(2020) LIVRO_ Procedimentos Estéticos Minimamente Invasivos

Prévia do material em texto

123
A Guide for Dermatologists and 
Plastic Surgeons
Adilson Da Costa 
Editor
Minimally Invasive 
Aesthetic 
Procedures 
Minimally Invasive Aesthetic Procedures 
Adilson Da Costa
Editor
Minimally Invasive 
Aesthetic Procedures 
A Guide for Dermatologists and 
Plastic Surgeons
ISBN 978-3-319-78264-5 ISBN 978-3-319-78265-2 (eBook)
https://doi.org/10.1007/978-3-319-78265-2
© Springer Nature Switzerland AG 2020
This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or 
part of the material is concerned, specifically the rights of translation, reprinting, reuse of 
illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, 
and transmission or information storage and retrieval, electronic adaptation, computer software, 
or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this 
publication does not imply, even in the absence of a specific statement, that such names are 
exempt from the relevant protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in 
this book are believed to be true and accurate at the date of publication. Neither the publisher nor 
the authors or the editors give a warranty, expressed or implied, with respect to the material 
contained herein or for any errors or omissions that may have been made. The publisher remains 
neutral with regard to jurisdictional claims in published maps and institutional affiliations.
This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Editor
Adilson Da Costa
Instituto de Assistência Médica ao 
Servidor Público Estadual (IAMSPE)
Tenured International Professor and 
Mentor for PhD and MSc Programs
São Paulo, SP, Brazil
https://doi.org/10.1007/978-3-319-78265-2
To my parents, who taught that I only needed to work hard 
and ethically to achieve whatever I want in my career and 
private life.
To my Professors and Teachers, who inspire me to share 
my knowledge without limits and with everyone.
To my husband, Watson Possato, and my three kids, 
Asher, Spencer, and Kyle DaCosta-Possato, who make me 
refresh my wish for life, new projects, and a long life every 
minute of the day.
vii
In a constant search for beauty, increasingly more people devote their time 
and resources to obtain the aesthetic standards of their time. The rise in aes-
thetic procedures around the world, especially in the United States of America, 
reflects this trend accurately. Although sometimes seen as frivolous, aesthetic 
improvements can bring significant improvement to the quality of life and 
general well-being of individuals.
I have devoted my career to the study and elaboration of innovative proce-
dures in dermatologic surgery, mainly focused on the aesthetic field, where I 
developed the subcision technique to treat cellulite and microcanullas to 
inject dermal fillers. Given that, along the course of my career, I have had the 
opportunity to meet and work with extraordinary professionals, such as Dr. 
Adilson Da Costa, who has extensive knowledge and research experience in 
clinical and cosmetic dermatology. His expertise in the field and eagerness to 
share scientific knowledge with other professionals have prompted him to 
publish, once again, an important book in our specialty.
I am glad to be part of Minimally Invasive Aesthetic Procedures: A Guide 
for Dermatologists and Plastic Surgeons, and to present this remarkable pub-
lication to our colleagues. This book addresses the needs of both dermatolo-
gists and plastic surgeons, providing the professionals with cutting-edge 
information and a practical step-by-step guide to the most broadly adopted, 
and possibly, most effective minimally invasive procedures.
Dr. Adilson Da Costa, thank you for sharing this outstanding accomplish-
ment with us!
 
Doris Hexsel, MD 
Porto Alegre, RS, Brazil
Foreword for Dermatoligist
ix
There is no doubt that minimally invasive aesthetic procedures have demon-
strated explosive growth over the past two decades. This growth is not limited 
to the numbers, types, and categories of procedures and products available, 
but includes growth in the number of dermatologists and plastic surgeons 
offering these procedures and the patients who seek them out. Because of the 
wide scope of treatments now available, their many variations, and the con-
tinuous introduction of new options, it is imperative that both fundamental 
principles and therapeutic specifics are readily understood by the practitioner. 
For this reason, Minimally Invasive Aesthetic Procedures: A Guide for 
Dermatologists and Plastic Surgeons is a timely and critical resource.
For plastic surgeons in particular, minimally invasive treatments represent 
a key sector of care that often must be integrated with surgical strategies. In 
some instances, a minimally invasive procedure, such as botulinum toxin or 
filler injections, may provide substantive patient benefits when surgery is not 
yet an indicated or optimal therapeutic option, as in the patient too young for 
a face-lift. In other instances, a minimally invasive procedure can become an 
important adjunct to a surgical procedure, exemplified by simultaneous autol-
ogous fat grafting or resurfacing. In still other circumstances, the minimally 
invasive procedure may be used to enhance or prolong the effects of treatment 
after a surgical procedure. To be most effective, plastic surgeons need to 
understand how to select the best procedure or set of procedures for the given 
patient and how to safely execute to optimize results.
The technique-driven format of Minimally Invasive Aesthetic Procedures: 
A Guide for Dermatologists and Plastic Surgeons will serve as a valuable 
guide to the practicing plastic surgeon in selecting and performing minimally 
invasive procedures. Each chapter focuses on a specific product or technique 
and provides a rationale for its selection, concise clinical guidance, and delin-
eation of side effects and complications. Tips contained within in each chap-
ter provide a key reminder of important areas of focus and attention. A broad 
spectrum of minimally invasive aesthetic procedures is represented, from 
chemical peels to toxins to fillers to threads and beyond, including variations 
in approach due to material selection or anatomical location. The direct, 
focused, and brief nature of each chapter means that the text also serves as a 
quick pretreatment review of a planned procedure in addition to more longi-
tudinal learning resource.
Foreword for Plastic Surgeons
x
I think plastic surgeons will find Minimally Invasive Aesthetic Procedures: 
A Guide for Dermatologists and Plastic Surgeons a valuable resource in their 
care of the aesthetic patient.
 
Felmont F. Eaves III, MD, FACS
Professor of Plastic Surgery, Emory University, Atlanta, GA, USA
Director, Emory Aesthetic Center
Medical Director, EAC Ambulatory Surgery Center
Past President, American Society for Aesthetic Plastic Surgery
Foreword for Plastic Surgeons
xi
According to the 2017 Cosmetic Plastic Surgery Statistics Report, minimally 
invasive cosmetic procedures accounted for 89.77% of all 17,504,950 cos-
metic procedures performed by plastic surgeons in the USA, per a survey 
conducted by the American Society of Plastic Surgeons. Moreover, in a simi-
lar survey conducted by the American Academy of Dermatology, procedures 
using laser, light, and energy-based devices, followed, respectively, by botu-
linum toxin, soft-tissue fillers, chemical peels, and body sculpting treatments 
were 2017s top cosmetic treatments among those specialists. This scenario 
makes it more than evident that minimally invasive aesthetic procedures 
dominatethe practices of the majority of medical doctors that work in the 
cosmetic field, and it is undoubtedly a trend that will continue in upcoming 
decades.
When I was first certified as a dermatologist, I began my practice at a time 
when minimally invasive aesthetic procedures were leaving the realm of dis-
belief and skepticism and entering the beginning stages of progression. 
Indeed, at that time, these procedures were first starting to follow scientific 
protocols in order to prove their real benefits and practical outcomes 
empirically.
I feel honored to have been among those pioneering dermatologists that 
helped to move forward the science behind minimally invasive aesthetic pro-
cedures, thereby transforming the creativity and observations in practice into 
clinical and in vitro protocols and publishing outcomes in international medi-
cal journals and several chapters of books. This groundwork helped give me 
the courage to step onto the stage at a conference and actively advocate and 
teach the role of these procedures in daily clinical practice.
I must say it was not an easy task. Many times, as happened to many of my 
colleagues that assumed that same role in their craft, this attitude attracted 
criticism from peers and former professors. However, I am delighted that I 
joined with so many of my colleagues around the world to make minimally 
invasive cosmetic procedures not only feasible, but now mainstream practice. 
I consider my work in having helped minimally invasive aesthetic procedures 
to be what they are today, aside from being one of the primary accomplish-
ments of my career!
This book, Minimally Invasive Aesthetic Procedures: A Guide for 
Dermatologists and Plastic Surgeons, is my new contribution to the world of 
aesthetic medicine. It is a 112-chapter, hard-copy book that compiles some of 
the most experienced authors and key procedural opinion leaders to share 
Preface
xii
with readers their expertise and knowledge on how to get the best outcome in 
the most difficult procedures. More than simply an overview of the most 
common cosmetic procedures performed by both dermatologists and plastic 
surgeons, it constitutes a practical, useful guide to the specialists who prac-
tice in outpatient clinics. Further, this book’s aspiration is to assist practitio-
ners preparing for each of these procedures in an easy, straight-to-the-point 
manner.
I do hope you enjoy reading this book and making it your best friend in the 
world of minimally invasive aesthetic procedures.
 
Adilson Da Costa, MD, MSc, PhD 
São Paulo, SP, Brazil
Preface
xiii
Part I Peelings
 1 Introduction: Classification of Peels . . . . . . . . . . . . . . . . . . . . . . 3
Carlos G. Wambier and Harold J. Brody
 2 Pearl Chapter: Basis of Photoaging and the Use 
of Chemical Peelings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
Suelen Montagner and Adilson Da Costa
 3 Tip Chapter: Peels for Ethnic Skin . . . . . . . . . . . . . . . . . . . . . . . 27
Renan Lage
 4 Blepharopeel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
Laura Bariquelo Buratini and Sergio Talarico Filho
 5 Cook Peel (70% Glycolic Acid + 70% Trichloroacetic 
Acid) for the Face . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
María del Pilar Del Río Navarrete Biot
 6 Cook Peel (70% Glycolic Acid +40% Trichloroacetic 
Acid) for Extra-Facial Areas . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
Carlos Gustavo Wambier
 7 Fluor-Hydroxy Pulse Peel for Face . . . . . . . . . . . . . . . . . . . . . . . 61
Erica Monteiro
 8 Fluor-Hydroxy Pulse Peel for Extra- Facial Areas . . . . . . . . . . . 67
Maria Paulina Villarejo Kede 
and Bruna Sabatovich Villarejo Iosifovich
 9 Genital Bleaching Peel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
Adriana Awada
 10 Glycolic Acid Peel for the Face . . . . . . . . . . . . . . . . . . . . . . . . . . 75
Jessica A. McCarrick and Valerie D. Callender
 11 Glycolic Acid Peel for Extra-Facial Areas . . . . . . . . . . . . . . . . . . 81
Caroline Silva Pereira, Beatrice Martinez Zugaib Abdalla, 
and Adilson Da Costa
 12 Jessner’s Peel for the Face . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87
Vanesa Piquero, Daniela Moya, and Edgar E. La Rotta
Contents
xiv
 13 Jessner’s Peel for Extra-Facial Areas . . . . . . . . . . . . . . . . . . . . . 95
Sarah Wilson, Howa Yeung, and Travis W. Blalock
 14 Phenol-Croton Oil Peels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
Fernanda Ayres de Morais e Silva Cardoso, 
Carlos Gustavo Wambier, and Adilson Da Costa
 15 Pyruvic Acid Peel for Face and Extra-Facial Areas . . . . . . . . . . 107
Bogdana Victoria Kadunc, Renan Lage, 
and Renata Cristina Vasconcellos
 16 Resorcin Peel for Face . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
Andrezza Facci
 17 Resorcin Peel for Extra-Facial Areas . . . . . . . . . . . . . . . . . . . . . 117
Erica Monteiro
 18 Salicylic Acid for Face (Facial Salicylic Acid Peel) . . . . . . . . . . . 121
Mercedes Florez White
 19 Salicylic Acid Peeling for Extra- Facial Areas . . . . . . . . . . . . . . . 127
Vanesa Piquero, Daniela Moya, and Edgar E. La Rotta
 20 Tretinoin Peel for Face . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
Luciane Scattone
 21 Tretinoin Peel for Extra-Facial Areas . . . . . . . . . . . . . . . . . . . . . 141
Renata Indelicato Zac and Adilson Da Costa
 22 Trichloroacetic Acid Peel for Facial 
and Extra-Facial Areas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
Natacha Quezada Gaón and María Isabel Herane Herane
 23 Thioglycolic Acid Peel for Dark Circles Under Eyes . . . . . . . . . 159
Vanessa Lucília Silveira Medeiros
 24 Thioglycolic Acid Peeling for Hemosiderin 
and Post- inflammatory Hyperchromia . . . . . . . . . . . . . . . . . . . . 165
Rossana Cantanhede Farias de Vasconcelos
Part II Botulinum Toxin
 25 Introduction: What Is Botulinum Toxin? . . . . . . . . . . . . . . . . . . 171
Doris Hexsel, Fernanda Camozzato, and Carolina Siega
 26 Tip Chapter: Histology and Physiology of the Skin . . . . . . . . . . 179
Renata Joffe, Jose A. Plaza, and Armineh Kajoian
 27 Botulinum Toxin for Craniofacial Hyperhidrosis . . . . . . . . . . . 193
Marcelo M. Bellini and Adriana de Cerqueira Leite
 28 Botulinum Toxin for Superior Third of the Face . . . . . . . . . . . . 197
Cristina Hachul Moreno, Aline Rodrigues Bragatto, 
and Caroline Moreira Albrecht
 29 Botulinum Toxin for Middle Third of the Face . . . . . . . . . . . . . 205
Loryart Marte Grullón and Javier Ruiz Ávila
Contents
xv
 30 Botulinum Toxin for Inferior Third of the Face . . . . . . . . . . . . . 209
Carlos Echevarria and Denise Durand
 31 Botulinum Toxin for the Neck . . . . . . . . . . . . . . . . . . . . . . . . . . . 217
Luciana R. Patricio Linhares and Adilson Da Costa
 32 Botulinum Toxin for Axillary Hyperhidrosis . . . . . . . . . . . . . . . 223
Clarissa Prati and Juliano Peruzzo
 33 Botulinum Toxin for Palmar and Plantar Hyperhidrosis . . . . . 229
Ada Regina Trindade de Almeida 
and Elisa Raquel Martins da Costa Marques
 34 Botulinum Toxin for Special Conditions: 
Chemical Rhinoplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235
Francisco Marcos Perez Atamoros 
and Alberto Avila Lozano
 35 Botulinum Toxin for Special Conditions: 
Facial Mesotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
Eloisa Leis Ayres
 36 Botulinum Toxin for Special Conditions: 
Gummy Smile – Advanced Points and Indications . . . . . . . . . . 245
Rosemarie Mazzuco and Beatrice Martinez Zugaib Abdalla
 37 Botulinum Toxin for Special Conditions: 
Masseter Hypertrophy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . 249
Caroline Romanelli T. A. Zelenika
 38 Botulinum Toxin for Special Conditions: 
Myomodulation to Body Contour . . . . . . . . . . . . . . . . . . . . . . . . 253
Roseli Andrade and Claudio Dias
Part III Hyaluronic Acid Filler
 39 Introduction: What Is Hyaluronic Acid Filler? . . . . . . . . . . . . . 261
Nelise Hans and Thais Sakuma
 40 Tip Chapter: Anatomy of the Face, Neck, Hands 
and Genital Areas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
Mirna Duarte Barros, Antonio Cardoso Pinto, 
Bianca Maria Liquidato, and Wagner Ricardo Montor
 41 Hyaluronic Acid for Dermic Hydration . . . . . . . . . . . . . . . . . . . 293
Adriana de Cerqueira Leite and Marcelo M. Bellini
 42 Hyaluronic Acid for Frontal and Glabella Areas . . . . . . . . . . . . 299
Maritza L. Kummerfeldt
 43 Filling Temporal and Eyebrow Areas . . . . . . . . . . . . . . . . . . . . . 305
Karina Colossi Furlan
 44 Hyaluronic Acid for Periocular Area . . . . . . . . . . . . . . . . . . . . . 313
Rodrigo Amaral de Lima and Adilson Da Costa
Contents
xvi
 45 Hyaluronic Acid for Malar Area and Zygomatic Arch . . . . . . . 321
Karina Colossi Furlan
 46 Hyaluronic Acid for Pre-auricular Area . . . . . . . . . . . . . . . . . . . 329
Liza R. Braun, Maxim Polansky, and Travis W. Blalock
 47 Hyaluronic Acid for Ear Lobe . . . . . . . . . . . . . . . . . . . . . . . . . . . 337
Adriana de Cerqueira Leite and Marcelo M. Bellini
 48 Hyaluronic Acid for the Nose . . . . . . . . . . . . . . . . . . . . . . . . . . . . 341
Carlos Echevarria and Denise Durand
 49 Hyaluronic Acid for Nasolabial Folds . . . . . . . . . . . . . . . . . . . . . 347
Aline Rodrigues Bragatto, Caroline Moreira Albrecht, 
and Cristina Hachul Moreno
 50 Hyaluronic Acid for Lips and Perioral Fine 
Lines and Wrinkles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 353
Luca Piovano
 51 Hyaluronic Acid Fillers for Treating Temporal 
Area Volume Loss . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359
Francisco de Melo and Carmelo Crisafulli
 52 Hyaluronic Acid for Chin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 367
Nark-Kyoung Rho
 53 Hyaluronic Acid for Neck Wrinkles . . . . . . . . . . . . . . . . . . . . . . 375
Caroline Romanelli T. A. Zelenika 
and Adilson Da Costa
 54 Hyaluronic Acid for Hands . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379
Tatiana Basso Biasi and Ricardo Limongi Fernandes
 55 Hyaluronic Acid for Genital Area . . . . . . . . . . . . . . . . . . . . . . . . 385
Shirlei Schnaider Borelli, Mariana Isis Wanczinski, 
and Nátalie Schnaider Borelli
Part IV Threads in Cosmetic Procedures
 56 Introduction: Threads in Cosmetic Procedures . . . . . . . . . . . . . 393
Thaísa Saddi Tannous Silvino, Ellem Tatiani de Souza 
Weimann, and Lissa Sabino de Matos
 57 Tip Chapter: Anesthesia in Cosmetic Procedures . . . . . . . . . . . 403
Gaurav P. Patel
 58 Eyebrow Thread Lifting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407
Iñigo de Felipe
 59 Threads for the Middle Third of the Face . . . . . . . . . . . . . . . . . 415
Tatiana Caloi
 60 Threads for the Inferior Third of the Face . . . . . . . . . . . . . . . . . 421
Flávio Rezende and Aline Vieira
 61 Threads for Chin Lifting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 427
Claudio Dias and Roseli Andrade
Contents
xvii
 62 Threads for the Neck . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 433
Paola Rosalba Russo and Gerhard Van Niekerk
 63 Threads for Corporal Areas: Upper and Inferior Limbs . . . . . 445
Gabriel Aribi, Cidia Vasconcellos, and Monica Aribi
 64 Threads for Abdomen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 455
Denise Rocha Luna Barcelos and Cyro Hirano
 65 Threads for Special Conditions: Buttocks . . . . . . . . . . . . . . . . . 461
Adriana Vilarinho, Raquel Cavalcante, 
and Renata Marques Sitler
Part V Chemical Substances for Injectable Cosmetic Neocollagenesis
 66 Introduction: Chemical Substances for Injectable 
Cosmetic Neocollagenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 467
Elisangela Samartin Pegas, Felipe Borba Calixto dos Santos, 
and Beatrice Martinez Zugaib Abdalla
 67 Tip Chapter: Improving Healing in Cosmetic Procedures . . . . 475
Maria da Glória Martin Sasseron, Renan Lage, 
Larissa Mondadori Mercadante, 
and Luiza de Castro Fernandes
 68 Calcium Hydroxyapatite for Face . . . . . . . . . . . . . . . . . . . . . . . . 487
Eliandre Costa Palermo and Alessandra Anzai
 69 Calcium Hydroxylapatite for Hands . . . . . . . . . . . . . . . . . . . . . . 499
Tatiana Basso Biasi and Vinicius Pollo Pires
 70 Calcium Hydroxyapatite For Unusual Body Areas . . . . . . . . . . 505
Gabriela Casabona
 71 Platelet-Enriched Plasma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 513
Abraham Benzaquén-Barchillón and Eduardo de 
Frutos-Pachón
 72 Poly-L-Lactic Acid for the Face . . . . . . . . . . . . . . . . . . . . . . . . . . 521
Carla Albuquerque, Kenia Calil, and Viviane Reis
 73 Poly-L-Lactic Acid for the Neck . . . . . . . . . . . . . . . . . . . . . . . . . 529
Renata Indelicato Zac and Adilson Da Costa
 74 Poly-L-Lactic Acid for Arms . . . . . . . . . . . . . . . . . . . . . . . . . . . . 533
Daniel Dal’Asta Coimbra and Betina Stefanello
 75 Poly-L-Lactic Acid for Hands . . . . . . . . . . . . . . . . . . . . . . . . . . . 539
Francisco Marcos Perez Atamoros and Alberto Avila Lozano
 76 Poly-L-Lactic Acid for the Gluteal Area . . . . . . . . . . . . . . . . . . . 543
Maria Helena Lesqueves Sandoval
 77 Polyacrylamide for the Face . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 549
Natacha Quezada Gaón, Cristián Vera-Kellet, 
and Ximena Wortsman
Contents
xviii
 78 Polycaprolactone for the Face . . . . . . . . . . . . . . . . . . . . . . . . . . . 555
Pierre Nicolau
 79 Polycaprolactone for Extrafacial Areas . . . . . . . . . . . . . . . . . . . 565
Natacha Quezada Gaón, Ximena Wortsman, 
and Patricia Apt
 80 Polyethylene Glycol for the Hands and Face . . . . . . . . . . . . . . . 575
Samira Yarak and Luis Henrique Barbizan de Moura
 81 Polymethylmethacrylate Microsphere Injections 
in the Face . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 581
Gottfried Lemperle
 82 Polymethyl Methacrylate for the Body . . . . . . . . . . . . . . . . . . . . 589
Marcio Soares Serra
Part VI Micro-aesthetic Surgery and Others
 83 Introduction: Dressings to Improve Healing 
in Cosmetic Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 595
Maria da Glória Martin Sasseron, Renan Lage, 
Larissa Mondadori Mercadante, 
and Luiza de Castro Fernandes
 84 Tip Chapter: How Might Cosmeuticals Improve 
Skin Aesthetic Procedures Outcome? . . . . . . . . . . . . . . . . . . . . . 605
Leslie Baumann and Erica Monteiro
 85 Chemical Liposculpture of the Chin . . . . . . . . . . . . . . . . . . . . . . 619
Valerie D. Callender and Jessica A. McCarrick
 86 Microneedling for Neocollagenesis of the Face . . . . . . . . . . . . . 625
Gabriella Fabbrocini, Caterina Mazzella, and Mirella 
D’Andrea
 87 Acne Scar: Shaving and Electrosurgery . . . . . . . . . . . . . . . . . . . 631
Joaquim José Teixeira de Mesquita Filho 
and Francine Papaiordanou
 88 Acne Scars: 5-Fluorouracil (MMP® Technique) . . . . . . . . . . . . 637
Maria Teresa Pereira Soares, Dirlene Melo Palmeira Roth, 
and Samir Arbache
 89 Acne Scars: Bleomycin Plus Triamcinolone Injection 
(MMP® Technique) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 643
Maria Teresa Pereira Soares, Dirlene Melo Palmeira Roth, 
and Samir Arbache
 90 Acne Scar: CROSS (Chemical Reconstruction 
of Skin Scar) . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . 649
Vito Abrusci and Valentina Benzecry
 91 Acne Scar: Dermal Graft . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 659
Sergio Schrader Serpa
Contents
xix
 92 Acne Scars: Dermabrasion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 667
Bogdana Victoria Kadunc
 93 Acne Scar: Hyaluronic Acid Filler . . . . . . . . . . . . . . . . . . . . . . . 673
Ada Regina Trindade de Almeida 
and Danielle Claudino de Oliveira Costa
 94 Acne Scar: Microneedling . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 677
Flávio Barbosa Luz and Tadeu de Rezende Vergueiro
 95 Acne Scar: Punch Elevation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 683
Caroline Silva Pereira, Beatrice Martinez Zugaib Abdalla, 
and Fábio Rebucci
 96 Acne Scars: Subcision . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 689
Jaime Piquero-Casals and Jaime Piquero-Martin
 97 Aspiration Curettage for Axillary Hyperhidrosis . . . . . . . . . . . 693
Rebeca Alvares Rodrigues Maffra de Rezende, 
Adilson Da Costa, and Flávio Barbosa Luz
 98 Autologous Fat Grafting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 699
Gabriele C. Miotto
 99 Autologous Fibroblasts Injections in Face . . . . . . . . . . . . . . . . . 705
Leticia de Chiara Moço, Fabio Antonio Abrantes Tuche, 
and Ricardo de Mendonça Filho
 100 Cellulite: Subcision . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 711
Camile L. Hexsel, Taciana Dal’Forno Dini, 
and Doris Hexsel
 101 Chemical Lipolysis of the Infraorbital Fat Pads . . . . . . . . . . . . 719
Patricia Rittes
 102 Electro-blepharoplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 723
Daniel Dal’Asta Coimbra, Betina Stefanello, 
and Natalia Caballero Uribe
 103 Submental Liposuction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 727
Aline Rodrigues Bragatto and Cristina Hachul Moreno
 104 Stretch Marks: Microdermabrasion and Superficial 
Localized Dermabrasion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 733
Taciana Dal’Forno Dini and Camile L. Hexsel
 105 Strech Marks: Transdermal Divulsion . . . . . . . . . . . . . . . . . . . . 741
Rogério Tércio Ranulfo, Marjorie Bezerra Porciúncula, 
and Lara Ranulfo de Mendonça
 106 Upper Blepharoplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 745
Aline Rodrigues Bragatto and Cristina Hachul Moreno
Contents
xx
Part VII Aesthetic Approach of Scalp
 107 Introduction: Clinical Emergency During Aesthetic 
Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 755
Merces Assumpcao-Morales and Javier Morales
 108 Pearl Chapter: Methods and Tips 
for a Better Scar Quality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 769
Luciana Takata Pontes, André Luiz Simião, 
and Arash Kimyai-Asadi
 109 Tip Chapter: Low-Level Light Therapy 
and High- Energy Lasers in Trichology . . . . . . . . . . . . . . . . . . . . 777
R. Minotto and L. Damiani
 110 Low-Level Light Therapy (LLLT) in Alopecia . . . . . . . . . . . . . . 781
R. Minotto and L. Damiani
 111 Scalp Mesotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 785
Renan Minotto and Rodrigo Vettorato
 112 Microneedling of the Scalp . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 791
Renan Minotto and Liliam Dalla Corte
 113 Tricopigmentation of the Scalp . . . . . . . . . . . . . . . . . . . . . . . . . . 795
Renan Minotto and Mariana Vale Scribel da Silva
 Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 801
Contents
xxi
Adilson Da Costa, MD, MSc, PhD Medical Doctor (1997) and Dermatology 
(2001) from the Santa Casa de São Paulo School of Medicine, Brazil.
Dr. Da Costa obtained his Master of Science degree in Clinical and 
Surgical Dermatology from the Federal University of São Paulo (2006) and 
doctorate’s (PhD) in Dermatology from the University of São Paulo Medical 
School (2012), both in Brazil, and he did his Postdoctoral Research Fellowship 
in Dermatology at Emory University School of Medicine (2016).
He is permanent professor and mentor of PhD and MSc at Instituto de 
Assistência Médica ao Servidor Estadual (IAMSPE), São Paulo, SP, Brazil.
He is the author of two books on Dermatology (Dermatology and 
Pregnancy, Elsevier; International Textbook of Cosmeceuticals, Guanabara- 
Koogan), as well as author of several book chapters, scientific articles, and 
scientific conference’s posters in the field of aesthetic and clinical-surgical 
dermatology.
He is a key opinion leader in dermatology, taking place as pharmaceutical 
and cosmetic companies’ advisory board member. Dr. Da Costa has given 
more than 200 lectures around world, aside of being principal investigator in 
about 200 clinical and in vitro trials.
About the Author
xxiii
Beatrice Martinez Zugaib Abdalla ABC School of Medicine, Santo André, 
SP, Brazil
2nd Year Resident of Internal Medicine at FMABC, Santo André, SP, Brazil
Vito Abrusci Private Practice, Milan, Italy
Caroline Moreira Albrecht São Paulo, SP, Brazil
Carla Albuquerque Carla Albuquerque Clinic of Dermatology, São Paulo, 
SP, Brazil
Roseli Andrade Clinical and Aesthetic Dermatology, Clínica Dermatológica 
Dra Roseli Andrade, Santos, SP, Brazil
Alessandra Anzai Hospital das Clínicas of University of São Paulo Medical 
School, Dermatology, São Paulo, SP, Brazil
Patricia Apt Las condes Clinic, Santiago del Chile, Chile
Samir Arbache Deparment of Dermatology, University of Mogi das Cruzes, 
Mogi das Cruzes, SP, Brazil
Gabriel Aribi Department of Dermatology of Hospital Ipiranga, São Paulo, 
SP, Brazil
Department of Dermatology of Centro Universitário Lusíada, Santos, SP, 
Brazil
Monica Aribi Department of Dermatology of Hospital Ipiranga, São Paulo, 
SP, Brazil
Merces  Assumpcao-Morales Garden City Primary Care, Garden City, 
NY, USA
NYU- Winthrop Hospital, Garden City, NY, USA
Francisco  Marcos  Perez  Atamoros Centro Dermatologico Tennyson, 
Mexico City, DF, Mexico
Javier Ruiz Ávila Dermédica Clinic of Dermatology, Mexico City, DF, MX
Adriana Awada Adriana Awada Clinic of Dermatology, Santo André, SP, 
Brazil
Brazilian Society of Dermatology, Rio de Janeiro, Brazil
Contributors
xxiv
Eloisa Leis Ayres EZskin Dermatologia, Niterói, RJ, Brazil
Fernanda Ayres de Morais e Silva  Cardoso Department of Medicine, 
Facid Wyden, Teresina, PI, Brazil
Denise Rocha Luna Barcelos Denise Barcelos Clinic of Dermatology, Rio 
de Janeiro, RJ, Brazil
Mirna Duarte Barros Department of Morphology, Santa Casa de São Paulo 
School of Medical Sciences, São Paulo, SP, Brazil
Leslie Baumann Baumann Cosmetic Dermatology Clinic, Miami, FL, USA
Marcelo M. Bellini Marcelo Bellini Clinic of Dermatology, São Paulo, SP, 
Brazil
Abraham Benzaquén-Barchillón Clínica Benzaquén, Málaga, Spain
Valentina Benzecry Private Practice, Milan, Italy
Tatiana Basso Biasi Brazilian Society of Dermatology, Florianópolis, SC, 
Brazil
Travis W. Blalock Emory University School of Medicine, Department of 
Dermatology, Atlanta, GA, USA
Nátalie Schnaider Borelli Brazilian Society of Dermatology, Private Office 
in São Paulo, São Paulo, SP, Brazil
Shirlei Schnaider Borelli Brazilian Society of Dermatology, Private Office 
in São Paulo, São Paulo, SP, Brazil
Aline  Rodrigues  Bragatto Aline Rodrigues Bragatto Clinic of Plastic 
Surgery, Valinhos, SP, Brazil
Department of Dermatology, Santa Casa of São Paulo University Hospital, 
São Paulo, SP, Brazil
Liza  R.  Braun Emory University School of Medicine, Department of 
Dermatology, Atlanta, GA, USA
Harold J. Brody Emory University School of Medicine, Atlanta, GA, USA
Laura Bariquelo Buratini Laura Bariquelo Buratini Clinic, Botucatu, SP, 
Brazil
Natalia  Caballero  Uribe Department of Dermatology, ABCSchool of 
Medicine, Santo André, SP, Brazil
Kenia Calil Kenia Calil Clinic of Dermatology, Marília, SP, Brazil
Valerie D. Callender Callender Dermatology and Cosmetic Center, Glenn 
Dale, MD, USA
Department of Dermatology, Howard University Hospital, Washington, DC, 
USA
Tatiana Caloi Tatiana Caloi Clinic of Plastic Surgery, São Paulo, SP, Brazil
Contributors
xxv
Fernanda Camozzato Brazilian Center for Studies in Dermatology, Porto 
Alegre, RS, Brazil
Antonio  Cardoso  Pinto Department of Morphology, Santa Casa de São 
Paulo School of Medical Sciences, São Paulo, SP, Brazil
Gabriela  Casabona Beauty Beyond Skin Clinic, Dermatology and 
Dermatologic Surgery, São Paulo, SP, Brazil
Jaime  Piquero-Casals Dermik: Clinica Dermatologica Multidisciplinar, 
Barcelona, Spain
Raquel Cavalcante Clínica Adriana Vilarinho, São Paulo, SP, Brazil
Liliam Dalla Corte Preceptor of Nail and Hair Diseases and Coordinator 
(Head) of the Nail and Hair Diseases Unit, Dermatology Department, 
UFCSPA, Hospital Santa Casa de Porto Alegre, Porto Alegre, RS, Brazil
Carmelo Crisafulli IMG Clinic, Dubai, UAE
Adilson  Da Costa Instituto de Assistência Médica ao Servidor Público 
Estadual, Tenured International Professor and Mentor for PhD and MSc 
Programs, São Paulo, SP, Brazil
Elisa  Raquel  Martins  da Costa  Marques Clínica de Dermatologia do 
Hospital do Servidor Público Municipal de São Paulo, São Paulo, SP, Brazil
Maria da Glória Martin Sasseron Department of Dermatology, Pontifical 
Catholic University of Campinas, Campinas, SP, Brazil
Mariana  Vale  Scribel  da Silva Department of Dermatology, Santa Casa 
Hospital, Porto Alegre, RS, Brazil
Mirella D’Andrea Dermatology Unit, Department of Clinical Medicine and 
Surgery, University Federico II, Naples, Italy
Daniel  Dal’Asta  Coimbra Daniel Coimbra Les Peaux Clinic of 
Dermatology, Rio de Janeiro, RJ, Brazil
Rubem David Azulay Institute of Dermatology, Santa Casa of Mercy of Rio 
de Janeiro, Rio de Janeiro, RJ, Brazil
Taciana Dal’Forno Dini Brazilian Center for Studies in Dermatology, Porto 
Alegre, RS, Brazil
Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, RS, Brazil
Ada Regina Trindade de Almeida Clínica de Dermatologia do Hospital do 
Servidor Público Municipal de São Paulo, São Paulo, SP, Brazil
Luiza de Castro Fernandes Medical Resident in Dermatology, Pontifical 
Catholic University of Campinas, Campinas, SP, Brazil
Adriana  de Cerqueira  Leite Adriana Leite Clinic of Dermatology, São 
Paulo, SP, Brazil
Leticia  de Chiara  Moço Cosmetic Dermatology Unit, Department of 
Dermatology, State University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil
Contributors
xxvi
Iñigo de Felipe Clinica Dermatológica De Felipe, Barcelona, Spain
Eduardo de Frutos-Pachón Clínica Kalos, Fundación Tejerina, Talavera, 
Spain
Rodrigo  Amaral  de Lima Servidor Público Estadual de São Paulo, São 
Paulo, SP, Brazil
Lissa  Sabino  de Matos Department of Dermatology, Pontifical Catholic 
University of Campinas, Campinas, São Paulo, SP, Brazil
Francisco de Melo ZO Skin Centre, Dubai, UAE
Ricardo  de Mendonça  Filho Paulo de Goes Institute of Microbiology, 
Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil
Lara  Ranulfo  de Mendonça Rogerio Ranulfo Clinic of Dermatology, 
Goiânia, GO, Brazil
Joaquim  José  Teixeira  de Mesquita  Filho Dermatologi Surgery Unit, 
Ruben David Azulay Institute, Santa Casa of Mercy of Rio de Janeiro, Rio de 
Janeiro, RJ, Brazil
Luis  Henrique  Barbizan  de Moura Dermatology  – UNIFESP EPM, 
Hospital São Paulo, São Paulo, SP, Brazil
Danielle Claudino de Oliveira Costa Clínica de Dermatologia do Hospital 
do Servidor Público Municipal de São Paulo, São Paulo, SP, Brazil
Tadeu  de Rezende  Vergueiro Department of Dermatology, University 
Hospital Pedro Ernesto, Federal Fluminense University, Niterói, RJ, Brazil
Rebeca Alvares Rodrigues Maffra de Rezende Rebeca Rezende Clinic of 
Dermatology, Rio de Janeiro, RJ, Brazil
Universidade Federal Fluminense (UFF), Niterói, RJ, Brazil
Ellem  Tatiani  de Souza  Weimann Universidade Federal de Roraima  – 
UFRR, Boa Vista, RR, Brazil
Children’s Hospital Santo Antônio, San Antonio, RR, Brazil
Rossana  Cantanhede  Farias  de Vasconcelos Dermatology Department, 
University of Santo Amaro, São Paulo, SP, Brazil
María del Pilar Del Río Navarrete Biot Clínica De Dermatológica Maria 
del Pilar Biot, Niterói, RJ, Brazil
Claudio Dias Clinical Aesthetic Medicine, Recife, PE, Brazil
Felipe  Borba  Calixto  dos Santos Department of Dermatology at PUC 
Campinas, Campinas, SP, Brazil
Denise Durand Clinica San Pablo, Lima, Peru
Carlos Echevarria Private Practice, Dermanova Clinic, Lima, Peru
Gabriella Fabbrocini Dermatology Unit, Department of Clinical Medicine 
and Surgery, University Federico II, Naples, Italy
Contributors
xxvii
Andrezza  Facci Clínica Andrezza Facci de Dermatologia, Barueri, SP, 
Brazil
Ricardo Limongi Fernandes Brazilian Society of Dermatology, American 
Academy of Dermatology, São Paulo, SP, Brazil
Sergio Talarico Filho Talarico Clinic of Dermatology, São Paulo, SP, Brazil
Mercedes  Florez  White Department of Dermatology, Herbert Wertheim 
College of Medicine, Florida International University, Miami, FL, USA
Karina Colossi Furlan Rush University Medical Center, Chicago, IL, USA
Natacha Quezada Gaón Department of Dermatology, Pontifical Catholic 
University of Chile, Santiago de Chile, Chile
Loryart Marte Grullón Department of Dermatology, Clinica Union Medica 
del Norte, Santiago de los Caballeros, Dominican Republic
Nelise Hans Private practice, Campo Grande, MS, Brazil
María Isabel Herane Herane University of Chile, Santiago, Chile
Camile  L.  Hexsel Brazilian Center for Studies in Dermatology, Porto 
Alegre, RS, Brazil
Madison Medical Affiliates, Mohs Surgery, Glendale and Waukesha, WI, 
USA
Madison Medical Associates, Glendale, WI, USA
Doris  Hexsel Brazilian Center for Studies in Dermatology, Porto Alegre, 
RS, Brazil
Hexsel Dermatologic Clinics, Porto Alegre/Rio de Janeiro, RS/RJ, Brazil
Cyro  Hirano Cosmetic Dermatology Unit, Policlínica Geral do Rio de 
Janeiro, Rio de Janeiro, RJ, Brazil
Bruna  Sabatovich  Villarejo  Iosifovich Federal University of Rio de 
Janeiro, Rio de Janeiro, RJ, Brazil
Renata Joffe Inform Diagnostics, Irving, TX, USA
Bogdana Victoria Kadunc Department of Dermatology, Pontifical Catholic 
University of Campinas, Campinas, SP, Brazil
Armineh Kajoian Inform Diagnostics, Irving, TX, USA
Maria Paulina Villarejo Kede Private Clinic, Rio de Janeiro, RJ, Brazil
Arash Kimyai-Asadi Department of Dermatology, Weill Cornell Medical 
College, Houston, TX, USA
Maritza  L.  Kummerfeldt Clinic of Dermatology, Guatemala City, 
Guatemala
Edgar  E.  La Rotta Centro Medico Buenaventura en Caracas, Guatire, 
Venezuela
Contributors
xxviii
Hospital Clinic Barcelona, Barcelona, Spain
Renan  Lage Cosmiatric Department, Department of Dermatology of the 
Pontifical Catholic University of Campinas - PUC Campinas, Campinas, SP, 
Brazil
Gottfried Lemperle Division of Plastic Surgery, University of California, 
San Diego, La Jolla, CA, USA
Bianca Maria Liquidato Department of Morphology, Santa Casa de São 
Paulo School of Medical Sciences, São Paulo, SP, Brazil
Alberto Avila Lozano Centro Dermatologico Tennyson, Mexico City, DF, 
Mexico
Flávio Barbosa Luz Universidade Federal Fluminense (UFF), Niterói, RJ, 
Brazil
Jaime Piquero-Martin Hospital Vargas de Caracas, Caracas, Venezuela
Caterina  Mazzella Dermatology Unit, Department of Clinical Medicine 
and Surgery, University Federico II, Naples, Italy
Rosemarie Mazzuco Private Practice, Carazinho, RS, Brazil
Jessica  A.  McCarrick Department of Dermatology, Howard University 
Hospital, Washington, DC, USA
Vanessa  Lucília  Silveira  Medeiros Department of Tropical Medicine of 
Federal University of Pernambuco, Recife, PE, Brazil
Instituto Davan Dermatologia, Recife, PE, Brazil
Larissa  Mondadori  Mercadante Medical Resident in Dermatology, 
PontificalCatholic University of Campinas, Campinas, SP, Brazil
Renan Minotto Preceptor of Nail and Hair Diseases and Coordinator (Head) 
of the Nail and Hair Diseases Unit, Dermatology Department, UFCSPA, 
Hospital Santa Casa de Porto Alegre, Porto Alegre, RS, Brazil
Dermatology Department, UFCSPA, Hospital Santa Casa de Porto Alegre, 
Porto Alegre, Rio Grande do Sul, Brazil 
Gabriele C. Miotto Division of Plastic and Reconstructive Surgery, Emory 
University School of Medicine, Atlanta, GA, USA
Suelen Montagner Private Clinic, Campinas, SP, Brazil
Erica Monteiro Department of Humanities and Medical Sciences, Federal 
University of São Paulo (UNIFESP), São Paulo, SP, Brazil
Wagner  Ricardo  Montor Department of Physiological Sciences, Santa 
Casa de São Paulo School of Medical Sciences, São Paulo, SP, Brazil
Javier Morales Advanced Internal Medicine Group, Greenvale, NY, USA
Donald and Barbara Zucker School of Medicine at Hofstra / Northwell 
University, University, NY, USA
Contributors
xxix
Cristina Hachul Moreno Department of Dermatology, Santa Casa of São 
Paulo University Hospital, São Paulo, SP, Brazil
Cristina Hachul Moreno Clinic of Plastic Surgery, São Paulo, SP, Brazil
Daniela Moya Hospital Universitario de Caracas, Caracas, Venezuela
Hospital Intercultural Kallvu Llank Chile, Cañete, Región del Bío Bío, Chile
Pierre Nicolau Pierre Nicolau Clinic of Plastic Surgery, Figueras (Girona), 
Spain
Eliandre  Costa  Palermo Faculty of Medicine of the ABC Foundation, 
Dermatology, São Paulo, SP, Brazil
Francine  Papaiordanou Francine Papaiordanou Clinic of Dermatology, 
Rio de Janeiro, RJ, Brazil
Gaurav P. Patel Department of Anesthesiology, Emory University School 
of Medicine, Atlanta, GA, USA
Luciana  R.  Patricio  Linhares Sociedade Brasileira de Dermatologia 
(SBD), São Paulo, SP, Brazil
Caroline Silva Pereira Pontifical Catholic University, São Paulo, SP, Brazil
ABC School of Medicine, Santo André, SP, Brazil
Sírio Libanês Hospital, São Paulo, SP, Brazil
Elisangela  Samartin  Pegas Leprosy, Phototerapy and Bullous Diseases 
Outpatient Clinic at PUC Campinas, Campinas, Brazil
Juliano Peruzzo Sociedade Brasileira de Dermatologia, Porto Alegre, RS, 
Brazil
Luca Piovano University of Camerino, Camerino, Italy
Plastic Surgeon, Rome, Italy
Vanesa Piquero Clinica Leopoldo Aguerrevere Caracas, Caracas, Venezuela
Clinica Dermik Barcelona, Barcelona, Spain
Vinicius Pollo Pires Brazilian Society of Dermatology, Florianópolis, SC, 
Brazil
Jose A. Plaza Inform Diagnostics, Irving, TX, USA
Maxim  Polansky Emory University School of Medicine, Department of 
Dermatology, Atlanta, GA, USA
Luciana Takata Pontes Department of Dermatology/Surgical Dermatology, 
Hospital De Clínicas – Unicamp – State University of Campinas, Campinas, 
SP, Brazil
Marjorie  Bezerra  Porciúncula Rogerio Ranulfo Clinic of Dermatology, 
Goiânia, GO, Brazil
Contributors
xxx
Clarissa  Prati Sociedade Brasileira de Dermatologia, Porto Alegre, RS, 
Brazil
Rogério Tércio Ranulfo Rogerio Ranulfo Clinic of Dermatology, Goiânia, 
GO, Brazil
Fábio Rebucci ABC School of Medicine, Santo André, SP, Brazil
Viviane Reis Viviane Reis Clinic of Dermatology, Bauru, SP, Brazil
Flávio Rezende Brazilian Society of Plastic Surgery (SBCP), International 
Society of Aesthetic Plastic Surgery (ISAPS), Rio de Janeiro, RJ, Brazil
Nark-Kyoung  Rho Leaders Aesthetic Laser & Cosmetic Surgery Center, 
Seoul, South Korea
Patricia Rittes Clinica Dermatológica Patricia Rittes, São Paulo, SP, Brazil
Dirlene  Melo  Palmeira  Roth Deparment of Dermatology, University of 
Mogi das Cruzes, Mogi das Cruzes, SP, Brazil
Paola Rosalba Russo Modena, Italy
Thais Sakuma Private practice, Campo Grande, MS, Brazil
Maria Helena Lesqueves Sandoval Department of Dermatology, Aesthetic 
Dermatology Unit, Cassiano Antonio Moraes Hospital, Vitória, ES, Brazil
Luciane Scattone Clínica Dermatológica Dra Luciane Scattone, São Paulo, 
SP, Brazil
Sergio Schrader Serpa Clínica Dermatológica Sergio Serpa, Rio de Janeiro, 
RJ, Brazil
Marcio Soares Serra Marcio Serra Clinic of Dermatology, Rio de Janeiro, 
RJ, Brazil
Carolina Siega Brazilian Center for Studies in Dermatology, Porto Alegre, 
RS, Brazil
Thaísa Saddi Tannous Silvino Universidade Federal do Mato Grosso do 
Sul – UFMS, Campo Grande, MS, Brazil
André Luiz Simião Department of Dermatology, Hospital E Maternidade 
Celso Pierro – Puccamp, Campinas, SP, Brazil
Renata Marques Sitler Clínica Adriana Vilarinho, São Paulo, SP, Brazil
Maria  Teresa  Pereira  Soares Maria Teresa Pereira Soares Clinic of 
Dermatology, São Sebastião do Paraíso, MG, Brazil
Betina  Stefanello Les Peaux Clinic of Dermatology, Rio de Janeiro, RJ, 
Brazil
Rubem David Azulay Institute of Dermatology, Santa Casa of Mercy of Rio 
de Janeiro, Rio de Janeiro, RJ, Brazil
Fabio Antonio Abrantes Tuche Pedro Ernesto Hospital, State University of 
Rio de Janeiro, Rio de Janeiro, RJ, Brazil
Contributors
xxxi
Gerhard  Van Niekerk Medical Aesthetic Clinic, Somerset West, South 
Africa
Cidia Vasconcellos Department of Dermatology of Hospital Ipiranga, São 
Paulo, SP, Brazil
Department of Dermatology of the University of São Paulo, São Paulo, SP, 
Brazil
Renata  Cristina  Vasconcellos Department of Dermatology, Pontifical 
Catholic University of Campinas, Campinas, SP, Brazil
Cristián  Vera-Kellet Department of Dermatology, Pontifical Catholic 
University of Chile, Santiago de Chile, Chile
Rodrigo Vettorato Department of Dermatology, Santa Casa Hospital, Porto 
Alegre, RS, Brazil
Aline Vieira Brazilian Society of Dermatology, Federal University of Rio de 
Janeiro (UFRJ), Rio de Janeiro, RJ, Brazil
Adriana Vilarinho Clínica Adriana Vilarinho, São Paulo, SP, Brazil
Carlos G. Wambier Yale University School of Medicine, New Haven, CT, 
USA
Carlos  Gustavo  Wambier Department of Dermatology, Yale University 
School of Medicine, New Haven, CT, USA
Department of Medicine, State University of Ponta Grossa, Ponta Grossa, 
PR, Brazil
Mariana Isis Wanczinski Brazilian Society of Dermatology, Private Office 
in São Paulo, São Paulo, SP, Brazil
Sarah  Wilson Emory University School of Medicine, Department of 
Dermatology, Atlanta, GA, USA
Ximena  Wortsman Department of Dermatology at University of Chile, 
Santiago del Chile, Chile
Samira  Yarak Dermatology  – UNIFESP EPM, Hospital São Paulo, São 
Paulo, SP, Brazil
Howa  Yeung Emory University School of Medicine, Department of 
Dermatology, Atlanta, GA, USA
Renata  Indelicato  Zac Dermatology Department, Minas Gerais Military 
Hospital, Belo Horizonte, MG, Brazil
Caroline  Romanelli  T.  A.  Zelenika Pontifical Catholic University of 
Campinas, São Paulo, SP, Brazil
Contributors
Part I
Peelings
3© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_1
Introduction: Classification 
of Peels
Carlos G. Wambier and Harold J. Brody
1.1 History/Background
Medical understanding and research followed the 
lay ancient and cultural formulas used to abrade 
or smooth the skin, such as sour milk, lemonade 
[6], vinegar, and even chemical formulas with 
phenol and croton oil [16]. Some peels are per-
formed on an empirical basis, such as the retinoic 
acid peel, also known as tretinoin peel [10], 
which is performed throughout Brazil but lacks 
more studies of its benefits in acne, rejuvenation, 
and the field of cancerization [29]. The 
International Peeling Society tries to set open 
study points in chemical peels research each year 
at its pre-American Academy of Dermatology 
meeting event. Main scientific contributions are 
summarized in Table 1.1.
