (a) without flashand (b) with flash: relief and lipwrinkles are flattened by the effectof the flash. The nasolabial folds, onthe other hand, are more clearlyvisible with flash.

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Phenol: pre-peel preparation 255

Box 32.1 Example of an informed consent form (originally drawn up by the Sociedad Española de Medicina yCirugía 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 beapplied on my skin, of its immediate effects, of the process of skin recovery, of the post-peel care after treatment and ofthe precautions to be taken during the months following the peel. I have also been informed that, because of the vari-ability of individual reactions, it is not possible to be given a precise date when normal activities may be resumed. I havealso 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 thislatter course of treatment with full knowledge of the facts.

Should any unforeseen situation or complication arise that requires medical intervention not described in the explanationsgiven 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 acceptthe 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 havereceived written in language I can understand and that I have read carefully or orally by the doctor during consultationsprior 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 twocopies: one for the patient and one for the doctor.

Signature, preceded in handwriting by the words ‘read and approved’.

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patient’s file. The patient should be given a cardiovascularexamination before the peel if there is any doubt as to theircardiovascular health, or merely as a precaution; the doctorthen has the opinion of a specialist to confirm that there isno cardiovascular contraindication to the peel. The patientshould be asked to have a biological examination. Theresults must be checked before the start of the peel. It isessential to check the patient’s blood count1 and liver andkidney function, to make sure there is no bacterial or viralinfection, diabetes or immunodeficiency.

The night before and themorning of the peelThe evening before the peel, patients should takelorazepam if they are worried about not getting to sleep.Patients who are very nervous or anxious can take anotherlorazepam tablet on the morning of the peel, together with10–20 mg of domperidone.

One hour before the peelThe patient should arrive at the clinic half an hour to anhour before the peel and not have eaten for more than 4hours.

� If the peel is to be done without deep sedation, thepatient should immediately be given premedication, asper the doctor’s usual practice: for example, one sublin-gual tablet of Temesta 2.5 mg (lorazepam) if the patienthas not taken any that morning and 15 drops of tilidine(a major analgesic) or any other strong analgesic thedoctor usually prescribes. It is best to use an analgesicthat the patient can tolerate easily.

� If the peel is to be performed under deep sedation orneuroleptanalgesia, the anesthetist should deal withpremedication.

Advantages of benzodiazepineUsing benzodiazepine as premedication is very worth-while. There are four obvious advantages:

� 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 producepartial amnesia that lasts for more than 10 hours. Mida-zolam produces short-term but deep amnesia thatmakes the patient forget any pain he or she may havefelt in the course of the treatment.


Box 32.3 Example of a general questionnaire andcoagulation questionnaire

Are you taking medication that contains aspirin or ananti-inflammatory?: Yes/No

Are you currently taking medication to thin theblood?: 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/NoDuring child birth?: Yes/NoDuring 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 cutyourself?: Yes/No

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 withbleeding?: 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

Have you ever had a pulmonary embolism?: Yes/No

Have you ever had an operation?: Yes/No

For what? (give details below):

.....................................................................................Have you ever had a local anesthetic?: Yes/No

If you did not tolerate it, what happened? (givedetails below):

.....................................................................................

Are you allergic?: Yes/No

To what?: .....................................................................

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� Benzodiazepines are neurostabilizers that can counter-act the initial toxic neurological effects of local anesthet-ics or phenol.

� A long-acting benzodiazepine greatly improves patientcomfort. It makes the patient feel drowsy, which reducesfacial movements and therefore helps keep the post-peelocclusive mask in place. Also, when a patient has taken2.5 mg of sublingual lorazepam as premedication, theywill feel much less pain immediately after the peel. A calmpatient is a patient who does not complain, does not fid-get, does not speak, does not smoke and does not scratch.

Preparing the occlusive mask

Sleek®, Micropore®, Blenderm® orLeukoflex®?The occlusive mask applied at the end of the peel will con-sist of either a single or a double layer, depending on whattype of dressing is used. Sleek® and Leukoflex®2 can be usedin a single layer. Leukoflex® has an advantage over otherbrands in being transparent. Micropore® can be applied intwo layers, or a layer of Blenderm® can be applied on top ofthe first layer of Micropore® (Figure 32.3).

Whichever dressing is used, the tape should be precutinto 3–5 cm strips (Figure 32.4) and placed within easyreach, ready for the occlusive mask (Figure 32.5) to beapplied at the end of the peel.

Settling the patient inThe patient is placed in a comfortable position to be main-tained for over an hour without moving,3 covered in awarm electric blanket or a metallic survival blanket.

Protecting the eyesA small quantity of sterile ophthalmic Vaseline® should beput in the conjunctival cul-de-sacs. The Vaseline® deacti-vates the phenol and protects the eyes from accidental con-tact. Terramycin® ointment or ophthalmic gentamicin canbe 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 outimmediately in case of contact with phenol (which is highlyunlikely if the peel is applied correctly).

VentilationKeeping the treatment room properly aired and ventilated4

and fanning the patient’s face help make the patient more


Figure 32.4The most common technique involves the use of occlusion for24 hours. An assistant prepares the strips of occlusive tape,cutting them to the right size (about 3–5 cm long) so that theocclusive mask can be applied immediately after the peel.

Figure 32.5After cutting, the pieces of occlusive dressings are installed ona sterile base, easy to take.

Figure 32.3Four different types of occlusive dressing that can be used forocclusive phenol.

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comfortable when the doctor goes through the essentialphase of carefully cleansing the skin with acetone and alco-hol before the peel (Figure 32.6). It is most unpleasant for apatient to have to inhale the fumes when these products arebeing wiped on the lips, cheeks and chin.

Good ventilation prevents sweating, especially in hot cli-mates: sweat overhydrates the superficial layers of the epi-dermis, which can lower the concentration of the activeproducts locally and increase skin permeability. Ventilationalso creates drafts that will stop the phenol vapors from stag-nating in the immediate vicinity of the patient and doctor.

Intravenous drip andmonitoringDiuresisOsmotic balance across the plasma membrane is regulatedby the concentration of proteins (albumin more than globu-lins). Relative dehydration would increase plasma oncoticpressure and capillary absorption of water and water-solublemolecules. Phenol is soluble in water, and its absorption ratecould be accelerated by the slightest dehydration.

Intravenous access should always be set up to help diure-sis by infusing 1 l of physiological saline or glucose solutionthroughout the procedure and for 1 hour afterwards. Properdiuresis is usually considered to be an effective way of reduc-ing the toxic effects of phenol by helping renal elimination.

Cardiorespiratory monitoringEvery patient must be properly monitored with pulse oxime-try and electrocardiography (ECG). Even if the peel is doneby the book and even when the simplest and least aggressivetechniques are used, stress can cause vagal reactions, lowblood pressure and tachycardia. Pulse oximeter monitoringcan pick up on any drop in oxygen saturation that couldaccentuate myocardial irritability and cause arrhythmias.

Without monitoring, a simple vagal reaction can goundetected, and if it is not treated correctly, the patient can

pass out or even stop breathing. The pulse oximeter is notvery effective at detecting arrhythmias; continuous ECGmonitoring is essential, even though some authors5 recom-mend simply checking the heartbeat and vital signs whenmore than half the face is treated with a phenol peel. Thisvague recommendation could be taken as encouraging anamateurish approach, while close and continuous moni-toring is essential as a simple precaution. Other authors,6

on the other hand, recommend monitoring the patient upto 4 hours after a phenol peel, which seems excessive giventhe results of toxicological studies showing how quicklyphenol is metabolized and detoxified. The blood levels ofphenol recorded by Deichmann and Litton during a full-face phenol peel show a rapid drop in plasma values 2hours after the beginning of the application. The bloodlevel of phenol always remains below toxicity thresholdswhen phenol is applied slowly. It is therefore not unreason-able to stop monitoring the patient shortly after the occlu-sive mask has been applied. By then, approximately 2 hoursafter the beginning of the application, the liver is detoxify-ing the phenol effectively, the kidneys are eliminating itand plasma levels are already going down.

Corticosteroids, atropine andantibioticsSome authors recommend injecting 125 mg of solumedrolintravenously before starting a phenol peel: injecting asteroid is said to reduce post-peel edema and to preventsome of the complications described above. However, I havenot noticed any advantage from this injection. The after-effects of the peel are similar with or without corticosteroids.However, it is worth considering an intravenous injection ofprednisolone for patients who smoke and do not have anyhistory of gastric ulcers. Smokers have an increased risk oflaryngeal edema immediately after a full-face phenol peel.

Atropine should not be injected automatically before afull-face phenol peel. It should be at hand, however, to treatany incidence of bradycardia. As a precaution, it has beenrecommended to inject a broad-spectrum antibiotic beforea phenol peel, although this is not essential for the correctpeel procedure.

Cleansing, degreasing anddisinfectingOnce the patient is settled in comfortably in the dorsaldecubitus position and put on a monitor and drip, the doc-tor can start cleansing the skin either before or after theanesthetist has started injecting the sedatives. The skin iscleansed and disinfected with a mixture of chlorhexidine,7

water and alcohol in equal parts (5 cm3 of each). It is thenrinsed and dried thoroughly. The whole area is carefully


Figure 32.6Ventilation during a local application of phenol (chemicalcheiloplasty: see Chapter 36).

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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 skinmust be degreased very carefully, applying medium pres-sure8 and paying special attention to the base of wrinklesand acne scars. The patient should be properly ventilated(with an electric or hand-held fan) to avoid inhaling theacetone and alcohol vapors. All told, it takes around 10minutes to cleanse the skin thoroughly. Applying mediumpressure helps extract and eliminate some of the residualsebum from the sebaceous glands, but should not take offthe stratum corneum: the doctor must be careful not toabrade the skin with the swab before a phenol peel. Acetonehas various functions: it degreases, cleans and helps thephenol penetrate; it also breaks down the barrier functionof the epidermis.9 This preliminary phase of careful cleans-ing, disinfecting and degreasing is essential to get perfectresults. Phenol does not penetrate as evenly and as wellthrough skin that has not been properly cleansed.

AsepsisIt is easier and more precise to hold the phenol-soaked cot-ton-tipped applicator with a bare, ungloved hand. It istherefore imperative for the doctor to disinfect his handssurgically to avoid infecting the patient’s skin. The assistantwho cuts the occlusive dressing and helps the doctor putthem in place should also disinfect his hands in the sameway, for the same reasons.

There are two reasons why a mask should be worn:firstly to avoid contaminating the patient’s skin with respi-

ratory bacteria, responsible for many of the cases of sec-ondary infection described, and secondly to protect thedoctor from partially inhaling the phenol vapors. Standingabove the phenol vapors for over an hour, the doctorinhales a fair amount of this volatile chemical, which canhave unpleasant side-effects such as dysgeusia or nausea.

Any person with any kind of infection should be keptaway from the treatment room: it is out of the question toperform a phenol peel when suffering from a sore throat,tracheitis, impetigo or a fungal infection on the hands.

Notes1. To screen for anemia, an obvious contraindication for a full-

face phenol peel.2. Leukoflex® is included in the Lip & Eyelid® formula kit.3. Particular care must be taken with patients who suffer from

lumbago, as they sometimes find it difficult to remain in adorsal supine position on a hard surface for a prolongedperiod of time.

4. By mechanical ventilation with an electric fan, air condition-ing, fanning by hand, etc.

5. Benatar D. Le peeling au phénol. J Med Esth Chir Derm1988; XV(60): 319–23.

6. Konior RJ, Kerth JD. Selected approaches to the aging face.Otolaryngol Clin North Am 1990; 23: 1083–95.

7. If there is no chlorhexidine, simple disinfection with 70%alcohol is sufficient.

8. The pressure should be equivalent to scratching.9. Simply applying acetone increases DNA synthesis as well as

synthesis of skin lipids


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Properties of coldCold has interesting anesthetic properties1 that developwhen the surface of the skin reaches 5°C. The temperatureof the dermis and hypodermis is then 15°C. Even if the skincan withstand this temperature for a long time without anyobvious damage, in practice it is unthinkable to usecryoanesthesia alone for a full-face phenol peel. Limitedareas can, however, be cooled before applying the acids2 tomake the application more bearable, when no other anes-thetic is being used. To do this, the practitioner can use3M® cold packs (Figure 33.1) or surgical gloves filled withan aqueous solution mixed with antifreeze (75% water and25% antifreeze). The skin must not be frozen, of course.Some doctors use a facial anesthetic technique that consistsin injecting Klein solution3 cooled to just a few degrees cel-sius under the skin of the face. This painful technique doesnot produce sufficient surface anesthesia, and changes allthe parameters of how the phenol penetrates through theskin. The skin itself, as opposed to the subcutaneous tissue,

is only partially anesthetized by this type of injection, andthe peel is still very painful. It is also impossible to injectthis solution in the lips, nose, eyelids, etc. Doctors who uselasers are familiar with the Dermacool® device: it generatescooled air that can be directed locally using a handpiece.This cooling device is sometimes used for local applicationsof phenol.

Anesthetic properties of phenolPhenol was used widely in the First World War as an anti-septic and a local anesthetic in surgery. Depending on theconcentration and the different adjuvants used, phenol caninduce coagulation or lysis of the membrane and intersti-tial proteins, which clinically manifests as the whitening ofthe skin that occurs when phenol is applied. An applicationof phenol immediately triggers intense pain followed bylocal anesthesia that takes effect within about 15 seconds, asthe skin whitens. The pain caused by an application of phe-nol is therefore very brief. The local anesthetic effect lastsfor 20–30 minutes, shortly after which the processes of der-mal inflammation intensify and trigger a painful, pulsingheat that, depending on the patient’s own perception, isrelatively intense. This pain gradually subsides over the fol-lowing few hours and goes completely once edema sets inand the inflammation has stabilized, usually the morningafter the peel. Phenol can therefore be applied on verysmall surface areas without any anesthetic: it is enough totell patients that they will feel an intense burning for 15seconds, immediately after the phenol has been applied onthe skin. The patient should be given painkiller tablets toalleviate the post-peel pain, which can last until the follow-ing morning.

The eyelids and upper lip can be treated with Lip & Eye-lid® formula, without any analgesic other than a paraceta-mol plus codeine tablet to be taken 1 hour beforetreatment. Patients should also be given a clear descriptionof the pain they will feel. By the time they have counted to15, the pain will have gone.

33Full-face phenol: nerve block anesthesia and/orsedation

Figure 33.13M® cold pack. This photo shows the forehead being cooledprior to a trichloroacetic acid peel to the papillary dermis(Unideep®).

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Type of anesthesia for a full-face peelUnlike a local application of phenol, a full-face phenol peelcannot be done without anesthetic.4 There are several dif-ferent possibilities.

General anesthesiaAccording to the medical literature, general anesthesia(GA) should not be considered as an additional cardiovas-cular risk factor during a phenol peel. However, there areother effective techniques that are less complex and alsoless dangerous.5 What is more, it is in the hours followingtreatment that the pain is at its height – a long time after theGA has worn off. GA is a needless source of stress.

GA does not make the patient more comfortable or anysafer. On the contrary, it adds the inherit risks of generalanesthesia to those of the phenol peel. GA is not the idealchoice for a full-face phenol peel. It is never indicated for alocal phenol peel.

Facial nerve blocksFacial nerve blocks (FNB see p. 265) are quick and easy toadminister, are not painful and cause few complications inthe hands of an experienced doctor. A drop of 2% lidocainecan be injected very superficially with a fine-gauge needle32G in precisely the same place that the nerve itself isinjected with a 25G5/8 gauge needle. It is not possible to seethe backflow of blood before injection with a 32G needle.

Allergy to local anestheticsAllergies to local anesthetics (LAs) are rare, and the term‘allergy’ is often used to describe numerous problems thatare more likely an overdose or a vagal reaction. Publica-tions report that the frequency of allergic reactions to LAsis no more than 1% of all the side-effects met with.6 Lido-caine is an amide local anesthetic that does not cause manyallergies.

Procaine, on the other hand, is an ester-type localanesthetic: when it is injected into the organism, it is trans-formed into N,N-diethylaminoethanol and para-amino-benzoic acid (PABA) when the ester link that binds thesetwo components of procaine is broken. PABA is a well-known allergen. Methyl para-hydroxybenzoate, whosestructure is similar to that of PABA, is also called PAB ormethylparaben. It is a preservative that binds, like a hapten,to the immunoglobulin E (IgE) on the surface of mast cellsand basophils and may be the cause of the few cases of ana-phylactic shock that have been described. Other patientsmay be allergic to metabisulfite conservative, found inpreparations containing adrenaline (epinephrine).

Toxicity of local anestheticsWhen nerve fibers depolarize, the sensation of pain is carriedfrom the periphery to the brain. LAs are molecules that sta-bilize the membranes of excitable cells that are susceptible todepolarization. Their general toxicity is directly linked to thisproperty. In cases of overdose, excessive cell membrane sta-bilization in the central nervous system (CNS) and the car-diovascular system produces severe side-effects. Differentfactors influence the risk of intoxication with LAs. For exam-ple, capillary absorption is more rapid in the face than on thebody. The large number of facial blood vessels is one factorthat speeds up absorption. Other factors that can causeintoxication include lack of adrenaline, low body weight(<45 kg), advanced age and competition with other mole-cules that use the same detoxification pathways. Intoxicationwith lidocaine is dose-related: unless there is a gross errorwhen injecting, the symptoms are gradual and do not startwith loss of consciousness or convulsions. The toxicity ofbupivacaine, on the other hand, can trigger cardiovascularsymptoms together with neurological symptoms.

The first signs of local anesthetic CNS toxicity are drowsi-ness, yawning and a general feeling of malaise. The patientmay complain of feeling lightheaded, anxious or dizzy. Theymay appear confused, pale, disoriented and complain ofvisual, auditory or gastric symptoms. When blood levels oflidocaine increase and reach 4–7 µg/ml, muscle spasms ortremors may start. The patient may have difficulty speakingand suffer from hallucinations, nystagmus and dizziness.Loss of consciousness follows, as blood levels of lidocainereach or go beyond 8 µg/ml. Muscle spasms and tremorscan develop into convulsions. Severe respiratory depressioncan lead to respiratory arrest, and the patient goes into acoma and dies if not properly ventilated. Death can comefrom both respiratory arrest and arrhythmia.

The cardiovascular system is actually more resistant toLAs than the CNS, and cardiac toxicity starts at muchhigher blood levels of lidocaine. The first stages of cardio-vascular toxicity are spontaneously reversible; they mani-fest in changes in blood pressure: stable or higher to startwith, due to vasoconstriction or the increase in cardiacsympathetic tone, it then drops because of the decrease incardiac output without any change in peripheral resis-tance.7 Circulatory collapse occurs as a result of negativeinotropic effects, bradycardia caused by the reducedexcitability of the myocardial cells, decreased intracardiacnerve impulse conduction and the direct myorelaxanteffect on the vascular fibers that causes peripheral vasodila-tion. Cardiorespiratory resuscitation should be carried outimmediately. Caution therefore dictates setting up venousaccess for fluid administration, an electrocardiograph, apulse oximeter and a sphygmomanometer.

The first thing a doctor faced with LA toxicity must do isto ensure good ventilation, at the same time as monitoringthe heartbeat. An upset stomach, one of the first signs of


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intoxication, can trigger vomiting. If the patient is notplaced correctly in the ‘safety’ position, the airways canbecome blocked, causing respiratory arrest and convulsionsor inducing hypoxemia, hypercapnia or acidosis, all condi-tions that can aggravate arrhythmias. The low quantities oflidocaine needed to do the facial nerve blocks for the hourthat the peel will last make CNS and cardiovascular toxicityto LAs almost impossible. It is nevertheless essential to rec-ognize the symptoms and to be able to treat them.

Choosing the right LA agent is also a safety factor, andwe will see below why simple lidocaine without adrenalineis the best choice of molecule for a phenol peel, both localand full-face.

BupivacaineBupivacaine is an amide-type anesthetic and rarely causesallergic reactions. It is stronger than lidocaine and has alonger duration of action (anesthesia for about 3–6 hours).It also has a slow onset of action, and it takes 20–30 minutesfor the anesthetic effect to develop. Mixing bupivacainewith lidocaine speeds up the onset of action, as lidocaineanesthetizes almost immediately. It is therefore very tempt-ing to combine the two products to achieve immediateanesthesia with the lidocaine as well as a longer duration ofanesthesia with the bupivacaine, which starts to take effectalmost as the lidocaine stops. Bupivacaine is far more toxicthan lidocaine, however, and no more than a total of 10 cm3

should be used for all of the nerve blocks on the face.8 Thethreshold value for the onset of neurological toxicity inhumans is 6.4 mg/kg for lidocaine and only 1.6 mg/kg forbupivacaine. The threshold value for the onset of neurolog-ical side-effects in a patient weighing 50 kg would thereforebe 80 mg. A 10 cm3 phial contains 50 mg of bupivacaine.Intravascular injection is instantly toxic to the heart and caninduce ventricular arrhythmias, ventricular tachycardia,ventricular fibrillation and cardiac arrest.

Moreover, injecting small quantities of bupivacaine inthe head or neck can cause symptoms of systemic toxicitysimilar to those caused by the accidental intravascularinjection of much larger quantities. If it is not possible toavoid using bupivacaine, it is essential to do an aspirationtest before each injection.

There are many drawbacks to using this product in afull-face phenol peel: its slow onset of action requirespatience, and the nerve block takes about 30 minutes to setup but lasts 180–360 minutes. This product is painful toinject. The doses required to produce a nerve block of thewhole face are lower than the neurotoxic doses, but not bymuch. As we saw above, the dose required for the face is atleast 50 mg, while the toxicity threshold starts at 80 mg andthe maximum allowed dose is 150 mg. As we saw in Chap-ter 28, Lalanne’s9 experiment clearly shows that perivascu-lar injections, even when the blood vessels have beenproperly dissected and are in plain view, can be followed by

vascular absorption and trigger serious rhythm disorders.It is therefore advisable not to use bupivacaine for facialnerve blocks, especially in a full-face phenol peel, when anymolecule likely to irritate the heart must be avoided.Besides, the most painful part of a phenol peel is the 20 sec-onds immediately following the direct application of phe-nol to the skin. The pain caused by post-peel inflammationis soon alleviated with painkiller tablets and lorazepam.

RopivacaineRopivacaine is an amide-type LA, a vasoconstrictor at lessthan 1% and a vasodilator at more than 1%.10 The fact thatit is the pure S-enantiomer reduces its toxicity. Like phe-nol, it is metabolized by the liver and eliminated by the kid-neys. When administered by dermal injection, it has a rapidonset of action (less than a minute) and the duration ofaction is longer than or equal to that of bupivacaine. Com-bining it with adrenaline does not prolong its duration ofaction, and a concentration of 0.75% provides longer anes-thesia than a concentration of 1%. Neurological and car-diovascular tolerance to ropivacaine is much better than tobupivacaine. What is more, there is a considerable differ-ence between the neurotoxic and cardiotoxic doses. Thetoxicity of ropivacaine is intermediate between that of lido-caine and bupivacaine. Direct intravascular injection ofropivacaine is still dangerous, however.

PrilocainePrilocaine is an amide-type LA, with a very low allergenicpotential and low toxicity11 and is non-vasodilating. Unfor-tunately, prilocaine is metabolized into ortho-toluidine, achemical that can induce methemoglobinemia. In doseshigher than 500 mg, it can cause cyanosis and reduce theoxygen-carrying capacity of the blood.

MepivacaineMepivacaine is intermediate between bupivacaine andlidocaine in its kinetics of action. The FNB is set up moreslowly than with lidocaine, in 10–15 minutes, although itlasts 90–180 minutes. Mepivacaine has no real advantageover lidocaine, as, at the same dose, its duration of action isonly slightly longer. Mepivacaine does not cause vasodila-tion but, unlike lidocaine, it does not have an antiarrhyth-mic action.

LidocaineLidocaine is an amide-type LA with a very short onset ofaction. It produces an immediate FNB that lasts from 25 to45 minutes, depending on whether it is combined withadrenaline.

Full-face phenol: nerve block anesthesia and/or sedation 263

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Unlike other LA, lidocaine has an anticonvulsant actionthrough the competitive inhibition of the subcorticalreceptors (0.5–4 mg/ml). It stabilizes the heartbeat:12 anintravenous injection of lidocaine is an effective treatmentfor heart arrhythmias resulting from phenol intoxication.

The toxicity of lidocaine is increased by beta-blockersand cimetidine, as they decrease blood flow in the liver, slowdown detoxification and increase plasma levels. Calciumchannel-blocking agents increase the risk of arrhythmia byaltering the electrical activity of the myocardial cells. Digi-talis glycosides also alter atrioventricular conduction andincrease the risk of rhythm disorders. Diphenylhydantoincan increase the free fraction of lidocaine by competing withthe plasma proteins at the binding site. Stabilization of theCNS with benzodiazepines can mask the first signs of lido-caine intoxication. However, the body easily eliminates thelow doses of lidocaine used in a series of FNB, and therehave been no reported cases of lidocaine intoxication dur-ing a full-face phenol peel performed with FNB.

Combination with adrenaline(epinephrine)Adrenaline stops LA spreading and shortens the onset ofaction; it prolongs the duration and improves the depth oflocal anesthesia. Adrenaline slows down capillary absorp-tion of LAs, and therefore makes metabolization anddetoxification easier.

Adrenaline is contraindicated in cases of diabetes, hyper-thyroidism, serious heart arrhythmias and coronary insuf-ficiency or in combination with beta-blockers ormonoamine oxidase (MAO) inhibitors. Lidocaine withadrenaline has a very rapid onset of action. Its duration ofaction is longer than that of lidocaine without adrenaline.However, inadvertent injection of a lidocaine–adrenalinesolution into the vessels located near the nerve trunksincreases the heart rate (immediate sinus tachycardia atover 130 beats per minute, spontaneously reversible inaround 15 minutes) and increases ventricular excitability(risk of fibrillation). It can trigger angina attacks that maylead to a heart attack. It is therefore preferable not to useadrenaline before a full-face phenol peel.

Topical anesthesia: EMLAThis ‘Eutectic Mixture of Local Anesthetics’ is used suc-cessfully 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 inthis indication:

� There is no denying that EMLA anesthesia for a phenolpeel is not as easy as it appears. It is a time- and space-consuming local anesthetic procedure: a large quantity

of EMLA must be applied to the whole face, in a thickand even layer, without occlusive dressing, for 1 hourand without any contact with the eyes.

� The skin on the face has a greater absorption capacitythan the rest of the body, and the duration of anesthesiamay not be long enough to finish applying the phenol intime and in optimal conditions of comfort, as it takesover an hour to apply phenol.

� Mixing lidocaine base and prilocaine base in equalparts, at room temperature, gives a ‘eutectic’ mixture.This mixture is emulsified in a base that consists mainlyof water and polyoxyethylene castor oil, and the anes-thetics are added to the oily phase. Phenol has an excel-lent oil/water partition coefficient. The oils lower thetoxicity of phenol, but also slow down its rate of pene-tration as well as absorption of the local anesthetics.There is a competition between the phenol solution andthe EMLA, which changes the activity and penetrationof the combined molecules.

� Applying an occlusive dressing, necessary for the EMLAcream to work, causes significant changes in the hydra-tion of the stratum corneum and increases permeability.Under occlusion, the corneocytes swell with water andbecome more permeable. The potential interactions areso complex that it is not possible to predict the results ofcombining EMLA and phenol peel formulations.

� With EMLA, liposoluble anesthetic molecules penetratethe stratum corneum and the rest of the epidermal barrierand soon reach the skin nerve endings. The phenol, whichis also liposoluble, can get through the epidermis morequickly. On the surface: the shorter contact time betweenthe epidermis and the phenol could reduce epidermal liq-uefaction. Deep down, a higher concentration of phenol inthe reticular dermis could cause the formation of retractilescar tissue. The concentration gradient created in theperivascular spaces of the dermis speeds up the absorptionof phenol. The risk of systemic toxicity can also increase.

� EMLA causes vasoconstriction followed by vasodila-tion. Vasodilation can sometimes be seen after only 30minutes of EMLA under occlusion. How will thesevasomotor changes affect the effectiveness or absorp-tion of phenol – and therefore its toxicity?

� There have been studies to prove that EMLA is nottoxic. Quantities of up to 150 g of cream applied on1300 cm2 of intact skin and left under occlusive dressingfor 7 hours did not produce toxic levels. Other studiesshow that injured skin allows EMLA to penetrate muchmore rapidly. Blood levels, although subtoxic, are thenmuch higher than when EMLA is applied on normal,healthy skin. When 10 g of EMLA is applied to healthyskin, maximum blood levels of the anesthetics arereached after 2–3 hours. Phenol substantially changesthe structure of the skin and causes intense vasodila-tion: how will it affect the absorption of the anestheticsin the EMLA?


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� The facial skin is more permeable than the skin on therest of the body. It allows the EMLA to penetrate twiceas quickly as the skin on other parts of the body.13

Proper anesthesia of large surface areas requiresapproximately 1–1.5 g of EMLA/10 cm2. The surfacearea of the face is around 500 cm2 (5% of the body sur-face area) and the maximum acceptable dose in an adultwith a healthy skin is 50 g.

� Because of the high cost of such large quantities of theproduct, practitioners have sometimes resorted to usingcopies that are not always standardized. It should benoted that there is an increased degree of uncertaintywith the use of non-standardized products.

� It is recommended not to use EMLA as an anestheticbefore doing epicutaneous allergy tests, as EMLA blocksthe vasodilation induced by certain mediators, such ashistamine and antigens.14

� The presence of prilocaine is a (relative) contraindica-tion to combining EMLA with products with a potentialto cause methemoglobinemia. Combined use withparacetamol (acetaminophen), for example, is to beavoided. Paracetamol is a derivative of phenol (N-acetyl-para-aminophenol) and is subject to the same detoxifi-cation pathways as phenol. Paracetamol inherits itsproperties of causing methemoglobinemia from phenol.Large doses of EMLA (>600 mg of prilocaine, or four 5 gtubes) should therefore not be applied prior to phenol.

� Eye contact with EMLA must be avoided, as it causesintense and painful irritation. Using EMLA on the eye-lids significantly increases the risk of eye contact. Thevehicle for EMLA contains carbomer 934, which onlygels in an alkaline environment. The alkalinity of themixture also contraindicates its use on the eyelid skin.

� The pH of EMLA cream is 9.4 (the excipient containssodium hydroxide). Phenol is more active in an acid envi-ronment. Impregnating the skin, for 1 hour, with a mix-ture at pH 9.4 will change the physiological balance of theskin, its acidity, its permeability and the activity of phenol.

� A few (unsuccessful) attempts to use EMLA as a topicalanesthetic before a trichloroacetic acid (TCA) peel havebeen published, but the authors reported that they werenot impressed by the results.

Therefore EMLA should not be used as an anestheticbefore a phenol peel.

The best choice of LA for FNB:lidocaine without adrenaline(epinephrine)Lidocaine without adrenaline is therefore the best choice ofLA for FNB before a full-face phenol peel. Lidocaine stabi-lizes the heartbeat, so accidental intravascular injection of

small quantities would not be dangerous during a phenolpeel. Its short duration of action is the only drawback, butwe have seen above that paracetamol plus codeine and coldpacks are enough to alleviate the post-peel pain in thehours following a phenol peel.

Sedation plus FNB with lidocainewithout adrenaline (epinephrine)This is the best technique for doing a full-face phenol peel.The patient and the doctor are at ease, under the benevo-lent protection of the anesthetist. Applying phenol to thewhole face is completely painless and the patient does notexperience or remember any stress or pain. Sedation andintravenous analgesia make up for the speed of sensoryrecovery after FNB with lidocaine without adrenaline.

How to apply facial nerve blocksBefore a full-face phenol peel, the patient is always put on adrip, electrocardiographic monitoring, pulse oximeter andblood pressure monitor. The doctor has everything he needsat his disposal in case of any allergic, vagal or other reactions.Although bupivacaine, ropivacaine or mepivacaine can beemployed for FNB, these products should not be used for thereasons set out above, and anesthesia should consist of FNBwith lidocaine without adrenaline and with deep sedation.

It takes approximately 15 minutes to do all the nerveblocks needed to anesthetize the whole face. If the skin hasnot been cleaned and degreased before the FNB, the phenolwill not be applied until about half an hour after the begin-ning of the first nerve block on skin that is already recover-ing sensation. The FNB should therefore be done after theskin has been cleaned and degreased. The FNB should bedone in a clockwise (or anticlockwise) sequence, as andwhere the phenol needs to be applied. This has the addedadvantage of diluting the doses of lidocaine in time andleaving a rest period between each zone. The hepatocytes,which initiate phenol detoxification by glucuronide andsulfate conjugation as soon as it is applied to the skin, ben-efit from these pauses between the different blocks.Administering the nerve blocks sequentially also helpsreduce the risks of systemic phenol toxicity.

Frontal and upper eyelid blockA frontal FNB anesthetizes the supraorbital nerve, thesupratrochlear nerve and the external nasal nerve (Figures33.2a–c, 33.3a,b). The quantities required to anesthetizethe 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 theanesthetic has been injected (with onset in around 1minute).


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Mid-face and outer eyelid block(Figures 33.4a,b, 33.5)The mid-face block anesthetizes the lower eyelid, part ofthe cheek, part of the nose and the upper lip. This secondphase is done after the phenol has been applied to thefrontal area. The infraorbital nerve can be reached from theoutside (Figure 33.4a,b) or from inside the mouth. Theinternal route is preferable, as it is easier to anesthetize theupper lip, the nostrils and the tip of the nose (Figure 33.5).It is best to anesthetize the upper eyelid from the outside,however.


Figure 33.2(a–c) Frontal and upper eyelid block.

A

B

C

Figure 33.3(a,b) Frontal and upper eyelid block.

A

B

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The small, outer eyelid nerve block (0.5 cm3 of lidocainewithout adrenaline) anesthetizes the zygomatic and lachry-mal branches of the facial nerve (Figures 33.6 and 33.7).

Approaching the infraorbital nerve internally allows theinjection to ‘fan out’ towards the tip of the nose. This tech-nique provides perfect anesthesia of the upper half-lip, thenostril and half of the tip of the nose on the same side:1–1.5 cm3 of 2% lidocaine without adrenaline is injected ineach side.

Lateral regionsThe temporal region can be anesthetized by blocking theauriculotemporal nerve (Figure 33.8a,b). After raising a


Figure 33.4(a, b) External route for blocking the infraorbitary nerve.

A B

Figure 33.5Internal route for blocking the infraorbitary nerve.

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skin wheal with a 32G needle just in front of the opening ofthe ear, a 25G1/2 needle is introduced perpendicularly,immediately in front of the tragus and behind themandibular condyle (Figure 33.8). It is essential to do anaspiration test because of the proximity of the superficialtemporal vessels. The injection should be done slowly andshould not meet with any resistance. Resistance would sig-nal that the injection had gone into the intracapsular jointor the posterior meniscus of the temporomandibular joint.If the peeling is performed under deep sedation, this area isusually not blocked.

The lower cheek region now needs to be anesthetized(Figure 33.9a,b). This area is not sensitized by the trigemi-nal nerve but by the ascending branches of the superficialcervical plexus. Sensitivity in the lower cheek can easily beblocked by injecting a ‘line’ of lidocaine under the skinalong the lower jaw (Figure 33.9). The pulse of the facialartery should be palpated over the jaw before injecting thelidocaine. The lidocaine should be injected in a line parallelto the lower jaw, on both sides of the pulse, over a few cen-timeters.

The anesthetist should inject a small dose of analgesicbefore phenol is applied on this area, which is less sensitiveand not protected by a nerve block.


Figure 33.6The small, outer eyelid nerve block (0.5 cm3 of lidocaine without adrenaline) anesthetizes the zygomatic and lachrymal branches ofthe facial nerve.

A B

Figure 33.7The small, outer eyelid nerve block (0.5 cm3 of lidocainewithout adrenaline) anesthetizes the zygomatic and lachrymalbranches of the facial nerve.

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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 lineparallel to the lower jaw, on both sides of the pulse, over a few centimeters.

A B

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Mental blockA drop of lidocaine is deposited in the gingival crevice sothat the injection will be painless. Bilateral injection of0.5–1 cm3 of 2% lidocaine without adrenaline (canine teethor premolar–canine junction) anesthetizes the whole of thechin region (Figures 33.10, 33.11). The lidocaine should beinjected in a line and slightly fanned. The older the patient,the further back the injection has to be, as the mental nerveforamen recedes as the bones age.

The nerve block anesthetic is applied gradually to thewhole face: the forehead and the right midface region fol-lowed by the right lateral region. The chin is then blockedand treated before blocking the left midface region andfinally the left lateral region. The lateral regions are oftentreated without nerve blocks; they are more complex andpatients can easily tolerate an application of phenol to thesides of the face thanks to analgesics, sedation or the anes-thetizing effect of the phenol itself. The quantities of lido-caine injected are thus diluted in time, and peak levels oflidocaine are not reached under these conditions. The phe-nol must be applied in over 1 hour to the whole face: thereis no justification for blocking all the sensory nerves in theface at the same time before starting to apply the phenol.This would also increase the risk of toxic peaks of lidocainein the blood.

Evolution of pain in the courseof the peelIn the course of a phenol peel performed under FNB withlidocaine without adrenaline and with no analgesic seda-tion, the patient gradually feels a painful, but bearable, sen-sation of heat develop in the treated areas. The patient willcomplain of this unpleasant sensation on the forehead astreatment of the midface region is ending. While the sec-ond midface region is being treated, the patient feels thisheat in the first midface region. The burning sensation onthe forehead is subsiding at this stage of the treatment, andso on and so forth. At the end of the peel, the effect of theFNB has worn off and if the patient has not been given ananalgesic before or during the peel, he or she will usuallyfeel a painful burning sensation over the whole face. Thiscan soon be alleviated with a strong analgesic administeredby mouth. It is important to check beforehand that thepatient can tolerate the analgesic.

At the end of the peel, the barrier function of the epider-mis is completely incapacitated and it is possible to achieverapid and effective analgesia by applying a few grams (atmost) of EMLA on the areas where the burning sensation ismost painful and where treatment has finished. EMLAshould be used only rarely in this indication. This recom-mendation does not conflict with the previous recommen-


Figure 33.10Mental block: external route.

Figure 33.11Mental block: internal route (better).

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dations, as the speed with which analgesia is produced inthis way means that only very small quantities of EMLAneed to be applied to the face after a deep peel – far fromtoxic plasma levels. Also at this point in the procedure, theinteractions between the small quantities of EMLA appliedand the quantity of active residual free phenol left on thesurface of the skin will be insignificant.

The burning sensation on the skin is much improved byapplying a cooling mask (Figure 33.12) in the hours or daysfollowing the peel.

SedationPremedication 30–60 minutes before the peel, a 100 mg tablet of hydrox-yzine or intramuscular promethazine is usually sufficient.The patient can also benefit from the rapid sedative prop-erties of sublingual lorazepam, as discussed earlier in thischapter. Atropine should not be injected automatically, butshould be available in case of bradycardia.

Analgesic sedation consists of minimal doses of midazo-lam or intravenous fentanyl, with blood pressure, cardiacand pulse oximeter monitoring.

FentanylThis is a strong, short-acting analgesic. The anesthetist‘titrates’ the analgesic slowly with repeated intravenousinjections of 25 µg when the patient complains about thepain. A total dose of 100 µg can be given safely. Someauthors administer 50 µg at a time to reach a maximumdose of 250 µg in 1.5 hours.15

Midazolam This is a strong sedative with a short onset of action that canbe administered intravenously, rectally, intramuscularly orsublingually. Midazolam can be used as premedication: 4 or5 drops are given sublingually as soon as the patient arrivesat the clinic. It has a short half-life. The anesthetist injects adose of 1 mg intravenously under pulse oximeter monitor-ing, even if the risk of respiratory depression is very rarewith a 5 mg dose. In case of overdose, flumazenil (Anex-ate®, which comes in 1 mg/10 ml phials) takes less than 1minute to compete with the central receptors occupied bythe midazolam: 0.2 ml is injected intravenously (15 sec-onds). Additional doses of 1 ml can be reinjected everyminute until the patient regains consciousness. Flumazenilhas very low toxicity, and doses of up to 100 mg have beeninjected intravenously without any signs of overdose.

Fintsi16 recommended simple intravenous sedation withoutFNB: 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 withthis procedure, but, without the FNB, the patient is in painduring the peel and this makes it uncomfortable for both thepatient and the doctor. The patient only has a vague memoryof the pain. Asken15 reported on a study by Litton showing anaccelerated heartbeat slowing down when deep sedation iscombined with nerve block anesthesia.


Figure 33.12A cooling mask (a) can be put in a freezer and placed on theface as soon as the peel is over (b).

A

B

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Notes1. Cold temperatures slow nerve conduction. What is more,

the vasoconstriction caused by cold temperatures slowsdown the rate at which local anesthetics are absorbed, andtheir effect is prolonged.

2. This is applicable to all types of peels.3. Klein solution: a mixture of saline solution, lidocaine, adren-

aline (epinephrine) and sodium bicarbonate normally usedas a local anesthetic in liposuction procedures.

4. Various phenol peel formulas can be found on the marketthat boast of the possibilities of doing a full-face peel ‘with-out anesthetic’. In some cases, this means ‘without generalanesthetic’ and in others the patient is put on strong anal-gesics, sedation and premedication. Some low-dose phenolpeels (around 30%) are no more painful than atrichloroacetic acid to the papillary dermis, but they are notmuch 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 tolidocaine in almost 30 years of my medical career.

7. Correct treatment consists in filling the blood vessels, raisingthe legs and putting the patient on oxygen.

8. It must be remembered that the large number of facial bloodvessels speeds up the absorption of LAs

9. Lalanne B, Baubion O, Sezeur A, Tricot C, Gaudy JH. Circu-latory arrest after splanchnic neurolysis with phenol in unre-spectable corner of the pancreas. Ann Chir 1994; 48(11):1025–8.

10. Which explains why the effect is not prolonged even whenthe 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 localanesthetic (EMLA) on normal and diseased skin. Acta DermVenerol (Stock) 1989; 69: 18–22.

14. Ferrari FP, Rosario Filho NA, Schmidt AV. Allergy skin test-ing after topical anesthesia. J Pediatr (Rio J). 1996; 72(4);215–20.

15. Asken S. Unoccluded Baker–Gordon phenol peels – previewand update. J Dermatol Surg Oncol 1989; 15: 998–1008.

16. Fintsi Y. Exoderm®, a novel, phenol based peeling methodresulting in improved safety. Am J Cosmet Surg 1997; 14:49–54.


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Preparing the solutionLip & Eyelid® formulaLip & Eyelid® formula is an oily solution of phenol, oftencalled phenol oil. The solution is ready for use and there isno preparation involved. The flask contains 3 ml of solu-tion, which is the quantity usually needed to treat thewhole face or do around 15 eyelid treatments.1 It is easy toplunge the applicator straight into the container and tosqueeze it out correctly on the neck of the flask. Lip & Eye-lid® formula remains stable for many years.

Baker–Gordon solutionThe four ingredients must be mixed immediately beforethe peel:

liquid phenol (88%) 3 mlcroton oil 3 dropsseptisol 8 dropsdistilled water 2 ml

Other formulas also have to be prepared immediatelybefore the peel: for more information, see Chapter 25.

Mixing the four ingredients of Baker’s solution producesan unstable emulsion rather than a truly stable solution. Itis recommended to keep strictly to the formula, as anyattempt at customizing it can lead to unexpected resultsand relatively serious complications. Because the emulsion(soap + oil + phenol + water) is unstable, the solution hasto be freshly prepared. It must be shaken continuouslythroughout the peel to keep the emulsion as homogenousas possible. This essential task should be given to an assis-tant who will be responsible for holding the containerthroughout the peel. If the Baker–Gordon solution is leftunattended, without being shaken, it separates into differ-ent phases. Each of these phases has a specific concentra-tion of phenol and produces different peel depths. If thesolution is not shaken continuously, each phase could be

applied in turn to the patient’s skin and the results wouldbe uneven: inadequate in some places and too deep in oth-ers. This could cause scarring, hypopigmentation or hyper-pigmentation. Not shaking the solution could certainlycause certain post-peel complications.