1.2 Histological Outcome
For superficial peels, such as Jessner’s solution 
(14% lactic acid, 14% salicylic acid, and 14% 
resorcinol in ethanol), also called a Combes’ 
C. G. Wambier (*) 
Yale University School of Medicine, 
New Haven, CT, USA 
H. J. Brody 
Emory University School of Medicine, 
Atlanta, GA, USA
1
Table 1.1 Theseminal advances in medical literature, 
updated from [4]
Authors and year Main contribution
Unna [30] Salicylic acid, resorcinol, 
phenol, and TCA descriptions
Fox [13] Phenol for facial freckles
Mackee and Karp [20] Phenol for scarring
Eller and Wolff [12] Sulfur, resorcinol, salicylic 
acid, phenol lotions, CO2 slush
Monash [21] Trichloroacetic acid peeling
Urkov [31] Resorcinol, lactic acid, salicylic 
acid, phenol, cantharidin
Max Jessner, 1950s Jessner’s solutions
Combes et al. [9] Buffered phenol formulas
Brown et al. [7] Phenol histology and buffered 
formulas
Ayres [1] TCA for actinic damage
Baker and Gordon [2] Phenol–croton oil formula
Litton [19] Phenol–croton oil formula
Resnik et al. [24] TCA peeling
Stegman [27] Histologic comparison of 
wounding agents
Van Scott and Yu [26] Alpha-hydroxy acids
Brody and Hailey [5] Medium-depth peeling, CO2 
slush, and 35% TCA
Monheit [22] Medium-depth peeling variation, 
Jessner, and 35% TCA
Griffin et al. [15] Pyruvic acid peel
Coleman and 
Futrell [8]
Medium-depth peeling 
variation, glycolic acid +35% 
TCA
Hetter [17] Croton oil strength paradigm. 
Phenol–croton oil formulas
Cucé et al. [10] Tretinoin peeling
Dainichi et al. [11] Salicylic acid in polyethylene 
glycol
Safoury et al. [25] Modified Jessner’s solution 
and TCA in melasma
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_1&domain=pdf
4
peel, there is only epidermal injury, with stratum 
corneum separation and upper epidermal intraep-
ithelial edema and spongiosis. No dermal changes 
are present. The upper dermal injury is the main 
characteristic of medium-depth peels. When 
necrosis reaches mid-dermis, the peel is consid-
ered deep [4].
Samuel Stegman’s work on the histological 
depth of chemical wounding [27] was a hall-
mark for more scientific and controlled chemi-
cal peeling [23]. The experiment involved a 
comparison between dermabrasion, a medium-
depth peel, comprising 60% trichloroacetic acid 
(TCA) and liquid phenol (88%), and a deep 
peel: Baker’s phenol mixture. Peels were per-
formed over the neck of a 55-year-old male, 
occluded for 24  h on the right side and unoc-
cluded on the left side; the skin was biopsied at 
3 days and 60 days after treatment. Histological 
outcomes were set: wound thickness (distance 
from basement membrane to the depth of the 
wound in the dermis), epidermal thickness, 
grenz zone (as a marker of sun damage: amor-
phous pale staining and elastosis), and distinct 
dermal scar formation. Dermabrasion produced 
more intense hypopigmentation clinically. 
Occluded peels on right side took longer to heal 
and apparently had slightly deeper wounding on 
the third day, and epidermis was thicker and still 
healing on the 60th day. At 120  days, peeled 
areas had normal ridge architecture, while 
dermabrasion produced an almost entirely flat 
epidermis. A dermal scar band from the middle 
to upper epidermis was formed at 60 days in all 
occluded specimens of sun- damaged skin. This 
band was not formed in non- sun- damaged con-
trol skin and was not formed in unoccluded pure 
phenol and TCA peels, with phenol–croton oil 
peel producing, noticeably, more dense collagen 
fibers and increased glycosaminoglycan density 
both above and beneath this scar tissue [27]. 
Although this experiment was done in the neck 
skin, which differs from facial skin in penetra-
tion and healing, it was an excellent starting 
point in methodology and histological basis of 
croton oil action in phenol formulas. Since we 
know that drivers usually have their left side 
more susceptible to sun damage [14], the dis-
cussion about tape occlusion effects remains 
open to debate.
1.3 Available Materials
• Degreasing agent: ethanol, acetone, or a mix-
ture of both (preferred by the author) although 
some experts prefer more complex degreasing 
formulas, with ether, resorcinol, or glycolic 
acid, for increasing degreasing and penetra-
tion effects of the peeling agent, which could 
also be replaced by a sequential combination 
of chemical peels (preferred by the authors). 
See Fig. 1.1a.
• Applicators: wooden or plastic, cotton-tipped 
applicators, cotton pads, or 4 × 4 gauzes. See 
Fig.  1.1b. Q-tips are better used for drying 
tears, because of the thin tube, which absorbs 
liquid by capillarity [34].
• Wounding agent: any chemical peel solution. 
See Table 1.1; Fig. 1.1c.
• Priming: Skin priming with topical retinoids 
is indicated for faster postoperative healing 
and increased penetration [32]. Other priming 
agents may be used, such as glycolic acid and 
azelaic acid; however, they lack scientific 
evidence.
• Post-peeling: Any moisturizer or ointment is 
safe enough not to cause further irritation or 
allergic reaction to the skin for superficial or 
medium-depth peels. Vaseline is very safe, 
from superficial to deep peels (Fig. 1.1d). For 
deep peels, there is still great debate on 
whether “tape occlusion” (originally, with 
Johnson & Johnson’s adhesive tape) dictates 
some extra strength or was just a costume 
derived from the first “phenolization” of war 
wounds during world war I. Although taping 
seems to increase the wound, it is still not 
clear if it is by occlusion and enhanced pene-
tration of the wounding agents, irritation from 
solvents and components of the glue, or simple 
debridement and maceration. Although baker 
and Gordon [28] have published an article 
stating that they had completely abandoned 
C. G. Wambier and H. J. Brody
5
taping since 1986, using a thick layer of 
Vaseline instead, for cases of very deep wrin-
kles, they still used taping (Brody, personal 
communication, 2017). Some specialists, such 
as Peter Rullan and Marina landau, adopt tap-
ing for the first 24 h, with a different tape, Hy- 
tape®, which is secured by surgical net, 
followed by debridement and a powder mask 
that hardens over 24 h (thymol-iodine). During 
this regimen, the patients eat and drink only 
by pushing their fluids and milk shakes 
through three to four hair dye plastic bottles. 
They cannot chew or suck. If they talk it has to 
be by mumbling or by writing it out. They 
cannot wash their face for 7–8 days, which is 
the period when the mask falls off. Mouth 
hygiene is done by gargling their mouth with 
Periogard® (Rullan, personal communication, 
2017). With Vaseline [3], patients are free to 
eat, drink, chew, and talk. Mouth hygiene is 
done as usual with toothbrush, dental floss, 
and gargle. And the main advantage to the sur-
geon is the direct observation of the skin dur-
ing the first week of critical follow-up [28, 
36]. One of the authors of this chapter, prof. 
Wambier, and Dr. Hetter agree that the croton 
oil concentration (cytotoxic fraction) is more 
important than post-peel regimens in deter-
mining rejuvenation [17, 18].
• Multiparameter monitors: Electrocardiogram, 
pulse oximeter, blood pressure, along with 
necessary advanced cardiologic life-support 
drugs, intravenous access, and defibrillator, in 
case of phenol peels in more than one cos-
metic unit, are advisable (Fig. 1.2; Table 1.2).
Fig. 1.1 Materials: acetone (a), multiple applicators (b), peeling agent disposed in a shot glass specific for that chemical, 
to avoid cross-contamination (c), Vaseline (d)
Fig. 1.2 Multiparameter monitor, showing left atrial flut-
ter caused by high-concentration topical anesthetic before 
the beginning of a phenol–croton oil peel, which was 
aborted. Safety always comes first in case of a cosmetic 
procedure
1 Introduction: Classification of Peels
6
1.4 Methods and Techniques
• Degreasing: it is important to remove all 
makeup, sebum, beard, topical anesthetic, and 
sunscreen by cleansing with mild soap and 
warm water. Before the procedure, the patient 
can be instructed to firmly apply acetone or 
ethanol to the face, by scrubbing with a gauze 
pad or what is preferable for controlled degreas-
ing; the physician may scrub the patient’s face 
with a semi-soaked gauze pad (Fig. 1.3).
• Applicationof the chemical agent: each physi-
cian has a preference of applicator for each 
chemical peel. Depending on the area of the 
face/body to be peeled, the physician may 
change the applicator for a semi-dry or soaked 
application, or, for extra penetration of the chem-
ical agent, the surgeon may use a rough applica-
tor, scrubbed with pressure and speed, multiple 
times. The number of passes, saturation of the 
applicator, and concentration of the chemical 
agent have direct effect on the aggression of the 
chemical peel. It is important to face the indica-
tion of each chemical agent for each classifica-
tion of peels. It is not wise to use a superficial 
peeling agent in multiple passes and with vigor 
to obtain a medium- depth peel, for example, or 
to use a deep-peel formula lightly to obtain a 
medium-depth peel (Figs. 1.4, 1.5, and 1.6).
• Washing or neutralization: in cases of excess 
superficial crystallization (pseudofrost) or 
when it is desired to stop the chemical reac-
tion to the skin, the chemical agent may be 
Table 1.2 Examples of chemical agents, classified by depth of peeling
Superficial chemical peels Medium-depth chemical peels Deep chemical peels
Salicylic acid 20–30% Monheit’s Jessner + TCA 35% Phenol–croton oil
Retinoic acid 2–8% Coleman’s glycolic + TCA 35% TCA >80% (CROSS)a
Glycolic acid 50–70% Brody’s solid CO2 + TCA 35%
Jessner’s solution MJS + TCA 35%
MJS Phenol 88%
Lactic acid 30–88% Pyruvic acid >50%
Pyruvic acid 40–50% TCA 40–60% (localized/CROSS)
Thioglycolic acid 10–35% Phenol–castor oil
Mandelic acid 30–40%
Resorcinol
TCA 10–35%
TCA trichloroacetic acid; MJS Mmodified Jessner’s solution
aTCA > 80% only indicated for rhinophyma or spot treatment of scars, xanthelasma, and actinic cheilitis
Fig. 1.3 Degreasing the face with acetone before phenol– 
croton oil peel
Fig. 1.4 Application of phenol–croton oil perioral peel 
with a cooler for patient comfort. The frosting is pro-
nounced in a deep chemical peel
C. G. Wambier and H. J. Brody
7
removed with a humid soft towel with water 
or 10% sodium bicarbonate (which is only 
imperative for glycolic acid and pyruvic acid 
peels) (Fig. 1.7).
• Post-peeling regimen: soon after the end of the 
desired effect of the chemical agent, the patient 
is started on a regimen to improve healing, by 
total avoidance of irritants, fragrances, aller-
gens, and sun exposure. The first step is the 
application of a moisturizing cream or petrola-
tum in the office. The author does not recom-
mend sunscreen in the first 24 h of superficial 
and medium-depth peels and in the first 7 days 
of deep peels to avoid allergen sensitization.
1.5 Clinical Outcome
• Superficial peels: there is thin scaling of the 
face. Some mild superficial peels such as sali-
cylic acid in polyethylenoglycol (PEG) cause 
imperceptible scaling but may have excellent 
action in the follicles and open comedos. Some 
patients may present irritation with minimal 
exposure to water or dry environment; thus, it 
is advisable to keep regular use of a moistur-
izer during the first 7 days of follow- up. Peels 
may be repeated every 7–14 days, depending 
on complete recovery. The desired clinical out-
come depends on the intention of the surgeon. 
And it is of pivotal importance to the clinical 
results that superficial peels have their effects 
enhanced on each repeated sequential session, 
with more noticeable clinical end points, such 
as erythema and mild frosting [4], which reflect 
on increased scaling after some days. Since 
melasma is a full-thickness epidermal melano-
sis, very light superficial peels, although safe, 
are less effective than low-concentration TCA 
peels, and modified Jessner’s solution (MJS) 
may be used to improve TCA penetration and 
decrease risks of post-inflammatory hyperpig-
mentation (PIH), which is very common in 
peels that reach the basal layer [25] (Fig. 1.8).
• Medium-depth peels: there is thick scaling of the 
face. Mild-to-moderate edema is to be expected, 
Fig. 1.5 Chemical reconstruction of scars (CROSS), 
with punctual application of 90% trichloroacetic acid by 
drilling with a toothpick into the icepicks and boxcars 
(focal deep peel). The full face was previously treated 
with superficial 40% pyruvic acid
Fig. 1.6 Application of solid carbon dioxide slush before 
sequential treatment with 35% trichloroacetic acid 
(Brody’s peel); in this case, the perioral area was demar-
cated for combination treatment with deep chemical peels 
by using Hetter’s formula with 1.1% croton oil in 33% 
phenol. (Courtesy of Dr. Harold Brody)
Fig. 1.7 Pseudofrosting of a modified Jessner solution 
peel (17% salicylic acid, 17% lactic acid, and 8% citric 
acid in ethanol). In superficial peeling, the end point is the 
background erythema. A hand-held ventilator was used 
for patient’s comfort. The pseudofrosting (crystals of sali-
cylic acid) may be removed with a wet soft towel or rinsed 
in tap water
1 Introduction: Classification of Peels
8
and the skin may be tender to touch for the first 
48 h. The patient must be counseled regarding 
herpes activation and advised not to pull on 
scales, because this can lead to erosions and 
delayed healing. The author, Wambier, advises 
his patients to cut only the bothering hanging 
scales with small, clean, scissors and to rub the 
face with hair conditioner in the shower, after 
the fourth or fifth day of peel to assist with thick 
scale removal. Complete recovery is expected in 
10 days. Peels may be repeated every 2 months 
if necessary. Regarding medium-depth peels’ 
modality, Brody’s peel is unique in a way that 
it combines a physical modality (CO2 slush) 
with 35% TCA, with increased efficacy for 
seborrheic keratoses, hypertrophic actinic 
keratoses, and superficial acne scars. Wambier 
prefers MJS over Jessner solution for sequen-
tial peel with 35% TCA for mild rejuvenation, 
because of fewer allergic reactions (resorcinol 
in Jessner’s); although there were no published 
biopsy data on the depth of peel, it seems to be 
as effective as Monheit’s peel for mild rejuvena-
tion [34] (Figs. 1.9 and 1.10).
Fig. 1.8 Superficial peel (modified Jessner’s solution) for 
rejuvenation and preparation for a medium-depth peel 
after 2 weeks. Uniform thin scales
Fig. 1.9 Medium- depth peel. Sequence of modified Jessner’s solution followed by 35% trichloroacetic acid for rejuve-
nation, sixth postoperative day
C. G. Wambier and H. J. Brody
9
• Deep chemical peels: there is intense edema, 
which usually lasts 72 h. Vesicles, blisters, and 
oozing occur in the first 48  h. Pustules and 
purulent exudate occur after 48–72 h. Crusts 
and eschars fall off by the 8th day. Careful 
debriding and crust removal are advised if 
there is liquid collection or localized pain. The 
patient may be started on systemic and topical 
combination antibiotic therapy if any sign of 
 infection is observed, such as odor, pus, 
increase in erythema, edema, or pain. 
Interestingly, a split-face study was performed 
with occluded Baker’s peel (50% phenol, 
2.1% croton oil) and Hetter’s medium-heavy 
peel (33% phenol, 0.7% croton oil), without 
clinically relevant differences at a short fol-
low-up [33]. This split-face experiment was 
criticized for short follow-up to observe 
chronic pigmentation changes and lack of side 
randomization [35] (Fig. 1.11).
Fig. 1.10 Medium-depth peel. Solid carbon dioxide fol-
lowed by 35% trichloroacetic acid (Brody’s peel) for 
treatment of moderate acne scars, third postoperative day
Fig. 1.11 Deep chemical peel. Phenol 35%, croton oil 
1.6%, and Septisol 5% for perioral area (one of Hetter’s 
formulas). The rest of the face was first peeled with 
Monheit’s medium-depth peel. Yellow crusts and exudate 
on the fourth postoperative day. Dry crusts illustrate this 
patient was not using Vaseline as instructed, which may 
result in fissures. Feathering was done to prevent demar-
cation marks between peels and to the neck
1 Introduction: Classification of Peels
10
Fig.1.12 Before and after two sessions of superficial chemical peels (modified Jessner’s solution) for treatment of 
melasma and facial melanosis
Fig. 1.13 Before and after medium-depth peel with modified Jessner’s solution followed by 35% trichloroacetic acid. 
Left to right: 0, 3, 5, 14 days
Fig. 1.14 Before and after deep chemical peels with 35% phenol and 1.6% croton oil (Hetter’s heavy formula). Left to 
right: 0, 3, 5, 7 days
1.6 Before and After 
(Figs. 1.12, 1.13, and 1.14)
C. G. Wambier and H. J. Brody
11
1.7 Side Effects, Complications, 
and Their Management
• Allergic reactions: They are most common 
with resorcinol and Jessner’s solution; thus, 
the author prefers modified Jessner’s solu-
tion, which is exempt of resorcinol. Acute 
urticarial reactions may occur with salicylic 
acid, so it is always advisable to have one shot 
glass for each solution, and disposable appli-
cators, to avoid cross-contamination. The 
office must be equipped with emergency 
crash medications (corticosteroids, anti-hista-
mines, epinephrine). Figure  1.15 illustrates 
Fig. 1.15 Allergic contact dermatitis following superfi-
cial retinoic acid (5%) peel blended with skin-tone 
makeup (top left) and blended with Curcuma longa, mela-
tonin, and golden colorant. Intense pruritus occurred after 
24 h. This patient, Dr. Wambier’s secretary, was managed 
with topical and systemic corticosteroids. Spot tests may 
be indicated in patients with known allergic contact der-
matitis or atopic dermatitis. Retinoic acid peels may exac-
erbate seborrheic dermatitis and rosacea
1 Introduction: Classification of Peels
12
an allergic contact dermatitis to retinoic acid 
peel formulas.
• PIH: This is the most common side effect of 
chemical peels in general. Predisposing fac-
tors are melasma, phototype, sun exposure. To 
minimize risks, skin preparation for 1 month 
and post-peel regimen with hydroquinone and 
corticosteroids may be indicated in some 
cases. Treatment is performed with low- 
fluency Q-switched Nd-YAG 1064  nm, 
Kligman’s formula, superpotent steroids, and 
very mild superficial peels, such as MJS, 10% 
TCA, or 20–30% salicylic acid.
• Convulsions: The odor of the chemicals, anxi-
ety, ventilators with flashing LEDs might pre-
dispose the patient with epilepsy to 
convulsions. It is advisable to have proper 
emergency medications (benzodiazepines, 
oxygen) and adequate environment when 
treating these patients.
• Eye irritation: It can occur from volatile 
chemicals and accidental splash or tearing. To 
maximize eye safety, it is always advisable to 
have saline bottles in the room, advise the 
patient to keep their eyes closed until the end 
of the procedure, keep eyelids dry with Q-tips 
during the procedure, and avoid general anes-
thesia or sedation. It is a general rule not to 
hold any applicator or chemical bottle directly 
above the patient’s eyes for accidents do hap-
pen. After deep peels, it is advisable to check 
the conjunctiva of the patient for any signs of 
erythema or chemosis and manage it properly 
with moisturizing gels, lubricating eye drops, 
and eyelash hygiene.
References
 1. Ayres S.  Dermal changes following application of 
chemical cauterants to aging skin. Arch Dermatol. 
1960;82:578.
 2. Baker T, Gordon H. The ablation of rhytides by chem-
ical means: a preliminary report. J Fla Med Assoc. 
1961;48:541.
 3. Beeson WH, McCollough EG.  Chemical face 
peeling without taping. J Dermatol Surg Oncol. 
1985;11(10):985–90.
 4. Brody HJ.  Chemical peeling and resurfacing 
[Internet]. 3rd ed. Atlanta: Emory University Digital 
Library Publications; 2009. p. 1–267. Available from: 
https://pid.emory.edu/ark:/25593/s2xpg
 5. Brody HJ, Hailey CW.  Medium-depth chemical 
peeling of the skin: a variation of superficial che-
mosurgery. J Dermatol Surg Oncol. 1986;12(12): 
1268–75.
 6. Brody HJ, Monheit GD, Resnik SS, Alt TH.  A 
history of chemical peeling. Dermatol Surg. 
2000;26(5):405–9.
 7. Brown AM, Kaplan LM, Brown ME. Phenol induced 
histological skin changes: hazards, techniques, and 
uses. Br J Plast Surg. 1960;13:158.
 8. Coleman WP, Futrell JM.  The glycolic acid tri-
chloroacetic acid peel. J Dermatol Surg Oncol. 
1994;20(1):76–80.
 9. Combes FC, Sperber PA, Reisch M. Dermal defects: 
treatment by a chemical agent. NY Physician Am 
Med. 1960;56:36.
 10. Cucé LC, Bertino MCM, Scattone L, Birkenhauer 
MC.  Tretinoin peeling. Dermatol Surg. 
2001;27(1):12–4.
 11. Dainichi T, Ueda S, Imayama S, Furue M, Ainichi 
TED, Eda ÃSEU, et  al. Excellent clinical results 
with a new preparation for chemical peeling in acne: 
30% salicylic acid in polyethylene glycol vehicle. 
Dermatol Surg. 2008;34(7):891–9; discussion 899.
 12. Eller J, Wolff S. Skin peeling and scarification. JAMA 
J Am Med Assoc. 1941;116:934–8.
 13. Fox G. Photographic atlas of the diseases of the skin, 
vol. 2. Philadelphia: Lippincott; 1905.
 14. Gordon JRS, Brieva JC. Unilateral dermatoheliosis. N 
Engl J Med. 2012;366(16):e25.
 15. Griffin T, Van Scott E, Maddin S. The use of pyru-
vic acid as a chemical peeling agent. J Dermatol Surg 
Oncol. 1989;15:1316.
 16. Hetter GP.  An examination of the phenol-croton 
oil peel: part II.  The lay peelers and their croton 
oil formulas. Plast Reconstr Surg. 2000a;105(1): 
240–8-51.
 17. Hetter GP. An examination of the phenol-croton oil 
peel: part IV. Face peel results with different concen-
trations of phenol and croton oil. Plast Reconstr Surg. 
2000b;105(3):1061–83; discussion 1084-7.
Tip Box
• Undisputed cost effectiveness.
• Hands-on training and supervision are 
mandatory for acquiring the correct 
technique.
• Dedication and chemical quality are 
vital for successful outcomes.
C. G. Wambier and H. J. Brody
https://pid.emory.edu/ark:/25593/s2xpg
13
 18. Larson DL, Karmo F, Hetter GP.  Phenol-croton oil 
peel: establishing an animal model for scientific 
investigation. Aesthet Surg J. 2009;29(1):47–53.
 19. Litton C. Chemical face lifting. Plast Reconstr Surg. 
1962;29:371.
 20. Mackee G, Karp F. The treatment of post acne scars 
with phenol. Br J Dermatol. 1952;64:456–9.
 21. Monash S. The uses of diluted trichloroacetic acid in 
dermatology. Urol Cutan Rev. 1945;49:119.
 22. Monheit GD.  The Jessner’s + TCA peel: a medium 
depth chemical peel. Dermatol Surg Oncol. 
1989;15:945–50.
 23. Orekoya O, Oremule B, Hanna T. Historical abstracts. 
Br J Dermatol. 2016;175:191–8.
 24. Resnik SS, Lewis LA, Cohen BH.  Trichloroacetic 
acid peeling. Cutis. 1976;17(1):127–9.
 25. Safoury OS, Zaki NM, El Nabarawy EA, Farag EA. A 
study comparing chemical peeling using modified 
Jessner’s solution and 15% trichloroacetic acid versus 
15% trichloroacetic acid in the treatment of melasma. 
Indian J Dermatol India. 2009;54(1):41–5.
 26. Van Scott EJ, Yu RJ.  Hyperkeratinization, corneo-
cyte cohesion, and alpha hydroxy acids. J Am Acad 
Dermatol. 1984;11(5):867–79.
 27. Stegman SJ.  A comparative histologic study of the 
effects of three peeling agents and dermabrasion on 
normal and sundamaged skin. Aesthet Plast Surg. 
1982;6(3):123–35.
 28. Stuzin JM, Baker TJ, Gordon HL.  Chemical 
peel: a change in the routine. Ann Plast Surg. 
1989;23(2):166–9.
 29. Sumita JM, Leonardi GR, Bagatin E. Tretinoin peel: a 
critical view. An Bras Dermatol Sociedade Brasileira 
de Dermatologia. 2017;92(3):363–6.
 30. Unna P. Therapeutiques generales des maladies de la 
peau. 1882.
 31. Urkov J.  Surface defects of skin: treatment by con-
trolled exfoliation. Ill Med J. 1946;89:75.
 32. Vagotis FL, Brundage SR. Histologic study of derm-
abrasion and chemical peel in an animal model 
after pretreatment with Retin-A. Aesthet Plast Surg. 
1995;19(3):243–6.
 33. Vasconcelos B, Figueira G, Fonseca J, Mendonça L, 
Fonseca C.  A splitface comparative study between 
two phenolbased peelings (BakerGordon and Hetter 
formulas) in the treatment of facial rhytids. Surg 
Cosmet Dermatol. 2013;5:40–4.
 34. Wambier CG.  My personal experience with peel-
ings. In: IssaMCA, Tamura B, editors. Chemical and 
physical procedures. Cham: Springer International 
Publishing; 2017. p. 1–9.
 35. Wambier CG, Brody HJ, Hetter GP.  Comments: 
Hemiface comparative study of two phenol peels 
(Baker-Gordon and Hetter formulas) for the cor-
rection of facial rhytids. Surg Cosmet Dermatol. 
2017;9(2):190–1.
 36. Wambier CG, de Freitas FP.  Combining phenol- 
croton oil peel. In: Issa MCA, Tamura B, editors. 
Chemical and physical procedures. Cham: Springer 
International Publishing; 2017. p. 1–13.
1 Introduction: Classification of Peels
15© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_2
Pearl Chapter: Basis of Photoaging 
and the Use of Chemical Peelings
Suelen Montagner and Adilson Da Costa
2.1 Intrinsic Aging
Intrinsic aging is the process of senescence that 
affects all body organs, and the skin clearly 
shows the action of time and is transformed by it 
[1]. In 1990, there were more than 300 theories of 
aging. Today, the situation is even more compli-
cated [2].
Intrinsic skin aging or chronologic aging is 
characterized by physiological changes geneti-
cally determined and includes structural, bio-
chemical, and functional alterations [3, 4]. These 
changes are complex, and there are many theo-
ries of skin pathophysiology, like shortening of 
telomeres, reduction of cellular DNA repair 
capacity [5], cellular senescence, and decreased 
proliferative ability [6] mutations of extranuclear 
mitochondrial DNA [7]. Some of them are 
highlighted.
2.1.1 Shortening of Telomeres
Telomeres are sequences of repeating nucleo-
peptides present at the end of chromosomes 
(Fig. 2.1) [8]. Because DNA polymerase cannot 
transcribe the final sequence of bases present in 
the DNA ribbon during replication, the telomeric 
size is reduced at each mitotic cycle [9]. This 
telomere reduction is associated with cellular 
aging [10–13]. This mechanism contributes to 
the regulation of growth arrest in senescent 
human cell cultures the same way as stress or 
aberrant signaling- induced senescence (STASIS) 
[14]. Telomeres themselves are regarded as pos-
sible biomarkers of biological aging and cellular 
senescence. Other possible biomarkers are the 
free radicals [15].
S. Montagner (*) 
Private Clinic, Campinas, SP, Brazil 
A. Da Costa 
Instituto de Assistência Médica ao Servidor Público 
Estadual, Tenured International Professor and Mentor 
for PhD and MSc Programs, São Paulo, SP, Brazil
2
Fig. 2.1 Representation of a telomere, highlighted
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_2&domain=pdf
16
2.1.2 Free Radicals 
and Antioxidizing Ability
In 1956, Denham Harman proposed a theory that 
free radicals are also involved in this aging pro-
cess: they would cause cellular damage, which 
would accumulate over the course of life and 
result in acceleration of dysfunctions [16]. Later, 
Yu and Yang described that not only the overex-
pressed production of reactive oxygen species 
(ROS) but also other oxidants, such as the reac-
tive nitrogen species and reactive lipid species, 
cause oxidative damage [17].
In other studies, the degradation of oxidized 
products was unraveled. The body can neutral-
ize ROS through the production of antioxidant 
enzymes, such as superoxide dismutase, catalase, 
and glutathione peroxidase, by an innate anti-
oxidant defense system [18, 19]. This function is 
exerted by proteasome (multicatalyctic protease), 
whose activity seems to diminish over the course 
of life. With this, an incomplete degradation of oxi-
dized proteins, increased protein aggregates, and 
the acceleration of cell dysfunction are observed, 
which, ultimately, lead to cellular aging [16, 20].
2.1.3 Cellular Senescence
The theory of cellular senescence has been demon-
strated in keratinocytes, fibroblasts, and melano-
cytes [21]. There is a reduction in the proliferative 
potential of cells after a certain amount of division 
[22–24]. Senescent cells can also produce several 
cytokines, chemokines, growth factors, proteases, 
and matrix metalloproteases, a phenomenon 
described as senescence- associated secretory phe-
notype (SASP) [25]. A hallmark of skin aging is 
the degradation of collagen and other extracellular 
matrix components in the dermal connective tissue 
and can be induced through chronic MMPs secre-
tion by senescent cells [26].
2.2 Intrinsic Factors
2.2.1 Genetic Characteristics
Many studies correlated genomes with the aging 
process [27, 28]. According to one of them, of all 
genes studied, 39 were regulated overlappingly 
in both sexes. They could serve as gender- 
independent biomarkers of endogenous skin 
aging. On the other hand, Wnt signaling pathway 
showed to be significantly downregulated in aged 
skin with decreased gene and protein expression 
for males and females [29].
Genic expression studies from aged sun- 
protected skins showed differential expression, 
possibly responsible for dysregulation of the 
insulin and STAT3 signaling pathway, the extra-
cellular matrix (PI3, S100A2, A7, A9, SPRR2B), 
and the cell cycle (CDKs, GOS2). There was also 
evidence of a high regulation of proapoptotic 
genes, in part by a dysregulation of FOXO1. An 
under-expression of the JUN and FOS family 
members and cytoskeleton genes (KRT2A, 
KRT6A, and KRT16A) is also affected by intrin-
sic aging [30].
Another alteration observed in skin aging is 
the reduced expression of type I collagen due to 
downregulation of the transcription growth factor 
(TGF) β-1 and the connective tissue growth fac-
tor (CTGF). This reduced collagen expression is 
even associated with increased nuclear factor-κB 
(NF-κB) activity and increased expression of 
matrix metalloproteinase (MMP)-1 [31, 32].
An interesting discovery is that DNA methyla-
tion measures the cumulative effect of an epigen-
etic maintenance system, like a “clock of aging,” 
and can determine the individual age with an 
error of less than 3.6 years. This additional infor-
mation can be used to address a host of questions 
in developmental biology, cancer, and aging 
research [33].
2.2.2 Sexual Hormones
With aging, the functional reserves of the endo-
crine system are reduced. As a result, the levels of 
sexual hormones decline. In females, hormonal 
changes are well documented. Women have a 
rapid decline of estrogen during menopause [34]. 
Estrogen is related to the stimulus of keratinocyte 
proliferation, which leads to the thickening of the 
epidermis, avoiding its atrophy [35]. In the der-
mis, the stimulus is of blood vessels and fibroblast 
production, thereby preserving collagen, elastic 
fibers, and glycosaminoglycans [36, 37]. With the 
S. Montagner and A. Da Costa
17
reduction of this hormone, the maintenance of 
these processes would be compromised.
The characterization of hormonal changes in 
males is a challenge, as there is not a remarkable 
hormonal decrease when compared with females. 
During the aging process, most men show a grad-
ual reduction of circulating testosterone—some-
thing around 1% a year after 30  years of age. 
However, this number substantially varies among 
men [38]. Testosterone reduction is related to 
intrinsic aging because it broadly interacts with 
the skin, the whole body, and the male behavior 
itself [39].
2.3 Extrinsic Aging
Extrinsic aging results from the exposure to envi-
ronmental factors—critical for the final result of 
the process [35]. Sun exposure intensifies skin 
aging due to ultraviolet radiation, a process 
referred to as photoaging [40]. Factors such as 
smoking and pollution may also lead to aging 
[41]. All these factors can lead to ROS genera-
tion, reducing collagen synthesis and increasing 
its degradation, contributing to premature skin 
aging (Fig. 2.2).
2.4 Extrinsic Factors
2.4.1 Air Pollution
The World Health Organization defines air pollu-
tion as contamination of the indoor or outdoor 
environment byany chemical, physical, or biologi-
cal agent that modifies the natural characteristics of 
the atmosphere [42]. The skin acts as a physical, 
chemical, and immunological barrier against the 
environmental factors. This barrier can fail when 
the exposure to stressors is prolonged and repeti-
tive, leading to the development of various skin 
diseases [43]. Major air pollutants which affect the 
skin are solar ultraviolet radiation, polycyclic aro-
matic hydrocarbons, volatile organic compounds, 
nitrogen oxides, particulate matter, cigarette 
smoke, heavy metals, and arsenic [44]. Air pollut-
ants damage the skin by inducing oxidative stress 
and can lead to aging of the skin [41, 44].
Some pollutants stand out, such as ozone, par-
ticulate matter (PM), and polycyclic aromatic 
hydrocarbons. Ozone can affect the integrity of the 
skin on murine cutaneous tissue, can act as a strong 
oxidative agent, and can induce the expression of 
MMP-9, indicating a role in matrix remodeling 
[45, 46]. Oxidation of epidermal lipids and dis-
turbed activity of matrix metalloproteinases con-
tribute to wrinkling and extrinsic skin aging [47].
Particulate matter in the air consists of com-
plex and varying mixtures of different sizes and 
composition. After penetrating the skin either 
through hair follicles or transdermally, PM exerts 
its detrimental effects through the generation of 
oxidative stress, contributing to extrinsic skin 
aging, characterized particularly by pigment 
spots on the face and nasolabial folds and less so 
by coarse wrinkles, solar elastosis, and telangiec-
tasia [48–50]. Furthermore, particles can serve as 
carriers for organic chemicals and metals that are 
capable of localizing in mitochondria and gener-
ating ROS directly in mitochondria [51], leading 
to skin aging by mitochondrial damage [41].
Polycyclic aromatic hydrocarbons (PAHs) are 
adsorbed on the surface of suspended PM in the 
air of urban areas [52] and are converted into qui-
nines, redox-cycling chemicals that produce 
reactive oxygen species [53]. They are associated 
with extrinsic skin aging, pigmentation, cancers, 
and acneiform eruption [52].
Collagen 
Generation of ROS
Premature Skin Aging
Syn
thes
is
Deg
radi
ng
Fig. 2.2 Air pollution, smoking, and sun exposure lead-
ing to ROS generation, reducing collagen synthesis and 
increasing its degradation, contributing to premature aging
2 Pearl Chapter: Basis of Photoaging and the Use of Chemical Peelings
18
2.4.2 Smoking
In 1969 it was recognized that smokers look older 
than non-smokers [54]. Later, smoking was 
found to be an independent risk factor for prema-
ture facial wrinkling even after controlling for 
sun exposure, age, sex, and skin pigmentation 
[55]. A dose–response relationship between 
wrinkling and smoking has been identified, with 
smoking being a greater contributor to facial 
wrinkling than sun exposure [56].
Reactive oxidants and free radicals from ciga-
rette smoke cause oxidative stress or secondary 
oxidative events and inhibition of antioxidant 
mechanisms [57–59]. Components of cigarette 
smoke increase transepidermal water loss, degen-
eration of connective tissue in the skin, and upreg-
ulation of matrix metalloproteinases-1 and -3 
which degrade collagen and elastic fibers, which 
causes skin to become less elastic [43, 60, 61].
2.4.3 Ultraviolet Radiation 
and Photoaging
Photoaging is a cumulative process that is depen-
dent on sun exposure degree and skin pigmen-
tation level. Clinical presentation of sun-aged 
skin includes dryness of the skin; yellowish, 
wrinkled, atrophic, irregular pigmentation; tel-
angiectasias; and pre-malignant lesions [62, 63]. 
Histologically there is thinning of the stratum 
spinosum, increased thickness of granular cell 
layer, flattening of the dermoepidermal junction, 
and an increased number of hypertrophic dopa-
positive melanocytes [62, 64].
In aging process it is observed that keratino-
cytes become resistant to apoptosis and suscepti-
ble to DNA mutations. The number of 
melanocytes is also reduced, and the melanocytic 
density is altered. Langerhans cells also decrease 
in number with aging, resulting in loss of anti-
genic ability [62].
The immediate effect of sun exposure on the 
skin is cutaneous hyperpigmentation with delay in 
the formation of new melanin, which is reversible. 
The prolonged, recurrent sun exposure implies 
definitive changes in the quantity and distribution 
of melanin in the skin. The deposition of amor-
phous material in the papillary dermis, in place of 
conjunctive tissue, is the main element in differen-
tiating chronologic aging and photoaging [62].
The morphological changes resulting from pho-
toaging are, essentially, different from those 
observed in intrinsic aging. A parallel between 
such changes is shown in Table 2.1 [62, 40, 64, 65].
Table 2.1 Skin changes caused by intrinsic and extrinsic aging
Intrinsic aging
(chronologic)
Extrinsic aging
(environmental factors)
Wrinkles Thin Deep
Stratum corneum Unchanged Tapered
Dysplastic cells Few Many
Collagen fibers Slight change in size and 
organization
Great change in size and organization
Elastic fibers Reorganized ↓ production and ↑ degeneration
Capillary follicle ↓ number and thinning ↓ number and structure: hair loss
Melanocytes Normal ↓ number and melanin
Sebaceous and sweat 
glands
↓ number ↓ number: dry skin
Dermoepidermal junction Slight flattening Major flattening
Microvasculature Reduced area Telangiectasias, ecchymoses, inflammatory 
perivascular infiltrate.
Benign changes Seborrheic keratosis Seborrheic keratosis
Pre-malignant changes _ Actinic keratosis
Malignant changes _ Basal cell carcinoma
Spindle cell carcinoma
Reprinted with permission from Montagner and Costa [65]
S. Montagner and A. Da Costa
19
The ultraviolet (UV) B (290–320 nm) and A 
(320–400 nm) fractions [66] as well as the infra-
red (IR) A (770–1400 nm) fraction [67–69] can 
induce the extrinsic skin aging process [41].
Ultraviolet radiation penetrates the skin, and 
in accordance with the wavelength, it interacts 
with the different cells located in the different 
strata. Shortwave radiation (UVB) is more 
absorbed in the epidermis and predominantly 
affects keratinocytes but is also able to cross this 
layer and reach the papillary dermis [70]. Longer 
waves (UVA) penetrate more deeply and hit 
 epidermal keratinocytes and dermal fibroblasts 
[71, 72]. IRA is able to penetrate through all 
three layers of the skin: the epidermis, dermis, 
and subcutis [41].
The UV-induced skin aging process is com-
plex and can occur by various pathways includ-
ing receptor-initiated signaling, mitochondrial 
damage, protein oxidation, DNA damage, and 
arylhydrocarbon receptor (AhR) signaling [41]. 
Table  2.2 compares the main mechanisms of 
intrinsic and extrinsic aging.
2.4.4 Receptor-Initiated Signaling 
Pathway
The reactive oxygen species produced by ultra-
violet radiation activate cell surface receptors of 
cytokines and growth factors in keratinocytes and 
fibroblasts, which activate kinases, that induce 
expression and transcription factors such as 
nuclear κB transcription factor (NF-κB) and pro-
tein 1 (AP-1) [41, 63].
The activated NFkB stimulates the transcrip-
tion of inflammatory cytokines (IL1, IL6, TNFa), 
attracting neutrophils and collagenases, associ-
ated in collagen degrading [73].
Increased AP-1, in turn, decreases the gene 
expression of dermal collagens I and III in fibro-
blasts, reducing collagen synthesis. Besides that, 
AP-1 stimulates the transcription of genes of 
matrix-disintegrating enzymes, such as metallo-
proteins (MMP-1, MMP-3, MMP-9), degrading 
mature dermal collagen [74, 75]. The radiation is 
not only related to collagen degradation but also 
contributes to reducing its synthesis. UVA ray 
exposure triggers two factors related to photoag-
ing: induction of matrix metalloproteinases 
(MMPs) and mitochondrial mutation [72, 76, 77].
2.4.5 Mitochondrial Damage
Actually,mitochondrial DNA damages are likely 
to be mediated through ROS.  Mitochondria 
 contain multiple DNA copies and generate ROS 
during energy production (adenosine triphos-
phate—ATP), by consuming oxygen via the 
respiratory chain. ROS can easily damage lipids, 
proteins, and even the mtDNA itself [78, 79]. The 
mitochondrial DNA shows a high mutation rate 
due to its histone deficiency, limited capacity 
of base excision repair, and proximity to ROS 
[79, 80].
UVA exposure can further increase ROS gen-
eration and induce mutations at the mitochon-
drial DNA [72, 81], like deletion of 4977  bp 
(base pair), the most often found mutation in 
aged tissues [63, 82–87]. While this genic change 
can be detected in tissues that are non-susceptible 
to solar rays [83], mtDNA mutations can be ten-
fold more frequent in photoaged skin in compari-
son to sun-protected skin [64, 78, 79, 88–92].
2.4.6 DNA Damage
Sunlight-induced DNA damage is considered the 
main cause for the genetic changes leading to 
skin lesions and carcinogenesis including malig-
nant melanoma [93]. DNA, the main intracellular 
Table 2.2 Main mechanisms involved in aging
Intrinsic aging
 Shortening of telomeres
 Reduction of cellular DNA repair capacity
 Cellular senescence and decreased proliferative 
ability
 Mutations of extranuclear mitochondrial DNA
Extrinsic aging
 Receptor-initiated signaling
 Mitochondrial damage
 Protein oxidation
 DNA damage
 Arylhydrocarbon receptor signaling
2 Pearl Chapter: Basis of Photoaging and the Use of Chemical Peelings
20
chromophore for UVB [70], absorbs photons 
from UVB. This interaction increases ROS pro-
duction and creates dimeric photoproducts, such 
as pyrimidines, which may be related to pre- 
malignant skin lesions [94, 95]. The DNA photo-
products that are induced by UVA are potentially 
more mutagenic than those induced by UVB, 
although UVB induces more cyclobutane pyrimi-
dine dimers than UVA [96].
Ultraviolet radiation also alters RNA and 
implies the formation of dysfunction-causing 
proteins. A blockade in RNA transcription by 
a DNA photoproduct allows p53 activation, 
thereby inducing the apoptosis of irradiated kera-
tinocytes [94].
These events activate multiple important sig-
naling pathways related to cell growth, differen-
tiation, senescence, DNA damage repair, 
connective tissue degradation, and inflammation 
[97]. This is followed by an irreversible blocking 
of cell cycle progression to prevent further DNA 
damage and increase the expression of senes-
cence-associated genes [97, 98].
2.4.7 Arylhydrocarbon Receptor 
Signaling
It is known that UVB also generates ROS species 
[99] initiating DNA damage, in the nucleus, once 
DNA is chromophore of UVB [100]. But, in the 
recent years, arylhydrocarbon receptor (AhR) 
was demonstrated to integrate part of the UVB 
stress response associated with photoaging.
This DNA damage-independent pathway is 
initiated outside the nucleus by the cluster ring 
and the internalization of cell membrane-bound 
growth factor receptors, such as the epidermal 
growth factor receptor (EGFR) [101]. AhR is 
activated in human epidermal keratinocytes upon 
exposure to UVB radiation, producing a series of 
photoproducts from tryptophan, which is free in 
the cytoplasm. These photoproducts are ligands 
of the AhR and activate it. This process leads to 
regulation of inflammation-associated genes, 
such as cyclooxygenase2 (COX2), that increase 
the expression of matrix metalloproteinases such 
as MMP-1 and MMP-3, among other proteases 
[102–105], melanocyte proliferation, and mela-
nin synthesis [58, 106]. In this scenario, the 
molecular response to solar aggression is evident. 
These mechanisms are briefly illustrated in 
Fig. 2.3.
2.4.8 Infrared Radiation
IRA irradiation is mainly absorbed by mitochon-
dria, where copper could serve as a chromo-
phore [107], and increases intra-mitochondrial 
production of ROS [108, 109]. ROS can increase 
intra- cytoplasmic calcium levels, activate the 
MAP kinases signaling pathway, and lead to 
elevated MMP-1 expression. Approximately 600 
genes are IRA responsive [110], and thus IRA 
radiation might further induce the extrinsic skin 
aging process through various other pathways. 
Important functions of the human skin which are 
characteristic for photoaging, such as angiogen-
esis [111] and production of mast cells [54], can 
be induced by IRA. Though IR does not induce 
tumorigenesis in the skin to the same extent as 
UVB, it is associated with a more aggressive 
tumor growth [112].
2.5 Conclusion
Ultimately, simply put, aging results from the 
modulation imbalance of collagen (with higher 
degradation and reduction of its synthesis) caused 
by excessive free radicals. Exposure to certain 
environmental factors, such as ultraviolet radia-
tion, smoking, and air pollution, induces or 
enhances this process, thereby leading to prema-
ture or exogenous aging.
Even with all biomolecular advances, preven-
tion is still the best way to fight aging and its con-
sequences, by avoiding the exposure to 
well-known exogenous factors. Endogenous and 
exogenous aging are objects of many research 
studies involving diet components in order to 
avoid or minimize the signs of time; however, 
there is still a lot to be proven. The advance in the 
knowledge of its pathogenesis is expected to cor-
roborate with new therapeutic findings.
S. Montagner and A. Da Costa
21
UVB UVA
ROS
Activate kinases
AP-1 NF-kB
Collagen
degrading
Deletion of
mitochondrial
4,977bp 
Photoaging
Dimeric
photoproducts
Pre-malignant
skin lesions
p53
activation
Cancer
Cells 
Cytoplasm
Nucleus
MMP1
MMP8
MMP9
TGF-β
type II
receptor
MMP1,3,9
Collagen
synthesis
Cell Membrane
EGFR
MMP
AhR
Fig. 2.3 Cellular effects of ultraviolet radiation. AhR sig-
naling pathway. UVB forming photoproducts that lead to 
pre-malignant lesions. UVA/UVB action on p53, produc-
ing cancer cells. Deletion of mitochondrial 4977 bp and 
ROS production by UVA radiation, ultimately, resulting 
in photoaging. (Adapted with permission from Montagner 
and Costa [65])
2 Pearl Chapter: Basis of Photoaging and the Use of Chemical Peelings
22
References
 1. Noh EM, Park J, Song HR, Kim JM, Lee M, Song 
HK, Hong OY, Whang PH, Han MK.  Skin aging- 
dependent activation of the PI3K signaling pathway 
via downregulation of PTEN increases intracellular 
ROS in human dermal fibroblasts. Oxidative Med Cell 
Longev. 2016;2016:6354261.
 2. Kanaki T, Makrantonaki E, Zouboulis 
CC.  Biomarkers of skin aging. Rev Endocr Metab 
Disord. 2016;17(3):433–42.
 3. Farage MA, Miler KW, Elsner P, Maibach HI. Intrinsic 
and extrinsic factors in skin ageing: a review. Int J 
Cosm Sci. 2008;30:87–95.
 4. Farage MA, Miler KW, Elsner P, Maibach 
HI.  Characteristics of the aging skin. Adv Wound 
Care. 2013;2:5–10.
 5. Allsopp RC, Vaziri H, Patterson C, Goldstein S, 
Younglai EV, Futcher AB, et al. Telomere length pre-
dicts replicative capacity of human fibroblasts. Proc 
Natl Acad Sci U S A. 1992;89:10114–8.
 6. Smith JR, Pereira-Smith OM. Replicative senescence: 
implications for in vivo aging and tumor suppression. 
Science. 1996;273:63–7.
 7. Michikawa Y, Mazzucchelli F, Bresolin N, Scarlato 
G, Attardi G. Aging-dependent large accumulation of 
point mutations in the human mtDNA control region 
for replication. Science. 1999;286:774–9.
 8. Meyne J, Ratliff R, Moyzis R.  Conservation of the 
human telomere sequence (TTAGGC)n among verte-
brates. Proc Natl Acad Sci U S A. 1989;86:7049–53.
 9. Yaar M, Eller MS, Gilchrest BA. Fifty years of skin 
aging. J Investig Dermatol Symp Proc. 2002;7:51–8.
 10. Kosmadari MG, Gilchrest BA. The role of telomeres 
in skin aging/photoaging. Micron. 2004;35:155–9.
 11. Dimri GP, Lee X, Basile G, Acosta M, Scott G, 
Roskelley C, et al. A biomarker that identifies senes-
cent human cells in culture and in aging skin in vivo. 
Proc Natl Acad Sci U S A. 1995;92:9363–7.
 12. Yaar M, Gilchrest BA. Skin aging: postulatedmecha-
nisms and consequent changes in structure and func-
tion. Clin Geriatr Med. 2001;17:617–30.
 13. Rabe JH, Mamelak AJ, McElgunn PJ, Morison WL, 
Sauder DN.  Photoaging: mechanisms and repair. J 
Am Acad Dermatol. 2006;55:1–19.
 14. Herbig U, Ferreira M, Condel L, Carey D, Sedivy 
JM. Cellular senescence in aging primates. Science. 
2006;311:1257.
 15. Green DR, Galluzzi L, Kroemer G. Mitochondria and 
the autophagy-inflammation-cell death axis in organ-
ismal aging. Science. 2011;333:1109–12.
 16. Widmer R, Ziaja I, Grune T.  Protein oxidation and 
degradation during aging: role in skin aging and neu-
rodegeneration. Free Radic Res. 2006;40:1259–68.
 17. Yu BP, Yang R. Critical evaluation of the free radical 
theory of aging. A proposal for the oxidative stress 
hypothesis. Ann N Y Acad Sci. 1996;786:1–11.
 18. Callaghan TM, Wilhelm KP. A review of ageing and 
an examination of clinical methods in the assess-
ment of ageing skin. Part I: cellular and molecu-
lar perspectives of skin ageing. Int J Cosmet Sci. 
2008;30:313–22.
 19. Finkel T, Holbrook NJ. Oxidants, oxidative stress and 
the biology of aging. Nature. 2000;408:239–47.
 20. Kraft DC, Deacaris CC, Rattan SI.  Proteasomal 
oscillation during mild heat shock in aging human 
skin fibroblasts. Ann N Y Acad Sci. 2006;1067: 
224–7.
 21. Hayflick L.  The limited in  vitro lifetime of human 
diploid cell strains. Exp Cell Res. 1965;37:614–36.