Litton’s solutionIf stored in the right conditions, away from sources of air,light and heat,2 Litton’s solution remains stable for severalyears. After shaking the flask,3 the quantity required for thepeel is drawn out (usually 3–5 ml, depending on how thickthe applicator is and how much of the product it retains).

Applying the peel solutionPreparing the applicatorThe applicator should not be too thick, so as not to retaintoo much of the product and to reduce the risk of drips.The doctor usually prepares it ‘by hand’ before startingapplication and after disinfecting his hands. Ideally, theapplicators should be prepared beforehand and left in ster-ile covers. The simplest and most efficient applicator con-sists of a wooden skewer approximately 15 cm long withcotton wound uniformly around one end to form a cylin-der of even diameter (Figure 34.1).

Other types of applicators can be used, depending on thedoctor’s experience. Some authors suggest applying phenolwith a brush to get a more superficial phenol peel.4 Thebristles 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 composi-tion of the phenol solution. A gauze pad should not be usedto apply a phenol peel, as the rough texture of this applica-tor could allow the phenol to penetrate too rapidly; besides,the large quantities of solution that gauze can absorb maycause drips and runs or deposit uneven quantities of theproduct on the skin too quickly; the most serious compli-cations can only be avoided by slow and even application.

34Full-face phenol: application

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The use of cotton balls is not advised, as they are not easy tohandle in ‘delicate’ areas such as the eyelids and alsobecause of the risk of runs. Cotton buds are not suitable forlarge surface areas, as they do not allow even application. Ina very localized phenol peel (i.e. eyelids or upper lip), how-ever, phenol is applied with a single cotton bud, as it ismore precise and uses up less of the product. The applica-tor should only ever be used once.

Some quick reminders about skinpreparationNo skin preparation is necessary during the weeks preced-ing 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 ofbotulinum toxin 8 days before the peel. Small benigntumors, in low numbers, can be treated by shave excisionimmediately before the peel and will therefore benefit fromthe local anesthesia induced by the nerve blocks. If thereare a large number of tumors, they can be excised after

frosting is obtained to avoid creating too many rapid tran-scutaneous penetration routes in the treated areas. Telang-iectasias can also be electrocoagulated immediately beforethe phenol is applied. Urkov applied phenol and cauterizeddeep wrinkles at the end of the peel, before putting on anocclusive mask.

Precautionary detailsThe flask of peel solution is put on a table, within reach ofthe doctor, and the top should be easy to take off and putback.

Replacing the top on the bottle after each use (the assis-tant’s responsibility) helps reduce the amount of phenol inthe air and prevents accidental spills.

There is a general rule for all peels: the doctor shouldavoid holding any vessel containing a chemical peel in hishand for a long time and should not hold the product infront of his face.

The air space above the face should not be violated. Onthe same table, a 20 ml syringe of sterile physiologicalsaline and a row of make-up remover pads (preferably ster-


Figure 34.1(a–c) Wooden skewer, approximately 15 cm long, with cotton wound uniformly around one end to form a cylinder of evendiameter.

A B C

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ile) are placed at hand. The doctor will use some of the padsto spread the phenol evenly on the skin, and the assistantwill use the rest to immediately sponge away any tears,often a unilateral reflex reaction. The patient is on a dripand monitors; the eyes are protected with ophthalmicVaseline®.

Setting the lower limits of thepeelBefore treatment, the lower limits of the peel must beestablished with the patient in a sitting position. The prac-titioner, with hand outstretched, places four fingers on theedge of the lower jaw, halfway between the chin and theangle of the jaw, and lifts the skin upwards. A surgical skinmarker is then used to draw the line marking the lower lim-its of the peel on the stretched skin: the line should start atthe angle of the jaw and go towards the chin. The lowerdemarcation line will be hidden in the shadow of the jaw(Figure 34.2). If the demarcation line is drawn when thepatient is lying down, the peel will not go far enough underthe jaw, and the line between treated and untreated skinmay be more visible.

Application techniqueThe applicator is soaked in Lip & Eyelid® solution andcarefully squeezed out on the inside of the neck of the bot-tle to get rid of any excess and avoid drips. The solutionmust be applied slowly and conscientiously to each squaremillimeter of the facial skin. The right hand5 holds the han-dle of the applicator between the thumb, index finger andmiddle finger. By moving the thumb smoothly over theother two fingers,6 the applicator can be rolled over the

skin: it is not a rubbing movement but a rolling one. Theapplicator is pressed on the skin with the same amount ofpressure that would be used for scratching. The solution isapplied uniformly and the pressure is firm and even. Thephenol is applied first in the base of the wrinkles. Thegloved left hand holds the skin taut to make it easier to treatapply the phenol and to help it penetrate. Care should betaken to avoid maceration in the bottom of skin folds. Afirst layer of phenol is gradually applied to the whole regionthat has been anesthetized. To even out penetration of thephenol that has just been applied, the area should be imme-diately gone over again with a make-up remover pad,moved perpendicular to the direction of application. Thesame cotton pad can be used throughout the peel, as it doesnot come into contact with the eyes. If the phenol is appliedhorizontally, the pad should be applied vertically and viceversa.

Around 3 ml of solution is applied on the skin in succes-sive coats to complete a full-face peel in over an hour. Theendpoint is the appearance of an even ‘gray–white’ frosting(see below). An assistant constantly sponges away anysmall reflex tears with a cotton ball or make-up removerpad, which is thrown away and replaced after each use tomake sure that the next time the eyes are wiped, no phenolis carried into them with the tears that have just beensponged away. Any touch-ups can be done the next day onthe same patient with the solution left in the bottle. Eventhough a phenol solution is antiseptic, it is out of the ques-tion 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 reachedits peak effect when a gray–white frosting appears. Some

Full-face phenol: application 275

Figure 34.2End of the third phase of treatment, up to the lowerdemarcation line. The phenol has gradually penetratedthrough the keratosis that was still visible at the end of thesecond phase of treatment.

Bad practice

A few doctors have been known to talk (sometimesproudly) of conduct that has more to do with greedthan good medical practice: they try to economize onthe volume of peel solution by whatever means theycan. Technically, it is of course possible to use lesssolution for a full-face peel, but this kind of misplacedeconomy is not to be recommended. The efficacy of aphenol peel is also dependent on the total quantity ofphenol that is applied to the skin and that reaches thedermis.7 If too little phenol is applied, the results willbe inadequate and in the long run it will cost the doc-tor more to do touch-ups than to apply the rightamount of good quality solution in the first place. As inmany other areas, false economies do not make a for-tune.

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patches of buff yellow may also appear when the maximumdepth has been reached (Figure 34.5). Pink–white or purewhite frosting occurs when the phenol has penetrated thepapillary dermis, and the results would be comparable tothose of a trichloroacetic acid (TCA) peel, which is not asgood as can usually be achieved with phenol. Some phenolpeel formulas need several coats of solution to achieve thistype of frosting. Lip & Eyelid® formula is usually applied ina single coat, and it only requires a little patience for thepure white frosting to turn gray–white.

Clinical signs of the phenolapplication

FrostingApplying Lip & Eyelid® formula to the skin triggers frosting8

(Figures 34.4–34.6) that is more or less intense and occursmore or less rapidly depending on the skin type. A thinner


Figure 34.3Pure white frosting after an application of Lip & Eyelid®formula to the right midface region. The frosting on theforehead has already faded during the rest period.

Figure 34.4Phenol penetrates more slowly on keratoses. A little patienceis required.

Figure 34.5When Lip & Eyelid® is being applied, a pure frosting appearstemporarily. It is soon replaced by gray–white frosting thatturns a buff yellow color in places, as can be seen here. Theappearance of buff yellow patches is a sign that the phenolhas reached maximum penetration.

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skin frosts more quickly than a thick and oily skin (Figure34.4). The rapidity of the onset of frosting is not alwaysrelated to the depth of the phenol peel. As soon as the skincomes into contact with an aqueous9 solution of highly con-centrated phenol, protein coagulation is abrupt (pure whitefrosting) but relatively superficial, and this stops the rest ofthe phenol applied on the skin from penetrating deeply.With an oily solution, on the other hand, frosting occursmore slowly and the color is less intense, which is a sign ofdeeper penetration.

Rapid frosting is often pure white in color, whereasslower frosting gradually turns into a gray–white color thatindicates deeper penetration of the phenol into the skin.The appearance of buff yellow patches signals even deeperpenetration (Figure 34.5). It is therefore relatively easy tojudge the depth of action of phenol: frosting that remainspure white shows that penetration is not as deep as withfrosting that turns gray–white. The appearance of buff yel-low patches shows that maximum penetration has beenreached. Any additional application of phenol would beassociated with a major risk of local complications.

EdemaSevere edema (Figure 34.7) occurs quickly after phenol hasbeen applied. The skin soon feels like cardboard because ofthe speed and extent of the edema that sets in and stretchesit.

Gradual applicationNerve block anesthesia is performed sequentially (anes-thetize one nerve trunk and apply phenol on the anes-

thetized area; anesthetize the next trunk and apply phenolon the corresponding area, etc.). This means dividing theface into as many areas as there are nerve trunks to block.The full-face phenol peel is thus done gradually, area byarea. Particular care must be taken not to leave thin strips ofskin untreated on the borders between the different areas:this would make the face appear ‘striped’, as the strip ofuntreated or undertreated skin would show up clearlybetween the areas regenerated by the phenol. It is easy to bemisled by the erythema and edema that develop around 10minutes after frosting and that extend beyond the area thathas been in physical contact with the phenol. When treatingthe next area, the applicator should be taken slightly into thearea of erythema and edema. The different cosmetic unitsare treated in turn, after each corresponding nerve block.

First phaseThe first phase covers the forehead, the upper eyelids and atemporal ‘extension zone’ on the right hand side (Figure34.8).

A frontal block and an outer eyelid block (see Chapter33) are done on each side of the face. The phenol is appliedvigorously in the base of each forehead wrinkle beforetreating the whole of the forehead. There are three borders


Figure 34.6All the colors associated with a phenol peel can be seen here.The chin has pure white frosting just after the phenol hasbeen applied. The cheeks have gray–white frosting after thesame amount of phenol as applied on the chin haspenetrated more deeply. The forehead is a pink color, wherethe frosting is fading, with patches of buff yellow. Figure 34.7

Edema is clearly visible on the left side of the face, which wastreated before the right side. The arch of the left eyebrow ismore prominent than the right. The left side of the nose isswollen, as well as the upper left half lip. The edema line isvery visible on the neck. Edema usually occurs at the sametime as the frosting fades. The erythema goes beyond thelimits of the edema, which in turn goes beyond the limits ofthe phenol application.

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to this first phase: the anterior hairline, the eyebrows andupper eyelids, and the temporal region.

Anterior hairlinePhenol is not toxic to the pilosebaceous units. To avoidcreating a visible demarcation line between the skin of theforehead and the hair, the applicator is taken 1 cm into theanterior hairline.

EyebrowsThe phenol is applied to the eyebrows against the lie of thehairs to ensure proper contact with the skin. Its action isnot deep enough to remove any permanent make-up.10

Upper eyelids (Figure 34.9)After the eyebrows, the doctor treats the upper eyelids. Anyexcess of phenol is avoided by using an applicator that hasalready been used to treat an adjacent area and that has notjust been soaked in phenol. The upper eyelid tarsus doesnot have to be treated: this would cause severe palpebraledema. When the eyelids are being treated, the assistantshould be ready to rinse the eyes out with a syringe of ster-ile physiological saline (prepared before the peel) andsponge away any reflex tears.

Temporal ‘extension zone’ (Figure 34.10)At the border between the frontal and temporal zones, it isworth making the most of the anesthesia that the phenol hasinduced and that extends about 1 cm beyond the frosting.

The skin of the forehead is thoroughly anesthetized bythe nerve blocks, and the phenol application should extendslightly into the temporal zone. Patients should be warnedthat they will feel a burning sensation on the temples for15–20 seconds as the phenol is applied to this unanes-thetized area. The temporal regions are treated graduallyup to a virtual horizontal line that goes through the centerof the pupils. The extension zone includes part of the wrin-kles of the crow’s feet: the phenol is first applied at the baseof these wrinkles; the left hand stretches the skin to make iteasier to reach the base of the wrinkles with the applicator.The peel solution is then applied to the rest of the area.

Rest periodThe phenol is applied slowly and carefully. A rest period of10–15 minutes is obligatory after the end of the first phase


Figure 34.8A single coat of Lip & Eyelid® has just been applied to thefirst zone. The frosting will turn gray–white without anotherapplication.

Figure 34.9Day 1 after a localized Lip & Eyelid® peel of the four eyelids.The upper eyelid tarsus was not treated with phenol: it doesnot show any skin change, just edema and severe erythema.

Figure 34.10End of first phase of treatment. The white line is the virtualborderline passing through the pupils. The area marked outby the colored line is the temporal ‘extension zone’.

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of treatment. It takes around fifteen minutes to treat thefrontal region, the upper eyelids and the temporal ‘exten-sion zone’. Twenty-five minutes after the beginning of thetreatment, the second phase can be started. Well-equippedclinics can make the most of the obligatory rest period totreat two patients at the same time, in two different rooms.

Second phaseThe second phase covers the central right-hand side: lowereyelid, midface region, half of the nasal pyramid, upper halflip, periauricular ‘extension zone’, earlobe and tragus (Fig-ure 34.11).

Lower right eyelidPhenol is applied up to 1–2 mm from the eyelashes. Nerveblocks do not always succeed in fully or properly anes-thetizing the eyelid skin. If intravenous sedation is notbeing used, patients should be warned that they might feelan intense but brief burning sensation. If the peel is donestep by step, very slowly, the anesthesia caused by the phe-nol itself, together with reduced sensitivity caused by theanalgesics, are sufficient to apply phenol on the eyelidswithout causing much pain. ‘Vocal’ anesthesia is essentialin this area, and I usually use the following ‘trick’ for theeyelids: the area is supposedly anesthetized by the nerveblocks; I tell the patient that I am going to test the depth ofthe anesthesia and that if it is not deep enough, it can beimproved. Inadequate anesthesia is signaled by a burning-type pain that lasts around 15 seconds. The phenol isapplied to the eyelid as if it were properly anesthetized. Thepatient interprets any pain as a simple test and finds it bear-able, whereas in fact the phenol has been applied. The phe-

nol itself produces sufficient anesthesia for treatment tocontinue without pain. As soon as the eyelid frosts, appli-cation can be completed painlessly.

The practitioner and assistant should watch out for anyreflex tears while the eyelids are being treated.

Nose and right midface regionThe right side of the nasal pyramid is treated, as well as theskin 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 connectingfibers, leads to loss of tip support. The resulting nasal tipptosis contributes to the classic impression of increasednose size with aging. There are surgical nose lift techniquesas well as a filling technique11 that raises the tip of the nose.A phenol peel is a valuable alternative: the tightened dermisoften gives the tip of the nose a clinically visible lift.

Upper right half lipThe upper lip requires careful treatment: several coats ofLip & Eyelid® should be applied. Before treating the wholelip, the solution is applied vigorously in the base of eachwrinkle, the skin of the lips is stretched between two fingersof the gloved left hand to open the wrinkles and make theatrophic base accessible (see Figure 34.12). Dermabrasioncan be performed after the phenol has been applied,12 whenfrosting is still apparent, if the doctor considers that phenolalone is inadequate. The term ‘chemabrasion’ can bereserved for this technique.13 After 24 hours of occlusion, ifsome lip wrinkles still persist, either the base of the wrinklescan be treated again with phenol or the whole lip can betreated with chemabrasion. To avoid creating a demarca-tion line on the vermilion portion of the lip, the phenolmust go 1–2 mm into the red lip. If the phenol does notpenetrate the red lip, not only will there be a demarcationline, but fine lines will also persist and lipstick can bleedinto the white lip area. Aging of the lips, combined with fatand jawbone atrophy, often starts with upper-lip ptosisthat hides the teeth. In young subjects (under 30 years old),


Figure 34.11The second zone being treated with Lip & Eyelid® formula.

Figure 34.12As for the upper lip, the base of the wrinkles on the chinshould be treated first before applying the phenol to thewhole chin area.

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1–2 mm of the upper teeth can often be seen when the faceis at rest and the mouth slightly open. Surgical techniquesthat reduce the height of the upper lip have been described,such as ‘moustache plastic surgery’:14 a simple techniqueperformed under local anesthetic that requires special carein the suturing to do a perfect edge-to-edge repair of theepidermis.

After a phenol peel, the upper white lip retracts slightly,and this is often enough to make the whole area lookyounger and the upper lip appear plumper without resort-ing to filling techniques.

Pretragal ‘extension zone’, earlobe, right tragus(Figure 34.13)A pretragal nerve block can be done to anesthetize thisarea, although it can easily be treated without a nerveblock, gradually, up to the virtual line between the cornerof the mouth and the earlobe. Lip & Eyelid® can be appliedmore vigorously in the pretragal folds, using the left handto stretch the skin and expose the base of the wrinkles tothe phenol. The earlobe and the tragus must be treated sothat the results are even over the whole area. If the earlobeand tragus are not treated, an area of sun-damaged skinwould be clearly visible on either side of the rejuvenatedface.

Rest periodAfter these areas have been treated, the 10–15 minute restperiod between the two phases can be used to apply theocclusive dressing to the first zone that was treated.15 Thethird phase starts around 50 minutes after the start of thetreatment.

Third phaseThis essential phase of the peel covers the rest of the right-hand side: half chin and lower lip and the right jaw ‘exten-sion zone’ to the neck (Figure 34.15).

Lower half lip and right half chinThe corner of the mouth requires careful treatment, as thewrinkles here are deep and atrophic. The fingers of the lefthand stretch the skin to expose the atrophic base of thewrinkles 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 treat-ment, and several coats may be required. Acne scars anddeep wrinkles are particularly resistant in this area, andsometimes require chemabrasion during the peel itself orafter 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 isperformed under deep sedation.

Lower limits of the peel and the neckPhenol is applied up to the lower limits set before the startof the peel; this forms the demarcation line (Figure 34.14).The skin on the neck is structurally different to that on theface: it has fewer appendages and pilosebaceous units. Aftera deep peel, the skin regenerates from these appendages. Aphenol peel on the neck carries an increased risk of scar-ring. What is more, the usual post-peel facial edema tendsto extend downwards to the neck, and if the neck is treated


Figure 34.13End of second phase of treatment. The white line shows thevirtual line from the corner of the mouth to the earlobe. Thecolored line shows the pretragal and cheek ‘extension zone’.The lower part of the extension zone shows a darker patch ofskin that comes from the slow penetration of the phenolthrough keratoses.

Figure 34.14End of the third phase of treatment, up to the lowerdemarcation line. The phenol has gradually penetratedthrough the keratosis that was still visible at the end of thesecond phase of treatment.

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at the same time then the edema that builds up in this areacan make patients feel as if they are suffocating – a veryunpleasant sensation. Therefore the neck could – possibly16

– be treated at a different time to the face. The best treat-ment for a sagging neck is still a surgical lift of the lowerhalf of the face, and a ‘medium-depth’ peel can improvethe photoaging: a phenol peel on the neck can be avoidedin the majority of cases. Nevertheless, some authors(including Baker) treat the neck at the same time as theface: they apply the product up to the clavicles on the ante-rior neck and up to the 7th cervical vertebra on the poste-rior neck. Other authors suggest treating the face on thefirst day and the neck the day after to reduce the risks oftoxicity associated with applying greater quantities of phe-nol to a larger surface area.

Rest periodAfter these areas have been treated, the 10–15 minute restperiod can be used to apply the occlusive dressing to thesecond zone that was treated .

Fourth phaseThis phase of the peel covers the left-hand side: lower eye-lid, midface region, half of the nasal pyramid, upper halflip, periauricular extension zone, earlobe and tragus (Fig-ure 34.16). See the details of application in the secondphase.

Rest periodAfter these areas have been treated, the 10–15 minute restperiod can be used to apply the occlusive dressing to thethird zone that was treated.

Fifth phaseThis phase marks the end of the peel, with an application ofphenol to the left-hand side, to half of the chin and theupper half lip, and to the jaw ‘extension zone’ to the neck(Figure 34.17).


Figure 34.15End of the third phase of treatment. The occlusive dressinghas been placed on the frontal region during the second restperiod; the second zone will be covered with an occlusivedressing during the third rest period. The color of the frostingwill gradually turn gray–white without any additionalapplication of phenol.

Figure 34.16Application of Lip & Eyelid®: fourth phase.

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Finishing the occlusive maskThe 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 beeven, as it will have developed phase by phase (Figure34.18). The patient may complain of a pulsing heat, whichcan soon be alleviated by applying a cold pack. New, long-acting analgesics can be used to reduce the pain.

Notes1. With one flask, it is possible to treat the upper or lower eye-

lids of 15 different patients, as approximately only 0.2 ml isneeded 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 toavoid all risk.

4. Though using phenol to do a superficial peel means bothpatient and doctor taking a pointless risk where less toxicagents are available (TCA, AHA, salicylic acid, etc.).

5. Left-handers will understand that they must reverse thehands used.

6. Making the gesture that universally means ‘to pay’.


8. As with TCA, the frosting is caused by protein coagulation:the three-dimensional structure of the proteins is changedand they become opaque. The same phenomenon is respon-sible 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 tooquickly and too deeply through skin whose permeability hasbeen significantly altered by the abrasion. Also, the diffusebleeding that accompanies the abrasion would partially neu-tralize the phenol.


14. Regis-Milano G. La plastie en moustache. XIX° réunion duGRCD, Paris, Janvier 1996: 17–18.

15. Information on the choice and preparation of the occlusivepost-peel mask can be found in Chapter 35.

16. See Chapter 31 for more information on the risks of treating theneck with phenol. The increased absorption area also carries anadditional and unnecessary risk of toxicity for the patient.


Figure 34.17End of application of the phenol peel. Occlusion dressing isnearly complete.

Figure 34.18Appearance of the face at the end of the peel (Lip & Eyelid®).The mask (here Leukoflex®) is complete. The appearance ofptosis of the right eyelid comes from the edema that startedearlier in this area as a result of the ‘phased’ application ofthe peel solution.

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Immediate post-peel careThe care required for the skin and patient after an applica-tion of phenol largely depends on the formulation and thedoctor’s experience.

Hospitalization or ambulatorypeel?The first question to ask is whether or not the patientshould be hospitalized. Some hospitals or cosmetic clinicslike to combine a phenol peel with other treatments: surgi-cal 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 post-peel care that can only be given if the patient is hospitalizedfor 8–10 days. It is clear that hospitalization can contributeto patients’ wellbeing, making life easier and helping themavoid any contact with the public, friends or relatives dur-ing the first week of – unsightly – skin regeneration. Somepractitioners, for fear of the potential toxicity of phenoland the possibility of heart rhythm disorders, prefer to hos-pitalize patients the first night after the peel until the occlu-sive mask has been removed 24 hours later. This briefperiod of hospitalization can also be beneficial to thepatient, who can be given a titrated intravenous analgesiauntil the morning after the peel. Some more recent tech-niques provide a phenol peel of the same quality and arecompletely ambulatory. Patients are taken home by afriend or relative. They can leave the clinic a few hours afterthe end of the phenol application,1 on condition that some-one stays with them around the clock for the first 72 hoursand that the patient can get to the doctor’s surgery quickly,2

whenever advised or necessary. The severity of the edemaon the first day means that the patient is completely depen-dent on others, and it is important that any localized treat-ment can be given rapidly. Cardiac toxicity has beendiscussed in Chapter 28: in summary, when the peel is per-formed 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 thatoccurs while the phenol is being applied. Detoxificationstarts immediately. A few hours after the peel, the risk ofphenol-induced arrhythmia is practically non-existent, ifthe liver has been able to detoxify the phenol and the kid-neys eliminate it normally (see Chapter 28). Peels of theBaker–Gordon or Litton type are often performed withhospitalization. Exoderm® or full-face Lip & Eyelid® peelsare usually ambulatory procedures. With the exception ofsome techniques, hospitalization, even if brief, no longerseems to be a necessity but is more of a comfort factor forboth patient and doctor. Patients are often happy to be ableto go home and be in familiar surroundings.

Occlusive or open technique?Publications on peels mention different possibilities, andonce again it is the formula used that determines the appli-cation procedure and the need for an occlusive or opentechnique.

Both techniques have been described as giving excellentresults. The following discussion weighs up the pros andcons of occlusion.

Ease and speedThe doctor may find it easier and quicker not to apply anocclusive mask, but this is a hasty conclusion: applying anocclusive mask is a simple procedure and can be done inthe obligatory rest periods between each treatment area.No time is wasted.

ComfortThe occlusive mask improves patient comfort: the skin liq-uefies beneath the mask, and the liquefied integuments donot drip on the skin. The occlusive mask prevents the skinfrom sticking to clothes or pillows. When an occlusive maskis put in place, the patient can apply a cooling cold pack toalleviate the painful burning sensation, whereas with theopen technique, direct contact with the skin is not possible.

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SafetyWith an occlusive mask, patients do not have to treatthemselves or be treated by anyone else; nothing has to beapplied to the skin, which reduces the risk of involuntaryerrors, allergies or secondary infections. The mask preventspatients from touching their skin and importing bacteriafrom their fingers. The mask prevents contact between theskin and any insects or pets carrying infectious agents,which may be dangerous to a skin deprived of its immunedefenses. With transparent occlusion (Leukoflex®), it ispossible to evaluate how the treated skin is developingthrough the mask.

When phenol is applied to healthy skin,3 occlusion slowsdown the absorption rate but does not alter the total quan-tity absorbed.4 The liver therefore has more time to detox-ify the phenol and the kidneys have more time to eliminateit. This increases the peel’s safety margin.

EffectivenessUnlike trichloroacetic acid (TCA), whose effect is restrictedby occlusion,5 the effectiveness of phenol is improved bymaceration. Stegman proved that applying an occlusivemask allows the phenol to penetrate more deeply andimproves the cosmetic results.6

Asken1 reported that it is possible to increase the pene-tration and effectiveness of phenol with occlusion, but thatthe same results can be achieved by vigorously cleansingand degreasing before the peel or by repeatedly applyinghydrating and covering agents (Vaseline®- or silicone-based products) after a phenol peel.7 This principle isapplied in certain phenol peel protocols that vaunt themerits of replacing 24-hour post-peel occlusion with con-tinual application of hydrating products. Using cream- orVaseline®-based occlusion rules out any possibility of atouch-up after 24 hours and deprives the doctor of a valu-able 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 asEucerin® that patients must continue applying themselvesthroughout the first night and up to 5 days after the peel.The face is washed with a showerhead with warm waterevery 4–5 hours, before each coat of cream is applied. Onthe 5th day, the Eucerin® is replaced with white Vaseline®until the 10th day. This procedure, more complicated forthe patient, often results in bacterial infections, which iswhy other authors9,10 have replaced the hydrating creamwith an antibiotic cream such as bacitracin. Fungal resis-tance or secondary infections are not uncommon, how-ever, and there have been reports of allergic reactions toantibiotic creams applied on skin that is completely perme-able. McCullough and Maloney9 recommend the followingmethod. During the first day and night, swabs of cold phys-

iological saline are applied. Thereafter, patients rinse theirfaces under the shower four times a day and apply a baci-tracin-type antibiotic cream up until at least the 8th day.Healing takes 10–14 days.11 Any scabs are rinsed under theshower and softened by the water, then coated in baci-tracin.

Another occlusive technique consists in applying sterilewhite Vaseline® after the phenol: the Vaseline® providesperfect occlusion, but can sometimes be unpleasant, as heatfrom the skin liquefies it, making it to drip and shifting bitsof skin debris. The patient is then led to wiping the skin fre-quently and the risk of secondary infection is increased.Prolonged use of Vaseline® after a peel is known to causeacneiform or milia lesions to appear.

Whichever technique is used instead of the occlusivemask, there is an increased risk of infection, injury, allergiesor errors, and a transparent occlusive mask is recom-mended during the first 24 hours to improve the peel’seffectiveness, reduce the need for patient participation inpost-peel care and lower the risk of secondary infection.

How to use the occlusive maskPitfalls to avoidThe occlusive mask must be perfectly even. The main pit-falls to avoid are as follows.

Air bubbles, pockets of maceration, tension linesThe presence of air bubbles reduces local maceration andtherefore effectiveness. Pockets of maceration increaselocal penetration of phenol (risk of dyschromia and scar-ring).

Any tension lines in the mask are transferred onto theskin; they can cause unnecessary pressure and may gener-ate areas of necrosis. Some protocols, however, take advan-tage of the benefits of intentional, well thought out andcontrolled tension on the skin while it is regenerating: forexample the Molding Mask (Dr Roige, Spain). Post-peelcare in this case includes the precise positioning of supportstrips.

Occlusive mask coming unstuckThe occlusive mask sometimes comes unstuck around theedges of the mouth, and lip wrinkles are among the mostdifficult to treat. Lack of maceration where the mask hascome unstuck can lead to inadequate results (Figure 35.1).

The mask comes unstuck all the more easily if the patienttalks, laughs, eats, chews or smokes. The patient shouldtherefore be kept in complete isolation for the first 24hours, without social contact, except for close friends orrelatives, who should be encouraged to help the patientavoid facial expressions and communicate without talking.Smoking is strictly contraindicated on the first day becauseof the lip movements required for puffing on a cigarette


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and inhaling the smoke. These movements soon make themask come unstuck around the mouth. However, it ispreferable to have a patient smoke calmly and cautiouslyrather than getting irritable and pulling off the mask toosoon in their haste for a cigarette or frantically and care-lessly inhaling smoke in secret.

Vigorous chewing motions also make the mask comeunstuck. The patient should therefore be put on a carbohy-drate and protein liquid diet so as to avoid chewing move-ments. A feeding cup should be used instead of a straw toavoid sucking movements. If the mask comes unstuckbefore the end of 24 hours, the patient should substitutethe Leukoflex® occlusion with Vaseline®.

Making the occlusive maskThe occlusive mask can be put on the lower part of the facewith the patient in a half-sitting position at the end of thepeel to make it hold better.

Precut Epstein maskEpstein recorded the facial measurements of 24 patients;from there, he worked out the average size and designed anadhesive mask that he considers ideal and that includes 10pieces of precut, standard-sized Steridrape®.8 This first

occlusive layer is covered with a second layer of adhesivetape. The Steridrape® is thin, very adhesive and completelyimpermeable, and is perfectly suited to the skin. It is quickto put on, as it only consists of 10 pieces and is easy to adaptto faces that are especially wide or narrow.

Classic mask: waterproof tapeChoice and preparation of these tapes are discussed inChapter 32. At the end of the peel, the doctor has severalrows of precut strips that can be picked up with the finger-tips. They are placed gradually on the skin, with severalmillimeters overlap between them, as on a tiled roof.

Only one layer of Sleek® is necessary. Garcia (Spain) hassuggested 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 recommendusing Leukoflex®, an impermeable and transparent dress-ing, which is applied in a single layer and through whichthe skin can be seen on the first day.

Specific areasThe anterior hairline is a special area. A first strip ofLeukoflex® is placed directly on the patient’s skin, at theedge of the hairline. Any hair sticking out over this edgeshould be cut off so that it does not get pulled out when themask is removed 24 hours later. A hairnet is placed on thepatient’s hair. An impermeable or plastic shower capshould not be used, as it holds the sweat on the scalp andmakes the occlusion very uncomfortable for the patient.The (loose) elastic edge of the hairnet is positioned on thefirst strip of Leukoflex®. A second layer of Leukoflex®holds the elastic of the hairnet in place; the net thus formsan integral part of the occlusive mask and can be used topull the whole dressing off smoothly and painlessly whenthe time comes to remove the mask.

A simple gauze pad can be used instead of a hairnet (Fig-ure 35.2). The gauze should be cut close enough to thedressing for the patient to be able to brush or comb thehair, and at the same time there must be enough gauze tohold onto to remove the occlusive mask later. Around theeyes, the occlusion should completely cover the eyebrows

Phenol: post-peel care 285

Figure 35.1An occlusive mask that has come mostly unstuck after 24hours; the results of this peel will be inadequate.

Figure 35.2Close-up of the top of the occlusive mask, near the anteriorhairline. 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 (Fig-ure 35.3). The eyelids, where occlusive dressing is not used,should be coated in ophthalmic antibiotic ointment orsterile Vaseline®. The nose must be properly covered – sev-eral thin strips of occlusive dressing are needed to do this.The area underneath the jaw, treated up to the pre-set lim-its, should only be partially occluded. Partial occlusion ofthe area under the jaw serves to create an area of featheringthat ends on the demarcation line on the neck.

The earlobes should not be occluded.

Medical post-peel treatmentA drop of artificial tears should be placed in the eyes at theend of the peel and several times a day over the followingfew days to reduce eye irritation, common after a phenolpeel.

An ophthalmic antibiotic cream should be applied to theeyelids. The patient must eat and drink as soon as possibleafter the peel to enhance elimination of the phenol. A seda-tive is recommended to reduce anxiety, which can amplifythe feeling of pain: lorazepam (2.5 mg) is highly indicatedand well tolerated by patients. Medication to regulate gas-tric emptying (domperidone) can be administered intra-muscularly or orally before the patient leaves to preventany nausea in the first few hours after the peel. In patientswith a history of herpes labialis, antiviral prevention shouldbe kept up. Patients should be given a telephone number orother means of communication so that they can contact thedoctor at any given moment. They should also have astrong analgesic to hand: paracetamol (acetaminophen)plus codeine is a good and most effective option and allevi-ates the pain during the first few days.13 Applying coldpacks can also alleviate the sensation of heat after the peel.

Post-peel care after 24 hoursAfter 24 hours, the occlusion has reached its full effect (Fig-ure 35.4). Maceration is finished and the superficial layersof the skin have been liquefied. It is not necessary for theocclusion to be kept on any longer, as after 24 hours the

skin has absorbed all the phenol and the risk of infectionincreases proportionally with the duration of the occlu-sion.

Removing the occlusive maskA phenol peel causes a liquid to form that unsticks andgradually lifts the occlusive mask during the first 24 hours,which means that it is often easy and relatively painless toremove, though this is not always the case. Removing theocclusive mask can certainly be painful (though onlybriefly) if the mask is ‘pulled off’ rather than pulled down.When the mask is made correctly, the first few centimetersare left loose on the anterior hairline. It is easy to take holdof the mask here and to pull it down hard, removing it inone swift movement. The patient might cry out at thispoint, but it is more from surprise than from pain. Thepatients who find the first 24 hours the most painful arealso the ones who find it more difficult to bear the occlusivemask being pulled off: they have a lower pain threshold andcan be given a strong analgesic or sublingual midazolam 30minutes before the mask is removed. Some practitionerssuggest (needlessly in my opinion) removing the mask


Figure 35.3Close view of the occlusive mask in the eyes area. Eyebrowsare covered but eyelids are not.

Figure 35.4The same patient as in Figure 35.3: appearance of the faceafter 24 hours of occlusion (Lip & Eyelid® formula).

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under anesthetic or sedation, which increases the overallrisks and the cost for the patient.

Appearance of the faceUnderneath the mask, the skin is coated in a thick liquid14

with a distinctive smell; this liquid results from the lique-fied epidermal layers mixed with inflammatory lymph(Figure 35.5). Good epidermal liquefaction seems to makefor a good prognosis, although the final results will notnecessarily be proportional to the amount of liquid foundbeneath the occlusion. After removing the mask, the face isvery swollen and looks severely burnt, but for all that thepatient does not feel much pain.15 The skin appears crum-pled in places, as the edema develops rapidly beneath therigid mask and the skin cannot stretch. This crumpledappearance soon disappears. The residual liquid is wipedfrom the rest of the face with a sterile cotton pad.

Touch-upsWhen the mask is removed, wrinkles and marks shouldhave disappeared completely. Any persistent marks orwrinkles can be touched up immediately after the mask hasbeen removed (Figure 35.6) by applying some more Lip &Eyelid® solution in the base of the wrinkles or on any resis-tant marks. Wrinkles on the upper lips are usually the most

resistant. Small touch-ups do not require anesthesia: thepain does not last long, as the phenol has produced neurol-ysis of the sensory nerves. Patients should just be warnedthat they might feel a brief burning sensation, and theundertreated areas should be treated again slowly. Moreextensive touch-ups (e.g. the whole of the midface region)might require short-term nerve block anesthesia in sensi-tive areas.

After 24 hours of occlusion, persistent wrinkles on theupper lip can be treated with chemabrasion: Lip & Eyelid®solution is once again applied to the whole of the lip, withspecial emphasis on the base of the wrinkles. Frostingoccurs relatively quickly. When the frosting has stabilized,the skin can be abraded with a diamond fraise or sandpaperon the frosting itself. The doctor then decides whether toreapply the occlusive dressing; the duration of occlusiondepends on the results achieved with the chemabrasion: ifthe 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 regenerationencouraged.


Figure 35.5Appearance of the face after the occlusion has been removedafter 24 hours (Lip & Eyelid® formula).

Figure 35.6Immediate touch-up of the upper lip and chin after theocclusive mask has been removed after 24 hours.

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Bismuth subgallate mask orantibiotic cream?

The advantages of moist or closed occlusive dressings havebeen extolled since ancient times. Ayurvedic doctors, theEgyptians, the Chinese and the Greeks all maintained that aclosed dressing, often coated in honey, enhanced woundhealing. At the beginning of the 20th century, doctors whotreated burns with gauze pads soaked in picric acid knewand made the most of the virtues of healing ‘under a scab’.Thomas Bayton (1797) was the first to rediscover the ben-efits of occlusion in treating venous ulcers after centuries ofmedical obscurantism. The latest studies confirm thatexposing a wound to the air slows down healing and thatocclusion accelerates healing and reduces the risk of infec-tion and pain.

The term ‘moist technique’ could lead to some confu-sion. A moist technique does not involve applying dress-ings soaked in physiological saline, for example. Thepresence of textile or skin debris can actually cause infec-tion and delay wound healing. Nor does a moist techniqueinvolve using antibiotic creams. What is referred to as amoist technique is actually any procedure that allows theskin to regenerate in conditions that are close to the skin’sphysiologically moist environment. Post-peel regenerationis radically different to the regeneration that followsmechanical abrasion or ablative laser treatment. Unlikeablative laser treatment or dermabrasion, a peel does notphysically remove the skin, even though it devitalizes itcompletely. The skin can be considered as the base of a‘moist’ dressing, even though using powder makes itappear rather dry (Figure 35.7). Sprinkling powder on skinthat has been devitalized by phenol but that still serves as a

protective layer creates the ideal conditions for rapid skinregeneration without infection.16

We will discuss the type of powder that can be usedbelow. One of the advantages of using a powder mask isthat the patient does not have to treat the skin at all. Thisreduces the risk of secondary infection, errors or allergies,and also means that the new epidermis, which is in the hor-izontal growth phase, will not be pulled away by the con-stant cleansing of the skin that goes hand in hand with theuse of antibiotic creams. As the skin begins to regenerate,the keratinocytes are not yet anchored by desmosomes andthe dermal papillae have not yet formed. This new, growingepidermis is an important source of cells with a greatpotential for regeneration and should not be removed byuntimely cleansing. Sprinkling bismuth subgallate on whatremains of the skin after removing the 24-hour occlusivemask anchors the dead cells in a sort of membrane andactually forms a kind of natural dressing that is dry on theoutside but physiologically moist on the inside.

Occlusive dressings have often been disparaged for fearof secondary infection that could delay healing. A phenolpeel has one big advantage over laser or abrasion in thatphenol is a powerful disinfectant in vivo even more than invitro. Infections are less common with phenol than withTCA, for example. Sprinkling on an antiseptic is preferableto applying an antibiotic cream. Indeed, antiseptics dis-courage the growth of any microorganisms in the wound,whereas antibiotics only work against certain strains ofbacteria. Bacterial resistance to antiseptics is much lowerthan it is to antibiotics. There have been no reports ofcross-resistance to different antiseptics, whereas this phe-nomenon has been widely reported with antibiotics. Aller-gies are far more common with antibiotics than withantiseptics. The presence of a large amount of exudate can,


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 notstick to the skin. (b) It comes off in one piece like an occlusive dressing under which the skin receives moisture.

A B

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on the other hand, render many antiseptics ineffective, buta phenol peel does not generate much liquid and any excessinflammatory liquid is soaked up when the skin is pow-dered. It is therefore far more advantageous to use a pow-der mask than antibiotic creams. When I have usedantibiotic creams on my patients, secondary infectionshave been very common, while this has rarely been the casewith a mask of bismuth subgallate powder.

Publications on peels describe several different powders.

ThymolThymol (thymic acid) is extracted from essence of thyme.It is four times more bactericidal than phenol and ten timesless toxic. Thymol iodide is used on burns in the same wayas iodoform, but has the advantage of not being absorbedand not having any odor. It is less irritating on wounds andmucous membranes than dithymol diiodide or aristol.Thymol iodide powder, an antiseptic that is used oftenafter a phenol peel, physically alters the selective perme-ability of plasma membranes. It is nevertheless a protoplas-mic poison that denatures enzyme proteins and is also anallergen.

Bismuth subnitrateBismuth subnitrate is an inert powder that has healing andabsorbent properties. It sticks well to the skin. It is not verytoxic by the systemic route, but can be more so by the localroute as a result of combining with proteins.

Gallic acid–iodoformGallic acid was used in the past to treat wounds, as was iod-oform. Iodoform was discovered in 1822 and used byHebra for its local anesthetic action – in the form of aniodoform gauze – on burns.

Bismuth gallateBismuth gallate (formerly known as Dermatol®) is antisep-tic, astringent and siccative. Gallium nitrate reduces metal-loproteinase activity in wounds and promotes themigratory phenotype of keratinocytes that can move moreeasily over the temporary protein matrix and close thewound more quickly. It reduces keratinocyte ability to syn-thesize the desmosomes that anchor the cell locally andlimit its movements.

Bismuth subgallateBismuth subgallate is also known as bismuth 3,4,5-trihy-droxybenzoate dihydroxide, basic bismuth gallate and gal-lic acid bismuth basic salt. Its molecular weight is 394.09. Ithas low toxicity; not much bismuth is absorbed. If bismuth

subgallate comes into contact with the eyes, eye dropsshould be used.

Zinc stearateUrkov used zinc stearate as a healing powder for 5 daysafter removing the occlusive mask.

Making the bismuth subgallatemaskBefore sprinkling the powder on the face, a drop of artifi-cial tears should be put in each eye and protective cottonpads placed on the eyes (Figures 35.8 and 35.10). Thepatient is placed in the dorsal decubitus position with eyesclosed. The face must not be completely dried before sprin-kling the powder on the face so that it sticks to the exudate(Figures 35.8–35.10). If the powder does not stick properlyon the skin, it should be sprayed with thermal water to helpthe powder stick. The mask must not be too rigid, how-ever.17

Bismuth subgallate comes in two formats: the Lip & Eye-lid® kit contains 12 separate sachets for deep localized peels(Figure 35.11a). A large bottle is also available (Figure35.11b) that allows for easy application by sprinkling thepowder directly on the skin. An assistant should gentlycompact the powder with sterile gauze.


Figure 35.8The eyes are protected before powdering with bismuthsubgallate.

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The bismuth subgallate mask should not be too thick.Too much powder makes the mask rigid, which is unpleas-ant for the patient and is sometimes difficult to removelater.

A mask that is too thick may also crack after the thirdday and form jointed plates that can leave visible linesimprinted on the skin and sometimes even wrinkles thatwere 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 toodry should be treated locally with an application of sterilewhite Vaseline®.