 22. Gilchrest BA.  In vitro assessment of keratinocyte 
aging. J Invest Dermatol. 1983;81:184s–9s.
 23. Cristofalo VJ, Pignolo RJ. Replicative senescence of 
human fibroblast-like cells in culture. Physiol Rev. 
1993;73:617–38.
 24. Gilchrest BA, Vrabel MA, Flynn E, Szabo G. Selective 
cultivation of human melanocytes from newborn and 
adult epidermis. J Invest Dermatol. 1984;83:370–6.
 25. Waldera Lupa DM, Kalfalah F, Safferling K, 
Boukamp P, Poschmann G, Volpi E, Götz- Rösch 
C, Bernerd F, Haag L, Huebenthal U, Fritsche E, 
Boege F, Grabe N, Tigges J, Stühler K, Krutmann 
J. Characterization of skin aging-associated secreted 
proteins (SAASP) produced by dermal fibroblasts 
isolated from intrinsically aged human skin. J Invest 
Dermatol. 2015;135:1954–68.
 26. Velarde MC, Demaria M. Targeting senescent cells: 
possible implications for delaying skin aging: a mini-
review. Gerontology. 2016;62(5):513–8.
 27. Kennedy SR, Loeb LA, Herr AJ. Somatic mutations in 
aging, cancer and neuro- degeneration. Mech Ageing 
Dev. 2012;133:118–26.
 28. Makrantonaki E, Pfeifer GP, Zouboulis CC. 
[Intrinsic factors, genes, and skin aging]. Hautarzt. 
2016;67(2):103–6.
 29. Makrantonaki E, Brink TC, Zampeli V, Elewa RM, 
Mlody B, Hossini AM, Hermes B, Krause U, Knolle 
J, Abdallah M, Adjaye J, Zouboulis CC. Identification 
of biomarkers of human skin ageing in both genders. 
Wnt signalling – a label of skin ageing? PLoS One. 
2012;7(11):e50393. https://doi.org/10.1371/journal.
pone.0050393.
 30. Lener T, Moll PR, Rinnerthaler M, Bauer J, Aberger 
F, Richter K.  Expression profiling of aging in the 
human skin. Exp Gerontol. 2006;41:387–97.
 31. Makrantonaki E, Zouboulis CC. William J. Cunliffe 
Scientific Awards. Characteristics and pathomecha-
nisms of endogenously aged skin. Dermatology. 
2007;214:352–60.
 32. Makrantonaki E, Bekou V, Zouboulis CC. Genetics 
and skin aging. Dermatoendocrinology. 2012;4: 
280–4.
 33. Horvath S.  DNA methylation age of human tissues 
and cell types. Genome Biol. 2013;14:R115.
 34. Labrie F, Belanger A, Cusan L, Gomez JL, Candas 
B. Marked decline in serum concentrations of adrenal 
C19 sex steroid precursors and conjugated androgen 
metabolites during aging. J Clin Endocrinol Metab. 
1997;82:2396–402.
S. Montagner and A. Da Costa
https://doi.org/10.1371/journal.pone.0050393
https://doi.org/10.1371/journal.pone.0050393
23
 35. Pereira S.  Dermatoses no idoso. In: Rotta O, edi-
tor. Guia de Dermatologia: clínica, cirúrgica e cos-
miátrica. São Paulo: Manole; 2008. p. 567–91.
 36. Verdier-Sevrain S, Bontè F, Gilchrest B. Biology of 
estrogens in skin: implications for skin aging. Exp 
Dermatol. 2006;15:83–94.
 37. Wolff EF, Narayan D, Taylor HS. Long-term effects 
of hormone therapy on skin rigidity and wrinkles. 
Fertil Steril. 2005;84:285–8.
 38. Bain J.  Epidemiology, evaluation and diagnosis of 
andropause. Geriatr Aging. 2003;6(Suppl 10):4–8.
 39. Tenover JL.  Testosterone and the aging male. J 
Androl. 1997;18:103–6.
 40. Wulf HC, Sandby-Møller J, Kobayasi T, Gniadecki 
R.  Skin aging and natural photoprotection. Micron. 
2004;35:185–91.
 41. Vierkötter A, Krutmann J. Environmental influences 
on skin aging and ethnic-specific manifestations. 
Dermato-Endocrinology. 2012;4(3):227–31.
 42. WHO air quality guidelines for particulate matter, 
ozone, nitrogen dioxide and sulfur dioxide, global 
update 2005, summary of risk assessment; 2006. 
Available from: http://www.who.int/phe/health_top-
ics/outdoorair/outdoorair_aqg/en/. Last accessed on 4 
Apr 2016.
 43. Valacchi G, Sticozzi C, Pecorelli A, Cervellati 
F, Cervellati C, Maioli E.  Cutaneous responses 
to environmental stressors. Ann N Y Acad Sci. 
2012;1271:75–81.
 44. Puri P, Nandar SK, Kathuria S, Ramesh V. Effects of 
air pollution on the skin: a review. Indian J Dermatol 
Venereol Leprol. 2017;83:415–23.
 45. Thiele JJ, Traber MG, Polefka TG, Cross CE, Packer 
L.  Ozone-exposure depletes vitamin E and induces 
lipid peroxidation in murine stratum corneum. J 
Invest Dermatol. 1997;108:753–7.
 46. Valacchi G, Pagnin E, Okamoto T, Corbacho AM, 
Olano E, Davis PA, et al. Induction of stress proteins 
and MMP-9 by 0.8 ppm of ozone in murine skin. 
Biochem Biophys Res Commun. 2003;305:741–6.
 47. Rittié L, Fisher GJ. UV-light-induced signal cascades 
and skin aging. Ageing Res Rev. 2002;1:705–20.
 48. Lademann J, Schaefer H, Otberg N, Teichmann A, 
Blume-Peytavi U, Sterry W. Penetration of micropar-
ticles into human skin. Hautarzt. 2004;55:1117–9.
 49. Vierkötter A, Schikowski T, Ranft U, Sugiri D, 
Matsui M, Krämer U, et  al. Airborne particle expo-
sure and extrinsic skin aging. J Invest Dermatol. 
2010;130:2719–26.
 50. Mills NL, Miller MR, Lucking AJ, Beveridge J, Flint 
L, Boere AJ, et  al. Combustion-derived nanopar-
ticulate induces the adverse vascular effects of 
diesel exhaust inhalation. Eur Heart J. 2011;32: 
2660–71.
 51. Li N, Sioutas C, Cho A, Schmitz D, Misra C, Sempf 
J, et al. Ultrafine particulate pollutants induce oxida-
tive stress and mitochondrial damage. Environ Health 
Perspect. 2003;111:455–60.
 52. Krutmann J, Jux B, Luecke S, Fritsche E, Abel J, 
Essel C, Rannug A. Involvement of arylhydrocarbon 
receptor (AhR-) signaling in skin melanogenesis. J 
Invest Dermatol. 2008;128:S220.
 53. Penning TM.  Dihydrodiol dehydrogenase and its 
role in polycyclic aromatic hydrocarbon metabolism. 
Chem Biol Interact. 1993;89:1–34.
 54. Daniell HW.  Smooth tobacco and wrinkled skin. N 
Engl J Med. 1969;280:53.
 55. Kadunce DP, Burr R, Gress R, Kanner R, et  al. 
Cigarette smoking: risk factor for premature facial 
wrinkling. Ann Intern Med. 1991;114:840–4.
 56. Kennedy C, Bastiaens MT, Bajdik CD, Willemze 
R, et  al. Leiden skin cancer study. Effect of smok-
ing and sun on the aging skin. J Invest Dermatol. 
2003;120:548–54.
 57. Chow CK. Cigarette smoking and oxidative dam-
age in the lung. Ann N Y Acad Sci. 1993;686: 
289–98.
 58. Boyd AS, Shyr Y, King LE Jr. Basal cell carcinoma 
in young women: an evaluation of the association of 
tanning bed use and smoking. J Am Acad Dermatol. 
2002;46:706–9.
 59. Dietrich M, Block G, Norkus EP, Hudes M, Traber 
MG, Cross CE, et al. Smoking and exposure to envi-
ronmental tobacco smoke decrease some plasma anti-
oxidants and increase gamma-tocopherol in vivo after 
adjustment for dietary antioxidant intakes. Am J Clin 
Nutr. 2003;77:160–6.
 60. Jorgensen LN, Kallehave F, Christensen E, Siana 
JE, Gottrup F. Less collagen production in smokers. 
Surgery. 1998;123:450–5.
 61. Just M, Ribera M, Monsó E, Lorenzo JC, FerrándizC.  Effect of smoking on skin elastic fibres: mor-
phometric and immunohistochemical analysis. Br J 
Dermatol. 2007;156:85–91.
 62. Binic I, Lazarevic V, Ljubenovic M, Mojsa J, 
Sokolovic D.  Skin ageing: natural weapons and 
strategies. Evid Based Complement Alternat Med. 
2013;2013:1–10.
 63. Landau M.  Exogenous factors in skin aging. Curr 
Probl Dermatol. 2007;35:1–13.
 64. Berneburg M, Grether-Beck S, Kürten V, Ruzicka 
T, Briviba K, Sies H, et al. Singlet oxygen mediates 
the UVA-induced generation of the photoaging- 
associated mitochondrial common deletion. J Biol 
Chem. 1999;274:15345–9.
 65. Montagner S, Costa A. Molecular basis of photoag-
ing. An Bras Dermatol. 2009;84(3):263–9.
 66. Kligman LH.  Intensification of ultraviolet-induced 
dermal damage by infrared radiation. Arch Dermatol 
Res. 1982;272:229–38.
 67. Schieke SM, Schroeder P, Krutmann J.  Cutaneous 
effects of infrared radiation: from clinical observations 
to molecular response mechanisms. Photodermatol 
Photoimmunol Photomed. 2003;19:228–34.
 68. Schroeder P, Haendeler J, Krutmann J.  The role of 
near infrared radiation in photoaging of the skin. Exp 
Gerontol. 2008;43:629–32.
 69. Schroeder P, Calles C, Benesova T, Macaluso F, 
Krutmann J.  Photoprotection beyond ultraviolet 
radiation--effective sun protection has to include 
2 Pearl Chapter: Basis of Photoaging and the Use of Chemical Peelings
http://www.who.int/phe/health_topics/outdoorair/outdoorair_aqg/en/
http://www.who.int/phe/health_topics/outdoorair/outdoorair_aqg/en/
24
 protection against infrared A radiation-induced skin 
damage. Skin Pharmacol Physiol. 2010;23:15–7.
 70. Sanches Silveira JEP, Myaki Pedroso DM. UV light 
and skin aging. Rev Environ Health. 2014;29:243–54. 
https://doi.org/10.1515/reveh-2014-0058.
 71. Debacq-Chainiaux F, Leduc C, Verbeke A, Toussaint 
O.  UV, stress and aging. Dermatoendocrinology. 
2012;4:236–40.
 72. Krutmann J. The role of UVA rays in skin aging. Eur 
J Dermatol. 2001;11:170–1.
 73. Reelfs O, Tyrrel RM, Pourzand C.  Ultraviolet a 
radiation- induced immediate iron release is a key 
modulator of the activation of NF-kappaB in human 
skin fibroblasts. J Invest Dermatol. 2004;122:1440–7.
 74. Angel P, Szabowski A, Schorpp-Kistner M. Function 
and regulation of AP-1 subunits in skin physiology 
and pathology. Oncogene. 2001;20:2413–23.
 75. Fisher GJ, Kang S, Varani J, Bata-Csorgo Z, Wan Y, 
Datta S, et al. Mechanisms of photoaging and chrono-
logical skin aging. Arch Dermatol. 2002;138:1462–70.
 76. Wang XY, Bi ZG.  UVB-irradiated human keratino-
cytes and interleukin-1alpha indirectly increase MAP 
kinase/AP-1 activation and MMP-1 production in 
UVAirradiated dermal fibroblasts. Chin Med J (Engl). 
2006;119:827–31.
 77. Watanabe H, Shindo K, Ida H, Tanaka H, Nagasaka T, 
Shiozawa Z. Aging effects of sympathetic reflex activ-
ities on skin nerves. Gerontology. 2003;49:366–73.
 78. Ray AJ, Turner R, Nikaido O, Rees JL, Birch- Machin 
MA. The spectrum of mitochondrial DNA deletions 
is a ubiquitous marker of ultraviolet radiation expo-
sure in human skin. J Invest Dermatol. 2000;115: 
674–9.
 79. Koch H, Wittern KP, Bergemann J. In human kerati-
nocytes the common deletion reflects donor variabili-
ties rather than chronologic aging and can be induced 
by ultraviolet A irradiation. J Invest Dermatol. 
2000;117:892–7.
 80. Ballard JW, Dean MD.  The mitochondrial genome: 
mutation, selection and recombination. Curr Opin 
Genet Dev. 2001;11:667–72.
 81. Hernandez-Pigeon H, Jean C, Charruyer A, Haure 
MJ, Baudouin C, Charveron M, et  al. UVA induces 
granzyme B in human keratinocytes through MIF: 
implication in extracellular matrix remodeling. J Biol 
Chem. 2007;282:8157–64.
 82. Shigenaga MK, Hagen TM, Ames BN.  Oxidative 
damage and mitochondrial decay in aging. Proc Natl 
Acad Sci U S A. 1994;91:10771–8.
 83. Eshaghian A, Vleugels R, Canter JA, McDonald MA, 
Stasko T, Sligh JE.  Mitochondrial DNA deletions 
serve as biomarkers of aging in the skin, but are typi-
cally absent in nonmelanoma skin cancers. J Invest 
Dermatol. 2006;126:336–44.
 84. Shoffner JM, Lott MT, Voljavec AS, Soueidan SA, 
Costigan DA, Wallace DC.  Spontaneous Kearns–
Sayre/chronic external ophthalmoplegia plus syn-
drome associated with a mitochondrial DNA deletion: 
a slip-replication model and metabolic therapy. Proc 
Natl Acad Sci U S A. 1989;86:7952–6.
 85. Lu CY, Lee HC, Fahn HJ, Wei YH. Oxidative dam-
age elicited by imbalance of free radical scavenging 
enzymes is associated with largescale mtDNA dele-
tions in aging human skin. Mutat Res. 1999;423:11–21.
 86. Cortopassi GA, Arnheim N. Detection of a specific 
mitochondrial DNA deletion in tissues of older 
humans. Nucleic Acids Res. 1990;18:6927–33.
 87. Cortopassi GA, Shibata D, Soong NW, Arnheim 
N. A pattern of accumulation of a somatic deletion 
of mitochondrial DNA in aging human tissues. Proc 
Natl Acad Sci U S A. 1992;89:7370–4.
 88. Harbottle A, Krishnan KJ, Birch-Machin MA. 
Implications of using the ND1 gene as a control 
region for real-time PCR analysis of mitochondrial 
DNA deletions in human skin. J Invest Dermatol. 
2004;122:1518–21.
 89. Krishnan KJ, Harbottle A, Birch-Machin MA. The 
use of a 3895 bp mitochondrial DNA deletion as a 
marker for sunlight exposure in human skin. J Invest 
Dermatol. 2004;123:1020–4.
 90. Berneburg M, Gattermann N, Stege H, Grewe M, 
Vogelsang K, Ruzicka T, et  al. Chronically ultra-
violet- exposed human skin shows a higher muta-
tion frequency of mitochondrial DNA as compared 
to unexposed skin and the hematopoietic system. 
Photochem Photobiol. 1997;66:271–5.
 91. Berneburg M, Krutmann J. Mitochondrial DNA dele-
tions in human skin reflect photo rather than chrono-
logic aging. J Invest Dermatol. 1998;111:709–10.
 92. Berneburg M, Plettenberg H, Medve-König K, 
Pfahlberg A, Gers-Barlag H, Gefeller O, et  al. 
Induction of the photoaging-associated mitochon-
drial common deletion in  vivo in normal human 
skin. J Invest Dermatol. 2004;122:1277–83.
 93. Schuch AP, Moreno NC, Schuch NJ, Menck CFM, 
Garcia CCM.  Sunlight damage to cellular DNA: 
focus on oxidatively generated lesions. Free Radic 
Biol Med. 2017;107:110–24.
 94. Svobodova A, Walterova D, Vostalova J. Ultraviolet 
light induced alteration to the skin. Biomed Pap 
Med Fac Univ Palacky Olomouc Czech Repub. 
2006;150:25–38.
 95. Gilchrest BA.  Photoaging. J Invest Dermatol. 
2013;133:E2–6. https://doi.org/10.1038/skinbio. 
2013.176.
 96. Runger TM, Farahvash B, Hatvani Z, Rees A. 
Comparison of DNA damage responses follow-
ing equimutagenic doses of UVA and UVB: a less 
effective cell cycle arrest with UVA may render 
UVA-induced pyrimidine dimers more mutagenic 
than UVB-induced ones. Photochem Photobiol Sci. 
2012;11:207–15.
 97. Bosch R, Philips N, Suárez-Pérez J, Juarranz A, 
Devmurari A, Chalensouk-Khaosaat J, González 
S. Mechanisms of Photoaging and cutaneous pho-
tocarcinogenesis, and photoprotective strategies 
with phytochemicals. Antioxidants. 2015;4:248–68. 
https://doi.org/10.3390/antiox4020248.
 98. Bhatia-Dey N, Kanherkar RR, Stair SE, Makarev 
EO, Csoka AB.  Cellular senescence as the causal 
S. Montagner and A. Da Costa
https://doi.org/10.1515/reveh-2014-0058
https://doi.org/10.1038/skinbio.2013.176
https://doi.org/10.1038/skinbio.2013.176
https://doi.org/10.3390/antiox4020248
25
nexus of aging. Front Genet. 2016;7:13. https://doi.
org/10.3389/fgene.2016.00013.
 99. Stege H, Roza L, Vink AA, Grewe M, Ruzicka 
T, Grether-Beck S, et  al. Enzyme plus light 
therapy to repair DNA damage in ultraviolet-B- 
irradiated human skin. Proc Natl Acad Sci U S A. 
2000;97:1790–5.
 100. Bender K, Blattner C, Knebel A, Iordanov M, Herrlich 
P, Rahmsdorf HJ. UV-induced signal transduction. J 
Photochem Photobiol B. 1997;37:1–2):1–17.
 101. Fritsche E, Schafer C, Calles C, Bernsmann T, 
Bernshausen T, Wurm M, Hubenthal U, Cline JE, 
Hajimiragha H, Schroeder P, Klotz LO, Rannug 
A, Furst P, Hanenberg H, Abel J, Krutmann J. 
Lightening up theUV response by identification of 
the arylhydrocarbon receptor as a cytoplasmatic tar-
get for ultraviolet B radiation. Proc Natl Acad Sci U 
S A. 2007;104(21):8851–6.
 102. Herrmann G, Wlaschek M, Lange TS, Prenzel 
K, Goerz G, Scharffetter-Kochanek K.  UVA irra-
diation stimulates the synthesis of various matrix- 
metalloproteinases (MMPs) in cultured human 
fibroblasts. Exp Dermatol. 1993;2(2):92–7.
 103. Brenneisen P, Oh J, Wlaschek M, Wenk J, 
Briviba K, Hommel C, Herrmann G, Sies H, 
Scharffetter- Kochanek K. Ultraviolet B wavelength 
dependence for the regulation of two major matrix- 
metalloproteinases and their inhibitor TIMP-1  in 
human dermal fibroblasts. Photochem Photobiol. 
1996;64(5):877–85.
 104. Brenneisen P, Sies H, Scharffetter-Kochanek K. 
Ultraviolet-B irradiation and matrix metalloprotein-
ases: from induction via signaling to initial events. 
Ann N Y Acad Sci. 2002;973:31–43.
 105. Krutmann J, Morita A, Chung JH.  Sun expo-
sure: what molecular photodermatology tells us 
about its good and bad sides. J Invest Dermatol. 
2012;132:976–84.
 106. Jux B, Kadow S, Luecke S, Rannug A, Krutmann 
J, Esser C.  The aryl hydrocarbon receptor medi-
ates UVB radiation-induced skin tanning. J Invest 
Dermatol. 2011;131(1):203–10.
 107. Karu TI.  Mitochondrial signaling in mamma-
lian cells activated by red and near-IR radiation. 
Photochem Photobiol. 2008;84(5):1091–9.
 108. Schroeder P, Pohl C, Calles C, Marks C, Wild S, 
Krutmann J. Cellular response to infrared radiation 
involves retrograde mitochondrial signaling. Free 
Radic Biol Med. 2007;43:128–35.
 109. Darvin ME, Haag S, Meinke M, Zastrow L, Sterry 
W, Lademann J.  Radical production by infrared A 
irradiation in human tissue. Skin Pharmacol Physiol. 
2010;23:40–6.
 110. Krutmann J, Schroeder P.  Role of mitochondria 
in photoaging of human skin: the defective pow-
erhouse model. J Investig Dermatol Symp Proc. 
2009;14(1):44–9.
 111. Chung JH, Eun HC. Angiogenesis in skin aging and 
photoaging. J Dermatol. 2007;34:593–600.
 112. Jantschitsch C, Weichenthal M, Maeda A, Proksch 
E, Schwarz T, Schwarz A. Infrared radiation does 
not enhance the frequency of ultraviolet radiation 
induced skin tumors, but their growth behaviour in 
mice. Exp Dermatol. 2011;20(4):346–50.
2 Pearl Chapter: Basis of Photoaging and the Use of Chemical Peelings
https://doi.org/10.3389/fgene.2016.00013
https://doi.org/10.3389/fgene.2016.00013
27© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_3
Tip Chapter: Peels for Ethnic Skin
Renan Lage
Created in 1976, the Fitzpatrick scale (FST) clas-
sified the skin into six types (I–VI). The classifi-
cation is based on each individual’s skin response 
to sun exposure and the susceptibility to tanning 
or burning when exposed to ultraviolet radiation 
(UVR) [1] (Table 3.1). Types IV, V, and VI are 
known as “skin of color” or ethnic skin, contem-
plating individuals who tan easily and usually do 
not burn [1, 3].
It is well established that there are no differ-
ences in the number of melanocytes in the skin, 
considering the different phototypes. Ethnic skin 
presents differences in the size, number, and 
aggregate of melanosomes, thus resulting in dif-
ferences in the epidermal distribution of melanin. 
That way, the greater the amount of melanin, the 
more pigmented the skin will be [1, 3, 4].
Structural differences in the epidermis and 
dermis are also observed. There is greater cohe-
sion between the epidermal layer cells, these 
being more compact and with an increase of the 
lipid layer. Fibroblasts are larger, multinucleated, 
and in greater quantity in the dermis. The bundles 
of collagen fibers are strongly attached, smaller, 
and parallel to the epidermis [1]. Skin with a 
higher phototype presents greater protection to 
the effects of the UVR as a result of melanin 
function and melanosome distribution, which 
reflects in signs of photoaging, presenting less 
expressive wrinkles, actinic keratoses, and photo- 
damaged skin. Pigmentation is another aspect to 
be considered on ethnic skin. It can consequently 
present pigmentary disorders like post- 
inflammatory hyperpigmentation (occurring 
commonly as a response to injuries) and melasma. 
A greater tendency to form keloid scars should 
also be considered [3, 5].
It is important to highlight existing ethnic dif-
ferences within the group of patients with higher 
skin phototypes. While Asian patients are more 
sensitive to chemical stimuli, probably due to a 
thinner stratum and higher density of the sweat 
glands, African descendant skin presents lower 
irritability, probably associated with a more 
R. Lage (*) 
Cosmiatric Department, Department of Dermatology 
of the Pontifical Catholic University of Campinas - 
PUC Campinas, Campinas, SP, Brazil
3
Table 3.1 Fitzpatrick phototypes [2]
Fitzpatrick 
phototype UVR response
I Always burns and never tans
II Always burns and tans with 
difficulty
III Sometimes mild burn, gradually 
tans
IV Rarely burns and tans with ease
V Very rarely burns and tans easily
VI Never burns
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_3&domain=pdf
28
cohesive stratum corneum. Other differences in 
African descendant skin that must be emphasized 
are the greater amounts of apocrine glands, larger 
glandular pores, sebaceous secretion, and bacte-
rial flora [4].
Considering that the world population is 
mostly composed of people of higher skin photo-
types (Asian, African, and Afro-descendant) and 
that noninvasive procedures, such as chemical 
peels, have become popular in recent years, it is 
important to study these procedures in this par-
ticular group of patients [6].
3.1 History/Background
The use of caustic substances for the preparation 
of chemical peels was first described in Ancient 
Egypt, in the Ebers Papyrus in 1550  BC [7]. 
Egyptians used animal oils, salt, and sour milk, 
whose active agent was lactic acid, to improve 
skin appearance [8].
In 1874  in Vienna, Dermatologist Ferdinand 
von Hebra, using a combination of exfoliative 
agents, performed the treatment of patients with 
melasma, Addison’s disease, and ephelides, and 
in 1882, Paul G.  Unna described the action of 
salicylic acid, resorcinol, trichloroacetic acid 
(TCA), and phenol on the skin. His work was fol-
lowed by many others [8].
Mackee in 1903 used phenol peel in acne 
scars, but it was only in 1952 that he, together 
with Florentine Karp, published the results [9]. 
During this period, in the 1940s in the United 
States, Eller and Wolff made the first systematic 
description on the use of phenol, salicylic acid, 
resorcinol, and cryotherapy spray for scar treat-
ment [8, 10].
The modern era of peeling began in the 1960s 
when Baker and Gordon developed the modified 
phenol formula (adding croton oil, Septisol, and 
water) and performed a histological evaluation of 
results, comparing effects between phenol and 
TCA [11].
In the 1970s and early 1980s, the scientific 
basis for TCA peelings was expanded by com-
paring the histological effects between three con-
centrations of the product. In parallel, 
alpha-hydroxy acids (AHA) were developed by 
Van Scott and Yu for more superficial peels, being 
indicated for the treatment of hyperkeratosis. 
Subsequently, peeling with glycolic acid was 
developed [11].
The combination of two substances for sur-
face peels (Jessner’s solution and 35% TCA) to 
reach medium depth was described in 1986 by 
Brody and Hailey and then by Monheit, provid-
ing a great deal of progress in the use of peels and 
reflecting on their current use [11].
3.2 Genesis
The action of chemical peeling is based on the 
application of a caustic substance causing skin 
layer destruction. The epidermis and the dermis 
react to the stimulus with repair mechanisms, 
culminating, respectively, in regeneration and 
remodeling, with consequent improvement of 
skin uniformity [6, 11].The indication of chemical peeling considers 
some criteria such as age, phototype, area to be 
treated, degree of photoaging, desired goals, 
medical practitioner’s habilitation, and inherent 
factors of each patient [12].
The benefits of the procedure vary according 
to phototypes, presenting differences in both indi-
cations and possible complications [6]. Unlike the 
pale skin in which the peels are mostly used to 
treat photoaging changes, in ethnic skin, the major 
indications are dyschromias, acne vulgaris, post-
inflammatory hyperpigmentation (PIH), melasma, 
and pseudofolliculitis barbae [5, 6].
3.3 Classification/Types
Peelings are classified according to the depth 
they reach the skin from superficial, medium, to 
deep. The first reaches the epidermis (preserving 
the basal membrane), the second to the papillary 
dermis, and the third to the reticular dermis. 
Superficial peels can still be subdivided into 
light, being able to reach to the spinosum, and 
deeper, when it reaches the entire epidermis. The 
depth is influenced by several factors: the type 
R. Lage
29
and concentration of the substance used, the pH 
of the solution, and exposure time to the sub-
stance [6, 11].
Superficial peelings can be used in all photo-
types, including IV, V, and VI.  Medium-depth 
peels may be indicated in some cases with ethnic 
skin; however, the deeper peels should be used 
very carefully in these patients considering the 
high risk of adverse effects like pigmentary dis-
orders and scars [6].
The substances used for superficial peelings 
are glycolic acid, salicylic acid, Jessner’s solu-
tion, and trichloroacetic acid (TCA) concentrated 
to 10–30%. TCA at concentrations of 35–50% 
and phenol at 88% comprise the substances used 
for medium depth. For deep peelings, the Baker- 
Gordon formula (88% phenol combination, tap 
water, liquid soap, and croton oil) is used [5, 11].
3.4 Available Materials
To indicate peeling, one should evaluate the 
patient’s profile, phototype, their professional 
activity, availability to be absent from work, and 
expectations. It is very important to explain, 
through educational material, the procedure that 
will be performed, as well as the previous prepa-
ration of the skin, period of desquamation, and 
the cosmetic results to be achieved. It is impor-
tant to carry out a detailed medical history, 
assessing the degree of sun exposure, personal 
history of herpes simplex, tendency for dyschro-
mia such as post-inflammatory hyperpigmenta-
tion, predisposition to keloid development, active 
smoking, inflammatory diseases, and isotretinoin 
use in the last 6 months and evaluating medica-
tions in use [5, 6].
The pre-peeling preparation starts 2–4 weeks 
earlier and is suspended within 3 days prior to the 
procedure. Formulations containing retinoic acid 
(0.025–0.1%) and/or glycolic acid (5–10%), 
associated or not with depigmenting agents, such 
as hydroquinone (2.5–5%), kojic acid (1–2%), or 
phytic acid in appropriate vehicles for each skin 
type, are used [13]. A study by Nanda et al. com-
pared the use of hydroquinone versus topical 
isotretinoin as an adjunct agent to peeling therapy 
in patients with melasma. Although both sub-
stances improve the skin within 12 weeks, after a 
6-month follow-up, hydroquinone showed a 
superior improvement [14].
Patients should be advised to the possibility of 
skin irritation, dryness, and erythema with the 
use of these products. Adequate photoprotection 
and pre-peeling preparation are extremely impor-
tant, reducing the risk of post-inflammatory pig-
mentation [6, 13].
Patients with a personal history of herpes sim-
plex must receive prophylactic therapy with anti-
virals. Aciclovir (1000  mg/day) or valaciclovir 
(1000 mg/day) is commonly used for a period of 
5 days. This preparation is unnecessary for super-
ficial peels [13].
Post-peeling care involves the use of photo-
protectors and mild emollients in all phototypes 
and the reintroduction of bleaching agents after 
1 week, especially in the higher skin phototypes 
[6, 11].
When applying a chemical peeling agent, 
some general observations are relevant for safety: 
avoid application to irritated, inflamed, or ery-
thematous skin; always have neutralizing sub-
stances available when necessary; assess the 
patient’s pain using a sensitive scale of 1–10; and 
be attentive to frosting, as it helps to identify the 
degree of penetration and depth of the substance 
on the skin [11].
3.4.1 Glycolic Acid
Glycolic acid belongs to the alpha-hydroxy acid 
(AHA) family. Its mechanism of action is by epi-
dermolysis, followed by scaling and dispersion 
of epidermal melanin. Epidermolysis usually 
occurs after a few minutes from application and 
is therefore applied for 3–5 min. It has commer-
cial concentrations ranging from 10% to 70%, 
needs to be neutralized with saline or sodium 
bicarbonate, and can be performed at intervals of 
2–3 weeks. It is possible to associate with 35% 
trichloroacetic acid when the goal is to perform a 
medium peel [5, 6, 15].
Its indications include acne, melasma, and 
post-inflammatory pigmentation [6, 16, 17]. In 
3 Tip Chapter: Peels for Ethnic Skin
30
acne, glycolic acid presents bactericidal and 
 anti- inflammatory actions and also corrects 
abnormal keratinization [6, 18, 19]. For melasma, 
a melanized keratinocyte is eliminated and a 
stimulus for skin renewal occurs. Treatment 
should be considered only for epidermal and 
mixed variants, since there may be an important 
increase in complication risks for the treatment 
of deeper forms [6, 20].
Wang et  al. [16] performed a study with a 
selection of 40 Asian patients with moderate to 
severe acne. Patients were divided into two 
groups and treated with four glycolic acid peel-
ing sessions of 30 and 50%, associated with daily 
topical 15% glycolic acid. The authors observed 
a significant decrease in the number of comedo-
nes, papules, pustules, and pore size, as well as 
improvement in the texture of the skin, giving a 
more rejuvenated appearance to the patients. 
Glycolic acid peeling was considered an effective 
therapy with minimal side effects [16].
Burns et al. [17] studied 19 patients with IV to 
VI phototypes, with post-inflammatory hyperpig-
mentation, randomly divided into two groups. 
Both groups received topical treatment with 
hydroquinone 2% associated with 10% glycolic 
acid, twice daily, with 0.05% isotretinoin at night. 
In one of the groups, six sessions of glycolic acid 
peeling (maximum concentration of 68%) were 
associated with a greater and faster improvement 
of pigmentation, with skin clearing [17].
Grover and Reddu [21] performed a study 
with 41 Indian patients (phototypes III–V) using 
10–30% glycolic acid to treat acne, melasma, 
post-inflammatory hyperpigmentation, and scar-
ring. Peeling has proven effective especially in 
the treatment of superficial scars and melasma, 
being moderately effective in acne and ineffec-
tive in dermal pigmentation. Adverse effects 
were irritation, post-inflammatory hyperpigmen-
tation, cold sores, and hypopigmentation [21].
Glycolic acid peels are usually well tolerated 
on ethnic skin and have few side effects, espe-
cially when applied in gradually titrated concen-
trations (from the lowest to the highest) [5, 6]. 
The most common side effect is post- 
inflammatory pigmentation, also erythema and 
desquamation [15, 22].
3.4.2 Lactic Acid
Lactic acid is also a member of the alpha-hydroxy 
acid family, which has similar activity to glycolic 
acid. It is used in the concentration of 85% and 
can be used in the treatment of melasma and acne 
scars [6, 13].
Sachdeva [23] conducted a study with seven 
Indian patients (phototypes IV and V) with acne 
scars; four peeling sessions were performed 
every 2  weeks using lactic acid. At the end of 
3 months, there was an important improvement in 
texture, pigmentation, and appearance of the 
scars [23].
Sharquie et  al. [24] conducted a study of 20Iraqi, phototype IV, patients with melasma. Six 
peeling sessions were performed with pure lactic 
acid every 3  weeks. Twelve patients completed 
the study and a significant improvement (as mea-
sured by Melasma Area and Severity Index 
(MASI)) was observed, with no reported adverse 
effects [24]. Another study, with the same authors 
[25], compared lactic acid with Jessner’s solution 
every 3 weeks in 30 patients with melasma (pho-
totype IV), each substance being applied to one 
half of the face. Twenty-four patients completed 
the study demonstrating that both treatments 
were statistically significant, with no reported 
adverse response [25].
Further studies with a greater number of 
patients are needed to evaluate the effectiveness 
of lactic acid in the treatment of melasma specifi-
cally in patients with ethnic skin.
3.4.3 Salicylic Acid
Salicylic acid (SA), another surface peeling 
agent, considered an ortho-hydroxybenzoic acid, 
belonging to the beta-hydroxy acid family, can be 
handled in a hydroalcoholic solution in concen-
trations of 20–30%. At concentrations of 3–5%, 
it presents keratolytic function. It can be used in 
6–8 sessions per week. It is lipophilic and pro-
duces desquamation of the superficial layers of 
the stratum corneum [5, 6].
It is useful in acne, post-inflammatory hyper-
pigmentation, melasma, pseudofolliculitis 
R. Lage
31
 barbae, and improvement of oily skin [5, 26]. In 
acne, it also has a comedolytic effect, with an 
improvement in inflammatory and non- 
inflammatory lesions [5]. A gradual bleaching 
effect with the use of salicylic acid peeling seri-
ally has been observed [27]. It is considered safe 
for use in patients with higher phototypes, pre-
senting a lower risk of post-inflammatory pig-
mentation when used in increasing titers and 
when associated with hydroquinone 4% [6, 28].
Lee and Kim [29] conducted a study about SA 
peeling in acne vulgaris in Asian patients to dem-
onstrate its safety and efficacy. Thirty-five 
Koreans with facial acne were selected and 
underwent the biweekly application of SA at 
30% for 12  weeks. In these patients, there was 
reduction of inflammatory and non-inflammatory 
lesions [29].
Other studies have found similar results, such 
as that conducted by Ahn and Kim [27], in which 
they demonstrated a skin clearing for Asian 
patients who underwent 30% SA peeling for 
3 months [27].
3.4.4 Tretinoin
It is a trans-retinoic acid and synthetic analogue 
of vitamin A.  It acts on collagen synthesis, 
increase in neovascularization, reversal of epider-
mal atypias, and dispersion of melanin. It can be 
used in concentrations of 5–12% for improve-
ment of acne, melasma, and post-inflammatory 
hyperpigmentation [6, 13]. Khunger et  al. [30] 
compared 70% glycolic acid peeling with 1% 
tretinoin in patients of Asian ethnicity, photo-
types III to V, demonstrating similar results in 
both groups [30].
3.4.5 Jessner’s Solution
The solution contains three keratolytic com-
pounds with synergistic action: salicylic acid 
(14 g), lactic acid (85%, 14 mL), and resorcinol 
(14 g) diluted in 100 ml of 95% ethanol. It also 
has a bleaching effect provided by the last com-
ponent. It can be used individually as a surface 
peeling agent or in combination with other agents 
such as TCA for medium peeling [5, 6].
The penetration varies according to the num-
ber of layers applied. The use of one layer reflects 
level I that forms slight erythema and whitish 
flocculation on the surface as an easily removable 
powder. If applied from two to three layers, a 
more lively erythema will form, as well as frost-
ing, accompanied by a burning sensation. Level 
III can be achieved with three to four layers and 
causes significant erythema, with areas of frost-
ing and mild burning. It is important to take into 
account the level to be achieved, being able to 
achieve up to medium depth [13].
This solution is indicated as an adjuvant treat-
ment for acne, pigmentary disorders, improve-
ment of oiliness and texture of the skin, fine 
wrinkles, and pseudofolliculitis barbae [5].
Some authors have shown that although 
Jessner’s peeling can be used individually, it is 
more effective when associated with other peels 
[31–33].
3.4.6 Trichloroacetic Acid (TCA)
Trichloroacetic acid is an inorganic compound 
and acts to cause protein denaturation with con-
sequent cell death by coagulative necrosis. It 
does not need to be neutralized, and it can be 
used in the concentrations of 10–65%, being 
applied in an isolated form in lower concentra-
tions as a superficial peeling agent (up to 35%) 
[6]. The depth achieved is associated with TCA 
concentration and exposure time to the product 
[11].
At the end of its application, the degree of 
depth reached can be divided into three levels. 
Level I is represented by erythema associated 
with light and irregular frost, level II by white 
coating and erythema, and level III by a solid 
white frost with little or no background erythema 
[34]. White frost (levels II and III) is not a desired 
effect for ethnic skin, since it increases the risk of 
complications such as scars and pigmentary dis-
orders. For this reason, although commonly used 
for lighter skin, it should be used more cautiously 
in patients with higher phototypes [15, 26].
3 Tip Chapter: Peels for Ethnic Skin
32
It is useful for the treatment of acne scars and 
for rejuvenation, generating more uniformity of 
skin color [26]. It can also be used focally for 
benign lesions such as seborrheic keratosis and 
solar lentigo [35].
Kalla et al. [36] performed a study with 100 
patients comparing trichloroacetic acid with gly-
colic acid in melasma treatment. The patients 
were divided into a group treated with glycolic 
acid peeling at 55–70% and the other with tri-
chloroacetic acid at 10–15%. The applications 
were carried out fortnightly. The authors of this 
study concluded that trichloroacetic acid is more 
effective compared to glycolic acid, but it has 
more adverse effects (burning sensation and 
hyperpigmentation), which must be considered 
when working with ethnic skin [36].
3.4.7 Other Agents
3.4.7.1 Thioglycolic Acid
It is an organic acid, is easily oxidizable, and has 
sulfur in its composition. It has iron affinity and 
the ability to chelate hemosiderin iron. It is used 
in concentrations from 5 to 10%. It can be used as 
a peeling agent in ochre dermatitis of the lower 
limbs and in constitutional periocular hyperpig-
mentation [13]. It presents as main side effects 
discreet erythema and transient desquamation 
and is considered a safe and effective agent. In a 
study by Costa et al. [37], when using 10% gel- 
containing thioglycolic acid, phototype IV 
patients presented improvement in constitutional 
periocular hyperpigmentation [37].
3.4.7.2 Resorcin
It is a caustic chemical peeling agent commonly 
used in association with other substances, its 
main combination being the Jessner’s solution. 
The concentrations range from 10 to 70%, and 
their indications include acne, dyschromias, fine 
wrinkles, and post-inflammatory hyperpigmen-
tation. Its advantages are low cost and stability, 
and potential side effects are intoxication and 
allergic reactions. Its use in ethnic patients and 
tendency to hyperpigmentation make it a viable 
option [13].
3.4.7.3 Mandelic Acid
It belongs to the alpha-hydroxy acid family, with 
a slow and safe penetration as a superficial peel-
ing agent. It can be used in acne for the treatment 
of active lesions and scars, especially when asso-
ciated with salicylic acid [38].
3.4.7.4 Pyruvic Acid
Pyruvic acid is an alfa-ketoacid, with keratolytic, 
antimicrobial, and antiseborrheic function and 
with capacity to stimulate the formation of neo-
collagen and elastic fibers. Its mechanism of 
action consists of epidermolysis, penetrating the 
skin in 1–2 min. Its penetration can be unpredict-
able and if too rapid can lead to the formation of 
scars. The main indications include acne,superfi-
cial scars, photoaging, and dyschromias in 
patients with low phototype. Additional studies 
in high-phototype patients are needed to indicate 
their efficacy and safety [6, 13, 15].
3.4.8 Salicylic-Mandelic Acid 
Combination
It consists of 20% salicylic acid and 10% man-
delic acid. It is a useful combination in the high-
est phototype skins, since mandelic acid has a 
slow penetration, being ideal for sensitive skin, 
and salicylic acid penetrates quickly, with the 
added benefit of preventing post-inflammatory 
pigmentation. Although still less widespread, it 
can be used in acne (active and scarring) and dys-
chromias [13, 15]. Sarkar et al. [39] demonstrated 
similar efficacy to glycolic acid for the treatment 
of melasma in patients with phototypes IV and V, 
with the benefit of better tolerance [39].
Some new compounds have been studied as 
chemical peeling agents such as beta- lipohydroxy 
acid and “amino fruit acids,” with good results. 
However, additional studies focusing on ethnic 
skin are still necessary [6].
3.4.9 Medium Peelings
Combination peels may be useful, the main 
example being the average peel performed with 
R. Lage
33
the combination of Jessner’s solution and TCA, 
indicated for moderate to severe photo-damaged 
skin. Another widely used option is the use of 
70% glycolic acid with 35% TCA, with the 
advantage of an important improvement of dys-
chromias and post-inflammatory hyperpigmenta-
tion from the use of glycolic acid [40]. An 
improvement in melasma is also reported with 
the use of Jessner’s solution and 15% TCA com-
bination [6, 15].
3.4.10 Fluor-hydroxy Pulse Peel
Fluor-hydroxy pulse peel is a combination of 
5-fluorouracil and 70% glycolic acid, used in the 
treatment of actinic keratoses. It has good cos-
metic results; however, to date, there are no stud-
ies applied to patients with higher phototypes 
[41, 42].
3.4.11 Deep Peelings
Deep peels reach the reticular dermis and act 
through the coagulation of proteins, leading to a 
restoration of dermis architecture [11].
They are considered aggressive because they 
provoke the formation of many thick crusts, 
being necessary the use of post-peeling dressings 
and presenting a more delayed recovery that lasts 
for months. However, a very significant cosmetic 
result is observed, with important skin renewal 
and reduction of deep wrinkles. The agents used 
are phenol and Baker’s solution. They should be 
avoided in higher phototypes by the risk of post- 
inflammatory hyperpigmentation and scar forma-
tion [13].
3.5 Phenol Peeling
Phenol when used at a concentration of 88% can 
penetrate to the depth of the upper reticular der-
mis. By coagulating keratin, it prevents its per-
meability to deeper levels. The best-known deep 
peeling formulation is Baker-Gordon. For this 
formulation, 3  ml phenol (88% phenol  +  12% 
water), 2 ml common/distilled water, 8 drops of 
0.025% soap (liquid hexachlorophene), and 3 
drops of croton oil are used. When diluted in this 
solution, phenol becomes capable of generating 
keratolysis and keratocoagulation, reaching 
deeper layers [13].
Its correct use requires anamnesis, physical 
examination, and laboratory tests. Phenol can be 
absorbed systemically, with potential cardiotox-
icity, nephrotoxicity, hepatotoxicity, and central 
nervous system depression. It should be per-
formed in a hospital environment due to the 
obligatory monitoring of the patient’s heart. 
Tachycardia, ventricular extrasystoles, atrial 
fibrillation, and ventricular fibrillation may be 
observed as adverse effects. Therefore, its use is 
avoided in cases of heart, kidney, or liver disease, 
herpes simplex, recent isotretinoin use, psycho-
logical instability, keloid predisposition, and con-
tinuous exposure to UV rays and in patients with 
phototypes IV to VI [40].
It is a very painful peeling due to the action of 
phenol in the intermediate reticular dermis, 
requiring sedation and analgesics. It is necessary 
to maintain good hydration before and during the 
procedure. Burning pain for up to 8 h and marked 
swelling may occur. In the postoperative period, 
it is recommended to use anxiolytics, analgesics, 
antibiotics, and ice packs. Epidermal regenera-
tion begins in 48  h and completes in around 
10 days [13, 40].
Pruritus is common during the healing process 
and can improve by applying low-potency corti-
costeroids and ice packs. Erythema and crusts 
may remain for up to 14 days, and milia forma-
tion is also possible [13, 40].
It can be said that phenol peel when well indi-
cated is considered extremely effective but should 
be avoided in patients with higher phototypes due 
to the high risk of complications [13].
3.5.1 Blepharopeeling
Parada et  al. [43] conducted a pilot study on 
blepharopeeling in the upper eyelid using the 
Baker-Gordon formula. For this, they applied the 
solution only in the region with excess skin. Eight 
3 Tip Chapter: Peels for Ethnic Skin
34
patients (phototypes I–III) were treated. These 
authors concluded that the procedure is effective 
and safe, with good aesthetic results; however, 
there were no studies in patients with higher pho-
totypes [43].
Table 3.2 shows the main agents indicated in eth-
nic skin for the different types of pathology [26].
3.6 Before and After (Figs. 3.1, 
3.2, and 3.3)
Table 3.2 Main indications for ethnic skin
Pathology Main agents indicated
Acne Salicylic acid 20–30%
Glycolic acid 30–50%
Post-inflammatory 
hyperpigmentation
Full face:
 Salicylic acid 20–30%
 Glycolic acid 30–50%
Spot peel:
 TCA 25%
 Jessner’s solution
 Salicylic acid 20–30%
Melasma (epidermal or 
mixed)
Salicylic acid 30%
Glycolic acid 50–70%
Acne scar Glycolic acid 70%
TCA 25%
Pseudofolliculitis barbae Salicylic acid 30%
a b c
d e f
Fig. 3.1 Patient with phototype V—melasma. (a–c) Image before Jessner’s solution peel (two layers). (d–f) 22nd day 
after peel
R. Lage
35
a b
Fig. 3.2 Patient with phototype IV—photoaged skin. (a) Image before Jessner’s solution and 35% TCA medium peel. 
(b) Sixth day after medium peel
a b c
d e f
Fig. 3.3 Patient with phototype IV—photoaged skin. (a–c) Images before Jessner’s solution and 35% TCA medium 
peel. (d–f) Sixth day after medium peel
3 Tip Chapter: Peels for Ethnic Skin
36
3.7 Side Effects, Complications, 
and How They May 
Be Handled/Managed
Post-peeling complications occur more fre-
quently in patients with a higher phototype and in 
larger depth (medium and deep) peels. In general, 
the factors that must be considered to avoid 
unwanted effects are adequate pre- and post- 
peeling care and proper selection of both patient 
and agent used [6].
Post-inflammatory pigmentation is more com-
mon in patients with ethnic skin, usually on a 
long-term basis [6]. They occur between 2 and 
3  days and up to 3  months after the procedure 
[40]. Syndromes can be avoided with proper 
choice of agent and depth (greater risk with 
greater depth) and performing correct photopro-
tection [6]. Treatment includes topical corticoste-
roids, tretinoin, hydroquinone, and even 
alpha-hydroxy acids [13].
Appropriate concentrations of the agent pre-
vent irritation, pruritus, or burning. However, if 
they occur, the use of emollients should be 
employed. Erythema and edema may be reduced 
with adequate photoprotection and, if pro-
longed, should be treated with topical cortico-
steroids to prevent the onset of pigmentary 
disorders [6].
Complications such as allergic reaction or tox-
icity can be avoided with retroauricular testing 
performed prior to peeling. Bacterial, fungal 
(Candida), and herpetic infections should be 
promptly treated, noting that the use of prophy-
lactic antivirals should be used in case of history 
of herpetic infections [6, 13].
Formation of hypertrophic scars, keloids, 
and delayed healing can be prevented with 
adequate collection of personal and family 
history and adequate choice of agent and depth 
[6, 13]. The treatment can be performedwith 
intralesional infiltration of corticoid, imiqui-
mod, surgical excision, laser, and silicone 
plates [6].
Other possible complications are acneiform 
eruption, milia, demarcation lines, and persistent 
erythema, and the latter should be treated with 
potent topical corticosteroids [13].
3.8 Conclusions/Findings
Chemical peeling is an important tool for the 
treatment of several conditions and is considered 
a safe, effective, and low-cost procedure. Ethnic 
skin has important peculiarities that reflect in 
some differences on the indication of peeling, use 
of materials, and various possible complications. 
Clinicians should therefore be well aware of the 
safety profile and potency of the different agents, 
applying them and adapting them in a way that 
respects the uniqueness of the ethnic skin.
Tip Box
• Fitzpatrick types IV, V, and VI are 
known as ethnic skin. They present 
differences in the epidermal distribu-
tion of melanin.
• Despite fewer signs of photoaging, it is 
more prone to post-inflammatory 
hyperpigmentation and melasma.
• Indications of ethnic skin peeling: dys-
chromias, acne vulgaris, post-inflamma-
tory hyperpigmentation (PIH), melasma, 
and pseudofolliculitis barbae.
• The superficial peeling can be used, 
the medium depth can be indicated, 
and the deeper peel used in special and 
well-selected cases, due to the high 
risk of adverse effects.
• Pre-peeling precautions include for-
mulations containing retinoic acid and/
or glycolic acid, associated or not with 
depigmenting agents, photoprotection, 
and antiviral prophylaxis.
• Post-peeling care includes photoprotec-
tors, mild emollients, and reintroduc-
tion of bleaching agents after 1 week.
• Glycolic acid: alpha-hydroxy acid, 
indicated for acne, melasma, and post-
inflammatory hyperpigmentation.
• Salicylic acid: beta-hydroxy acid, 
 indicated for acne, post-inflammatory 
hyperpigmentation, melasma, pseudo-
folliculitis barbae, and improvement of 
oily skin.
R. Lage
37
References
 1. Zaidi Z. Skin of colour: characteristics and disease. J 
Pak Med Assoc. 2017;67(2):292.
 2. Fitzpatrick TB. The validity and practicality of sun- 
reactive skin types I through VI.  Arch Dermatol. 
1988;124(6):869–71.
 3. Taylor SC. Skin of color: biology, structure, function, 
and implications for dermatologic disease. J Am Acad 
Dermatol. 2002;46:S41–62.
 4. Rawlings AV. Ethnic skin type: are there differences 
in skin structure and function? Int J Cosmet Sci. 
2006;28(2):79–93.
 5. Grimes PE. Agents for ethnic skin peeling. Dermatol 
Ther. 2000;13:159–64.
 6. Salam A, Dadzie OE, Galadari H. Chemical peeling in 
ethnic skin: an update. Br J Dermatol. 2013;169(Suppl 
2):82–90.
 7. Bryan CP.  Ancient Egyptian medicine: the Papyrus 
Ebers [translation]. Chicago: Ares Publishers; 1974. 
p. 158–61.
 8. Brody HJ, Monheit GD, Resnik SS, Alt TH. A history 
of chemical peeling. Dermatol Surg. 2000;26:405–9.
 9. Mackee GM, Karp FL.  The treatment of post acne 
scars with phenol. Br J Dermatol. 1952;64:456–9.
 10. Eller JJ, Wolff S.  Skin peeling and scarification. 
JAMA. 1941;116:934–8.
 11. Fischer TC, Perosino E, Poli F, Viera MS, Dreno 
B, Cosmetic Dermatology European Expert Group. 
Chemical peels in aesthetic dermatology: an update 2009. 
J Eur Acad Dermatol Venereol. 2010;24(3):281–92.
 12. Khunger N.  Standard guidelines of care for chemi-
cal peels. Indian J Dermatol Venereol Leprol. 
2008;74(Suppl):S5–12.
 13. Yokomizo VMF, Benemond TMH, Chisaki C, 
Benemond PH. Peelings químicos: revisão e aplica-
ção prática. Surg Cosmet Dermatol. 2013;5(1):58–68.
 14. Nanda S, Grover C, Reddy BS.  Efficacy of hydro-
quinone (2%) versus tretinoin (0.025%) as adjunct 
topical agents for chemical peeling in patients of 
melasma. Dermatol Surg. 2004;30:385–8.
 15. Sarkar R, Bansal S, Garg VK.  Chemical peels for 
melasma in dark-skinned patients. J Cutan Aesthet 
Surg. 2012;5(4):247–53.
 16. Wang CM, Huang CL, Hu CT, Chan HL. The effect of 
glycolic acid on the treatment of acne in Asian skin. 
Dermatol Surg. 1997;23(1):23–9.
 17. Burns RL, Prevost-Blank PL, Lawry MA, Lawry TB, 
Faria DT, Fivenson DP. Glycolic acid peels for postin-
flammatory hyperpigmentation in black patients. A 
comparative study. Dermatol Surg. 1997;23(3):171–4.
 18. Lee SH, Huh CH, Park KC, Youn SW.  Effects of 
repetitive superficial chemical peels on facial sebum 
secretion in acne patients. J Eur Acad Dermatol 
Venereol. 2006;20(8):964–8.
 19. Takenaka Y, Hayashi N, Takeda M, et al. Glycolic acid 
chemical peeling improves inflammatory acne erup-
tions through its inhibitory and bactericidal effects on 
Propionibacterium acnes. J Dermatol. 2012;39:350–4.
 20. Erbil H, Sezer E, Taştan B, Arca E, Kurumlu 
Z.  Efficacy and safety of serial glycolic acid peels 
and a topical regimen in the treatment of recalcitrant 
melasma. J Dermatol. 2007;34(1):25–30.
 21. Grover C, Reddu BS.  The therapeutic value of gly-
colic acid peels in dermatology. Indian J Dermatol 
Venereol Leprol. 2003;69:148–50.
 22. Javaheri SM, Handa S, Kaur I, Kumar B. Safety and 
efficacy of glycolic acid facial peel in Indian women 
with melasma. Int J Dermatol. 2001;40(5):354–7.
 23. Sachdeva S.  Lactic acid peeling in superficial 
acne scarring in Indian skin. J Cosmet Dermatol. 
2010;9:246–8.
 24. Sharquie KE, Al-Tikreety MM, Al-Mashhadani 
SA. Lactic acid as a new therapeutic peeling agent in 
melasma. Dermatol Surg. 2005;31:149–54.
 25. Sharquie KE, Al-Tikreety MM, Al-Mashhadani 
SA. Lactic acid chemical peels as a new therapeutic 
modality in melasma in comparison to Jessner’s solu-
tion chemical peels. Dermatol Surg. 2006;32:1429–36.
 26. Roberts WE.  Chemical peeling in ethnic/dark skin. 
Dermatol Ther. 2004;17(2):196–205.
 27. Ahn HH, Kim IH.  Whitening effect of sali-
cylic acid peels in Asian patients. Dermatol Surg. 
2006;32:372–5.
 28. Grimes PE.  The safety and efficacy of salicylic 
acid chemical peels in darker racial-ethnic groups. 
Dermatol Surg. 1999;25(1):18–22.
 29. Lee HS, Kim IH. Salicylic acid peels for the treatment 
of acne vulgaris in Asian patients. Dermatol Surg. 
2003;29:1196–9.
• Jessner’s solution: adjuvant treatment 
for acne, pigmentary disorders, 
improvement of oiliness and texture of 
the skin, fine wrinkles, and pseudofol-
liculitis barbae.
• TCA: indications include acne scars 
and rejuvenation.
• Post-peeling complications occur more 
frequently in patients with a higher 
phototype and in larger depth peels.
• Post-inflammatory hyperpigmentation 
is the major complication that can be 
avoided with proper choice of agent, 
depth, and correct photoprotection.
• Other complications include erythema 
and edema, allergic reactions, toxicity, 
infections, scars, and demarcation 
lines, among others.
3 Tip Chapter: Peels for Ethnic Skin
38
 30. Khunger N, Sarkar R, Jain RK. Tretinoin peels versus 
glycolic acid peels in the treatment of Melasma in dark- 
skinned patients. Dermatol Surg. 2004;30(5):756–60.
 31. Kim SW, Moon SE, Kim JA, et al. Glycolic acid ver-
sus Jessner’s solution: which is better for facial acne 
patients? A randomized prospective clinical trial of split-
face model therapy. Dermatol Surg. 1999;25:270–3.
 32. Safoury OS, Zaki NM, El Nabarawy EA, et  al. A 
study comparing chemical peeling using modified 
Jessner’s solution and 15% trichloroacetic acid versus 
15% trichloroacetic acid in the treatment of melasma. 
Indian J Dermatol. 2009;54:41–5.
 33. Abdel-Mequid AM, Taha EA, Ismail SA. Combined 
Jessner solution and trichloroacetic acid ver-
sus trichloroacetic acid alone in the treatment of 
melasma in dark-skinned patients. Dermatol Surg. 
2017;43(5):651–6.
 34. Mangat DS, Tansavadti K, Garlich P. Current chemi-
cal peels and other resurfacing techniques. Facial 
Plast Surg. 2011;27(1):35–49.
 35. Chun EY, Lee JB, Lee KH. Focal trichloroacetic acid 
peel method for benign pigmented lesions in dark-
skinned patients. Dermatol Surg. 2004;30(4 Pt 1): 
512–6.
 36. Kalla G, Garg A,Kachhawa D. Chemical peeling – 
glycolic acid versus trichloroacetic acid in melasma. 
Indian J Dermatol Venereol Leprol. 2001;67:82–4.
 37. Costa A, Basile AVD, Medeiros VLS, Moisés TA, Ota 
FS, Palandi JAC. 10% thioglycolic acid gel peels: a 
safe and efficient option in the treatment of consti-
tutional infraorbital hyperpigmentation. Surg Cosmet 
Dermatol. 2010;2(1):29–33.
 38. Kontochristopoulos G, Platsidaki E.  Chemical 
peels in active acne and acne scars. Clin Dermatol. 
2017;35(2):179–82.
 39. Sarkar R, Garg V, Bansal S, Sethi S, Gupta 
C. Comparative evaluation of efficacy and tolerability 
of glycolic acid, salicylic mandelic acid, and phytic 
acid combination peels in melasma. Dermatol Surg. 
2016;42(3):384–91.
 40. Camacho FM.  Medium-depth and deep chemical 
peels. J Cosmet Dermatol. 2005;4(2):117–28.
 41. Marrero GM, Katz BE. The new fluor-hydroxy pulse 
peel. A combination of 5-fluorouracil and glycolic 
acid. Dermatol Surg. 1998;24(9):973–8.
 42. Teixeira SP, de Nascimento MM, Bagatin E, Hassun 
KM, Talarico S, Michalany N.  The use of fluor- 
hydroxy pulse peel in actinic porokeratosis. Dermatol 
Surg. 2005;31(9 Pt 1):1145–8.
 43. Parada MB, Yarak S, Gouvea LG, Hassun K, Talarico 
S, Bagatin E. “Blepharopeeling” in the upper eyelids: 
a nonincisional procedure in periorbital rejuvenation 
FA pilot study. Dermatol Surg. 2008;34:1435–8.
R. Lage
39© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_4
Blepharopeel
Laura Bariquelo Buratini and Sergio Talarico Filho
4.1 Materials
• A large number of different formulas of phe-
nol intended for peeling are available in the 
literature.
• The most commonly used is the Baker and 
Gordon formula, which consists of (Fig. 4.1):
 – Phenol USP 88%—3 ml
 – Liquid soap (Septisol®)—8 drops
 – Croton oil—3 drops
 – Distilled water—2 ml
• It should be prepared for immediate use only.
• All formulas include adjuvants to increase 
phenol penetration.
• Solutions with high concentrations of phenol 
cause rapid coagulation of skin proteins, 
translated clinically by immediate skin frost-
ing. The coagulated layer acts as a barrier, 
reducing skin permeability, thus interrupting 
phenol penetration and preventing phenol 
from reaching the reticular dermis. For this 
reason, solutions with high concentrations of 
phenol can produce more superficial peels 
than one could expect.
• Solutions at lower concentrations (15–20%), 
on the other hand, penetrate the skin more 
 easily, reach drainage routes, and are rapidly 
metabolized. Small amounts of free phenol 
acting for a short time may not be sufficient 
for good results. However, if large volumes 
of these solutions are applied in an attempt to 
correct this problem, the saturation of dis-
posal mechanisms increases the risk of 
toxicity.
• Croton oil (extracted from the plant Croton 
tiglium) has the capacity to increase phenol 
absorption by intensifying the inflammatory 
process.
• Septisol®, as a surfactant agent, reduces sur-
face tension, delaying phenol penetration and 
absorption and thus providing greater unifor-
mity in peeling.
L. B. Buratini (*) 
Laura Bariquelo Buratini Clinic, Botucatu, SP, Brazil 
S. T. Filho 
Talarico Clinic of Dermatology, São Paulo, SP, Brazil
4
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_4&domain=pdf
40
4.2 Methods and Techniques
Even in the case of application in a restricted 
area, with much lower risk of toxicity, the proce-
dure must be performed in a surgical center 
(which can be ambulatory with good ventilation 
to dissipate phenol vapors) and with the patient 
always monitored.
4.2.1 The Prepeeling
• Laboratory: Even when it is a localized appli-
cation restricted to the eyelid region:
 – Hepatic function
 – Renal function
 – Electrolyte dosage
 – Electrocardiogram
• Photography:
 – Face: front and oblique and profile on both 
sides.
 – Orbital region with eyes open and closed.
• Written consent post-information and 
guidelines:
 – Detailed guidelines on the procedure to 
be performed, including description of 
the evolution and aspect of the treated 
area that will be experienced by the 
patient and all the care that should be 
followed.
 – Post-informed consent should be obtained 
after complete clarification of the proce-
dure, possible intercurrences, risks, possi-
ble complications, and results that should 
be expected.
 – It is of fundamental importance that the 
relatives and other people of the patient’s 
conviviality are also prepared to support 
the evolution and to help the patient and the 
doctor.
• Skin preparation:
 – When peeling is applied in restricted/local-
ized areas, such as blepharopeel, skin 
 preparation is not mandatory as when per-
formed in the whole face but might be done.
 – Consists of previous use, for 3–4  weeks 
prior to the peeling, of products commonly 
recommended in protocols for home reju-
venation, such as retinoic acid, glycolic 
acid, vitamin C, kojic acid, etc. This may 
allow more uniform penetration of the 
chemical agent and decrease the risk of 
inflammatory hyperpigmentation by the 
use of bleaching agents.
• Antiviral therapy
• If the patient has a previous history of recur-
rent herpes simplex, prophylaxis with acyclo-
vir (400 mg orally every 8 h, starting 2 days 
before the procedure and maintained for a 
total of 5–7 days) must be done.
Destilled
Water
Phenol
USP 88% Croton oil Septisol
Fig. 4.1 Components 
of the Baker and 
Gordon formula
L. B. Buratini and S. T. Filho
41
4.2.2 The Peeling
• Degreasing:
 – Cleansing and disinfection with chlorhexi-
dine solution or water and alcohol in equal 
parts.
 – The skin is degreased with gauze soaked in 
acetone or ether, vigorously scrubbed, pro-
viding adequate cleaning and mild surface 
sanding that removes deposited debris on 
the skin.
 – This preliminary phase is essential to 
achieve best results. Phenol will not be able 
to penetrate ideally if the skin is not prop-
erly cleaned.
• Application technique:
 – The solution should be prepared at the time 
of starting the peeling and be stirred con-
tinuously to obtain the ideal homogeneous 
mixture of its components, since it is an 
unstable solution (Fig. 4.2).
 – The application should be made with a cot-
ton swab, which should be moistened in the 
solution with care, always completely 
removing the excess.
 – The application should be started at the 
deepest wrinkles that must be distended in 
order to achieve the most uniform distribu-
tion as possible, avoiding irregularities.
 – In the upper eyelids, the solution should be 
applied until the eyelid folds and in the lower 
eyelids, up to 2 mm from the tarsal border.
 – In the eyebrow area, the solution must be 
applied in the opposite direction in relation 
to the eyebrow hair.
• Dressing:
 – The peeling may or may not be occluded 
with tape. Several papers describe excel-
lent results with both techniques, each pre-
senting advantages and disadvantages.
 – Occlusion should be done with narrow 
strips of adhesive tape, which should be 
placed immediately after peeling applica-
tion. The strips should be short so that 
greater mobility and consequent greater 
adhesion are allowed. In the first layer, one 
or two extra strips may be applied so that 
the mask gains greater stability. All areas 
must be covered to avoid irregularities.
4.3 Clinical Follow-Up
• Almost immediately after the application, 
whitening of the skin is noted, which then pro-
gresses to pinkish hue and, subsequently, to 
grayish coloring (Fig. 4.3).
• Edema can be noticed in a few minutes, wich 
will gain great intensity, implying difficulty of 
ocular opening even after 48–72 h (Fig. 4.4).
• There is intense pain after application of the 
peeling solution, which stops after a few sec-
onds, due to the transient neurotoxic effect of the 
phenol. The pain returns after about half an hour, 
which remainsintense for more or less 8 h.
• Psychological comfort and psychological sup-
port should be offered to the patient the day 
after the procedure. The application of ice 
packs may play an auxiliary role in relieving 
the burning sensation and reducing edema.
Before stirring (non homogeneous solution) After stirring
Fig. 4.2 Freshly prepared solution
4 Blepharopeel
42
• Special attention should be given to the use of 
drugs that promote analgesia and the use of 
hypnotics to allow the patient to sleep.
• The tape, when applied, should be removed 
after 48 h, when it is usually practically loose 
due to the large amounts of exudate produced. 
The skin should be cleaned with sterile saline 
solution. There is no evidence that an earlier 
removal (24 h) of the tape cannot be made, if 
desired, because of the discomfort.
• The area should be washed three to five times 
daily with running water and soap. For com-
fort, this can be done by standing under the 
shower with warm water. It is essential that 
fibrin crusts (Fig. 4.5) are removed mechani-
cally at this stage and, if necessary, a topical 
fibrinolytic agent can be used.
• Antibiotic ointments may be used until com-
plete re-epithelialization. The risk of infection 
is always lower when you can successfully 
prevent the formation of scabs.
• The recommendation for the patient not to 
manipulate the skin inappropriately is vital for 
good healing.
• Between 7 and 10  days, complete re- 
epithelialization occurs.
• Intense erythema and great skin sensitivity 
remain for about 2–3 months (Fig. 4.6). The 
use of cosmetics that camouflage this aspect 
should be recommended, as well as the use of 
moisturizers, which give great comfort to the 
patient.
• Sun exposure must be avoided for 3 months 
after the peeling.
• Sunscreen should be used daily with rigor 
since complete reepithelialization has 
occurred, and it should be associated with 
accessories like sunglasses, caps, and hats.
Fig. 4.3 Immediate whitening
Fig. 4.4 Twenty-four hours after peeling Fig. 4.5 Large amount of fibrin
Fig. 4.6 Two months after peeling: intense erythema
L. B. Buratini and S. T. Filho
43
4.4 Before and After (Figs. 4.7, 
4.8, 4.9, 4.10 and 4.11)
Fig. 4.7 (a) Before; (b) 24 h after; (c) 4 days after; (d) 6 months after
a b
c d
Fig. 4.8 (a) Before; (b) 3 days after; (c) 2 months after
a b c
4 Blepharopeel
44
Fig. 4.9 (a) Before; (b) 6 months after
a b
Fig. 4.10 (a) Before; (b) 11 months after
a
b
a b
Fig. 4.11 (a) Before; (b) 18 months after
4.5 Side Effects, Complications, 
and Their Management
• Conjunctivitis
 – Usually chemically induced, caused by a pri-
mary irritant, not necessarily by direct contact 
with the peeling agent in the conjunctiva but 
due to evaporation and proximity of the eye-
ball to the area in which the product is applied.
 – There is often lacrimation and, sometimes, 
secretion.
 – We recommend cleaning with saline or 
boricated water and the use of antibiotic 
and corticosteroid eye drops.
L. B. Buratini and S. T. Filho
45
 – In general, it improves within 1–2  days 
without major repercussions.
• Pigmentation changes
 – Perhaps the most frequent of the possible 
complications, hyperpigmentation is usually 
transient and represents an excellent response 
to depigmenting and tretinoin treatment.
 – Phenol always leads to a permanent and 
generalized hypopigmentation in the 
treated area, caused by the permanent 
reduction of melanin synthesis by melano-
cytes. It is important to take this fact into 
account when selecting patients.
• Hypertrophic scars
 – Complication not very rare.
 – They occur within the first 3 months after 
peeling and are most common in isolated 
sites, particularly in the perioral region 
(Fig. 4.12).
 – They usually respond well to topical treat-
ment with corticosteroids and, if necessary, 
with intralesional infiltrations of triamcino-
lone (Fig. 4.13).
• Infections
 – They are not frequent.
 – They may be bacterial, fungal, or viral.
 – Avoiding the formation of crusts can help 
prevent this complication.
 – Complaint of intense pain after the first day 
should always remind the possibility of 
developing viral infection.
• Persistent ectropion
 – A mild ectropion occurs most often and is 
transient. It is due to intense cutaneous 
retraction and resolves within 1 month.
 – A more intense and persistent ectropion 
(Fig. 4.14) may occur more rarely, some-
times requiring surgical correction 
(Fig. 4.15).
 – A way to avoid this complication is to 
scrub the swab almost dry on the lower 
eyelids at the moment of peeling 
application.
 – In patients who have previous surgical 
inferior blepharoplasty, the risk/benefit of 
peeling should be considered in this 
region.
• Persistent erythema
The patient should be aware that the erythema 
may last for a period of about 90 days and may 
extend further in some cases.
Fig. 4.13 The same patient in Fig. 4.12, after two intral-
esional infiltrations of triamcinolone, plus three sessions 
of treatment with Intense Pulsed Light
Fig. 4.14 Persistent ectropion post-phenol blepharopeel
Fig. 4.15 Surgical correction of the ectropion
Fig. 4.12 Hypertrophic scar, 3 months after peeling
4 Blepharopeel
46
Bibliography
 1. Alt TH. Occluded Baker-Gordon chemical peel: review 
and update. J Dermatol Surg Oncol. 1989;15(9):980–93.
 2. Asken S.  Unoccluded Baker-Gordon phenol 
peels--review and update. J Dermatol Surg Oncol. 
1989;15(9):998–1008.
 3. Brody H.  Peeling profundo. In: Peeling químico e 
resurfacing. 2nd ed. Rio de Janeiro: Reichman & 
Affonso; 2000. p. 163–89.
 4. Deprez P.  Textbook of chemical peels: superficial, 
medium and deep peels in cosmetic practice. England: 
Informa Healthcare; 2007. p. 193–313.
 5. Fintsi Y. A novel, phenol-based peeling method resulting 
in improved safety. Am J Cosm Surg. 1997;14:49–54.
 6. Kligman AM, Baker TJ, Gordon HL. Long-term his-
tologic follow-up of phenol face peels. Plast Reconstr 
Surg. 1985;75:652–9.
 7. Landau M.  Deep chemical peels for photoaging. In: 
Tosti A, Grimes PE, de Padova MP, editors. Color atlas 
of chemical peels. Germany: Springer; 2006. p. 69–88.
 8. Lawrence N, Brody HJ, Alt TH. Chemical peeling. In: 
Coleman III WP, Hanke CW, Alt TH, Asken S, edi-
tors. Cosmetic surgery of the skin. 2nd ed. St. Louis: 
Mosby; 1997. p. 85–111.
 9. Park JO, Choi YD, Kim SW, Kim YC, Park 
SW. Effectiveness of modified phenol peel (Exoderm) 
on facial wrinkles, acne scars and other skin problems 
of Asian patients. J Dermatol. 2007;34:17–24.
Tip Box
• Patient choice: adequate psychological 
profile to pass safely and calmly through 
the postoperative period; low phototype.
• Post-peeling occlusion: we observed in 
our clinical practice very similar results 
with or without occlusion. Therefore, 
we have no longer used it.
• Formulation used: we use half amount 
of the croton oil (peeling penetration 
agent) proposed by Baker, and we have 
observed less post-peeling hypopigmen-
tation as well as low incidence of hyper-
trophic scars.
• Removal of fibrin: we advise the patient 
to apply a solution constituted of a glass 
of water with a spoon of white vinegar 
in a compress in the areas containing 
fibrin for 15 min before cleaning. This 
facilitates the removal of fibrin crusts 
that should be then achieved by gently 
scrubbing of the area with a gauze 
embedded in water with antiseptic soap.
• After cleaning, we advise the use of an 
ointment composed of fibrinolysin, 
deoxyribonuclease, and chlorampheni-
col in these areas. This procedure should 
be repeated at least three times a day.
L. B. Buratini and S. T. Filho
47© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_5
Cook Peel (70% Glycolic 
Acid + 70% Trichloroacetic Acid) 
for the Face
María del Pilar Del Río Navarrete Biot
5.1 Materials
• Topical anesthetic—while some authors con-
traindicateits use, as it can affect the frost 
observation [1], others recommend it [2]. In 
order to minimize pain and discomfort, we 
always use it.
• Alcohol or acetone—for degreasing
• A small fan or a skin cooler
• Gloves
• 70% glycolic acid gel
• 35% TCA solution
• Tap water or 10% bicarbonate solution—to 
neutralize the GA
• A gel mask to be used when the procedure is 
performed
• Petrolatum product or panthenol cream—to 
be used after the peeling (Fig. 5.1)
5.2 Methods and Techniques
• Medium-depth peeling is a four-step proce-
dure: pre-peel preparation, peeling itself, 
recovery phase, and maintenance phase [1].
• The pre-peel preparation begins at the initial 
consultation, when it is important to deter-
mine the patient’s expectations, Fitzpatrick 
skin type, and skin conditions [2].
• Patients with rosacea, atopic dermatitis, seb-
orrheic dermatitis, psoriasis, vitiligo, and 
active retinoid dermatitis are at a greater risk 
of having post-procedural complications.
• Fitzpatrick skin types IV to VI are not good 
candidates, as they have a greater risk of 
developing hyperpigmentation or 
hypopigmentation.
• Check the patient’s history for medium-depth 
or deep chemical peels within the last 
3 months, recent facial surgery with extensive 
undermining, treatment with isotretinoin 
within the last 6 months, hypertrophic scars, 
and keloids. These findings increase the risk 
of complications. Investigate a history of 
recurrent herpes simplex infection.
M. d. P. Del Río Navarrete Biot (*) 
Clínica Dermatológica Maria del Pilar Biot, 
Niterói, RJ, Brazil
5
Fig. 5.1 Materials used for the peeling
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_5&domain=pdf
48
• Never forget to ask about the patient’s work 
and social life, as there will be a downtime of 
at least 7 days.
• Begin the pre-peeling preparation 2–6 weeks 
before the procedure. These should include 
topical retinoid acid preparations, alpha 
hydroxy acids, hydroquinone, and other skin- 
lightening agents.
• The pre-peeling preparation is important to 
thin the stratum corneum, improve active 
agent penetration, accelerate healing, reduce 
the risk of post-inflammatory hyperpigmenta-
tion (PIH), and scarring. It contributes to 
achieving a more homogeneous effect and 
more predictable results [2, 3].
5.2.1 The Peeling Itself
• Remove all makeup, wash the face with a mild 
soap or a Syndet gel, and degrease with alco-
hol or acetone.
• Patients with a seborrheic, thick skin may ben-
efit from a gentle microdermabrasion, prior to 
the peeling.
• Apply 70% glycolic acid (GA) gel using 
gloved fingers and leave it for 2–4  min. Be 
careful not to exceed this time interval, and be 
ready to neutralize it when time is over or as 
soon as erythema appears.
• Neutralize the GA with tap water or with a 
10% sodium carbonate solution [4].
• After neutralizing the GA, dry the skin thor-
oughly before applying the TCA.
• Using a 7.5  ×  7.5-cm gauze, apply the 35% 
TCA solution. It can be done in two different 
ways: applying over the entire face at once, 
waiting a couple of minutes, and then applying 
another layer until the desired frost is achieved 
or segmentally, treating one anatomic region at 
a time and going to the next only when the final 
frost is achieved. In this way, the application 
begins on the forehead, going to the cheeks, the 
nose, the chin, and finally, the perioral and peri-
ocular regions [1, 4]. Do not forget to feather 
into the hairline and eyebrows [5].
• Be careful not to double treat the nasolabial 
folds when treating the cheeks and the perioral 
region. Within 1 cm of the lower lid eye lashes, 
use a small cotton swab to apply the TCA.
• During the procedure, dry the tears, as they 
may create stripes over the cheeks and carry 
the solution to the neck.
• TCA causes protein precipitation in the skin 
resulting in frost, which is a whitish hue of the 
skin. The depth of the peel can be correlated 
with the intensity of the frost. The develop-
ment of diffuse homogeneous erythema indi-
cates epidermal penetration. A white frost 
indicates coagulative necrosis of the papillary 
dermis and a gray–white frost, a coagulative 
necrosis of the reticular dermis [2, 4]
• The number of coats applied and the pressure 
used during the application are important fac-
tors influencing the depth of the peeling.
• There is no need to neutralize the TCA, as the 
protein coagulation induced limits its penetra-
tion and prevents systemic absorption [3].
• When the desired frost is achieved, cool com-
presses or a cold gel mask should be used to 
minimize the burning sensation.
• The patient should be sent home only after 
complete frost disappearance using a 
petrolatum- based product or panthenol cream. 
Be sure that all post-peeling instructions are 
clearly understood (Figs. 5.2 and 5.3).
Fig. 5.2 Final homogeneous white frost
M. d. P. Del Río Navarrete Biot
49
5.3 Clinical Follow-Up
• At home, the patient should wash the face 
twice daily with a mild soap or a Syndet gel. 
Dry gently without rubbing, and apply the pet-
rolatum product or panthenol cream at least 
two times a day or as many times as needed to 
feel comfortable.
• On the day of the procedure, there will be just 
edema and erythema. During the next 2 days, 
the skin will be dark and extremely dry, with 
an aggravation of all the spots and rhytides.
• By the third day, the skin begins to crack and 
desquamate at the more dynamic areas of the 
face, beginning at the perioral region. By that 
day, the edema will be probably gone.
• Shedding continues from the fourth until the 
seventh day, when it will be complete. The last 
areas to peel will be the pre-auricular region 
and the hairline.
• The petrolatum or panthenol cream should be 
used until the third day, when the shedding 
begins, and a non-comedogenic moisturizer 
can be prescribed.
• The use of sunscreen during the first days of 
post-peeling is difficult and uncomfortable, 
but it is recommended whenever the patient 
has to leave home during daylight hours. In 
this case, the use of chemical-free products is 
safer, minimizing the risk of contact 
dermatitis.
• Prophylactic treatment for herpes simplex 
infection with valacyclovir 500 mg twice daily 
or acyclovir 400 mg three times a day should 
be prescribed to all patients, beginning 1 or 
2 days before the peeling and maintained for 
10–14 days [2, 6].
• When the re-epithelialization is complete and 
skin appearance is back to normal, the patient 
can restart the treatment used in the preparation 
phase. Sun exposure has to be avoided for at 
least 6 weeks [4].
• The patient will return for consultation on the 
seventh day post-procedure, and until then a 
daily phone call is recommended and sending 
selfies is encouraged.
• Generally, due to the level of injury and con-
tinued clinical improvement, one single 
medium-depth peel is enough. However, if 
necessary, it can be repeated after 3  months 
(Figs. 5.4, 5.5, 5.6, and 5.7).
Fig. 5.3 Final homogeneous white frost
Fig. 5.4 Third day post procedure
5 Cook Peel (70% Glycolic Acid + 70% Trichloroacetic Acid) for the Face
50
Fig. 5.5 Third day post procedure. Desquamation begin-
ning by the perioral region
Fig. 5.6 Fourth day post peeling
Fig. 5.7 Fourth day post peeling
M. d. P. Del Río Navarrete Biot
51
5.4 Before and After (Figs. 5.8, 
5.9, 5.10, and 5.11)
Figs. 5.8 and 5.9 Before treatment. After two medium depth peelings
Figs. 5.10 and 5.11 Before treatment. After two medium depth peelings. Complete clearance of the forehead 
lentigines
5 Cook Peel (70% Glycolic Acid + 70% Trichloroacetic Acid) for the Face
52
5.5 Side Effects, Complications, 
and Their Management
• Complications can occur during or post proce-
dure. Intraprocedural complications are com-
monly due to improper technique or problems 
with the chemical agent used. Post-procedural 
complications are the result of inadequate care 
during healing,contact dermatitis, and local 
infections. A correct selection of the patient 
and the peeling agent and a good technique 
are essential for minimizing the occurrence of 
complications.
• The most feared intraprocedural complication 
is ocular accidents, and to avoid them, some 
safety rules should be followed. Sit the patient 
in a confortable position with eyes closed. 
Keep the container with the peeling agent on 
the side of the patient to avoid inadvertent 
dropping. Always have appropriate eye rinse 
solutions ready to use in case of unintended 
eye exposure to the chemical agent. 
Specifically, saline is used to dilute TCA and 
bicarbonate or water to neutralize GA [2, 4].
• Post-inflammatory hyperpigmentation (PIH) 
remains the most common complication, 
especially in darker skin types [6]. It can be 
treated with retinoids, alpha hydroxy acids 
(AHA), hydroquinone, and other skin- 
lightening agents. If necessary, superficial 
peelings can be done. Avoiding sun exposure 
in the pre-procedural and post-procedural 
phases and preparing the skin with retinoids, 
AHA, hydroquinone, and other bleaching 
agents for at least 2 weeks before peeling and 
restarting this treatment as soon as possible 
after re-epithelialization will diminish the 
chances of developing hyperpigmentation.
• Although rare after medium-depth peelings, 
hypertrophic scarring is another possible 
complication, and when it occurs, it is usu-
ally seen along the mandibular and perioral 
regions. To prevent this complication, any 
area of persistent erythema must be treated 
with topical steroids [5]. For a medium-
depth peel, the erythema should disappear 
in 15–30  days, and persisting erythema 
beyond this time is a predictor of potential 
scarring [6].
• Herpes simplex infection can occur after 
medium peelings and should be treated with 
antiviral agents. Prescribing valacyclovir or 
acyclovir to all patients, as previously 
described in this chapter, will reduce the risk 
of this complication.
• Bacterial infections are rare in TCA peels, as 
this agent is bactericidal [6]. The use of thick 
occlusive ointments, prolonged use of topical 
steroids, and poor wound care are predispos-
ing factors.
• Contact dermatitis, milia, and areas of hypopig-
mentation, where the peel was deeper than 
planned, are other possible complications.
• Frequent return visits and daily phone calls 
are recommended to closely monitor the heal-
ing evolution. Give the patient your personal 
cellphone number and encourage him to send 
selfies. Complications may occur, but early 
diagnosis and immediate treatment are essen-
tial for a good resolution.
Tip Box
• Be familiar with the procedure and the 
peeling agents you are using.
• Work in a safe manner. Keep a bottle of 
thermal water and saline by your side 
during the application.
• Never pass the peeling agent container 
over the patient’s head.
• GA complications are related to exposure 
time. So, when applying the GA gel, pay 
attention to the watch to control exposure 
time and to minor changes on the skin.
• TCA complications are related to the 
product concentration, pressure during 
the application, and number of coats. 
So, when applying the TCA solution, 
squeeze the gauze or the cotton swab 
tip, to prevent product excess, and wait a 
couple of minutes between the layers.
• Take time to explain your patient the 
post-procedure evolution.
• Be sure that your instructions are clearly 
understood.
• Keep in touch with your patient, espe-
cially during the first 72 h.
M. d. P. Del Río Navarrete Biot
53
References
 1. Pelletier-Louis M-L.  Peelings chimiques et prise 
en charge du vieillissement cutané. Ann Chir Plast 
Esthet. 2017;62:520–31.
 2. Jackson A.  Chemical peels. Facial Plast Surg. 
2014;30:26–34.
 3. Truchuelo M, Cerdá P, Fernández LF.  Chemical 
peeling:a useful tool in the office. Actas Dermosifiliogr. 
2017;108:315–22.
 4. Fabbrocini G, Padova MP, Tosti A. Chemical peels: 
what’s new and what isn’t new but still works. Facial 
Plast Surg. 2009;25:329–36.
 5. Coleman H, Futrell J.  The glycolic acid trichloro-
acetic acid peel. J Dermatol Surg Oncol. 1994;20: 
76–80.
 6. Nikalji N, Godse K, Sakhiya J, et al. Complications 
of medium depth and deep chemical peels. J Cutan 
Aesthet Surg. 2012;5:254–60.
5 Cook Peel (70% Glycolic Acid + 70% Trichloroacetic Acid) for the Face
55© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_6
Cook Peel (70% Glycolic Acid 
+40% Trichloroacetic Acid) 
for Extra-Facial Areas
Carlos Gustavo Wambier
6.1 Materials
• Degreasing agent: standardized acetone–etha-
nol (3:1 mixture) or 70% ethanol.
• Applicators: 4 × 4 gauzes (Fig. 6.1).
• Peeling agents: large stock bottles of GA 70% 
(cosmetic grade) and TCA 40%. Pour the con-
tents of the acids in two different shot glasses 
or beaker glasses with units of measure. For 
patients with atrophic skin, the author recom-
mends TCA 30–35% instead of TCA 40% 
(Fig. 6.2).
• Neutralizing agent: sodium bicarbonate solu-
tion 10% in a large glass. Dry disposable soft 
towels are soaked in this cup and are ready to 
be used.
• Post-peeling regimen: Vaseline and 
sunscreen.
6.2 Methods and Techniques
• Degreasing: the importance of removal of all 
make-up, sebum, beard, topical anesthetic, 
and sunscreen before any chemical peel is 
unquestionable. The physician scrubs the 
body surface to be treated with semi-soaked 
gauze pads.
• Peeling solution application: the left hand is 
used for GA 70% solution and the right hand 
for TCA 40% solution (the dominant hand for 
TCA); if the author is left handed, he would 
change the disposition of the shot glasses and 
bowls as well in the table. Fold gauzes in half 
C. G. Wambier (*) 
Department of Dermatology, Yale University School 
of Medicine, New Haven, CT, USA
e-mail: carlos.wambier@yale.edu
6
Fig. 6.1 Materials. Two shot glasses for soaking 4 × 4 
gauzes, folded in half twice. After excess solution is 
removed from the gauze, the saturated gauze is placed in 
small bowls (red plastic for glycolic acid and ceramic for 
TCA). A large glass containing three soft towels is placed 
in the right side of the picture. These compressed “magic 
towels” are dry and compressed in individual packages 
(large container in the back). After each area is done, 
everything is refilled. Gloves used for neutralization 
(assistant) are changed after each neutralization to avoid 
cross-contamination of the neutralizing solution
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_6&domain=pdf
mailto:carlos.wambier@yale.edu
56
twice, soak, and squeeze to remove excess 
solution. Place in each bowl one saturated 
gauze of each solution for every 5% of body 
surface area. Begin with GA, fast application 
to cover the whole designated area, throwing 
away semi-dry gauzes, and changing to a new 
saturated gauze. As soon as the process is 
over with GA, start the application of TCA 
with the dominant hand, starting from the 
same point and covering exactly the same 
area, changing the gauzes in the same 
position.
• Endpoint visualization: the surgeon waits for 
the endpoint. For higher phototypes, above 
Fitzpatrick III, due to risk of post- inflammatory 
hyperpigmentation, in the first session, the 
endpoint is erythema. For lower phototypes, 
the endpoint is speckled frosting. Usually, ery-
thema is achieved at 2 min after TCA applica-
tion, and frosting starts in 3  min. Once the 
solution is dry, wait at least 3 min before using 
another application of TCA, which is always 
less saturated than the first application 
(Figs. 6.3 and 6.4).
• Focal treatment: if there is a specific goal for 
the treatment session, for example, to remove 
actinic keratosis, this waiting time is the 
Fig. 6.2 Application of 40% trichloroacetic acid solution 
with the dominant hand as soon as 70% glycolic acid solu-
tion has been applied with theother hand. Watch uniform 
layer of solution
Fig. 6.3 Endpoint observation at 2 min. Actinic keratoses 
presented early frosting, which is expected; this patient’s 
desired endpoint at the first session was erythema, with 
speckled frosting over hand melanoses with denser frost-
ing over actinic keratoses
C. G. Wambier
57
time to perform local treatments, such as 
cryotherapy for hypertrophic keratoses or 
cotton- tipped applicator peel with 40% TCA 
with increased pressure and passes, over 
superficial keratoses, to achieve uniform 
frosting.
• Neutralization: once the endpoints are 
achieved, the area treated is dried with a gauze 
(if still wet) and subsequently neutralized with 
soft towels saturated in 10% bicarbonate solu-
tion by the assistant. Three disposable towels 
are necessary for each limb, passing all tow-
els at the whole area, starting with the area 
where there is increased frosting (hot spots) 
(Fig. 6.5).
• Post-peeling regimen: a thick layer of 
Vaseline is applied to the peeled areas as 
soon as the desired chemoabrasion end-
points were achieved. The patient is 
instructed to use broadband sunscreen over 
the Vaseline layer twice a day if the skin 
needs to be sun-exposed, otherwise, only 
Vaseline (Fig. 6.6).
6.3 Clinical Follow-Up
• There is pain after 2 min of TCA application, 
which usually lasts until complete frosting or 
erythema is achieved. Neutralization stops the 
pain almost instantly.
• The skin becomes dry after about 1  week for 
limbs and 3 days for the neck and chest. The cor-
neal layer becomes thick and darker after about 
10 days, when it starts to peel, very slowly. For 
the hands and feet, expect about 3–4 weeks for 
peeling to start, while the shoulders, chest, and 
neck usually peel after about 2 weeks (Fig. 6.6). 
It is very important to avoid pulling or scratching 
the dark peeling skin because it protects deeper 
layers from light and chemicals. Moisturizing 
with either Vaseline or fragrance-free hypoaller-
genic creams is fundamental to avoid fissures.
• Vesicles, blisters, and oozing are not expected; 
if any of those signs are present during follow-
 up, diagnosis must be made of either herpes 
reactivation, bacterial infections, or eczema-
tous reactions.
Fig. 6.4 Endpoint observation at 4 min after the solution 
was dry revealed no frosting over hand melanoses and 
superficial pigmented seborrheic keratoses. This patient’s 
desired endpoint at first session was erythema, with 
speckled frosting over hand melanoses with denser frost-
ing over actinic keratoses. Another focal layer of 40% tri-
chloroacetic acid was applied to the melanoses
Fig. 6.5 Neutralization with 10% sodium bicarbonate 
after erythema endpoint was achieved (about 4  min). 
Three applications of 10% are performed to ensure com-
plete neutralization and removal of the acids
6 Cook Peel (70% Glycolic Acid +40% Trichloroacetic Acid) for Extra-Facial Areas
58
6.4 Before and After (Figs. 6.7, 
6.8, 6.9, and 6.10)
Fig. 6.7 Two-week follow-up of Cook’s peel applied to 
the forearms and hands of a patient with multiple sebor-
rheic keratoses and lentigines. This patient was peeled 
with 70% glycolic acid followed by 35% trichloroacetic 
acid with a large feathering area due to phototypes III–IV 
and concerns of demarcation marks to the arms
Fig. 6.8 Two-month follow-up of Cook’s peel applied to 
the forearms and hands with 70% glycolic acid followed 
by 35% trichloroacetic acid of a patient with multiple seb-
orrheic keratoses and lentigines; skin texture improved, 
superficial actinic keratoses were removed, and most of 
the melanoses peeled off. The patient was scheduled for a 
second session after one more month
Fig. 6.6 Two-week follow-up. Pinching the skin reveals the thick corneal layer which will peel in about 2 more weeks. 
The areas which achieved frosting are darker (melanoses)
C. G. Wambier
59
Fig. 6.9 Before and after 2 months of a single Cook’s peel with 70% glycolic acid, followed by 40% trichloroacetic 
acid
Fig. 6.10 Before and after 4 months of two Cook’s peels in the dorsal hands with 70% glycolic acid followed by 40% 
trichloroacetic acid
6 Cook Peel (70% Glycolic Acid +40% Trichloroacetic Acid) for Extra-Facial Areas
60
6.5 Side Effects, Complications, 
and Their Management
• Post-inflammatory hyperpigmentation: the 
most common side effect of chemical peels in 
general. If erythema endpoint is respected for 
higher phototypes, this adverse reaction is 
minimized, along with the results; therefore, 
multiple treatments are recommended.
• Infection: any oozing or edema must be treated 
with topical steroids, along with systemic 
antibiotics, especially in the lower limbs, 
where erysipelas is not rare. This peel is 
 contraindicated in patients with venous insuf-
ficiency or lymphedema.
Tip Box
• Hands-on training mandatory for acquir-
ing the correct technique, as in any peel.
• In patients with atrophic skin or higher 
phototypes, use 30–35% TCA instead of 
40% to minimize the adverse effects of 
hotspots.
• Understand the limitations of extra-facial 
resurfacing treatments. Expect multiple 
treatments with safer interventions.
• Realistic expectations and patience 
must be taught to every patient undergo-
ing body peels.
C. G. Wambier
61© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_7
Fluor-Hydroxy Pulse Peel for Face
Erica Monteiro
7.1 Materials [1–5]
7.1.1 Reagents
 – Correctly labeled peeling agents in various 
concentrations: Jessner’s solution or 70% gly-
colic acid (GA) gel and 5% 5-fluorouracil 
(5-FU) propylene glycol emulsion.
 – Alcohol and/or acetone to clean and degrease 
the skin.
 – Syringes filled with normal saline for irriga-
tion of the eyes in case of accidental spillage.
 – Neutralizing solutions: only for glycolic acid 
peel.
7.1.2 Equipment (Fig. 7.1)
 – Glass cup or beaker in which the required 
agent is poured.
 – Head band or cap for the patient.
 – Gloves.
 – Cotton-tipped applicators or swab sticks.
 – 2″ × 2″ cotton gauze pieces.
7.2 Methods and Techniques
7.2.1 Patient Selection
The success of a chemical peel depends on a 
careful selection of patients and individualization 
of the treatment.
Men or women with hyperkeratotic AK target 
lesions of moderate/severe intensity are eligible 
for the treatment.
7.2.2 Technique Using Glycolic Acid 
Peel (Standard Fluor-hydroxy 
Pulse Peel for the Face)
 – At first, the patient’s skin is cleaned (by 
 impregnated cotton with 70% ethanol and/or 
acetone).
 – In the next step, the solution of 70% glycolic 
acid gel is applied on the patient’s face with a 
cotton applicator.
 – The forehead, the sides of the face and cheeks, 
chin, and nose are impregnated (Fig. 7.3). The 
eyes, nostrils, mouth, ears, and mucosa must 
be avoided.
 – After 3–5 min, the glycolic acid is neutralized 
with water or normal saline.
E. Monteiro (*) 
Department of Humanities and Medical Sciences, 
Federal University of São Paulo (UNIFESP), 
São Paulo, SP, Brazil
e-mail: erica@dermatologia.com.br
7
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_7&domain=pdf
mailto:erica@dermatologia.com.br
62
 – Finally, 0.5% 5-FU is full face applied. The 
eyes, nostrils, mouth, ears, and mucosa must 
be avoided.
 – The treatment can be continued once a week 
or every 2 weeks, for 4–8 weeks.
7.2.3 Technique Using Jessner’s 
Solution (Alternative Fluor- 
hydroxy Pulse Peel 
for the Face)
 – At first, the patient’s skin is cleaned (by 
impregnated cotton with 70% ethanol and/or 
acetone).
 – In the next step, Jessner’s solution is applied 
on the patient’s face with a cotton 
applicator.
 – The forehead, the sides of the face and cheeks, 
chin, and nose are impregnated (Fig. 7.2). The 
eyes, nostrils, mouth, ears, and mucosa must 
be avoided.
 – Neutralization is not necessary.
 – Finally, 0.5% 5-FU is full face applied. The 
eyes,nostrils, mouth, ears, and mucosa must 
be avoided.
 – The treatment can be continued once a week 
or every 2 weeks, for 4–8 weeks.
3
2
5
9
7
6
1
48
Fig. 7.1 Materials used for the fluor-hydroxy pulse peel. 
(1) Alcohol-based solution of 30% salicyclic acid, (2) 
alcohol and/or acetone to clean and degrease the skin, (3) 
cold water, (4) syringes filled with normal saline for irri-
gation of the eyes, in case of accidental spillage, (5) cap 
for the patient, (6) gloves, (7) cotton-tipped applicators or 
swab sticks, (8) cotton gauze pieces, (9) ice for cooling
1
6
5
2
4
3
Fig. 7.2 Cosmetic units to treat – First, protect the eye 
area (6). Apply the chemical peel solutions following the 
below (1)–(5) cosmetic area. Cosmetic units: (1) forehead, 
(2) the sides of the face and cheeks, (3) chin, (4) peri 
buccal, (5) nose, (6) protect the eye area
E. Monteiro
63
7.3 Clinical Follow-Up
7.3.1 Prepeeling Preparation 
(Table 7.1)
 – For optimal results, preparation of the skin in the 
weeks before the procedure is very important.
 – Topical retinoic acid preparations used daily 
for 3–6 weeks prior to the procedure may cre-
ate better and more even penetration of the 
peeling solution in sebaceous and hyperkera-
totic skins.
 – Standard photography and informed consent 
should always be obtained before the proce-
dure for all types of peelings.
 – Generally, it is not necessary to discontinue 
use of any of the patient’s medications 
including anticoagulants, aspirin, or nonste-
roidal anti-inflammatory or antihypertensive 
drugs.
 – According to our experience with superficial 
peeling, smoking does not have any adverse 
effect on post-peel healing or on the extent of 
the results.
Table 7.1 Pre- and post-fluor-hydroxy pulse peel recommendations [1–7]a
Considerations Benefits/recommendations
Pre
(at least 
2–4 weeks 
prior to the 
procedure)
Post
(immediate)
Post
(long after 
complete 
reepithelization)
Priming Reduces wound healing time, facilitates 
uniform penetration, detects intolerance 
to any agent, enforces patient 
compliance, and reduces the risk of 
complications
+
Infections Control any active infection or 
dermatoses
In patients with history of herpes simplex 
posted for medium-depth and deep peels, 
antiviral therapy with acyclovir or 
famciclovir is recommended, beginning 
2 days prior to the procedure and 
continued for 7–10 days until complete 
reepithelization
+ + +
Photoaging Topical retinoids, alpha hydroxy acids + − +
Post-inflammatory 
hyperpigmentation
Topical retinoids, hydroquinone, alpha 
hydroxy acids, vitamin C
+ − +
Photoprotection Broad-spectrum sunscreens and clothes + + +
Moisturization + + +
Fast healing Tretinoin 0.025% + − +
(after 
reepithelization)
Maintenance
(agents which are 
likely to be used in 
postprocedure 
maintenance)
Tretinoin 0.025%, glycolic acid 6–12%, 
5-FU
+
(after 
reepithelization)
aTretinoin is known to reduce healing time after resurfacing. The choice of the priming agent depends on the individual 
physician’s preference and individualized patient requirements
7 Fluor-Hydroxy Pulse Peel for Face
64
7.4 Before and After: 
Illustrations (Fig. 7.3)
Fig. 7.3 Before and after fluor-hydroxy pulse peel, three sessions, every 2 weeks
7.5 Side Effects, Complications, 
and Their Management
• Intense scaling.
• Xerosis.
• Erythema.
• Contact dermatitis.
• Small ulcers.
• Post-inflammatory hyperchromia.
7.5.1 Post-Peeling 
Recommendations (Table 7.1) 
[1–7]
 – The goal of a chemical peel is to cause the 
outer layer of the skin to peel and flake, reveal-
ing the fresh, smooth layer underneath.