Following daysDays 1–6 (Figure 35.13)During the first two days, the patient puts artificial tears inboth eyes. During 48 hours, it is the patient that puts thesubgallate powder on the areas that need it, that is, wherethe powder appears moist. Where the powder has notstuck, because of a lack of skin liquefaction, a little Ter-ramycin® ointment or sterile white Vaseline® should beapplied.

The patient and doctor should be in contact – even if it isonly by telephone – every day, as the appearance of the faceis very worrying for both the patient and friends and rela-tives (Figure 35.13). The person in contact with the patientmust be able to answer any questions, allay any fears andpossibly examine the patient: it is essential that the patientshould be regularly reassured by the doctor that things areproceeding as normal (Figure 35.14).


Figure 35.9Bismuth subgallate powder mask: end of making the mask.Note that the peri ophthalmic area is covered withpetrolatum jelly.

Figure 35.10Eye protection before sprinkling the bismuth subgallatepowder on the skin.

Figure 35.11(a) The Lip & Eyelid® kit contains 12 sachets of bismuthsubgallate. (b) A sprinkler is also available. This makes iteasier to apply the powder.

A B

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Figure 35.12(a) A bismuth subgallate mask that is too dry. (b) Applicationof sterile white Vaseline® around the eyes and mouth.

B

Figure 35.13(a) Bismuth subgallate mask on day 1. (b) Day 3: the edema isgoing down quickly. (c) Day 3: close-up of the mask on theeyelids. The upper eyelids are coated in an antibioticointment instead of the powder.

A

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The pain usually intensifies suddenly on the 3rd and 4thdays: patients generally consider the night of the 3rd day tobe the most ‘unpleasant’ of the whole week. Strong anal-gesics might be necessary: paracetamol (acetaminophen)plus codeine, which the patient should have at hand, is suf-ficient to ease the pain in most cases.

Cold packs – chilled but not frozen – can help alleviatethe sensation of burning or pulsing heat. Many patientscomplain of severe itching that can be relieved with a seda-tive antihistamine such as promethazine. In some cases, theantihistamine can be combined with lorazepam. A patientwho is asleep on promethazine and lorazepam does notscratch!

No other specific treatment should be applied on theface during the first week. The patient should be seen againon 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 hesees the patient on the 6th day (Figure 35.16). The doctorcan also help flaking along, but must take care not to dam-age the skin. Anything that is not stuck to the regeneratingskin can be removed. Once the patient is back home, he orshe continues to apply a thick coat of sterile white Vase-line® to the face and gently rubs it in after carefully washingthe hands with antiseptic soap. A thick coat of Vaseline®creates an impermeable dressing that prevents transepider-mal water loss (TEWL). The water accumulates betweenthe Vaseline® and the skin – that is, in the bismuth subgal-late powder. It hyperhydrates the powder mask, helping itcome away without the patient having to do anything otherthan pick up the strips (skin plus powder) that fall away bythemselves. Throughout the first week, the patient shouldbe told quite firmly to sleep on his or her back instead of onthe side, so that the skin on the face does not stick to thepillow (see Chapter 37).

Day 7 (Figure 35.17)The doctor can use forceps to remove any small bits of themask that are still on the face. On some patients, the pow-der mask has not come off by the 7th day, and the doctorshould then remove it, taking care not to damage the skin.The skin sometimes appears a bit crumpled under themask, but the crumpling, caused by the pressure of themask, can be seen to disappear within moments.

If the skin is in good enough condition, camouflagemake-up (Avene® or Cover Mark®) can be applied imme-diately after sun protection. Sun avoidance and the use of a


Figure 35.14The lower demarcation line on the neck should be given special attention and should be coated with Vaseline® in case movementis awkward (patient on the 3rd day). (b) The same patient after repeated applications of Vaseline® on the 4th and 7th days. Theedema that could be seen in (a) has gone.

A B

Figure 35.15An infection may occur in the form of a papular reaction onthe neck. Oral antibiotics are essential in this case.

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total sunblock must be kept up for 3–6 months. Patientswho are averse to the idea of having to put any productwhatsoever on the skin should be ruled out from a phenolpeel. Flaking does not stop on the 7th day, and it is com-mon 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 weeksThe patient applies a hydrating cream with vitamin E (seeChapters 2 and 3) four or five times a day to stop the skindrying out and becoming itchy and to prevent scratchingand/or complications. The patient can continue to apply athin layer of Vaseline® as long as it is needed to improvedryness or itching.

On the 10th day, the patient can usually return to nor-mal activities, making sure that the skin is protected withan effective sunscreen and wearing make-up to hide thevery pink color of the skin. A colorless sunscreen can bemixed with the patient’s usual foundation as well as a col-

ored sunscreen (metablock HSP 50 color). Erythemaremains severe for the first few weeks, but gradually fadeswithin 4–8 weeks. Patients with dark skin or who live insunny climates should apply Blending Bleaching® creamonce or twice a day to reduce the incidence of pigmentarychanges.

Sun avoidanceSun avoidance should be ‘aggressive’ and ‘permanent’ dur-ing the first 3 months after the peel. Patients who work out-doors are most likely to suffer from uneven skin color orpost-inflammatory hyperpigmentation. ‘Permanent sunprotection’ does not mean that patients should keep out ofthe sun for the rest of their lives, but that they shouldactively protect their ‘new’ and more sensitive skin.Patients have a natural tendency to avoid sun exposure forsome time after a peel. After strict sun avoidance for up to2–3 months, outdoor activities can be resumed with totalsunblock, although sunbathing is forbidden during the firstyear after a peel.


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 firstcoat of Vaseline® and can help flaking along, taking care not to damage the skin. (b) Immediately after an application ofVaseline® and doctor-assisted flaking.

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During the first few months, wearing sunglasses (that donot 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 notrecommended for use before then, as recent studies showthat although retinoids improve post-peel skin regenera-tion when used before the peel, it seems that they can delayregeneration when they are applied too quickly after a peelor dermabrasion. The patient should be seen again duringthe 3rd week to make sure there are no pigmentary changesor other complications and to treat them if necessary. It issometimes necessary to use a depigmenting cream duringthe first 6 weeks, especially in patients who live in verysunny climates.

Touch-upsPhenol peels do not always produce the results hoped for,but fortunately it is rare that the results are so inadequate asto require extensive touch-ups or a complete re-peel. Anextensive touch-up can be done 6 weeks after the peel.Fintsi18 reported an incidence of 30% of local touch-upsafter Exoderm®. In his study, 21 cases out of 558 had to begiven more extensive touch-ups: 20 times for acne andonce for a hyperpigmentation problem.

Notes1. 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 1–2hours at the most.

3. As opposed to the use of phenol in the past as a disinfectantfor wounds, when occlusion does not slow down the rate ofpenetration of phenol.

4. Ruedemann R, Deichman WR. Blood phenol level after top-ical application of phenol-containing preparations. JAMA1953; 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 occlu-

sion. It is in fact cosmetic occlusion rather than physicalocclusion.

8. Beeson WH, McCollough EG. Chemical face peeling with-out taping. J Dermatol Surg Oncol 1985; 11: 985–90.

9. McCulloch EG, Langsdon PR, Maloney BP. Chemical peelwith phenol. In: Roenigk RK, Roenigk HH (Eds.), Dermato-logic 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 takes7–8 days.

12. This is a sterile adhesive plastic used in surgery to cover afield of operation and through which the surgeon can makeincisions.

13. Paracetamol must not be injected intravenously during thepeel, however, to avoid any competition among the enzymesresponsible for liver detoxification.

14. Patients often complain that some liquid has leaked outfrom the bottom of the occlusive mask and that they havehad 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 pro-mote infections. If the mask is too thick or rigid, it must becovered immediately in sterile white Vaseline® to soften it.

18. Fintsi Y. Exoderm-lift – liquid formula. 1996.


Figure 35.17The usual appearance of the skin, 7 days after a phenol peel.The skin is thin, sensitive and red. The demarcation line isparticularly visible between the face and the neck. A TCA peel(Easy TCA®) has actually been applied to the neck anddécolletage on the 3rd day after the peel and these areas arenow flaking (see also Figure 30.8).

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Chemical blepharoplastyIntroductionSurgical blepharoplasty is a technique that has become pro-gressively easier as it has been taken out of the strict frame-work of surgery requiring hospitalization. Once performedreadily under general anesthesia, it soon moved onto localanesthesia combined with neuroleptanalgesia, then deepsedation, and is now often carried out under simple localanesthesia with lidocaine. Lip & eyelid formula allows a treat-ment without any kind of anesthesia. Surgical blepharo-plasty, when performed by a skilled surgeon, should giveexcellent results that last several years, after which patients goback to the doctor, as they are no longer happy with theresults. A second blepharoplasty is then decided on and theresults will be no different to the last. It is common to comeacross patients who have ‘benefited’ from three successivesurgical blepharoplasties over 15 years. It has to be admittedthat the cosmetic results of multiple surgical blepharoplastiesare not always of good quality and patients who have beenoperated on too often are as easy to spot as patients with rota-tion flap hair transplants or large cylindrical punch grafts.

Surgical blepharoplasty can change the look of thepalpebral aperture, especially when patients want their eyesto look more ‘cat-like’. A second blepharoplasty can makethe tarsal region of the upper lid slightly darker. A thirdblepharoplasty can be disastrous: the palpebral apertureloses its elasticity and narrows, the eye becomes smallerand less mobile, the skin above the tarsus of the upper eye-lid takes on a very dark color that stops abruptly on the scarbecause of the altered distribution of dilated vertical bloodvessels (Figure 36.1). Lagophthalmia entropion or ectro-pion can develop.

I performed my first chemical blepharoplasty with local-ized phenol in the 1990s to treat blepharochalasis that haddeveloped just a few years after a surgical blepharoplasty ofthe four eyelids. The blepharoplasty had been done perfectlycorrectly, well before the patient had reached 40, and 4 yearslater there was once again a significant excess of skin on theupper eyelid that made the patient’s eyes look heavy and sad.The patient preferred to have non-surgical treatment.

Clinically, it was reasonable to investigate the problemwith her. Apart from surgery, what treatment options werethere to lift the ‘curtain’ of the upper eyelids? After a quicklook at the question, a peel seemed to be the only option.Alpha-hydroxy acids (AHAs) were ruled out immediatelybecause of the risks involved and the fact that they are inef-fective on the eyelids. Trichloroacetic acid (TCA) was ruledout, as the high concentrations needed to get the skin toretract would be dangerous and in any event ineffective.There was therefore only one option left: phenol. I have notencountered many problems with regular use of full-facephenol peels and, on the contrary, have found them to bevery successful. The results achieved locally on the eyelidshave often been remarkable (Figure 36.2).

36Phenol: chemical blepharoplasty and cheiloplasty

Figure 36.1Typical abnormalities of the upper eyelid after several surgicalblepharoplasties.

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Phenol therefore seemed to be an excellent option fortreating drooping eyelids. In fact, the general toxicity ofphenol is non-existent when treating limited areas, and alocal anesthetic is all that is needed given the anestheticproperties of the phenol itself.

AnesthesiaChapter 33 is devoted to the details of anesthesia for a phe-nol peel. Lip & Eyelid® formula can be applied without anyanesthetic on small areas, however. Patients feel an intenseburning sensation a few seconds after application. Theywill have been told that the burning sensation only lasts for15 seconds and that they can have a nerve block if theywant. Vocal anesthesia plays an important part, and thepatient can take a paracetamol (acetaminophen) pluscodeine tablet 1 hour before the treatment. Nerve blocksare often used to increase patient comfort: 2% lidocainewithout adrenaline (epinephrine) is used, and its durationof action is sufficient. The patient should be given para-cetamol plus codeine tablets for the post-peel pain, whichis inevitable during the first 24 hours because of the sever-ity and rapidity of inflammation caused by the peel.

Protecting the eyesA small quantity of ophthalmic Vaseline® is put in the con-junctival cul-de-sacs to protect the cornea, before the bot-tle of phenol has even been opened. The Vaseline® actuallydeactivates the phenol. The patient has eye drops (artificialtears) to put in the conjunctivae as soon as the phenol hasbeen applied and several times a day over the followingdays.

Phenol solutionThere are many different phenol formulations, and differ-ent combinations have been tested with varying results.The Baker–Gordon or Litton formulas potentially pose an

increased risk because of their depth of penetration in thethin eyelid skin. After using several different formulas, Igradually came to develop a phenol oil that meets my ownhigh standards of safety and effectiveness. Adapted for thetreatment of the eyelids and lips, this solution is called Lip& Eyelid® Formula. The eyelids and the lips do not, ofcourse, have the same thickness, resistance, permeability orreactivity; they are very different, and this is why the appli-cation protocol is also different in each case.

Application to the eyelids (Figures36.3–36.5)The choice of applicator is important: the large cotton budsnormally used in a full-face phenol are not precise enoughand absorb too much of the product. Cotton wool or gauze


Figure 36.2Full-face Lip & Eyelid® peel: close-up of the eyelids 30 daysafter treatment – note the significant retraction of the eyelid.

Figure 36.3(a) Lip & Eyelid® to the lower eyelids and an application ofOnly Touch® (lentigo to the forehead and right cheek) plusEasy TCA® as an evening-out peel. (b) Lip & Eyelid® on all foureyelids. The tarsus of the lower lid is not treated.

A

B

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soaked in solution is not suitable because of the risk ofdrips on the neck, or, even worse, in the eyes (let us not for-get that phenol is a protein coagulant and any contact withthe cornea could damage it irreversibly).

A double cotton bud would not be precise enough eitherand the ideal applicator is a single cotton bud: it is light,precise and simple – all of which are good qualities when itcomes to using phenol. Using a 1 cm3 syringe, 0.2 cm3 isdrawn up from the 3 cm3 bottle of Lip & Eyelid® and the

cotton bud is soaked by ‘injecting’ 0.10–0.14 cm3 of thepeel solution directly onto it. After disinfecting the areawith alcohol and carefully degreasing with acetone, Lip &Eyelid® is applied carefully on the lower lids with the cot-ton bud. Distinct frosting occurs rapidly and marks the endof the phenol application. The tarsus of the upper eyelid isnot usually treated. Applying Lip & Eyelid® on the eyelidtarsus induces severe edema that is very uncomfortable forthe patient and does not significantly improve results. Totreat the second eyelid, the remaining 0.06 cm3 should be‘injected’ onto the end of the same cotton bud. A bottle ofLip & Eyelid® formula provides enough solution to treattwo eyelids on 15 patients.

The same quantity of solution is needed to treat theupper eyelids. An assistant should be present whose soleduty is to mop up any tears as soon as they appear to pre-vent any diluted phenol dripping onto the face or going upinto the conjunctivae by capillarity. A fresh cotton padshould be used for each tear.

An evening-out peel is necessary to prevent demarcationlines, it should be applied on the rest of the face when theLip & Eyelid® application has finished and before anyocclusion is applied. Patients with a light skin type could begiven four weekly sessions of Easy TCA® (to the Grenzzone) or a single session of Unideep® (to the papillary der-mis).

Occlusion versus open techniqueOcclusion causes the phenol to macerate, which is oftenunnecessary on the eyelids. The lower eyelid can be coveredwith impermeable tape (there is a roll of tape in the peelkit) if a greater depth of action is required (Figure 36.6), if

Phenol: chemical blepharoplasty and cheiloplasty 297

Figure 36.4Lip & Eyelid® to the upper eyelids.

Figure 36.5The upper and lower eyelids have been treated with Lip &Eyelid®, and the frosting has already faded. The rest of theface has been treated with a Unideep® as an evening-outpeel: note the even pink–white frosting from the Unideep®and the post-peel Unideep® cream on the forehead.

Figure 36.6Occlusion can be applied if necessary, although this is rarelythe case. Here, occlusion has been applied using Sleek® (seeChapter 32).

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the wrinkles are deep or if there is xanthelasma for exam-ple. No occlusion is applied otherwise.

Occlusion of the upper eyelid, which is only indicated toincrease the depth of action of the peel, will always beessentially extratarsal (Figure 36.6). In the large majority ofcases, a chemical blepharoplasty is done without occlusion.

After applying the phenol, the doctor applies anevening-out peel, either Easy TCA® or Unideep®, to therest of the face. Both of these peels consist of an acid solu-tion and a post-peel cream that stimulates healing, isantioxidant and tyrosinase-inhibiting. This special post-peel cream should be applied once only by the doctor at theend of the facial peel. When the phenol is used withoutocclusion and without impermeable dressing, the EasyTCA® or Unideep® post-peel cream is applied on the areatreated with Lip & Eyelid® at the same time as it is appliedto the rest of the face.

Immediate post-peel careImmediate post-peel careWith occlusionAny occlusion is removed after 24 hours and the dermis isusually laid bare (Figure 36.7) and needs protecting.Applying bismuth subgallate, although highly effective atwound healing in general and in phenol peels in particular,has always caused minor problems for me on the mobileregion of the upper eyelid. The powder easily falls into theeyes (Figures 36.8 and 36.9). When the powder, which has

first been soaked with the products of epidermal liquefac-tion, dries on the skin, it can form crusted plates that hingeon the skin and that (in my experience) have occasionallycreated wrinkles that did not exist before the peel. I there-fore do not put any powder on the mobile part of the uppereyelid, and rather use a ‘moist’ technique, namely anantibiotic ointment (e.g. ophthalmic Terramycin®) duringthe first week after the peel) or just Vaseline®. Applying thistype of ointment is in any event equivalent to occlusion.1

Without occlusionThe patient’s skin, dried out by the phenol, provides anideal physiological dressing. The doctor can, however, tryapplying some bismuth subgallate (with a cotton bud), asbeads of serous fluid can often ooze unseen through the


Figure 36.7(a) After 24 hours of occlusion, the dermis has been destroyed. Note the significant amount of skin liquefaction. (b) Destruction ofthe dermis after 24 hours of occlusion.

A B

Figure 36.8Bismuth subgallate powder on lower eyelid.

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skin that has been ‘mortified’ by the phenol. If the powdersticks to the treated area, it can be concluded that it wasnecessary. If it does not stick, it was not necessary and thereis no point trying to force it to stick. In this case, the patientshould be seen again the next day to check whether thepowder is now required by trying to apply it again. Bismuthsubgallate (or Vaseline® or an antibiotic ointment) willprotect the skin for around 6 days. After that, the patientshould apply Vaseline® (ophthalmic if possible) severaltimes a day so that the bismuth subgallate powder comesaway from the skin by itself, without any outside help.

Subsequent post-peel carePatients should be given a small sachet of bismuth subgal-late (there are some small sachets in the Lip & Eyelid® kit),which they should apply with a cotton bud to any area thatappears moist. The patient should be seen as often as nec-essary, usually on the 1st, 3rd, 6th and 10th days. The

treated area is usually dry within 48 hours, at the most. Ifadditional bismuth subgallate powder will not stick to theskin, it is not necessary (Figure 36.10). Patients should nottouch their skin with their bare hands to avoid any risk ofinfection. In cases where the doctor has opted for a ‘moist’post-peel technique and has applied an antibiotic ointmentor Vaseline®, the patient should wash the area with thermalwater spray or with a showerhead before each applicationof cream. The different layers of antibiotic ointment orVaseline® should be not allowed to accumulate withoutwashing in between.

Patients sometimes feel some considerable discomfortthat they describe as a pulling sensation, a tightening of theskin, caused by the powder mask. This sensation is usuallylocalized around the edge of the mask, where it meets theskin that has not been treated with phenol. Applying Vase-line® with a cotton bud to the edge of the treated area canhelp alleviate this feeling of tightness (see the yellow dots inFigure 36.10: on day 5, the subgallate is dry). From the 5thday onwards (or the 4th day if needs be), and as long or asoften as necessary, sterile white Vaseline® or ophthalmicVaseline® should be applied on the bismuth subgallate sothat 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 feelpainful or just uncomfortable. The doctor should apply alittle Vaseline® on this area to soften it, even if it is only afew days since the peel was applied.


Figure 36.9Application of bismuth to all four eyelids: chemicalblepharoplasty and evening-out peel (Unideep®). TheUnideep® post-peel cream is applied to the face immediatelyafter the peel, the evening of the peel and the followingmorning. This photograph was taken on day 1.

Figure 36.10Day 3: the bismuth subgallate is dry.

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Post-peel developmentsEyelid edema Severe eyelid edema, which goes down quickly and lasts 7days at the most, appears immediately after the solutionhas been applied (Figure 36.12). It peaks on the morning ofthe 1st and 2nd days. The edema goes down during the daywhen the patient is no longer lying down. It spreads to theupper cheek on the 2nd day, the lower cheek on the 3rdday, the lower jaw on the 4th day, and on the 5th day isbarely noticeable. It is not uncommon for the patient to beunable to open their eyelids on the morning of the 1st day.If the edema lasts longer than 10 days, it is not normal.

ErythemaErythema develops equally rapidly, a few minutes after Lip& Eyelid® has been applied. It peaks during the first fewweeks (Figure 36.13), and fades, more or less slowlydepending on the patient, in 3 weeks to 3 months. The ery-thema takes longer to fade on lighter, more transparentskin. It always resolves, however, and is easily covered upwith make-up (a green make-up stick should be appliedfirst, followed by camouflage make-up, e.g. Couvrance® byAvène).

The bismuth subgallate powder comes away from theskin automatically (Figure 36.14) with the Vaseline® thatprevents transepidermal water loss (TEWL) evaporation.

The downtime is 8–10 days maximum.


Figure 36.11From the 5th day, Vaseline® should be applied on thebismuth subgallate so that it comes off without any outsidehelp.

Figure 36.12Normal edema over the first 2 days that has spread to thecheek area. (a) Chemical blepharoplasty of the four eyelids.(b) Chemical blepharoplasty of the upper eyelid only. (c)Chemical blepharoplasty of the lower eyelids only.

C

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Effectiveness and indicationsThe results of a chemical blepharoplasty may be inadequateif there is a large amount of excess skin or for lower eyelidfat pads. In these cases, surgical blepharoplasty is indicated.Applying Lip & Eyelid® to the eyelids treats wrinkles andfine lines, dyschromia, keratoses, and sagging eyelids (Fig-ure 36.15), but only improves eye bags when they arecaused by sagging skin rather than the presence of subcuta-neous fat. Surgery is indicated in this case.


Figure 36.13Normal erythema on the 13th day.

Figure 36.14Vaseline® has been applied the night before, on the 5th day,to remove the subgallate powder.

Figure 36.15Examples 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 thelower lids and Easy TCA® as an evening-out peel.

A B

C

D

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ComplicationsLip & Eyelid® is one of the safest phenol peels on the mar-ket, but incorrect application can lead to the usual localside effects of chemical peels.

PainTaking a painkiller tablet half an hour before treatmentalleviates the pain resulting from the inflammatory edema.A second tablet, taken before going to bed, ensures thepatient gets a good night’s sleep. The following morning,the pain will have almost completely gone. It is commonfor some pain to recur on the third day.

Risk of pigmentation disorders andpre-peel preparationEven if it is generally accepted that phenol has more of adepigmenting than a hyperpigmenting effect, the doctormust be prepared for any reactional hyperpigmentation.If the skin being treated is a very ‘melanin-reactive’ pho-totype or might have a severe inflammatory reaction, themelanocytes should be ‘sedated’ with tyrosinaseinhibitors and antioxidants (Blending Bleaching® cream)before and after Lip & Eyelid®, both on the areas to betreated and on the surrounding areas. The cream shouldbe applied twice a day for 2 weeks before the peel and assoon after the peel as possible. The skin can usually toler-ate Blending Bleaching® cream from the 10th day afterthe peel. Melanocyte ‘sedation’ should be continued for aminimum of 6 weeks.

If the peel is being performed on a skin phototype I to IIIand if the patient follows advice to keep out of the sun anduse sun protection, there should be no post-inflammatoryhyperpigmentation, but there is an increased risk of pro-longed erythema on lighter skin types. The sun should beavoided completely, and effective sun protection(Melablock HSP® SPF 50+) should be used for up to 3–6months. Exposure to UV light should be gradual thereafter.Even when the peel is applied correctly, there is still a riskof pigmentary changes, which are always reversible withBlending Bleaching® cream. Avoiding pigmentary changesis mainly a matter of pre- and post-peel care. Local depig-mentation, which can only be treated with a full-face appli-cation of Lip & Eyelid®, can be avoided by careful patientselection.

Demarcation lineThere is clearly a risk of a demarcation line on skin withsevere dyschromia or sun damage, a lot of wrinkles, freck-les, keratoses, or lentigines, as the skin treated with Lip &Eyelid® will look rejuvenated and stand out clearly fromthe surrounding damaged skin. In these cases, it is espe-

cially important to combine the peel with Easy TCA® orUnideep® to minimize the demarcation line if the skinphototype has been properly selected (see above). Ahealthy skin without dyschromia, of phototype I to III, IVat the most, does not pose the risk of a marked demarca-tion line. The demarcation line can be seen most clearly onthe edges of the occlusion. When using the occlusive tech-nique, it is best not to cover the whole of the treated area,but to leave an area unoccluded in order to create a gradu-ated area of penetration. If results prove inadequate, theycan be touched up or avoided altogether through properpatient selection.

Delayed healing When a chemical blepharoplasty is performed withoutocclusion, the increased depth of action of the phenolsometimes translates into a persistent moist scab in theinside corner of the upper eyelid (Figure 36.16), where thephenol has macerated more intensely. Applying an antibi-otic cream or ointment remedies the problem, and itshould resolve before the 15th day. There are no sequelaefrom this slow healing. If the scab persists for more than 2weeks, the doctor should remain alert and monitor thepatient more closely.

Other complicationsPoor 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 healmore quickly than the first.

I have never experienced scarring, entropion or ectro-pion with this treatment, but in theory they are possible.Prolonged erythema of several months can be treated, if itbothers the patient, with alternating applications every 2


Figure 36.16Benign delayed healing after chemical blepharoplasty.

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weeks of corticosteroids (hydrocortisone) and antioxidantcreams (Renutriv ACE Lipoic Complex®). Bacterial infec-tions should not occur if the technique is correct and post-peel care is conscientious. Herpes prevention is essential inpatients with a history of herpes.

Post-peel anxiety is common, not to say usual, and theextent of anxiety depends on the patient’s state of mindbefore the peel. Patients should be able to contact the doc-tor whenever they feel the need.

Record of resultsA photographic record of results is shown in Figures 36.17and 36.18.

In conclusionChemical blepharoplasty of the upper and/or lower eyelidswith Lip & Eyelid® formula is a relatively simple technique


Figure 36.17Developments and results: (a) before; (b) +24 hours; (c) +3weeks; (d) +6 weeks; (e) +14 months.

A B

C D

E

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that does not cause bleeding and is very quick (a few min-utes). It does not change the appearance of the eyes, but, onthe contrary, restores their original qualities. It is easy toperform without local anesthetic or with nerve blocks oflidocaine without adrenaline. Results are inadequate fortreating fat pads, but are excellent, if not perfect, in allresurfacing indications. The low rate of local complicationsand the lack of general complications make it an ideal tech-nique to rejuvenate the eyes, when the patient does notwant laser treatment or surgery and if the doctor is experi-enced in performing peels in general and in using phenol inparticular. It is obvious that a chemical blepharoplastyshould not be the first peel performed by a doctor who isinexperienced in this branch of medicine or cosmetic der-matology.

Chemical cheiloplastyA chemical cheiloplasty or labioplasty treats wrinklesaround the lips. The principle of the treatment is identicalto that of a chemical blepharoplasty, but it is easier to treatwrinkles on the upper lip than on the eyelids. It is also lessstressful for an inexperienced doctor.

The skin on the lips is more resistant than the skin on theeyelids. It has more appendages and is more apt to healwell.

Chemical resurfacing of the upperlip in combination with Easy TCA®

Lip & Eyelid® can be applied to the upper lip without nerveblock anesthesia. A first quick coat of peel solution induces

local anesthesia within 15 seconds. Subsequent applica-tions of phenol will therefore be painless.

Easy TCA® is applied without anesthetic, and Lip &Eyelid® and Easy TCA® can be combined when the wrin-kles are mainly located around the lips and the skin onthe rest of the face does not require a peel to the papillarydermis, which is often the case. The procedure is thenvery quick. Figure 36.19 shows an example of thisapproach. When there is more extensive sun damage, it ispreferable to combine Lip & Eyelid® with Unideep®. Fig-ure 36.20 shows an example of a case of upper lip wrin-kles in a patient who does not require a peel to thepapillary dermis on the rest of the face. Upper lip wrin-kles are more common in smokers and in patients whosemouths are very mobile and who use the orbicular mus-cle of the mouth too often or too vigorously: an injectionof botulinum toxin reduces upper lip mobility and pro-duces better results in combination with a deep peel.Because of the severe inflammation resulting from a deeppeel, the toxin is injected before the peel (at least 24hours previously). 15 units of Dysport® or 4 units ofBotox® are usually enough, injected at four differentpoints on the upper lip (Figure 36.20).

Chemical resurfacing of the upperlip in combination with a peel tothe papillary dermisWhen sun damage is more severe or if the patient has askedfor an evening-out peel at the same time to minimizesometimes long journeys, Lip & Eyelid® can be combinedwith Unideep® (Figure 36.20).


Figure 36.18Long-lasting results: (a) before treatment; (b) 1 year after alocalized peel with Lip & Eyelid® on the lower lid; Unideep®was employed as an evening-out peel

A

B

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A B

C D

E F

Figure 36.19Chemical 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 ofgray–white frosting (Easy TCA® is applied after the lip has frosted and before occlusion). (f) Occlusion, beginning of occlusion.

continued

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G H

I J

K L

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 upperlip. (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 wherethe botulinum toxin was injected 8 days before the phenol peel.

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A

B

C

D

Figure 36.20(a) Appearance of the patient’s upper lip before the peel. Therest of the skin is quite badly sun-damaged and requires anapplication of Unideep®, a TCA peel to the papillary dermis, ifnot a full-face phenol peel. (b) After disinfecting anddegreasing the whole face, Unideep® is applied gradually insequence. (Unideep® is applied in sequence, like phenol, butwithout 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 patientfeels a slight burning sensation that can be alleviated with acold pack placed directly on the acid before it has dried. Thecold pack must be completely dry so that it does not dilutethe peel solution.

continued

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E

G

F H

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 peelhas penetrated more deeply (there is a chance of infection or scratching etc. later on). The pinpoint frosting is similar to thatproduced by One Touch® peel. The midface and cheek region have been treated as described above. Unideep® is applied to thechin at the same time as the jaw area, where the patient also benefited from a cold pack. The Unideep® post-peel cream hasbeen 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® isapplied to the left midface region and the cheek. The post-peel cream is applied. The chin region as well as the jaw area aretreated with Unideep®. This photograph shows an impermeable keratosis that will be treated with a single application of OnlyTouch®.

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Although both peels can be done without nerve blocks,patients often appreciate them, as they make the whole proce-dure more comfortable, especially when TCA is being applied.

Patients who are very squeamish may benefit from seda-tion.

ResultsResults, as we have seen elsewhere in this chapter and thisbook, can sometimes be perfect. Others are less perfect,although still appreciated by the patient. Results can last3–10 years. More superficial peels should be done on ayearly basis to maintain the results.

ComplicationsSee Chapter 37.

Summary of the ‘chemicalresurfacing’ techniquePre-peel� If risk of pigmentary changes:

– Skin phototype I to III: Blending Bleaching® twice aday, 2–3 weeks before the peel


I

J

K

Figure 36.20 continued(i) Application of Only Touch®. (j) Immediate induction oflocal frosting. (k) The upper lip is occluded with theimpermeable tape provided in the Lip & Eyelid® kit. It mustgo at least 1 cm beyond the area treated with phenol. Thepatient should be told not to make any mouth movementsfor the next 24 hours. At the end of treatment, a coolingmask is applied for around 15 minutes. The patient can gohome, having made an appointment for the next day toremove the occlusive mask on the lip.

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– Skin phototype IV: blending and bleaching creamand 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 thepeel

Preparation and application of thepeel

� 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 phe-nol.

� 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 thewrinkles and then apply to the whole area

� Without nerve block anesthesia: apply a quick coat ofLip & Eyelid® to the whole area; warn the patient howlong the burning will last (15 seconds)

� Apply in the base of the wrinkles and to the whole area.

Eyelids immediately after the peel

� (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

Upper lip and chin immediately afterthe peel

� 24 hours of occlusion: the transparent occlusive dress-ing can be found in the Lip & Eyelid® kit

� If the occlusive dressing comes off accidentally before24 hours, apply Vaseline® as emergency occlusion

� A painkiller tablet for the evening or night (more ifpainful)

� Lorazepam 2 mg to be taken before going to bed

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 Vase-

line®)� 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 Vase-

line® to be applied four times a day; rinse the skin underthe showerhead before applying another layer of cream

� Patients should wash their hands thoroughly beforetouching their skin

� If there is an unpleasant sensation of tightness in thearea treated with phenol: apply neutral sterile Vaseline®to the edges of this area

The 3rd day� Normal recurrence of pain for several hours: paraceta-

mol plus codeine tablet

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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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 tol-

erate 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 daysand 1 month� If there are pigmentary changes (after approximately 1

month):

– Do a few sessions of Easy TCA® (pinpoint or cloudywhite frosting)

– May be combined with a corticosteroid such as clo-betasol

See the patient again after 3 monthsfor the end of treatment

Note1. See Chapter 32 for further remarks on the use of Vaseline®

immediately after a peel.


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General remarksWe must humbly accept the fact that there is still no magicformula that even the most experienced practitioner coulduse on all skin types without taking precautions and with-out risk and whose results would be both spectacular andpermanent. Some formulations are of course more simpleand less dangerous to use than others, but there is no guar-antee of automatic success and complete safety. The practi-tioner must follow the rules of application for each peel, beaware of its limitations, risks and indications, and knowhow to avoid and treat any complications. ‘Artistic’ impro-vization usually leads to disastrous results. It is vital to readthe instructions for use for each peel before applying it. Athorough knowledge of the symptomatology and physicaland chemical mechanisms of peels is essential for the prac-titioner to be able to work confidently, safely and effi-ciently. It is child’s play for any competent doctor to applyliquid to a patient’s skin, but the true skill lies in anticipat-ing the complications, being able to prevent them and, ifprevention fails, being able to treat them. Patients deserveto be treated with respect, optimum safety and conscien-tiously by true professionals. Any peel, even a superficialone that is neutralized quickly and even in the most experi-enced hands, can lead to complications that are not neces-sarily serious or permanent, but that are more than what aparticular patient is prepared to put up with. The deeper apeel penetrates, the sooner it is effective and the greater therisk of serious and permanent complications.

We will look at each complication in detail, how to pre-vent it and how to treat it. Systemic complications,1 exclu-sive to phenol peels, are dealt with in Chapter 28.

The magnitude of the risk depends on the following fac-tors:

� the type of peeling agent used, its concentration, how itis applied, and the depth it reaches

� the doctor’s (lack of) experience, the monitoring andtreatment equipment used

� skin preparation (when necessary) and post-peel carerecommended by the doctor

� the patient’s own sensitivity and compliance with thepre- 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 factorsIf there were a secret to safety, it would lie in a thoroughknowledge and understanding of this type of treatment.For doctors to give patients a wide range of choice, theymust know how to use at least the three main types of con-ventional peels correctly: alpha-hydroxy acids (AHAs),trichloroacetic acid (TCA) and phenol (for phenol, thedoctor should at least know how to apply it locally). Foreach type of peel, the doctor must be perfectly acquaintedwith its indications, results, limitations and complicationsto be able to choose the right product for a given patientand to be able to apply it correctly. The patient should beinformed of alternative techniques, their possibilities, con-traindications, side-effects and cost.

The application technique must be flawless and in keep-ing with the particular procedure for each peel, appropriateto the patient’s skin type and the results expected. The doc-tor must be aware of and acquainted with the risks of com-plications and the means to prevent and treat them. It isbetter to avoid complications through prevention ratherthan treat them. Each patient is different and each peel mustbe suited to each patient, which in no way means tryingdangerous experiments with different formulas on a case-by-case basis. On the contrary, it is a matter of choosingamong tried and tested treatments the one that is most suit-able for the patient’s skin structure and that will give thebest results with a minimum of inconvenience. For exam-ple, the practitioner should be able to decide whether it is

37Complications of chemical peels

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preferable to carry out several more superficial treatmentsor, on the contrary, to do a single phenol peel. If the latteroption is chosen, which formula should be used:Baker–Gordon, Grade’s or Litton’s, Verner, Hetter, mold-ing mask, Cora Valenti, Exoderm® or Lip & Eyelid? Shouldan occlusive mask be applied? Should the peel be neutral-ized? Should occlusion be left on for 24, 36 or 48 hours? Ispost-peel care necessary? If so, what? If TCA is the treatmentselected, should it be medium or deep or is it better to doseveral sessions with Easy TCA® or Unideep®? If an AHApeel seems the best choice, should it be glycolic acid, man-delic acid or lactic acid? Or Easy Phytic® peel? Should thepeels be combined with other treatments, such as botu-linum toxin, dermabrasion, filling, surgery, coagulation oftelangiectasias, shave excision, mesotherapy, etc.? Whichorder should the combined treatments be performed in?Peel before toxin or vice versa? Peel before a face-lift or viceversa? Peel before mesotherapy or vice versa?

Most peels carry a risk of one of the complications dealtwith in this chapter. The likelihood of these complicationsoccurring largely depends on the type of peel and thepatient. Classifying peels as very superficial, superficial,medium or deep is purely theoretical and should not makethe doctor any less vigilant. A low-concentration TCA or asimple glycolic acid peel can penetrate deep into the dermisif the peel is applied repeatedly and vigorously, or, as far asglycolic acid is concerned, if the peel is not neutralized intime. Depending on the agent and technique used, compli-cations can be systemic or local, permanent or temporary,serious or not.

Inadequate resultsInadequate results are an acceptable complication whenthe patient has been forewarned and the practitioner is pre-pared to compensate and do a proper touch-up. It is unac-ceptable when the patient has not been warned of thispossibility and the doctor does not provide the care thepatient deserves.

Reasons for inadequate resultsWrong indicationIf the doctor’s aim is to improve the texture of the skin,treat hyperpigmentation and even-out the complexion, asingle peel to the papillary dermis or four Easy TCA® peelsto the basal layer Grenz zone are good indications. On theother hand, it would be dreaming to expect to get rid ofsurgical or acne scars or the wrinkles on the cheek of thepatient in Figure 37.1 with glycolic acid or even TCA. Scarsare treated with deep peels, often in combination withother treatments (punch elevation, dermabrasion, subci-sion, laser, filling, etc.). Wrinkles are treated with phenol.

Poor product knowledgeAttempting to use glycolic acid or TCA to achieve a visiblelifting effect on ‘Sharpei skin’ is inviting disappointment:cosmetic and plastic surgery alone can achieve a liftingeffect. It is better to warn patients of the possibility of inad-equate results with any peel, even a deep one, if their skin isvery thick, oily and sagging. It is likely that a deep peelwould have to be repeated (locally or completely) to achievethe desired results. In these cases, it is worth considering acombination of a surgical face-lift and a peel.

Sagging, thick skin is not a good indication for peels ingeneral (Figure 37.2). Peels can get rid of fine lines, hyper-pigmentation and keratoses and improve the quality ofsun-damaged skin.

Lack of pre-peel preparation, propercleansing and/or degreasing the skinThe presence of a lipid film on the skin partially deactivatesmany peels and limits their penetration. An unprepared stra-tum corneum may be too thick – too impermeable – inplaces. This relative local impermeability means that the acids


Figure 37.1Wrinkles on the cheeks that will not respond or respondpoorly to superficial or medium peels.

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do not penetrate evenly and the results will also be uneven.Pre-peel preparation is essential for certain peels,2 but unnec-essary, or even dangerous, for others.3 It is essential to followthe recommendations for each peel solution to the letter.

Facial expressionsAfter a deep peel, facial expressions imprint lines in thenewly regenerating dermis and epidermis (Figure 37.3).Injecting botulinum toxin (before or after a peel) preventsdynamic wrinkles reappearing after a peel. Smoking shouldbe forbidden after a deep peel to prevent the rapid reap-pearance of ‘accordion folds’ around the mouth. As well asthe sucking movements required, smoking reduces theoxygen supply to the newly regenerating skin at the sametime as dramatically increasing the number of free radicals.Smoking accelerates skin aging and slows down healing.

Combined techniquesNon-surgical facial rejuvenation often requires a combina-tion of different techniques, such as (micro)dermabrasion,

filling treatments, shave excision, prior surgical removal ofsmall benign tumors, punch elevation of scars, stimulatingfacial mesotherapy, peels of different depths, etc. The doc-tor can only learn by experience what results to expect,which techniques should be combined and how best to usethe chosen peel on a particular patient. Therein lies the artof peeling.

Histology of lesions undergoingtreatmentLentigines, for example, result from a problem in the basallayer of the epidermis. Let us not forget, however, that theepidermis extends to varying depths into the dermis to formthe dermal papillae. If a lentigo originates in a relativelysuperficial papilla, a peel to the Grenz zone will solve theproblem,4 but if the lentigo originates in a deep papilla, itwould take a very deep peel to dislodge it. Histologically,lentigines often have a deep ‘golf club’ structure that makesthem difficult to reach. In this way, some problems that arehistologically epidermal can only be treated by deep peels.In the diagram in Figure 37.4, a peel to the Grenz zone canresolve problem ‘A’, whereas problem ‘B’ will only respondto a peel to the reticular dermis. This reticular peel can be

Complications of chemical peels 315

Figure 37.2Sagging skin that does not respond well to peels.

Figure 37.3Reappearance of dynamic wrinkles 10 days after a full-facephenol peel.

A

B Reticular dermis

Grenz zone

Figure 37.4Lentigines at different depths,

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localized (e.g. with Only Touch®) or full-face (phenol peel).Repeated intraepidermal peels, no matter how often theywere performed, would do nothing to solve the problem.Stretch marks, to give another example, are characterized byepidermal and dermal atrophy. They can only be improvedby combining epidermal resurfacing with strong and deepdermal stimulation.

Prevention of inadequate resultsThis involves:

� 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

In all cases, caution dictates that the patient should bepromised less dramatic results that might be hoped for. Inthis way, in the best-case scenario, the patient will get a nicesurprise and be happy with the better than expected results.In the worst-case scenario, the doctor will not have madepromises he cannot keep.

Patients should be made fully aware of the limitations oftheir treatment. They should be shown photographs – andnot necessarily the ones showing the best results. It isalways essential to talk with patients before treatment tofind out what they want and make sure they get the resultsthey are looking for. It would be pointless to suggest a seriesof superficial peels to patients who want to get rid of crow’sfeet, when a botulinum toxin injection would providethem with the quick results they want. False hopes alwayscreate problems for the doctor that raised them. Somepatients’ disappointment can turn into a nightmare for thedoctor.

TreatmentTouch-up or different techniqueIf the selected peel turns out not to be strong enough, a dif-ferent peel should be used or it should be combined withother treatments. Local or general touch-ups can be doneas soon as the condition of the skin permits, that is, whenthe skin has completely regenerated and when all erythemaand flaking has finished. The ‘rest’ time between two peelsis usually between 4 and 6 weeks.5 Many peels only produceresults after fairly frequent repetition.

Repeating peels� Very superficial (stratum corneum) and superficial

(intraepidermal: Easy Phytic®) peels have to be repeatedto produce visible results. Results usually only show

after a certain number of sessions, as they are stimulat-ing 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. Thedoctor should always wait for the skin to recover beforere-peeling. Skin that is actively flaking should not haveanother peel applied to it. Some patients need a fifthpeel (oily skins, resistant hyperchromia, squeamishpatients who do not allow the doctor to apply the solu-tion properly, etc.).