 – Patients will experience some level of dryness 
and flaking for 2–5 days after treatment.
 – During this time of dryness and flaking, their 
skin is more sensitive (more redness and sting-
ing), and they cannot use vitamin C, retinol, 
avobenzone, glycolic acid, and lactic acid.
 – In this 2–5-day period, using a soothing gel or 
mask helps calm and soothe the skin. Other 
great options to use in this postprocedure time 
period are heparan sulfate and hyaluronic acid.
 – Patients should be advised to stay out of sun 
and to avoid picking at dry, flaking skin.
 – Exfoliating scrubs and other facial brushes 
and other forms of friction, including 
 microdermabrasion, should be avoided during 
the healing process.
 – Avoid any products with hydroxy acids, reti-
nol, and 5-FU until the skin barrier has been 
restored.
 – Use calming skincare products with anti- 
inflammatory ingredients such as green tea, 
argan oil, and chamomile to help alleviate any 
stinging or redness while the skin recovers.
E. Monteiro
65
References
 1. Marrero GM, Katz BE. The new fluor-hydroxy pulse 
peel. A combination of 5-fluorouracil and glycolic 
acid. Dermatol Surg. 1998;24(9):973–8.
 2. Teixeira SP, de Nascimento MM, et  al. The use of 
fluor-hydroxy pulse peel in actinic porokeratosis. 
Dermatol Surg. 2005;31(9 Pt 1):1145–8.
 3. Bagatin E, Teixeira SP, et al. 5-Fluorouracil superfi-
cial peel for multiple actinic keratoses. Int J Dermatol. 
2009;48(8):902–7.
 4. Guimarães CO, Miot HA, Bagatin E.  Five percent 
5-fluorouracil in a cream or for superficial peels in the 
treatment of advanced photoaging of the forearms: a 
randomized comparative study. Dermatol Surg. 2014 
Jun;40(6):610–7.
 5. Simon JC, Dominicus R, et  al. A prospective ran-
domized exploratory study comparing the efficacy of 
once-daily topical 0.5% 5-fluorouracil in combination 
with 10.0% salicylic acid (5-FU/SA) vs. cryosurgery 
for the treatment of hyperkeratotic actinic keratosis. J 
Eur Acad Dermatol Venereol. 2015;29(5):881–9.
 6. Monteiro EO. Acne e fotoproteção. RBM. 2009;66(6): 
6–9. Edição Especial Dermatologia link: http://
www.moreirajr.com.br/revistas.asp?fase=r003&id_ 
materia=4083.
 7. Monteiro EO.  Filtros solares e fotoproteção. RBM 
Esp Dermatol Cosm. 2010;67:5–18.
Tip Box
• To ensure the best outcome from fluor- 
hydroxy pulse peel, patient education is 
crucial.
• Retinoids should be used 2–3 times 
prior to procedures to speed healing.
• Retinoids should not be used after the 
procedure until reepithelization has 
occurred.
• Standard photography and informed 
consent should always be obtained 
before the cosmetic procedures.
• The fluor-hydroxy pulse peel applied in 
a pulse dose regimen not only provides 
cosmetic improvement but, more impor-
tantly, has a therapeutic effect on ablat-
ing premalignant AKs.
7 Fluor-Hydroxy Pulse Peel for Face
http://www.moreirajr.com.br/revistas.asp?fase=r003&id_materia=4083
http://www.moreirajr.com.br/revistas.asp?fase=r003&id_materia=4083
http://www.moreirajr.com.br/revistas.asp?fase=r003&id_materia=4083
67© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_8
Fluor-Hydroxy Pulse Peel 
for Extra- Facial Areas
Maria Paulina Villarejo Kede 
and Bruna Sabatovich Villarejo Iosifovich
8.1 Materials
A 5% 5-FU solution in propylene glycol is used 
along with Jessner’s solution (salicylic acid 14 g, 
resorcin 14  g, lactic acid 14  g, ethanol qsp). 
Salicylic acid is photosensitive, and lactic acid 
absorbs the water in the air, so the solution is sen-
sitive to light and air. Its mechanism of action is 
based on the keratolytic properties of salicylic 
acid and resorcinol and on the action of epider-
molysis of lactic acid. The penetration depends 
on the number of layers and can reach average 
peelings. It causes burns and may or may not be 
removed with water. It can be performed on the 
face and in extra-facial areas, but for the risk of 
salicylism, evaluate the extent to be treated. It can 
be applied evenly with gauze or cotton. Reapply 
new layer after 3 or 4 min. Remove crystals of 
salicylic acid with water. the glycolic acid 70% 
gel (the highest concentration of glycolic acid is 
70% and the solutions are made with water or the 
combination of water, alcohol, and propyleneglycol) is used. It is an alpha hydroxy acid found 
in sugar cane or synthesized from formaldehyde. 
It has a variable penetration and can penetrate 
more in sensitive areas, being little recommended 
for medium, deep, and combined peels. The pen-
etration is dependent on the pH, number of lay-
ers, and time of application. The application can 
be made with gauze or gloved fingers quickly and 
evenly. The applicator should remain in the room, 
and the appearance of erythema, which is the 
endpoint, should be observed and neutralized. 
Neutralization is mandatory and can be done 
with 10% sodium bicarbonate solution.
8.2 Methods and Techniques
The author prefers the combination of 5-FU to 
Jessner’s solution to glycolic acid. It is a superfi-
cial and combined peeling in which a solution of 
5-FU 5% in propylene glycol is applied after 
Jessner’s solution. Apply a layer of Jessner’s 
solution gauze or cotton in a uniform way. 
Reapply the new layer after 3 or 4 min. Remove 
crystals of salicylic acid with water. After a 5-min 
interval, a 5% 5-FU solution layer is applied in 
gloved-fingers propylene glycol, remaining on 
the skin for 12 h, depending on the tolerability. 
After the interval of 12 h, it is advised to remove 
the peeling in the domicile with water and neutral 
soap and the application of a Vaseline cream and 
photoprotection. The treatment is performed in 
eight pulses, and the interval between sessions 
can be weekly, biweekly, or monthly, depending 
on the tolerability of the patient. It is an effective, 
M. P. V. Kede (*) 
Private Clinic, Rio de Janeiro, RJ, Brazil 
B. S. V. Iosifovich 
Federal University of Rio de Janeiro, 
Rio de Janeiro, RJ, Brazil
8
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_8&domain=pdf
68
low-cost, and well-tolerated peeling for treatment 
of actinic keratoses on the face and in extra-facial 
areas. When it comes to extensive body areas, 
staggered intervals between sessions should be 
performed to minimize the risk of toxic compli-
cations depending on the agent used. Treatment 
is ideal until complete bleaching of the lesions. 
Hypertrophic lesions should be treated with other 
procedures prior to or between intervals. 
Squamous cell carcinoma should be excluded. Its 
main indication is the treatment of moderate-to- 
severe photoaging with multiple actinic keratoses 
and correlated conditions. Katz described the 
fluor-hydroxy pulse peel for treatment of multi-
ple actinic keratoses as a superficial and com-
bined peeling in which a solution of 5-FU 5% in 
propylene glycol is applied after Jessner’s solu-
tion and compared it to the isolated use of 
Jessner’s solution, in eight weekly pulses. 
Efficacy was assessed by counting lesions and 
photographs. At 6 months follow-up, the differ-
ence was significant, and the combined peeling 
produces.
8.3 Follow-Up at the Clinic 
(Figs. 8.1, 8.2, 8.3, and 8.4)
Figs. 8.1 and 8.2 Application of three layers of solution and after 5 min, application of one layer of 5-FU solution in 
the neck and breastplate
Figs. 8.3 and 8.4 Skin peeling after 4 days of the combined peeling of Jessner’s solution and 5-FU
M. P. V. Kede and B. S. V. Iosifovich
69
Figs. 8.5 and 8.6 Pre- and post-eight fortnightly sessions of combined peeling of Jessner’s solution and 5-FU on 
breastplate
8.4 Before and After (Figs. 8.5, 
8.6, 8.7, 8.8, 8.9, and 8.10)
Figs. 8.7 and 8.8 Pre- and post-eight fortnightly sessions of combined peeling of Jessner’s solution and 5-FU on 
breastplate
8 Fluor-Hydroxy Pulse Peel for Extra-Facial Areas
70
Figs. 8.9 and 8.10 Pre- and post-eight fortnightly sessions of combined peeling of Jessner’s solution and 5-FU on 
breastplate
8.5 Side Effects, Complications, 
and Their Management
Allergic reactions (less than 0.1%), systemic tox-
icity (not done in very extensive areas by resor-
cinol and salicylic acid), infection, and persistent 
erythema, by use of Jessner’s solution, along 
with irritant dermatitis and 5-FU discomfort are 
observed [1, 2, 3–7], which must be treated with 
symptom-oriented products in accordance with 
each kind of side effect observed.
References
 1. Bagatin E, Hassun KM, Teixeira SP, Talarico S. 
Systematic review of chemical peelings. Surg Cosmet 
Dermatol. 2009;1(1):37–46.
 2. Brody HJ, Monheit GD, Resnik S, Alt TH.  A his-
tory of chemical peeling. Dermatol Surg. 2000; 
26:405–9.
 3. Kede MPV, Sabatovich O. Dermatologia Estética. São 
Paulo: Ed Atheneu; 2015.
 4. Monheit GD.  Chemical peels. Skin Therapy Lett. 
2004;9:6–11.
 5. Katz BE. The fluor-hydroxy pulse peel: a pilot evalu-
ation of a new superficial chemical peel. Cosmet 
Dermatol. 1995;8:24–30.
 6. Marrero GM, Katz BE. The new fluor-hydroxy pulse 
peel. A combination of 5-fluorouracil and glycolic 
acid. Dermatol Surg. 1998;24:973–8.
 7. Teixeira SP, Nascimento MM, Bagatin E, et  al. The 
use of fluor-hydroxy pulse peel in actinic porokerato-
sis. Dermatol Surg. 2005;31:1145–8.
Tip Box
• The penetration of this peel depends on 
the number of layers
• To remove the peel after 12 hours of its 
application on the skin.
• On average, eight peel pulses are indi-
cated and the interval between sessions 
a be weekly, biweekly, or monthly, 
depending on the tolerability of the 
patient
• Side effects must be treated with symp-
tom-oriented products in accordance 
with each kind of side effect observed
M. P. V. Kede and B. S. V. Iosifovich
71© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_9
Genital Bleaching Peel
Adriana Awada
9.1 Materials
• Spectra laser (Q-switched Nd/Yag laser; 
Lutronic Co., Gyeonggi-Do, Korea) (Fig. 9.1)
• Cool masks
• Bleaching cream Dermamelan (Mesoestetic 
Inc., Viladecans, Barcelona, Spain) (Fig. 9.2)
A. Awada (*) 
Adriana Awada Clinic of Dermatology, 
Santo André, SP, Brazil 
Brazilian Society of Dermatology, 
Rio de Janeiro, Brazil
e-mail: awada@adrianaawada.com.br
9
Fig. 9.1 Spectra laser (Q-switched Nd/Yag laser; Lutronic 
Co., Gyeonggi-Do, Korea) 
Fig.  9.2 Bleaching cream Dermamelan (Mesoestetic 
Inc., Viladecans, Barcelona, Spain) 
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_9&domain=pdf
mailto:awada@adrianaawada.com.br
72
9.2 Methods and Techniques 
[1–21]
• Five sessions of Spectra laser in the area, six 
passes each time (Fig. 9.3).
• Cool down the area with ice immediately.
• Apply Dermamelan mask in the area and leave 
there for 6–8 h.
• Wash the area after that.
• Apply calming cream twice a day, for 6 days.
9.3 Clinical Follow-Up [1–21]
See the patient every 7 days and when other ses-
sions are applied, for 5 weeks.
9.4 Before and After
Before treatment
 
Second treatment (after 7 days)
 
Fig. 9.3 Instrumental parameters of Spectra laser used in 
each session
A. Awada
73
Third treatment (after 14 days)
 
Fourth treatment (after 21 days)
 
Final result (after 28 days)
 
9.5 Side Effects, Complications, 
and Their Management [1–21]
We only noticed the patient experienced a lot of 
pain during laser treatment, but we did not use 
any kind of anesthetic. We would stop and cool 
the area when it was too painful. No complica-
tions or side effects were reported.
Tip Box
• Respect the patient’s pain.
• Cool the area before, during, and after 
each pass with the laser.
• Apply the peeling mask all over the area 
and cover with plastic, so the cream 
remains in the skin and acts better.
9 Genital Bleaching Peel
74
References
 1. Alharbi MA. Q-switched double-frequency Nd:YAG 
(532 nm) laser is an effective treatment for racial lip 
pigmentation. J Cosmet Dermatol. 2019 Apr 9.
 2. Won KH, Lee SH, Lee MH, Rhee DY, Yeo UC, 
Chang SE. A prospective, split-face, double-blinded, 
randomized study of the efficacy and safety of a 
fractional1064-nm Q-switched Nd:YAG laser for 
photoaging-associated mottled pigmentation in Asian 
skin. J Cosmet Laser Ther. 2016;18(7):381–6.3. Ergun S, Saruhanoğlu A, Migliari DA, Maden I, 
Tanyeri H. Refractor Pigmentation Associated with 
Laugier-Hunziker Syndrome following Er:YAG Laser 
Treatment. Case Rep Dent. 2013;2013:561040.
 4. Simşek Kaya G, Yapici Yavuz G, Sümbüllü MA, 
Dayi E. A comparison of diode laser and Er:YAG 
lasers in the treatment of gingival melanin pigmen-
tation. Oral Surg Oral Med Oral Pathol Oral Radiol. 
2012;113(3):293–9.
 5. Ostovari N, Mohtasham N, Oadras MS, Malekzad 
F. 532-nm and 1064-nm Q-switched Nd:YAG laser 
therapy for reduction of pigmentation in macular 
amyloidosis patches. J Eur Acad Dermatol Venereol. 
2008;22(4):442–6.
 6. Poon VK, Huang L, Burd A. Biostimulation of der-
mal fibroblast by sublethal Q-switched Nd:YAG 532 
nm laser: collagen remodeling and pigmentation. J 
Photochem Photobiol B. 2005;81(1):1–8.
 7. Cisneros JL, Del Rio R, Palou J. Sclerosis and 
the Nd:YAG, Q-switched laser with multiple fre-
quency for treatment of telangiectases, reticular 
veins, and residual pigmentation. Dermatol Surg. 
1998;24(10):1119–23.
 8. Bernstein EF, Koblenzer C, Elenitsas R. Minocycline 
pigmentation following carbon dioxide laser resurfac-
ing: treatment with the Q-switched Nd:YAG laser. J 
Drugs Dermatol. 2015;14(4):411–4.
 9. Zarzoso I, Bodet D, García-Patos V. A peculiar inheri-
tance: the patient had a net-like pattern of pigmen-
tation on her vulva and perianal skin. Am J Obste 
Gynecol. 2013;208(6):506.e1–2.
 10. Loesch M, Jordan L, Honda KS, Rezaee R, Cooper 
K. Minocycline pigmentation of the vulva masquer-
ading as a melanocytic lesion. JAAD Case Rep. 
2016;2(4):337–9.
 11. Garg S, Vashisht KR, Makadia S. A prospective ran-
domized comparative study on 60 Indian patients 
of melasma, comparing pixel Q-switched NdYAG 
(1064 nm), super skin rejuvenation (540 nm) and 
ablative pixel erbium YAG (2940 nm) lasers, with 
a review of the literature. J Cosmet Laser Ther. 
2019;21(5):297–307.
 12. Jo DJ, Kang IH, Baek JH, Gwak MJ, Lee SJ, Shin MK. 
Using reflectance confocal microscopy to observe in 
vivo melanolysis after treatment with the picosecond 
alexandrite laser and Q-switched Nd:YAG laser in 
melasma. Lasers Surg Med. 2018. [Epub ahead of print].
 13. Choi JE, Lee DW, Seo SH, Ahn HH, Kye YC. Low-
fluence Q-switched Nd:YAG laser for the treatment 
of melasma in Asian patients. J Cosmet Dermatol. 
2018;17(6):1053–58.
 14. Kwon HH, Choi SC, Jung JY, Park GH. Combined treat-
ment of melasma involving low-fluence Q-switched 
Nd:YAG laser and fractional microneedling radiofre-
quency. J Dermatolog Treat. 2019;30(4):352–6.
 15. Lee MC, Lin YF, Hu S, Huang YL, Chang SL, Cheng 
CY, Chang CS. A split-face study: comparison of 
picosecond alexandrite laser and Q-switched Nd:YAG 
laser in the treatment of melasma in Asians. Lasers 
Med Sci. 2018;33(8):1733–38.
 16. Kong SH, Suh HS, Choi YS. Treatment of Melasma 
with Pulsed-Dye Laser and 1,064-nm Q-Switched 
Nd:YAG Laser: A Split-Face Study. Ann Dermatol. 
2018;30(1):1–7.
 17. Saleh F, Moftah NH, Abdel-Azim E, Gharieb MG. 
Q-switched Nd: YAG laser alone or with modified 
Jessner chemical peeling for treatment of mixed 
melasma in dark skin types: A comparative clinical, 
histopathological, and immunohistochemical study. J 
Cosmet Dermatol. 2018;17(3):319–27.
 18. Alavi S, Abolhasani E, Asadi S, Nilforoushzadeh M. 
Combination of Q-Switched Nd:YAG and Fractional 
Erbium:YAG Lasers in Treatment of Melasma: A 
Randomized Controlled Clinical Trial. J Lasers Med 
Sci. 2017;8(1):1–6. 
 19. Ustuner P, Balevi A, Ozdemir M. A split-face, inves-
tigator-blinded comparative study on the efficacy and 
safety of Q-switched Nd:YAG laser plus micronee-
dling with vitamin C versus Q-switched Nd:YAG 
laser for the treatment of recalcitrant melasma. J 
Cosmet Laser Ther. 2017;19(7):383–90.
 20. Gokalp H, Akkaya AD, Oram Y. Long-term results 
in low-fluence 1064-nm Q-Switched Nd:YAG laser 
for melasma: Is it effective? J Cosmet Dermatol. 
2016;15(4):420–26.
 21. Alexiades M. Randomized, Double-Blind, Split-Face 
Study Evaluating Fractional Ablative Erbium:YAG 
Laser-Mediated Trans-Epidermal Delivery of 
Cosmetic Actives and a Novel Acoustic Pressure 
Wave Ultrasound Technology for the Treatment 
of Skin Aging, Melasma, and Acne Scars. J Drugs 
Dermatol. 2015;14(11):1191–8.
A. Awada
75© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_10
Glycolic Acid Peel for the Face
Jessica A. McCarrick and Valerie D. Callender
10.1 Materials (Fig. 10.1)
10.1.1 Glycolic Acid
• Peels are available as free acids, neutralized, 
buffered, or esterified GA.  Buffered or par-
tially neutralized GA is safer and recom-
mended over free GA [1].
• GA peels are available in concentrations rang-
ing from 20% to 70%. Peel intensity is deter-
mined by glycolic acid concentration and 
vehicle [5]. Typically, gel formulations are 
easier to control due to slower penetration [1].
• Check GA peel expiration, as potency 
decreases with time [7].
• Glycolic acid peels require neutralization. 
Neutralizing agents include sodium bicarbonate, 
8–15% solution, or water. Sodium bicarbonate 
10% solution is most commonly used [5].
• Other materials to be available include a gen-
tle cleanser, timer, degreasing agent (isopro-
pyl alcohol, acetone) hand-held fan, and a 
hairnet or headband (Figs. 10.2 and 10.3).
J. A. McCarrick 
Department of Dermatology, Howard University 
Hospital, Washington, DC, USA 
V. D. Callender (*) 
Callender Dermatology and Cosmetic Center, 
Glenn Dale, MD, USA 
Department of Dermatology, Howard University 
Hospital, Washington, DC, USA
e-mail: drcallender@callenderskin.com
10
Fig. 10.2 Glycolic acid peel procedure: glycolic acid 
application
Fig. 10.1 Materials
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_10&domain=pdf
mailto:drcallender@callenderskin.com
76
10.2 Methods and Techniques
10.2.1 Patient Selection
• Select patients carefully (dermatologic indica-
tion, Fitzpatrick skin type, lifestyle) prior to 
performing GA peels. Ideal patients should be 
motivated to comply with pre- and post- 
treatment regimens [5].
• Ideal candidates for GA peels may have mild 
to moderate photodamage, actinic damage, 
acne vulgaris and rosacea, and pigmentary 
disorders (melasma, PIH).
• GA peels should be avoided in current smok-
ers and patients with eczema.
• It is important to assess the history of hyper-
trophic scars or keloids, along with history 
and dates of facelifts, laser treatments, derm-
abrasion, and radiation treatments, as these 
can affect healing and predispose to scarring.
• Assess the history of herpes simplex and pre-
treat with prophylactic antiviral medication as 
appropriate, to be continued for 10 days (pre- 
procedure until full reepithelialization) in a 
medium-depth peel [5, 7]. In patients under-
going superficial GA peels, consider valacy-
clovir 2 g po BID × 1 day as prophylaxis on 
the day of procedure, with the first dose given 
prior to peel.
• Peels are contraindicated in patients undergoing 
isotretinoin therapy [5]. Discontinue isotretinoin 
at least 6–12 months prior to any peel [2, 5].
• Hormone replacement therapy, oral contra-
ceptives, and tetracyclines may predispose 
patients to PIH [2]. The risk of PIH should be 
discussed.
• It is advisable to take preoperative and postop-
erative photographs for each patient. Consider 
usage of a complexion analysis software, such 
as VISIA® Complexion Analysis System, for 
monitoring patients’ results.
10.2.2 Priming of Skin 
and Preoperative Instructions
• GA peel efficacy may be optimized by proper 
patient selection and priming of skin.
• Skin priming may be achieved with hydroqui-
none, topical retinoids, and products contain-
ing low concentrations of glycolic acid.
• In patients with Fitzpatrick skin types III–VI or 
with PIH, pretreat with hydroquinone for at least 
2 weeks prior to procedure [3]. In patients with 
skin of color,a test spot should be performed.
• Consider topical retinoids daily for 3–6 weeks 
prior to GA peel [3, 5].
• Glycolic acid 8–12% products may be used up 
to BID and may unmask a GA sensitivity in 
some patients prior to peel procedure [3].
• Stop all topicals and pretreatment products 
3–5 days before peel.
• Total sun protection routine—educate patients 
on the necessity of sunscreen, protective cloth-
ing, and sun avoidance every day [2].
• Educate patients to avoid facial manipulation 
(picking/scratching, buff puffs, use of OTCs) [2].
• Patients should avoid waxing of the face (eye-
brows, upper lip, etc.) 1 week prior to peel.
• Provide instructions to patient regarding the 
night before and day of procedure. Skin should 
be cleansed with non-residue soap the day 
before and day of procedure. Advise patients 
to not apply cosmetics or moisturizers on the 
day of procedure.
10.2.3 Steps of Glycolic Acid Peel 
Procedure
Glycolic acid peel procedure consists of four 
main steps—cleansing and defatting of the skin, 
time-dependent application, and neutralization.
Fig. 10.3 Glycolic acid peel procedure: cleansing of the 
skin with a non-residue liquid cleanser
J. A. McCarrick and V. D. Callender
77
• Cleansing and defatting—Immediately before 
procedure, assess the skin for dry, scaly 
patches and open sores [1].
• Wash face with a gentle, non-residue cleanser 
to remove any residual make-up or moisturiz-
ers [5].
• GA is hydrophilic [1]. Thus, it is important to 
degrease the skin to ensure an even peel.
• Degrease (“defat”) the skin using isopropyl 
alcohol or acetone. If using acetone, test a 
small area, and assess for any potential irrita-
tion. Acetone should be avoided in patients 
with irritation [2].
• Glycolic acid application—Patient should be 
in a comfortable position, keep their eyes 
closed, delicate areas protected, and have a 
hairnet or headband in place [1, 5].
• Delicate areas, such as eyes, corners of the nose, 
and lips, may be protected with Aquaphor®, zinc 
oxide paste, or damp gauze, in order to avoid 
irritant contact dermatitis [1, 3, 5].
• In order to avoid inadvertent spilling, keep 
container of GA to the side of the patient.
• Peel may be applied with cotton-tip applica-
tor, gauze, sponge, or a brush, but brush appli-
cation is typically preferred [1, 3]. Apply 
liquid formulations using a fan brush and gel 
formulations with either cotton or a gloved 
hand.
• Sequential application in the order of the fore-
head, cheeks, nose, chin.
• GA peel depth is both time dependent and 
concentration dependent—highly superficial 
depth (GA 30–50%, 1–2-min application), 
superficial depth (GA 50–70%, 2–5-min 
application), and medium-depth (GA 70%, 
3–15-min application) peels may be achieved 
[1, 5].
• It may be necessary to perform multiple 
passes in order to achieve medium-depth 
peeling.
• Contact time should be tailored to each patient, 
and the first peel should last no longer than 
2–3  min, followed by immediate neutraliza-
tion, or sooner, if uniform erythema is seen 
prior to 2–3 min [1, 2].
• Other factors affecting peel intensity include 
amount of acid applied, vehicle, and technique 
used [1].
• Patients may experience erythema or burning 
sensation during procedure, which can be 
minimized by use of a hand-held fan.
• Neutralization/rinse off—Set timer to antici-
pated duration of peel, but it is also important 
to consider erythema and degree of discomfort 
in assessing endpoint, as frosting is unreliable 
[3, 5].
• Use sodium bicarbonate or water to neutral-
ize peel. Allow patient to rinse with tepid 
water [2].
• Use application of cold, wet compresses until 
stinging and burning subside [3].
• Apply a mild steroid or an emollient cream 
[3].
Post-peel care, moisturization, and postopera-
tive instructions—For patient comfort, recom-
mend soothing cool compresses for 1–2  days 
after the procedure. Patients may cleanse using a 
bland, gentle cleanser and keep skin moist with 
petroleum-based emollients. Sun should be 
avoided and sun protection employed [2].
• Consider necessity of mild steroids or antibi-
otic creams as required [3].
• Instruct patient to avoid inflammatory agents 
for at least 1 week and to avoid sun exposure 
for 4–6 weeks post-peel [3].
• After complete re-epithelialization at 5–7 days, 
patients may restart usual regimen with topical 
medications (topical retinoids, bleaching 
creams, moisturizers, AHA creams, etc.).
10.3 Clinical Follow-Up
• A series of glycolic acid peels is recommended 
for most patients. Usually, 6–8 peels are rec-
ommended for optimal results [2].
• Start with GA 20–30% and increase concen-
tration with subsequent sessions. Increase the 
concentration by 10% with each peel as 
tolerated.
• Repeat GA peel using 2–4-week intervals [2].
• Post-procedure visit—to assess peel response, 
infection, persistent erythema, early hypertro-
phic scars [7].
• Infection: unhealed crusting at days 7–10.
10 Glycolic Acid Peel for the Face
78
• Persistent erythema: erythema lasting after 
day 14.
• Scarring: raised or elevated areas at 10–14 days 
may herald early hypertrophic scar formation 
[2, 7].
10.4 Before and After
See Fig. 10.4
10.5 Side Effects, Complications, 
and Their Management
Anticipated side effects during peel application 
include burning sensation and erythema. Other 
complications and side effects include technical 
complications, infections, PIH, scarring, and per-
sistent erythema.
10.5.1 Technical Complications
• Improper application may lead to uneven 
peels with suboptimal results.
• There is increased risk of necrotic ulceration 
with prolonged applications or higher concen-
trations of GA.
• Inappropriate or inadvertent placement of GA 
peel may be managed with immediate neutral-
ization [7].
10.5.2 Infection
• Signs of local infection include excessive crust-
ing, purulent drainage, and odor. This may be 
prevented through the use of soaks to debride 
crusting. Treat with appropriate antibiotic selec-
tion, topical or oral antibiotics as appropriate [7].
• Herpes simplex virus (HSV) reactivation pre-
scribes prophylactic antivirals in patients with 
a history of HSV, starting either 1–2  days 
before peel or on the day of peel and continu-
ing for 7–14  days until complete re- 
epithelialization [5, 7].
10.5.3 Cosmetic Side Effects 
and Complications
• Pigmentary changes—PIH is the most com-
mon side effect of GA peels in treatment of 
melasma [4]. Pre-peel and maintenance ther-
apy with topical retinoids and hydroquinone 
or other bleaching agents can reduce the risk 
of and treat post-peel PIH.
• Scarring—Consider daily silicone gel and 
topical or intralesional steroids [7].
• Persistent erythema—Erythema lasting 
>3–5  days in superficial peels and >15–
30  days in medium-depth peels. Treat with 
daily sunscreen to prevent inadvertent and fur-
ther UV exposure, along with the use of topi-
cal steroids and/or systemic steroids [7].
Before After
Fig. 10.4 African–American 
female with melasma treated 
with a series of three glycolic 
acid 30% peels before and after. 
(Photos Courtesy of Portia 
Love, MD)
J. A. McCarrick and V. D. Callender
79
10.5.4 Allergic Reactions 
and Contact Dermatitis
• Glycolic acid is a reported contact allergen. 
Allergic reactions and contact dermatitis 
may be managed with topical corticosteroids 
[2, 7].
References
 1. Sharad J.  Glycolic acid peel therapy  – a current 
review. Clin Cosmet Investig Dermatol. 2013;6:281–
8. https://doi.org/10.2147/CCID.S34029.
 2. Tung RC, Bergfeld WF, Vidimos AT, Remzi 
BK.  Alpha-Hydroxy acid-based cosmetic proce-
dures. Guidelines for patient management. Am J Clin 
Dermatol. 2000;1:81–8.
 3. Zakopoulou N, Kontochristopoulos G.  Superficial 
chemical peels. J Cosmet Dermatol. 2006;5:246–53.
 4. Sheth VM, Pandya AG.  Melasma: a comprehensive 
update: part II.  J Am Acad Dermatol. 2011;65:699–
714. https://doi.org/10.1016/j.jaad.2011.06.001.
 5. FabbrociniG, De Padova MP, Tosti A.  Chemical 
peels: what's new and what isn’t new but still works 
well. Facial Plast Surg. 2009;25:329–36. https://doi.
org/10.1055/s-0029-1243082.
 6. Green BA, Yu RJ, Van Scott EJ.  Clinical and cos-
meceutical uses of hydroxy acids. Clin Dermatol. 
2009;27:495–501. https://doi.org/10.1016/j.
clindermatol.2009.06.023.
 7. Monheit GD.  Chemical peels. Skin Therapy Lett. 
2004;9:6–11.
Tip Box
• Advantages of GA peels include mini-
mal downtime, minimal risk, and mini-
mal discomfort.
• To reduce the risk of PIH and to increase 
peel efficacy, prime with topical reti-
noids, hydroquinone, or non- 
hydroquinone cosmeceuticals.
• Stop all topicals ~5 days prior to peel.
• Perform test spot in patients with skin of 
color.
• Start low and titrate up: Start with GA 
20–30% and increase concentration by 
10% as tolerated with subsequent sessions.
• Depth of the GA peel is dependent on 
both time and pH, which is determined 
by GA concentration.
• GA peels do not exhibit frosting as a 
true endpoint. Monitor time, erythema, 
and degree of patient discomfort to 
assess endpoint.
• Duration of contact with the skin (time 
from application to neutralization) 
affects peel depth.
• Very superficial depth (GA 30–50%, 
1–2-min application), superficial depth 
(GA 50–70%, 2–5-min application), 
and medium depth (GA 70%, 3–15-min 
application).
• Medium-depth peels may require mul-
tiple passes.
• GA peels require neutralization with 
either water or sodium bicarbonate.
• Less frequent intervals between peels in 
patients at higher risk for post-peel 
complications.
• Hand-held fan may reduce patient 
discomfort.
10 Glycolic Acid Peel for the Face
https://doi.org/10.2147/CCID.S34029
https://doi.org/10.1016/j.jaad.2011.06.001
https://doi.org/10.1055/s-0029-1243082
https://doi.org/10.1055/s-0029-1243082
https://doi.org/10.1016/j.clindermatol.2009.06.023
https://doi.org/10.1016/j.clindermatol.2009.06.023
81© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_11
Glycolic Acid Peel for Extra-Facial 
Areas
Caroline Silva Pereira, 
Beatrice Martinez Zugaib Abdalla, 
and Adilson Da Costa
11.1 Materials (Fig. 11.1)
• Procedural gloves
• Nonsterile gauze or brush
• 70% alcohol
• 30–70% GA peel (solution with water; a mix-
ture of water, alcohol, and propylene glycol or 
gel)
• 10% sodium bicarbonate solution
11.2 Methods and Techniques
• Pre-peel anamnesis: Patients with a history of 
herpes simplex should take prophylactic anti-
viral therapy.
• Skin preparation: It should be started at least 
2 weeks before the procedure, since it reduces 
healing time, allows a uniform absorption of 
the agent, and reduces the risk of post- 
inflammatory hyperpigmentation. It can be 
performed with glycolic acid (5–10%), associ-
ated or not with depigmenting agents, such as 
hydroquinone (2.5–5%), kojic acid (1–2%), or 
phytic acid, in vehicles suitable for each type 
of skin [1].
• It is mandatory to obtain the informed consent 
form of the patient and to perform a photo-
graphic documentation.
• Different from face application, wherein 
imaginary aesthetic unit areas are created and 
GA peel is applied, generally, in a centrifuge 
direction, body application is done randomly 
since the entire area is covered by the sub-
stances and undesirable overlapping is 
avoided.
C. S. Pereira (*) 
Pontifical Catholic University, São Paulo, SP, Brazil 
ABC School of Medicine, Santo André, SP, Brazil 
Sírio Libanês Hospital, São Paulo, SP, Brazil 
B. M. Z. Abdalla 
ABC School of Medicine, Santo André, SP, Brazil 
2nd Year Resident of Internal Medicine at FMABC, 
Santo André, SP, Brazil 
A. Da Costa 
Instituto de Assistência Médica ao Servidor Público 
Estadual, Tenured International Professor and Mentor 
for PhD and MSc Programs, São Paulo, SP, Brazil
11
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_11&domain=pdf
82
• Cleaning the skin with 70% alcohol-soaked 
gauze.
• GA application is done with brush or gauze, 
quickly and evenly, after cleaning the skin 
with alcohol.
• The observation of the skin must be con-
stant and rigorous to prevent intense epider-
molysis and secondary burns. The 
appearance of whitish- gray color means 
epidermolysis and frosting means dermal 
lesion (Fig. 11.2).
• In case of epidermolysis or frosting, a 10% 
sodium bicarbonate solution is sprayed on the 
skin, when a mandatorily observed sparkling 
reaction shows up.
11.3 Clinical Follow-Up
• Patient must leave the medical office with 
minimum-SPF-15 product on the exposed 
area where GA peel was applied. It’s better 
when it’s used in the hydrating vehicle, which 
needs to be reapplied every 2 h.
• If scaling occurs in the next few days, a night 
hypoallergenic, moisturizing product can be 
used before going to bed.
• Patients need to be evaluated after 2, 5, and 
10 days to treat and/or follow-up any subse-
quent epidermolysis.
• Another GA peel can be performed every 
15 days.
Fig. 11.2 Epidermolysis pattern under glycolic acid peel 
application
Fig. 11.1 Material used for glycolic acid peel on extrafa-
cial areas
C. S. Pereira et al.
83
11.4 Before and After
Figures 11.3 and 11.4.
a b
c d
Fig. 11.3 Clinical improvement of skin treated with gly-
colic acid peel. 70% Glycolic acid peel at pH  -0.6 for 
post-inflammatory hypercromia. (a) Pre-peel; (b) 
Immediately after peel application; (c) Peel sparkles after 
being sprayed with 10% sodium bicarbonate; (d) Skin 
appearance immediately after the first peel session; (e) 
After the second session (60) days. (Courtesy: Molinaro 
[2])
11 Glycolic Acid Peel for Extra-Facial Areas
84
a b
Fig. 11.4 Clinical improvement of skin treated with 70% glycolic acid peel. 70% Glycolic acid peel at pH -1.5 for 
Civatte poikiloderma. (a) Pre-peel; (b) After the third session (45 days)
eFig. 11.3 (continued)
11.5 Side Effects, Complications, 
and Their Management
The complications and side effects vary accord-
ing to the GA’s absorption depth, professionals’ 
skills, and patient characteristics [3, 4], as the 
following:
• Pigmentary alterations from post- 
inflammatory hyperpigmentation and 
hypopigmentation, which may be treated with 
daily-use topical corticosteroids, tretinoin, 
hydroquinone, or alpha-hydroxy acids
• Infections: bacterial (Staphylococcus, 
Streptococcus, Pseudomonas), viral (herpes 
C. S. Pereira et al.
85
simplex), and fungal (candida), treated with 
agents’ specific medications
• Allergic reactions, which can be overcome 
with topical or systemic steroids
• Acneiform eruptions, which can be treated 
with systemic antibiotics
• Lines of demarcation between treated areas 
and non-treated areas, which can be improved 
with tretinoin, hydroquinone, or alpha- 
hydroxy acids’ daily use
• Textural modifications, which are better 
treated with topical tretinoin or GA-based 
cream
In general, side effects and complications can 
be avoided if GA peel isn’t performed during 
pregnancy, lactation, active herpetic lesions, bac-
terial or fungal infections, dermatitis at the site of 
application, use of photosensitizing medications, 
and allergies to peeling components [4, 5].
References
 1. Velasco MVR, Ribeiro ME, Bedin V, Okubo FR, 
Steiner D.  Rejuvenescimento da pele por peel-
ing químico: enfoque no peeling de fenol. An Bras 
Dermatol. 2004;79(1):91–9.
 2. Molinaro MC.  Peelings corporais. In: MPV K, 
Sabatovich O, editors. Dermatologia Estética. 3rd ed. 
Sao Paulo: Editora Atheneu; 2015. p. 639.
 3. Fischer TC, Perosino E, Poli F, Viera MS, Dreno 
B, Cosmetic Dermatology European Expert 
Group. Chemical peels in aesthetic dermatology: 
an update 2009. J Eur Acad Dermatol Venereol. 
2010;24(3):281–92.
 4. Berson DS, Cohen JL, Rendon MI, Roberts WE, 
Starker I, Wang B.  Clinical role and application of 
superficial chemical peels in today’s practice. J Drugs 
Dermatol. 2009;8(9):803–11.5. Mendonça MC, Aarestrup FM, Aarestrup BJ. Clinical 
protocol for punctuated 88% phenol peels in the treat-
ment of photoaging: a histopathological study of three 
cases. Dermatol Surg. 2012;38(12):2011–5.
 6. Oremović L, Bolanca Z, Situm M. Chemical peelings – 
when and why? Acta Clin Croat. 2010;49(4):545–8.
 7. Khunger N.  Standard guidelines of care for chemi-
cal peels. Indian J Dermatol Venereol Leprol. 
2008;74(Suppl):S5–12.
Tip Box
The following observations are important 
for safety when applying peels:
• Avoid applying to irritated, erythema-
tous, or inflamed skin [3].
• Always have the neutralizing substance 
of the chemical agent in use [3].
• Always be aware of visual signs, such as 
erythema and frosting, which help iden-
tify the degree of substance absorption 
and depth being reached [3].
• GA peel’s main indications are treatment 
of spots, scars, and fine wrinkles, either 
on the face or on body skin [6, 7].
11 Glycolic Acid Peel for Extra-Facial Areas
87© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_12
Jessner’s Peel for the Face
Vanesa Piquero, Daniela Moya, 
and Edgar E. La Rotta
12.1 Materials (Fig. 12.1)
• Patient headband or cap
• Astringent cleansing or soap solution or facial 
tonic
• Alcohol, acetone, and degreasing lotion
• Mask of cleaning clay and/or ozone vaporizer
• The traditional formula of Jessner’s peeling 
consists of salicylic acid 14 grams, resorcinol 
14 grams, and lactic acid (85%) 14 grams in 
95% ethanol 100 ml
• Jessner’s modified peel: 17% lactic acid, 17% 
salicylic acid, and 8% citric acid with ethanol 
base; another 5% lactic acid, 15% citric acid, 
2–3% salicylic acid, and 3–5% kojic acid, also 
adding 2% hydroquinone or adding 14% res-
orcinol [1–3]
• Gloves
• Disposable applicators or gauze
• A manual fan is used
• Vaseline
• Criogel and rose or spring water [4, 5]
• Jessner’s peeling is often combined with other 
subsequent peels, such as 35% trichloroacetic 
acid, 3% retinoic acid or retinol, vitamin C 
serum, or other techniques such as micronee-
dling, for best results
• Sunscreen [2, 3, 5]
12.2 Methods and Techniques
12.2.1 Prepeeling
• Interrogation and physical examination: avoid 
in case of inflammation, dermatitis, substance 
allergies, infection of the area, treatment with 
isotretinoin, delayed healing, pregnancy, or 
lactation [2].
• Pre-preparation of the skin: at least 2 weeks 
before indicate the use of bleaching agents, 
topical retinoids, alpha-hydroxy acids, and/or 
other topical exfoliating agents, as these 
increase the penetration of the chemicals with 
which the peeling is performed.
• Interrupt topical treatments 24–48 h prior to 
peeling application [2, 5, 6].
V. Piquero (*) 
Clinica Leopoldo Aguerrevere Caracas, 
Caracas, Venezuela 
Clinica Dermik Barcelona, Barcelona, Spain
e-mail: v.piquero@dermik.es 
D. Moya 
Hospital Universitario de Caracas, 
Caracas, Venezuela 
Hospital Intercultural Kallvu Llank Chile, 
 Cañete, Región del Bío Bío, Chile 
E. E. La Rotta 
Centro Medico Buenaventura en Caracas, 
Guatire, Venezuela 
Hospital Clinic Barcelona, Barcelona, Spain
e-mail: elarothi23@alumnes.ub.edu
12
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_12&domain=pdf
mailto:v.piquero@dermik.es
mailto:elarothi23@alumnes.ub.edu
88
• The interval between peelings is from 15 days 
to 1 month.
• Wait at least 30 days to perform a peel if you 
have undergone facial surgery.
• Do not perform in case of active herpes, and 
take precaution in case of recent herpes.
• Avoid applying these peels on tanned skin or 
with sun exposure 15 days before.
• Avoid epilation of the skin, since the skin is 
still sensitive [2, 7].
• Shaving on men should not have been per-
formed on the same day of peeling.
• Explain the patient’s real expectations of results 
and have them sign an informed consent.
• Any phototype and cutaneous surface can be 
treated, but phototypes IV and V always have 
a higher risk of post-peeling hyperpigmenta-
tion [1, 5, 8].
• We must know the product that we are going 
to use when we are preparing for the peeling, 
since gelled substances or with higher pH will 
be smoother than alcoholic with resorcinol 
and pH plus acid.
• In patients with chemical contact dermatitis, we 
can perform a prior epicutaneous test [6, 7, 9].
12.2.2 Peeling
• Remove hair from the area and put on a cap.
• Remove debris from the skin area to be treated, 
and clean/wash with neutral cleanser or soap 
and/or facial tonic.
• Apply a degreaser based on ethanol, alcohol, 
or acetone.
• The eye, paranasal areas, and mouth can be 
protected with Vaseline.
• Eye and mouth protection is with wet gauze or 
glasses [4, 9].
• In oily skins, ozonated water vaporizer can be 
recommended to dilate the pores and promote 
acid penetration.
• Remove comedones and milia and complete 
facial cleansing.
• Apply the peeling of Jessner with 10 × 10-cm 
gauze. It should be applied evenly, putting 
Fig. 12.1 Materials for 
chemical peel
V. Piquero et al.
89
some pressure on the skin; the gauze should 
be sufficiently wet but without draining the 
substance (Fig. 12.2).
• Cotton-tipped applicators are used to touch up 
small areas or around the eyes or papules 
(Fig. 12.3).
• A manual ventilator is given to the patient to 
be directed to areas where he or she feels 
burn [7].
• This peeling is applied by layers; the greater 
the number of layers, the greater the depth of 
penetration and the greater the aggressiveness. 
In general, 3–5 layers are applied.
• It should be applied in order, for example, fol-
lowing the hands of the clock or by anatomical 
areas (frontal, cheeks, and nasal), up to the 
area of hair implantation and 0.5 cm below the 
mandibular border [4, 9, 10].
• Jessner’s solution is applied in 1–3 coats to get 
even frosting; the endpoint is erythema or 
even frosting. The greater the number of lay-
ers applied, the greater the depth of peeling.
• In case of erythema and intolerable burning 
sensation, peeling should be removed and the 
application discontinued [3, 10].
• In the case of the modified Jessner formu-
las, the action of these formulas can be 
modified according to the concentration of 
the active ingredients, pH, vehicle, and the 
combination being less aggressive and irri-
tating [5, 6, 10].
• While the product is working, we can calm it 
with a manual fan (Fig. 12.2).
• Once the product acts, we can indicate to wash 
with fresh water, thermal water, or rose water. 
Although it does not require neutralizing by 
bicarbonate, it provides rapid relief.
• Place Criogel or a cold soothing mask, ther-
mal water, or a firm natural yoghurt mask.
• In case of combined Jessner peeling, apply the 
following chemicals: TCA, retinoic acid, gly-
colic, and vitamin C serum, and follow the 
steps of the application of these substances
• Apply cool and soothing moisturizer followed 
by sunscreen (Fig. 12.4) [5, 10].
Fig. 12.2 Uniform application of the peeling around the 
face; the white frosting helps us to show the places of 
application
Fig. 12.3 Use of manual fan to counteract pain and burn-
ing and use of cotton applicators to apply on comedones, 
lower eyelid, etc
Fig. 12.4 Refresh with cold or rose water, cryogel, and 
apply cold soothing cream like aloe vera gel and them fin-
ish with a sunscreen
12 Jessner’s Peel for the Face
90
12.2.3 Post-peeling
• Indicate four glasses of water on the first day 
to avoid salicylism.
• Avoid makeup for 6  h; only loose and inert 
powders can be used.
• Use photo-protection, especially in the first 
48–72 h after the application of peeling and up 
to 15 days.
• Keep the skin moisturized, especially in the 
scaly stage [7].
• In case of redness, intense inflammation, or 
risk of hyperpigmentation, we can indicate 
medium-power steroids 3–5  days post 
peeling.
• Avoid heat and saunas for 3–7 days [6, 7,9].
• The patient will experience skin redness for 
2  days and subsequent chemical desquama-
tion; all of this is resolved within 2–7  days 
after application.
• Firm cold yogurt mask and topical steroids 
post-peeling can be recommended at 
home.
• Indicate oral acyclovir prophylactic in case of 
history of cold sores, particularly in cases with 
high relapse and last crisis less than 1 month 
[7, 10].
• Avoid intense physical activity and sweating 
for at least 5 days.
• Avoid abrasive soaps and scrubs for a period 
of at least 7 days.
• Restart topical treatment after resolved peel-
ing symptoms (approximately 5 days).
• Basic moisturizing cream and sunscreen for 
5–7 days post-peeling are indicated, and then 
the rest of the treatment is resumed.
• Peeling can be repeated between 15 days and 
1 month, with an average of 3 weeks.
• All these recommendations could change 
according to the intensity of the applied peel-
ing, the characteristics of the skin that is 
treated, and climatic or environmental factors. 
(Figs. 12.5 and 12.6) [2, 10].
Fig. 12.5 Facial erythema after 24 h of Jessner’s peeling 
plus TCA 15% for acne scars
Fig. 12.6 Mild to moderate peeling after 72 h of apply-
ing Jessner’s peel for acne
V. Piquero et al.
91
12.3 Before and After (Figs. 12.7, 12.8, 
12.9, 12.10, 12.11, and 12.12 )
Before: After 7 days:
Figs. 12.7 and 12.8 Jessner’s peeling for melasma
Before: After 5 months:
Figs. 12.9 and 12.10 Results after six peelings, every 3 weeks: Jessner, Jessner combined with retinoic acid, Jessner 
combined with 25% TCA, Jessner plus 35% TCA, monthly sessions in addition to home treatment
12 Jessner’s Peel for the Face
92
12.4 Side Effects, Complications, 
and Their Management 
(Figs. 12.13, 12.14, and 12.15)
• The most frequent side effects in the use of 
Jessner’s peeling solution are prolonged red-
ness, hyperpigmentation, and solar lentigines.
• Some days (3 to 7 days) after the peeling pro-
cedure the patient may feel scaly skin redness, 
burning. [3, 4].
• Jessner’s peeling solution is a superficial peel-
ing, which makes it very safe in all cutaneous 
phototypes, but phototypes IV and V have a 
higher risk of post-inflammatory hyperpig-
mentation [2, 9, 10].
• Risk of herpetic spread in patients with 
herpes.
• Risk of impetigo or pyoderma in patients who 
do not have adequate skin hygiene, environ-
mental, makeup, exercise.
• Alteration in healing in patients receiving 
isotretinoin, heavy cigarette smoking, history 
of hypertrophic scarring, connective tissue 
disorders, diabetics, and immunosuppression.
• Risk of hyperpigmentation in patients with 
regular sun exposure [5, 8, 9].
• The Jessner solution is extremely safe and 
well tolerated despite concerns that the toxic-
ity of resorcinol and salicylate could cause.
• Resorcinol is a sensitizer that could cause 
allergy and induce hypothyroidism, syncope, or 
methemoglobinemia in high concentrations.
• Resorcinol stains light brown hair with light 
brown surfaces (furniture, stretchers, hair 
bands).
• The systemic effects of salicylic acid in high 
concentrations and extensive areas of the skin 
causing salicylism are tinnitus, vertigo, head-
ache [3, 5, 10].
• In case of allergy to any of its ingredients, it 
can be treated with topical or systemic steroids 
according to intensity and oral antihistamines.
• Excessive peeling, erythema, or post-peel irri-
tation can be treated with low- or high-potency 
steroids for 5–7 days [6, 9, 10].
• Post-peeling post-inflammatory hyper-
pigmentation can be treated with high-
potency steroids first and then with topical 
depigmenting.
• NSAIDs or antihistamines may be indicated 
in case of edema, inflammation or pruritus 
[3, 6, 9].
Before: After:
Figs. 12.11 and 12.12 Results after four Jessner peelings alone, or combined with glycolic acid, and TCA for acne 
scars and melasma
V. Piquero et al.
93
Fig. 12.13 Intense facial erythema with burning sensa-
tion in the first 24 h of Jessner peeling for photoaging
Fig. 12.14 Acneiform eruption and perioral eczema in 
Jessner peeling application area
Fig. 12.15 Onset of supralabial herpes simplex and 
facial edema after 7 days of Jessner facial peeling
Tip Box
• This peeling can be used on all skin 
types.