� TCA peels to the papillary dermis (Unideep®) should notbe repeated until at least 1 month later and on condi-tion that the skin has completely recovered from theprevious session.

� Localized TCA to the reticular dermis (Only Touch®): insome cases, lentigines or keratoses do not disappear afterthe first session of Only Touch®. The application proto-col for Only Touch® provides for a second applicationwhere necessary. The Only Touch® peel should be com-bined with Easy TCA® to avoid pigmentary changes andcan be applied before the first and the fourth Easy TCA®peels. If some lesions resist or recur, a complete cycle ofOnly Touch® plus Easy TCA® can be started again aftera 6-week rest period. Resistant lesions on the face can betreated locally with a spot application of Lip & Eyelid®.However, applying very localized phenol often produceslong-lasting (3–6 months or more), localized erythema.This erythema tends to resolve naturally, but should beaccompanied with protective measures against post-inflammatory hyperpigmentation.

� Phenol (Lip & Eyelid® formula): if a full-face phenol peeldoes not produce adequate results, a second peel can beapplied to the areas that did not respond to the firstpeel. The touch-up can be localized or full-face, if thecondition of the skin permits and if there has been along rest period. Skin regeneration after the second peelis much quicker, there is less edema and post-peel ery-thema is of a much shorter duration (2 weeks at themost). If a third phenol peel were indicated (inextremely rare cases of very thick skin, patients whosmoke, or rapid resumption of facial expressions), itwould most often be localized. The author has onlyonce had to do a third phenol peel on the lip and cheekarea after inadequate results on skin that was extremelyoily and thick. Recovery was even faster after a thirdapplication of phenol and there was hardly any ery-thema. It should be noted that if a second phenol peelcan boost inadequate results, a third phenol peel onlybrings a very slight improvement over the second.

Melanocyte toxicityMelanocytes are located in the basal layer of the epidermisand 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 ker-atinocytes and thus provide a homogenous photoprotec-tive layer of pigments on the surface of the epidermis. It hasbeen shown6 that melanocytes have three different ways oftransporting melanin to keratinocytes:

� melanocyte phagocytosis: transfer of melanin plus cyto-plasm plus melanocyte dendrites to the keratinocyte

� membrane fusion between melanocytes and ker-atinocytes, leading to direct exchanges betweenmelanocytes and keratinocytes

� exocytosis of melanosomes by melanocytes to the extra-cellular environment, where they are picked up again bykeratinocyte endocytosis

Each melanocyte communicates with 35–40 keratinocytesthrough its dendrites and forms one ‘melanization unit’. Ifthe melanocyte transmits eumelanosomes, the keratinocytesreceive effective sun protection. On the other hand, ifpheomelanosomes are transmitted to the keratinocytes, theywill not be properly protected against UV rays. Keratinocytescan synthesize active substances that alter the proliferation,differentiation and certain biological functions ofmelanocytes.6 An agent’s melanocyte toxicity is an advantagewhen treating melanin hyperpigmentation. On the otherhand, it is an adverse effect when melanocyte toxicity resultsin partial, complete, localized or generalized depigmenta-tion. Complete, generalized and permanent depigmentationresults in ‘porcelain’ skin and, according to Litton,7 occurs in3% of phenol peels with his formula. This complication hasnot been described to date with the Lip & Eyelid® formula.

Melanocyte toxicity of differenttypes of peelsAHAsAHAs are not considered toxic to melanocytes. Therefore,there is little fear of depigmentation when these peels areapplied according to the rulebook. When these peels areneutralized, their effect stops, and AHAs cannot thereforedo any irreversible damage to melanocytes. If they are notneutralized soon enough, they can, however, causemelanocytic lesions and areas of depigmentation as a result.

Uneven penetration of AHAs can damage melanocyteslocally. 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, glycolicacid, benzoyl peroxide, etc.9

� the patient has used abrasive or hair-removing tech-niques that alter the relative impermeability of the skinbefore the peel

In general, the appearance of frosting during an AHA peelis a sign of overpeeling, and pigmentation problems maywell occur. An AHA peel should always be neutralized aftererythema and before frosting.

TCATCA is not considered toxic to melanocytes. High concen-trations of TCA can, however, coagulate melanocytes anddestroy them. Areas of depigmentation can thereforeappear if TCA has been too aggressive locally. Aqueoussolutions of TCA in particular can penetrate more deeplythan they should, as they are neither homogeneous nor sta-ble. An even, intraepidermal TCA peel to the basal layer orGrenz zone does not cause depigmentation. Easy TCA®, inthe basic protocol, does not produce depigmentation.

A TCA peel to the papillary dermis, if applied evenly,does not usually cause permanent, pathological depigmen-tation. If the TCA penetrates too deeply into the dermis,depigmentation is sometimes accompanied by scarring.Three different degrees of TCA penetration cause three dif-ferent complications: scarring results from the deepestpenetration; depigmentation without scarring results whenthe TCA penetrates too deeply (but not deep enough tocause scarring) and is melanolytic; and a hyperpigmentedhalo results from an untreated, peripheral inflammatoryreaction (Figure 37.44).

PhenolPhenol is considered toxic to melanocytes, although pig-mentary changes can sometimes occur after a phenol peel(see later in this chapter). Phenol is by far the most effectiveagent when it comes to treating many facial hyperpigmen-tations. In general, a slight loss of pigment should be con-sidered as normal after a phenol peel, and not as acomplication. For a given concentration, depigmentationis proportional to the total quantity of phenol applied tothe skin. That is to say that several coats of the same prod-uct will cause depigmentation more often than a moresmaller number of coats. The presence of adjuvants canalso be a risk factor for depigmentation: croton oil is acommon adjuvant in phenol formulas and enhances pene-tration of the phenol. If there is too much croton oil, thephenol can penetrate more deeply and cause depigmenta-tion. The use of thymol iodide as a post-peel mask isanother risk factor, as thymol is a phenol derivative thatcan have a toxic effect on melanocytes in the period imme-diately following the phenol peel. This risk can be avoidedby using bismuth subgallate as a post-peel mask. Phenol isnot melanolytic, however: it does not physically destroy


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melanocytes. Melanocytes are not simply melanin-produc-ing organelles, but play an active part in many of the bio-logical processes in the skin:

� production of cytokines� mediators of inflammation� enzyme production� synthesis of molecules in the extracellular matrix

Histological sections taken after phenol peels show thatmelanocytes are still present, though many of them areinactive. Clinically, fewer melanocytes are rendered inac-tive with the latest formulas (e.g. Lip & Eyelid®). Thismeans that long-term prognosis for sun exposure can bebetter with these peels than with older phenol formulationsand that a few months or even a year after the peel, it isoften difficult to see a demarcation line.10 The melanocytetoxicity of phenol means the practitioner must choose theproduct most suited to the patient’s complexion.

When persistent (absolute or relative) depigmentation islikely after a phenol peel and it is essential to warn patientsthat the texture of their skin will be rejuvenated, but that inall likelihood they will have to wear foundation on a per-manent basis to hide the difference in color between thetreated and untreated skin.

The risk of depigmentation can pose a problem withbadly sun-damaged skin, but, at the same time, this is oneof the best indications for phenol. The extraordinaryresults achieved on photoaged skin are often accompaniedby a more visible demarcation line between the areas ofhealthy, treated skin and the old, untreated skin. Com-bined use of phenol on the face and Easy TCA® orUnideep® on the neck help attenuate this demarcation line(Figure 30.1). The melanocyte toxicity of phenol poses dif-ferent problems depending on whether the treatment hasbeen applied to the whole face or just locally (e.g. the upperlip). Depigmentation of the whole face is easier to hide withmake-up than localized depigmentation, and this shouldbe discussed with the patient. Usually, older patients whoseupper lip is very damaged will accept this local depigmen-tation, easily disguised with camouflage make-up, whereasyounger patients find it more difficult to accept being con-demned to wearing make-up every day, and often preferother treatment options.

PreventionThe selected peel must be applied in strict accordance withthe instructions for use. The practitioner should alwaysbear in mind that the deeper the peel, the more effective itis, but also the more dangerous it is and that phenotypedoes not always correspond to genotype: an individual whoappears to have a light complexion may react dermatologi-cally like a much darker phenotype. With this in mind,family anamnesis might well prove worthwhile. Examining

the areas of the body that have never been tanned can pro-vide a clue to the patient’s ‘base’ color, and the area treatedwith phenol may well return to this original color.

Melanocyte toxicity depending onskin phototypeBlack patientsBlack patients can be treated with correctly neutralized gly-colic acid or with Easy Phytic® solution. Easy TCA® canalso be used (pinpoint or cloudy-white frosting): TCAshould never be allowed to penetrate reticulary dermis (seeChapter 16). Phenol should not be applied on patients witha skin phototype above IV.

Asian patientsAsian patients might pose a problem of residual depigmen-tation with deep peels. Dark Asian skins are treated likeblack skins. Lighter Asian skins can be treated with deeperpeels. Fintsi69 and Professor Damiano Kim (Korea) appliedphenol successfully to light Asian skins. AHAs, EasyPhytic® and Easy TCA® can be used in all cases. TCA insimple aqueous solution (TCA–SAS) often triggers post-inflammatory hyperpigmentation on Asian skin. Unideep®should be used with caution on Asian skin phototypes.

Dark-skinned patientsMediterranean or Latin American skin types can be treatedwith AHAs, superficial TCA or Easy TCA®. A TCA peel tothe papillary dermis can be used with caution, avoidingoverpeeling and post-peel inflammatory reactions. Patientswith skin phototype IV can be treated with phenol if thepatient is warned of the possibility of depigmentation inthe treated skin. Results can be very satisfactory, as the dif-ference in color between the treated and untreated areasmay not be too marked.

Red-haired patientsRed-haired patients, whose skin is often covered in freck-les, do not pose any problems with AHA peels or EasyTCA®. A TCA peel to the papillary dermis gets rid of mostof the freckles and Easy TCA® in the basic protocol lightensthem.

In principle, the texture of their skin makes them goodcandidates for phenol, as they get wrinkles sooner thandarker skin phototypes and do not often suffer from post-inflammatory hyperpigmentation after a medium or deeppeel. All the freckles will disappear, however, leaving theskin 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 oftentake on the color of areas that have never been exposed tothe sun.

Treating melanocyte toxicityAs yet there is no easy and effective treatment to returncolor to a skin that has lost it. No doubt in the futuremelanocyte grafts will be a possibility. For now, make-up isthe only solution.

ErythemaPost-peel erythema can be perfectly normal (Figure 37.5)or a warning sign of a more serious complication. Ery-thema can occur as a reaction even after simply cleansingthin and sensitive skin before a peel. If an erythema devel-ops after the skin has been cleansed gently and without acidproducts, it may be concluded that it is hypersensitive andshould be treated with caution.

Chronologically, the skin’s first response to an applica-tion of acid is usually erythema. This erythema is caused bythe inflammatory vasodilation of the blood vessels in thedermis in response to chemical injury. The vasodilationtriggers transient dermal edema. This edema is largelyresponsible for the rapid disappearance of fine lines after

superficial peels. The dermis fills with extravasated fluids asa result of vasodilation, and this stretches the epidermis.The fine lines disappear temporarily. Erythema may there-fore be the only clinical sign of a superficial peel. Thedeeper the peel, the more erythema is replaced by frostingdue to protein coagulation. The speed with which ery-thema is replaced by frosting largely depends on thestrength of the acid used. Some very strong acids triggerfrosting even before erythema becomes apparent.

AHAs and erythemaAHAs in aqueous solutionEssentially, AHAs trigger erythema – a sign that the peelshould be neutralized. Erythema appears more quicklywhen the skin has been prepared (certain products increasethe permeability of the stratum corneum) during the weeksbefore the peel.

� Very localized, isolated erythema signals an area wherethe AHAs have penetrated rapidly. The doctor shouldkeep a close eye on this area and neutralize it withsodium bicarbonate or another alkaline solution, whileleaving the peel to work a little longer on the rest of thetreated area that has not yet reached the stage of ery-thema. Great care should be taken not to let the acidpenetrate too deeply locally and trigger frosting, whichcan lead to complications. After neutralizing, it can helpto apply a little cortisone cream on an area of erythema.

� Even and light erythema is a clear sign that it is time toneutralize the peel with an alkaline solution preparedbefore the peel has been applied. After the acid has beenproperly neutralized, the erythema should be transientand last one hour at the most.

� If the practitioner ignores the erythema and does not neu-tralize, the AHA peel can cause localized pinpoint frost-ing that will gradually converge and become relativelyuniform. An AHA peel that is not neutralized causesscabbing and, in the most serious cases, dyschromia andscarring. Patients often give up on the treatment if thepeel is not properly neutralized. Erythema from over-peeling can last for several weeks or months and leaveareas of skin that are ‘smoother’ than the surroundingskin.

Easy Phytic® solutionThis peel deserves special attention because of the fact thatit does not need neutralizing (see Chapter 11). It triggerslight and uniform erythema that lasts for a few hours at themost. Neutralizing this peel would reduce its effectivenessand take away any benefit. If any abnormal frosting occurs,the peel should be neutralized immediately.


Figure 37.5Normal erythema after a full-face phenol peel.

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TCA and erythema

TCA in simple aqueous solution(TCA–SAS)The appearance of light, uniform and widespread erythemaafter a TCA–SAS peel does not usually lead to any prob-lems and has a natural tendency to resolve gradually with-out treatment. The appearance of localized erythema,especially on the cheekbones, should alert the doctor, as itcan be a sign of local overpeeling or one or more of the fol-lowing:

� 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 fol-lowing clinical signs: erythema, pinpoint frosting, cloudy-white frosting, converging cloudy frosting, evenpink–white frosting, pure white frosting and finallygray–white frosting. The speed with which one signreplaces another is dose-dependent.

These signs should appear in sequence when a low-con-centration TCA peel is applied in successive coats. A moreconcentrated TCA peel will trigger converging clouds offrosting at the same time as erythema around the frosting(Figure 37.6). Higher concentrations trigger pink frostinginstead of erythema and erythema, only then appears as thefrosting fades in the treated areas.

Highly concentrated TCA triggers immediate ‘purewhite’ frosting without any hint of pink or gray, which sig-nals coagulation of the skin proteins and the walls of thedermal blood vessels.

Although the erythema from TCA is often less severethan that from phenol, it can be vivid and last 15 days toseveral months.

TCA–SAS peels sometimes produce prolonged andspectacular erythema, as can be seen in Figure 37.7. Thesesimple aqueous solutions do not penetrate evenly, anduneven pathological erythema often results. Erythema aftera peel to the papillary dermis with TCA in simple aqueous


Figure 37.6Normal erythema around an area of frosting during a TCApeel to the papillary dermis (Unideep®) on the décolletage.

Figure 37.7Uneven, pathological erythema after TCA in aqueous solution– a peel to the papillary dermis. (Courtesy of Dr A Carvajal,Colombia.)

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solution is usually expected to last 1–2 months. A peel tothe top of the reticular dermis can last 1–3 months. Persis-tent erythema is often followed by inflammatory hyperpig-mentation that is aggravated by sun exposure. Effective sunprotection (see Chapter 3) is therefore essential as long asthe erythema persists.

Indurated erythema might lead to scarring, and preven-tive treatment should be started (see the section on scarringlater in this chapter). When intraepidermal TCA peels orTCA peels to the basal layer are repeated too often,11 ery-thema can last even longer. Using tretinoin during theweeks before or after a TCA peel is also likely to trigger orexacerbate erythema.

Easy TCA®Basic protocol (pinpoint or cloudy white frosting)Light erythema develops immediately after the peel anddisappears in around 30 minutes (Figure 37.8). The skinmay appear ‘sunburned’, and this can last up to a maxi-mum of 48 hours in patients with thin and sensitive skin.Because of the action of the post-peel cream, there is oftenno observable erythema during the days following this peelif it has not gone beyond pinpoint or cloudy white frosting.The post-peel mask scavenges free radicals and breaks thevicious inflammatory circle that sets in after any peel.Scratch lesions can, as with TCA–SAS solution, cause local-ized erythema resulting from local infection (Figure 37.9),which should be treated.

Treating stretch marksThis more aggressive protocol involves sandpaper abrasionprior to the application of Easy TCA® solution and 12–24hours’ occlusion of the post-peel mask cream. It causessevere erythema within the first few hours of occlusion.After the occlusion has been removed, the skin looks

swollen and red (Figure 37.10). During the first week, over-all developments are comparable to those of a phenol peel.The erythema can last for several weeks and the next peelcan only be performed after the erythema has completelyresolved. As with TCA–SAS, persistent localized erythemais a sign of local complications and should be monitored,while uniform erythema has a natural tendency to resolvegradually without treatment (Figure 37.11).


Figure 37.8Normal and transient erythema 30 minutes after Easy TCA®.

Figure 37.9Localized erythema around scratch lesions after an Easy TCA®peel to the papillary dermis.

Figure 37.10Erythema 24 hours after treatment of stretch marks: abrasion-occlusion protocol.

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Unideep®Unideep® is a TCA peel to the papillary dermis. Adaptedfrom Easy TCA® technology, it consists of a peel solutionand a post-peel mask. Thanks to the post-peel mask, theerythema following the peel does not last as long as the ery-thema after a peel with TCA–SAS to the same depth. Theerythema following Unideep® lasts around 5–8 days (Fig-ure 37.12), and the only treatment that it requires is anapplication of antioxidant cream (e.g. Renutriv ACE LipoicComplex®) and Vaseline® (see Chapter 23). If there is per-sistent localized erythema, there might be a local complica-tion, and treatment is necessary. Effective sun protectionmust be used.


Figure 37.11Erythema totally disappeared 5 weeks after Lip & Eyelid®formula of upper eyelid and unideep (TCA peel to papillarydermis) in the rest of the face.

Figure 37.12Erythema 5 days after Unideep® on the face, apart from thearea around the mouth, which was treated with occlusive Lip& Eyelid®.

A B

Figure 37.13Normal erythema after Only Touch®and Easy TCA® for lentigines: (a)before; (b) 2 weeks after treatment.

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Only Touch®Only Touch® is an adjuvanted, stabilized and concentratedTCA peel, used to reach the reticular dermis locally. Itshould be applied in strict accordance with the recommen-dations for use (see Chapter 22).

The erythema that always follows an application of OnlyTouch® usually lasts 2–3 weeks and gradually resolveswithout treatment (Figure 37.13). Only Touch® should beapplied carefully, avoiding any excess product and limitingcontact time between the applicator and the skin: the skinshould just be touched lightly, with the same pressure as forpushing the buttons on a telephone to dial a number. Ifcontact time is any longer, the acid solution will penetratetoo deeply. Too much solution and too long a contact timecan cause small, erythematous lesions that do not lastlonger than 3–4 months and that gradually resolve withtreatment. The erythema caused by Only Touch® can eas-ily turn into post-inflammatory hyperpigmentation if theproduct is used alone,12 but post-inflammatory hyperpig-mentation is rare if Only Touch® is combined with an‘evening-out’ Easy TCA® peel. Any erythema warrantseffective sun protection. Any erythema lasting longer than2 weeks must be treated.

Phenol and erythema

Full-face phenolPhenol peels are always accompanied by severe erythema(Figures 37.14 and 37.15). The erythema appears imme-diately around the edges of the frosting caused by the phe-nol and can then be seen on all of the treated area, as soonas the frosting fades. This immediate erythema resultsfrom inflammatory vasodilation that follows chemicalinjury and is normal. After 24 hours, the patient appearsseverely burnt, as can be seen in Figure 37.14. The classi-cal phenol formulas often cause erythema that last morethan 3 months, or sometimes even several years. It can bepermanent (in some rare cases). Lip & Eyelid® causes ery-thema 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 visiblethrough the transparent skin. Within a few weeks ormonths, the restructured epidermis will cover up thehypervascularization, which tends to gradually dimin-ish.

Local phenolThe eyelids, upper lip and the area around the mouth canall be treated locally, in combination with an ‘evening-out’peel on the rest of the face.

The usual erythema caused by phenol appears locallyand lasts from 3 weeks to 3 months (Figure 37.16). Thelocalized erythema, surrounded by skin of a normal color,


Figure 37.14Normal erythema and edema 24 hours after full-face phenol.

Figure 37.15Normal erythema 15 days after full-face phenol.

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is more visible than with a full-face peel, where the demar-cation line is in less visible areas. It is essential to warn thepatient of the need to wear camouflage make-up. Persis-tent, localized erythema in the treated area means that com-plications are likely and should be closely monitored.Figure 32.17 shows erythema of the whole area treated withphenol. This is not a dangerous, ‘localized’ erythema.

PreventionThe basic rule is ‘the deeper the peel, the more severe andlonger-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 ery-thema (e.g. tretinoin).

� Avoid secondary infections and skincare products thatare too aggressive. Beware of ‘scrubs’ used too soonafter a peel. Some patients cannot tolerate flaking, andtry to pull off the strips of flaking skin. Others try to getrid of the ‘dead skin’ with abrasive creams. In bothcases, the skin can be damaged and localized erythemaor hyperpigmentation can occur. With Easy TCA®(pinpoint frosting), there may be some light exfoliationbefore the end of the first week after the peel.

� Do not repeat peels more often than necessary, and waitfor the erythema from the previous peel to subsidebefore applying the next peel.

� Apply the peel evenly, using a stable and homogenizedformulation.

� Avoid peeling techniques that do not allow monitoringof 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, makesure that they have done so regularly and evenly.

AHAs: erythema preventionThe practitioner should monitor the whole peel procedureclosely and carefully and make sure that the acid is neutral-ized at the right time (except for Easy Phytic®, which doesnot require neutralization). Any frosting will result in pro-longed erythema. The neutralizing solution should be pre-pared before the start of the peel.


Figure 37.16Normal erythema 15 days after localized phenol (Lip &Eyelid® formula). Rest of the face treated with Unideep®.

Figure 37.17Normal erythema 7 days after Lip & Eyelid® around themouth and chin. The whiteness comes from an application ofantioxidant cream and the shine from Vaseline®. The rest ofthe face has been treated with Unideep® (TCA peel to thepapillary dermis)

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TCA: erythema preventionTCA–SASThe peel should not be applied more often than thepatient’s skin can tolerate it. After a peel to the papillarydermis, erythema cannot be avoided. Flaking should not beforced prematurely by pulling off strips of flaking skin. Onthe 8th or 10th day after a peel to the papillary dermis, per-sistent erythema and/or slightly infected areas without anytrace of flaking suggest that the skin has been pulled off orthat the patient has been scratching, sometimes completelyunconsciously at night. A TCA–SAS peel can be repeatedafter 4–6 weeks at the earliest, once the erythema has com-pletely disappeared. Effective sun protection is essential.

Easy TCAThe very light erythema that follows Easy TCA® disappearsvery rapidly. It is the only peel where it is not strictly for-bidden to help flaking along. Bleeding should, of course, beavoided, as this would trigger erythema. The erythemasoon subsides and does not cause any adverse sequelaeunless there is a secondary infection. The maximum fre-quency for repeating the basic protocol (pinpoint frosting)is four peels at 5-day intervals. The ideal frequency is fourpeels at 8-day intervals. Effective sun protection is essential.

Only Touch®Local erythema is inevitable after a peel to the reticular der-mis. Pulling off scabs must be avoided at all costs. OnlyTouch® can be combined with Easy TCA® to reduce ery-thema and hyperpigmentation. The maximum frequencyfor repeating the peel is when the erythema has completelydisappeared. Effective sun protection is essential.

Unideep®Erythema clears up rapidly after this peel to the papillarydermis – usually within 8 days. The maximum frequencyfor repeating the peel is 3–4 weeks and once the erythemahas completely cleared. Effective sun protection is essential.

Phenol–ResorcinolErythema is inevitable after a phenol peel (Figure 37.18). Itcan sometimes be less severe and of a shorter duration if a cor-ticosteroid is injected intravenously at the beginning of thepeel. Its intensity varies from patient to patient, from light andimperceptible to severe and deep. Resorcinol is a potentiallyallergenic phenol derivative: persistent, pruritic erythemaafter a resorcinol peel might be a sign of contact dermatitis.

Treating erythemaErythema has a natural tendency to resolve spontaneouslywithout treatment. The patient should be told to see thedoctor if there is any abnormal, localized and persistent

erythema. A peel can reveal a subclinical condition ofeczema or lupus. Clinical examination and close question-ing of the patient is of prime importance to bring theseproblems to light before treatment.

Treat until complete resolutionPersistent, localized erythema means that there is a risk ofhyperpigmentation or scarring. Erythema can be extremelyunpleasant for patients, and they might ask for a treatmentto get rid of it more quickly. Localized erythema requirestopical treatment, and erythema in the whole treated arearequires systemic treatment.

Recommended treatmentsTopical cosmeticsEffective sun protection is always indicated with erythema,as it tends to develop into hyperpigmentation after UVexposure. Antioxidant creams can limit the negative effectsof 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 EasyTCA® post-peel mask provides effective protection againsterythema.

Local corticosteroidsTreatment consists in prescribing a cream containingsteroid anti-inflammatories. The sooner treatment isstarted, the more effective it is with low-dose products. Iftreatment is delayed, higher doses of fluoro-corticosteroidshave to be used, and the results are less satisfactory. A(2.5%) hydrocortisone cream or a topical clobetasone


Figure 37.18Normal, localized erythema 8 days after Lip & Eyelid® on theupper lip and Unideep® on the rest of the face. Note the lighterythema from the Unideep® on the 8th day.

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cream applied three or four times a day for 2 weeks shouldbe sufficient. If treatment is started later still, fluocinoloneor halcinonide must be prescribed. Some authors recom-mend preventive application of a cortisone cream immedi-ately after a peel, although these creams do not help skinregeneration and penetrate far more readily and rapidlythrough skin that is far more permeable. Applying a corti-costeroid during the first week after a peel does not pose anyproblems. On the other hand, excessive use of cortico-steroids increases the risk of acne and bacterial, viral andfungal infections, and can cause telangiectasia. What ismore, long-term use of topical corticosteroids thins theskin, causing atrophy that defeats the purpose of a peel. Incases of indurated erythema likely to lead to scarring, corti-costeroids can be repeatedly injected locally into the ery-thema, and the lesion can be covered with a silicone sheetpressure dressing, day and night, until the lesion disappears.

General treatmentsCorticosteroids by the systemic route will only be neededvery rarely to treat erythema. They can be administered ina single and preventive injection at the start of a phenolpeel. Promethazine can be recommended, at a maximumdose of six times 25 mg/day, when the erythema causespruritus and reflex scratching that could lead to unsightlyscars, infections or dyschromia.

LasersRubin describes using the Candela pulsed dye laser to goodeffect to reduce persistent erythema. Intense pulsed lightcan also be used to treat post-peel erythema.

TelangiectasiasTelangiectasias result from vasodilation and a proliferationof dermal blood vessels. There are many different causes:sun aging, hormone therapy, inflammatory dermatosis,corticosteroids, alcohol, etc.

AHAsThese do not usually have any effect on telangiectasias anddo not cause neovascularization.

TCAIn the month following a TCA peel to the papillary dermis,pre-existing telangiectasias can be seen more clearlythrough the relatively transparent epidermis because of thetemporary loss of thickness and pigmentation. It is rare fornew telangiectasias to develop, and this does not often posea problem after a peel, even a deep one.

The doctor can coagulate the telangiectasias immediatelybefore applying an Easy TCA® peel (Figures 37.19 and37.20). The fact that the solution will penetrate into the smallholes left after coagulating the blood vessels does not causeany complications. On the contrary, this prevents the usualscabs that form after the coagulation of telangiectasias andthat can last up to 2 weeks. The duration of scabbing is morethan halved and there is less risk of secondary infection.

PhenolPhenol can improve the appearance of very fine, superficialtelangiectasias through coagulation. Deeper telangiectasias


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), anapplication of Only Touch® to the lentigines and finally an application of Easy TCA® to the whole face. Coagulation and OnlyTouch® will be repeated just before the fourth session of Easy TCA®. (b) Results of these combined treatments. The lack ofnasolabial folds in (a) comes from the patient’s position.

A B

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may be pushed deeper into the skin by the synthesis of newcollagen in the upper part of the dermis, and will be less vis-ible. On the other hand, inflammatory vasodilation canalso aggravate them. The patient should be warned thattelangiectasias are not in themselves an indication for a peeland that results vary. The doctor should be wary of raisedtelangiectasias that are difficult to hide. There are reportedcases of deep peels being performed despite the presence oftelangiectasias, which remain unchanged by the peel, but aphenol peel can also cause numerous small telangiectasiasto appear during the first weeks after the peel. These telang-iectasias must be treated to stop them turning into hyper-pigmented marks.

PreventionThe type of peel must be carefully chosen. These vasculardilations must be treated preventively as indicated above(see Figure 37.20).

TreatmentThis can involve electrocoagulation, Surgitron® (Ell-man),15 scarification, microsclerosis, laser or flashlamp.These treatments should be carried out 1–2 weeks beforethe peel. The one exception is Easy TCA®, where thetelangiectasias can be treated immediately (a few minutes)before the peel solution is applied.

Scarring and dyschromia

Intraepidermal peel (Figure 37.21)An intraepidermal peel is characterized by the followingsymptoms: erythema without frosting after an AHA peelor erythema and maybe some pinpoint frosting after aTCA peel. Phenol is not indicated for this depth ofaction.


Figure 37.20(a) Telangiectasia on the tip of the nose, treated by coagulation with a Kobayashi needle mounted on the handpiece of an Ellmanunit (radiofrequency). Immediately after coagulation, Easy TCA® solution is applied. (b) When it is dry, the post-peel cream isapplied. (c) The almost total lack of scabbing on the fourth day after the combined treatment.

A B C

Figure 37.21Intraepidermal peel.

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Risk of scarringThis is non-existent. Re-epithelialization after an intraepi-dermal peel is rapid and easy, as it comes from growthstimulation in the still intact basal layer of the epidermis.The epidermis ‘feels’ the loss of the stratum corneum as adangerous attack and reacts by sending a clear growth mes-sage to the ‘mother’ keratinocytes in the basal layer. Thesekeratinocytes divide16 and rebuild a normal epidermis asquickly as possible. A local increase in the concentration oftumor necrosis factor alpha (TNF-α) stimulates the ker-atinocytes to transform themselves into corneocytes andrestore the skin’s initial state of impermeability. The stra-tum corneum is largely responsible for the skin’s totalimpermeability (maybe >70%). This relative impermeabil-ity not only affects the fluids coming in and going out, butalso fungal, bacterial or viral invasion. The constant shed-ding of dead cells from the stratum corneum is in itself aphenomenon of great importance to homeostasis: it getsrid of epidermal garbage and a large quantity of xenobioticmicroorganisms.

Risk of dyschromiaIntraepidermal peels do not stimulate melanocytes andnever cause achromia. There is no risk of skin discol-oration. However, some sensitive skins react to any inflam-mation by stimulating melanogenesis. The risk of post-peelhyperpigmentation cannot therefore be ruled out com-pletely.17

Peel to the basal layerA peel to the basal layer (Figure 37.22) is characterized byerythema and the appearance of pinpoint frosting afterTCA or generalized erythema after AHAs. Phenol is notindicated for this depth of peel.

The acids destroy most of the epidermis. Histologically,the basal layer does not form the perfect sine wave that isusually shown in diagrams. On the contrary, the ker-atinocytes are embedded deeply and unevenly in the der-mis and form the deep ‘dermal papillae’.

Even if the acid reaches the papillary dermis in places, alarge number of keratinocytes survive, allowing the skin toregenerate very quickly. The process of re-epithelializationis the same as for intraepidermal peels: the basal layer ker-atinocytes are stimulated to grow.

Risk of scarringThis is non-existent. The skin can easily repair itself with-out having to rely on stimulation of the myofibroblast sys-tem to contract an area that is taking too long to heal.

Risk of dyschromiaThere is no risk of achromia. Melanocytes are stimulatedmore directly, and the risk of hyperpigmentation is higher.The inflammatory reaction that follows any peel to thebasal layer can cause post-inflammatory hyperpigmenta-tion, even if it is slight. A vicious circle can set in that hasthe potential to cause post-peel pigmented marks: the peelcauses inflammation – that is, among other things, vasodi-lation that brings oxygen as well as pro-inflammatory sub-stances to the treated areas. Free radicals are formed thatdamage the structures regenerating the skin. The structuraldamage maintains inflammation, and post-peel hyperpig-mentation may occur on dark and reactive skins. It isimportant to break this vicious inflammatory circle byscavenging free radicals as soon as they are produced. Largequantities 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 (Figure37.23)The Grenz zone19 is a transition area between the epidermisand the dermis. A TCA peel to the Grenz zone is characterizedby the appearance of cloudy-white frosting in which spots ofnormal skin color can be seen where the keratinocytes of thedeepest dermal papillae have not been coagulated by the acid.AHA and phenol peels are not appropriate for this depth, andTCA is ideal for a peel to the Grenz zone. The process of skinrepair is slightly more complex, and relies both on the manysurviving keratinocytes being stimulated to divide and thekeratinocyte reserve in the pilosebaceous units.

Risk of scarringThe keratinocyte reserves allow rapid and easy regenera-tion of the epidermis. The retractile myofibroblast systemis not stimulated. There is no risk of scarring.


Figure 37.22Peel to the basal layer.

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Risk of dyschromiaThe skin becomes lighter simply because of the epidermalmelanin stock being eliminated. Enough melanocytes sur-vive for the skin not to lose its natural color permanently.There are substantial reserves of melanocytes in the pilose-baceous units. Hypochromia is therefore rare after a peel tothe Grenz zone, and there is no reason why achromiashould occur. On the contrary, melanocyte stimulation isrelatively strong and the risk of hyperpigmentation isincreased. With this kind of peel, the preventive measuresdescribed in the section on hyperpigmentation later in thischapter should be heeded.20

Peel to the papillary dermis(Figure 37.24)AHAs and phenol are not indicated, and TCA is again thegold-standard peel to the papillary dermis. The followingsigns show that the papillary dermis has been reached:

even, pink–white frosting and epidermal sliding sign. Re-epithelialization after a peel to the papillary dermis isslower as it relies on:

� 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 sparedby 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 differ-

entiated keratinocytes that specialize in sebum produc-tion; they must first dedifferentiate before they canregenerate the epidermis

Risk of scarringThe papillary fibroblasts are stimulated directly.22 They willproduce a layer of collagen that can differentiate histologi-cally from the collagen that is naturally present in the pap-illary dermis. The fibrils of the new collagen are alignedhorizontally. This more complex process of skin regenera-tion can give rise to more complications than more super-ficial peels.

In principle, only the fibroblasts in the papillary dermisare stimulated, and an effective keratinocyte layer can beregenerated quickly enough to avoid activation of themyofibroblast system and scar retraction. Only overpeelingcan cause localized scarring. A peel to the papillary dermisis still very safe as far as scarring is concerned.

Risk of dyschromiaA peel to the papillary dermis causes severe inflammationand strongly stimulates melanogenesis, often irregularly,with a risk of post-inflammatory hyperpigmentation. Pre-ventive treatment of this is one of the most importantphases in a peel to the papillary dermis. Areas of achromiamay also appear when the peel has penetrated too farlocally.

A peel to the papillary dermis therefore marks the safetylimit beyond which the risks are higher, though most oftencontrollable. How far this limit can be stretched depends –among other things – on how permeable the skin is: in localareas of increased permeability, the TCA can penetrate toodeeply.

Peel to the reticular dermis(Figure 37.25)Phenol is the ideal agent for a peel to the reticular dermis.The following signs indicate that the peel has reached thereticular dermis: even, pure white or gray–white frosting.


Figure 37.23Peel to the Grenz zone.

Figure 37.24Peel to the papillary dermis.

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Occasionally, small, buff-yellow patches may appear. Epi-dermal sliding is soon replaced by edema.

Skin repair after a peel to the reticular dermis is slower, asall the basal layer keratinocytes have been destroyed and theskin can only rely on the differentiated keratinocytes of thepilosebaceous units and the intradermal excretory ducts ofthe sweat glands. To repair the dermis, the sebocytes in thepilosebaceous units must dedifferentiate, and horizontalgrowth is required to ‘close’ the skin quickly. Next comes aphase of vertical growth whose purpose is to regenerate aphysiologically sound epidermis that will maintain home-ostasis and restore the vital barrier function after the ker-atinocytes have differentiated into corneocytes.

Risk of scarringUnder ideal conditions, healing after a peel should be sup-ple and constant, leaving skin that is rejuvenated, hydrated,even in texture and without scars. The risk of scarring ismuch higher after a peel to the reticular dermis than after apeel to the papillary dermis. Delayed healing, resultingfrom excessive local penetration or local infection, stronglystimulates all of the skin’s regeneration mechanisms; theycan trigger the phenotypic conversion of simple fibroblastsinto myofibroblasts and start retractile-type healing. Par-ticular attention must be paid to scar prevention measures(see later in this chapter).

Risk of dyschromiaThere is a major risk. Achromia is possible.

Difference between a facial peeland a body peelIt is conventionally accepted that post-peel regeneration onthe body takes twice as long as on the face. With peels to the

papillary dermis, and especially the reticular dermis, it isimportant to consider the number of pilosebaceous units.The more pilosebaceous units there are, the greater thechances of healing without major problems (Figure 37.26).It is easier for the skin to heal on the scalp than on the faceand easier on the face, than on the neck or décolletage.

Rapid skin regeneration means that there is little chanceof infection and retractile scar formation. Slow and diffi-cult regeneration sharply increases the risk of retractilescars, infection and dyschromia.

HyperpigmentationGeneral considerationsThe skin responds to any lesion, burn or abrasion with aninflammatory reaction that may be accompanied bymelanocyte stimulation and excessive melanin production.This reaction is generally considered to last for 3 months atthe most.

Different types of pigmentation disorders can occurafter a peel:

� partial or total depigmentation (see melanocyte toxic-ity).

� local or general hypopigmentation (see melanocyte tox-icity).

� local or general, absolute or relative hyperpigmenta-tion.


Figure 37.25Peel to the reticular dermis.

Figure 37.26(a, b) Papillary dermis on body skin: only few pilosebaceousunits are able to regenerate the destroyed layers of skin.Healing is slow and risk is higher.

A

B

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Fitzpatrick skin phototypes I to III rarely develop post-inflammatory hyperpigmentation (PIH), whereas skinphototypes IV to V carry a much higher risk. PIH can be‘absolute’ or ‘relative’ to the surrounding skin. RelativePIH occurs when some areas of skin do not lighten as muchas the surrounding areas and therefore appear darker. Anarea of normal skin color surrounded by an area of a lightertone can look like PIH. Absolute PIH consists of a patch ofskin that is hyperpigmented in relation to the normal skincolor that surrounds it. Figure 37.27 shows an absolute PIHreaction.

Risk depending on peel typeOn the whole, the risk of PIH is proportional to the depthof the peel.

AHAsThe risk of hyperpigmentation is low, and often resultsfrom localized overpeeling or delayed neutralization thatleads to excessive penetration and possibly epidermolysis.There is still a risk of PIH, however, even if the peel hasbeen neutralized correctly (Figure 37.28).

TCA–SASAs the risk increases with the skin phototype, it is obviousthat a patient with Fitzpatrick skin type III will have fewerpigmentary changes than a patient with Fitzpatrick type V.Skin type V most often develops hyperpigmentation. That


Figure 37.27Post-inflammatory hyperpigmentation (PIH): TCA peel,aqueous solution with uneven penetration to the papillarydermis.

Figure 37.28PIH after a peel with 70% unbuffered glycolic acid; neutralization with a sodium bicarbonate solution as soon as erythemaappeared. There is no visible frosting. Postoperative developments were normal. On the 8th day, the patient consulted the doctorabout the appearance of PIH 3 days before (a). Treatment consisted of tyrosinase inhibitors, topical antioxidants, sun avoidanceand protection. (b) The patient after 5 weeks. (c) After 8 weeks. The hyperpigmentation has improved significantly. A telephonecall revealed that the problem has cleared up completely after 3 months.

A B C

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is why some authors maintain that TCA cannot be used totreat hyperpigmentation, whereas in fact it produces excel-lent results when used correctly and as part of an overalltreatment program for the patient, possibly includingrepeated peels and the use of appropriate topical treat-ments between and after the TCA peels. Patients withdyschromia always require an overall treatment program,not matter which type of peel is used. TCA in aqueous solu-tion is nevertheless a molecule that carries a higher risk ofPIH (see Figure 37.27). Many publications stress theabsolute necessity to prime the skin for an application ofTCA in aqueous solution. Any peel of this type requires 3–4weeks of preparation, with tretinoin (to speed up recoveryand even out penetration) and hydroquinone (to inducemelanocyte sedation).

Easy TCA®One of the four weekly peels sometimes causes transientand limited PIH (Figure 37.29), often on the sides of theface, and mainly occurs when the patient has not usedeffective sun protection from the morning after the firsttreatment. This PIH is easily reversible, erased by the fol-lowing treatment, and can be avoided with good applica-

tion techniques: the cotton bud should be partiallysqueezed out before applying the solution and only thebeginnings of pinpoint frosting should be achieved. Thedeeper Easy TCA® is allowed to penetrate, the greater is therisk of hyperpigmentation: pinpoint frosting is far lesslikely to trigger PIH than even, pink frosting. Repeating thepeel 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®Applying Only Touch® peel too deeply can cause pro-longed punctiform erythema that has a strong tendency tocause hyperpigmentation when exposed to daylight. Thecontact time between the applicator and the skin must bebrief – the equivalent of the contact time between the fin-gers and a phone keypad (Figure 37.30).

If an application of Only Touch® is followed by pro-longed, punctiform erythema, treatment consists in avoid-ing pulling off the small scabs, effective sun protection ofthe whole face and sun avoidance, applying a cortisonecream locally, applying an antioxidant cream and tyrosi-nase-inhibitors on the whole face and close monitoring.

Heavy-handed application of Only Touch® triggers ede-matous and hard gray–white frosting that, on palpation,feels frozen, as if with dry ice. This type of reaction is a signthat scarring is likely.

Phenol in alcohol solutionManquat23 relates the following: ‘Hayem tried phenic acidas a counterirritant. A brush is dipped in a solution of 9parts crystallized phenic acid [phenol] to 1 part 90% alco-hol and is painted on evenly and without letting the solu-tion run. After these applications, the skin often becomespigmented and retains the burn marks indefinitely.’

As a result of the almost immediate formation of animpenetrable protein coagulum, solutions with a high con-centration of phenol (88%) that are ‘untamed’, asdescribed above, do not penetrate deeply enough tobecome fully toxic to melanocytes, and the skin becomeshyperpigmented in reaction to the chemical burn.

Baker–Gordon and Litton formulasLitton7 reported that 67% of practitioners who answeredhis questionnaire have had to deal with pigmentation dis-orders. It should not be concluded from this that 67% ofpatients have problems with dyschromia, but that 67% ofpractitioners have come across it at least once, which is dif-ferent. What is more, it is surprising that not all the practi-tioners questioned have been confronted with it at onetime or other. Melanocyte toxicity appears to be more fre-quent than PIH with these formulas.


Figure 37.29Transient local PIH after the first Easy TCA® peel. The secondpeel will erase this pigmentation. Combine with BlendingBleaching® and Melablock HSP®.

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A C

Figure 37.30(a) Lentigines before Only Touch®. (b) Only Touch® applied too deeply: frosting has turned buff yellow. The contact time betweenthe applicator and the skin was too long. (c) Prolonged erythema (6 weeks), abnormal after Only Touch®: the contact timebetween the applicator and the skin was too long. (d) Three months after treatment: almost complete resolution of erythematousspots and no PIH. Lentigines have gone.

B D

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Oily formulasThese formulas (e.g. Lip & Eyelid®) seem to cause hyper-pigmentation disorders rather than melanocyte toxicity,which is a good thing, as it is easier to treat PIH, and depig-mentation is not readily reversible. Post-peel cosmeceuticalcare is therefore extremely important. Hyperpigmentaryreactions often go hand in hand with inadequate results(Figure 37.31) and this particular combination means thatthe peel solution did not penetrate far enough (see the sec-

tion above on inadequate results). PIH resulting from anapplication of phenol is readily treated with Easy TCA®and tyrosinase-inhibiting creams.

PreventionProper patient selectionSensitivity testIf there is a personal history of PIH, a sensitivity test could becarried out on a hidden area. It is worth bearing in mind thatif the test is negative, patients will be convinced that they aresafe from complications and it is far more likely that any prob-lem that might arise will be put down to the practitioner’s pre-sumed incompetence rather than any particular skinsensitivity. Different areas of the face do not react to peels inthe same way: a patch test behind the ear does not really sayanything about how the area around the mouth will react.Sensitivity tests should therefore be seen more as a means ofdissuading a patient who is likely to have complications ratherthan a means of preparing for any potential problems. Apatient with a pigmentary reaction to a test should be ruledout for treatment with medium or deep peels and be orientedtowards a peel that causes less melanocyte stimulation.

Genetic factorsThe capacity to develop PIH is largely dependent ongenetic factors. Patients who suffer from pigmentarychanges after a peel often develop hyperpigmentation frominsect bites or small operative scars, and it is worth ques-tioning patients before starting treatment.

Skin phototypeThe risk of pigmentary changes increases with the skinphototype: as a general rule, Fitzpatrick skin types I to IIIdevelop little or no hyperpigmentation and are thereforeexcellent candidates for deep peels. The lighter and moreeven the complexion, the fewer problems there will be withpigmentary changes. The darker the skin, the greater is therisk of pigmentary changes. Phototypes IV to V rapidlydevelop hyperpigmentation after any inflammation, evenwithout sun exposure. A medium-depth peel (to the papil-lary dermis) on a dark skin phototype should always bepreceded by skin preparation. These treatments will notstop all PIH, however. It is therefore wise only to performless aggressive peels on patients with a dark skin type. Asianskins and patients whose genotype does not correspond tophenotype24 are more susceptible to PIH.

Preparing the skinPrevention of infectionsIf there is any history, no matter how transient, of herpes,valaciclovir should be prescribed (two times 500 mg/daybefore and after the peel). In principle, herpes outbreaks do


Figure 37.31Unexpected pigmentary change after a full-face phenol peel.Note also the inadequate results.

Box 37.1

Not counting the importance of skin preparation, theadjuvants used, technical errors and preventive post-peel care and treatment, the risk of pigmentarychanges can be quantified diagrammatically as fol-lows: Phenol < TCA > AHA > Easy TCA®

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not leave scars, but they can sometimes leave some local-ized pigmentation for months or even years. To avoid sec-ondary infections, medium or deep peels should not beperformed during infectious outbreaks of acne.25

Cleansing and degreasing the skinIf the skin is not cleansed and degreased evenly or notproperly prepared before a TCA–SAS peel, the acid canpenetrate unevenly and PIH may occur. Organic matterinactivates the acids,26 and the presence of lipids or surfacedebris can alter the depth of penetration. Easy TCA® solu-tion was designed not to be affected by the presence of thissurface organic debris. It is a saponified solution of TCAthat is applied without prior degreasing and cleansing.

Over-cleansing should be avoided: the skin must not bemechanically abraded when disinfecting and degreasing;the stratum corneum must not be destroyed by overenthu-siastic wiping.27 This manual abrasion would be unevenand create areas of deeper penetration, increasing the riskof scarring and pigmentation.

The pressure applied when cleaning the skin should befirm and above all even.

Even application of the peelAHAsAHAs must be applied quickly, since if they are appliedslowly, the areas treated first should also be the first areas tobe neutralized. Partial and gradual neutralization is diffi-cult and a source of errors. AHAs should therefore beapplied as quickly as possible, starting with the most resis-tant areas, such as the forehead. If the acid is appliedquickly, all areas can be considered to have had almostexactly the same contact time and the whole face can beneutralized at one go. The whole treatment area should bemonitored extremely closely to make sure that the peel isneutralized as quickly as possible if it is about to penetratetoo deeply in any specific area.

TCA–SASThe more force applied on the applicator, the more deeplywill the TCA penetrate. Applying TCA with a brush gives amore superficial peel than applying the same concentrationwith a gauze pad. The number of coats must be the same allover: the depth of the peel increases with the successive num-ber 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 intoaccount: with the same number of coats, a more highlyconcentrated TCA will give a deeper peel. It is important towatch out for any teardrops that may dilute the TCA andits action. Tear tracks on the cheeks can leave a line of moresuperficial penetration. Tears can also carry TCA onto theneck, where it can produce an unwanted linear peeltogether with PIH.

EasyTCA®The ease of application and weekly repetition of this peelguarantee 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®, seeabove and Chapter 22.

PhenolPhenol must be applied evenly. The depth of the peeldepends on the number of coats and the type of solutionused. Chapter 34 describes in detail the application meth-ods needed to get an even result. It is extremely importantto follow the application methods for each particular for-mula carefully. In all cases, any occlusive mask must beeven and not form ‘bubbles’ or areas of pressure. Any tearscould carry phenol onto the neck (linear peel and increasedprobability of PIH).

Sun avoidance and protectionThe sun is not the only cause of post-peel hyperchromia.Rubin14 describes coming across cases of hyperpigmenta-tion where there has been no sun exposure. For moreinformation on sun protection, see Chapter 3.

Some medicines can causepigmentationThese include estrogens, and progestins (including oralcontraceptives), phenothiazines, thyroid hormones andphotosensitizers, among others.

Close monitoring Pigmentation disorders (as well as scars) are often pre-ceded by persistent localized erythema that must be treatedas quickly as possible (see above). Once again, the patientshould have an overall treatment program. The patient


Figure 37.32Pseudo-hyperpigmentation of the forehead: photograph takenon 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. Thepractitioner is not being asked for a treatment but for aresult, especially one that does not damage the skin.Patients should be seen as often as required. Generally, thedeeper the peel, the more frequent the checkups should be.A phenol peel, for example, requires daily monitoring forthe first 8–10 days after treatment. Over the first few daysafter a TCA peel to the basal layer of the epidermis or theGrenz zone, a pseudo-pigmentary change can be seen toappear (Figure 37.32) that actually results from dehydra-tion of the epidermal layers where melanin is found. Acidsbind readily with water molecules and dehydrate the skin.The melanin granules are brought closer together and theskin appears darker in places.28 It is not possible for a gen-uine pigmentary change to set in within 2 or 3 days.

Prevention through re-peelingTCA–SASFouque and Seban29 limit pigmentary changes by automat-ically applying an AHA peel after a TCA in aqueous solu-tion. Although AHAs are not toxic to melanocytes, thesesuperficial peels can – partially or completely – put a stopto any pigmentary changes that are common between the2nd and 4th week following a TCA peel in aqueous solu-tion, especially in countries with very sunny climates. Theprotocol includes three phases:

� First phase: the patient applies a depigmenting creamfor 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 sen-sitivity.

� Third phase: the following week a 70% unbuffered peelis applied for 1 minute, then neutralized.

As soon as the condition of the skin permits, a peel to thebasal layer of the epidermis can be envisaged to reduce thequantity of intraepidermal melanin and improve the pene-tration and action of depigmenting agents. Any additionalinflammation must, of course, be avoided, as this wouldcreate a second wave of hyperpigmentation. I use only EasyTCA® to treat pigmentary changes: application of the peelsolution to the start of pinpoint frosting and application ofthe post-peel mask cream, whose main properties areantioxidant, tyrosinase-inhibiting and anti-inflammatory.

Easy TCA®

If there should be a pigmentary change after one session ofEasy TCA®, the next session will ‘stop it in its tracks’ andtreat it.

PregnancyCortez30 relates that if a patient falls pregnant in the firstfew months after a phenol peel, dyschromia disorders may

occur. Pregnancy is contraindicated in the months follow-ing a deep peel, especially in patients with a high risk of pig-mentary changes.

TreatmentIf prevention fails, treatment must follow. The more super-ficial the pigmentation, the better will it respond to treat-ment. If the hyperpigmentation originates in the dermis, itwill not respond as well to treatment. It is often necessaryto treat the actual inflammation that is maintaining thepigmentation.

Examining the skin under a Wood’s lamp (354 nm) –also called ‘black light’ – can help determine the depth ofthe lesions. The more pigmented the skin appears in theWood’s light, the more superficial is the pigmentation. Theangle of the light should be varied to improve the visualaccuracy of the diagnosis. Skin that looks washed out by theWood’s light will not respond well to depigmenting treat-ment.31

Whatever the case may be, my first choice of treatmentfor epidermal or dermal post-peel PIH is always four ses-sions of Easy TCA® to the basal layer (pinpoint frosting) incombination with Blending Bleaching® cream. Results canoften be seen after the first re-peel.

Topical depigmenting agentsMonobenzoneMonobenzone (Figure 37.33), also known as monobenzylhydroquinone, benoquin and hydroquinone monobenzylether, has a molecular weight of 200.27 and is a stable chem-ical compound under normal conditions. It is not a newdepigmenting molecule: the Journal of the American Med-ical Association published an article about it in 1956.Monobenzone is used to completely inhibit the productionof melanin from tyrosine, mainly in certain severe cases ofvitiligo. However, it is rare to resort to this rather extremetreatment. Doctors are, in fact, more willing to use tech-niques for repigmenting areas of vitiligo than techniques forcomplete depigmentation of normally pigmented areas.33


HO

O

Figure 37.33Monobenzone.

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Monobenzone34 should only be applied after attempts atrepigmentation have failed and when the vitiligo makessocial life difficult. Patients with severe vitiligo are happy tobe one color again. However, the cosmetic risks are high:the skin becomes completely white, burns in the sun, andany hope of normal repigmentation, if for example a curefor vitiligo were discovered, vanishes as soon as monoben-zone is applied. This product should never be used a simplewhitening agent, at any concentration.

In any event, complete depigmentation usually onlydevelops after 6 months to 4 years, with three daily applica-tions, and the depigmentation protocol, which is very precise,is full of pitfalls.35 The patient must also be aware that therecan be permanent and complete depigmentation in areasother than those being treated; the hair can go gray, but theeyes do not change color. Nevertheless, 11 out of 15 vitiligopatients treated with monobenzone developed conjunctivalmelanosis; and one patient had a line of corneal pigmentdeposit in each eye after one year of monobenzone.36

Monobenzone can cause contact allergies37 that, oddlyenough, occur mainly on areas of normal color skin andvery rarely on the vitiligo patches. Fifteen per cent ofpatients develop skin rashes. Sun protection must be wornpermanently, as the skin loses all its melanin protection.

Depigmentation does not occur systematically, andsome patients who respond well at first do less well later on.Others regain pigmentation in patches over the summermonths. A few rare vitiligo patients repigment, sometimesfairly evenly, without the underlying mechanism beingunderstood, when monobenzone is stopped and they nolonger need to depigment.

Nevertheless, there are still some monobenzone depig-menting creams on the market: they have low concentra-tions of monobenzone (around 1.5%). Nevertheless, somehighly concentrated means at 20% can be found on themarket. When applied to the hands, there have been casesof permanent, confetti-like depigmentation that has spreadto the forearms.38

Monobenzone is therefore not indicated in the treat-ment of freckles, melasma, age spots, PIH and otherdyschromias, apart from cases of severe vitiligo that resistsattempts at repigmentation.

Other topical depigmenting agentsConventional topical depigmenting agents (hydroquinone,kojic acid, Morus alba, arbutin, azelaic acid, lactic acid, etc.)do not destroy the melanin in the skin, but inhibit tyrosi-nase and the oxidative stages of the chemical reactions thatturn tyrosine (Figure 37.34) into indole groups during thefirst stages of melanogenesis. AHAs, retinoic acid, salicylicacid, etc. increase flaking and eliminate the intraepidermalmelanin stock more quickly. Corticosteroids and non-steroidal anti-inflammatory agents combat inflammation.

Topical depigmenting agents cannot be expected to pro-duce rapid results: the active products have to penetrate the

skin and change the metabolism of the melanocytes, reduc-ing melanogenesis or changing the quality of the melanin.29

A completely new epidermis then has to be built from cellgrowth in the basal layer, which takes 4–6 weeks. Depig-mentation is therefore gradual, and topical depigmentingagents are often combined with products that accelerateepidermal flaking.

HydroquinoneHydroquinone is closely related to phenol and can reducemelanin production. It appears that it can also degrademelanosomes. It has a tyrosinase-inhibiting activity andcan change the membrane structure of the intracellularorganelles of melanocytes. Hydroquinone acts mostly onthe first stages of melanin synthesis. Its action is thereforegradual, like any tyrosinase inhibitor.

Is it worth using preventively? Applying hydroquinonecreams during the weeks before a peel reduces melanin syn-thesis, and the patient will slowly see a certain improvementin the hyperpigmentation, depending on how long and howpotent the treatment is. However, it is not certain that thepreventive application of hydroquinone before a peel canreduce the reactive potential of melanocytes during inflam-mation. I never apply hydroquinone before a peel for twomain reasons: firstly because of the problems associatedwith hydroquinone itself, which we shall consider below,and secondly because of its low anti-inflammatory poten-tial. On the other hand, it can be advantageous using hydro-quinone after a peel to inhibit melanin synthesis. It shouldbe applied as soon as possible after the peel: during the re-epithelialization stage. It can therefore be applied immedi-ately after a glycolic acid peel or Easy Phytic® solution,40 5–7days after a peel to the papillary dermis41 and 8–10 days aftera peel to the reticular dermis. The concentration normallyused is between 2% and 6%. It should be noted that Euro-pean legislation limited hydroquinone to 2% in cosmeticproducts for many years and finally banned it altogether.Concentrations of less than 4% hydroquinone are less effec-tive. Concentrations higher than 4% are more effective butalso more irritating.


OH

COOH

NH2

Figure 37.34Tyrosine. Note the resemblance to the usual tyrosinaseinhibitors.

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It takes several months to achieve an acceptable clinicalresult when hydroquinone is used as monotherapy, butabnormal epidermal and dermal pigmentation can even-tually be reduced. There are reports in the literature thathydroquinone has been prescribed in high doses (up to10–15%) to counter dramatic pigmentary changes; atthese doses, it must not be applied for more than 8 daysand a more conventional concentration of 3–5% shouldbe used for the rest of the treatment. The effect is dose-dependent, and it might be concluded that a high concen-tration is always required to get a rapid and clinicallysatisfactory result. However, it is important to bear inmind the problems that have been associated with the useof 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. Ochronosiscan appear even if the patient has not had a peel before-hand. Ochronosis usually appears after concentrationshigher than 4% have been applied, but lower concentra-tions can cause it in patients with Fitzpatrick skin type Vor VI.

� It can cause confetti-like depigmentation.� It is potentially mutagenic.

Hydroquinone has also been combined with other mole-cules to increase its penetration and effectiveness, as in theKligman 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 gtretinoin 0.05%ascorbic acid 0.1 gdexamethasone acetate 0.05 geucerin O/W ad 50 g(or natural unguent La Roche–Posay ad 50 g)in an opaque tube

Other depigmenting formulas can be prescribed:

tretinoin 0.1%hydroquinone 4% ana(+ triamcinolone acetonide to combat inflammation ifdesired)

twice daily until the local problem is resolved.30

Rubin,14 quite rightly, highly recommends the following,less irritating formulation:

glycolic acid 10%hydroquinone 4%

Substituting 0.1% tretinoin with 10% glycolic acid removesan irritant and potentially photosensitizing factor at thesame time as enhancing penetration and therefore theeffectiveness of hydroquinone.

Lower concentrations have been tested successfully.Their synergy means that the concentrations of each activeproduct can be reduced and hence their side effects are alsoreduced. The formula is as follows:14

citric acid 3%lactic acid 3%hydroquinone 2%kojic acid 2%

Many prescription formulas have been developed, combin-ing, for example, vitamin C and indomethacin:

hydroquinone 5%tretinoin 0.025%vitamin C 0.2%dexamethasone acetate 0.01%indomethacin 2%cream O/W ad 30 g

All of these hydroquinone creams are still fairly irritating tothe skin, and many commercial formulations have beendeveloped with new cosmeceutical technologies that arenot available in pharmacies.44

Finally, it should be noted that hydroquinone poses aserious galenical problem, as it tends to oxidize quickly:preparations containing hydroquinone have to be mixedand packaged in an oxygen-free atmosphere (in nitrogen).Preparations packaged in jars oxidize too quickly and losemost of their effectiveness within a few days. The idealpackaging for hydroquinone cream is a hermetically sealed,double-layer, aluminum tube.

Kojic acidKojic 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


OH

O

O

OH

Figure 37.35Kojic acid.

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(through copper chelation and caseinase inhibition). It hasbeen isolated from Aspergillus, Acetobacter and Pencilliumspecies. It has antibacterial properties and reduces the pro-duction of free radicals (iron chelation). It has been usedsince 1988 (Japan) as a bleaching agent, for both the skinand teeth and in the food industry. It also has antisepticand antioxidant properties. Kojic acid is more stable andbetter tolerated than hydroquinone, but prolonged use hascaused contact dermatitis, especially on Asian skin types. Itis usually used in doses 2–4%. It can be combined with gly-colic acid, and enhances the penetration and action of thelatter. 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 bloodconcentrations in thyroid hormones and stimulating thy-roid-stimulating hormone (TSH). As a result, the thyroidgland increases in volume and weight and there is diffusethyroid follicular hypertrophy/hyperplasia.

Azelaic acidAzelaic acid (Figure 37.36), also known as nonanedioicacid, 1-7-heptanedicarboxylic acid, anchoic acid, lepargylicacid and azelainic acid, has a molecular weight of 188.22,which limits its penetration through the skin. Azelaic acidis therefore more effective when it is combined with othermolecules that can enhance its penetration (AHA,retinoids, etc.). It has antibacterial45 properties used in thetreatment of acne or rosacea. At doses of 20% (Skinoren®),azelaic acid has tyrosinase-inhibiting properties46 throughcompetition. Even though its tyrosinase-inhibiting activityis not as strong as that of hydroquinone, it is useful fortreating melasma or PIH. It reduces DNA synthesis inhyperproliferating melanocytes in hyperpigmentation.Unfortunately, it is slow-acting (several months) and haslittle effect on old PIH and on deep, dermal pigmentation.Azelaic acid does not act on normal melanocytes or fibro-blasts and does not cause leukodermia or ochronosis. Testson animals show that azelaic acid is not cytotoxic, muta-genic or teratogenic.47,48

Glabridin, licorice extractGlabridin (Figure 37.37) is the most active depigmentingcomponent of licorice extract. It has an inhibiting action

on melanogenesis, without affecting melanocyte DNA orRNA synthesis. It is therefore not cytotoxic. Glabridin0.5% inhibits erythema and UVB-induced pigmentation. Italso has anti-inflammatory properties through the inhibi-tion of superoxide anion production and throughcyclooxygenase activity.49 It is therefore a good indicationin the treatment of PIH.

ArbutinThe arbutin molecule (Figure 37.38) consists of hydro-quinone labeled to glucose, and is also known as hydro-quinone-β-D-glucopyranoside. It mainly works byinhibiting tyrosinase activity rather than suppressing thesynthesis or expression of this enzyme. Apparently, arbutindoes not hydrolyze to release hydroquinone, which is nottherefore directly responsible for the inhibition of melaninsynthesis.50 Nevertheless, it has not been officially provedto have a strong depigmenting effect, and one study evenshows that applying arbutin can increase pigmentation.51


O OH

OH

O

Figure 37.36Azelaic acid.

O O

H

HO OH

Figure 37.37Glabridin.

OH

O

OH

OHHO

HO

O

Figure 37.38Arbutin.

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4-Hydroxyanisole (4-HA)4-HA is a cytotoxic molecule that inhibits melanogenesis (at2%), but only seems to be effective when combined withtretinoin (at 0.01%). Used alone, it appears not to be active.

Vitamin E (αα-tocopherol)Vitamin E (α-tocopherol: Figure 37.39) is one of the bestantioxidants for cell and organelle membranes. It stabilizesand prevents the destruction of the lipids that make upthese membranes, which are very susceptible to oxidation.It blocks the chain reactions that cause intracellularlipoperoxides to form, thus protecting the nucleic acidsand proteins. It also inhibits the peroxidation of membranearachidonic acid, which prevents the subsequent formationof pro-inflammatory prostaglandins.

Vitamin E has a beneficial antioxidant effect during thepost-peel period. One single molecule of vitamin E protects3000 membrane phospholipids: stabilization of the lyso-some membranes prevents the release of histamine, whichreduces the duration of solar erythema.

Vitamin E has other actions:

� protection of the superoxide dismutase (SOD) enzymethat neutralizes superoxide radicals

� limitation of the formation of links that make the colla-gen protein chains rigid

� limitation of the production of malonedialdehyde,whose action on the glycation of proteins is linked tothe aging process

� acceleration of the healing of burns

Japanese publications report that vitamin E can be usedeffectively in the treatment of facial pigmentation. Itinhibits tyrosinase indirectly by inhibiting its hydroxylaseactivity. It also acts by limiting the oxidative phasesrequired in the first stages of the transformation of tyrosineinto indole derivatives. Vitamin E oxidizes easily, and morestable derivatives than pure α-tocopherol have to be usedin cosmetic preparations. Tocopheryl acetate is one of themore stable derivatives of vitamin E. Tocopheryl ferulate isalso frequently used.

Vitamin A (retinol)It has been proved that vitamin A (retinol: Figure 37.40)and its analogs,52 used in topical applications, enhance skinregeneration by increasing the rate of keratinocyte division.Retinol induces cell differentiation in the basal layer of theepidermis and enhances apoptosis of old cells, which inturn facilitates the regeneration of healthy keratinocytes.Retinol controls cell migration in the skin epithelium; thismigration is an essential stage in skin regeneration. Manydifferent mechanisms of action have been suggested: one isthat the retinol acts as a signal that facilitates the interac-tion of epidermal growth factor (EGF) with the cells of theskin epithelium. Retinol also modulates the transcriptionof certain genes. Many other effects have been attributed toretinol in topical application: it is a hydrating molecule thatincreases the thickness of the epidermis through selectivemultiplication of living keratinocytes at the expense of thekeratinocytes that make up the stratum corneum. Becausethe stratum corneum is thinner, the skin appears softer andmore hydrated. Retinol also prevents the formation ofcomedonal acne by preventing corneocytes from buildingup in the outlets of the pilosebaceous units and formingplugs. Retinol counters post-inflammatory hyperpigmen-tation by accelerating keratinocyte turnover, which helpseliminate epidermal melanin more quickly. Topicalretinoic acid (tretinoin) has a well-known irritant effect,due to the fact that it builds up in places where it does notexist naturally in these concentrations. Pure, encapsulatedretinol in cyclodextrins can be an effective replacement. Infact, pure retinol penetrates more readily than its palmitateor acetate esters. Pure, encapsulated retinol in cyclodextrinreaches the deep layers of the skin in a few hours andarrives at its target without being oxidized. Bearing in mindthe stages of retinoic acid synthesis in the skin, it is clearlyworthwhile to use retinol.

Retinoic acid is synthesized inside keratinocytes. Theretinol is first converted into retinal (retinaldehyde), whichis in turn converted into retinoic acid. Both of these stagesare enzyme-dependent.

Retinoic acid regulates the transcription of genes thatcode for the synthesis of important intracellular proteins.Retinol also induces the expression of the protein thattransports retinoic acid. Retinol encapsulated in cyclodex-trins (Renutriv ACE Lipoic Complex®–SkinTech) hasgreater bioavailability and its antioxidant action is of betterquality.


HO

O

Figure 37.39Vitamin E (α-tocopherol)

OH

Figure 37.40Vitamin A (retinol).

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Vitamin C (L-ascorbic acid)Vitamin C (L-ascorbic acid: Figure 37.41) can limitmelanin production, as it has a tyrosinase-inhibiting andantioxidant activity. Skin cells naturally use ascorbic acid inenergy metabolism and when synthesizing collagen. A defi-ciency in vitamin C is a well-known cause of many disor-ders, including hyperkeratotic folliculitis and delayedwound healing.

Ascorbic acid is unstable in aqueous solution and is notliposoluble. It oxidizes rapidly, losing its protective proper-ties, and more stable derivatives are generally used. Magne-sium ascorbyl phosphate is one of the most stable andhydrophilic vitamin C derivatives. On the surface andinside the skin, it is rapidly converted into vitamin C by aphosphatase enzyme found in abundance both on andinside the skin. Magnesium ascorbyl phosphate is a moreeffective antioxidant and longer lasting than the derivativeascorbyl palmitate, often used in topical preparations. Thisis because the enediol function53 of the second carbon atomof ascorbyl phosphate is protected, while the palmitatederivative has no protection for this area of the molecule,which is responsible for the acid and antioxidant propertiesof vitamin C. Magnesium ascorbyl phosphate can be usedon the most sensitive skins, such as skin that has just bene-fited from a peel. It is readily absorbed by the topical routeand lasts for a long time inside the skin, which gives it a sus-tained tyrosinase-inhibiting action and therefore a lighten-ing and depigmenting effect. Topical vitamin C(Purascorbol aesthetic dermal) also has an antiaging effectthat works in different ways:

� It modulates the three genes responsible for the synthe-sis of procollagen leading to an increase in type III col-lagen synthesis. This action is very important forpost-peel healing and maintaining normal skin struc-ture.

� It is a cofactor of prolyl and lysyl hydroxylase enzymesin the first stages of collagen synthesis; these are neces-sary 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.

� It protects vitamin A from oxidation and prevents pro-tein chains from breaking.

� It has a protective action on other antioxidant systems,which is beneficial in situations where free-radical pro-duction is increased (e.g. during post peel oxidativestress). This is also the case with infected or uninfectedwounds and areas exfoliated by peels or other abrasiveor resurfacing techniques.

� It enhances re-epithelialization.

Morus alba (mulberry or white mulberry) extractsMulberroside F (also known as 3′-di-O-β-D-glucopyra-noside and moracin M-6), extracted from mulberry leaves,inhibits tyrosinase activity, in the conversion of dopa (3,4-dihydroxy-β-phenylalanine) into dopachrome (dopa oxi-dase activity). This tyrosinase-inhibiting activity has beenmeasured as 4.5 times more powerful than that of kojicacid.45 Mulberroside F also has an antioxidant activity onthe superoxide anion.

AHAsThe melanogenesis-inhibiting properties of lactic acid andglycolic acid have been shown55,56 in the treatment ofmelasma as well as solar lentigines and PIH. The mechanismof action not only lies in the faster dispersion of pigments ina more rapidly renewed epidermis, but also in the inhibitionof tyrosinase activity. This inhibition has no relation to theacidity of these products, as studies show that tyrosinase-inhibiting activity is constant, even below pH 5.6.

Important observations on the use of topicaldepigmenting agentsOne of the explanations for the failure of depigmentingtreatments is that they are often applied extremely locally, tothe hyperpigmentation itself, whereas they should be appliedevenly to the whole face in the morning, for example, andagain in the evening on the hyperpigmentation alone.

Sun avoidanceComplete sun avoidance can by itself resolve many hyper-pigmentation problems within 6–18 months. See alsoChapter 3.

Local corticosteroidsWhen a peel causes localized inflammation that visiblydevelops into hyperpigmentation, even with sun protectionand avoidance, a corticosteroid (preferably a fluoro-corticosteroid) should be applied. It should be appliedtwice a day locally to the erythema before it develops intohyperpigmentation and should not be used long term (1week at the most), to avoid the side-effects associated withcorticosteroids. This treatment should of course be com-bined with sun protection/avoidance measures and a topi-cal depigmenting agent.


HOP

OH

OO

O

O

HO

HO OH

Figure 37.41Vitamin C (L-ascorbic acid), in the form of ascorbyl phsophate.

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ScarringUnlike pigmentation problems that are common aftermany peels, scarring is fortunately a rare complication.Some areas of the face are more sensitive. Scars can arisedirectly from excessively deep, chemical destruction of thedermis57 or can be the ‘logical’ result of neglecting a sign –for example, ignoring and not treating persistent erythemaproperly. Treatment needs to start as soon as possible: assoon as scarring seems likely, as a stabilized scar is unfortu-nately a permanent scar.

The deeper the peel, the more effective it is, but also themore dangerous. A deep peel, when performed correctly,produces exceptional results in the majority of cases. I havenever come across any report of complete facial necrosis aftera peel. Fortunately therefore, the problem remains localized.Scarring can be atrophic, hypertrophic or retractile, depend-ing on the depth of the burn and the area treated. To have abetter understanding of the risk of post-peel scarring, wemust take another look at the physiology of skin healing.

Brief chronology of healingInitial phenomenaThe process starts almost immediately: neutrophils enterthe treated area during the peel and stay there for 3–5 days.Macrophages are present from day 3 to day 10 and lym-phocytes from day 6 or 7.

Re-epithelializationThis starts 24 hours after the peel and begins with cen-tripetal keratinocyte migration followed by accelerated cellproliferation. It should be effective within a week – that is,protect (partially, as there is only one layer of cells) the der-mis.

Collagen regenerationAfter re-epithelialization, dermal collagen is regeneratedover a 2- to 3-month period.

Various facts about post-peelhealingOpen healing is slower than when the re-epithelializingwound is covered. This does not matter for intraepidermalpeels, as the dermis is still covered by several layers of livingand protective keratinocytes. On the other hand, when itcomes to medium or deep peels,58 this is of major impor-tance. Peels have an advantage over laser or mechanicalabrasive treatments in that they leave a layer of skin inplace. This layer of skin is of course dead, but it offers pro-

tection against external aggressions and enhances re-epithelialization. The strips of skin that survive after amedium or deep peel should therefore be left in place, asthey protect the regenerating skin. Lasers gradually vapor-ize the layers of skin to be eliminated, and if it were not forcolloid dressings, the skin would have to heal in the open.The colloid dressings on the market (Convatec®, Omni-derm®, Vigilon®, etc.) allow better-quality healing in amoist environment after laser treatment. Totally occlusivedressings (including Vaseline®) carry an increased risk ofinfection and have to be monitored actively, as bacteriaproliferate far more rapidly under occlusion than in theopen air. Because of the increased bacterial proliferationand the skin’s lowered immune defenses after a medium ordeep peel,59 it is preferable to use a moist healing methodafter a phenol peel. A mask of bismuth subgallate or thymoliodide is used for this after a phenol peel (see Chapter 35).

Post-peel hydration is also important. The skin shouldnot be allowed to dry out while it is re-epithelializing aftera 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 der-mis

� after the healing mask has been removed (from the7th–8th day) after a phenol peel.

Only a thin layer of Vaseline® need be applied to stop anypruritus triggered by surface keratinocytes (that have notyet differentiated into corneocytes) drying out. Vaseline®creates an impermeable layer on the surface of the skin andprevents water evaporating from the epidermis (TEWL:transepidermal water loss). Water accumulates under thelayer of Vaseline® and provides immediate natural hydra-tion that soon relieves the pruritus caused by the ker-atinocytes drying out. Patients on whom Vaseline® isapplied should be monitored particularly closely, becauseof the increased risk of secondary infection under occlu-sion. Aloe vera extracts appear to accelerate healing afterdermabrasion, but have the disadvantage of potentiallycausing contact allergies. The use of antioxidant creamsmay also be indicated during the first few weeks after a peel(Renutriv ACE Lipoic Complex®–SkinTech).

Risk of scarring depending on themolecule usedAHAsWhen an AHA peel is strictly intraepidermal,61 the risk ofscarring is non-existent, as there is no phenotypic conver-


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sion of fibroblasts into myofibroblasts (see above). Duringthe 1990s, when the use of AHAs in cosmetic medicine firsttook off, women’s magazines carried reports of real disas-ters with gruesome photographs. At the time, a patient gaveme a copy of a popular German magazine62 (Brigitte –19/95: 62–8) that told the story of a journalist who, out ofprofessional conscientiousness (or curiosity?), decided totest a peel of 70% glycolic acid in simple aqueous solutionin a reputable cosmetic surgery clinic. After a few monthsof preparation with tretinoin,63 the doctor quickly appliedseveral coats of 70% glycolic acid and left his nurse to takecharge of the immediate follow-up. According to the jour-nalist, the peel was not neutralized, but simply rinsed withwater64 several times, even though the patient complainedof persistent burning. The eyes also had to be rinsed, as thecopious amounts of water used on the face had carried theacid into the conjunctival cul-de-sacs. The patient wenthome and the doctor left on vacation the very same day.The next day, alarmed by the condition of her skin, thepatient wanted to see the doctor and, as her surgeon wasaway, saw one of his colleagues, who was of course horri-fied to see that a product as strong as an AHA at 70% hadbeen applied on such lovely skin. The danger was so greatthat he had to prescribe manual lymphatic drainage! Othercolleagues told the patient that ‘it would last for years’.

The article goes on to say that three months later not allthe after-effects had gone, but it omits to describe the stateof the skin, and the results of a single AHA peel obviously islittle. The journalist concluded that she would never againlet herself be treated with any acid whatsoever, given the‘daily horror’ she had to live through after trying the light-est one. This is confirmation once again that a thoroughknowledge of the techniques, together with a high degree ofprofessional conscientiousness, is essential to avoid prob-lems and that any peel, even a superficial one, can causecomplications.

TCAPublications often present this molecule as being the mostlikely to penetrate too deeply and cause scars. Books andjournals about peels are full of photographs of complica-tions and scars resulting from peels with TCA–SAS (Fig-ures 37.42 and 37.43).7 According to Litton7 and Stone,65

‘deep’ TCA has a natural tendency to cause hypertrophicscars. In reality, it must be used in accordance with preciserules, and practitioners must be aware of and respect itssymptomatology and TCA should never leave any scars.

The risk of scarring after a TCA peel is linked to the acidpenetrating too deeply.

The total quantity of TCA applied to the skin during apeel determines the depth of the peel. This quantitydepends (among other things) on the concentration of thesolution and the number of coats applied. Applying ahighly concentrated TCA peel means that a lot of acid goes

into the skin in one go and it is impossible to control thedepth. The more concentrated the TCA is, the more deeplyit penetrates. One of the major problems stems from thefact that the concentration is calculated in different ways indifferent parts of the world: although percentages are


Figure 37.42(a,b) A scar probably due to uneven application of TCA–SAS,50% m/m.

A

B

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always given, a concentration in mass per mass (m/m) isnot the same as in mass per volume (m/v) or mass plus vol-ume (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 theskin in a little more TCA, which will combine with moreproteins and destroy other cells.

The risk of scarring is also linked to the thickness of theskin. The thinner the skin, the more deeply will the TCApenetrate; the thicker the skin, the less it will penetrate.Nevertheless, scars do not only form where the skin isthinnest. On the contrary, they can also form in areaswhere the skin is thicker, with areas of thin skin remainingscar-free. These ‘paradoxical’ scars can often be explainedby an intentionally ‘forceful’ application on an area that ismistakenly believed to be more resistant and in an attemptto get better results.

Dry skin allows TCA to penetrate more rapidly andmore deeply than hydrated or oily skin, which is usuallythicker than dry skin. Skin lipids deactivate TCA and well-hydrated skin dilutes it. TCA that penetrates well-hydratedskin encounters more water than it does when it penetratesdry skin. The more aggressively the skin is prepared, themore permeable will it be and the TCA will penetrate morerapidly: caution must be observed with regard to pre-peel

degreasing and disinfecting, which abrade the skin andwhich are not recommended for all peels. Patients shouldbe questioned before a peel to find out if they regularly useproducts on their skin that reduce the thickness or imper-meability of the stratum corneum (AHAs, tretinoin, ben-zoyl peroxide, salicylic acid, etc.)

The type of applicator also plays a role in determiningthe depth of penetration of the acid: gauze abrades the skinas the acid is applied and promotes quicker and deeperpenetration, while a brush spreads the TCA on the stratumcorneum without enhancing penetration and thereforeproduces a more superficial peel.

TCA penetrates more readily where the skin has beendamaged. TCA–SAS should therefore not be appliedimmediately after hair removal, coagulation of telangiec-tasias, a session of mesotherapy, filling wrinkles, etc. EasyTCA® is not a simple aqueous solution of TCA, but rathera ‘tamed’ solution that can be applied safely after the treat-ments listed above. An aqueous solution of TCA is unsta-ble; a tamed solution67 is far more stable and penetratesmore evenly.

The risk of scarring after a TCA peel is also linked to thequality of the care surrounding it. Apart from some seriouscases, scars do not form immediately, but are preceded byprolonged local erythema and/or infection that should bediagnosed and treated appropriately. Many problems (seebelow) can be avoided by proper patient selection, andpost-peel monitoring can limit others.

Scars usually – but not always – occur in patients withdry and thin skins that have been treated with too muchTCA–SAS with an inappropriate concentration or qualityand when monitoring and post-peel care have beenneglected or inadequate. They can also occur in patientswith thicker skin, with a history of hypertrophic scars.

PhenolIt is reported that, at the same depth of injury, phenolcauses fewer problems with scarring than TCA.68 Accord-ing to Fintsi,69 the Exoderm® formulation is ‘self-blocking’:it somehow recognizes the reticular dermis and stops itsaction there. Other new formulations (e.g. Lip & Eyelid®)have this advantage. Although some phenol peels withrather exotic or inappropriate protocols have producedscar reactions, certain current phenol peel formulations areless aggressive, kinder to the skin and just as effective. Thefact that the phenol automatically stops acting at the retic-ular dermis should be treated with caution: it cannot besafely assumed that a phenol formula will stop in every caseright at the most superficial part of the reticular dermis,even if technically phenol is self-blocking, as it neutralizesitself by combining with proteins. We still do not know atwhich depth it is completely neutralized! Our ‘self-block-ing’ also depends on the total amount that was applied inthe skin.


Figure 37.43Scarring after TCA in aqueous solution of unknownconcentration: probably 50% m/m.

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General prevention of scarringPatient selectionSpecial care should be taken with patients who haveextremely thin, dry or sun-damaged skin, as the acids pen-etrate this very permeable skin more quickly and moredeeply and the skin can sometimes overreact. Carefulanamnesis will reveal any personal or family history ofkeloids or any tendency to scar hypertrophy. Insulin-dependent diabetics should be ruled out from a peel to thereticular dermis (because of the increased risk of scarringand infection), whereas diabetic patients (type 2, non-insulin-dependent) who are stabilized on oral antidiabeticdrugs can have a deep peel on condition that they are mon-itored more closely than usual.

Ehlers–Danlos syndromeIt would be more appropriate to talk of Ehlers–Danlos syn-dromes,70 as this is a heterogeneous group of connective tis-sue disorders, a ‘diffuse hereditary’71 disease, of which to dateten groups and different subgroups have been identified.Paganini is suspected to have suffered from it.72 Types I to IVand type VIII can be diagnosed clinically, while types VI, VII,IX and X require laboratory diagnosis.73 The different sub-groups are characterized by deficiencies at different levels:there are mutations of genes coding for type I or III collagenor for certain enzymes.70,74 In certain subgroups (VIIC), elec-tron microscopy shows that the collagen is laid down insheets rather than fibrils and takes on a hieroglyphic pat-tern.75 The incomplete or light forms of the syndrome arecertainly more common than reported in the literature71 andsome authors suggest a worldwide incidence of 9% of thepopulation.68 It typically manifests as fragility and hyperelas-ticity of the skin and joint hypermobility. The skin can bestretched further than normal skin and returns to its originalstate when let go. Minor traumas cause disproportionate lossof substance and atrophic, parchment-thin scarring. Theskin eventually loses its elasticity, and its appearance resem-bles ‘cutis laxa’ – loose, hanging and wrinkled.

From a clinical point of view, the coexistence of at leasttwo 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 foldschange facial morphology; the skin is hyperelastic and cansometimes hang on the face.77 It is especially important tobe aware of this syndrome and try to detect borderline

cases in patients wanting rejuvenating techniques. Sur-geons should be particularly wary because of the possiblyfatal vascular complications.78,79

Treatment with isotretinoinPatients who have used isotretinoin (13-cis-retinoic acid,Roaccutane®) or other more recent retinoids during theprevious year or are going to use it within the next 12months should be ruled out from medium or deep peels.Some authors even suggest leaving a gap of 2–3 yearsbetween 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 tomechanical injury as much as physical injury and infection,and there is a risk of hypertrophic, star-shaped scars on thecheeks that can form months after a peel has been carriedout too soon after isotretinoin.

Patients whose skin has been significantly changed byisotretinoin and who still complain of dry or fragile skinshould not be given any type of peel.80 It is absolutely vitalto wait for the skin to heal completely with restitutio adintegrum before performing any kind of peel, even if ittakes years. Common sense dictates that it is better to live afew more years with wrinkles than live the rest of one’s lifewith scars. Intraepidermal peels or peels to the basal layertheoretically do not pose such a serious risk, as regenera-tion 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 TCAin aqueous solution should be considered likely to causescarring in combination with isotretinoin.

Skin preparationSkin preparation must be even, suitable to the skin typeand not excessive. Some peels are only really effective afterseveral weeks’ of skin preparation (TCA–SAS), whereasfor other products (Exoderm®, Easy TCA® and Lip & Eye-lid®) pre-peel preparation is pointless, and in some casesany pre-peel preparation is contraindicated (EasyPhytic®82).

If preparation is too rough, the skin will be too perme-able to the acids – overall and locally. Results might some-times be better, of course, but if preparation is tooaggressive, the safety factor is reduced. It is essential to fol-low the instructions provided with each formulation andeach technique. They are based on the experience anderrors of their authors and help avoid pitfalls and acci-dents.


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Avoiding injuries� Except in cases where the doctor wishes to increase the

depth of peel penetration intentionally,83 patients mustbe warned not to use ‘exfoliating scrubs’ on their skinduring the days before a peel. If the patient uses an exfo-liating scrub, or a ‘home-peel’, as it is known for mar-keting purposes, it may be uneven and enhancepenetration of the acid locally.

� Secondary infections must be avoided: close post-peelmonitoring is necessary.

� Premature re-peeling should be avoided: a re-peel shouldnot be done if re-epithelialization is not complete.

� A full face deep peel should not be done at the sametime as a face-lift; however, it is possible to do a chemi-cal cheiloplasty84 or a chemical blepharoplasty at thesame time as a surgical face-lift, for example.

� Scratch lesions should be avoided.

Persistent localized erythemaAs we have seen earlier in this chapter, persistent localizederythema (especially in high-risk areas) is more often thannot a sign of dyschromia rather than scarring. Induratederythema poses a risk of scarring more than PIH.

Specific prevention depending onpeel type

AHAsAHA peels are superficial peels that do not have a naturaltendency to cause scarring. If the doctor himself monitorsthe peel and the neutralization stage as usual, in principlethere is no chance of scars forming. If the peel is neutral-ized as soon as erythema appears, there is no risk of scar-ring. A peel that is neutralized too late, however, can causescarring. Neutralization (acid + base) should not be con-fused with dilution (acid + water). Dilution is not alwaysenough: the recommendations given in the protocol foreach particular product must be followed.

Easy Phytic® solutionEasy Phytic® solution (see Chapter 11) is a slow-release andself-neutralizing mixture of fruit acids and phytic acid (pH<1). The peel solution can only be applied on an intactstratum corneum, where it will concentrate and graduallybe released. The gradual penetration of the acids does notoverwhelm the skin’s buffer capacity.85 Any prior treatmentlikely to accelerate or increase penetration of the acidscould overwhelm the skin’s buffer capacity and cause prob-lems. There have been no reports of scarring to date, and

Easy Phytic® can be considered extremely safe as far asscarring is concerned.