• It has antiseptic effect if a single soft 
coat is applied.
• It is especially useful on very thick and 
oily skins.
• It is used in actinic skin, acne, and 
melasma.
• This peeling is essential to improve the 
efficacy and safety of peeling with tri-
chloroacetic acid, making use of lower 
concentrations of TCA.
• This peeling is applied by layers, vary-
ing the depth according to its method of 
application, skin type, and formula used.
• This peeling is not timed, it is not neu-
tralized, it does not generate labor casu-
alties, the result is fast, and it is easy to 
control its penetration.
12 Jessner’s Peel for the Face
94
References
 1. Rendon MI, Berson DS, Cohen JL, Roberts WE, 
Starker I, Wang B.  Evidence and considerations in 
the application of chemical peels in skin disorders 
and aesthetic resurfacing. J Clin Aesthet Dermatol. 
2010;3(7):32–43.
 2. Safoury OS, Zaki NM, El Nabarawy E, Farag EA. A 
study comparing chemical peeling using modified 
Jessner’s solution and 15%trichloroacetic acid versus 
15% trichloroacetic acid in the treatment of melasma. 
Indian J Dermatol. 2009;54(1):41–5. https://doi.
org/10.4103/0019-5154.48985.
 3. Serrano G, Lloret G, Tomas R, Millan F, Janes 
C. Nuevos peelings con AHAs. Piel y Dermocosmetica 
Ibero-Americana. 1997;1:26–44.
 4. Rubin MG.  Exfoliación química. España: Elsevier 
Saunders; 2007.
 5. Grimes P. Jessner’s solution. In: Tosti A, Grimes PE, 
De Padova MP, editors. Color atlas of chemical peels. 
Berlin: Springer; 2006. p. 23–9.
 6. Ortiz Y, Ortega G.  Quimiodermoexfoliaciones 
(Peelings). In: Perez Atamoros F, Enriquez Merino 
J, editors. Dermatologia Cosmética, vol. P0. Mexico: 
Elsevier; 2011. p. 247–62.
 7. Figueiredo M, Henneberg T, Chisaki C, Henneberg 
P. Chemical peels: review and practical applications. 
Surg Cosmet Dermatol. 2013;5(1):58–68.
 8. Fischer T, Perosino E, Poli F, Viera M, Dreno B, For 
the Cosmetic Dermatology European Expert Group. 
Chemical peels in aesthetic dermatology: an update 
2009. J Eur Acad Dermatol Venereol. 2010;24:281–
92. https://doi.org/10.1111/j.1468-3083.2009.03409.
 9. Kontochristopoulos G, Platsidaki E.  Chemical 
peels in active acne and acne scars. Clin Dermatol. 
2017;35(2):179–82. https://doi.org/10.1016/j.clinder-
matol.2016.10.011. Epub 2016 Oct 27.
 10. Puri N. Efficacy of modified Jessner's peel and 20% 
TCA versus 20% TCA peel alone for the treatment 
of acne scars. J Cutan Aesthet Surg. 2015;8(1):42–5. 
https://doi.org/10.4103/0974-2077.155082.
• Ventilation helps to reduce burning or 
pain and is necessary in your application.
• It allows a better penetration of other 
substances such as trichloroacetic acid 
and other peeling, hence its use in com-
bination with glycolic acid, retinoic 
acid, mandelic acid, citric acid, lactic 
acid, pyruvic acid, etc.
V. Piquero et al.
https://doi.org/10.4103/0019-5154.48985
https://doi.org/10.4103/0019-5154.48985
https://doi.org/10.1111/j.1468-3083.2009.03409
https://doi.org/10.1016/j.clindermatol.2016.10.011
https://doi.org/10.1016/j.clindermatol.2016.10.011
https://doi.org/10.4103/0974-2077.155082
95© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_13
Jessner’s Peel for Extra-Facial 
Areas
Sarah Wilson, Howa Yeung, and Travis W. Blalock
13.1 Materials
• Alcohol and acetone solutions for degreasing 
the skin.
• Jessner’s solution—composed of salicylic 
acid 14 g, 85% lactic acid 14 g, and resorcinol 
14 g in a 100 cc 95% ethanol base.
 – Salicylic acid is light-sensitive; thus, JS 
needs to be stored in a dark bottle.
• Applicators such as sable brush, gauze sponge, 
and cotton-tip applicators can beused.
13.2 Methods and Techniques 
[1, 2]
13.2.1 Indications
• Pigmentation of the neck and chest responds 
well to JS chemical peels alone (Fig. 13.1) [1].
 – JS can be used as monotherapy for mild 
dyspigmentation of the neck and chest.
 – Application of JS to the neck and chest 
once a month for 3 months total is an effec-
tive superficial peel schedule, as it provides 
predictable results in the least amount of 
time in this peeling category.
 – JS is tolerated well, as opposed to some 
other peels in its category. In 1 study [3], 
16 patients of varying Fitzpatrick skin 
types were treated for melasma with 70% 
unbuffered glycolic acid on 1 cheek and 
JS on the other for 3 monthly peels. 
Blinded clinical observation showed sim-
ilar statistically significant improvement 
with both modalities; however, 10 of 16 
patients reported more pain with glycolic 
acid.
 – For patients with more severe actinic dam-
age, combination with 35% TCA is usually 
more effective.
• Actinic keratoses can be treated using a com-
bination treatment approach [1]:
 – Monotherapy with JS chemical peel is not 
typically effective for actinic keratoses.
 – Combination therapy with JS chemical 
peel followed by topical 5-fluorouracil 
(5-FU) can enhance the depth of 5-FU 
penetration to allow potentially increased 
efficacy [4–6]. One author has anecdotally 
reported over 80% clearing of actinic ker-
atosis lesions and overall improvement of 
photodamaged skin using this JS and 
5-FU combination [4]. A similar combina-
tion treatment for actinic keratosis using 
glycolic acid has been described as the 
fluor- hydroxy pulse peel with 91% of 
actinic keratoses clearing at 6-month fol-
low-up [5].
S. Wilson · H. Yeung · T. W. Blalock (*) 
Emory University School of Medicine, Department 
of Dermatology, Atlanta, GA, USA
e-mail: sarah.jo.wilson@emory.edu; 
howa.yeung@emory.edu; twblalo@emory.edu
13
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_13&domain=pdf
mailto:sarah.jo.wilson@emory.edu
mailto:howa.yeung@emory.edu
mailto:howa.yeung@emory.edu
mailto:twblalo@emory.edu
96
 – In patients with severe sun damage and 
multiple actinic keratoses, the use of 35% 
trichloroacetic acid peel after JS to areas 
such as the arms or legs can be consid-
ered. However, high level of caution and 
appropriate informed consent should be 
obtained since there are higher risks of 
dyspigmentation and scarring for 
medium-depth chemical peels off the 
facial areas due to poorer wound-healing 
capacity.
13.2.2 Procedures on a Step-by-step 
Way
• The skin is degreased using alcohol and then 
subsequently with acetone solution, both 
applied using cotton balls or gauze sponges.
• Application with a sable brush is preferred to 
ensure an even, light-white frost. In our expe-
rience, frosting can sometimes be weak, slow, 
and/or uneven when applied using two cotton- 
tipped applicators, cotton balls, or a gauze 
sponge.
• The extent of frosting will be evident 3–4 min 
after application.
 – It is important to differentiate whitening 
from salicylic acid precipitation rather than 
a true frost due to tissue coagulation. 
 Whitening can be wiped off easily with a 
damp cotton ball.
• A second coat is then applied, and this process 
can be repeated until the end-point—a thin 
pale to pinpoint white frost, which evolves 
slowly, is reached. The patient may experience 
mild stinging and burning.
• Neutralization is not required.
• Heavier pressure and increased coats of JS 
applied increase the depth of penetration, as 
does pre-treatment with topical tretinoin lead-
ing up to the peel.
13.3 Clinical Follow-Up
• It is important to counsel the patient about 
expected exfoliation and subsequent care [7]:
 – Mild red-brown to streaky erythema and 
darkening of pigmentation for 1–3 days
 – Non-vesicular exfoliation for 2–4  days 
afterward, mostly with flaking but rarely 
with peeling
• The peel should be repeated to produce the 
best results. Some regimens include once a 
month for 3  months. Others suggest every 
6–8 weeks [1, 8].
• Strict photo-protection should be advised fol-
lowing the procedure.
13.4 Before and After (Fig. 13.1)
a
b
c
Fig. 13.1 (a) Freckles and lentigines with hypopig-
mented macules from actinic damage and previous kera-
tosis removal on the chest before sable brush application 
of two coats of Jessner’s solution. (b) Immediately after 
frosting. (c) Two months after two monthly peels with 
resulting fading of freckling and lentigines [1]
S. Wilson et al.
97
13.5 Side Effects, Complications, 
and Their Management 
[6–9]
• Similar to other superficial peeling agents, JS 
is generally well tolerated in a wide variety of 
skin types with few contraindications and very 
rare incidence of toxicity. However, it is con-
traindicated in pregnancy and during lactation 
[7, 8].
• Potential side effects include persistent or 
streaky erythema, dyspigmentation, scarring, 
allergic contact dermatitis, and systemic tox-
icity from resorcinol or salicylic acid 
absorption.
• Rare potential side effects of resorcinol 
include contact dermatitis, dyspigmentation, 
pallor, dizziness, tremor, syncope, and hypo-
thyroidism, described mostly with higher con-
centrations and repeat application [6]. 
Exogenous ochronosis has been described as 
well.
• Contact dermatitis to resorcinol may occur 
and manifest as edema out of proportion to the 
peel, which can be effectively treated with oral 
prednisone.
• Rare potential side effects of salicylic acid 
include salicylate toxicity or “salicylism” (e.g., 
pallor, fatigue, tinnitus, nausea, vomiting, diz-
ziness, hyperpnea, and other neurologic distur-
bances) seen at higher concentrations and 
widespread exposure [7]. Increased oral fluid 
intake can be recommended in the first 12  h 
after JS peel to potentially assist with salicylic 
acid excretion [2].
• Because Jessner’s peel is a mixture of multiple 
ingredients, slight variations in efficacy or 
composition may be experienced depending 
on the manufacturer of the peel.
References
 1. Brody HJ. Chemical peeling and resurfacing. 3rd ed. 
Emory University Digital Library Publications; 2008. 
amazon.com and open.library.emory.edu.
 2. Rubin MG. Manual of chemical peels : superficial and 
medium depth. Philadelphia: J.B.  Lippincott; 1995. 
187 p.
 3. Lawrence NL, Cox SE, Brody HJ. A comparison of 
Jessner’s solution and glycolic acid in the treatment 
of melasma in dark skinned patients: a double blind 
study. J Am Acad Dermatol. 1997;37:589–93.
 4. Tosti A, Grimes PE, Padova MPD.  Color atlas of 
chemical peels. 2nd ed. Heidelberg/New York: 
Springer; 2012. 211 p.
 5. Marrero GM, Katz BE. The new fluor-hydroxy pulse 
peel. A combination of 5-fluorouracil and glycolic 
acid. Dermatol Surg. 1998;24(9):973–8.
 6. Cassano N, et  al. Peeling agents: toxicological and 
allergological aspects. J Eur Acad Dermatol Venereol. 
1999;13(1):14–23.
 7. Arif T.  Salicylic acid as a peeling agent: a compre-
hensive review. Clin Cosmet Investig Dermatol. 
2015;8:455–61.
 8. Tannous Z, Avram MM, Tsao S, Avram MR. The color 
atlas of cosmetic dermatology. 2nd ed. New  York: 
McGraw-Hill Publishing; 2011.
 9. Grimes PE, Rendon MI, Pellerano J.  Superficial 
chemical peels. In: Grimes PE, editor. Aesthetics and 
cosmetic surgery for darker skin types. Philadelphia: 
Lippincott Williams & Wilkins; 2008. p. 154–69.
Tip Box
• Jessner’s solution chemical peels are 
safe and effective as monotherapy for 
pigmentation on the face and neck.
• When used in combination with 5-FU or 
35% TCA, Jessner’s solution can effec-
tively treat actinic keratoses.
• Application of JS with a sable brush 
may produce more uniform, light frost-
ing more effectively than a cotton-tip 
applicator or gauze sponge.
• The effects of each coat of JS will be 
evident 3–4  min after application; 
patients may experience tingling or mild 
burning.
• The expected end-point of a Jessner’s 
peel is a thin, pale to pinpointlight frost.
• It is important to counsel patients that 
hyperpigmentation is expected for 
1–3  days, followed by non-vesicular 
exfoliation for 2–4 days after the peel.
• Jessner’s solution is a superficial peel 
that is typically well tolerated in a wide 
variety of skin types with few contrain-
dications and very rare incidence of 
toxicity.
13 Jessner’s Peel for Extra-Facial Areas
http://amazon.com
http://open.library.emory.edu
99© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_14
Phenol-Croton Oil Peels
Fernanda Ayres de Morais e Silva Cardoso, 
Carlos Gustavo Wambier, and Adilson Da Costa
14.1 Materials
• Degreasing agent: standardized acetone- 
ethanol (3:1 mixture) or any nail polish 
removal solution containing acetone and no 
castor oil in the composition (castor oil is 
derived from another Euphorbiaceae, Ricinus 
communis, which also contains phorbols) [1].
• Applicators: wooden, cotton-tipped applica-
tors (swabs or split tongue depressors) or 
4 × 4 gauzes (Fig. 14.1).
• Peeling agent: freshly made mixture of stock 
solution (below), carbolic acid 88% (phenol 
88% in water), 5.5 mL of water for injection, 
and 0.5  mL of Septisol, the standard soap, 
contains triclosan in aqueous base (Fig. 14.2).
• Stock solution, containing 1  mL of Croton 
 tiglium oil (Delasco), mixed with 24  mL of 
carbolic acid 88% (from compounding 
pharmacies).
• Post-peeling preparation: Vaseline.
• Multiparameter monitor: electrocardiogram, 
pulse oximeter, blood pressure, along with 
necessary advanced cardiologic life support 
drugs, intravenous access, defibrillator 
(Fig. 14.3). The new multiparameter monitors 
also include heart rate-corrected Q-T interval 
(QTc), which is probably the most interesting 
F. A. de Morais e Silva Cardoso (*) 
Department of Medicine, Facid Wyden, 
Teresina, PI, Brazil 
C. G. Wambier 
Department of Medicine, State University of Ponta 
Grossa, Ponta Grossa, PR, Brazil 
A. Da Costa 
Instituto de Assistência Médica ao Servidor Público 
Estadual, Tenured International Professor and Mentor 
for PhD and MSc Programs, São Paulo, SP, Brazil
14
Fig. 14.1 Materials. Multiple cotton-tipped wooden 
applicators, freshly made peel solution, plastic cotton- 
tipped swabs for drying tears, and 4 × 4 gauze for drying 
excessive solution
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_14&domain=pdf
100
for phenol peels, because of recent evidence 
of severe yet reversible within 15  min QTc 
prolongation during peels [2].
• Activated carbon masks: the staff and surgeon 
must avoid repeated inhalation of volatile 
organic compounds during the peels [3]. 
Therefore, the appropriate personal protection 
equipment are masks with chemical filters 
(Fig. 14.4).
Fig. 14.2 Freshly made peel solution, containing 
1.6% croton oil and 35% phenol. When let still for 
some minutes, it presents two phases: upper phase 
with less phenol and lower phase with more phenol. It 
must be mixed before every single application for con-
sistent results. Upper phase is too weak for achieving 
effects
Fig. 14.3 Defibrillator, which may also include a multi-
parameter monitor. Another option is to have both simple 
defibrillator and a multiparameter monitor
Fig. 14.4 Disposable N95 mask with activated carbon 
filter for volatile organic compounds
F. A. de Morais e Silva Cardoso et al.
101
14.2 Methods and Techniques
• Degreasing: the importance of removal of all 
make-up, sebum, beard, topical anesthetic, 
and sunscreen before any chemical peel is 
unquestionable. The physician scrubs the 
patient’s face with semi-soaked gauze pads.
• Peeling solution preparation: mix phenol with 
croton oil first, since croton oil is completely 
soluble in liquid phenol. By keeping a standard 
of 10 mL of the final volume, to reach 35% 
phenol, 4 mL of this solution will be a mixture 
of phenol 88% and croton oil, and the remain-
ing 6 mL will be fixed as 5.5 mL of water and 
0.5 mL of Septisol.
• Strength by croton oil concentration: the 
amount of croton oil drawn from the stock 
solution, which contains 4% croton oil in phe-
nol (described in Materials), determines the 
inflammation and rejuvenation effects caused 
by its phorbol esters. This is set by the amount 
of stock solution in 4 mL of phenol 88%/cro-
ton oil mixture (peeling solution preparation, 
above). Thus, by adding only 4  mL of the 
stock solution, the final concentration of cro-
ton oil will be 1.6%, a very strong formula, 
adequate for perioral area, nose, and deep 
wrinkles. By adding 3 mL of stock solution to 
1 mL of 88% carbolic acid, the croton oil con-
centration will be 1.2%, a strong formula, 
adequate for forehead and moderate wrinkles. 
By adding 2 mL of stock solution to 2 mL of 
88% carbolic acid, the croton oil concentra-
tion will be 0.8%, a medium-strength formula, 
adequate for overall use and adequate for mild 
wrinkles. By adding 1 mL of stock solution to 
3 mL of 88% carbolic acid, the croton oil con-
centration will be 0.4%, a light formula, ade-
quate for eyelids and neck.
• Application: the saturation of the applicator, 
pressure, and number of strokes are the main 
variables for increasing damage by the peeling 
solution. The applicator is constantly rubbed 
with gentle yet firm pressure, while the other 
hand secures the skin from movement and 
holds a gauze pad for drying drips (Fig. 14.5).
• Post-peeling regimen: a thick layer of Vaseline 
is applied to the peeled areas as soon as the 
desired chemoabrasion endpoints were 
achieved. The patient and family member are 
instructed to keep a regimen to improve heal-
ing, by total avoidance of irritants, fragrances, 
allergens, and sun exposure and taking diet 
rich in proteins and vitamins. Sunscreen must 
be avoided during the first 7 days of deep peels 
to avoid allergen sensitization.
Fig. 14.5 Application of full-face phenol-croton oil peri-
oral peel with a cooler for patient comfort and blankets to 
minimize chances of hypothermia. The frosting is the end-
point for deep peels, with an even white color
14 Phenol-Croton Oil Peels
102
14.3 Clinical Follow-Up
• There is intense edema for 72 h. Vesicles, blis-
ters, and oozing may occur in the first 48 h. 
Purulent exudate may occur after 48–72  h. 
Crusts usually fall off by the 8th day. Careful 
debriding and crust removal are advised if 
there is liquid collection or localized pain. The 
patient may be started on systemic and topical 
combination antibiotic therapy if any sign of 
infection is observed, such as odor, pus, 
increase in erythema, edema, or pain.
• Days 0–2: Vaseline, cold saline compresses, and 
thermal water sprays. Keep opioids as needed 
(codeine 30–60 mg q6h, tramadol 100 mg q8h, 
or oxycodone 10 mg q8h) (Fig. 14.6).
• Days 1–3: Optional use of systemic steroids if 
edema is too severe.
• Days 2–4: Allow facial washes with baby 
shampoo or non-irritant cleaning lotions 
(Cetaphil or similar), and change saline com-
presses for either boric acid 3% solutions or 
dilute vinegar (1 desert spoon of vinegar in 
250 mL of cold, filtered water).
• Days 3–8: Careful evaluation for the need of 
antibiotic therapy, with topical silver sulfadia-
zine 1% and systemic Cefaclor 750  mg bid, 
with temperature and pulse monitoring by the 
patient at home if needed (Figs. 14.6 and 14.7).
Fig. 14.7 Deep chemical peel. Phenol 35% with croton 
oil 1.6% full face and 0.4% over the neck. Mild edema 
with purulent exudate on the third post-operative day. 
Compresses were changed to 3% boric acid solutions, and 
the patient was advised to apply silver sulfadiazine 1% 
over the green exudative areas
Fig. 14.6 Deep chemical peel. Phenol 35% with croton 
oil 1.6% full face and 0.4% over the neck. Intense edema 
on the first post-operative day
F. A. de Morais e Silva Cardoso et al.
103
14.4 Before and After (Figs. 14.8 
and 14.9)
Fig. 14.8 Close-up of unrivaled resultsof a single 
phenol-croton oil peel application to face (1.6% croton 
oil in 35% phenol). The rejuvenation process is so 
intense that even intradermal nevi become compound 
nevi
Fig. 14.9 Skin elastosis caused by sun damage and 
smoking is reversed by using the right technique. After 
6 months of the application (right), the patient presented 
natural skin color, which is the main difference of Hetter’s 
peels and Baker’s peels
14 Phenol-Croton Oil Peels
104
14.5 Side Effects, Complications, 
and Their Management
• Bronchoconstriction and lung edema: the 
patient is exposed to high levels of fumes of 
phenol, which may cause bronchial edema 
and asthma attacks. The office must be 
equipped with emergency crash medications 
(corticosteroids, epinephrine, beta-adrenergic 
inhalants, such as albuterol).
• Post-inflammatory hyperpigmentation: the 
most common side effect of chemical peels in 
general. Predisposing factors include 
melasma, phototype, and sun exposure. Skin 
preparation for 1  month with hydroquinone 
may be used. Treatment is performed with 
low-fluency Q-switched Nd-YAG 1064  nm 
and cosmeceuticals (vitamin C, ferulic acid). 
Kligman’s formula is used only after erythem-
atous phase, usually 4  months; superpotent 
steroids such as clobetasol may also be used in 
severe cases.
• Hypopigmentation: usually “pseudo- 
hypopigmentation,” which means skin color is 
actually normal but younger than the photo-
aged surrounding skin. Therefore, the key to 
success with Hetter’s formulas is to always 
perform long feathering zones to untreated 
areas (about 4–10 cm). Sub-epidermal fibrosis 
from manipulation or excessive rubbing in 
deep wrinkles may cause true focal hypomela-
nosis, which is best addressed by using 
5- fluoruracil tattooing technique, in the same 
way as idiopathic guttate hypomelanosis else-
where [4].
• Eye irritation: intraoperative exposure to vol-
atile chemicals and accidental splash or tear-
ing. To maximize eye safety, eyes should 
remain shut throughout the whole peeling 
session, eyelids must remain dry with cotton-
tipped plastic swabs during the procedure, 
and avoidance of general anesthesia or seda-
tion, which abolish natural tearing reflex, and 
patient’s conscience to keep the eyes closed. 
A standard eye-opening procedure is done 
with the patient in seated position, with Q-tips 
in the corners of the eyes to dry the tears 
which fall. The use of opioids reduces tearing 
by anticholinergic effects and should be used 
even in patients with excellent pain tolerance. 
No applicator or chemical bottle shall pass 
directly above the patient’s face. Always 
check the conjunctiva during the post-opera-
tive period for any signs of erythema or che-
mosis. If it is caused by lagophthalmos, 
exudate, or ointments, the management is 
done with moisturizing gels, lubricating eye-
drops, and hygiene.
• Prolonged erythema: erythema starts during 
the first week and is greater in the second 
week post-operative. The erythema must be 
regarded as normal healing process of deep 
injury and is actually a superficial sign of col-
lagen production which is undergoing in the 
deep dermis. The patient must be warned of 
its benign nature even before the peel and also 
hope that it lasts for months. If erythema sub-
sides before the first month, which is com-
mon in 0.4–0.8% croton oil formulas, there is 
usually less neocollagenesis than the cases 
where erythema was prolonged. Topical reti-
noids and irritants must be avoided, because 
inflammation can cause burning sensation 
and prolong erythema for longer than 
4 months.
• Ectropion and scars: when performed with 
adequate technique by avoiding excessive rub-
bing and pressure in areas prone to hypertro-
phic formation, such as the zygomatic arch, 
pre-auricular area, medial upper eyelids, and 
lateral lower eyelids. Some patients with 
lower eyelid wrinkles may also have laxity, 
which is accessed by the snap-back test. If the 
test is negative, avoid superficial treatments, 
which will induce cicatricial ectropion. Also, 
patients who have previously undergone plas-
tic surgery and deep peels in the lower eyelids 
may be accessed by opening their mouth to 
check for lower eyelid retraction. These 
patients, with lateral lower eyelid inferior 
retraction, will present increased retraction 
and ectropion or lagophthalmos after a deep 
peel in this area. Evaluation by an oculoplastic 
surgeon is mandatory in these cases.
• Milia: after full epidermal healing, the milia 
which are a common consequence of 
F. A. de Morais e Silva Cardoso et al.
105
 resurfacing in oily and thick skin may be 
removed after needle pricks.
• Cardiac arrhythmias: safety pauses of 10 min 
between each cosmetic unit of the face (fore-
head, perioral, nose, periocular, each cheek) 
usually prevent cardiac conduction events. 
The authors also recommend checking all 
medications that the patient takes for QT- 
prolongation potential. This can be done by 
CredibleMeds website http://www.credi-
blemeds.com or smartphone apps. Withdraw 
all possible medications and check for QTc 
prolongation in the preoperative period. The 
presence of frequent extra-systolic beats is a 
signal that phenol is affecting repolarization. 
Give longer pauses, ventilate the room bet-
ter, increase intravenous (IV) drip, and 
reduce area of exposure before each 10-min 
pause.
• Infection: any systemic sign of infection or 
increased edema past the first 48  h must be 
treated promptly by coverage of 
Staphylococcus aureus and Pseudomonas 
aeruginosa; usually, antibiotic prophylaxis is 
not indicated, unless the patient has prosthesis 
or other conditions.
References
 1. Piamphongsant T. Phenol-castor oil: modified peel for 
dermal melasma. Dermatol Surg. 2006;32(5):611–7; 
discussion 617.
 2. Wambier CG, Brody HJ, Hetter GP.  Comments: 
Hemiface comparative study of two phenol peels (baker-
Gordon and Hetter formulas) for the correction of facial 
rhytids. Surg Cosmet Dermatol. 2017;9(2):190–1.
 3. Wambier CG, Beltrame FL.  Air safety and personal 
protective equipment for phenol-croton oil peels. 
Dermatol Surg. 2017;44(7):1035–7.
 4. Wambier CG, Wambier SP de F, Pilatti LEP, 
Grabicoski JA, Wambier LF, Schmidt A.  QTc pro-
longation during phenol-croton oil peels. J Am Acad 
Dermatol. 2018;78(4):810–2.
Tip Box
• Hands-on training is mandatory for 
acquiring the correct technique.
• Patient selection and adequate cardiol-
ogy assessment before peel are the keys 
to a safe procedure.
• Learning curve is long. Constant prac-
tice takes the dedicated physician to 
perfection.
14 Phenol-Croton Oil Peels
http://www.crediblemeds.com
http://www.crediblemeds.com
107© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_15
Pyruvic Acid Peel for Face 
and Extra-Facial Areas
Bogdana Victoria Kadunc, Renan Lage, 
and Renata Cristina Vasconcellos
15.1 Materials
• Acetone in a soft cotton pad or gauze for 
cleaning and degreasing the skin and improv-
ing its penetration.
• Fifty to eighty percent pyruvic acid in 
hydroalcoholic solution, most recommended 
for being more effective, should be kept air-
tight in the refrigerator (2–8 °C) because it is 
very unstable. In addition, although the 
vapors are non- toxic, they can irritate the eyes 
and airways, so a fan can be used during the 
procedure.
• Soft cotton, soft brush, or a folded 4 × 4 gauze 
sponge, in crescent order of penetration.
• 8.4% sodium bicarbonate in water solution for 
neutralization (Fig. 15.1).
15.2 Methods and Techniques
• It is described in the literature that the penetra-
tion is usually uniform even on unprepared 
skin, but it is advisable to use at least 2 weeks 
before, once a day, topical tretinoin (0.025%) 
and topical bleaching agents (4% hydroqui-
none, 20% azelaic acid) to decrease the risk of 
post-inflammatory hyperpigmentation and 
promote wound healing [1, 2].
• The skinshould be cleansed to ensure uniform 
penetration by removing the excess sebum of 
the skin with acetone in a soft cotton 
(Fig. 15.2).
• PA is applied with a gauze, and the area was 
gently scrubbed for approximately 1 min and 
left in the skin for 10 min or until erythema 
appeared (Fig. 15.3) [1–6]. It must be applied 
in a faster manner in each cosmetic unit and 
neutralized with 8.4% sodium bicarbonate 
solution, if localized frosting areas are 
observed (Fig. 15.4).
• After 10 min or when the erythema appears, 
the entire face is washed in a sink with copi-
ous amounts of water [1, 2, 5–8].
• Immediately after the procedure, a facial 
cream emollient can be applied.B. V. Kadunc · R. C. Vasconcellos (*) 
Department of Dermatology, Pontifical Catholic 
University of Campinas, Campinas, SP, Brazil 
R. Lage 
Cosmiatric Department, Department of Dermatology 
of the Pontifical Catholic University of Campinas - 
PUC Campinas, Campinas, SP, Brazil
15
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_15&domain=pdf
108
a b c
d e f
Fig. 15.1 The materials to be used. (a) Acetone. (b) Gauze. (c) Fifty to eighty-percent pyruvic acid in hydroalcoholic 
solution. (d) Cotton swabs. (e) 8.4% sodium bicarbonate solution. (f) Water
Fig. 15.2 The skin should be cleansed with acetone
Fig. 15.3 The pyruvic acid should be applied with a 
gauze
B. V. Kadunc et al.
109
15.3 Clinical Follow-Up
• The erythema persists for about 4–6  h after 
the procedure. During this period, some 
patients may feel tingling or burning sensa-
tions, especially in periorificial areas 
(Fig. 15.5).
• The skin does not get dry and scaly, unless it is 
combined with a second peel such as retinoic 
acid or trichloroacetic acid (TCA).
• A mild desquamation lasting 7–10 days can be 
observed [5].
• During the first 3 days after peel care, facial 
shower or bathing should be restricted for up 
to two times a day with a mild cleanser lotion 
(Fig. 15.6).
• The patients should be instructed to apply 
moisturizing cream twice a day for a week, 
avoid sun exposure, and use sunscreens 
daily.
• Another peeling session can be performed 
once every 2 weeks.
• Because collagen remodeling takes 60–90 days, 
the final evaluation of the patient should be done 
after 90 days (Figs. 15.7 and 15.8) [1, 3–5, 8].
Fig. 15.4 The frosting areas must be neutralized with 
8.4% sodium bicarbonate solution Fig. 15.5 The erythema persists for about 4–6 h after the 
procedure
Fig. 15.6 One day after de procedure. The skin usually 
does not get dry and scaly
15 Pyruvic Acid Peel for Face and Extra-Facial Areas
110
15.4 Before and After (Figs. 15.7 
and 15.8)
a b
Fig. 15.7 (a) Before the procedure. (b) Two months after two sessions with 60% pyruvic acid
a b
Fig. 15.8 (a) Before the procedure. (b) Two months after one session with 80% pyruvic acid
15.5 Side Effects, Complications, 
and Their Management
The effect of PA depends on the concentration 
used and the duration of the application before 
the neutralization.
In general, the response occurs faster in 
women and in younger skin.
If any frosting is observed, immediate neutraliza-
tion with 8.4% sodium bicarbonate solution must be 
done (Fig. 15.9), and extreme care should be taken 
to the hot area, with the use of healing creams and 
tinted, high sun protection factor sunscreens.
Other side effects are:
• Persistent erythema (Fig.  15.10) that can be 
treated with super-potent steroid gels such as 
clobetasol 0.05% with only few descriptions 
in the literature [9].
• Scarring. A very low risk is presented.
B. V. Kadunc et al.
111
• Post-inflammatory hyperpigmentation. It may 
be treated with Kligman formulas, sunscreen, 
oral tranexamic acid, and Q-switched 1064- 
nm laser [2, 6, 7, 9, 10].
References
 1. Ghersetich I, Brazzini B, Peris K, Cotellessa C, 
Manunta T, Lotti T. Pyruvic acid peels for the treatment 
of photo- aging. Dermatol Surg. 2004;30(1):32–6.
 2. Berardesca E, Cameli N, Primavera G, Carrera M. 
Clinical and instrumental evaluation of skin improve-
ment after treatment with a new 50% pyruvic acid 
peel. Dermatol Surg. 2006;32(4):526–31.
 3. Wambier CG.  Pyruvic acid peel. In: Chemical and 
physical procedures. Cham: Springer; 2017. p. 1–10.
 4. Bruce A, Roberts W, Teller C, Colvan L. The effects 
of a daily skincare regime non maintaining the ben-
efits obtained from previous chemical resurfacing 
treatments. J Drugs Dermatol. 2016;15(9):1145–50.
 5. Cotellessa C, Manunta T, Ghersetich I, Brazzini B, Peris 
K. The use of pyruvic acid in the treatment of acne. J 
Eur Acad Dermatol Venereol. 2004;18(3):275–8.
 6. Marczyk B, Mucha P, Budzisz E, Rotsztejn H. 
Comparative study of the effect of 50% pyruvic and 
30% salicylic peels on the skin lipid film in patients with 
acne vulgaris. J Cosmet Dermatol. 2014;13(1):15–21.
 7. Yu RJ, Scott EJV. Alpha-hydroxyacids and carboxylic 
acids. J Cosmet Dermatol. 2004;3:76–87.
 8. Kadunc BV. Pyruvic acid: standardization technique 
for the use in chemical peelings by means of experi-
mental study. University of Sao Paulo; 1998.
 9. Kontochristopoulus G, Platsidaki E.  Chemical 
peels in active acne and acne scars. Clin Dermatol. 
2017;35:179–82.
 10. Jaffary F, Faghihi G, Saraeian S, Hosseini SM. 
Comparison the effectiveness of pyruvic acid 50% 
and salicylic acid 30% in the treatment of acne. J Res 
Med Sci Off J Isfahan Univ Med Sci. 2016;21:31.
Tip Box
• PA is a good alternative for the treat-
ment of acne, oily skin, folliculitis, mild 
photodamage with superficial wrinkles 
(Glogau I–II), and superficial scarring.
• Anti-inflammatory and antibiotic effects 
are its greater advantage.
• The risk of post-inflammatory hyperpig-
mentation can be minimized by prepara-
tion of the skin.
Fig. 15.10 Persistent erythema
a
b
Fig. 15.9 (a) Frosting by unforeseen deepening. (b) 
Neutralization with 8.4–10% sodium bicarbonate 
solution
15 Pyruvic Acid Peel for Face and Extra-Facial Areas
113© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_16
Resorcin Peel for Face
Andrezza Facci
16.1 Materials
• Hoffmann solution
• Resorcinol peel 22.5%
• Gauze
• Soap
• Physical sunscreen
16.2 Methods and Techniques
The skin is scrubbed and cleansed with 
Hoffman Solution in order to remove the 
remaining surface oils, which permits a better 
absorption. A resorcinol peel solution of 22.5% 
was applied with a gauze rubbing gently the 
skin. Mild tingling and burning sensation were 
noticed by the patients in the first minutes and 
then followed by paresthesia that lasts about 
30 min (Fig. 16.1).
In this superficial chemical peel, mild ery-
thema and very light scaling are the usual clinical 
picture (Table 16.1).
16.3 Clinical Follow-Up
Resorcinol peel doesn’t present any special 
adverse condition, with no downtime, despite 
absence of symptoms and scaling.
A. Facci (*) 
Clínica Andrezza Facci de Dermatologia, 
Barueri, SP, Brazil
16
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_16&domain=pdf
114
16.4 Before and After (Figs. 16.2 
and 16.3)
Fig. 16.1 Method to apply resorcinol peel on the skin
Table 16.1 Steps of the peeling procedure
Degreasing – cleansing
Application of peeling agent
Rinse off
After all apply, Physical sunscreen
Fig. 16.2 Acne patient before and after 15 days of last session of resorcinol peel for face
A. Facci
115
16.5 Side Effects, Complications, 
and Their Management
Overpeeling and systemic toxicity are very rare. 
Complications are generally mild and do not 
occur often [1].
But the references listed are transitory hyper-
pigmentation, dizziness, sweating, pallor, and 
methemoglobin if in higher concentrations. I 
found none of them [2, 3].
References
 1. Lynch BS, Delzell ES, Bechtel DH.  Toxicology 
review and risk assessment of resorcinol: thyroid 
effects. Regul Toxicol Pharmacol. 2002;36:198–210.
 2. Kede MPV, SabatovichO. Dermatologia Estética. 3rd 
ed: Ed Atheneu. Rio de Janeiro; 2015. p. 589–621.
 3. Palermo E, et al. Tratado de CIrurgia Dermatológica, 
cosmiatria e laser: Elsevier. Rio de Janeiro; 2012. 
p. 311–32.
Tip Box
• Benefit Clinical onset
• Easy to 
perform
Must be repeated or com-
bined to achieve any satis-
factory result
• Mild or no 
scaling
Comfortable due to 
absence of desquamation 
and burning post-peeling
• Well- 
tolerated
No skin-type restriction
Fig. 16.3 Patient with post-inflammatory acne lesions before and after 15 days of last session of resorcinol peel for 
face
16 Resorcin Peel for Face
117© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_17
Resorcin Peel for Extra-Facial 
Areas
Erica Monteiro
17.1 Materials [1–5]
17.1.1 Reagents
• Correctly labeled peeling agents in various 
concentrations: resorcinol solution (ethanol) 
10%, 20%, or 50%.
• Alcohol and/or acetone to clean and degrease 
the skin.
• Neutralizing solutions: not required.
17.1.2 Equipment (Fig. 17.1)
• Glass cup or beaker in which the required 
agent is poured.
• Gloves.
• Cotton-tipped applicators or swab sticks.
• 2″ × 2″ cotton-gauze pieces.
17.2 Methods and Techniques
17.2.1 Patient Selection
The success of a chemical peel depends on a 
careful selection of patients and individualization 
of the treatment.
Patients with extra-facial (hands, trunk) dys-
chromia and photoaging. It can be useful to com-
plement laser, IPL, and other treatment 
technologies (Fig. 17.2).
E. Monteiro (*) 
Department of Humanities and Medical Sciences, 
Federal University of São Paulo (UNIFESP), 
São Paulo, SP, Brazil
e-mail: erica@dermatologia.com.br
17
2
1
4
5
3 7
6
Fig. 17.1 (1) Resorcinol 20% (ethanol solution). (2). 
Alcohol to clean and degrease the skin. (3). Glass cup or 
beaker in which the required agent is poured. (4). Cotton- 
gauze pieces. (5). Cotton-tipped applicators or swab 
sticks. (6). Gloves. (7). Sunscreen after the procedure
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_17&domain=pdf
mailto:erica@dermatologia.com.br
118
17.2.2 Technique Using Resorcinol 
20% (Ethanol Solution)
• At first, the patient’s skin is cleaned (by cotton 
impregnated with 70% ethanol and/or acetone).
• Laser or IPL is performed.
• In the next step, the solution of resorcinol 20% 
is applied on the hands with a cotton 
applicator.
• Neutralization is not necessary.
• Finally, sunscreen is applied.
• The treatment can be repeated after 4–8 weeks, 
if necessary.
17.3 Clinical Follow-Up
17.3.1 Pre-peeling Preparation 
(Table 17.1)
• For optimal results, preparation of the skin in 
the weeks before the procedure is very 
important.
• Topical retinoic acid preparations used daily 
for 3–6 weeks prior to the procedure may cre-
ate better and more even penetration of the 
peeling solution in sebaceous and hyperkera-
totic skins.
• Standard photography and informed consent 
should always be obtained before the proce-
dure for all types of peelings.
• Generally, it is not necessary to discontinue 
use of any of the patient’s medications 
including anticoagulants, aspirin, or nonste-
roidal anti-inflammatory or antihypertension 
drugs.
• According to our experience with superficial 
peeling, smoking does not have any adverse 
effect on post-peel healing or on the extent of 
the results.
17.4 Before and After (Fig. 17.2)
a b
Fig. 17.2 (a) Before and (b) after resorcin 20% peel. (Courtesy: Andrezza Facci, MD; Barueri, SP, Brazil)
E. Monteiro
119
17.5 Side Effects, Complications, 
and Their Management
17.5.1 Post-peeling 
Recommendations 
(Table 17.1) [1–6]
• The goal of a chemical peel is to cause the 
outer layer of the skin to peel and flake, reveal-
ing the fresh, smooth layer underneath.
• Patients will experience some level of dryness 
and flaking for 2–5 days after treatment.
• During this time of dryness and flaking, their 
skin is more sensitive (more redness and sting-
ing), and they cannot use vitamin C, retinol, 
avobenzone, glycolic acid, and lactic acid.
• In this 2–5-day period, using a soothing gel or 
mask helps calm and soothe the skin. Other 
great options to use in this post-procedure 
time period are heparan sulfate and hyaluronic 
acid.
• Patients should be advised to stay out of the 
sun and to avoid picking at dry, flaking skin. 
Resorcinol is an ultraviolet light absorber and 
can cause allergic contact dermatitis reactions. 
Avoiding the sun is mandatory [6].
• Exfoliating scrubs and other facial brushes 
and other forms of friction, including micro-
dermabrasion, should be avoided during the 
healing process.
• Avoid any products with hydroxy acids, reti-
nol, and 5-fluoruracil (5-FU) until the skin 
barrier has been restored.
• Use calming skincare products with anti-
inflammatory ingredients such as green tea, 
argan oil, and chamomile to help alleviate 
any stinging or redness, while the skin 
recovers.
Table 17.1 Pre- and post-resorcinol 20% peel, after IPL/laser, recommendations [1–6]*
Considerations Benefits/recommendations
Pre (at least 
2–4 weeks prior 
to the procedure)
Post 
(immediate)
Post (long after 
complete 
reepithelization)
Priming Reduces wound healing time, facilitates 
uniform penetration, detects intolerance 
to any agent, enforces patient 
compliance, and reduces the risk of 
complications
+
Infections Control any active infection or 
dermatoses
+ + +
Photoaging Topical retinoids, alpha-hydroxy acids + − +
Post-inflammatory 
hyperpigmentation
Topical retinoids, hydroquinone, 
alpha-hydroxy acids, vitamin C
+ − +
Photoprotection Broad-spectrum sunscreens and clothes + + +
Moisturization + + +
Fast healing Tretinoin 0.025% + − + (after 
reepithelization)
Maintenance (agents 
which are likely to be 
used in post-procedure 
maintenance)
Tretinoin 0.025%, glycolic acid 6–12% + (after 
reepithelization)
* Tretinoin is known to reduce healing time after resurfacing. The choice of the priming agent depends on the individual 
physician's preference and individualized patient requirements
17 Resorcin Peel for Extra-Facial Areas
120
References
 1. Khunger N, IADVL Task Force. Standard guidelines 
of care for chemical peels. Indian J Dermatol Venereol 
Leprol. 2008;74 Suppl:S5–12.
 2. Faghihi G, et al. Solution of azelaic acid (20%), res-
orcinol (10%) and phytic acid (6%) versus glycolic 
acid (50%) peeling agent in the treatment of female 
patients with facial melasma. Adv Biomed Res. 
2017;6:9.
 3. Karam PG. 50% resorcinol peel. Int J Dermatol. 
1993;32(8):569–74.
 4. Monteiro EO. Acne e fotoproteção. RBM Rev Bras 
Med. 2009;66(6, n. esp):6–9.
 5. Monteiro EO.  Filtros solares e fotoproteção. RBM 
Especial Dermatologia e Cosmiatria. 2010;67:5–18.
 6. Ongenae K, Matthieu L, Constandt L, Van Hecke 
E.  Contact allergy to resorcinol monobenzoate. 
Dermatology. 1998;196(4):470–3.
Tip Box
• With the advent of lasers and newer 
techniques, the use of some chemical 
peels has declined, as resorcinol peel for 
extra-facial treatment.
• Nowadays, the use of resorcinol peel 
alone to rejuvenate the hands or other 
extra-facial areas is not common. But it 
can be useful to complement laser, IPL, 
and other treatment technologies.
• Resorcinol is an ultraviolet light 
absorber and can cause allergic contact 
dermatitis reactions. Avoiding the sun is 
mandatory.
• Retinoids should be used 2–3  weeks 
prior to procedures to speed up healing.
• Retinoids should not be used after the 
procedure until reepithelization has 
occurred.
• Standard photography and informed 
consent should always be obtained 
before the cosmetic procedures.
E. Monteiro
121© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_18
Salicylic Acid for Face (Facial 
Salicylic Acid Peel)
Mercedes Florez White
18.1 Materials
A variety offormulations of salicylic acid have 
been used for skin care products, for chemical 
peeling, and for keratolytic agents.
• SA has been used in concentrations from 0.5% 
to 50% (Table 18.1) [1].
• The most common concentrations for chem-
ical peels are 20% and 30% in hydroalco-
holic solution, as well as newer formulations 
with different vehicles, including one with 
SA 30% in a gel of polyethylene glycol, 
which has shown to be safer (less absorption) 
[1–3].
18.2 Methods and Techniques
The procedure includes three stages or phases: 
The preparation before the peel, the actual proce-
dure or peeling technique, and the post-peeling 
care and management of complications.
18.2.1 Indications 
and Contraindications
• SA peels are useful in a variety of skin condi-
tions. The list of these conditions is shown in 
Table 18.2, being acne as the main and most 
studied indication.
• One of the advantages of the SA peel is that it 
is safe to be used in any skin photo-type, since 
Fitzpatrick photo-type I to VI.
• SA peel is safe and effective in patients with 
skin photo-types V and VI.
• They can also be combined with other proce-
dures, such as microdermabrasion or as a part 
of a rejuvenating program, alternating with 
lasers, lights, and other technologies.
• Could be used in combination with oral isotret-
inoin treatment showing significantly better 
M. F. White (*) 
Department of Dermatology, Herbert Wertheim 
College of Medicine, Florida International University, 
Miami, FL, USA
e-mail: mflorez@fiu.edu
18
Table 18.1 Concentrations of SA used in dermatology 
and cosmetics (Modified from Arif T)
SA 
concentration Uses
0.5–10% Topical treatment of acne (skin care 
products: cleansers, lotions, solutions)
3–6% Topical treatment of hyperkeratotic 
disorders (psoriasis, ichthyoses, 
keratosis pilaris)
5–40% Warts – corns
50% Actinic damage
20–30% Superficial chemical peeling of the 
face
SA salicylic acid
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_18&domain=pdf
mailto:mflorez@fiu.edu
122
clearance of acne than monotherapy with 
isotretinoin and with no abnormal scarring.
• SA peel is contraindicated in patients with 
contact dermatitis or allergy to salicylates, 
active infection, including viral at the site of 
the peeling, active dermatitis on the face, 
intense erythema and dryness due to retinoids 
or AHA, and pregnancy. A very good clinical 
history including all previous reactions to 
medications and procedures is mandatory to 
avoid complications.
18.2.2 Preparation Before Peeling
• Proper patient selection is crucial before con-
sidering a chemical peel.
• Detailed history and cutaneous examination 
are performed in all patients prior to chemical 
peeling.
• Standardized photographs of the areas to be 
peeled should be taken, including full-face 
frontal and lateral views. If the condition 
treated requires it (e.g., melasma), UV photo-
graphs could help in the assessment of the 
evolution and results of the treatment.
• Pretreatment with tretinoin, retinol, AHA, or 
poly-hydroxy acids at least 2 weeks before the 
procedure should be discontinued 2  days 
before the peel.
• For patients with hyperpigmented disorders and 
those prone to have post-inflammatory hyper-
pigmentation, pretreat with 4% hydroquinone or 
triple combination (hydroquinone 4%, fluocino-
lone acetonide 0.01% and tretinoin 0.05%) for at 
least 2 weeks before the procedure, and stop the 
medication at least 2 days before the peel.
• Use broad-spectrum inorganic sunscreens 
(UVA-UVB) with an SPF 30 or more, are 
mandatory and should be applied frequently 
before and after the procedure.
• The simultaneous use of antioxidants (e.g., 
vitamin C or combinations of vitamin C plus 
E) with sunscreens may help in preventing 
post-inflammatory hyperpigmentation.
18.2.3 Peeling Techniques
Before starting the procedure, the physician 
should be having ready the following (Fig. 18.1):
• The peeling compound – 20% or 30% SA peel 
in alcoholic solution or gel
• A gentle cleanser for sensitive skin or a lipo- 
hydroxy acid (LHA) or SA cleanser for oily 
skin
• Isopropyl alcohol to degrease the skin or ace-
tone if the skin is very oily
• Gloves
• 4 × 4 non-woven gauzes to clean the skin
• “Harsh” standard 4  ×  4 gauze to apply the 
peeling substance
• 1 inch paint sponge
• A surgical cap and a headband to cover the 
patient’s head
• Petrolatum to protect sensitive areas of the 
face such as the lips and folds
• Soothing mask (optional)
• Bland moisturizer (optional)
• Sunscreen
• Portable handheld fan (battery operated or 
electrical)
Table 18.2 Main indications of salicylic acid peels
Acne
Melasma
Rosacea
Excessive oiliness of the skin
Solar lentigo
Photodamage (mild to moderate)
Fine lines
To improve skin texture of the face
Fig. 18.1 Material for salicylic acid peel procedure
M. F. White
123
18.2.4 Directions
• Before starting the procedure, the patient 
must sign an informed consent with the 
explanation of the procedure and post- 
procedure care, including possible 
complications.
• Take pictures of the area that will be peeled, if 
not taken during a previous visit.
• Patient should cover the head with a surgical 
cap and should also use a headband to pull 
back the hair from the face.
• Clean very well facial skin using the cleanser 
according to the skin type: A gentle cleanser 
for a sensitive to dry skin and a cleanser with 
SA or LHA for oily skin.
• The face is then degreased using a non- woven 
gauze piece socked with alcohol or acetone. 
Some SA peel kits bring a pre-peel cleanser 
that may be used at this time instead of alcohol 
or acetone.
• Apply a thin layer of petrolatum on sensitive 
areas of the face such as the lips, the nasal- 
alar cheek junction, and the preauricular 
fold.
• Apply the salicylic acid solution or gel with 
a wedge sponge or a “harsh” gauze. (The 
author starts with 20% concentration to 
assess the skin reaction of the patient.) The 
application should be uniform on the entire 
face and upper neck, starting from the fore-
head and progressing to the zygomatic 
cheeks, chin, upper lip, nose, and lower eye-
lids. The whole application should be com-
pleted within 30 s. At this point the subject 
experiences a stinging and burning sensa-
tion, which increases over the next 2  min-
utes, reaches a crescendo at 3 minutes, and 
then rapidly decreases to baseline over 
5 minutes after the application; this is con-
sidered the end point of the peel. The burn-
ing sensation and stinging can be reduced 
using a portable handheld fan. As the hydro-
ethanolic vehicle evaporates, it leaves behind 
a white precipitate of salicylic acid on the 
surface of the face, due to the crystallization 
of the SA which is termed as salicylic acid 
frost (Fig.  18.3). This should not be con-
fused with frosting or whitening of the skin, 
which represents protein agglutination. 
There is very little penetration of the active 
agent once the vehicle has volatilized. At 
this point, there is no burning or stinging as 
the agent causes a superficial anesthesia to 
light touch. In patients with acne, this is the 
time to perform the comedo extraction to 
take advantage of the temporary superficial 
anesthesia.
• Since SA peel is self-neutralized, patient’s 
face is now rinsed thoroughly with water and 
a bland cleanser to remove any residual of SA 
precipitate.
• Use a soothing mask – optional. (The author 
uses a refreshing cellulose mask for 15 min-
utes after the final cleansing.)
• Apply UVA-UVB inorganic (physical) 
sunscreen.
• Patient should be instructed to use daily sun-
screen and a wide brim hat all the time, espe-
cially when the skin exfoliation starts.
• Give the patient a written post-procedure 
instructions that should be signed by the 
patient and a copy should be included in the 
patient’s chart.
18.3 Clinical Follow-Up
• Use gentle cleansers and bland moisturizers 
for the first 48 hours.
• Peeling usually begins2  days post-peel. At 
this time patients can resume their topical 
skin care formulations, which may include 
topical hypopigmenting agents, topical anti-
acne medications, and/or retinoids, AHA or 
PHA.
• Permanent use of an inorganic, broad- 
spectrum sunscreen is mandatory.
• Antioxidants. There is enough evidence that 
the concomitant use of antioxidants, such as 
vitamin C, may minimize the effects of ultra-
violet and visible light, as well as the forma-
tion of free radicals by the infrared A rays. 
Its use can help reducing the inflammation 
and, therefore, the post-inflammatory 
hyperpigmentation.
18 Salicylic Acid for Face (Facial Salicylic Acid Peel)
124
• Excessive desquamation and irritation in the 
post-peel period can be treated with low- to 
high-potency topical steroids. Topical steroids 
are very effective in resolving post-peel 
inflammation and mitigating the complication 
of post-inflammatory hyperpigmentation.
• Any residual post-inflammatory hyperpig-
mentation resolves with the use of topical 
hydroquinone formulations following sali-
cylic acid peeling.
18.4 Before and After
Results of salicylic acid peels in acne and melasma 
are shown in Figs. 18.2 and 18.3, respectively.
Fig. 18.3 Salicylic acid 
precipitate (salicylic 
acid frost)
Fig. 18.2 Patient with 
acne under treatment 
with oral isotretinoin 
and three treatments 
with 30% salicylic acid 
peel in hydroalcoholic 
solution
M. F. White
125
18.5 Side Effects, Complications, 
and Their Management
Hypergpigmentation: Which can be easily treated 
with daily photoprotection and combination of 
retinoids and hydroquinone.
Prolonged erythema, exfoliation, and dry skin: 
Use of photoprotection and local moisturizing; in 
severe cases, the use of topical corticoids can be 
well indicated.
Salicylism: Although it is a rare side effect when 
this peel is applied onto small skin area, as the face, 
if symptoms are absorbed (such as nausea, vomit, 
dizziness, psychosis, and stupor), to administrate 1 
liter of water after finishing the peel can be a good 
alternative. In intense clinical manifestations, the 
referral to an urgent care unit is mandatory.
Fig. 18.4 Melasma. 
Treatment with 
hydroquinone 4% and 
three sessions of 30% 
salicylic acid peel in gel
Tip Box 
Indications
• Salicylic acid 20–30% is the peeling 
agent of choice in acne.
Preparation
• Pretreatment, at least 2 weeks before the 
procedure, is important to enhance the 
penetration of the SA and to prevent 
future complications.
• Acne and photoaging are pretreated, 
with tretinoin, retinol, AHA, or poly- 
hydroxy acids and should be discontin-
ued 2 days before the peel.
• Hyperpigmented conditions (melasma, 
post-inflammatory hyperpigmenta-
tion) are pretreated with hydroquinone 
4% or triple combination (hydroqui-
none 4%, fluocinolone acetonide 
0.01%, and tretinoin 0.05%) and dis-
continued 2 days before the procedure 
(Fig. 18.4).
• It is safe and effective in all types of 
active acne due to its comedolytic and 
anti-inflammatory properties.
18 Salicylic Acid for Face (Facial Salicylic Acid Peel)
126
References
 1. Arif T.  Salicylic acid as peeling agent: a compre-
hensive review. Clin Cosmet Investig Dermatol. 
2015;8:455–61.
 2. Dainichi T, Ueda S, Isoda M, et al. Chemical peeling 
with salicylic acid in polyethylene glycol vehicle sup-
presses skin tumor development in hairless mice. Br J 
Dermatol. 2003;148:906–12.
 3. Davies M, Marks R. Studies of the effect of salicylic 
acid in normal skin. Br J Dermatol. 1976;95:187–92.
 4. Grimes PE.  Salicylic acid. In: Tosti A, Grimes PE, 
Padova MP, editors. Color atlas of chemical peels. 2nd 
ed. New York: Springer-Verlag; 2006.
 5. Imayama S, Ueda S, Isoda M. Histologic changes in 
the skin of hairless mice following peeling with sali-
cylic acid. Arch Dermatol. 2000;136:1390–5.
 6. Kontochristopoulos G, Platsidaki E.  Chemical 
peels in active acne and acne scars. Clin Dermatol. 
2017;35:179–82.
 7. Lazo ND, Meine JG, Downing DT. Lipids are cova-
lently attached to rigid corneocyte protein envelope 
existing predominantly as beta-sheets: a solid state 
nuclear magnetic resonance study. J Invest Dermatol. 
1995;105:296–300.
 8. Lee HS, Kim IH. Salicylic acid peels for the treatment 
of acne vulgaris in Asian patients. Dermatol Surg. 
2003;29:1196–9.
Post-peeling Care
• Patients must avoid sun exposure after 
the procedure.
• Daily use of a broadband (UVA-UVB) 
inorganic, mineral sunscreen with SPF 
30 or more and other measures like 
using a wide brim hat are key to prevent 
post-inflammatory hyperpigmentation.
M. F. White
127© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_19
Salicylic Acid Peeling 
for Extra- Facial Areas
Vanesa Piquero, Daniela Moya, 
and Edgar E. La Rotta
19.1 Materials
• Cleaning solution, alcohol, and acetone for 
degreasing.
• Cleansing clay mask and ozone vaporizer 
(optional use) [1].
• Salicylic acid concentrations ranging from 
10% to 50% in solutions of ethanol, polyeth-
ylene glycol, ointment, paste, or ethyl alcohol. 
Amber bottle, closed. Shake before using.
• 30% salicylic acid is used for chest and back 
acne, keratosis, and pigmented photodamage.
• 40% to 50% salicylic acid is used for warts, 
calluses, psoriasis, and actinic lesions [2].
• 50% salicylic acid ointment with croton oil 
buffered with methyl salicylate is useful in 
photodamage in hands or palmoplantar hyper-
keratosis [3–5].
• Applicators or gauze (preferably disposable) 
or brush (not recommended for risk of con-
tamination), are used to apply the salicylic 
peel.
• A manual fan is used to relieve burning but in 
corporate areas sometime is not necessary 
because the peeling is well tolerated.
• Cryogel and rose or thermal water is used 
[2, 6].
• It can be finished by applying another sub-
stance to be taken to home, such as retinoic 
acid, hydroquinone, and vitamin C occluding 
with transparent film. If not, apply sunscreen 
or soothing cream of witch hazel (Fig. 19.1) 
[1, 7, 8].
19.2 Methods and Techniques
19.2.1 Pre-peeling
• Ensure that the patient is not allergic to 
salicylates.
• Avoid applying in dermatitis, active infec-
tions, pregnancy, tanning, and in patients with 
isotretinoin medications (suspended for at 
least 3 months).
• To prepare the skin, you must consider the 
area and the lesion to be treated.
V. Piquero (*) 
Clinica Leopoldo Aguerrevere Caracas, 
Caracas, Venezuela 
Clinica Dermik Barcelona, Barcelona, Spain 
D. Moya 
Hospital Universitario de Caracas, 
Caracas, Venezuela 
Hospital Intercultural Kallvu Llank Chile, 
Cañete, Región del Bío Bío, Chile 
E. E. La Rotta 
Centro Medico Buenaventura en Caracas, 
Guatire, Venezuela 
Hospital Clinic Barcelona, Barcelona, Spain
19
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_19&domain=pdf
128
• In case of back and chest acne; is recomended 
the previous application (2–6 weeks) of topi-
cal retinoids or benzoyl peroxide.
• For hyperpigmented lesions is recomended 
to previously prepare the skin with kojic 
acid, alpha-hydroxy acids, hydroquinone 
before.
• In case of actinic damage, use topical retinoids 
before salicylic peeling [1, 2].
• Substances used for the preparation of skin 
conditions should be suspended 24 h prior to 
the application of the peeling.
• A detailed consent form listing details about 
the procedure and possible complications 
should be signed by the patient [1, 9].
• Select patients from any phototype, but greater 
caution should be exercised in IV and V pho-
totypes [2].
• Explain to the patient the actual peeling 
results, such as reinforcement of home treat-
ment and the need for several sessions.
• Photographic control of the area to be treated 
(Figs. 19.2, 19.3, 19.4, and 19.5).
19.2.2 Peeling
• Remove debris from the skin area to be treated, 
clean or wash with cleaner or mild soap, or 
applya degreaser based on ethanol, alcohol, 
or acetone.
• Apply the peeling of salicylic acid with 
5 × 5  cm gauze or cotton applicator, always 
Fig. 19.1 Materials
Fig. 19.2 Salicylic paste for palmar hyperkeratosis. Step 
1: clean/wash beforehand with cleaner
Fig. 19.4 Step 3—applied occlusive with clear plastic 
paper for 24–48  h. Come back 1 week after the 
procedure
Fig. 19.3 Step 2—apply peeling agent; in this case was 
used salicylic acid paste at 50%
V. Piquero et al.
129
adapting the amount applied to the skin type 
[1, 7, 9].
• The number of layers varies between 2 and 4 
layers of the product in each session. For exam-
ple, in the neck and neckline usually need only 
two layers, for the arms and hands are neces-
sary three layers, and for the back four layers.
• If the patient feels intolerable burning sensation 
or have an intense erythema, stop the applica-
tion and the peeling must be removed [1].
• Each layer should be applied uniformly, through-
out the area, following an order in its application, 
so as not to omit an area and avoid being irregu-
lar, in a circle or in a square, for example.
• The time of contact with the skin will depend 
on the type and area of skin to be treated, with 
an approximate of 3–5 min.
• After 1–3 min, the burning and itching sensa-
tions are sought to reduce using a portable 
hand fan or cryogel.
• Use rose water or thermal water to reduce 
symptoms.
• This peeling doesn’t need to be neutralized 
and produces a frosty product of the precipita-
tion of salicylic acid on the skin, becoming a 
whitish frost.
• We recommended a time of 3–4  weeks to 
repeat the application, although it could be 
every 2 weeks if the skin is not sensitive and 
the results were lighter than desired.
• In the case of 30% salicylic acid, it is advis-
able not to apply in a body extension greater 
than 10%. As examples of extension, we can 
cite the whole back or both arms or middle 
back and chest.
• In all cases, it is recommended to ingest water 
to avoid salicylism, during or after the 
procedure.
• After relieving the symptoms, another chemi-
cal can be added, or the area is rinsed with 
thermal water, and a moisturizer and sun-
screen are applied.
• The 50% salicylic paste form can be applied 
with plastic film during 24–48 h, and the 
patient has to remove at home, this should be 
repeated 7 days after the first application in 
the doctors office.; this is useful in hyperkera-
tosis palmar or plantar.
19.2.3 Post-peeling
• Use photo protection, especially in the first 
48–72  h after the application of the peeling 
and up to about 15 days.
• Keep the skin moisturized.
• This peeling reddens a little and peels a lot.
• It is advisable to ingest 1 l of water in the post- 
peeling hours.
• The effects of extra-facial salicylic peeling not 
only depend on the concentration of the acid 
but also depend on the area to be treated, for 
example, in neck area, the erythema and the 
renovation of the skin will be slower than 
 others parts of the body, while in stretch marks 
of the legs the effect of this peeling is smooth. 
[1, 4, 5, 7, 10].
Fig. 19.5 Application of 30% salicylic acid peeling in 
dorsal acne lesions
19 Salicylic Acid Peeling for Extra-Facial Areas
130
19.3 Clinical Follow-Up (Figs. 19.6, 
19.7, 19.8, and 19.9)
• The application of superficial peels, as is the 
case of salicylic acid, partially eliminates the 
epidermis, without reaching the basement 
membrane.
• It causes an improvement in the skin surface 
and results in a smoother and cleaner skin.
• The first 48–72  h will result in redness and 
desquamation of the treated area [8].
• The improvement of the treated skin can be 
observed up to 1 month after the application of 
the treatment, since the process of remodeling 
elastin and collagen fibers needs a period of 
approximately 21 days [2, 5, 8].
Fig. 19.6 Peeling for back acne
Fig. 19.7 Salicylic acid peeling for back folliculitis in 
men
Fig. 19.8 Peeling for erythematous striae in the abdo-
men. Peeling of salicylic acid + retinoic acid 5% occlusive 
with transparent film for 6 h
Fig. 19.9 Peeling for erythematous stretch marks—24 h 
post-application of salicylic peeling in stretch marks
V. Piquero et al.
131
• Good benefits have been proven in the 
treatment of comedones, inflammatory 
lesions, as well as photodamage and 
hyperkeratosis.
• It is used in the treatment of acne vulgaris in 
the chest and back, obtaining good results in 
comedones as in residual hyperpigmented 
spots [6, 7].
• It is also used in extra-facial hyperpigmenta-
tion and lesions due to actinic damage, pilar 
keratosis, psoriasis, and callosity, among 
others.
• Another indication of salicylic peeling is for 
red streaks, with proven effectiveness when 
combining microdermabrasion plus salicylic 
peeling plus occlusive retinol for 6 h.
• We must inform the patient that he should con-
tact us in case of any type of complication.
• In the case of salicylic acid paste, ask patient 
to return in 7 days [1, 8].
• For the peeling of traditional salicylic only or 
combined in general, the patient is requested 
to return to the office within 3  weeks or 
21 days of application [2].
19.4 Before and After
See the Figs.  19.10, 19.11, 19.12, and 19.13. 
After three treatments, one peel per month, and 
with sun protection and domiciliary treatment, 
the results are very satisfactory.
Figs. 19.10 and 
19.11 Before and after 
salicylic peeling and 
domiciliary treatment 
for hyperpigmentation 
post-intense pulsed light 
(IPL)
Figs. 19.12 and 19.13 Before and after one-session salicylic peel for chest acne
19 Salicylic Acid Peeling for Extra-Facial Areas
132
19.5 Side Effects, Complications, 
and Their Management
• Peeling with salicylic acid is safe, rarely 
involves adverse effects, and is not very com-
plicated. If any complication is present, that is 
mild and transient [3].
• Salicylic acid may cause prolonged local ery-
thema, exfoliation or severe flaking, and dry-
ness. In areas such as the chest, back, hands, 
and forearms, the main complications are dry-
ness and dyschromia [2, 3].
• Patients with skin phototypes IV and V are 
most likely to develop erythema of the treated 
area and should be disciplined with post- 
peeling care, since these skins types are more 
vulnerables to develop hyperpigmentation; 
hypopigmentation such as pityriasis alba 
occurs in these phototypes when associated 
with dry skin [2, 6].
• Use moisturizing creams, to soften the skin 
with desquamation.
• In case of excessive scaling and irritation in 
the post-exfoliation period, topical steroids 
can be treated (Fig. 19.15).
• The main precaution to take with body peeling 
is the risk of percutaneous absorption toxicity, 
especially if we use high concentrations in 
very large areas of the skin. That is why we 
must recommend ingesting 1 l of water after 
the application [2, 5–7].
• Salicylism, which may occur due to rapid 
absorption (especially when combined with a 
base or is occluded in large areas), could 
become toxic to the central nervous system, 
manifesting itself with nausea, vomiting, dizzi-
ness, psychosis, stupor, and, consequently, 
coma and death [2].
• Salicylism produces cellular glucose con-
sumption with the consequences described 
above for the organism [2] Some locals com-
plications can be observed in the attached fig-
ures (Figs. 19.14 and 19.15).
Fig. 19.15 Complication with salicylic peel plus plate-
let-rich plasma for stretch marks
Fig. 19.14 Complication with salicylic paste peel—pro-
longed local erythema, exfoliation or severe flaking, dryness
Tip Box
• The most frequent indications are body 
acne and keratosis pilaris.
• This peeling can be popular in summer 
for plantar keratosis.
• In pilar keratosis and folliculitis of men, 
it is a good choice.
• We must be careful with the extensions 
of the skin to be treated. Do not apply in 
very large areas.
V. Piquero et al.
133
References
 1.Bosniak S, Cantisano-Zilkha M. Tecnicas minimam-
ente invasivas. New York: Amolca; 2007.
 2. Arif T.  Salicylic acid as a peeling agent: a compre-
hensive review. Clin Cosmet Investig Dermatol. 
2015;8:455–61. https://doi.org/10.2147/CCID.
S84765.
 3. Fischer T, Perosino E, Poli F, Viera M, Dreno B, For 
the Cosmetic Dermatology European Expert Group. 
Chemical peels in aesthetic dermatology: an update 
2009. J Eur Ac Derm and Ven. 2010;24:281–92. 
https://doi.org/10.1111/j.1468-3083.2009.03409.
 4. Salam A, Dadzie OE, Galadari H. Chemical peeling in 
ethnic skin: an update. Br J Dermatol. 2013;169:82–
90. https://doi.org/10.1111/bjd.12535.
 5. Grajqevci-Kotori M, Kocinaj A.  Exfoliative skin- 
peeling, benefits from this procedure and our expe-
rience. Med Arch. 2015;69(6):414–6. https://doi.
org/10.5455/medarh.2015.69.
 6. Nikalji N, Godse K, Sakhiya J, Patil S, Nadkarni 
N. Complications of medium depth and deep chemi-
cal peels. J Cutan Aesthet Surg. 2012;5(4):254–60. 
https://doi.org/10.4103/0974-2077.104913.
 7. Rendon MI, Berson DS, Cohen JL, Roberts WE, 
Starker I, Evidence WB. Considerations in the appli-
cation of chemical peels in skin disorders and aesthetic 
resurfacing. J Clin Aesth Dermatol. 2010;3(7):32–43.
 8. Pearl E.  Grimes. Exfoliaciones con ácido salicí-
lico. In: Rubin MG, editor. Exfoliación química. 
Barcelona, España: Elsevier Saunders; 2007.
 9. Khunger N, IADVL Task Force. Standard guidelines 
of care for chemical peels. Indian J Dermatol Venereol 
Leprol. 2008;74 Suppl:S5–12.
 10. Karia UK, Padhiar BB, Shah BJ.  Evaluation of 
various therapeutic measures in striae rubra. J 
Cutan Aesthet Surg. 2016;9(2):101–5. https://doi.
org/10.4103/0974-2077.184056.
• Remove with water or bicarbonate 
immediately, in case of excessive 
redness.
• This peeling is a good option when the 
patient wants to peel the skin.
• The 50% salicylic paste form is applied 
occlusive with clear plastic paper and is 
useful in callus, psoriasis, and 
hyperkeratosis.
• Another curious application of the 
occlusive salicylic paste is in the case of 
hedgehog spicules in the soles of divers; 
when left for 48  h and removed, the 
spicules are removed in a painless 
manner.
• This peeling can be associated with oth-
ers, such as making a general peel of 
glycolic acid and subsequent specific 
application of salicylic acid in the com-
edones or inflammatory lesions. Or you 
can apply salicylic acid in the entire area 
to be treated and then apply retinoic acid 
5% with plastic film occlusive for 6 h.
19 Salicylic Acid Peeling for Extra-Facial Areas
https://doi.org/10.2147/CCID.S84765
https://doi.org/10.2147/CCID.S84765
https://doi.org/10.1111/j.1468-3083.2009.03409
https://doi.org/10.1111/bjd.12535
https://doi.org/10.5455/medarh.2015.69
https://doi.org/10.5455/medarh.2015.69
https://doi.org/10.4103/0974-2077.104913
https://doi.org/10.4103/0974-2077.184056
https://doi.org/10.4103/0974-2077.184056
135© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_20
Tretinoin Peel for Face
Luciane Scattone
20.1 Materials
The peel is prepared with powder retinoic acid 
(RA) dissolved in ether, alcohol, and propylene 
glycol solution up to the desired concentration 
(ranging from 1% to 12%). We can add light or 
dark pigment dye to mask the yellow color of the 
product (Figs. 20.1 and 20.2) [1, 2].
20.2 Methods and Techniques
Even considering the fact that it is a superficial 
peeling, with epidermal exfoliation of the granu-
lar layer up to basal layer (0.45 mm), we should 
comply with the indication criteria for RA peel. 
The clinician should properly assess the patient, 
analyze his/her psychological profile, check the 
integrity of dermal barrier, and take into consid-
eration photoaging, age, gender (in women the 
penetration is higher because the skin is finer), 
clinical presentation, skin thickness, skin photo-
type (type I people experience deeper penetration 
than the others), whether the patient can go to 
work showing skin desquamation, etc. [2].
When greater, faster, and more homogeneous 
penetration of the product is desired, the patients 
should prepare the skin by applying lighter acids 
10 days before the peel session [2, 3].
L. Scattone (*) 
Clínica Dermatológica Dra Luciane Scattone, 
São Paulo, SP, Brazil
20
Fig. 20.1 Material used—finger protector, brush, and 
peel
Fig. 20.2 RA peel with dye. (A) and RA peeling without 
dye (B)
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_20&domain=pdf
136
20.2.1 How to Apply
There is no need to have previous topical 
anesthesia.
After applying make-up remover, the entire 
face is cleaned with gauze soaked with chlorhexi-
dine, ketone, or alcohol [3], to degrease the skin. 
The peel may be formulated as gel, lotion, cream, 
or propylene glycol with color dye or in its natu-
ral color (yellowish) [1].
Using a cotton swab, brush, or finger protec-
tor [2], apply the product homogeneously on 
the entire face, avoiding areas close to the nose, 
mouth, and eyelids. There is no need for neu-
tralization; each clinician should standardize 
the peels preferably by buying products always 
by the same supplier to avoid undesirable 
results.
The peel remains on the patient’s skin for 
3–12 h, provided that it does not cause any burn-
ing sensation or discomfort.
Removal of the peeling should be made with 
liquid soap, and moisturizer is applied only when 
desquamation starts as of day 3. However, if the 
patient needs immediate moisturizing due to dis-
comfort, it does not affect the expected result.
Daily use of broad-spectrum sun protection is 
recommended [2, 4, 5], as well as the use of 
physical protection such as caps and glasses, 
especially for subjects that play sports.
Normally, the process of desquamation finishes 
in 7 days, which may vary according to skin type.
According to the indication, 3–5 weekly or 
monthly sessions are required until the expected 
result is reached.
The patient should necessarily be informed in 
writing and verbally about the post-peel care. It is 
important to emphasize that the patient may have 
to avoid social gatherings until the desquamation 
is over and avoid sun exposure for at least 
1 month after the last serial peel.
Patients with previous history of herpes may 
perform prophylactic antiviral therapy with acy-
clovir or valacyclovir (per os [PO] for 5 days) at 
the clinician’s discretion [2].
Photographic documentation should be made 
before and after each peel, always with the same 
lighting (Figs. 20.3, 20.4, and 20.5).
Fig. 20.3 Aspect of the skin during RA peel application 
with color dye (B) and without color dye (A)
Fig. 20.4 Application of RA peel with finger protector
L. Scattone
137
20.3 Before and After (Figs. 20.6, 
20.7, 20.8, 20.9, 20.10, 20.11, 
20.12, and 20.13)
Fig. 20.5 Application of RA with brush
Figs. 20.6 and 20.7 Melanosis and photodamage after first and fifth sessions of 5% RA peel
20 Tretinoin Peel for Face
138
Figs. 20.8 and 20.9 Melasma after first and third sessions of 7% RA peel
Figs. 20.10 and 20.11 Periorbicular wrinkles before after fourth session of 5% RA peel
L. Scattone
139
Figs. 20.12 and 20.13 Melasma on the upper lip before after fourth session of 5% RA peel
20.4 Side Effects, Complications, 
and Their Management
Adverse events are normally mild and transient, 
and the most frequent one is erythema, followed 
by burning sensation, desquamation, simplex 
herpes episodes, post-inflammatory pigmenta-
tion, and flare of rosacea [2, 4, 6, 7].
Management may include cold thermal water, 
topical low-power corticoid, Vaseline gel, and 
herpes treatment, if applicable (Figs. 20.14 and 
20.15). Fig. 20.14 Fine and marked desquamation after 3 days 
post-application of RA peel. 5%
20 Tretinoin Peel for Face
140
References
 1. Kong R, Cui Y, Fisher GJ, Wang X, Chen Y, Schneider 
LM, Majmudar G. A comparative studyof the effects 
of retinol and retinoic acid on histological molecu-
lar, and clinical properties of human skin. J Cosmet 
Dermatol. 2016;15:49–57.
 2. Yokomizo VMF, Benemond TMH, Chisaki C, 
Benemond PH.  Chemical peels: review and pratical 
applications. Dermatol. 2013;5(1):56–68.
 3. Guerra FMRM, Krinsk GG, Campiotto LG, 
Guimaraes KMF.  Applicability of chemical peels 
facial at treatments  – study review. Brazilian 
Journal of Sugery and Clinic Research  - BJSCR 
2013;4(3):33–6.
 4. Magalhães GM, Borges MFM, Queiroz ARC, 
Capp AA, Pedrosa SV, Diniz MS.  Estudo duplo-
cego e randomizado do peeling de ácido retinóico 
a 5% e 10% no tratamento do melasma: avaliação 
clínica e impacto na qualidade de vida. Dermatol. 
2011;3(1):17–22.
 5. Denise S, Camila F, Mediana B, Fernanda 
AMS.  Treatment of melasma: systematic review. 
Surg Cosmet Dermatol. 2009;1(2):87–94.
 6. Yildirim S, Gurel MS, Gungor S, Tekeli O, Canat 
D.  Comparison of efficacy of chemical peeling 
with 25% thichloroacetic acid and 0,1% retinoic 
acid for facial rejuvenation. Adv Dermatol Allergol. 
2016;XXXIII(3):199–205.
 7. Park SE, Kim SS, Kim CW, Her Y. A prospective split- 
face comparative study of periorbital wrinkle treat-
ments: fractional erbium-doped yttrium aluminum 
garnet laser, intense pulsed light, and topical 0.1% 
tretinoin cream. Ann Dermatol. 2016;28(5):650–2. 
https://doi.org/10.5021/ad.2016.28.5.650.
Fig. 20.15 Erythema, burning, and desquamation after 
3 days post-application of RA peel. 5%
Tip Box
• Comply with the real indication of RA 
peel.
• Type I people experience deeper pene-
tration than the others.
• The patients should prepare the skin by 
applying lighter acids 10 days before the 
peel session.
• It is recommended daily use of broad-
spectrum sun protection in the following 
days after the peel session.
• From 3–5 weekly or monthly sessions 
are required until the expected result is 
reached.
L. Scattone
https://doi.org/10.5021/ad.2016.28.5.650
141© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_21
Tretinoin Peel for Extra-Facial 
Areas
Renata Indelicato Zac and Adilson Da Costa
21.1 Materials
• Acetone 3% in alcohol
• Tretinoin 5% cream
• Gloves
• Gauze
21.2 Methods and Techniques 
[1–7]
• Before application, use acetone 3% in alcohol 
with gauze or cotton to remove all skin oils 
(Figs. 21.1 and 21.2).
• Apply the tretinoin 5% cream as a uniform 
mask with gloved fingers (Fig. 21.3).
• Wrap the skin with a plastic and leave the tret-
inoin cream on the skin for 4–6 h (Fig. 21.4).
• Remove it with water and mild soap or cleans-
ing solution.
R. I. Zac (*) 
Dermatology Department, Minas Gerais Military 
Hospital, Belo Horizonte, MG, Brazil 
A. Da Costa 
Instituto de Assistência Médica ao Servidor Público 
Estadual, Tenured International Professor and Mentor 
for PhD and MSc Programs, São Paulo, SP, Brazil
21
Fig. 21.1 Materials
Fig. 21.2 Preparation
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_21&domain=pdf
142
21.3 Clinical Follow-Up [1–7]
• Do not apply over erupted or broken skin.
• For the first 72 h post-peel or until all post- 
peel irritation has ceased, bland moisturizers, 
cleansers, and sunscreens are continued.
• After this time, patient can then resume their 
topical skincare formulations, which may 
include topical demelanizing agents, anti- acne 
medications, and retinoids.
• Excessive desquamation and irritation in the 
post-peel period can be treated with topical 
steroids.
• Hyperpigmentation remaining after the peel-
ing procedure responds to topical hydroqui-
none and frequent use of sunscreens.
• The peels are repeated at an interval of 
2–4 weeks.
• Peak results are visible after a series of 3–6 
chemical peels, depending on the severity of 
the condition being treated and skin type.
21.4 Before and After
Figures 21.5 (before) and 21.6 (after).
21.5 Side Effects, Complications, 
and Their Management [1–7]
• Pruritus, burning, and irritation can be avoided 
by previously using moisturizers on dry and 
sensitive skin and treated with calamine 
lotion.
• Persistent erythema can be prevented by fre-
quently using a broad-spectrum sunscreen 
and attenuated by using topical steroids.
• Picking, scratching, and scrubbing the skin 
can predispose to secondary infections. Use 
antibiotics as soon as crusts, oozing, pustules, 
or blisters appear.
Fig. 21.3 Application
Fig. 21.4 Wrapping
Fig. 21.5 Before
Fig. 21.6 After
R. I. Zac and A. Da Costa
143
• Acneiform eruption can be treated with topi-
cal antibiotics or benzoyl peroxide.
• Milia should be extracted.
• Post-inflammatory hyperpigmentation and 
hypopigmentation should be prevented with 
adequate priming and frequent use of broad- 
spectrum sunscreen. Topical corticosteroids, 
hydroquinone, or alpha-hydroxy acids can be 
used if necessary.
• Allergic reactions can be treated with antihis-
tamines, corticosteroids, and epinephrine in 
severe cases.
References
 1. Anitha B. Prevention of Complications in Chemical 
Peeling. J Cutan Aesthet Surg, 2010;3(3):186–8.
 2. Faghihi G, Fatemi-Tabaei S, Abtahi-Naeini B, 
et  al. The Effectiveness of a 5% Retinoic Acid Peel 
Combined with Microdermabrasion for Facial 
Photoaging: A Randomized, Double-Blind, Placebo-
Controlled Clinical Trial. Dermatology Research and 
Practice 2017;
 3. Cucé LC, Bertino MC, Scattone L, Birkenhauer MC. 
Tretinoin peeling. Dermatol Surg. 2001;27(1):12–4.
 4. Hexsel D, Mazzuco R, Dal’Forno T, Zechmeister D. 
Microdermabrasion followed by a 5% retinoid acid 
chemical peel vs. a 5% retinoid acid chemical peel for 
the treatment of photoaging - a pilot study. J Cosmet 
Dermatol. 2005;4(2):111–6.
 5. Kang S, Kim KJ, Griffiths CE, et al. Topical tretinoin 
(retinoic acid) improves early stretch marks. Arch 
Dermatol. 1996;132:519–26.
 6. Ud-Din S, Mc George D, Bayat A. Topical manage-
ment of striae distensae (stretch marks): preven-
tion and therapy of striae rubrae and albae. JEADV 
2016;30:211–22.
 7. Yokomiso VMF, Benmond TMH, Chisaki C, et al. 
Chemical peels: review and practical applications. 
Surg Cosmet Dermatol. 2013;5(1):58–68.
Tip Box
• Use acetone 3% in alcohol with gauze.
• Apply the tretinoin 5% cream as a uni-
form mask with gloved fingers.
• Leave it on the skin for 4–6 h.
• Remove it with water and mild soap or 
cleansing solution.
21 Tretinoin Peel for Extra-Facial Areas
145© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_22
Trichloroacetic Acid Peel for Facial 
and Extra-Facial Areas
Natacha Quezada Gaón 
and María Isabel Herane Herane
22.1 Materials
• Sterilized gauzes and cotton tips of different 
sizes.
• Sterilized, nonmetal, and disposable recipient 
for the acid.
• Ether, acetone, and alcohol mixed in equal 
proportion for facial cleansing.
• Solid petroleum jelly, to protect the lips, 
angles, and sensitive areas.
• Trichloroacetic acid-base lotion 15%, 20%, 
25%, 30%, and 35%.
• Cold fan.
• Baking soda, 10%, acts as buffer (its efficacy 
is not well accepted) (Fig. 22.1).
22.2 Methods and Techniques 
[1–10]
• Choose correctly the patient for indications 
such as photodamage, scars, keratoses, and 
others [1–3].
• Patient must have a fair-skin phototype (I–IV) 
and no history of keloid scars, hepatitis, HIV 
infection, active herpes simplex, or any other 
active dermatologic condition.
• Patient must be out of isotretinoin treatment 
for 3–6 months or no history of radiotherapy 
in the last 2 years.
• Previous skin preparation should be with topi-
cal retinoids or Kligman formula, at least 
2 weeks before the procedure.
• The previous education of the patient on using 
photoprotection SPF 50+ to avoid complica-
tions is very important.
• Detailed explanation of the procedure is nec-
essary. Patients must be aware that a stinging 
sensationwill be normal for 15–30  min and 
that a dark crust will develop that will resolve 
in different times in several days.
N. Quezada Gaón (*) 
Department of Dermatology, Pontifical Catholic 
University of Chile, Santiago de Chile, Chile 
M. I. Herane Herane 
University of Chile, Santiago, Chile
22
Fig. 22.1 Materials: gauzes, cotton tips of different sizes, 
sterilized, nonmetal, disposable recipient
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_22&domain=pdf
146
• An informed consent that explains the proce-
dure, complications, and risks should be 
signed before.
• Standard photography registry is authorized 
by the patient.
• Start the procedure with a deep facial skin 
cleansing using a gauze and the degreasing 
solution, taking off residual cosmetics and 
skin grease.
• Apply solid petroleum jelly in the mouth angles 
and other areas we would like to protect.
• Pour trichloroacetic acid in the recipient, and 
soak the gauze or cotton tip in the acid not let-
ting the acid drain.
• The use of TCA for performing chemical extra-
facial peels has been reported mainly in two vehi-
cles: aqueous solution and water- soluble paste.
• Apply a first layer of TCA (15–35%) in a 
homogeneous way considering the cosmetic 
units; this can be done in the whole extra- 
facial or only in the areas to be treated [4] 
(Figs. 22.2 and 22.3).
a b
Fig. 22.2 (a) Homogeneous application with cotton tip of TCA 35% peeling in keratosis area. (b) Homogeneous 
application with gauzes of TCA 20% peeling in a back of the hand in cosmetic unit
a b c
Fig. 22.3 (a) Homogeneous application with gauzes of TCA 15% peeling in a cheek cosmetic unit. (b) Homogeneous 
application with cotton tip of TCA 20% peeling in periocular area. (c) Homogeneous frosting in cosmetic unit
N. Quezada Gaón and M. I. Herane Herane
147
• For cross peel (TCA 75%–95%), cotton tips of 
different sizes are useful, and it must be very 
carefully applied depending on the area that 
will be treated (Fig. 22.4) [5–8].
• TCA produce stinging and burning sensation 
that can be minimized with the use of a cold 
fan.
• Always remember that frosting with TCA 
appears very soon; we must be patient before 
applying a second or third layer.
• Depth will depend on the percentage of acid, 
the number of passes, the pressure on the 
application, and the previous treatment of the 
skin.
• The more homogeneous and white the frost-
ing, the greater the penetration.
• It is advisable to decide the cosmetic units to 
be treated with more or less intensity previ-
ously and individually.
• Once you obtain the frosting and stinging is 
controlled, we can associate other chemical 
peels or laser to maximize results (Figs. 22.5, 
22.6, and 22.7) [9, 10].
• If we decide not to associate other procedures, a 
photoprotector SPF 50+ should be applied to 
finish.
22.3 Clinical Follow-Up [1–10]
• Post-procedure indications should be given in 
written form, pointing the importance of crust 
evolution.
• Crusts will drop by themselves in different times 
leaving erythema and temporary sensitive areas 
(Figs. 22.8, 22.9, 22.10, 22.11, 22.12, and 22.13).
• Medical staff should insist in a strict photo-
protection and the regular use of a repair 
healing cream, moisturizing cream, or petro-
leum jelly.
• Do not forget all patients having herpes sim-
plex infection prophylaxis (valaciclovir 
500 mg twice a day for 5 days)
• If the patient has a history of recurrent herpes 
simplex infection, it is advisable to prescribe 
valaciclovir 500 mg twice a day until desqua-
mation is over.
• The use of steroids will be necessary if the 
peeling is too intense. Prescribe prednisone 
1 mg/kg, and taper the dose every 3–7 days.
• Telephone calls or visits to the clinic the fol-
lowing days reinforce the management.
• A week control plus standardized photogra-
phy post-procedure is necessary.
a b c
Fig. 22.4 (a) Application of TCA 90% cross peeling technique in the earlobe. (b) Frosting. (c) Before two sessions 
TCA peeling 90% for repair earlobe
22 Trichloroacetic Acid Peel for Facial and Extra-Facial Areas
148
a b
Fig. 22.5 (a) 
Application of cross 
peeling technique in ice 
pick. (b) Frosting
a b
Fig. 22.6 (a) 
Homogeneous 
application of 20% TCA 
peeling facial. (b) 
Combination of 5% 
retinoic acid peel facial
N. Quezada Gaón and M. I. Herane Herane
149
a b
c d
Fig. 22.7 Before (a), post-peeling TCA 30% (b), after dermabrasion (c), and 1 week later (d)
a b
Fig. 22.8 (a) Peeling 
TCA 20% 1 week after 
with desquamation in 
different times. (b) Two 
weeks after
22 Trichloroacetic Acid Peel for Facial and Extra-Facial Areas
150
a b
Fig. 22.9 (a) 
Three weeks after 
peeling TCA 30% with 
desquamation and 
erythema. (b) 
Four weeks later, 
erythema in some areas 
is still present. The 
patient does not follow 
the instructions
a b c
Fig. 22.10 (a) Before peeling TCA 20% in the cheeks. (b) Desquamation in different times, 3 days. (c) A week after
a b c
Fig. 22.11 (a) Before peeling TCA 30% in the cheeks. (b) Desquamation in different times, 4 days (c) A week after. 
Erythema in some areas is still present
N. Quezada Gaón and M. I. Herane Herane
151
a b c
Fig. 22.12 (a) Before periocular peeling TCA 20%, (b) crust 2 days after, and (c) final result after a week
a b c
Fig. 22.13 (a) Before. (b) After a week of peeling TCA 30% in cheeks with discrete remaining erythema. (c) After 
1 year, good results are still noticeable
• Keep strict photoprotection for 3  months 
 post- procedure to avoid hyper- or 
hypopigmentation.
• Desquamation post-peeling lasts 7–15  days, 
leaving temporary patches that are normal.
• Once desquamation is gone, a discrete-to- 
moderate erythema remains for approximately 
4  weeks; if it lasts longer, we are facing a 
 persistent erythema.
22.4 Before and After (Figs. 22.14, 
22.15, 22.16, 22.17, 22.18, 
22.19, 22.20, 22.21, 22.22, 
22.23, and 22.24)
22 Trichloroacetic Acid Peel for Facial and Extra-Facial Areas
152
a b
Fig. 22.15 (a) Before. 
(b) Four weeks after one 
session of cross peeling 
TCA 30% in keratosis of 
the hand
a bFig. 22.16 Before (a) 
and after (b) three 
sessions TCA 90% cross 
peeling technique in 
earlobe area
a bFig. 22.17 Before (a) and after (b) three 
sessions TCA 90% cross 
peeling technique in 
earlobe area. (Pictures in 
traction)
a b
Fig. 22.14 (a) Before. 
(b) Four weeks after one 
session peeling TCA 
20% in a back of the 
hand in a patient with 
photodamage
N. Quezada Gaón and M. I. Herane Herane
153
a b
Fig. 22.18 Before (a) 
and after (b) one session 
peeling TCA 35% in 
cosmetic units of the 
cheeks in a patient with 
photodamage
a b
Fig. 22.19 Before (a) 
and after (b) one session 
TCA 30% in the cheeks 
in a patient with acne 
scarring and 
photodamage
a b
Fig. 22.20 Before (a) 
and after (b) one session 
of peeling TCA 20% in 
periocular area
a b
Fig. 22.21 Before (a) 
and after (b) one session 
TCA 30% plus 
dermabrasion of 
superior perioral area 
(Pictures in rest)
22 Trichloroacetic Acid Peel for Facial and Extra-Facial Areas
154
a b
Fig. 22.22 Before (a) 
and after (b) one session 
TCA 30% plus 
dermabrasion of 
superior perioral area 
(Pictures in contraction)
a b
Fig. 22.23 Before (a) 
and after (b) three 
sessions of cross peel 
TCA 90% in ice pick 
technique
a b c
Fig. 22.24 Before (a) and after (b) three sessions of cross peel TCA 90% in ice pick technique
22.4.1 Side Effects, Complications, 
and Their Management [1–10] 
(Figs. 22.25, 22.26, 22.27, 
22.28, 22.29, and 22.30)
• Immediate complications are mainly sore and 
pain that is different among individuals. Cold 
fan helps a lot.
• Hyperpigmentation or hypopigmentation can 
be seen after complete desquamation and 
even after 1  month; it can be prevented 
strictly.
• Persistent erythema. If present over 2 months, 
we must use IPL or vascular lasers plus photo-
protection to resolve.
• Atrophic, hypertrophic, and keloid scars.
N. Quezada Gaón and M.I. Herane Herane
155
Fig. 22.25 Eight weeks after treatment TCA 30% in a 
back of the hand with persistent erythema
Fig. 22.26 Four  weeks after treatment TCA 30% in a 
back of the hand area with persistent erythema and atro-
phic and hypertrophic scars
a b
Fig. 22.27 Edema 24 h 
after TCA 30% 
treatment in the cheeks 
(a), control 2 weeks 
after (b)
a b c
Fig. 22.28 (a) Before. (b) Two  weeks after treatment TCA 30% in perioral area with persistent erythema. (c) At 
12 weeks and after six sessions of IPL improvement of erythema
22 Trichloroacetic Acid Peel for Facial and Extra-Facial Areas
156
a b c
Fig. 22.30 Before (a) and after 2 weeks of treatment TCA 15% (b). Hyperpigmentation can be seen at 2 weeks (b) that 
is almost resolved 6 weeks after using Kligman’s depigmenting formula (c)
• Infections: herpes simplex infection is the 
most common. Secondary bacterial infection 
has been reported.
• Acneiform reactions and milium cysts can be 
developed.
References
 1. Rendon M, Berson D, Cohen J, Roberts WE, Starker 
M, Wang B.  Evidence and considerations in the 
application of chemical peels in skin disorders and 
a b c
Fig. 22.29 (a) Before. (b) Four weeks after treatment TCA 30% in perioral area with persistent erythema at week 4. 
(c) At 10 weeks and after six sessions of IPL improvement of erythema but hypopigmented areas remain
Tip Box
• Sectorial peel helps for a better control 
of the procedure. It is possible to per-
form a deeper peel in more affected 
areas and less aggressive in the rest.
• Sectorial peel has a faster and better 
healing process.
• If a patient is phototype IV and might 
react with hyperpigmentation applica-
tion of 3 mm, TCA 20% in preauricular 
area is a good proof method to confirm 
if hyperpigmentation might occur.
• The extra-facial peeling heals slower 
than the facial peeling and has more risk 
of complication.
N. Quezada Gaón and M. I. Herane Herane
157
aesthetic resurfacing. J Clin Aesthet Dermatol. 
2010;3(7):32–42.
 2. Orso Rebellato P, Rodrigues Lisbon Faucz L, Vilaverde 
Schmitt J, Araujo Scharf Pinto C.  Trichloroacetic 
acid peeling in the treatment of actinic melanosis 
in the back of the hands: a comparative randomized 
study between two vehicles. Surg Cosmet Dermatol. 
2015;7(4):294–7.
 3. Puri N.  TCA peel versus glycolic acid peel for the 
treatment of melasma. Indian Dermatol Online J. 
2012;3(2):109–13.
 4. Yildirim S, Salih Gurel M, Gungor S, Tekeli O, 
Canat D.  Comparison of efficacy of chemical peel-
ing with 25% trichloroacetic acid and 0.1% retinoic 
acid for facial rejuvenation. Adv Dermatol Allergol. 
2016;33(3):199–205.
 5. Ribeiro de Oliveira AR, Cardoso de Mendonça MC, 
Figueiredo Machado R, Tavares Lopes Silva M, Vieira 
Arestrup B. Minimally invasive technique for repair-
ing complete earlobe cleft. Surg. Cosmet Dermatol. 
2011;3(3):254–6.
 6. Mradula PR, Sacchidanand S. A Split-face compara-
tive study of 70% trichloroacetic acid and 80% phenol 
spot peel in the treatment of freckles. J Cutan Aesthet 
Surg. 2012;5(4):261–5.
 7. de Mendonça MC, de Oliveira AR, Araújo JM, Silva 
MD, Gamonal A. Nonsurgical technique for incomplete 
earlobe cleft repair. Dermatol Surg. 2009;35(3):446–50.
 8. Garg S, Baveja S. Combination therapy in the man-
agement of atrophic acne scars. J Cutan Aesthet Surg. 
2014;7(1):18–23.
 9. Simões Alves F, Nakandakari S. Trichloroacetic acid 
matricectomy: a retrospective study. Surg Cosmet 
Dermatol. 2011;3(3):254–6.
 10. Gomes Meski A, Cucé L. Chemabrasion for the treat-
ment of perioral wrinkles: clinical analysis and epi-
dermal Langerhans cells qualification. Surg Cosmet 
Dermatol. 2009;1(2):74–9.
22 Trichloroacetic Acid Peel for Facial and Extra-Facial Areas
159© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_23
Thioglycolic Acid Peel for Dark 
Circles Under Eyes
Vanessa Lucília Silveira Medeiros
23.1 Materials
Thioglycolic acid (TA) or mercaptoacetic acid 
[1–3].
• Microruptures in the vessels lead to the accu-
mulation of hemoglobin metabolites like iron 
in the skin of the eyelid. The deposition of iron 
in tissues activates many enzymes and has a 
catalytic effect by the conversion of superox-
ide and hydrogen peroxide into a highly active 
free radial (OHo) capable of damaging organic 
molecules. The damage stimulates melanogen-
esis, causing secondary melanic pigmentation.
• Glycolic acid is the smallest alpha-hydroxy 
acid; therefore, it has the high capability to pen-
etrate the skin. Thioglycolic acid is a derivate of 
glycolic acid with a higher molecular weight.
• Thioglycolic acid is formed by the replace-
ment of an oxygen atom by a sulfur atom in an 
acid radical of glycolic acid. This chemical 
reaction receives the name “Thio.” The new 
acid then receives the addition of this prefix to 
the original compound name.
• It has ability to penetrate the skin between 
glycolic acid and trichloroacetic acid. The 
more limited penetration promotes a lighter 
burn and cell renewal with greater safety than 
glycolic acid.
• Thioglycolic acid is classified as a carboxylic 
acid with a simple sulfur group and a carboxyl 
group. The former reacts with bases, acids, 
ketones, and organic halogen compounds. The 
latter reacts with amines and alcohols.
• Thus, thioglycolic acid has an antioxidant 
activity and the capability to eliminate iron 
accumulation, verified by the presence of 
metabolite reaction (carboxyethylcysteine).
• The concentration of the peeling varies with 
the place of application. Twenty percent acid 
is indicated for corporal vascular discolor-
ations and 10% for the eyelid. The vehicle 
used is non-alcoholic gel.
• Non-sterile disposable gloves, mask, sterile 
gasses, swabs, 50% alcohol, and 10% gel-free 
thioglycolic acid are used for eyelid peeling 
(Fig. 23.1).
V. L. S. Medeiros (*) 
Department of Tropical Medicine of Federal 
University of Pernambuco, Recife, PE, Brazil 
Instituto Davan Dermatologia, Recife, PE, Brazil
23
Fig. 23.1 Material used in the peeling 
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_23&domain=pdf
160
23.2 Methods and Techniques
• The choice of the patient is crucial to get bet-
ters results. The best candidate is one with ery-
thema in the eyelids (vascular discoloration), 
little hyperpigmentation, and slight change in 
skin texture (Fig. 23.2). If the patient has tear 
trough depression, treat first the depression 
and the superficial iron.
• Program three to five peeling sessions with a 
minimum interval of 15 days. Use a whitening 
cream with vitamin C at least 15 days before 
the first session to prevent post-inflammatory 
pigmentation.
• In the procedure, the patient should wash the 
face and eyelids with a gentle soap. After, 
clean the area with 50% alcohol to degrease 
the skin. Prevent the patient from opening the 
eyes at this moment (Fig. 23.3).
• Apply thioglycolic acid 10% and spread with 
a cotton swab. Start with the lower eyelid 
because sometimes to reach the affected area, 
it is necessary to ask the patient to look up 
(Fig. 23.4). The endpoint of the first session is 
a burning sensation or at most a very light 
frost (Fig. 23.5). The time to reach this result 
is between 3 and 5 min. Do not go beyond this 
time to get frost in the first session.
• Clean the area with a dry gauze and after that 
with gauze soaked in 0.9% physiological solu-
tion. Repeat the process in the upper eyelid. In 
the end, the patient should wash the eyelids 
again.
• Add 3–5  min in each subsequent session 
according to the evolution presented after the 
first session. The maximum time is 15  min. 