TCA–SASTCA penetrates very rapidly through the skin. If it pene-trates too deeply, it is often too late before it is noticed, andsurface neutralization is not enough to reverse the caustic,scarring processes triggered deep down. In reality, TCA isonly partially neutralized, even if base solutions are appliedimmediately: only the excess TCA on the skin surface canbe neutralized. In high-risk areas or on thin and permeableskin, it is therefore recommended to use lower concentra-tions of TCA and to apply the product less vigorously (cf.choice of applicator). Care should be take to avoid anyinadvertent drips of TCA86 or the acid stagnating in thebase of deep wrinkles: there is a risk of linear overpeeling,traces of which can remain visible for many months oreven be permanent in cases of large excesses. Scars can beavoided 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-peelcream. A specific quantity of TCA in aqueous solution at50% 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 thebasal layer of the epidermis. Moreover, applying the post-peel cream limits or stops the immediate post-peel inflam-matory reaction. If the application procedure is followedcorrectly, there is no risk of overpeeling and no risk of scar-ring. Care should be taken not to use the aqueous solutionof TCA 50% m/m as it is, without mixing it with the adju-vant, base solution. There is no doubt that applying anaqueous solution of TCA 50% m/m directly to the skin car-ries a high risk of scarring.

This error has been made several times,87 but if the doc-tor follows the recommended application technique, hewill notice that with 50% m/m TCA, an unusually intenseand rapid frosting appear on the forehead and the patientwill feel an intense pain; the doctor will stop the applicationbefore starting to treat the more sensitive areas of skin,where the risk of scarring is greater. As we have alreadyseen, the skin on the forehead is more resistant to chemicalinjury. If this wrong concentration is used, applying plentyof Easy TCA® post-peel cream immediately after washingthe skin with copious amounts of water will limit the injuryand prevent serious complications in the majority of cases.

Only Touch®Only Touch® consists of a base solution whose qualita-tive 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 isvery aggressive, cannot of course be applied directly tothe skin at the risk of penetrating too deeply and causingpermanent scarring. Following the application proce-dure is absolutely essential: Only Touch® is dabbedquickly88 on lentigines and keratoses of less than 1 cm indiameter. Treating larger areas rapidly increases the riskof scarring.

It is easy to avoid scarring if the following rules areobserved:

� Be careful not to apply 80% m/m TCA directly to theskin.

� 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 smallvariations in preparation causes unwanted local or sys-temic effects.

Baker–Gordon solution is unstable. Applying phasesof different concentrations to different areas of the facecan be avoided by shaking the solution constantlythroughout the whole peel procedure and keeping thesolution homogeneous. If the solution is not shaken, itcan produce an uneven peel: undertreated areas will benext to overpeeled areas, where scars might form. Forthis reason, it is preferable to use formulas that remainhomogeneous (Lip & Eyelid®). When an occlusive maskis used, it should be applied evenly, without air bubblesor excessive pressure:

� If there are air bubbles in the occlusive dressing, thephenol cannot macerate evenly, and some areas will beundertreated, whereas if the occlusive mask is too tight,scars can form where the severe edema that develops inthe first few hours after a phenol peel causes too muchlocal pressure.

� The occlusive mask does not usually go under the jaw,as the movements and traction to which the dressingwill be subjected will cause the same phenomenon asdescribed above.

� The patient must be closely monitored, as bacterial,viral or fungal infections can develop unnoticed overthe days after a phenol peel.

� Any pruritus should be treated to avoid scratch lesions,a source of scarring.

� The application protocol recommended with one typeof peel formula cannot necessarily be used withanother. Nevertheless, although phenol is a deep peel, it

does not cause scarring as readily as TCA at the samedepth.

� Applying Vaseline® as occlusion after phenol is just aseffective as a dressing, and does not carry the risk of airbubbles or areas of pressure. However, Vaseline®increases the risk of infection and rules out any touch-up 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 in1984,89 and surgical correction was successful. No doubtthere are other previous cases that have not been publishedor that I have not heard of.

Severe cases have also been reported90 after eyelid peels;however, ectropion is not a specific complication of deepeyelid peels.

Ectropion can also be a complication of:

� Surgical treatment: it is in fact the most common com-plication after surgical blepharoplasty. Particular careshould be taken when doing a peel if the patient has ahistory of blepharoplasty and even more so in cases ofmultiple blepharoplasties. Patients with lagophthalmiashould in principle be ruled out from deep peels,although some cases can be treated cautiously.

� Various cosmetic treatments: ectropion can occur afterdeep peels with TCA or phenol and after laser treatmentor mechanical abrasion.

� Systemic medication: 5-fluorouracil (5-FU) by the sys-temic route can cause ectropion. A case of ectropionthat occurred after topical application of 5% 5-FU hasbeen described.91 The complication was bilateral andresolved when treatment was stopped.

� Topical treatments: the appearance of ectropion afterlong-term treatment with tretinoin has been described.In this case, it is reversible when treatment stops.

Prevention of ectropionIf ectropion seems to be developing:

� A flexible silicone dressing that will resist the pull of thescar should be applied (Figure 37.44).

� A strong corticosteroid should be rubbed gently andslowly into the affected area.

� Corticosteroid injections in situ may prove effective.


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Prevention and treatment of scarsStrong, topical corticosteroids should be applied, twicedaily, very locally. A self-adherent silicone dressing (Silas-tic® or Mepiform®/Mepitel®92: Figure 37.44) should beworn 24 hours a day that adapts to the curves of the skinand does not pull away growing cells when the dressing ischanged.

Corticosteroids (e.g. Celestone®–Depomedrol®) can beinfiltrated. The injection technique is important:

� Location: the corticosteroids must be injected into thescar tissue itself and not in the tissue surrounding thescar. Not only is an injection underneath or beside thescar ineffective, it can also cause fat atrophy underneathor 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. Thescar should become soft and non-adherent. Scars oftenrespond well to this treatment within 1 month.

If no treatment seems to be working and the scar is perma-nent, there are a few solutions:

� surgical excision combined with a preventive siliconepressure dressing to avoid local recurrences – as forectropion, Litton and Trinidad7 recommend simplywaiting for a few months instead of rapid surgical exci-sion

� laser treatment� concealing with special camouflage make-up (e.g.

Cover Mark®)

The prognosis is much better if the scar results from over-peeling (technical error) rather than the nature of the skinitself (e.g. with Ehlers–Danlos syndrome). A technicalerror can be put down to experience, and there is no reasonwhy it should happen again during a repeat peel. If thescarring results from the patient’s genetic make-up, she orhe should not be given another peel.

Secondary infectionsSkin that has just been treated with a peel93 is more proneto all types of infection, as it can no longer rely on its dif-ferent defense mechanisms being intact. The risk mainlydepends on the depth of the peel and how carefully it isapplied. However, other factors come into play. Secondaryinfections rarely cause major problems, and do not reallyleave scars if treatment is started in time. Infections aremost often local, but can become generalized in some seri-ous cases or after a peel to the reticular dermis.

Risk of infection depending onpeel typePeel to the epidermis and basallayer:94 very low riskOne of the skin’s defenses against infection is ‘neutralized’by all peels: the destruction of the stratum corneum makesthe skin more permeable to microorganisms. The cells ofthe stratum disjunctum – the outermost cells in normal


Figure 37.44Silicone sheets: (a) Mepiform®. (b) Mepitel®.

A B

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skin – are shed regularly and take with them a large amountof microbial fauna. This desquamation, which is a naturaldrainage route for the skin, cannot take place immediatelyafter a peel, as the epidermis tends to keep its cells in orderto regain its normal thickness and form a physical barrierto microorganisms. Without regular desquamationmicroorganisms that have managed to penetrate throughthe skin’s first line of defense cannot be physically elimi-nated.

The majority of the skin’s immune defenses are found inthe deep layers of the epidermis and dermis. An intraepi-dermal peel lets in many xenobiotic microorganisms, butall of the skin’s defenses remain viable and usually stop anylocal infection from developing. After an intraepidermalpeel, skin regeneration is very rapid and there is not reallyenough time for infection to set it. Intraepidermal peels areusually repeated once a week or every 2 weeks. Eachintraepidermal peel stimulates the skin’s regenerativecapacities, and the skin finds it more and more easy toresist infection. Therefore, these peels do not increase therisk of infection (or only very little). The risk of herpes isnot increased.

Peel to the Grenz zone:95 fairly lowriskThe risk of infection increases with the depth of action ofthe acids: the absence of the stratum corneum explains theincreased penetration of microorganisms; the destructionof many of the skin’s immune defenses gives more freedomto microorganisms to grow. However, the epidermal bar-rier is still partially effective;96 the dermal barrier is com-pletely active and even stimulated.

Apart from scratch lesions that can develop into verylocalized infections, a peel to the Grenz zone is not partic-ularly dangerous as far as infection is concerned. If aninfection should develop after a peel to this depth, a topicalantibiotic is usually enough to control it.

Easy TCA® applied to pinpoint or cloudy white frostingcauses virtually no infections, apart from a few potentialtransient infections of scratch lesions (the frequency isaround 1 in a 1000).

Peel to the papillary dermis:97

significant riskThe acid puts the majority of the skin’s immune defensesout of action. The doors are wide open to microorganisms(there is no stratum corneum or epidermis): they are nolonger eliminated by the continual shedding of dead cells,and the immune system cannot fight against them. Theacids have burned the Langerhans cells and other defensesin the papillary dermis, and the skin is waiting for itsimmune defenses to be renewed. The risk of infection issignificantly higher than with a peel to the Grenz zone. It is

essential to take all necessary precautions to avoid, preventand/or treat any infection.

Peel to the reticular dermis:98 verysignificant riskThe skin no longer has any physical or immune defenses,and is at the mercy of any microbe attack. The patient’shealth depends entirely on the hygiene measures takenduring 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 infectionsLocal and loco-regional bacterialinfectionsLocal and loco-regional infections occur in cases of localoverpeeling99 above all or after scratch lesions (Figure37.45). Although peels to the papillary or reticular dermisare more likely to become infected, infections can never-theless develop after a more superficial peel.

Fortunately, serious local infections are rare, as the peel-ing agents, especially phenol, are germicidal.100 Moreover,the skin on the face is rich in blood vessels and has effectivedefenses against infections. With age, however, there arefewer blood vessels in the face and the skin becomes moresusceptible to external aggression. Infections seem todevelop more readily and are more serious when peels areperformed in a hospital setting, because of the presence ofmultiresistant strains. I am fortunate enough not to haveany dramatic photos of post-peel infections to show, butmany cases of secondary infection and scratch lesions fromstreptococci, staphylococci and Pseudomonas have been


Figure 37.45Secondary infection: scratch lesions after Easy TCA®.

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described in the literature.68 The result of following ruleswill allow you to perform secure peelings with a very lowinfection rate.

Pruritus must be treated rapidly to prevent infections.Deep peels, to the reticular dermis, obviously pose a partic-ular risk of secondary infection during the first week aftertreatment.

Conventional care often includes the application of anantibiotic cream or ointment. This local antibiotic cannotbe applied in superimposed layers, and patients shouldwash their skin before applying a new layer of antibiotic.Cleaning the skin is a problem in itself, as it may injure theextremely sensitive skin and is often painful. As a result,patients do not always clean their skin before each newapplication, and put one layer of ointment on top ofanother. After a few days of maceration, it is almostinevitable that a secondary infection will develop.

Other patients clean the skin too vigorously before eachapplication of antibiotic: the regenerating skin gets dam-aged, severe inflammation is maintained and secondaryinfections develop more readily. The antibiotic ointmentshould therefore be cleaned off carefully and evenly, usinga showerhead to gently spray tepid water directly onto theskin. The skin can be degreased with a gentle cleansinglotion before showering.

Using a ‘powder mask’ (bismuth subgallate or thymoliodide) during the first week after a peel to the reticulardermis (Lip & Eyelid®) limits or even prevents secondaryinfections – not only because of the properties of the pow-der itself, but also because the patients have absolutelynothing to do themselves: they will not have to touch theskin directly and therefore cannot import any infectiousagents (Figure 37.46). The powder protects the skin fromexternal aggression and from microorganisms in particularlong enough (6–7 days) for the skin’s defenses to be suffi-

ciently restored by the time the powder mask is removed. Ihave never come across any infection when using this ‘dry’technique, while I have often met with small infectionswhen using antibiotic creams.

General bacterial infections: toxicinfectionsA few cases of toxic shock were reported after facial peelswith Baker’s solution in 1982, 1983 and 1987 and afterrhinoplasty in 1983. Todd and colleagues described the firstcases of toxic shock syndrome in 1978 as a result of the useof certain tampons. It appears to be caused by an entero-toxin F and/or exotoxin C with the same molecular weight(22 000), secreted by Staphylococcus aureus. Other authorssuspect that the two toxins are really one and the same.101

SymptomsThe following symptoms should alert the practitioner:

� a temperature over 39°C in the first 2–4 days after amedium or deep facial peel; the patient’s temperaturemay, however, rise slightly and innocuously (37–38°Cmaximum) in the first 12 hours after the peel

In cases of toxic shock, other symptoms follow the rise intemperature:

� skin rash� low blood pressure (systolic <90 mmHg)� vomiting and diarrhea� muscle pain� mucous membrane infection� kidney damage� liver damage� hematological problems (anemia or thrombocytope-

nia)� damage to the central nervous system

TreatmentTreatment is aggressive and requires hospitalization.Patients should be taken to hospital as soon as there is anysuspicion of toxic shock (raised temperature) and beforeany other symptoms appear. The symptoms of infectionare often hard to spot: there was no visible sign of infectionbeneath the thymol iodide powder before the start of toxicshock described in the 1980s after a phenol peel (Baker’ssolution). Toxic shock syndrome can come like a bolt fromthe blue. In the cases described, the skin recovered nor-mally and no scars were left after recovery.

Prevention of bacterial infectionsIntraepidermal peels to the basal layer or the Grenz zone donot require such stringent precautions as deep peels, and


Figure 37.46Protective mask of bismuth subgallate powder after treatmentof wrinkles on the upper lip with Lip & Eyelid® formula.

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treatment can be monitored as normal. There should be noparticular 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 cottonbuds. The skin should never be touched with the barehands during or after the peel.

Special precautions for phenol peelsThe phenol solution is ‘rolled’103 onto the skin with a cot-ton bud soaked in the product. If the doctor makes theapplicator himself, he should check that his hands are ster-ile beforehand. It is difficult to make this rolling movementwith gloved hands, as the glove can wind around the appli-cator and make application awkward, or even dangerous.Only the left hand should be gloved, and the right handshould be surgically disinfected and not come into contactunnecessarily with the skin.

Infections are more common with the ‘moist’104 healingtechnique than with the ‘dry’105 technique.

The drawback to using creams when the epidermis isregenerating is that skin debris builds up and forms a basefor the infection underneath the occlusive layer. The

advantage, however, is that it is possible to see how the epi-dermis is progressing during the first week, which is notpossible with an occlusive mask of thymol or bismuth. Ifpractitioners prefer the ‘moist’ technique, they should pre-scribe an antibiotic cream, preferably without cortico-steroids, and bear in mind the possibility of contactallergies. Patients have to wash their skin under a shower-head four times a day to get rid of the skin debris and thenapply a new layer of antibiotic cream (e.g. bacitracin). Spe-cial care must be taken not to damage the growing epithe-lium. Not cleaning the skin properly has led to alarmingsecondary infections from Pseudomonas,106 in the form ofpyoderma. Proper debridement and cleaning together withappropriate antibiotic treatment stop this infection.

Treating bacterial infectionsIt is enough to proceed logically: topical or systemic antibi-otic treatment should be used. A bacteriological sampleshould be taken before any treatment in order to make aculture and an antibiogram. Treatment should start beforethe results of the culture arrive.

Small, localized infectionIf the patient does not have a temperature, they should betreated with local antibiotics.

In the particular case of phenol used in combination witha ‘dry’ healing technique, topical antibiotics can be applieddirectly onto the powder mask. The powder will come away(not a serious consequence) and the epidermis will be laidbare. A ‘moist’ technique should then be used locally.

Loco-regional bacterial infectionFigure 37.47 shows a case of loco-regional infection begin-ning at the end of the occlusive regeneration phase of a full-face phenol peel. The patient did not have a temperature, but


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 acneiformdermatitis has been cured with oral antibiotics.

A B

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had numerous painless, papular lesions on the neck. Oralantibiotic treatment cleared the problem up in a few days.

Post-peel acneiform dermatitisPost-peel acneiform dermatitis occurs readily under agreasy ‘dressing’ (e.g. Vaseline®), and should be treatedwith oral antibiotics. It clears up in 6–8 days.

Suspected toxic shockThe patient should be hospitalized immediately.

Secondary herpes infectionsSecondary herpes infections are very widespread107 and therisk of ‘waking up’ the virus is very real, especially for peelsto the papillary dermis.

Risk depending on peel typePeel to the epidermis or basal layerThe risk of herpes activation is minimal.108 The skin is notbadly injured and its defenses are still strong enough. AHA,Easy Phytic® or Easy TCA® peels can therefore be carriedout – no further than the basal layer – without any fear of aherpes outbreak.

Peel to the Grenz zoneDepending on how prone the patient is to herpes, valaci-clovir can be used to prevent it. Patients who say they haveonly had one outbreak of herpes, ‘20 years ago’, can quitereasonably be treated without any herpes prevention if thepeel 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 atthe drop of a hat’ should, of course, automatically receiveHerpes prevention.

Peel to the papillary or reticular dermisA person who has had even just one outbreak of labial herpesin their life is at serious risk of a recurrence in the days fol-lowing a peel to the papillary or reticular dermis. This cannotbe considered as just a potential complication. On the con-trary, it should be considered as an almost certain side-effectof peels to these depths. Herpes prevention is thereforeobligatory. Only Touch® is a deep peel that reaches the retic-ular dermis, but because its use is limited to areas of 1 cm indiameter at most, the immune defenses are not damagedenough to trigger herpes, and there have been no cases ofherpes described after this peel. No prevention is necessary.

Specific herpes symptoms after a peelDiagnosing a herpes outbreak is relatively complex in thedays following a peel, because the superficial layers of the

epidermis have been removed and this is where the blistersthat allow easy diagnosis form. Sometimes herpes will man-ifest only as painful erythema (Figure 37.48b), but some-times also in a clearly necrotic form. The herpes outbreakmay be delayed and occur after the 8th day. In general, thesudden onset of pain accompanied by erythema betweenthe 4th and 7th days is a sure sign of herpes. The herpes canspread over the whole face within a few hours, but fortu-


Figure 37.48(a) Secondary herpes infection 5 days after a TCA peel to thepapillary dermis. No herpes prevention treatment was used.(b) Close-up of the upper lip: only painful erythema can beseen; treatment with valaciclovir brings rapid remissionwithout hyperpigmentation or scarring.

A

B

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nately does not usually leave any scars109 and it appears thatthere have been no cases of herpes spreading to the eyesafter a medium or deep facial peel.106 Severe local outbreakscan, however, leave local hyper/hypopigmentation.

Differential diagnosis: herpes/bacterialinfectionAn infection can be assumed to be herpes if the patient hasa personal history of herpes. If pain is felt on the upper lipfirst, this also suggests herpes, while pain felt on the cheekwould rather suggest a bacterial infection, especially if thereare scratch lesions and pus. Given that the epidermis hasbeen exfoliated by the medium or deep peel, the doctorshould not expect to see herpes blisters.

Pain is an important clinical sign: herpes is painful evenbefore it is visible, whereas a bacterial infection is usuallypainless or only becomes painful after it has developedclinically for a certain amount of time.

Differential diagnosis:herpes/overpeelingIn addition to the signs and symptoms described above,overpeeling does not usually cause much pain at first,whereas herpes does.

Prevention of herpes outbreaksHerpes prevention is sometimes advisable with a peel to theGrenz zone, and is essential with peels to the papillary orreticular dermis (except for Only Touch®; see above).

Questioning the patient and clinical examinationIn the majority of cases, patients forget that they once hada ‘cold sore’ when they had ’flu several years ago, and thedoctor should of course look very carefully for anydyschromia in places where herpes is usually located, andshould not forget that herpes may develop in other areasapart from the upper lip, as can be seen in Figure 37.49,which shows herpes located in the ear.

Preventive treatmentThis comprises:

� aciclovir: two times two tablets a day, 3 days before and5 days after a medium or deep peel

� valacyclovir: two times 500 mg/day, 2 days before and 5days after a medium or deep peel

Treating post-peel herpes outbreaksOral antiviral treatmentThis comprises aciclovir by mouth from four times400 mg/day to 800 mg five times a day or valaciclovir by

mouth: three times 500 mg to three times 1 g per day. Thehigher doses are for treatment of herpes outbreaks thathave occurred in spite of proper preventive treatment.

Topical treatmentTopical aciclovir is not well tolerated by patients after adeep peel because of the burning sensation it triggers.109 Ifpain is very local, EMLA cream can be used cautiously, as itis absorbed more readily through skin that has no stratumcorneum and is damaged by herpes. Local corticosteroidsshould not be used.

Treating pain and/or pruritusNerve blocks can be given in cases of very painful out-breaks. A mixture of lidocaine with adrenaline (epineph-rine) and ropivacaine or bupivacaine110 can be used. Insome cases, the doctor will have to prescribe opioids torelieve severe pain. However, treatment with opioids mightwell get rid of the pain but will not affect the itching. Itcould even aggravate the pruritus. The itching sometimesresists hydroxyzine and diphenhydramine. Asken109

reported that he once had to inject propanolol intra-venously to relieve unbearable pruritus.

Benzodiazepines111 and strong analgesics112 sedatepatients and prevent scratching, secondary infections, pig-mentation problems and permanent scars. Dailydoctor–patient contact is essential to reassure the patientthat the herpes lesions are healing properly.


Figure 37.49Unusual location of herpes blisters in the helix above thetragus.

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Special case of herpes under post-phenol occlusivemaskIt is difficult to diagnose and impossible to monitor herpesoutbreaks, large or small, beneath an opaque occlusivemask of bismuth subgallate or thymol iodide. If there is anyhint of herpes, any acute pain between the 4th and 7th dayafter the phenol, the powder mask113 should be removedimmediately in order to examine the skin thoroughly. If thedoctor’s suspicions are confirmed, the herpes should betreated as described above. Once the diagnosis has beenmade, the powder mask should not be replaced, and the‘moist’ technique should be used instead, with regularapplication of an antibiotic cream (e.g. bacitracin) to avoidsecondary bacterial infection.

PruritusAll peels destroy at least part of the epidermis and stimulatekeratinocyte growth. The rapid dehydration of the non-cornified keratinocytes can cause pruritus, which, however,is easily controlled.

Superficial peelsIntraepidermal peels or peels to the basal layer rarely causepruritus, except in overpeeled areas, where it may be tem-porary. Peels to the Grenz zone do not cause much pruri-tus. There have been no reports of severe pruritus with EasyTCA®, except for two cases of allergy to the post-peelcream.114

Dermal peelsPruritus is a logical result of a dermal peel. It sometimesstarts very quickly, towards the 3rd day, or later, betweenthe 8th and 30th days. It gradually becomes less severe, andeventually disappears on its own.

Medication is sometimes necessary for patients whotend to scratch and are at risk of causing lesions, secondaryinfections or scars. Sublingual lorazepam (2.5 mg) orpromethazine (25 mg/tablet, 2–6 tablets a day) usuallystops post-peel pruritus. A calm or sleepy patient tends notto scratch! Cool compresses can also be applied. Cold com-presses help the patient cope with the pruritus, but frozencompresses are not advised immediately after a dermalpeel.

Following a phenol peel, pruritus usually starts graduallyunderneath the bismuth subgallate powder mask. Thepatient must be told not to scratch, since if the powdermask is pulled off accidentally when scratching, it may cre-ate bleeding lesions that could become infected (Figure37.50). Fortunately, these lesions heal rapidly and onlyleave a few areas of dyschromia. Instead of scratching, thepatient should gently tap any area that is itching.

Facial edemaAll peels cause edema in the treated area. In fact, all peelstrigger an inflammatory reaction whose cardinal signs are‘rubor, dolor, tumor, calor’.115 The redness (rubor) andheat (calor) come from vasodilation that enhances the pas-sage of liquids through the vascular endothelium andcauses swelling (tumor), whose rapid onset can be painful(dolor). The pain can of course be superficial and be nomore than a feeling of tightness when the inflammation islimited. The inflammation is also due to the presence ofpro-inflammatory components in the dermis, which,together with the increased oxygen supply (because of thevasodilation), promotes the formation of free radicals. Thefree radicals damage the neighboring structures and main-tain the inflammation. The result is a ‘vicious circle’ inwhich vasodilation promotes inflammation that causesvasodilation.

From a physiological point of view, the movement offluids follows Starling’s hypothesis (1896):116

movement of fluid = K [(CP + IO) – (IP + PO)]

where CP and IP are the capillary and interstitial hydrosta-tic pressure, IO and PO are the interstitial and plasmaosmotic pressures, and K is the filtration constant for thecapillary membrane. If the resultant is positive, there isplasma filtration into the interstitial space. If the resultantis negative, there is absorption into the capillary lumen.

The edema creates an additional barrier to capillaryabsorption by increasing the physical distance between thecapillary wall and the molecules to be absorbed.116 If theedema resolves rapidly by itself, it does not need treatment.

The rapid onset of edema dilutes the acids that arrive inthe immediate surroundings of the blood vessels and pre-vents protein coagulation in the vessel walls: blood contin-ues to circulate. When there is too much acid, extravascularplasma 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 whiteor even gray.

Severity of edema depending onpeel type

Peels to the epidermis or basal layerEdema comes from dermal inflammation, and peels thatdo not cause inflammation in the papillary dermis do notcause much edema. If the patient has an allergic reaction toone of the components used (e.g. resorcinol), then severeedema can set in rapidly, however. Any severe edema aftera peel that does not go beyond the basal layer is most likelyassociated with an allergy or infection.


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Peel to the Grenz zoneMild and short-lived edema (48 hours) might develop.117 Itdoes not require treatment. Edema that lasts any longercould be an allergy, and, if so, should be treated accord-ingly.

Peels to the papillary or reticulardermisA peel to the papillary dermis always causes edema, whoseseverity depends on the inflammatory reaction followingthe peel (Figures 37.51–37.53). An inflammatory reactionis desirable insofar as it sets in train the skin regenerationprocess; it is therefore responsible for the rejuvenatingeffect of a peel. But, at the same time, it generates free rad-icals that have well-known negative effects. Inflammationtherefore has its downside and must be controlled byantioxidants in order to limit the negative side and makethe most of the restructuring effect. This is why Easy TCA®,Unideep® and Easy Phytic® are rich in antioxidants, bothin the peel solution and in the cream ‘mask’ that the doctor

applies immediately after the peel. These antioxidantsreduce post-peel inflammation, allowing patients toresume their social activities more quickly and allowingmore frequent repetition of the peels. In general, the deeperthe peel, the more severe is the edema, as the edema trans-lates the severity of the dermal inflammation into visiblesigns. It is therefore logical that edema is more severe aftera phenol peel. The extent of the ‘lifting effect’ of a peeldepends on the depth of the peel and the severity of theedema. It can therefore be concluded that the overall liftingeffect of a peel will be proportional to the edema it triggers.Edema is sometimes so severe as to cause the lips to pro-trude118 or prevent patients from opening their eyes.

Deep peels therefore give rise to dramatic edema that cansometimes be very worrying for patients and their immedi-ate friends and family. A case has been reported of a patientwho was rushed to the nearest hospital by the family, whowere worried by what appeared to be severe burns.

It is essential to warn patients of the severity of theedema and to show them photographs of the post-peelperiod so that they do not worry. If a detailed explanationis not given beforehand, anything the doctor might say


Figure 37.50(a) Scratch lesion after a phenol peel – treated with bismuth subgallate. Note the intense and uneven erythema 10 days after thepeel. (b) The scratch lesion has completely healed. This photograph was taken about 5 years after (a), during the course of othertreatment.

A B

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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.

A B

A B

Figure 37.52(a) Before a TCA peel to thepapillary dermis. (b) facial edema24 hours after TCA to the papillarydermis (Unideep®).

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after treatment will ring hollow to patient, friends and fam-ily! It is extremely important for the doctor to have regularcontact with the patient during the first week after the peel,as the doctor can check on progress every day and reassurethe patient that everything is normal.

Link between pain and edemaFortunately for the patient, there is no linear relationbetween the pain felt and the severity of the edema. It is notpainful even when it is so severe that patients cannot opentheir eyes for anything from a few hours to several days,depending on the formula used. If after the 3rd day theedema is painful, there might be a secondary infection.

Edema and local phenol peelA local phenol peel on the eyelids or lips (Lip & Eyelid®)also gives rise to severe edema (Figure 37.54) that can makeit difficult for patients to eat or open their eyes, which canmake some patients extremely anxious. This edema reachesits peak, locally, during the first 2 days and then subsidesaccording to the laws of gravity. During the 3rd and 4thdays, edema of the eyelids migrates downwards to thecheeks and then the jaw, reaches the neck on the 5th day,and disappears on the 6th or 7th day. The edema that fol-lows a localized phenol peel on the lips subsides morequickly, as it has less distance to cover before it reaches theneck.


Figure 37.53(a) Before the peel. (b) Facial edemathe day after a TCA peel to thepapillary dermis (Unideep®): notethat the edema on the first day notonly gets rid of the cheek wrinklesbut also the facial sagging. Theerythema is reduced by antioxidantsin the post-peel cream.

A B

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®.

A B

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Prevention of edemaPeels to the papillary dermis and especially to the reticulardermis trigger the most dramatic edema, and it is only inthese cases that prevention should be considered. Theseverity of the edema is hard to predict; some patients have(relatively) little swelling, whereas others have severeedema even before the whole face has been treated. Preven-tive, intravenous injections of corticosteroids before thepeel do not appear to make much difference, and theedema develops in spite of the corticosteroids.

With phenol peels, it is often possible to limit edema inthe upper eyelids by not treating the skin of the upper eye-lid tarsus (Figure 37.55). The eyelid edema is then lessuncomfortable for the patient.

When the impermeable dressing (occlusive phenol) isbeing applied, it should not be placed too close to the eyes,to avoid excessive swelling on the part of the eyelids notcovered by the occlusive dressing.

Treating edemaSmall, paper or textile bags containing China tea, after theyhave been boiled and cooled in the refrigerator, makeexcellent, refreshing compresses that can be used to allevi-

ate the discomfort of eyelid edema. The patient shouldsleep in a half-sitting position to help the edema go down.The doctor should wait for some months before judgingthe permanent effect of the peel. As the swelling goes down,wrinkles that have not responded to the medium or deeppeel reappear on the patient’s skin.

It is not necessary to prescribe diuretics in the largemajority of cases. Edema associated with an infection or anallergy should be treated accordingly.

Steroids and non-steroidal anti-inflammatories shouldbe avoided so as not to interfere with collagen generation.Oral Varidase®119 can be used to help the swelling subside.

MiliaThese small epidermal inclusion cysts120 are a relativelycommon and fortunately benign complication of mediumor deep peels, and occur mainly when the peels have beenfollowed by greasy occlusion or occlusive make-up. Theycan 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 beforethey become visible, and it takes 6–12 weeks of patience forthem to disappear, unless patients run out of patience andremove them themselves or ask the doctor to do it.

Prevention of miliaTopical tretinoinApplying topical tretinoin (all-trans-retinoic acid) before apeel can often reduce the incidence of milia. However, theundesirable effects of retinoic acid in combination with adeep or medium peel must be taken into account. Retinoicacid increases the depth of penetration of caustic agents,could increase the risk of hyperpigmentation68 and, if it isapplied too soon after a medium or deep peel, slows downthe rate of re-epithelialization.

Dry technique for phenolDuring the phase of skin regeneration that follows a phenolpeel, 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 isused, and if they do, they are small, few in number andleave no marks after excision.

Treating miliaPatients should not try to remove these small, white, subcu-taneous cysts themselves. If they are handled unnecessarilyor too roughly, sometimes with the help of unorthodoxinstruments, secondary infections and/or scars can follow,


Figure 37.55Frosting of the skin after application of Lip & Eyelid®formula: note that the skin of the upper eyelid tarsus has notbeen treated, to limit the post-peel edema.

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and the milia can remain deeply embedded in the skin. Atthe most, patients can use a Buf-Puf® (3M) sponge to gen-tly 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: aperiod of 1 month is left for them to clear, by which timere-epithelialization is complete. The doctor should care-fully make an incision in the top of each cyst with the tip ofa No. 11 scalpel or an 18G needle, which will make it easierto extract them with a blackhead remover without leavingany marks, as the cut is strictly intraepidermal. This treat-ment is carried out with sterile equipment after disinfec-tion, and there is no need for local anesthetic.

AcneAcne can be either treated or triggered by a peel. Anintraepidermal peel (Easy Phytic®) or a peel to the basallayer (Easy TCA®) is usually a good treatment for come-donal, papular or even papulopustular acne. Intraepider-mal peels or peels to the basal layer do not usually triggerpost-peel acne, unlike peels to the papillary dermis, whichcan promote secondary infections.

Active acne must be treated in the weeks before a peel tothe papillary or reticular dermis, and the medium or deeppeel can only be started once the infection has completelycleared. The increased epidermal permeability resultingfrom prescription treatments must be taken into account.

Doing a papillary or reticular dermal peel during theactive phase of pustular acne would trigger a potentiallyserious infection of the whole treated area that could evendevelop into toxic shock. A fortiori, peels should not beperformed on patients suffering from active acne conglo-bata, necrotica, etc.

Some comedones may occur in certain patients duringthe post-peel period: they should be extracted with a black-head remover.

It is common for acneiform dermatitis to develop undergreasy dressings (see also the section above on microbialinfections) after deep peels treated with the ‘moist’ tech-nique. Vaseline® in fact creates an impermeable layer thatacts as total occlusion. It is known that bacterial prolifera-tion is much more rapid under occlusion than in the openair. Antibiotics and standard local treatments are used totreat post-peel acne.

PainThe pain threshold is virtually the same for all humanbeings, who perceive the stimulation of their nociceptorsfrom the same intensity threshold. Pain tolerance, how-ever, varies considerably from one patient to another. It isvery important to consider patient psychology, especially

during the first peel session. Patients have absolutely noidea what they are about to go through, and words like‘chemical’ or ‘burn’ evoke images that contribute to thegeneral anxiety generated by the first sensation of pain.Peels that do not go beyond the Grenz zone have to berepeated several times in order to be effective. The first ses-sion is the most painful, as the patient feels the pain‘blindly’, not knowing what is going to happen next, andbecomes increasingly anxious, which amplifies the sensa-tion of pain. Patients find the following sessions lesspainful, as they can anticipate when the pain will stop. Ingeneral, pain tolerance seems to increase with age. Con-trary to rumor, men have a slightly higher pain sensitivitythreshold than women, but women, who are more used topain, tolerate it (much) better. It is personality more thanrace or gender that influences how a person experiencespain, and it is often difficult to draw the line between painand suffering, sensation and emotion, pain experiencedand pain felt, as regardless of a person’s pain threshold, inthe end the pain always feels real.

Pain during application of thepeelThe pain caused by a peel is largely proportional to itsdepth. The type of pain, its intensity and its duration varydepending on the peel used. It is recommended to givepatients details about the pain they will feel, how intense itwill be, how it will develop, and how long it will last. It isessential to tell them about any change in technique, aspatients may become anxious if the pain they feel is differ-ent to what has been described.

AHAsPartially buffered glycolic acid at 50% or 70% is notpainful. Unbuffered 70% glycolic acid (with pH <1)causes a burning sensation that is as bearable as it is short-lived. Neutralization with a solution saturated in sodiumbicarbonate immediately stops any burning sensation.Other AHAs are less aggressive on the skin and lesspainful. The pain decreases as the molecular weight of themolecules increases, as larger molecules have more diffi-culty penetrating the skin. Lactic acid is sometimes used totest skin sensitivity (the STINGING test): applying a 10%solution triggers a burning sensation in patients with sen-sitive skin. Easy Phytic® solution (glycolic, lactic, mandelicand phytic acids in a self-neutralizing solution) produces aspecific type of pain that starts with rapid burning fromthe glycolic acid, quickly followed by a relatively painlesstingling sensation that soon decreases in intensity. Thesesensations arise from the successive and gradual penetra-tion of the different acids and their natural neutralizationby the skin.


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TCA

Peels to the papillary or reticular dermisThe pain caused by TCA is directly proportional to theconcentration of the acid in the solution applied: a solutionat 20% m/m burns less than a solution at 30% m/m. Pain isone of the signs that alerts the doctor immediately to anyerror in the formulation used. If the patient complains of avery intense burning sensation when a solution that is notsupposed to be too aggressive has been applied, it is impor-tant to stop the application and check whether the solutionhas been properly prepared. A peel to the papillary dermisis always painful, but the intensity of the pain does notalways warrant local anesthesia; it is often enough to talk tothe patient, explain the pain, and the different phases of thetreatment and anticipate when the pain will stop. Patientsare grateful, however, when the doctor administers nerveblocks before applying the acid. It is not necessary to blockthe whole face, and supraorbital, suborbital and mentalblocks significantly reduce the intensity of the pain. Withthese nerve blocks, application to the forehead and midfaceregion is completely painless. To avoid overreactions, moresqueamish patients could be given mild premedication orsometimes, although rare, deep sedation before a peel tothe papillary dermis. When TCA is applied to the reticulardermis, premedication, deep sedation and/or nerve blockswill be necessary, as peels of this depth are very painful. Theanti-prostaglandin action of aspirin reduces the burningsensation and provides relief to many patients:500–1000 mg of aspirin taken 45–60 minutes before thepeel can therefore be recommended if the peel is to reachthe papillary dermis. There is a greater risk of bruising,however.

The Unideep® peel (TCA to the papillary dermis com-bined with an antioxidant, stimulating and analgesic post-peel mask) has the advantage in that it can be appliedregion by region and the patient benefits from the almostimmediate analgesic effect of the post-peel cream maskthat is applied as soon as frosting is achieved. The foreheadis treated first until even pink–white frosting appears, andthe post-peel cream is applied on this area before startingtreatment on the next area. Patients soon experience therapid relief brought by the post-peel cream, which makesthem less anxious about the rest of the treatment.

Using cold packs (ColdHot Pack® by 3M) before apply-ing the Unideep® solution can be effective: cooling the skinbefore applying the solution alleviates most of the pain. Itseems that most of the pain comes from the sudden warm-ing of the papillary dermis after vasodilation; the heat-sen-sitive nociceptors in the papillary dermis cannot, of course,react as strongly when they are cooled beforehand withcold packs. Using cold packs is therefore effective bothbefore applying the peel solution and immediately after-wards – the plastic of the cold packs can come into directcontact with the acid in Unideep® (Figure 37.56). Some

patients, however, find the cold almost as unpleasant as thebite of the acids, and prefer simply to have their skinfanned with a hand-held or electric fan. Squeamishpatients will appreciate a frontal nerve block. TheUnideep® solution is applied to the forehead first andtaken beyond the anesthetized region towards the temples.The post-peel cream immediately stops the sensation ofpain, and the rest of the face can be treated easily, without


Figure 37.56Cryoanesthesia with a cold pack during combined chemicalblepharoplasty (Lip & Eyelid®) and TCA to the papillary dermis(Unideep®).

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nerve blocks, as patients can accept pain that they know tobe short-lived and bearable, having felt it on the templesand expecting it to be ‘blocked’ by the post-peel cream.

Only Touch® is an adjuvanted and saponified solutionwith a concentration of 45% m/m of TCA. Localized appli-cation to small, benign lesions with a maximum diameterof 1 cm triggers intense burning that is not too unpleasant,as it is limited in extent. Only Touch® does not require anytype of anesthesia. When treating a large number of lesions,as is often the case with lentigines on the hands or décol-letage, the patient may appreciate the use of cold packs toreduce the burning sensation (Figure 37.57). The cold packcan be used in two ways: either the doctor waits for the acidto dry before applying the cold pack on the skin with asheet of paper in between or applies the plastic of the coldpack directly on the acid as it is taking effect. The acids useddo not damage the plastic of the cold pack, and this type ofimmediate and direct application seems to be the mosteffective at reducing the pain.

Peels to the basal layer or Grenz zoneEasy TCA®, an adjuvanted and saponified solution with15% m/m TCA,112 only produces a sensation of heat ormild burning that the vast majority of patients find easy tobear. More squeamish patients will complain of feelingsome pain, but it is short-lived, as the post-peel cream alle-viates it immediately.123 After the post-peel cream has beenapplied, there is only a feeling of tightness.

PhenolPhenol is used to regenerate the skin down to the reticulardermis. It has useful neurolytic and anesthetic properties.The pain is therefore short-lived (around 15 seconds), asthe phenol produces local numbness that lasts from 20–30minutes. After this time, the inflammatory phenomena in

the dermis become powerful enough to trigger a painfuland intense sensation of heat that will slowly subside overthe next few hours and days.

Recently, some phenol formulas have been presented asallowing a full-face peel without any anesthetic. A phenolpeel that can be applied to the whole face without any typeof anesthetic is a more superficial phenol peel that does notinduce regeneration of the reticular dermis of the samequality as the ‘classic’ phenol peels. Less pain goes hand inhand with inadequate results: the results of this type ofphenol peel are the same as for a TCA peel to the papillarydermis and may not have much effect on wrinkles. Thepain caused by these peels is also the same as for a TCA peelto the papillary dermis. It is pointless to put a patientthrough the risks of phenol toxicity only to get the resultsthat a simple, non-toxic molecule (TCA) can achieve. Aneffective, full-face phenol peel should therefore be usedwith an anesthetic (see Chapter 33).

A localized Litton or Baker–Gordon peel can be carriedout with short-acting nerve blocks with 2% lidocaine with-out adrenaline (epinephrine). The pain is also short-lived.Phenol provides anesthesia that extends about 1 cmbeyond the frosting, and the phenol can be applied slowly,step by step.

Chemical blepharoplasty and cheiloplasty124 are ideallycarried out with Lip & Eyelid® formula: its action is moregradual than that of Baker–Gordon or Litton phenol, and itcan be applied locally without any anesthetic since the painonly lasts 12–15 seconds.

Phenol is neurolytic; it makes the skin less sensitive forseveral days, and it is possible to touch up certain areaswithout causing any real pain after the nerve block anes-thesia has worn off, even the day after the peel. Even if deepinflammatory phenomena make the dermis painful, theepidermis remains insensitive.

Post-peel painAHAsNeutralization, which relieves the pain, can sometimes beunpleasant, as the process of AHA neutralization is slightlyexothermic. The pain subsides very quickly after anyintraepidermal peel.

Easy TCA® and Unideep®The Easy TCA® (to the basal layer or Grenz zone) andUnideep® (to the papillary dermis) post-peel mask creamhas the major advantage of relieving the burning sensationcaused by the acids almost immediately.

Using cold packs as soon as the peel is over usually pro-vides relief to the patient.

No specific treatment is necessary for the pain thatcomes immediately after peels to the papillary dermis.


Figure 37.57Use of a cold pack during treatment of lentigines on thehands with Only Touch®.

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Only Touch®There is almost no residual pain after Only Touch®.

Peel to the reticular dermisThe fact that patients look as if they have third-degreeburns after a peel to the reticular dermis has no relation tothe pain they actually feel (Figure 37.58).

After a phenol peel, the type of pain experienced variesenormously, and descriptions given by different patients ofthe intensity of the pain go from ‘completely painless’ to‘extremely painful’. Opioids are sometimes necessary torelieve severe pain.

A combination of paracetamol (acetaminophen) pluscodeine is especially well suited to post-peel pain, butshould not be used in the hours following a phenol peel, asparacetamol (a phenol derivative) goes through the samedetoxification pathways as phenol, which could createmetabolic competition and the risks of toxicity associatedwith phenol might be increased. Preventive administrationof benzodiazepines (lorazepam 2.5 mg before the peel andon the night of the peel before going to bed) relieves theanxiety caused by these unpleasant sensations and reducesthe need for analgesics after the peel. In case of very severe,localized pain (extremely rare), a nerve block could beused.

Often, the pain described by the patient is an unpleasantsensation of heat, due to extensive vasodilation that imme-

diately follows a deep peel. A cold pack can help the patientget through this phase.

The pain that occurs after a phenol peel can be summa-rized 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 sensitivityAll peels, even if they do not cause any visible flaking, dam-age the skin’s protective stratum corneum and make itmore sensitive to all types of aggression. Light consists ofhigh-energy particles called photons. Photons are absorbedby the ozone layer and oxygen in the atmosphere and only7.1% of solar energy reaches the Earth. Photons move inwaves and have a characteristic wavelength and frequency.They are absorbed in the skin, where they cease to exist andare converted into energy. UV rays have wavelengthsbetween 100 and 400 nm, but only UVA (320–400 nm)and UVB (290–320 nm) reach the Earth, as the ozone layerblocks UVC.125 High frequencies have the most energy(gamma rays have the most energy and UV rays have moreenergy 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 sunon the equator stronger than the sun in Lapland, and themidday sun burns more than the afternoon sun. Fog doesnot slow down UV penetration, but urban pollution is, onthe contrary, a powerful sunblock because of the presenceof aromatic hydrocarbons, which make excellent UVblocks. Altitude in itself has less influence than the angle ofincidence, but snow, on the other hand, reflects 85% of UVrays, whereas dry sand only reflects 17%, water 5% andgrass 2%. Therefore, places lying between snow-coveredmountains on a very sunny day are particularly dangerous.

After penetrating the skin, photons are absorbed by spe-cific molecules called chromophores. Each chromophoreabsorbs a set wavelength. Photons that penetrate the skinare converted into energy, and this produces biochemicalchanges that make certain molecules unstable by puttingthem in a higher-energy state. Some molecules can convertthis energy into heat and/or vibrations and thus regaintheir original stable state (eumelanins behave in this way,for example). The energy absorbed can also break certainintramolecular bonds and convert some molecules into


Figure 37.58After a phenol peel, patients look as if they have third-degreeburns, but in fact feel no pain at all.

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free radicals. These free radicals are very reactive and willbind rapidly with other chemical species.

Free radicals can also attack the DNA molecule andblock its replication locally. They can sometimes break theDNA molecule during the replication phase of the cellcycle, before the mitosis phase, or if photosensitizing mol-ecules are used. Fortunately, human cells contain mecha-nisms for the repair of damaged DNA, involving DNApolymerase and other enzymes.

The polyunsaturated fatty acids that make up cell mem-branes are very sensitive to free-radical attacks. The CH2

group that is located between the double bonds of arachi-donic acid degrades as a result of free-radical attacks; itforms unstable peroxides, and at the end of these chain reac-tions a malonedialdehyde molecule is released at the sametime as two new free radicals, and these spread the reactionsto the rest of the membranes. Once the free-radical reactionhas started, the damage spreads quickly. Some amino acids,either free or as components of proteins, can absorb UVrays, leading to photoionization and releasing electrons thatinitiate reactions that damage proteins. Moreover, in thepresence of oxygen, oxygen free-radicals are formed thatthen react with organic molecules to produce hydroperox-ides. These can then damage proteins both by breakingpolypeptide chains and by forming bridges between them.

In short, sunlight damages the genetic code, cell mem-branes, intracellular organelles, proteins, enzymes, etc.What is more, only 25% of the erythema dose is needed tocause 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 thedamage caused by photons. Some of the light from the sunis reflected off the fatty layer covering the corneocytes. Theoutermost layers of the stratum corneum also reflect light,and the photons that manage to penetrate this layer are dif-fused as they reflect off the different layers of cells.

The UV photons that have not been reflected or absorbedreach the basal layer of the epidermis, the papillary dermisand the reticular dermis. UVA rays that are emitted perpen-dicular to the skin penetrate deeply: 66% get through thestratum corneum and 44% reach the basal layer. They haverelatively little effect on the epidermis, but do severe damageto the dermis. Some 17% of UVB rays get through the stra-tum corneum and 3% reach the basal layer. They cause moredamage to the epidermis than to the dermis. The thicknessof the stratum corneum is therefore an important part of theskin’s defenses, and treatments that damage it (dermabra-sion, laser, AHA creams, peels, etc.) allow photons in andpromote the free-radical damage described above.

The angle of incidence of solar rays is important: at ver-tical incidence, the photons only have to cover 15 µmthrough the corneocytes, while, at oblique incidence, theyhave to cover up to 35 µm to reach keratinocytes. Themorning or late afternoon sun is therefore less dangerousthan the midday sun.

Skin color is in itself a defense mechanism: white skinlets in up to 64% of rays that touch it and black skin is onlypermeable to 18% of these rays. White skin suffers fromphotoaging much more quickly than black skin. Yellowskin has fewer pigments than black skin, but the stratumcorneum is thicker than Caucasian skin and is better atreflecting and diffusing photons.

Beta-carotene, superoxide dismutase (SOD) and catalase(CAT) are vital free-radical defenses. Epidermal beta-carotene diffuses from the dermis and can scavenge freeradicals. SOD and CAT block the oxidative action of UVphotons. SOD blocks the first stage of oxidation, the forma-tion of the superoxide anion. The level of SOD in the bodyhas been directly correlated with life expectancy. Organismswith the most SOD live the longest. Some cosmetic prepara-tions 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 foreffective sun protection. Just one peel, of whatever kind,makes the skin more sensitive to the sun: patients soon feelthe difference just hours after treatment, and complain thatthey can no longer expose their skin to direct sunlightbecause of the burning sensation this causes. The deeperthe peel, the more sensitive the skin is to the sun. Thethinned or absent stratum corneum cannot provide pro-tection against the sun’s rays until the epidermis has com-pletely 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 there-fore recommended to keep using total sunblock126 andavoid the sun for a duration that is directly proportional tothe depth of the peel.

Demarcation lineA deep peel restructures the skin permanently and changesthe quality and structure of the skin irreversibly. Treated skinis cleared of actinic lesions and there is a visible line betweenthe treated and untreated skin. This is called a ‘demarcationline’ and can result from a difference in the quality or color ofthe skin (Figure 37.59). A difference in color is more obviousthan 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 (withphenol) or hyperpigmenting (with TCA) properties of dif-ferent peeling agents, the parameters that should be takeninto account are the depth of the peel and the patient’s skintype.

Depth of peelIntraepidermal peels or peels to the basal layer of the epi-dermis do not create a demarcation line. TCA peels to thepapillary dermis can change the texture and color of the


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skin, but there is often no visible demarcation line afterTCA to the papillary dermis. TCA is not toxic tomelanocytes. It can, however, get rid of the majority offreckles if it reaches the papillary dermis, and there will bea visible demarcation line between the skin with and theskin without freckles. A phenol peel is deep127 and toxic tomelanocytes, and it is with this type of peel that there is agreater risk of a demarcation line.

Skin typeHigh skin phototypes (IV to VI), dark or Asian skins,tanned or very sun-damaged skins are the most at risk of ademarcation line after a medium or deep peel. Skin photo-types I to III only very rarely suffer from permanent post-peel pigmentation problems: the only possible visibledifference would be in the texture of the skin. Figure 37.60shows the absence of a color demarcation line in a patientwith a light skin type who has had a combination of a local-ized deep phenol peel on the eyelids (Lip & Eyelid®) and aTCA peel to the papillary dermis on the rest of the face(Unideep®). The results shown are after 1 year. The phenolhas clearly made the skin firm again, and the medium-depth TCA has significantly improved the sun damage.Nevertheless, there is still a slight visible difference in thestructure of the skin between the areas treated with phenoland those treated with TCA to the papillary dermis. Thereis a particular risk with very sun-damaged skin, as themedium or deep peel restructures the skin to such an

extent that it leaves a very visible difference in the quality ofthe treated and untreated areas. Loss of tanning is propor-tional to the depth of the peel: intraepidermal peels lightena tan and deeper peels get rid of it altogether. A deep andlocalized treatment on tanned skin will always take awaythe color in the treated area that will appear all the lighteragainst the surrounding, tanned skin. Tanned, sun-dam-aged skins with a high phototype and dark or Asian skinsshould always be treated in such a way that the inevitabledemarcation lines will not be visible.

This is where the finer details of peel application count,as certain areas are more likely to develop demarcationlines than others.


Figure 37.59Neck demarcation line after a full face phenol peel.

Figure 37.60(a) Eyelid aging before treatment. (b) Results 1 year afterapplication of Lip & Eyelid® formula (upper and lower eyelids)and Unideep® to the rest of the face to even out the results.

A

B

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High-risk areasThe foreheadPrevention consists in applying the peel in the hair, about1 cm beyond the hairline. Neither phenol nor TCA are toxicto the hair bulb. There is no danger of localized alopecia.

The eyebrows should be treated against the lie of the hairso that the peel comes into contact with the skin under-neath the eyebrows.

White lip–red lip, nostrilsPrevention consists in taking the peel slightly over onto theoral mucous membrane and treating the skin on the edgesof the nostrils, up to the junction of the mucous mem-brane. Contact between phenol and the first millimeter ofthe lip mucous membrane does not pose any problem, andallows the doctor to treat fine lines at the same time asavoiding a visible and unsightly demarcation line aroundthe lips. Aged lips might take advantage of carefully appliedphenol on the red lip.

The earPrevention consists in feathering the tragus and the ear-lobe.

The neckPrevention consists in clearly setting the lower limit of thepeel before treatment, with the patient in the sitting posi-tion. If an occlusive phenol peel is used, the occlusive dress-ing should not be put under the lower jaw. The absence ofocclusion 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 beneaththe jaw (Figure 37.61).

Dilated poresBenatar128 describes this complication when doing deep-peel treatments on patients with thick, oily skins anddilated pores. The results of deep peels – and especiallymedium peels – are mediocre compared with the dramaticresults seen when treating drier and thinner skins. Thick,oily skin with dilated pores benefits more from ablativelaser resurfacing than a peel, even a deep one.

Epidermal peels and peels to the dermoepidermal junc-tion and the papillary dermis do not usually cause the pores


Figure 37.61(a) Demarcation line 1 month after afull face phenol peel (lip and eyelids)formula; (b) same patient 4 monthsafter the peel: the demarcation lineis fading.

A B

Figure 37.62Areas at risk of a demarcation line.

Go to 1 cm beyondthe hairline

Treat thetrages and

earlobe

Do not forgetthe nostrils

Treat theeyebrowsagainst thelie of thehair

Go to 1 cminto thered lip

Phenol: setthe lower limitwith patientupright

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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

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) Fourmonths after full-face Lip & Eyelid®: the nevi have become hyperpigmented. (d) Six months after full-face Lip & Eyelid®: the neviare still hyperpigmented.

A B

C D

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to dilate. On the contrary, more often than not, theytighten the pores.

Purpura, petechiaePetechiae are small skin hemorrhages characterized by tinybright red, purple or bluish spots that range in size from apinpoint to several millimeters in diameter. They arecaused by the rupture of small, dermal blood vessels andthe extravasation of red blood cells. Purpura, unlike atelangiectasia, does not blanch when pressed with glass.Vitamin C and K deficiencies promote petechiae. Purpurausually tends to fade slowly and gradually, but recurrentpurpura can leave spots of iron deposit on the skin. It is arare complication, but petechiae can appear rapidly after aphenol peel if the patient has bouts of severe coughing orvomiting that trigger a sudden increase of pressure in thedermal blood vessels that have been damaged and tem-porarily dilated by the inflammatory reaction to the phenolpeel (Figure 37.63).

Once again, treatment is essentially preventive and con-sists in avoiding movements or maneuvers that mightincrease capillary pressure in the facial blood vessels:coughing, vomiting and even, as I was told recently, wash-ing the hair with the head bent forwards or nighttimescratching. There are some herbal medicinal plants thatmay be fairly effective and that are mainly used to treatvenous stasis: witch hazel, horse chestnut and red vine canincrease resistance in the vessel walls and reduce their per-meability, and have an anti-inflammatory and anti-edemaaction. These plant extracts can be taken by mouth, andvitamins C and K can be prescribed at the same time.

Benign nevoidhyperpigmentationAlthough phenol peels have been described as a possibletreatment for nevi,129 benign nevoid hyperpigmentationcan develop after a phenol peel (Figure 37.64). After aperiod of depigmentation of approximately 6 to 8 weeks,some nevi might become hyperpigmented. This hyperpig-mentation is benign. No skin cancer potentially induced bypeelings has been reported in medical publications.

Notes1. Heart, liver, kidney, larynx, neurological, digestive compli-

cations, 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.

4. Easy TCA® to cloudy white frosting.5. Although this ‘rest’ time varies considerably.6. Schmitt D. Biologie de la peau. Les éditions INSERM, 1995.7. Litton C, Trinidad G. Complications of chemical face peel-

ing as evaluated by a questionnaire. Plast Reconstr Surg1981; 67: 738–43.

8. Easy Phytic® solution is a slow-release and self-neutralizingmixture of AHAs that work gradually and is not thereforecompatible with any preparation technique that mightincrease the permeability of the stratum corneum.

9. Beware of young patients who overuse aggressive anti-acnepreparations.

10. Except for skin that is badly sun-damaged, as the area treatedwith phenol will have completely regenerated and will be offar better quality than the untreated, neighboring skin,which will still look old.

11. With less than a week in between for Easy TCA®.12. See the photographs in the section on hyperpigmentation

later in this chapter.13. Renutriv ACE Lipoic Complex® (see Chapter 3).14. Rubin MG. Manual of Chemical Peels, Superficial and

Medium Depth. Philadelphia: JB Lippincott, 1995.15. It is preferable to use partially insulated needles, such as

Kobayashi.16. There is an overall increase in the quantity of newly synthe-

sized DNA in the epidermis.17. It should be remembered that any peel removes at least the

stratum corneum, the first UV barrier. Effective sun protec-tion should be used to make up for the loss of the stratumcorneum.

18. This is partly what Easy TCA® post-peel cream is for: it pen-etrates more easily when it is applied immediately after thepeel solution and scavenges the free radicals as soon as theyare produced. In Easy Phytic® solution, phytic acid, with its12 free-electron-binding sites, plays this role.

19. Grenz is the German word for ‘border’: the border betweenthe dermis and the epidermis.

20. Easy TCA® does not cause hyperpigmentation when it isapplied to the Grenz zone, because of the anti-free-radical,anti-inflammatory and tyrosinase-inhibiting action of thepost-peel cream, applied immediately after the acid solution.Weekly repetition of Easy TCA® is also a contributing factorto avoiding post-inflammatory hyperpigmentation.

21. Epidermal sliding: the acids coagulate the proteins that bindthe epidermis to the dermis and the epidermis slides over thedermis. Sliding is the pathognomonic sign of a peel to thepapillary dermis.

22. Whereas with a superficial peel, they are stimulated indirectly.23. Manquat A. Traité élémentaire de thérapeutique de matière

médicale et de pharmacologie, 5° ed, tome 2. 1903: 193.24. For example, a patient with light skin with a dark-skinned

parent or grandparent. Their skin appears not to react muchto inflammation, but they can soon develop pigmentarychanges.

25. Easy TCA® or AHAs can, on the other hand, be applied incases of standard papulopustular acne.

26. Girond JP, Mathé G, Meyniel G. Pharmacologie clinique.1590–1. Expansion Scientific Français, 2003.

27. Some formulations do require this kind of manual abrasionin immediate preparation for peeling.


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28. It is not uncommon for the patient to phone the doctorcomplaining that their melasma has gone from brown toalmost black during the first 3 days after Easy TCA®. This isnot a pigmentary change, but normal local dehydration ofthe epidermis, a sign of a positive effect on the pigmentationproblem being treated.

29. Fouque L, Seban D. Peelings associé TCA et acide glycolique.18° réunion du GRCD, Perpignan, 25–27 Septembre 1995.


31. The Wood’s lamp (350–390 nm) can, however, revealintraepidermal pigmentation that is lying over another der-mal pigmentation. In this case, it gives a false sense of safety,and there is a risk of promising the patient rapid resultswhen only the epidermal pigmentation can be readily elimi-nated.

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 pharma-

ceuticals, Costa Messa, CA, USA). In the case of resistance,the dermatology department at Yale University School ofMedicine uses concentrations of up to 40%.

35. For example, if the product is applied at night, there is a riskof depigmenting other parts of the body through involun-tary movements when asleep or by rubbing the eyes with thehand while applying the treatment, etc.

36. Hedges TR, Kenyon KR, Hanninen LA, Mosher DB. Cornealand conjunctival effects of monobenzone in patients withvitiligo. Arch Ophthalmol 1983; 101: 64–8.

37. Nordlund JJ, Forget B, Kirkwood J, Lerner AB. Dermatitisproduced by application of monobenzone in patients withactive vitiligo. Arch Dermatol 1985; 121: 1141–4.

38. Catona A, Lanzer D. Monobenzone, superfade, vitiligo andconfetti-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 solu-

tion.42. Inhibition of homogentisic acid oxidase, leading to local

accumulation of homogentisic acid followed by polymeriza-tion 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 lipo-

somes, cyclodextrins, nanosomes or multilayers and usingspecific molecules such as arbutin, magnesium ascorbylphosphate, etc.

45. The chemical composition of the base cream can alter theantibacterial effectiveness of azelaic acid: Charnock C,Brudeli B, Klaveness J. Evaluation of the antibacterial effi-cacy 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 ofaction. Effect of azelaic acid on melanoma and other tumoralcells 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. Toxicityof azelaic acid. Drugs under experimental and clinicalresearch [Drugs Exp Clin Res] 1983; 9(6): 447–55.

49. Yokota T, Nishio H, Kubota Y, Mizoguchi M. Theinhibitory effect of glabridin from licorice extracts onmelanogenesis 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 applicationseems to be 1–2%.

51. Nakajima M, Shinoda I, Fukuwatari Y, Hayasawa H. Arbutinincreases the pigmentation of cultured human melanocytesthrough mechanisms other than the induction of tyrosinaseactivity. 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 ofretinol or retinaldehyde can be just as effective as tretinoin,without being irritating. Keratinocytes have the necessaryenzyme arsenal to convert these precursors into retinoicacid, 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. BiolPharm Bull 2002; 25: 1045–8.

55. Ando S, Ando O, Suemoto Y, Mishima Y. Tyrosinase genetranscription and its control by melanogenic inhibitors. JInvest Dermatol 1993; 100: 1505–55.

56. Usuki A, Ohashi A, Sato H et al. The inhibitory effect of gly-colic acid and lactic acid on melanin synthesis in melanomacells. Exp Dermatol 2003; 12(Suppl 2): 43–50.

57. Excessive application on the doctor’s part, too high a con-centration 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 isneutralized 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 morerapidly and more deeply.

64. Water does not neutralize acids, but dilutes them, which isnot enough in this case. An acid is neutralized by combiningit with a base to produce a salt.

65. Stone PhA. Peelings au phénol Baker/Gordon et modifiés. JMed 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 thanthe second. See Chapter 12 for more information.

67. In addition to TCA and water, a tamed solution containsother ingredients that change or regulate its activity. Resultsare therefore more predictable.

68. Collins PS. Chemical face peelings. In: Elson ML (Ed.), Eval-uation and Treatment of the Aging Face, 34–67. 1995, Ger-many, 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. Inher-

ited disorders of connective tissue. In: Braunwald E, FauciAS, Kasper DL et al. Harrison’s Principles of Internal Medi-cine, 15th edn. New York, McGraw-Hill, 2001: 2290–300(specifically 2295–7).

72. Yusel D. Was Paganini born with Ehlers–Danlos syndromephenotype 4 or 3? Clin Chem 1995; 41: 124–5.

73. Byers PH. Ehlers–Danlos syndrome: recent advances andcurrent understanding of the clinical and genetic hetero-geneity. J Invest Dermatol 1994; 103(5 Suppl): 475–525.

74. Lloyd J, Narcisi P, Richards A, Pope FM. A T+6 to C+6mutation in the donor splice site of COL31A IVS7 causesexon skipping and results in Ehlers–Danlos syndrome typeIV. J Med genet 1993; 30: 376–80.

75. Wertelecki W, Smith LT, Byers P. Initial observation ofhuman dermatosparaxis: Ehlers–Danlos syndrome typeVIIC. 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 clinicalfeatures of Ehlers–Danlos syndrome type VIIB resultingfrom a base substitution at the splice acceptor site of tiatron5 of the Col1A2 genes. J Med Genet 1994; 31: 306–11.

78. Mattar SG, Kumar AG, Lumsden AB. Vascular complica-tions in Ehlers–Danlos syndrome. Am Surg 1994; 60:827–31.

79. Berney T, La Scala G, Vetterel D et al. Surgical pitfalls in apatient with type IV Ehlers–Danlos syndrome. Dis ColonRectum 1994; 37: 1038–42.

80. AHAs or TCA in aqueous solution could penetrate toodeeply; phenol would certainly cause scarring. Easy TCA®could possibly be used, on the strict condition that it doesnot go beyond the basal layer of the epidermis (pinpointfrosting).

81. Although some doctors like to prepare the skin.82. As this peel is slow-release, anything that accelerates pene-

tration must be avoided. The AHAs in this peel build up inthe stratum corneum before being slowly released into theepidermis.

83. This type of dangerous procedure consists in reaching thelimits of a peel’s possibilities; the safety factor gets lower asthe peel gets closer to this limit.

84. A deep peel of the radial folds of the lips (Lip & Eyelid®); seeChapter 36.

85. The skin’s buffer capacity is its physiological capacity toresist 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 solu-

tions himself. The nurse ‘forgets’ to mix the TCA in aqueoussolution with the base solution and actually prepares onlyTCA 50% m/m for the doctor, who applies it directly to thepatient’s skin.

88. The surface to be treated should be touched in the same wayas when touching a keyboard: quickly and precisely. There isno delete key with Only Touch®!

89. Wojno T, Tenzel RR. Lower eyelid ectropion followingchemical face peel. Ophthalmic Surg 1984; 14: 9–12.

90. McKinney P, Zukowski ML, Mossie R. The fourth option: anovel approach to lower lid blepharoplasty. Aesth Plast Surg1991; 15: 293–6.

91. Hecker D, Hacker SM, Ramos-Caro FA, Flowers FP. Tem-porary ectropion due to topical fluorouracil. Cutis 1994; 53:137–8.

92. Ideally, of course, this dressing should be worn as a preven-tive 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 alcohol-

and acid-resistant (mycobacteria, for example).101. LaVerme WE, Drapkin MS, Courtiss EH, Wilson RM. Toxic

shock syndrome after chemical face peel. Plast Reconstr Surg1987; 80: 115–19.

102. Patients with herpes, active acne or active seborrheic der-matitis, for example. These disorders should be treatedbefore the peel.

103. The rolling movement is similar to that used when rolling acigarette.

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.), Dermato-logic 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 anti-bodies in 70% of the population and HSV-2 antibodies in17% of subjects. Overall, 20% of subjects test positive foranti-HSV-2 antibodies in developed countries, and this ratecan reach 60% in developing countries. In France, labial her-pes, or cold sores, affect around 12 million people.

108. Only 2 cases of post-peel herpes were counted in 5280 EasyTCA® peels to the basal layer, performed in Spain, on 1320patients, each treated for 1 month, at all times of the year.


110. Bupivacaine and ropivacaine have a much longer durationof action than lidocaine. Ropivacaine poses a far lower risk ofcardiac arrhythmias.

111. For example, sublingual lorazepam (Temesta®) 2.5 mg of1/2 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 ery-

thema and pruritus, responsive to the topical application ofhydrocortisone 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


ch37 7/11/06 9:07 am Page 369

the Grenz zone in places and can trigger a local edematousreaction that looks like an allergy, but disappears by itself in48 hours.

118. This is a rare, but reported, side-effect.119. Varidase® = 10 000 IU streptokinase and 2500 IU

streptodornase. Streptokinase is a protein, an enzyme pro-duced by beta-hemolytic streptococci. It has indirect fibri-nolytic properties by binding with plasminogen. It is a fibrinnon-specific thrombolytic.

120. Small, whitish and firm formations that form epidermalcysts. They are formed from an accumulation of keratin inthe pilosebaceous units.

121. Bismuth subgallate or thymol iodide powder mask (seeChapter 35).

122. Easy TCA® solution contains AHAs, antioxidants, vitaminsand saponins, and can be applied on all skin types, withoutpreparation and prior cleaning of the skin.

123. The cream does not contain any local anesthetic, however,and its pH is slightly acidic. It therefore does not neutralizethe solution.

124. Chemical blepharoplasty is treatment of the eyelids with alocalized deep peel. Chemical cheiloplasty is treatment of thelips with a localized deep peel (see Chapter 36).

125. The nucleic acids in the thymus have the same absorptioncurve as the ozone layer. If there were no ozone layer, thesenucleic acids would absorb UVC, and the free-radical dam-age caused by this absorption would destroy the body’simmune defenses.

126. Melablock HSP®: physical and chemical protection, SPF 50+and HSP inducers.

127. The possibility of using phenol as a more superficial peel hasbeen broached elsewhere in this book. Because of the relativelyhigh risk of toxicity and complications, this agent should onlybe used for deep peels carried out under strict control.

128. Benatar D. Le peeling au phénol. J Med Esth Chir Derm1988; XV(60): 319–23.

129. Hopkins JD, Smith AW, Jackson IT. Adjunctive treatment ofcongenital pigmented nevi with phenol chemical peel. PlastReconstr Surg 2000; 105: 1–11.


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A trichloroacetic acid (TCA) peel, even if it reaches thepapillary dermis, is not always enough to correct thepatient’s cosmetic problem, and experienced doctors areoften led to combining several techniques to achieve theresults they want. Peels can be combined to work togetheror with other surgical or non-surgical techniques. Usinganother technique or another peel before a TCA peel isoften intended to remove part of the epidermis to enhancepenetration of a lower-concentration TCA. The first tech-nique provides the equivalent of a superficial peel that willenhance the action of the TCA applied afterwards. Someauthors maintain that using a combination of peels lowersthe frequency of complications compared with using moreconcentrated TCA, in aqueous solution. Not all combina-tions are safe, however, and a combination of differentpeels on the same surface often tends to make the symp-toms more complex and increase the risk of complicationscompared with the safer formulations of today.

Post-peel care is also more complex when peels arecombined, as the injury is deeper: 6–7 days of post-peelcare are usually required, when the patient will use Vase-line®, antioxidant creams or antiseptic washes (e.g. povi-done–iodine solution). Post-peel care should include adepigmenting cream (Blending Bleaching®) and effectivesun protection (Melablock HSP®). Prolonged erythemalasting more than 15 days is common. If it is focal – andtherefore suspicious – it can be treated with a strong corti-costeroid cream two or three times a week. The risk ofscarring and pigmentary changes is greater when peels arecombined (on the same surface), because of the increasedpenetration of TCA. Cosmetics that are suitable for thepost-peel period should be used as soon as the skin cantolerate them. Tretinoin, alpha-hydroxy acid (AHA)creams or benzoyl peroxide must not be used again for 6weeks.

Alpha-hydroxy acids plustrichloroacetic acidAHA peels make the skin more permeable because theyreduce corneocyte cohesion and induce partial epider-

molysis. The depth of action of a TCA peel is increased bythe prior application of an AHA peel. Glycolic acid 70%in aqueous solution has been tried before TCA. After theusual application, the glycolic acid is quickly diluted withplenty of water. It cannot be neutralized, as if there is anybicarbonate – for example – on the skin before the TCAis applied, it will ‘pre-neutralize’ the TCA. After the gly-colic acid has been diluted, the skin is wiped with a papertissue or gauze swab and 25% m/m TCA is applied. Theuneven penetration of glycolic acid in aqueous solutionposes a significant problem, as it affects the penetrationof the TCA that is applied afterwards. Where the glycolicacid has penetrated more deeply, the TCA will penetrateeven more deeply. Where the glycolic acid has not pene-trated far, the depth of action of the TCA is barelyimproved. A combination of AHAs and TCA cannottreat wrinkles or scars, and the indications are much thesame as those for TCA in simple aqueous solution(TCA–SAS) used alone. There is no clear advantage tousing this combination.

Resorcinol plus trichloroaceticacidThis combination has been described in the treatment ofphotoaging, fine lines, actinic keratoses and on skin photo-types lower than V. It can be used to treat some hyperpig-mentations, although there is a high risk ofpost-inflammatory pigmentary changes. Pre-peel prepara-tion and post-peel care must be rigorous in the latter indi-cation. Jessner’s (or Combes’) solution, described inChapter 24, is a mixture in equal parts (14 g) of resorcinol,salicylic acid and lactic acid, mixed in ethanol to give100 ml of solution. It is therefore a mass per volume (m/v)calculation. Jessner’s solution can be used to deepen TCApenetration. After degreasing and disinfecting the skin, acoat of Jessner’s solution is applied and left to dry. A sec-ond coat can be applied if the skin is oily and thick. Next,25% m/m TCA is applied until even frosting is achieved. Acold pack can be applied to the skin at the end of the peel toalleviate the burning sensation that the patient feels.

38Combination of techniques

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Dry ice plus trichloroaceticacidA ‘reasonable’ application of dry ice on its own usually pro-vides a superficial peel; if the dry ice is followed immedi-ately by an application of 25% m/m TCA, the papillarydermis is easily reached, as the prior application of dry icedeepens the lesions created by the TCA. This technique(also called the Coleman technique) can be used on skinphototypes I to III, possibly IV, but never on V or VI. Therisk of developing hypertrophic, atrophic or depigmentedscars is high if more than 30% m/m TCA is applied afterdry ice, especially on the cheeks or around the eyes.

Given the inherent risks of this combination, its indica-tions are restricted to the treatment of keratoses ordepressed scars, in which the dry ice, applied locally andcombined with TCA, produces very good results, compara-ble to those of a phenol or Only Touch® peel.

The technique is as follows: a block of dry ice is held inthe hand, protected by several gauze pads to stop it fromfreezing. The block of dry ice is dipped in a solution of ace-tone (2/3) and alcohol (1/3) so that it will slide easily overthe skin without sticking. The skin is then rubbed vigor-ously. The depth reached depends on the contact time: thelonger the dry ice is left in contact with the skin, the deeperis the lesion caused (Figure 38.1).

The action of the dry ice is considered ‘superficial’ if thecontact time is 3–5 seconds, ‘medium’ after 5–8 secondsand ‘deep’ after 8–15 seconds.1 An experienced doctor willinduce different depths of injury, depending on the type ofdisorder being treated, by allowing longer contact timebetween the dry ice and the skin and/or by following thedry ice treatment with a TCA peel of varying concentra-tions. For example, contact time on keratoses2 will belonger to enhance penetration of the acid afterwards, or amore concentrated acid will be used after an even applica-tion of dry ice. This technique requires very thoroughpreparation: the doctor must examine the problem beforethe peel and, using a photograph of the patient’s face, drawup a precise chart clearly showing the contact times withthe dry ice and the different concentrations of TCA thatmay be applied after the dry ice. When dry ice that is

soaked in acetone is applied on the skin, fumes are let offthat are unpleasant for the patient, who should be properlyventilated to avoid inhalation.

It soon becomes clear that it is difficult to control thedepth of injury caused by dry ice, and therefore the depthof treatment overall, which is a significant risk factor.

Combination of differentconcentrations oftrichloroacetic acidIt is common to combine different concentrations of TCAduring the same peel session: a TCA peel to the papillarydermis (Unideep®) can be applied locally for dermalmelasma on the forehead, for example, while a TCA to theGrenz zone (Easy TCA®) is applied to the rest of the face(to even out the results) after focal treatment of keratosesor lentigines with a TCA to the reticular dermis (OnlyTouch®).

Phenol plus trichloroaceticacidUsing peels to different depths on the same patient is indi-cated when disorders of different depths coexist. Considera patient who presents with early elastosis, a few lentiginesand deep wrinkles on the upper lip: only phenol can get ridof the wrinkles on the upper lip, but it would be unneces-sarily deep to treat the early elastosis on the rest of the face.The phenol would of course get rid of the few senile lentig-ines, but a deep and very localized treatment with OnlyTouch® can also get rid of them and with less risk. Thispatient would therefore benefit from the following combi-nation (Figure 38.2):

• First session: combined peels: application of Lip & Eye-lid® formula (occlusive protocol) on the upper lip,immediately followed by an application of OnlyTouch® peel on the lentigines. Next, Easy TCA® isapplied to the whole face, except for the area treatedwith phenol.

• 8 days later: a second Easy TCA® application to theGrenz 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 Grenzzone (cloudy-white frosting) to the whole face, exceptfor the area treated with phenol.

• Last peel session: if the lentigines have not completelydisappeared, Only Touch® is reapplied locally. A fourthEasy TCA® is then applied to the Grenz zone (cloudy-white frosting), except for the area treated with phenol.


Figure 38.1 Depth of injury caused by the application of dry ice.

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Repetition of combined peelsCombined peels usually reach the dermis. We have justseen that the papillary dermis is easily reached, but it is alsopossible to reach the reticular dermis using more aggressivecombinations locally. This type of peel cannot be repeateduntil the skin has completely recovered, and not before 3months. Any persistent erythema, a sign of even the slight-est inflammation, rules out another peel.

Face-lift plus peelThe high risk of focal or widespread facial necrosis con-traindicates a phenol peel immediately after a face-lift. If aface-lift and a deep peel have to be combined, the surgicalface-lift must be done first and the chemical peel after-wards to avoid the demarcation line being surgically liftedto the cheek. Caution usually dictates a gap of 6 monthsbetween a surgical face-lift and a deep peel. It is of coursepossible to perform a face-lift without blepharoplasty and aphenol peel around the mouth and eyelids at the same time

of operation. There is no particular risk of necrosis3 inthese areas, as they have not been treated surgically.

TCA, on the other hand, has been applied successfully bydifferent authors to the whole face at the end of a surgicalface-lift. The depth of peel determines the risk of necrosis.

Trichloroacetic acid plusbotulinum toxinCan botulinum toxin be injected in the same session as apeel?

Thoughts on the possibility ofinjecting toxin before a peelSpeed of absorptionSymptoms of botulism have been reported as soon as 2hours after ingestion of contaminated food, which means

Combination of techniques 373

1

Lip & Eyelid®upper lip

Possibly secondOnly Touch® before

fourth East TCA®

2

Only Touch® peel,senile lentigines

3

Full-face Easy TCA®,one per week

8 days 8 days 8 days

Lip

& E

yelid

® fo

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Figure 38.2 Graph representing the way to associate different types of peelings and the period for repeating these peelings. A local phenol isfirst applied (on the upper lid for example). Immediately after, Only Touch® treats lentigines. When local frosting due to the deepTCA (Only Touch®) is perfect, Easy TCA® is applied on the whole face, but not on the phenol treated area.

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that intoxication is very rapid considering the time takenfor digestion and intestinal absorption. Uptake of thetoxin by the synapse is a rapid phenomenon that takesplace in several stages, the first of which is the binding ofthe toxin with an ectoreceptor/acceptor. Next comesinternalization in the presynaptic membrane, the forma-tion of endosomes and the intracytoplasmic interactionsthat eventually block the release of acetylcholine inresponse to a nerve impulse.

The internalization and ‘internal actions’ are slower andmore complex phenomena than simple binding at thereceptor/acceptor site. Vesicles that mediate internaliza-tion can be seen after 30 minutes through an electronmicroscope. Uptake of toxin at the receptor site is thereforevery rapid and starts within the first few minutes (or sec-onds?) after the toxin has been injected into their immedi-ate environment.

Different depths of actionBotulinum toxin (discovered in 1895 by Ermengem fromBelgium) is injected deep down in the facial muscles,whereas peels do not injure the skin beyond the reticulardermis at the most.

Influence of inflammationThe inflammatory reaction and edema that follow TCApeels (especially in simple aqueous solution) seem to be thedetermining risk factor of this combination. There is a riskof the toxin traveling or diluting in the post-peel edema.Therefore, under no circumstances should botulinumtoxin be injected after any peel whatsoever, as long as theinflammatory reaction and edema are still active.

Injecting the toxin before a peelIt is generally accepted (but not officially specified) thatbotulinum toxin should be injected at least 1 week before apeel. The obvious advantage of this prior injection is thatthe toxin blocks muscle movements and allows the dermisand epidermis to regenerate on a ‘smooth base’. Eight daysafter the toxin has been injected, its effect is complete andthe peel can be applied without any risk of the toxin beingmoved or diluted.

However, this technique means an extra journey andmore lost time for the patient.

After 10 years of clinical experience in the simultaneoususe of botulinum toxin and Easy TCA®, I can safely say thatthere is no risk in combining these two procedures duringthe same session. The botulinum toxin is injected first, anda rest period of 10 minutes is left to give time for the uptakeof the toxin at the presynaptic acceptor site. The EasyTCA® peel is then applied according to the basic protocol(see Chapter 15). There has never been any change in dura-

tion or depth of action, nor has the toxin moved duringthis combined procedure.

To my knowledge, injection of botulinum toxin imme-diately before other peels has not been tested, and it isadvisable to leave a rest period of 1 week after injection ofthe toxin if a peel other than Easy TCA® is applied.

Trichloroacetic acid and fillersHyaluronates and papillary peels clash on the battlefield ofthe dermis, and it is generally recommended not to injectsensitive polymers before applying a peel. Hyaluronic acidis a large carbohydrate polymer that is sensitive to externalaggressions such as free-radical attacks. Peels that producea severe inflammatory reaction generate a large number offree radicals that can break the hyaluronate polymers,shorten their lifespan in the dermis and introduce a greatmany macrophage cells into the dermis that can phagocy-tose the hyaluronates.

Under these conditions, the lifespan of the hyaluronicacid is shortened and filler injections with sensitive poly-mers should be given some time after a peel. This tech-nique also means an extra journey and more lost time forthe patient. I have therefore also used Easy TCA® at thesame time as injections of collagen and different reticu-lated hyaluronic acids (Restylane®, Juvederm®, Esthélis®,etc.) and have not seen any difference in the behavior ofwrinkles, whether or not these injections are combinedwith Easy TCA®. The filler injection is given first and EasyTCA® (solution plus post-peel mask) is applied immedi-ately afterwards. The antioxidant qualities of the post-peel mask seem to explain the fact that there is nointeraction.

Trichloroacetic acid andabrasionWe saw in Chapter 21 that it is possible to combine sand-paper abrasion with Easy TCA®.

Microdermabrasion withcorundum crystalsIn reality, the advantage of preceding a peel with microder-mabrasion is far from clear, as microdermabrasion doesnot provide abrasion as even as that produced by simplesandpaper. The handpiece of the microdermabrasion unitis comparable to a pencil, and its action can be likened todrawing a criss-cross of lines with clear spaces in between.The TCA solution penetrates more deeply in the base of theabrasion lines, giving a linear and uneven peel.


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LaserLaser treatment is not a simple alternative to sandpaperabrasion. Unlike sandpaper, it is painful and requires prioranesthesia. Besides, it is most likely that gentle and gradualabrasion with sandpaper has a clear advantage over laserabrasion in that it does not put any heat stress on the skin.

Notes1. Here, 3–5 seconds means in practice: 3 seconds on thin skin

and 5 seconds on thick skin.2. Or around the edges of scars to attenuate the difference in

height.3. Asken S, Unoccluded Baker–Gordon phenol peels – review

and update. J Dermatol Surg Oncol 1989; 15: 998–1008.

Combination of techniques 375

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ch38 7/11/06 9:07 am Page 376

abrasion 152erbium laser 152keratosis pilaris treatment 165, 166microdermabrasion 152scar treatment 162–3, 163

body scars 163–5uneven 161with phenol peel 279, 280with TCA peels 374see also sandpaper abrasion

accordion effect 33acetaminophen 195–6, 195acetic acid 79, 79acetone, skin preparation 54, 92, 149, 259acetylcholine (ACh) 21–3

esterase 22achromia, following AHA peels 68aciclovir 353acne 16, 27–8, 34, 34, 73, 359

comedonal 8, 33–4, 33, 125–6, 125macrocomedones 33–4

conglobata 102fulminans 102microcystic 126, 126necrotica 102papulopostular 73, 74, 126, 126rosacea 8scars 31, 127, 162

back 145, 163, 165décolletage 142ECTA treatment 163, 165ice-pick scars 55phenol treatment 241–3, 242, 243TCA treatment 100, 103see also scars

treatment 15, 31, 359AHAs 17, 55combined treatment 127Easy Phytic® 73–4ETCA 125–9, 125–8isotretinoin 102, 103Jessner’s formula 188maintenance treatment 127multifocal treatment 128–9phenol peels 240–3, 242, 243

post-peel care 126–7, 127problems 127, 128side-effects of acne 127TCA 102–3, 103, 109–10

actinic keratoses see keratosesadrenaline

phenol peels and 249with lidocaine 152–3, 153, 264

aging skin 36, 36AHA peels and 55–6

Easy Phytic® 71–3free radical aging 31hands 135–8, 136–9prevention 97–8, 120treatment 17–18

over 40–45 years old 18sagging skin 18–23under 40–45 years old 17–18

see also photoagingAhronson formula 196alcohol

phenol resistance and 212skin preparation 54with phenol peels 201

all-trans-retinoic acid (ATRA) 7see also tretinoin

allergiesto AHAs 67to antibiotic cream 27to local anesthetics 262to resorcinol

test for 185Unna’s paste 189–90

alpha-hydroxy acids (AHAs) 47, 48, 69application of 54

number of sessions 61buffers 49–50, 61, 63classification of peels 2combination treatment 59–60

hydroquinone 60TCA 371tretinoin 56, 59–60

contact time 49–50, 54, 62–3depth of peel 2

skin appearance and 62

Index

Page numbers in italics refer to illustrations or tables

alpha-hydroxy acids (AHAs) (cont.)effectiveness 57–8factors influencing penetration 53–4, 70histological effects 53

dermis 53epidermis 53

hyperpigmentation treatment 341indications for use

acne 55aging 55–6hyperkeratotic eczema 57ichthyosis 56–7melasma 56warts 56–7xerosis 56–7

mechanism of action 51neutralization 50, 54, 63–4, 69

partially buffered solutions 64preparation of neutralizing solution 63

pKa 50–1post-peel care 15, 65pre-peel preparation 5–6, 11, 54

Jessner’s formula as 189repeat peels 54, 61side-effects 67–8

achromia 68allergies 67dryness, desquamation, sensitization 67erythema 67, 319, 324hyperpigmentation 67, 331, 335infections 67–8melanocyte toxicity 317pain 67, 359, 361scarring 68, 342–3, 346shiny skin 68telangiectasias 67

slow-release complex see Easy Phytic® solution (EPS)see also glycolic acid; lactic acid

alpha-tocopherol see vitamin Ealuminium oxide 89, 184amino acids, dietary 30analgesics

following stretch mark treatment 161phenol peels and 253, 256, 292, 362TCA peels and 43

Unideep® 179see also pain

anaphylactic shock 262anesthesia

abrasion and 151with ETCA 152–3

allergy to local anesthetics 262checking effectiveness of 153chemical blepharoplasty 296phenol anesthetic effect 203, 203, 261phenol peels 262–5, 361

bupivacaine 263combination with adrenaline 264EMLA 264–5general anesthesia 262

lidocaine 263–4mepivacaine 263prilocaine 263repivacaine 263

scalp 131–2scar treatment 162TCA peels 43, 106, 360

Unideep® 179–80, 179toxicity of local anesthetics 262–3see also nerve blocks

angina 249angiogenesis 7, 8

retinoid effects 59antibiotic treatment 350, 351–2

acne 127allergies to antibiotic cream 27phenol peels and 258, 284, 288–9post-peel care 16

apoptosis 18heat stress and 14

Aptos® threads 231, 231arbutin 6, 17, 339, 339Argentofenol® 214arginine 30arrhythmias

anesthesia and 262, 263phenol and 216–20, 217, 258

bradycardia 220premature ventricular contraction 217, 217tachyarrhythmias 217, 217, 220

ascorbic acid 41–2, 49in ETCA 112see also vitamin C

ascorbyl palmitate (AP) 110, 341ascorbyl phosphate 341asepsis 259Asian skin, melanocyte toxicity 318asiaticosides 82aspirin 360atropine 220, 258, 271Ayres formula 196azelaic acid 6, 339

acne treatment 17hyperpigmentation treatment 339melasma treatment 98, 339

backacne treatment 55

scars 145anti-aging treatment 72

bacterial infections see infectionBaker–Gordon solution 273, 332Baker’s formulas 196, 206

toxic shock and 350basal layer peel 328, 328, 348–9, 354bentonites 89benzene 184benzodiazepine

herpes infection and 353pain management 362

378 Index

phenol peels and 253advantages of 256–7

benzoic acid, in resorcinol peels 184–5benzoin

in resorcinol peels 184tincture of 186

benzoyl peroxide 8, 9AHA peel preparation 54

Easy Phytic® 75TCA peel preparation 87

beta-blockers 219, 264betamethasone 28bigeminy 217biosaccharides 18biotin, in ETCA post-peel mask 111bismuth gallate 289bismuth subgallate (BSG) 147, 156–7, 156, 288–90, 342

chemical blepharoplasty and 298–9, 298–300making a mask 289–90, 289–91

bismuth subnitrate 289bisphenols 195black skin

hyperpigmentation treatment 8melanocyte toxicity and 318TCA sensitivity 91

bleeding, abrasion and 151, 152, 152Blenderm® occlusive mask 257, 257, 285Blending Bleaching® cream 17, 123, 167

chemical blepharoplasty and 302melasma treatment 121, 122post-inflammatory hyperpigmentation treatment 124stretch mark treatment 158Unideep® treatment and 182

blepharoplastysurgical 295, 295see also chemical blepharoplasty

blood pressure, phenol and 220body peels 32, 330

AHA peels 61Easy Phytic® 72–3, 72

resorcinol peel 186see also specific areas of the body

botulinum toxin (BTX) 11, 21combination treatment 43

Easy Phytic® 71–2phenol 233–4, 233TCA 43, 373–4

expression wrinkles and 31, 36prevention 315

perioral wrinkles and 36pre-peel preparation 61, 253, 274

chemical cheiloplasty 304botulism 373–4Bowen’s disease 170, 172bradycardia 220, 262Brown and Kaplan solution 196buffering

AHAs 49–50, 61, 63importance in the body 50phenol peels 201

bupivacaine 263burns 24

calluses 81carbachol 21, 21carbamide see ureacarbolic acid see phenolcarbon dioxide laser resurfacing 232carboxylic acids 49carcinoma 240

TCA treatment 102cardiac arrest, phenol and 220–1cardiorespiratory monitoring, phenol peels 258cardiovascular complications, phenol 215, 216–21

blood pressure 220bradycardia 220cardiac arrest 220–1prevention 219–20tachyarrhythmias 217, 217, 220treating arrhythmia during peel 220

catechin 194catechol 193, 193ceramides 18ceyssatite, in resorcinol peels 184chaperonins 14cheilitis, actinic 60cheiloplasty see chemical cheiloplastychelation 89

chelated TCA 89iron chelation by lipoic acid 18

chemabrasion 145, 162, 279, 280chemical blepharoplasty 235, 235, 295–304, 361

anesthesia 296application 296–7, 296, 297complications 302–3

delayed healing 302, 302demarcation line 302pain 302pigmentation changes 302

effectiveness 301, 301, 303, 304eye protection 296indications 301occlusion 297–8, 297–9phenol solution 296post-peel care 298–9, 300, 310–11post-peel developments 300

edema 300, 300erythema 300, 301

pre-peel care 309–10chemical cheiloplasty 36, 235, 304–11, 305–9, 361

post-peel care 310–11pre-peel care 309–10results 309

chemical peelsclassification criteria 1–3

chemical dependence 2doctor dependence 1patient dependence 2–3

definition 1depth of 2

Index 379

chemical peels (cont.)deep 3medium 3skin appearance and 62superficial 3very superficial 3

see also specific peelschemical sympathectomies 245–6chemical tanning 16chloasma 98–9

see also melasmacholine acetyltransferase 22cholinergic receptors 21cimetidine 264citric acid 41, 47, 48

in ETCA 112in ETCA post-peel mask 111

clay 89, 89clay masks, TCA in 89–90, 90coal tar 194coconut fatty acid monoethanolamide (cocamide) 41

in ETCA 112coenzyme Q-10 18coenzyme R, in ETCA post-peel mask 111cold

anesthetic properties 261cold packs 251, 261, 292, 360cooling mask 271, 271

collagenAHA effects 71production by fibroblasts 7, 53

vitamin C effect 341regeneration 342TCA effects 91, 95

colloid dressings 28, 342Combes’ solution 187Combes, Sperber and Reisch solution 196comedonal acne 8, 33–4, 33

macrocomedones 33–4treatment

comedone extraction 125ETCA 125–6

see also acneconfetti-like depigmentation 6, 6, 338conjunctivitis, phenol and 221contact time 49–50

AHA peels 54, 62–3glycolic acid 55, 56, 62–3, 63

resorcinol 186cooling mask 271, 271corneal opacity 20corneocytes 209corneodesmosomes 6, 51

AHA effects 67corticosteroids

intravenous 28, 258, 348oral 28topical 9, 28

erythema treatment 325–6following AHA peel 64

hyperpigmentation treatment 341scar treatment 348

cortisone 60erythema and 319

corundum crystal microdermabrasion 374cosmetics see post-peel cosmeticscresols 194, 194, 200croton oil 199–200, 317Croton tiglium 199, 199crow’s feet 38cryoanesthesia 360

Unideep® and 179, 179, 360cumene 193, 193cyclohexanehexyl hexaphosphate 70cysteine 18

dansyl chloride 51dark skin

melanocyte toxicity and 318pigmentary changes 8, 11TCA sensitivity 91

deanol see DMAEdécolletage

AHA peels 61ETCA treatment 142–4, 142–4Jessner’s formula use 189lentiginosis 141, 142photoaging 141, 142–4, 142–4, 145scars 163–5, 165

acne scars 142dehydration 27demarcation line 275, 278, 279, 280, 292, 318, 363–5, 364

chemical blepharoplasty 302depth of peel and 363–4high-risk areas 365, 365prevention 365skin type and 364

depigmenting agents 336–41dermabrasion see abrasion; sandpaper abrasionDermacool® 261dermal atrophy 36–7, 38dermal filling 11

combination treatment 43–4dermatitis

acneiform 9, 351, 352, 359berloque 99retinoid 8, 9–10seborrheic 9, 10, 54

TCA treatment 100–1, 103dermis

AHA effects 53phenol effects 206–7

desquamation, AHA peels and 67glycolic acid 61

diabetes 30as contraindication for phenol peels 249as contraindication for TCA peels 104scarring and 345

dicarboxylic acids 49

380 Index

dichloroacetic acid (DCA) 80–1, 80application protocol 80–1chemistry 80toxicity 80

dichlorophene 195N,N-diethylaminoethanol (DEAE) 20dihydrolipoate (DHLA) 18dihydrotestosterone 16dilated pores 32, 365–7

phenol treatment 245TCA treatment 100

N,N-dimethylaminoethanol see DMAEdimethylethanolamine see DMAEN,N-dimethylisopropanolamine (DMIPA) 20Dioscorea (Mexican wild yam) 18diphenol 193, 194discoloration see pigmentary changesdisinfection, phenol 204diuresis, phenol peels and 258dizziness, resorcinol peels and 190DMAE (N,N-dimethylaminoethanol) 18–23

chemistry of 19historical use of 20modes of action 21–3

action on striated facial muscles 21dermal action 22effect on myofilaments and smooth muscle cells 22–3epidermal action 21–2exocrine glands 23vasomotor effect 22

sagging skin treatment 19, 21–3, 33topical skin application 21

side-effects 19–20toxicity 20

DMIPA (N,N-dimethylisopropanolamine) 20dry ice treatment 372dry skin 55

following AHA peels 67Dubreuilh’s melanosis 102dyschromias 34, 34, 56, 327–30

phenol treatment 237–9, 237resorcinol application 183

Jessner’s formula 188risk of 328, 329, 330see also specific dyschromias

Easy Phytic® solution (EPS) 69–78, 70application 76–7, 76body treatments 72–3, 72combination treatment 71–2

botulinum toxin 71–2flashlamp therapy 72mesotherapy 71

contraindications 77erythema and 319indications 71–4

acne 73–4aging skin 71–3

post-peel care 77pre-peel preparation 75–6

cleansing 75, 76, 76precautions 74–5, 75repeat peels 77scar prevention 346see also alpha-hydroxy acids (AHAs)

Easy TCA® (ETCA) 40–5, 86, 109–20, 110acne treatment 125–9, 125–8

combined treatment 127comedonal acne 125–6microcystic acne 126papulopustular acne 126scars 145side-effects of acne 127

actinic keratosis treatment 174–5application 115–18, 115–17, 122

applicator 114–15base solution 111–12complications

erythema 321, 321–2, 325hyperpigmentation 332, 332, 335, 336pain 361scar prevention 346

décolletage treatment 141, 142–4, 142–4depths of action 116, 117hand treatment 136–40

photoaging 136–8, 136–7solar lentigines 137, 137, 138, 168warts 139, 140

indications 112keratosis pilaris treatment 165, 166lentigine treatment 137, 137–8, 170, 171, 174–5, 175lip treatment 304, 305–6maintenance of results 119, 123melasma treatment 121–4, 121–2, 123

problems 123–4neck treatment 141, 141photoaging treatment 119post-inflammatory hyperpigmentation treatment 124post-peel care 117–18, 122–3, 137, 144

post-peel mask 110–11, 117, 122, 154, 154sun protection 118

pre-peel preparation 114repeat peels 118–19, 122, 144scalp keratoses treatment 131–3, 131, 133scar treatment 162–3, 162, 163

body scars 163–5, 164smokers’ skin and 119solution preparation 112–14, 113, 114stretch mark treatment 145, 152–61, 321, 321

anesthesia 152–3, 153complications 161post-peel care 160–1protocol 153–8, 153–9results 158–60, 159–60

with Only Touch® 169with sandpaper abrasion 146–7, 146

anesthesia 152–3see also trichloroacetic acid (TCA)

ectropion 347prevention 347

Index 381

eczema 183hyperkeratotic 57

edema 28, 319, 354–8, 356eyelid, following chemical blepharoplasty 300, 300pain and 357phenol peel and 203, 277, 277, 357, 357–8prevention 358severity 354–7stretch mark treatment and 155, 155TCA peel and 356, 357treatment 358

Ehlers–Danlos syndrome 345elastin 95elastosis 56

phenol treatment 236elderly patients 27

see also aging skinelectrocardiography (ECG) 258electrocoagulation 11, 327Eller and Wolf’s solutions

phenol 196resorcinol 187

EMLA cream 152herpes treatment 353phenol peels and 264–5

enzymatic TCA 88epidermal sliding 153, 181epidermis

AHA effects 53phenol effects 206regeneration 53

epidermolysis 53, 206epinephrine see adrenalineepistaxis 80epithelioma

basal cell (BCE) 170squamous cell (SCE) 170

Epstein mask 285erbium laser abrasion 152erythema 319–26

AHA peels and 62, 67, 319, 324following chemical blepharoplasty 300, 301phenol peels and 319, 323–4, 323–4, 325prevention 324–5resorcinol peels and 190TCA peels and 320–3, 320, 325

Easy TCA® 321, 321–2Only Touch® 173, 322, 323Unideep® 322, 322

treatment 325–6corticosteroids 325–6cosmetics 325laser treatment 326

tretinoin treatment and 10esterification reaction 53–4estradiol benzoate 60estrone 60ether, skin preparation 54excipients, in ETCA 112Exoderm® 197, 197

acne scar treatment 242, 243wrinkle treatment 234

expression wrinkles 31, 36, 315, 315phenol treatment 234

eye contactEasy Phytic® solution 75TCA 81

eyebrows, phenol application 278eyelids, phenol application 278, 278, 279, 296–7, 296–7

see also chemical blepharoplasty

face-liftcombined with peel 373

phenol peel 230–1, 230scars 243–4, 244versus phenol peel 228–30, 228–9

facial nerve blocks (FNB) 265–9frontal and upper eyelid block 265, 266–8lateral regions 267–8, 269mid-face and outer eyelid block 266–7, 267

fentanyl 271fibroblasts 22, 44, 206

abrasion effects 146AHA effects 51collagen production 7, 53resorcinol effects 184

fibronectin 22–3fillers 43–4, 374fine lines 56

AHA effectiveness 58phenol treatment 233

flaking skin, post-peel care 15, 16flashlamp treatments 14

combination treatment 44Easy Phytic® 72

flavonoids 193, 194flumazenil 271fluocinolone 3265-fluorouracil (5-FU) 60, 347

keratosis treatment 102, 102folds

AHA effectiveness 58nasolabial 34phenol treatment 233–4TCA effectiveness 95

folliculitis 183folliculitis barbae 128forced diuresis 219forearms

aging 135AHA peels 61tretinoin treatment 8

freckles 29, 36, 99, 100, 318removal 177, 178, 238TCA treatment 99–100, 100

frontal nerve 132frosting

AHA peels 62Jessner’s formula 188phenol peels 276–7, 276–7

382 Index

TCA peels 107, 108, 320ETCA 115, 116, 123, 137, 153, 154, 163, 321scalp treatment 131, 131Unideep® 180, 181

fruit acids see alpha-hydroxy acids (AHAs)furosemide 219, 220

gallic acid 289gastrointestinal symptoms, phenol intoxication 215giant hairy nevus 245ginsenoids 82glabridin 17, 339, 339gluconic acid 48glutamine 30glutathione 18glycerol 48, 82, 87

adjuvanted to phenol 201adjuvanted to TCA 87–8

glyceryl monooleate 88, 88glycolic acid 31, 47–8, 55, 69

acne treatment 17, 55application technique 62as pre-peel treatment 57classification of peels 1, 2contact time 49–50, 55, 56, 62–3, 63cosmetic application 59desquamation 61effectiveness 58factors influencing penetration 53–4histological effects 53hyperpigmentation treatment 341neutralization 64, 64pH 49post-inflammatory hyperpigmentation 331post-peel care 65pre-peel preparation 60–1see also alpha-hydroxy acids (AHAs)

glycosaminoglycans 7, 30AHA effects 53TCA effects 91

glycyrrhetinic acid 17, 18Grade’s formulas 196Grenz zone 206, 328–9, 329, 355

infection risk 349guaiacol 194–5, 194

hairline, phenol application 278halcinonide 326haloacetic acids 79, 79

see also specific acidshands 32

aging 135–8, 136–9AHA peels 61solar lentigines 137, 137–8, 168TCA treatment 95, 96

ETCA 136–40, 136–9, 168warts 101, 101

tretinoin treatment 8healing process 28, 342

chronology 342

delayed healing 302, 302heat stress 13–14

sublethal damage 14heat-shock proteins (HSPs) 13–14

sun protection and 14–15hectorites 89hemorrhoids 247hepatic toxicity, phenol 222herpes

Easy Phytic® and 77following AHA peels 68phenol peels and 249pigmentary changes and 334–5prevention 6, 10, 109

ETCA versus TCA–SAS 42resorcinol peels and 190secondary 352–4, 352, 353

differential diagnosis 353prevention 353risk of 352symptoms 352–3under occlusive mask 354

Hetter formulas 197–8, 197hexachlorophene 195, 195hormone replacement therapy (HRT), phenol peels and 250Hutchinson’s freckle 102hydrocortisone 28, 105

erythema treatment 325–6hydroquinone 6, 56, 187, 193, 193

combination treatment with AHAs 60hyperpigmentation treatment 17, 337–8phenol oxidization to 209TCA peel preparation 105tolerance 11

4-hydroxyanisole (4-HA) 340hydroxybenzene 193hydroxyproline 53hydroxyzine 271hyperkeratinization 55hyperkeratosis 10, 55

hand 139pigmented 56treatment 57

hyperpigmentation 8, 330–41following chemical blepharoplasty 302following keratosis treatment 173, 174following resorcinol peels 190following stretch mark treatment 87, 161monitoring 335–6post-inflammatory (PIH) 13, 16, 35–6, 35, 39, 100, 331

AHA peels 67, 331phenol peels 237–8, 332–4, 334sensitivity test 334TCA peels 44–5, 173, 174, 331–2, 331–2

pregnancy and 336prevention 334–6

even application of peel 335re-peeling 336skin preparation 334–5sun protection and avoidance 335

Index 383

hyperpigmentation (cont.)treatment 17, 31–2, 336–41

corticosteroids 341pre-peel treatments 60sun avoidance 341TCA treatment 99, 124topical depigmenting agents 336–41

hypertrophic scars 32hypervitaminosis A 10hypothyroidism, secondary 189

ichthyosis 47treatment 56–7

inadequate results 314–16facial expressions 315, 315histological regions 315–16inadequate preparation and 314–15poor product knowledge 314prevention of 316treatment 316

repeat peels 316wrong indication 314, 314, 315

infection 27, 348–54bacterial 67–8, 349–52

treatment 351–2following AHA peels 67–8following resorcinol peels 190following stretch mark treatment 161pigmentary changes and 334–5prevention 6, 10, 350–1

post-peel care 16TCA peels 42, 44

risk of 348–9see also herpes

inflammation 30stretch mark treatment and 149, 155, 155tretinoin treatment reaction 9with Easy Phytic® treatment 74–5with phenol treatment 203

informed consent form 253, 255inositol hexaphosphoric acid 70insulin-dependent diabetes see diabetesintense pulsed light (IPL) 72intraepidermal peel 327, 327involucrin 209iodoform 289iron oxide 184isotretinoin 8, 87

acne treatment 102, 103, 128phenol peels and 250scarring and 345TCA peel preparation 105

jaundice, phenol and 221Jessner’s solution 183, 187–9

application 188as preparation for a TCA peel 188–9as preparation for an AHA peel 189classification of peels 2formulations 187

indications for use 188keratosis treatment 189post-peel care 187safety 188see also resorcinol

kaolin, in resorcinol peels 184Karp’s formulas 196keloids 241

phenol peels and 250keratinocyte touch, abrasion and 152keratolytic effect, phenol 214keratoses 7, 10, 102, 167

actinic 60, 170–2, 171ETCT treatment 174–5Only Touch® treatment 167, 172, 172, 173phenol treatment 240post-peel care 172precautions 174TCA treatment 96, 97, 102treatment complications 173tretinoin preparation and 10

impermeability of 132scalp 131, 131

ETCA treatment 131–3, 131, 133local anesthesia 131post-peel care 132, 132preparation for treatment 131

seborrheic 174, 239, 239senile 10treatment 61, 81, 102

Jessner’s formula 189phenol peels 239–40, 239

keratosis pilaris 154, 166kidney disease, phenol peels and 249kidney insufficiency 30Klein solution 152, 196Kligman’s formulas 17, 338Köbner phenomenon 161kojic acid 6, 11, 60, 187, 338

hyperpigmentation treatment 17, 338–9

lactic acid 11, 48–9, 187hyperpigmentation treatment 341skin sensitivity testing 359see also alpha-hydroxy acids (AHAs)

lactic acidosis 80Langerhans cells (LC) 42, 109, 206Langerhans, Paul 109lanolin, in resorcinol peels 184laser treatments 14, 28, 375

erythema 326versus phenol peel 232

lentigines 8, 22, 34, 34, 56, 167, 169–70, 170hands 137, 137–8, 168histology effect on results 315, 315treatment 32, 61, 169

ETCA 137, 137–8, 170, 171, 174–5, 175Only Touch® 137, 138, 167, 168, 170, 171resorcinol 183

384 Index

lentiginosisdécolletage 141, 142TCA effectiveness 96, 97, 97see also lentigines

lentigo maligna 102, 170phenol treatment 238–9, 239

Leukoflex® occlusive mask 257, 257, 285licorice extracts 6, 339

hyperpigmentation treatment 17, 339lidocaine 20, 152, 262, 263–4

arrhythmia prevention 220phenol peels and 262, 263–4

nerve blocks 265–70tachyarrhythmia treatment 220with adrenaline 152–3, 153, 264

linoleic acid 30linolenic acid 30Lip & Eyelid® formula 198, 228, 235, 273, 296

application 276–9, 296–7, 296–7dyschromia treatment 237edema and 357, 357–8photoaging treatment 227post-peel care 293use with Unideep® 228wrinkle treatment 233, 235

upper lip 304, 305–9see also chemical blepharoplasty; phenol peels

lipofuchsin 22lipoic acid 18

iron chelation 18lips see chemical cheiloplastyliquiritin 17Lister, Lord 196, 214–15Litton’s solution 197, 273, 332liver disease, phenol peels and 249lorazepam

phenol peels and 253, 256, 271pruritis and 354

lunchtime peel 71Lysol® 194, 200, 215

macrocomedones 33–4magnesium ascorbyl phosphate (MAP) 110, 341magnesium oxide 89, 184make-up 29

phenol peels and 227, 250malic acid 48mandelic acid 47, 48marionette lines 34medizolam 271melanocyte toxicity 316–19

AHAs 317phenol 317–18prevention 318skin phototype and 318–19TCA 317treatment 319

melanocytes 206exocytosis 317membrane fusion 317

phagocytosis 317see also melanocyte toxicity

melasma 8, 98, 98, 121post-peel care 15, 16skin preparation 121–2treatment 31–2, 39, 40

AHA peels 56persistent dark ring 123, 124phenol peel 237–8recurrence 124TCA 98–9, 99, 121–4, 121–2, 123

Melonin® 156, 156men, phenol peels 29, 226, 226mental block 270, 270mental retardation 29Mepiform® 348, 348Mepilex® 156, 156Mepitel® 348, 348mepivacaine 263mesolift see mesotherapymesotherapy 11

post-peel care 15with Easy Phytic® treatment 71

methemoglobinemia 189, 263microdermabrasion 152

corundum crystals 374Micropore® occlusive mask 257, 257, 285milia 358–9

prevention 358treatment 358–9

moist technique 288molecular chaperones 14Monheit technique 188–9monoamine oxidase (MAO) inhibitors, phenol peels and 250,

253, 264monobenzone 336–7, 336monochloroacetic acid (MCA) 79–80, 79

poisoning 79–80monofluoroacetic acid 80Morus alba 6, 11

hyperpigmentation treatment 17, 341Moy technique 189mucopolysaccharides 71mulberroside F 17, 341myofibroblasts (MFBs) 22–3, 204–5, 205

abrasion effects 146myofilaments

DMAE effects 22–3

nasolabial folds 34natural moisturizing factor (NMF) 18nausea

phenol peels and 215resorcinol peels and 190

neck 31, 141AHA peels 61demarcation line prevention 365ETCA treatment 141, 141Jessner’s formula use 189phenol peels 250–1, 280–1

Index 385

neck (cont.)photoaging 141, 141

neoangiogenesis see angiogenesisneomycin allergies 27nerve blocks

herpes infection treatment 353phenol peels and 262, 265–70, 361

facial nerve block application 265–9, 266–9mental block 270, 270

TCA peels 360–1Unideep® 179, 180

neuroablation 246–7neurological symptoms, phenol intoxication 215neurolysis 245–6neutralization, AHAs 50, 54, 63–4, 69

partially buffered solutions 64preparation of neutralizing solution 63

nevi 245, 366, 367norcholine see DMAEnormal skin characteristics 25nutrition 30

occipital nerve of Arnold 132occlusive dressing 15, 342

chemical blepharoplasty 297–8, 297–9EMLA cream and 264herpes infection under 354phenol application and 211, 282, 282, 283–6, 285, 286

bismuth subgallate mask 288–90, 288–91removal 287, 386–7

TCA application and 92ETCA 147, 154–5, 154, 155

ochronosis 338oily skins, tretinoin treatment 8older patients 27

see also aging skinoliganuria, phenol and 221olive skin, pigmentary changes 11Only Touch® 167, 167

application 168–9combination treatment with ETCA 169complications

erythema 173, 322, 323, 325hyperpigmentation 332, 333, 335scar prevention 346–7

indications for use 167keratosis treatment 139, 167, 172, 172, 173

complications 173post-peel care 172precautions 174

lentigine treatment 137, 138, 167, 168, 170, 171pre-peel preparation 167solution preparation 167–8wart treatment 139, 140see also trichloroacetic acid (TCA)

ophthalmic toxicity, phenol 221

p-aminobenzoic acid (PABA) 20, 20pain 359–62

abrasion and 152

AHA peels 67, 359, 361edema and 357herpes infection 353phenol peels 203, 292, 361, 362

evolution of 270–1stretch mark treatment 161TCA peels 43, 360–1

scalp treatment 133see also anesthesia

painkillers see analgesicspapillary dermis peel 329, 329, 349, 355–7papillomas 80paracetamol 195–6, 195, 362partition coefficient 201perioral wrinkles 36, 37petechiae 366, 367petrolatum, in resorcinol peels 184PFPE 18pH 49, 49

effect of dilution of solution 50phenol 184

administration routes in the past 215anesthetic effect 203, 203, 261aqueous versus oil vehicle 211capillary absorption 209carcinogenicity 203chemical neuroablation 246–7chemical sympathectomies 245–6chemistry of 193, 193–4derivatives 194–6disinfection 204halogenated phenols 195hemorrhoids and 247lymphatic absorption 209medications containing 213–14

dental wick 214gargles 213mouthwash 214soap 213

metabolization 209–10, 210urinary elimination 212

neurolysis 203, 245–6peels see phenol peelsprotein coagulation 203–4sensitivities 212spasticity and 246–7toxicity 211, 213–22

animal studies 213antidotes 216by inhalation 221hepatic toxicity 222lessons from medical history 214–15lessons from toxicology centers 216melanocyte toxicity 317–18ophthalmic toxicity 221paradoxical toxicity 214renal toxicity 222symptoms of intoxication 215

urinary incontinence and 246see also chemical blepharoplasty; chemical cheiloplasty

386 Index

phenol peels 233adjuvants 198–201

cresol (Lysol®) 200croton oil 199–200glycerol 201resorcinol 199salicylic acid 199saponins 200septisol 200TCA 199

age of patient 225–6, 225aging and 36, 36

photoaging 34–5anesthesia 262–70

general 262local 262–4nerve blocks 265–70topical 264–5

antibiotics and 258application 273–82, 278–82

applicator preparation 273–4, 274clinical signs of 276–7, 276–7demarcation line 275, 278, 279, 280, 292

Aptos® threads and 231, 231asepsis 259atropine and 258buffers 201cardiorespiratory monitoring 258cardiovascular complications 216–21

arrhythmias 217, 220blood pressure 220cardiac arrest 220–1prevention 219–20treatment during peel 220

classification of 2cleansing and disinfection 258–9combination treatment

botulinum toxin 233–4, 233face-lift 230–1, 230, 373TCA 372, 373Unideep® 228

complicationsedema 203, 277, 277, 357, 357–8erythema 319, 323–4, 323–4, 325hyperpigmentation 332–4, 334, 335infection prevention 351milia prevention 358pain 203, 270–1, 292, 362pruritis 354scarring 204, 344, 347

contraindications 249–51cost 251heart condition 249herpes 249insulin-dependent diabetes 249isolated patients 250kidney disease 249liver disease 249mental or behavioral risks 250patient history 249–50

sun exposure 251corticosteroid injection 258diuresis 258formulations 196–8

Exoderm® 197, 197Hetter formulas 197–8, 197historical 196–7Lip & Eyelid® formula 198oil versus aqueous formulations 200–1

frosting 276–7, 276–7hepatic and renal integrity requirement 210histological effects 204–6

dermal changes 206–7epidermal changes 206long-term 207

hospitalization 283indications for 233–47

acne 240–3, 242, 243dilated pores 245dyschromias 237–9, 237keratoses 239–40, 239laxity and skin elastosis 236, 237nevus 245scars 162, 243–5, 244, 245superficial cancers 240telangiectasias 240wrinkles 233–6xanthelasma 240, 240, 241

male skin 29, 226, 226shaving and 226–7

neck 250–1, 280–1occlusive mask 282, 282, 283–6, 285, 286

advantages and disadvantages 283–4bismuth subgallate mask 288–90, 288–91occlusion effects 211precautions 284–5preparation of 257, 257, 285–6removal 286–7, 287

patient selection 251phototype influence 227–8, 228post-peel care 16, 283–94, 292–4

antibiotic cream 288–9bismuth subgallate mask 288–90, 288–91medical treatment 286sun avoidance 292–4touch-ups 287, 294

pre-peel preparation 253–7, 274benzodiazepine 256–7botulinum toxin 253, 274clinical examination 253–6eye protection 257legal documents 253, 255medication 253photographs 253

precautions 250–1safety factors 251sagging skin and 31, 228, 230, 236, 237sedation 265, 271skin regeneration 251skin thickness and 226

Index 387

phenol peels (cont.)smoking and 29solution preparation 273storage of solution 198ventilation 257–8, 258versus face-lift 228–30, 228–9versus laser resurfacing 232see also chemical blepharoplasty; chemical cheiloplasty;

phenolphenolic acids 195phenoxyethanol 89

in ETCA post-peel mask 111phosphatidylcholine 32photoaging 31, 32, 32, 34–5, 35, 56, 95

AHA peels and 55–6décolletage 141, 142–4, 142–4, 145hands 136–8, 136, 139neck 141, 141phenol peel treatment 225, 227, 237resorcinol application 183TCA application 95–8, 96, 97, 98

ETCA 119–20, 136–8, 136–9, 142–4, 142–4lentiginosis 96, 97, 97perioral wrinkles 97prevention 97–8solar elastosis 95–7, 96

tretinoin treatment and 10see also aging skin; sun-protection

phototherapy 72see also flashlamp treatments

phytic acid 70–1, 70in ETCA post-peel mask 111

picric acid 195, 195pigmentary changes

confetti-like depigmentation 6, 6following chemical blepharoplasty 302following keratosis treatment 173, 174

pigmented ring 173following stretch mark treatment 158, 158, 159, 161, 161monitoring 335–6post-acne pigmentation 127, 128pregnancy and 336prevention 6, 11, 334–6

even application of peel 335skin preparation 334–5sun avoidance and protection 335

treatment 8, 17, 182, 336–41corticosteroids 341sun avoidance 341topical depigmenting agents 336–41

see also hyperpigmentation; melanocyte toxicitypinpoint bleeding, abrasion and 151, 152, 152pKa 50–1poikiloderma of Civatte 121poisoning

MCA 79–80TCA 81

polyphenols 193, 194polyunsaturated fatty acids 363porcelain skin 206

post-inflammatory hyperpigmentation see hyperpigmentationpost-peel care

AHA peels 15, 65Easy Phytic® 77

cosmeceuticals used 23–5, 24phenol peels 16, 283–94

medical treatment 286resorcinol peels 15, 186–7

Jessner’s formula 188sensitive skin 25sun protection 13–15TCA peels 15–16, 43, 108see also occlusive dressing

post-peel cosmetics 16–18acne treatment 17aging treatment 17–18

sagging skin 18–23erythema treatment 325hyperpigmentation treatment 17

postoperative wounds, phenol peels and 249pre-peel preparation see preparationpregnancy

Easy Phytic® and 77pigmentary changes and 336tretinoin treatment and 10

premature ventricular contraction 217, 217preparation 28–9

AHA peels 5–6, 11, 54Easy Phytic® 75–6glycolic acid 60–1

avoidance of side-effects 10benefits of 10–11combination treatment 11for even penetration 6, 10immediate pre-peel preparation 5inadequate 314–15infection prevention 6, 10Jessner’s formula as preparation 188–9medium- and long-term preparation 5melasma treatment 121–2monitoring 11phenol peels 253–7, 274pigmentary change prevention 6, 11, 334–5pre-peel sun protection 6resorcinol peels 185

Jessner’s formula 188scar prevention 345stimulation of skin regeneration 6–7, 11stretch mark treatment 149TCA peels 5, 6, 42, 92, 106

ETCA 114Only Touch® 167Unideep® 179

testing patient compliance 11tretinoin 7–10

prilocaine 263procaine 20, 20, 262promethazine 271, 326, 354propylene glycol 88, 88

in ETCA post-peel mask 111

388 Index

proteoglycans 30protomyofibroblasts 205pruritis 28, 161, 347, 354

herpes infection and 353phenol peels and 354treatment 350, 353with Easy Phytic® peel 74

psoriasis 183ptosis 230

nasal tip 279pulse oximetry 258Purifying cream® 127

intolerance 128purpura 367pyruvic acid 36, 48, 48

quadrigeminy 217Quillaja, tincture of 186

radiotherapy, phenol peels and 249re-epithelialization 7, 11, 13–14, 28, 342red-headed patients, melanocyte toxicity 318–19renal toxicity, phenol 222resorcinol 183, 183, 193, 193

allergies to 185, 189–90application 185–6as adjuvant of phenol peels 199classification of peels 2combination treatment with TCA 371contact time 186histological effects 184indications for use 183ingredients of peels 184–5pastes 185, 185post-peel care 15, 186–7pre-peel preparation 185properties of 183repeat peels 187side-effects 189–90toxicity 189

reticular dermis peel 329–30, 330, 349, 355–7retinaldehyde 7retinoids 6–7, 87retinol 7

in ETCA post-peel mask 111see also vitamin A

rinsingAHAs 50, 54, 63TCA 87–8

ropivacaine 263

safety factors 313–14sagging skin 15, 33, 33

choice of peel and 31DMAE treatment 18–23, 19, 33phenol peels and 228, 230, 236, 237

salicylate derivatives 24–5salicylic acid 48, 48, 187, 195, 195

as adjuvant of phenol peel 199salicylism 189

sandpaper abrasion 145, 146, 147acne scars 100acne treatment 132equipment 146grade 0 abrasion 149–51, 149grade I abrasion 149, 151grade II abrasion 149, 151, 151grade III abrasion 149, 151, 152guiding signs 152

bleeding 152keratinocyte touch 152pain 152

scar treatment 162–3, 163stretch mark treatment 146

depth of abrasion 149with ETCA 146–7, 146

anesthesia 152–3saponins 41

as adjuvants of phenol peels 200in ETCA 112

scabbing 51scalp 131

keratoses, ETCA treatment 131–3, 131, 133local anesthesia 131–2see also keratoses

scars 145, 328–30, 342–8acne 31, 55, 162

back 145, 163, 165treatment 100, 103, 241–3, 242, 243

AHA peels 68, 342–3, 346body scars 163–5, 164

back 145, 163, 165décolletage 163–5, 165

dermabrasion 245, 246face-lift 243–4, 244facial 162hypertrophic 32keratosis treatment 173, 174phenol peels 204, 344, 347post-traumatic 35–6, 36, 244, 245prevention 345–7, 348

Ehlers–Danlos syndrome 345injury avoidance 346isotretinoin and 345patient selection 345skin preparation 345

resorcinol peels 190risk of 328, 329, 330, 342–4TCA peels 44, 91–2, 317, 321, 343–4, 343–4, 346–7treatment 162–6, 347–8

corticosteroids 348dermabrasion 162–5, 163ETCA 162–3, 162, 163phenol peels 162, 243–5, 244, 245, 246resorcinol 183

scratch lesions 349, 349, 355sebaceous glands

acne and 55AHA effects 68

seborrheic dermatitis see dermatitis

Index 389

seborrheic keratoses see keratosessebum production, reduction of 7

biotin effect 111sedation

phenol peels 265, 271fentanyl 271medizolam 271premedication 271

TCA peels 360selenium, in ETCA post-peel mask 111senile atrophy 8sensitive skins

combined AHA/tretinoin treatment 59–60TCA treatment 101–2

sensitization, AHA peels 67septisol 195

as adjuvant of phenol peel 200serborrheic dermatitis 9, 10, 54shaving 226–7shiny skin, following AHA peels 68silicion, in ETCA post-peel mask 111silicon dioxide 89, 184silicone dressing 348, 348silicone ointment 60sinus rhythm 216skin cancers

tretinoin treatment and 10see also carcinoma

skin color 29see also pigmentary changes

skin necrosis 53, 53TCA and 81, 91, 92

skin permeability 7penetration of chemicals 209tretinoin treatment and 9

skin phototypemelanocyte toxicity and 318–19phenol peels and 227–8, 228pigmentary changes and 334

skin regeneration cycle 119, 119skin thickness 116, 116Sleek® occlusive mask 257, 257, 285smokers’ skin 119smoking 29

aging and 135expression lines and 315

smooth muscle cells (SMCs), DMAE effects 22–3sodium bicarbonate 63

neutralization of AHAs 63–4sodium glycolate 50sodium laureth sulfate (SLES) 41

in ETCA 112sodium oxide 184Soft Peel® 87solar elastosis 95–7, 96solar lentigines see lentiginessolumedrol 258sorbitan monolaurate 89spasticity 246–7Starling’s hypothesis 354

stratum corneum 209hydration 23, 209increasing permeability of 92thinning 10, 13

AHA effects 51for body anti-aging treatment 72–3

stratum disjunctum (SD) 109stretch marks 32, 57, 145, 316

abrasion treatment 146depth of abrasion 149depth of abrasion, grade 0 sandpaper abrasion 149–51, 149depth of abrasion, grade I sandpaper abrasion 149, 151depth of abrasion, grade II sandpaper abrasion 149, 151,

151depth of abrasion, grade III sandpaper abrasion 149, 151,

152classification 145, 146ETCA treatment 145, 152–61, 321, 321

anesthesia 152–3, 153complications 161post-peel care 160–1protocol 153–8, 153–9results 158–60, 159–60

hyperpigmentation following treatment 87origin of 147position of 148, 149preparation for treatment 149TCA treatment 103treatments summary 148, 150–1

Styrax benzoin tree 184sun sensitivity 362–3sun-protection 6

heat-shock proteins and 14–15phenol peels and 251, 292–4pigmentary change prevention 335, 341post-peel care 13–15

effective sun protection factor 13glycolic acid peels 59TCA peels 16, 43, 118, 122

tretinoin treatment and 9, 10surface tension 200, 200surfactants 5, 41surgical scars see scarssweat glands 23

tachyarrhythmias, phenol and 217, 217, 220tartaric acid 47, 48taspine 200tea tree oil 17TEAS see trolaminetelangiectasias 7, 240, 326–7, 326

AHA peels and 67, 326phenol peels and 326–7prevention 327TCA peels and 326, 326treatment 11, 327, 327

teratogenicityDMAE 20tretinoin 10

Tercinol® 213

390 Index

testosterone 16, 60tetrachlorophene 195thiosome 129thymol 289, 317titanium dioxide 184tocopheryl acetate 17

see also vitamin Etopical corticosteroids 28

following AHA peels 64tretinoin treatment and 9

touch-ups 316phenol peels 287, 294

toxic shock 350Transcutol® 11, 17trehalose 14–15, 15tretinoin 6–10, 17

age for starting treatment 9AHA peel preparation 54combination treatment 56, 59–60histological effects 7indications for use 7–8mechanism of action 7milia prevention 358post-peel care 13precursors 11prescription of 8–9recommendations 9side-effects 9–10TCA peel preparation 87, 92, 105teratogenicity 10

trichloroacetic acid (TCA) 81–92, 177adjuvanted TCA 86–90

chelated TCA 89enzymatic TCA 88glycerol 87–8glyceryl monooleate 88phenoxyethanol 89propylene glycol 88sorbitan monolaurate 89TCA in clay masks 89–90, 90

anesthesia 43, 106aqueous solutions 81–6

calculating the concentration of 82–6, 83–5hydrophilicity of TCA crystals 81–2inhomogeneity of 82, 83see also TCA–SAS (below)

as adjuvant of phenol peel 199bacterial infection prevention 42chemistry 81choice of 39–40classification of peels 2combination treatments 43–4

abrasion 374AHAs 371botulinum toxin 43, 373–4different TCA concentrations 372dry ice 372fillers 43–4, 374flashlamps 44phenol 372, 373

resorcinol 371complications 44–5

downtime 45edema 356, 357erythema 320–3, 320–2, 325exhausting the skin’s resources 44hyperpigmentation 44–5, 173, 174, 331–2, 331–3, 335,

336infections 44melanocyte toxicity 317pain 43, 133, 360–1scarring 44, 91–2, 317, 343–4, 343–4, 346–7telangiectasias 326, 326

contraindications 103–4depth of penetration 42–3, 91, 91Easy TCA see Easy TCA® (ETCA)herpes prevention 42histological effects 91–2indications for use 96–103

acne 102–3, 103actinic keratoses 102berloque dermatitis 99dilated pores 100folds and wrinkles 95freckles 99–100, 100melasma/chloasma 98–9, 99oncological indications 102photoaging 34–5, 95–8, 96, 97, 98post-acne scarring 100post-inflammatory hyperpigmentation 99seborrheic dermatitis 100–1sensitive skin 101–2stretch marks 103warts 101, 101xanthelasma 103

length of peel 43occlusion of 92post-peel care 15–16, 43, 108pre-peel preparation 5, 6, 42, 92, 106

Jessner’s formula as 188–9repeat peels 43solution mix 42symptomatology of application 106–8, 106, 107–8TCA–SAS (TCA in simple aqueous solution) 5, 15–16,

40–5, 86, 320, 346application 105–6

toxicity 81see also Only Touch®; Unideep®

trigeminy 217trimethylsilanol monomannuronate 111trolamine (triethanolamine salicylate, TEAS) 24–5

application 24mode of action 24precautions 25

Truppman and Maschek solution 197tumor necrosis factor (TNF) 200tyrosinase inhibitors 11tyrosine 337, 337

under-eye bags 32, 32

Index 391

Unideep® 177, 177, 360application 179–81, 180

anesthesia 179–80, 179complications

erythema 322, 322, 325pain 361

indications for use 177–9lip treatment 304, 307–9post-peel care 181–2post-peel mask application 181preparation 179removal of freckles 177, 178with phenol peel 228see also trichloroacetic acid (TCA)

Unna paste 183allergies to 189–90classification of peels 2see also resorcinol

urea 48in ETCA post-peel mask 111

urinary incontinence 246Urkov’s solution

phenol 197resorcinol 187

vagal reaction 258valacyclovir 353vascular endothelium 201Vaseline® 27, 60, 342

chemical blepharoplasty and 296in resorcinol peels 184phenol peels and 211, 253, 284, 292, 347

eye protection 257stretch mark treatment 156–8, 156, 158

Verner Kellson’s solution 197Vit E Antioxidant ® 17–18vitamin A 30, 340, 340

hyperpigmentation treatment 340in ETCA post-peel mask 111see also retinol

vitamin C 30, 49, 341, 341hyperpigmentation treatment 341in ETCA post-peel mask 110

recycling 18see also ascorbic acid

vitamin E 18, 39, 158, 340, 340hyperpigmentation treatment 340in ETCA post-peel mask 111

vitamin H, in ETCA post-peel mask 111vomiting, local anesthetic toxicity 263

warts 174hands 139, 140seborrheic 10treatment 139, 140

AHAs 56–7DCA 81MCA 80TCA 101, 101

Wood’s light 98, 238, 238, 336wool fat, in resorcinol peels 184wrinkles 56

AHA effectiveness 58deep 37–8, 38, 39expression 31, 36filling 43–4perioral 36, 37, 97phenol treatment 225, 233–6

around mouth and eyes 235, 235, 236deep wrinkles 233, 233, 234, 235expression lines 234folds and furrows 233–4radial wrinkles 236, 236

TCA effectiveness 95upper lip 304

see also chemical cheiloplasty

xanthelasma 81, 240phenol treatment 240, 241TCA treatment 103

xanthoma 161xerosis 55

treatment 56–7

zinc oxide, in resorcinol peels 184zinc stearate powder 187, 289

392 Index

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