Fig. 23.2 Best patient to be chosen—eyelids with vascu-
lar discoloration without pigmentation and tear trough 
atrophy
Fig. 23.3 Step two—apply a thick layer of 10% thiogly-
colic acid and spread with a cotton ball
Fig. 23.4 Step 
one—clean the area with 
50% alcohol
V. L.S. Medeiros
161
The time should not be increased if the patient 
reaches a moderate frost or experiences 
increased burning sensation.
23.3 Clinical Follow-Up
• In the next 1–3 days, there will be a light ery-
thema and a descript edema in the treated area 
(Figs. 23.5 and 23.6). They are being progres-
sively replaced by parchment skin. The color 
can range from skin color to light brown 
depending on the melanin content of the skin 
(Fig. 23.7).
• Skin desquamation begins on the fourth day 
and ends 7–10  days after the session 
(Fig. 23.8). In this period, the patient can use a 
vitamin C eyelid cream twice a day and 
sunscreen.
• The patient should avoid sun exposure during 
the entire treatment. In addition to vitamin C, 
prescribe sunscreen and sunglasses in situa-
tions when exposure is unavoidable (e.g., 
driving).
• After desquamation, the patient can return to 
the use of whitening cream until the next 
session.
Fig. 23.5 Step 
three—stop the session 
in the scheduled time or 
reach an opaque skin 
appearance with light 
erythema
Fig. 23.6 Light erythema 24 h after the session Fig. 23.7 Brownish skin with parchment-like appear-ance 48 h after the session
Fig. 23.8 Onset of skin 
peeling on the fourth 
day after the session
23 Thioglycolic Acid Peel for Dark Circles Under Eyes
162
23.4 Before and After
 1. Patient 1 (Figs. 23.9 and 23.10)
 2. Patient 2 (Figs. 23.11 and 23.12)
23.5 Side Effects, Complications, 
and Their Management
Most of the adverse effects are related to exces-
sive skin peeling contact time. Burning sensation 
and frost are guides to the endpoint of the 
session.
• Pain: The patient should not feel pain during 
or after the session. If the patient complains 
about pain, stop the application immediately 
and clean the area. The patient may have very 
thin skin or low pain tolerance. If the com-
plaint occurs after the application, consider 
the possibility of infections (bacterial or 
herpetic).
• Lead the patient to return for frequent reas-
sessment until the cause is determined.
• Burning sensation: A light burning sensation 
is normal and should stop within a few min-
utes after the end of the session. If the patient 
complains of increased burning, stop the 
application and clean the site. Prolonged burn-
ing sensation is similar to the pain of a first- 
degree burn. The treatment is to apply 
moisturizing, low-potency corticosteroids, or 
topical immunomodulators.
• Edema: Some patients may experience mild 
swelling simultaneously with erythema after 
the frost. This is transient and should disap-
pear in 24  h. If the swelling is important or 
persists after a few days, consider very thin 
skin, error in application time, or in the acid 
formula. If this repeats or increases in the next 
application, it may be due to acid sensitiza-
tion. If the edema is mild to moderate, the 
treatment is low-potency corticosteroids or 
topical immunomodulators until complete 
improvement. If the edema is severe, the treat-
ment is prednisone 0.5 mg/kg/day until reso-
lution of the condition.
• Erythema: Mild erythema occurs in all cases 
and disappears within 24–48 h. The absence 
of erythema indicates that the time of the acid 
in the skin was very short. Excessive burning 
of the skin may prolong the erythema and is 
indicative of other possible problems such as 
post-inflammatory hyperpigmentation. The 
Fig. 23.9 Patient 1 before—vascular discoloration with 
few wrinkles. Absence of pigmentation and tear trough 
atrophy
Fig. 23.10 Patient 1 after—improvement of vascular dis-
coloration and skin texture
Fig. 23.12 Patient 2 after—improvement of vascular dis-
coloration, skin texture, and hyperpigmentation
Fig. 23.11 Patient 2 before—vascular discoloration with 
secondary hyperpigmentation and mild tear trough 
atrophy
V. L. S. Medeiros
163
treatment is low-potency corticosteroids or 
topical immunomodulators, sunscreen, and 
vitamin C cream.
• Post-inflammatory pigmentation: It is an 
uncommon side effect. It is related to the previ-
ous melanin content of the skin or prolonged 
erythema after the session. Increasing the time 
of peeling application may not improve pig-
mentation and induce post-inflammatory 
hyperpigmentation. If the patient has a very 
pigmented look, first schedule treatment for 
that factor. If the patient develops post- 
inflammatory hyperpigmentation, the treat-
ment is performed with bleaches such as 
vitamin C and inhibitors of tyrosinase activity.
References
 1. Tullii R, Izzo M.  El papel del ácido tioglicólico en 
las pigmentaciones férricas/the role of thioglycolic 
acid in ferric pigmentations. Ver Panam Flebol Linfol. 
2001;41:57–63.
 2. Costa A, Basile DVA, Medeiros VLS, Moisés AT, Ota 
SF, Palandi JAC. 10% thioglycolic acid gel peels: a 
safe and efficient option in the treatment of consti-
tutional infraorbital hyperpigmentation. Surg Cosmet 
Dermatol. 2010;2(1):29–33.
 3. http://www.chemicalland21.com/specialtychem/
finechem/THIOGLYCOLIC%20ACID.htm
Tip Box
• Eyelid dark circles have many etiologies 
and different clinical presentations. For 
the correct treatment, it is important to 
identify the predominant type of eyelid 
dark circles and start treatment for it.
• The blood vessel microruptures in the 
skin of the eyelid lead to the deposition 
of hemoglobin metabolites and release 
free radicals. This leads to eyelid vascu-
lar discoloration and causes secondary 
melanic pigmentation.
• Thioglycolic acid has the capability to 
react with iron and other hemoglobin 
metabolites and promotes desquama-
tion. For this reason, it is indicated for 
treatment of the vascular type of dark 
eyes circles.
• The protocol is three to five sessions 
with a minimum interval of 15  days. 
The use of creams with haloxyl, mela-
nogenic inhibitors, resorcinol, and vita-
min C helps to prevent complications. 
After the session, the patient should use 
eyelid cream, sunscreen, and sunglasses 
and avoid sun exposure.
• Most of the adverse effects are related to 
excessive contact time. Burning sensa-
tion and frost are guides to the endpoint 
of the session before the planned time. 
Generally, the side effects can be treated 
with low-potency corticosteroids or top-
ical immunomodulators, followed by 
vitamin C cream and sunscreen.
23 Thioglycolic Acid Peel for Dark Circles Under Eyes
http://www.chemicalland21.com/specialtychem/finechem/THIOGLYCOLIC ACID.htm
http://www.chemicalland21.com/specialtychem/finechem/THIOGLYCOLIC ACID.htm
165© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_24
Thioglycolic Acid Peeling 
for Hemosiderin and Post- 
inflammatory Hyperchromia
Rossana Cantanhede Farias de Vasconcelos
24.1 Materials (Fig. 24.1)
• 50–70% alcohol
• 0.9% saline solution
• Gauze or cotton pad
• Swabs
• 10–20% thioglycolic acid gel packed in drop-
per vials with 20  ml done in manipulation 
pharmacy
24.2 Methods and Techniques 
(Figs. 24.2 and 24.3)
• Degrease the region with 50–70% ethanol.
• Apply 10% or 20% thioglycolic acid gel in the 
area.
• Allow 2 min of contact. Remove it with gauze 
and water or 0.9% saline in abundance.
R. C. F. de Vasconcelos (*) 
Dermatology Department, University of Santo 
Amaro, São Paulo, SP, Brazil
24
Fig. 24.1 Materials to be used 
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_24&domain=pdf
166
• Keep an interval of 7, 15, and 30 days between 
sessions.
• Repeat the sessions 3–8 times, increasing the 
contact time by 3 min. Do not exceed 15 min 
of contact in the periocular area.
• Stop if there is burning or adverse effects.
24.3 Clinical Follow-up (Fig. 24.4)
• The clinical results of thioglycolic acid peels 
to treat periocular hyperpigmentation show 
improvement in recent works, assessed on a 
scale from 0 to 10.
• The use of 10% gel in the periocular hyperpig-
mentation had an average clinical satisfaction 
of 6.8, reported by Costaet al. [1] and Souza 
et al. [2].
• Initial results of a work in progress at the hos-
pital of University of Santo Amaro, with peel-
ing of 20% thioglycolic, showed an average 
satisfaction of 6.3.
• When we evaluate only patients with pigmen-
tary and vascular components, an increase in 
the average satisfaction, up to 7.05, is noticed.
• This superiority in the darkest circles shows 
the greatest effect of thioglycolic acid in the 
hemosiderotic component (Vasconcelos et al. 
unpublished).
• In the treatment of hyperpigmentation of the 
lower limbs triggered by venous insufficiency, 
Goldman et al. [3] showed 40% good or very 
good improvement.
• In Schamberg disease, Hammerschmidt et al. 
[4] reported the use of 10% thioglycolic acid 
peeling gel resulting in improved lightening of 
lesions by 68.7%.
• For use in post-inflammatory hyperpigmenta-
tion, Reinehr et al. [5] reported the use of 30% 
thioglycolic acid peels in association with 
topic depigmentant with good results.
Fig. 24.2 Application of 10% or 20% thioglycolic acid 
peeling 
Fig. 24.3 Removal with 0.9% saline solution 
Fig. 24.4 Immediate appearance after the removal: gray48 
frosting, mild erythema 
R. C. F. de Vasconcelos
167
24.4 Before and After (Figs. 24.5, 
24.6, and 24.7)
24.5 Side Effects, Complications, 
and Their Management 
(Figs. 24.8 and 24.9)
Erythema, swelling, and peeling are described as 
adverse effects after the procedure by Goldman 
et al. [3] and Costa et al. [1]. Varying degrees of 
erythema and edema appear immediately after 
application and revert on the second day, whereas 
mild peeling appears lasting 3–4 days. Crusting 
may occur in case of intense frosting or technical 
error. Complications are not related to the num-
ber of sessions and are rare.
Some patients do not get better or have little aes-
thetic improvement of hyperpigmentation. These 
are individuals who may benefit from the most 
number of sessions with thioglycolic acid or com-
bined treatment with use of other depigmentants 
that act more effectively on deposits of melanin.
• Not related to the number of sessions.
• Spontaneous reversion.
• The most common are erythema, edema, and 
peeling.
• Crusts and dyschromias may rarely occur.
Fig. 24.5 Post-inflammatory hyperpigmentation before 
application 
Fig. 24.6 Peeling appearance 1  week after the 
application 
Fig. 24.7 Appearance after 1 month of the last session in 
a total of five sessions 
Fig. 24.8 Erythema and mild flaking 
Fig. 24.9 Mild flaking and thin crust with partial 
whitening 
24 Thioglycolic Acid Peeling for Hemosiderin and Post-inflammatory Hyperchromia
168
Tip Box
• A total of 20% thioglycolic acid serial 
peeling for hemosiderosis and 
hyperchromia
• Quite an advantageous option for use in 
office
• Very common complaint
• Quick method
• Easy application and access
• Little risk of adverse effects
• Low cost
• High level of patient satisfaction
References
 1. Costa A, Basile AVD, Medeiros VLS, Moisés TA, Ota 
FS, Palandi JAC. 10% thioglycolic acid gel peels: a 
safe and efficient option in the treatment of consti-
tutional infraorbital hyperpigmentation. Surg Cosmet 
Dermatol. 2010;2(1):29–33.
 2. Souza DCM, Ludtke C, ERM S, Rocha NW, Weber 
MB, Manzoni APD, Lorenzini FK. Comparação entre 
ácido tioglicólico 2.5%,hidroquinona 2%, haloxyl 2% 
e peeling de ácido glicólico 10% no tratamento da 
hiperpigmentação periorbital. Surg Cosmet Dermatol. 
2013;5(1):4651.
 3. Goldman N, Neto B, Goldman K.  Tratamento 
das Hiperpigmentações de Membros Inferiores 
Desencadeadas pela Insuficiência Venosa com o 
Uso de Ácido Tioglicólico. [acesso 05 jun 2009]. 
Disponível em: www.sbme.org.br/portal/download/
revista/14/04_Tratamento_das_Hiperpigmentacoes.
pdf.
 4. Hammerschmidt M, Gentili AC, Hepp T, Mukai 
MM.  Peeling de ácido tioglicólico na doença de 
Schamberg. Surg Cosmet Dermatol. 2013;5(2):165–8.
 5. Reinehr CPH, Boza JC, Horn R.  Peeling de ácido 
tioglicólico como terapêutica para hipercromia pós- 
inflamatória. Surg Cosmet Dermatol. 2015;7(4):350–2.
R. C. F. de Vasconcelos
http://www.sbme.org.br/portal/download/revista/14/04_Tratamento_das_Hiperpigmentacoes.pdf
http://www.sbme.org.br/portal/download/revista/14/04_Tratamento_das_Hiperpigmentacoes.pdf
http://www.sbme.org.br/portal/download/revista/14/04_Tratamento_das_Hiperpigmentacoes.pdf
Part II
Botulinum Toxin
171© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_25
Introduction: What Is Botulinum 
Toxin?
Doris Hexsel, Fernanda Camozzato, 
and Carolina Siega
25.1 History
Botulism was first described in the mid-1800s, but 
its etiologic agent, Clostridium botulinum, and 
mechanism of action were identified almost a cen-
tury later. The botulinum toxin (BoNT) has long 
been considered the most poisonous of poisons, 
and efforts to purify, isolate, and describe the 
molecular structure of the botulinum toxin date 
back to the 1940s [1–4]. Onabotulinumtoxin A 
(Botox, Botox Cosmetic; Allergan, Irvine, Calif.) 
is the first available botulinum toxin type A 
(BoNT-A) preparation initially purified in the 
crystalline form by Dr. Shantz and adapted for 
clinical use by Dr. Scott [5]. In the 1970s, after 
promising results from preclinical trials, Dr. Alan 
Scott conducted clinical trials to assess the effects 
of BoNT-A as a nonsurgical treatment of strabis-
mus [6]. Botulinum toxin type A was first 
approved in 1979 by the US Food and Drug 
Administration (FDA) for treatment of strabismus 
[5] and was subsequently approved in 1989 for 
treating hemifacial spasm and blepharospasm.
The cosmetic use of BoNT-A was first reported 
by Carruthers and Carruthers in 1992 [7], who 
have, afterward, extensively studied and expanded 
cosmetic indications [6]. The improvement in 
facial rhytids on the upper face, around the sites 
injected to treat hemifacial spasm and blepharo-
spasm, led to the development of the technique to 
treat glabellar lines. Approximately 10 years later, 
the cosmetic treatment for glabellar hyperkinetic 
lines with onabotulinumtoxin A was approved by 
the Food and Drug Administration in the USA 
and by other surveillance health authorities from 
different countries. It represents one of the most 
important contributions to the approach for the 
aging face in recent years.
25.2 Botulinum Toxin Types
Clostridium botulinum is an anaerobic, gram- 
positive, spore-forming bacillus that produces 
exotoxins grouped into eight serotypes: A, B, C, 
D, E, F, G, and H [8]. The latter, however, has been 
recently described as a chimeric toxin mainly 
because it was neutralized by available antitoxins, 
being also denominated as BoNT-FA [9].
Botulinum neurotoxins are 150-kDa proteins 
composed of a heavy chain (HC—100 kDa) and a 
light chain (LC—50 kDa). The domain structure is 
shared by all BoNT serotypes. The heavy chain is 
D. Hexsel (*) 
Brazilian Center for Studies in Dermatology, 
Porto Alegre, RS, Brazil 
Hexsel Dermatologic Clinics, 
Porto Alegre/Rio de Janeiro, RS/RJ, Brazil
e-mail: doris@hexsel.com.br 
F. Camozzato · C. Siega 
Brazilian Center for Studies in Dermatology, 
Porto Alegre, RS, Brazil
25
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_25&domain=pdf
mailto:doris@hexsel.com.br
172
composed of two functional domains, the receptor 
binding domain and the translocation domain. The 
light chain is a zinc metalloprotease that cleaves 
specific sites of the SNARE complex, blocking the 
release of acetylcholine in cholinergic nerves. 
BoNT types A, C, and E cleave the synaptosomal-
associated protein (SNAP-25), whereas BoNT 
types B, D, F, G, and H (or FA) cleave the vesicle-
associated membrane protein (VAMP), also known 
as synaptobrevin II. BoNT type C also cleaves the 
syntaxin [8]. The blockage of acetylcholine release 
is reversible, and while active, it promotes a differ-
ent spectrum of action varying from muscle relax-
ation tomuscular palsy, depending on the subtypes 
and doses used [8].
In addition, it has been found that the effects 
of BoNT-A enable not only the muscles’ chemi-
cal denervation but also neurologic modulation in 
sweat glands, leading to reduction or ceasing of 
sweating in the treated areas [10, 11]. Other 
effects of BoNTs have been studied and dis-
cussed, such as neurologic modulation in seba-
ceous glands [12], vascular regulation [13], 
regulation of mood states [14–18], and regulation 
of the expression levels of genes relevant to inva-
sive growth in keloid fibroblasts [19, 20]. 
However, no definite elucidation of mechanism 
of action for each of these indications has been 
reached up to now.
Currently, serotypes A and B are approved for 
use in humans, but only serotype A is approved 
for cosmetic use [8]. The BoNT serotype E is 
under testing in phase II in the USA [21].
25.2.1 Commercial Preparations
Different formulations of BoNT-A are available 
worldwide, which are neither identical nor inter-
changeable. The commercial formulations of 
BoNT-A approved for cosmetic indications are 
onabotulinumtoxin A (ONA; Botox®, Allergan 
Inc., Irvine, USA); abobotulinumtoxin A (ABO; 
Dysport®, Ipsen, France; Azzalure® in Europe); 
and incobotulinumtoxin A (INCO; Merz 
Pharmaceuticals, Frankfurt, Germany; as 
Bocouture® in Europe) (Fig. 25.1) [22].
Onabotulinumtoxin A is a homogenous 900- 
kDa complex of BoNT-A and nontoxic proteins, 
purified through ethanol precipitation and crys-
tallization. Abobotulinumtoxin A is a 500–900- 
kDa heterogeneous complex of neurotoxin and 
protein that is purified through an ion-exchange 
process. And INCO is a homogenous solution of 
150-kDa BoNT-A, purified through ion exchange 
and pH elution free from complexing proteins.
The dose of BoNT-A is measured in units of 
biological activity (U), which is verified in ani-
mal models. The units of different products are 
not equivalent, but proportional doses between 
different products can be established to obtain 
similar results. A dose equivalence of up to 
1:2.5  U between ONA or INCO and ABO is 
adopted by the most experienced physicians 
when using different products, as supported by 
the literature [23–25]. Injections of ONA and 
ABO at the dose equivalence of 1:2 U can also be 
used, as it results in similar fields of muscular and 
anhidrotic effects [24]. Most researchers support 
the dose equivalence between ONA and INCO 
around 1:1 [26–28]. Diffusion or the fields of 
anhidrotic and muscular effects are considered to 
be a dose-dependent effect rather than related to 
intrinsic characteristics of each product [29]. By 
using a proper dose equivalence, all the men-
tioned products can produce similar results in 
terms of duration and field of muscular and anhi-
drotic effects.
Fig. 25.1 Most used commercial preparations of 
BoNT-A in the cosmetic field
D. Hexsel et al.
173
25.3 Before and After
Successful outcomes depend mainly on the phy-
sicians’ knowledge of facial anatomy, skill, and 
proper doses and technique. The aging process in 
the mid- and lower face is more associated with 
volumetric changes, more sagging, fat and skin 
atrophy, and laxity [30], while dynamic wrinkles 
are predominant in the upper face (Figs. 25.2 and 
25.3). Moreover, gender and ethnic features, as 
well as patients’ preferences, have to be consid-
ered to reach optimal results [31–33].
Currently, the trend in rejuvenation with BoNT-A 
comprises the use of lower doses and techniques to 
deliver natural results (Figs. 25.4 and 25.5), avoid-
ing complete paralysis of facial muscles [31, 34]. 
Indications are cited in Table 25.1.
Combined treatments have been considered as 
a standard approach to obtain facial harmony 
[35]. The combination of BoNT-A and hyal-
uronic acid dermal fillers provides optimized out-
comes, with better results than BoNT-A alone. 
Both techniques can be done at the same time 
[36]. Lasers, radiofrequency, chemical peels, 
a b
Fig. 25.2 (a) Glabellar 
lines at baseline and (b) 
2 weeks after treatment. 
Stronger glabellar 
muscles may require 
high doses
a b
Fig. 25.3 (a) Upper 
forehead lines at 
baseline and (b) 2 weeks 
after treatment. The 
treatment is tailored 
according to each 
patient’s characteristics 
and needs
a b
Fig. 25.4 (a) Mild 
asymmetric smile before 
and (b) 2 weeks after 
treatment with 
BoNT-A. The right side 
was treated with 2.5 U 
of ABO injected in a 
single point 1 cm 
laterally to the nasal ala
a b
Fig. 25.5 (a) A 34-year-old patient at rest before treatment and (b) the same patient 2 weeks after treatment showing 
eyebrow repositioning. The treatment of glabellar muscles raises the tail of the brow
25 Introduction: What Is Botulinum Toxin?
174
microdermabrasion, microneedling, and other 
superficial techniques can be used to improve 
results. The authors recommend the use of these 
techniques and the toxins at different times.
The “microbotox” or “microtoxin” technique 
consists in delivering multiple intradermal or 
subdermal injections of very small doses of 
BoNT-A into the overlying skin and superficial 
layer of the facial and neck muscles [37]. It can 
be used to treat some aesthetic conditions, includ-
ing fine lines, mild neck laxity, rosacea, and oily 
skin [12, 13, 37–40]. It can also slightly treat 
muscles that cannot be paralyzed.
Recently, the treatment of keloids and hyper-
trophic scars with BoNT-A was reported. Results 
are controversial, and more evidence is needed to 
support its efficacy [41–44].
25.4 Side Effects, Complications, 
and How They May 
Be Managed
Although BoNT-A injections for cosmetic use 
have a well-described safety profile [45, 46], side 
effects may occur. In general, they occur within 
the first few days following injection and are usu-
ally transitory. Since most of the studies assess 
the aesthetic effects of BoNT-A in the upper face, 
most frequently reported side effects concern the 
upper face such as headache, eye disorder, eyelid 
ptosis, and heavy eyelids [46]. The majority of 
the side effects can be avoided by using the con-
sensus doses [31, 47, 48] and injection sites 
described in the literature, also considering the 
patient anatomy and the desired results.
Side effects can be considered cosmetic and 
non-cosmetic. Whereas non-cosmetic side effects 
can be related to the technique, the injections, or 
the product, cosmetic side effects are most of the 
times technique related. Cosmetic side effects are 
related to unnatural look, an undesirable ana-
tomic position of a facial structure or asymmet-
ric, unwanted movements.
25.4.1 Non-cosmetic Side Effects
As expected for any injection procedure, pain, 
discomfort, burning, erythema, edema, pruritus, 
and bruising may be observed (Fig. 25.6) [22, 45]. 
Topical anesthetics, small gauge needles, cooler 
systems, and cold compress [49] can be used to 
minimize pain and bruising. These side effects are 
expected and resolve within a few days. 
Hematomas and ecchymosis (Fig. 25.7) also can 
occur after any injection procedure. They can be 
prevented with more superficial injections and 
can be controlled by compression of the treated 
area for a few minutes when reaching a vessel. 
Avoiding the use inhibitors of platelet aggregation 
for at least 7 days before treatment prevents the 
formation of hematomas and ecchymosis.
Paresthesia and dysesthesia in the treatment 
area are infrequent and may be produced by 
Fig. 25.6 Erythema and edema may occur at the injec-
tion sites. They are transitory and resolve within a few 
hours
Table 25.1 Hyperkinetic lines and other aesthetic indi-
cations are treated in three-thirds of the face and also in 
extrafacial areas
Area Indications
Upper face Glabellar lines
Lateral canthal lines
Horizontal forehead lines
Middle 
face
Infraorbital rhytids
Nasal oblique lines (“Bunny” lines)
Nasal tip elevation
Lower face Perioral rhytids
Gummy smile
Asymmetric smile
Masseter overactivity
Mentalis overactivity
Mandibularcontour or “Nefertiti lift”
Extrafacial Platysmal bands
Décolleté lines
Leg contour (hypertrophy of the 
gastrocnemius muscle)
D. Hexsel et al.
175
nerve trauma. Infections are rare and can be pre-
vented by skin antisepsis.
Headache is a common side effect after 
BoNT-A treatment of the upper face [45, 46, 50]. 
It is usually mild and spontaneously resolves 
within a few days after injection. There are 
reports of idiosyncratic severe headaches lasting 
2–4  weeks. Headaches are managed based on 
severity with analgesic, nonsteroidal anti- 
inflammatory drugs, or opioids.
Allergic reactions or immediate hypersensi-
tivity, although rare, may occur. Care should be 
taken with drugs that may potentiate BoNT-A 
effects such as aminoglycosides, quinidine, anti-
cholinergics, and muscle relaxants.
More severe side effects due to distant spread 
of BoNT-A have been reported with large doses 
and include generalized muscle weakness, dys-
phagia, dysarthria, dysphonia, and respiratory 
difficulties.
Clinical non-responsiveness to BoNT-A is 
rare. It may be primary, due to individual factors, 
errors related to drug preparation or administra-
tion, improper muscle selection, inadequate 
doses per injection site or area, or secondary to 
antibody formation after BoNT-A injections. A 
recent meta-analysis [51] showed that the fre-
quency of neutralizing antibodies (NAbs) was 
higher in secondary non-responsive patients 
compared with clinically responsive patients. 
However, almost half of secondary non- 
responsive patients did not have NAbs, suggest-
ing other factors rather than NAbs that may cause 
non-responsiveness. Moreover, NAb frequency 
was generally higher among conditions usually 
treated with higher BoNT doses [51].
BoNT-A treatment for cosmetic indications 
is associated with a low rate of NAb formation 
[51, 52]. The use of the lowest effective doses, 
waiting for at least 16 weeks between treatments 
and avoiding frequent touch-ups, may prevent 
BoNT-A clinical non-responsiveness [52].
Blepharoptosis is usually unilateral and char-
acterized by a 2–3 mm lowering of the affected 
upper eyelid. It may appear 2–10 days after the 
injections, lasting for up to 40  days [45]. This 
side effect is caused by spread of the toxin 
injected at the glabellar region through the 
orbital septum fascia to the levator palpebrae 
superioris. The incidence of this side effect can 
be reduced by injecting BoNT-A at least 1  cm 
above the supraorbital ridge, using a small vol-
ume to reconstitute the products and avoiding 
excessive manipulation of the area. 
Blepharoptosis can be treated using ophthalmic 
solutions with alpha-adrenergic effects, such as 
apraclonidine 0.5% (Iopidine®).
Brow ptosis or heavy eyelids is associated 
with overtreatment of the frontalis muscle. This 
side effect is temporary and spontaneously 
resolves as BoNT-A effects diminish, with no 
additional treatment required.
Diplopia or double vision is uncommon and 
may occur when injections are close to the ocular 
globe with consequent paralysis of the lateral 
rectus muscle.
In the lower face, undesirable paralysis in the 
musculature can occur if high doses of BoNT-A 
are used, leading to incompetence of the sphinc-
ter of the mouth, asymmetries, and impaired 
muscular support of the lower face [31]. The low-
est efficacious doses and low volumes of BoNT-A 
should be used in the lower face indications [53]. 
The most common side effects in the treatment of 
the neck are dysphagia, difficulties in flexing the 
neck, and dry mouth [31].
25.4.2 Cosmetic Side Effects
Frozen look or mask appearance of the face after 
BoNT-A treatment was quite common in the past 
decades. Currently, the natural look of the 
Fig. 25.7 Ecchymosis may also occur at the injection 
sites. This side effect is transitory and resolves spontane-
ously within a few days
25 Introduction: What Is Botulinum Toxin?
176
patients is targeted by most of the experienced 
physicians. The use of low doses and partial 
treatment of some facial muscles, especially the 
frontalis muscle, may be the best option for some 
patients. These simple measures provide a more 
natural look.
Excessive brow elevation (Fig.  25.8) can be 
avoided with an injection point at the lateral part 
of the frontalis muscle or at the middle pupillary 
line, 1  cm above the eyebrow. Excessive eleva-
tion of the malar region occurs due to injection 
points placed in the lower lateral parts of orbicu-
laris oculi muscles. This is a risky area, as the 
effects might target the zygomaticus major mus-
cle and provoke the drooping of mouth corners.
The “Botox sign” is produced by the excessive 
recruitment of the nasalis muscle when a patient 
smiles, after BoNT-A treatment of the upper third 
of the face. The treatment of the nasalis muscle is 
recommended when treating glabellar and fron-
talis muscles for patients who already present 
these lines before treatment.
Changes in the gender features give an unnat-
ural look to patients. Toxin injections in the gla-
bella can change the brow shape and position, 
giving a feminine look to male patients, with 
arched eyebrows or excessive elevation of the tail 
of the brow [33]. They can be avoided by keeping 
the original position and avoiding excessive ele-
vation with linear injections of BoNT-A in fron-
talis muscle in men.
25.5 Conclusions
More than 20 years of cosmetic use of BoNT-A 
consolidate it as a safe, predictable, and very 
effective treatment for a number of cosmetic 
facial and extrafacial indications. Side effects are 
mild to moderate and usually transitory. 
Currently, the trend in aesthetic treatments with 
BoNT-A comprises the use of proper doses and 
techniques, giving natural results. Combinations 
with fillers and other procedures should also be 
considered for better cosmetic results.
a b
Fig. 25.8 (a) Brow 
position before BoNT-A 
treatment and (b) 
excessive brow elevation 
after BoNT-A treatment. 
This cosmetic side effect 
can be resolved with a 
touch-up
Tip Box
• Clostridium botulinum is an anaerobic, 
gram-positive, spore-forming bacillus 
that produces exotoxins grouped into 
eight serotypes: A, B, C, D, E, F, G, 
and H.
• BoNT-A blocks the release of acetylcho-
line causing muscles’ chemical denerva-
tion and also neurologic modulation in 
sweat glands, leading to relaxation of 
muscles and decreasing sweating in the 
treated areas.
• Different formulations of BoNT-A are 
available worldwide; they are not inter-
changeable although are equally 
efficient.
• The three main commercial formula-
tions of BoNT-A approved for cosmetic 
indications are onabotulinumtoxin, abo-
botulinumtoxin A, and incobotulinum-
toxin A.
• BoNT-A is an effective treatment to 
enhance facial beauty by modulating 
facial muscle activity.
• BoNT-A remains the gold-standard 
treatment for upper facial dynamic 
wrinkles and presents benefits for some 
indications at middle and lower facial 
wrinkles.
D. Hexsel et al.
177
References
 1. Lamanna C, McElroy OE, Eklund HW. The purifica-
tion and crystallization of clostridium botulinum type 
A toxin. Science. 1946;103(2681):613–4.
 2. Kegeles G. The molecular size and shape of botulinus 
toxin. J Am Chem Soc. 1946;68:1670.
 3. Putnam FW, Lamanna C, Sharp DG.  Molecular 
weight and homogeneity of crystalline botulinus A 
toxin. J Biol Chem. 1946;165(2):735.
 4. Putnam FW. Physical chemical properties of crystal-
line botulinus A toxin. Fed Proc. 1947;6(1 Pt 2):284.
 5. Scott AB, Rosenbaum A, Collins CC. Pharmacologic 
weakening of extraocular muscles. Investig 
Ophthalmol. 1973;12:924–7.
 6. Carruthers A, Carruthers J. You want to inject what? 
Dermatol Surg. 2015;41(Suppl 1):S2–8.
 7. Carruthers JD, Carruthers JA. Treatment of glabellar 
frown lines with C. botulinum-A exotoxin. J Dermatol 
Surg Oncol. 1992;18:17–21.
 8. Peck MW, Smith TJ, Anniballi F, et  al. Historical 
perspectives and guidelines for botulinum toxins 
neurotoxin subtype nomenclature basel.Toxins. 
2017;9(1):pii: E38.
 9. Pellett S, Tepp WH, Bradshaw M, et al. Purification 
and characterization of botulinum neurotoxin FA 
from a genetically modified clostridium botulinum 
strain. mSphere. 2016;1(1):pii: e00100–15.
 10. Shelley WB, Talanin NY, Shelley ED.  Botulinum 
toxin therapy for palmar hyperhidrosis. J Am Acad 
Dermatol. 1998;38(2 Pt 1):227–9.
 11. Schnider P, Binder M, Auff E, Kittler H, Berger T, 
Wolff K. Double-blind trial of botulinum A toxin for 
the treatment of focal hyperhidrosis of the palms. Br J 
Dermatol. 1997;136(4):548–52.
 12. Li ZJ, Park SB, Sohn KC, et al. Regulation of lipid-
production by acetylcholine signalling in human seba-
ceous glands. J Dermatol Sci. 2013;72(2):116–22.
 13. Khan TT, Herne K, Dayan SH, Woodward JA. Facial 
blanching due to neurotoxins: proposed mechanisms. 
Dermatol Surg. 2013;39(1 Pt 1):24–9.
 14. Finzi E, Rosenthal NE. Treatment of depression with 
onabotulinumtoxinA: a randomized, double-blind, 
placebo controlled trial. J Psychiatr Res. 2014;52:1–6.
 15. Heckmann M, Teichmann B, Schröder U, 
Sprengelmeyer R, Ceballos-Baumann AO. 
Pharmacologic denervation of frown muscles 
enhances baseline expression of happiness and 
decreases baseline expression of anger, sadness, and 
fear. J Am Acad Dermatol. 2003;49(2):213–6.
 16. Hexsel D, Brum C, Siega C, et  al. Evaluation of 
self-esteem and depression symptoms in depressed 
and nondepressed subjects treated with onabotu-
linumtoxinA for glabellar lines. Dermatol Surg. 
2013;39(7):1088–96.
 17. Magid M, Reichenberg JS, Poth PE, et  al. 
Treatment of major depressive disorder using botu-
linum toxin A: a 24-week randomized, double-
blind, placebo- controlled study. J Clin Psychiatry. 
2014;75(8):837–44.
 18. Wollmer MA, de Boer C, Kalak N, et  al. Facing 
depression with botulinum toxin: a randomized con-
trolled trial. J Psychiatr Res. 2012;46(5):574–81.
 19. Xiao Z, Zhang M, Liu Y, Ren L. Botulinum toxin type 
a inhibits connective tissue growth factor expression 
in fibroblasts derived from hypertrophic scar. Aesthet 
Plast Surg. 2011;35(5):802–7.
 20. Xiaoxue W, Xi C, Zhibo X. Effects of botulinum toxin 
type A on expression of genes in keloid fibroblasts. 
Aesthet Surg J. 2014;34(1):154–9.
 21. ClinicalTrials.gov [Internet]. Bethesda (MD): 
National Library of Medicine (US). 2000 Feb 29  – 
Identifier NCT02939326, Evaluate safety and efficacy 
of a single treatment cycle of EB-001 in subjects with 
Glabellar Frown Lines; 2016 Oct 11 [cited 2017 Aug 
21]; [about 5 screens]. Available from: https://clini-
caltrials.gov/ct2/show/study/NCT02939326?term=bo
nti&rank=2.
 22. Dessy LA, Fallico N, Mazzocchi M, Scuderi 
N.  Botulinum toxin for glabellar lines: a review of 
the efficacy and safety of currently available products. 
Am J Clin Dermatol. 2011;12(6):377–88.
 23. Karsai S, Raulin C.  Current evidence on the unit 
equivalence of different botulinum neurotoxin A for-
mulations and recommendations for clinical practice 
in dermatology. Dermatol Surg. 2009;35(1):1–8.
 24. Hexsel D, Brum C, do Prado DZ, et al. Field effect of 
two commercial preparations of botulinum toxin type 
A: a prospective, double-blind, randomized clinical 
trial. J Am Acad Dermatol. 2012;67(2):226–32.
 25. Carruthers J, Fournier N, Kerscher M, Ruiz-Avila J, 
Trindade de Almeida AR, Kaeuper G.  The conver-
gence of medicine and neurotoxins: a focus on bot-
ulinum toxin type A and its application in aesthetic 
medicine--a global, evidence-based botulinum toxin 
consensus education initiative: part II: incorporat-
ing botulinum toxin into aesthetic clinical practice. 
Dermatol Surg. 2013;39(3 Pt 2):510–25.
 26. Dressler D. Comparing Botox and Xeomin for axillar 
hyperhidrosis. J Neural Transm. 2010;117:317–9.
 27. Dressler D, Mander G, Fink K. Measuring the potency 
labelling of onabotulinumtoxinA (Botox®) and inco-
botulinumtoxinA (Xeomin®) in an LD50 assay. J 
Neural Transm (Vienna). 2012;119(1):13–5.
• BoNT-A injection is a minimally inva-
sive surgical procedure with good safety 
and tolerability profiles in aesthetic 
indications.
• The potential side effects are usually 
transitory, and their incidence can be 
minimized with proper patient selec-
tion, techniques, and doses.
25 Introduction: What Is Botulinum Toxin?
http://clinicaltrials.gov
https://clinicaltrials.gov/ct2/show/study/NCT02939326?term=bonti&rank=2
https://clinicaltrials.gov/ct2/show/study/NCT02939326?term=bonti&rank=2
https://clinicaltrials.gov/ct2/show/study/NCT02939326?term=bonti&rank=2
178
 28. Sattler G, Callander MJ, Grablowitz D, et  al. 
Noninferiority of incobotulinumtoxinA, free from 
complexing proteins, compared with another botuli-
num toxin type A in the treatment of glabellar frown 
lines. Dermatol Surg. 2010;36:2146–54.
 29. Hexsel D, Hexsel C, Siega C, Schilling-Souza J, Rotta 
FT, Rodrigues TC.  Fields of effects of 2 commer-
cial preparations of botulinum toxin type A at equal 
labeled unit doses: a double-blind randomized trial. 
JAMA Dermatol. 2013;149(12):1386–91.
 30. Fagien S, Raspaldo H. Facial rejuvenation with botu-
linum neurotoxin: an anatomical and experiential 
perspective. J Cosmet Laser Ther. 2007;9(Suppl 1): 
23–31.
 31. Sundaram H, Signorini M, Liew S, et  al. Global 
aesthetics consensus: botulinum toxin Type 
A--evidence-based review, emerging concepts, and 
consensus recommendations for aesthetic use, includ-
ing updates on complications. Plast Reconstr Surg. 
2016;137(3):518e–29e.
 32. Sundaram H, Huang PH, Hsu NJ, et  al. Aesthetic 
applications of botulinum toxin A in Asians: an inter-
national, multidisciplinary, Pan-Asian consensus. 
Plast Reconstr Surg Glob Open. 2016;4(12):e872.
 33. de Maio M. Ethnic and gender considerations in the 
use of facial injectables: male patients. Plast Reconstr 
Surg. 2015;136(5 Suppl):40S–3S.
 34. Dayan SH, Ashourian N. Considerations for achiev-
ing a natural face in cosmetic procedures. JAMA 
Facial Plast Surg. 2015;17(6):395.
 35. Sundaram H, Liew S, Signorini M, et al. Global aes-
thetics consensus: hyaluronic acid fillers and botuli-
num toxin type A-recommendations for combined 
treatment and optimizing outcomes in diverse patient 
populations. Plast Reconstr Surg. 2016;137(5): 
1410–23.
 36. Carruthers A, Carruthers J, Monheit GD, Davis PG, 
Tardie G.  Multicenter, randomized, parallel-group 
study of the safety and effectiveness of onabotu-
linumtoxinA and hyaluronic acid dermal fillers 
(24-mg/mL Smooth, Cohesive Gel) alone and in com-
bination for lower facial rejuvenation. Dermatol Surg. 
2010;36:2121–34.
 37. Wu WT. Microbotox of the lower face and neck: evo-
lution of a personal technique and its clinical effects. 
Plast Reconstr Surg. 2015;136(5 Suppl):92S–100S.
 38. Steinsapir KD, Rootman D, Wulc A, Hwang 
C.  Cosmetic microdroplet botulinum toxin A fore-
head lift: a new treatment paradigm. Ophthal Plast 
Reconstr Surg. 2015;31(4):263–8.
 39. Bloom BS, Payongayong L, Mourin A, Goldberg 
DJ.  Impact of intradermal abobotulinumtoxinA 
on facial erythema of rosacea. Dermatol Surg. 
2015;41(Suppl 1):S9–16.
 40. Rose AE, Goldberg DJ. Safety and efficacy of intra-
dermal injection of botulinum toxin for the treatment 
of oily skin. Dermatol Surg. 2013;39(3 Pt 1):443–8.
 41. Jeong HS, Lee BH, Sung HM, et  al. Effect of bot-
ulinum toxin type A on differentiation of fibro-
blasts derived from scar tissue. Plast Reconstr Surg. 
2015;136(2):171e–8e.
 42. Shaarawy E, Hegazy RA, Abdel Hay RM. Intralesional 
botulinum toxin type A equally effective and better 
tolerated than intralesional steroid in the treatment 
of keloids: a randomized controlled trial. J Cosmet 
Dermatol. 2015;14(2):161–6.
 43. Prodromidou A, Frountzas M, Vlachos DE, et  al. 
Botulinum toxin for the prevention and healing of 
wound scars: a systematic review of the literature. 
Plast Surg (Oakv). 2015;23(4):260–4.
 44. Haubner F, Leyh M, Ohmann E, Sadick H, Gassner 
HG.  Effects of botulinum toxin A on patient- 
specific keloid fibroblasts in  vitro. Laryngoscope.2014;124(6):1344–51.
 45. Cavallini M, Cirillo P, Fundarò SP, et  al. Safety of 
botulinum toxin A in aesthetic treatments: a sys-
tematic review of clinical studies. Dermatol Surg. 
2014;40(5):525–36.
 46. Jia Z, Lu H, Yang X, et  al. Adverse events of botu-
linum toxin type A in facial rejuvenation: a system-
atic review and meta-analysis. Aesthet Plast Surg. 
2016;40(5):769–77.
 47. Ascher B, Talarico S, Cassuto D, et al. International 
consensus recommendation on the aesthetic usage 
of botulinum toxin type A (Speywood unit)--part I: 
upper facial wrinkles. J Eur Acad Dermatol Venereol. 
2010;24(11):1278–84.
 48. Ascher B, Talarico S, Cassuto D, et al. International 
consensus recommendations on the aesthetic usage 
of botulinum toxin type A (Speywood Unit)--
Part II: Wrinkles on the middle and lower face, 
neck and chest. J Eur Acad Dermatol Venereol. 
2010;24(11):1285–95.
 49. Hexsel DM, Dal Forno T, Soirefmann M, Porto MD, 
Hexsel CL.  Effective, low-cost, simple, disposable 
cooling tool for patient comfort in common dermato-
logic procedures. Dermatol Surg. 2013;39(9):1402–4.
 50. Carruthers J, Rivkin A, Donofrio L, et  al. A multi-
center, randomized, double-blind, placebo-controlled 
study to evaluate the efficacy and safety of repeated 
onabotulinumtoxinA treatments in subjects with 
Crow’s Feet Lines and Glabellar Lines. Dermatol 
Surg. 2015;41(6):702–11.
 51. Fabbri M, Leodori G, Fernandes RM, et  al. 
Neutralizing antibody and botulinum toxin therapy: a 
systematic review and meta-analysis. Neurotox Res. 
2016;29(1):105–17.
 52. Naumann M, Boo LM, Ackerman AH, Gallagher 
CJ.  Immunogenicity of botulinum toxins. J Neural 
Transm (Vienna). 2013;120(2):275–90.
 53. Cohen JL, Dayan SH, Cox SE, Yalamanchili R, 
Tardie G.  OnabotulinumtoxinA dose-ranging study 
for hyperdynamic perioral lines. Dermatol Surg. 
2012;38(9):1497–505.
D. Hexsel et al.
179© Springer Nature Switzerland AG 2020 
A. Da Costa (ed.), Minimally Invasive Aesthetic Procedures, 
https://doi.org/10.1007/978-3-319-78265-2_26
Tip Chapter: Histology 
and Physiology of the Skin
Renata Joffe, Jose A. Plaza, and Armineh Kajoian
26.1 Epidermis
The epidermis is the outermost layer of the skin. 
It is a stratified, squamous epithelium layer 
composed primarily of two types of cells: kera-
tinocytes, melanocytes, Langerhans cells, and 
Merkel cells, but keratinocytes constitute the 
major cell population of the epidermis (80%). 
The epidermis commonly is divided into four 
layers according to keratinocyte morphology 
and position: the basal cell layer (stratum germi-
nativum), the squamous cell layer (prickle cell 
or stratum spinosum), the granular cell layer 
(stratum granulosum), and the cornified or 
horny cell layer (stratum corneum) [1, 2]. The 
last three layers that constitute the living, nucle-
ated cells of the epidermis are sometimes 
referred to as the stratum malpighii and rete 
malpighii [2].
The epidermis is a continually renewing layer 
and gives rise to derivative structures, such as 
pilosebaceous apparatus, nails, and sweat glands. 
The basal cells of the epidermis undergo a verti-
cally oriented proliferation cycle that helps in the 
renewal of the outer epidermis.
26.2 Keratinocytes
Approximately 85% of cells in the epidermis are 
the ectodermally derived keratinocytes, which are 
cells that produce keratin. The differentiation pro-
cess that occurs as the cells migrate from the basal 
layer to the surface of the skin is called keratiniza-
tion. This process occurs for a period of about 
14  days, where the epidermal keratinocytes are 
transformed from undifferentiated basal cells to 
fully differentiated cornified cells. The keratino-
cyte first passes through a synthetic and then a deg-
radative phase [3]. In the synthetic phase, the cell 
builds up a cytoplasmic supply of keratin, a fibrous 
intermediate filament arranged in an alpha-helical 
coil pattern that serves as part of the cell cytoskel-
eton. Bundles of these keratin filaments converge 
on and terminate at the plasma membrane, thereby 
forming the intercellular attachment plates known 
as desmosomes. During the degradative phase of 
keratinization, cellular organelles are lost, the con-
tents of the cell are consolidated into a mixture of 
filaments and amorphous cell envelopes, and, 
finally, the cell is known as a horny cell or a corneo-
cyte. The process of maturation resulting in cell 
death is known as terminal differentiation [1].
R. Joffe (*) · J. A. Plaza · A. Kajoian 
Inform Diagnostics, Irving, TX, USA
26
http://crossmark.crossref.org/dialog/?doi=10.1007/978-3-319-78265-2_26&domain=pdf
180
26.2.1 Basal Layer
The basal layer, also known as the stratum ger-
minativum, consists of a single layer of cuboi-
dal/columnar keratinocytes that attach to the 
basement membrane zone with their long axis 
perpendicular to the dermis. These basal cells 
adhere to one another and to more superficial 
squamous cells through desmosomal junctions 
[2]. The basal layer is the primary location of 
mitotically active cells in the epidermis that give 
rise to cells of the outer epidermal layers. 
Kinetic studies demonstrate that the basal cells 
of the epidermis include three populations: stem 
cells, transit- amplifying cells, and the commit-
ted cells.
Stem cells Undifferentiated cells with unlimited 
capacity for cell division
Transit- 
amplifying 
cells
Cells with a limited capacity for 
mitosis before becoming committed to 
terminal differentiation
Committed 
cells
Cells that have irreversibly lost their 
capacity to divide and progress along 
keratinization pathways
Migration of a basal cell from the basal layer 
to the cornified layer in humans takes at least 
14  days, and the transit through the cornified 
layer to the outermost epidermis requires another 
14 days.
26.2.2 Squamous Cell Layer
The squamous cell layer or stratum spinosum 
overlies the basal cell layer and has a thickness of 
typically 5–10 cells [2]. The keratinocytes located 
immediately above the basal layer have a polyhe-
dral shape and a rounded nucleus, whereas the 
ones present in the upper spinous layers have a 
generally larger size, become flatter as they are 
pushed toward the surface of the skin, and con-
tain lamellar granules [3]. The granules are 
membrane- bound organelles containing glyco-
proteins, glycolipids, phospholipids, free sterols, 
and a number of acid hydrolases including 
lipases, proteases, acid phosphatases, and glyco-
sidases. Although the lamellar granules are pri-
marily active in cells at the interface between the 
granular and cornified layers, they also function 
in cells of the upper spinous layer to deliver pre-
cursors of stratum corneum lipids into the inter-
cellular space [4].
Intercellular spaces between spinous cells are 
bridged by numerous desmosomes, which pro-
mote a mechanical connection between cells of 
the epidermis and provide resistance to physical 
stresses. The spine-like appearance of the numer-
ous desmosomes along cell margins is where the 
stratum spinosum derives its name [3]. Gap junc-
tions are another type of connection between epi-
dermal cells. These junctions allow for 
physiologic communication through chemical 
signals, which is vital in the regulation of cell 
metabolism, growth, and differentiation [5].
26.2.3 Granular Layer
The granular layer, or stratum granulosum, is 
composed of flattened cells containing abundant 
keratohyalin granules in their cytoplasm. These 
cells are responsible for further synthesis and 
modification of proteins involved in keratiniza-
tion [3]. The granular layer varies in thickness in 
proportion to that of the overlying horny cell 
layer. For example, under thin cornified layer 
areas, the granular layer may have thickness of 
only 1–3 cell layers, whereas under the palms of 
the hands and soles of the feet, the granular layer 
may have a tenfold thickness as the above- 
mentioned areas. The keratohyalin granules are 
deeply basophilic andhave irregular shape and 
size, and they are necessary in the formation of 
both the interfibrillary matrix, which holds kera-
tin filaments together, and the inner lining of the 
horny cells. Lysosomal enzymes are found at 
high levels in the stratum granulosum because 
the granular layer is a keratogenous zone of the 
epidermis.
R. Joffe et al.
181
26.2.4 Cornified Layer
The cornified layer comprising horny cells (cor-
neocytes) is the most superficial layer of the epi-
dermis. It provides mechanical protection to the 
underlying epidermis and acts as a barrier to pre-
vent water loss and invasion by foreign substances 
[6]. The corneocytes, which are rich in protein 
and low in lipid content, are surrounded by a con-
tinuous extracellular lipid matrix [3]. The large, 
flat, polyhedral-shaped horny cells have lost their 
nuclei during terminal differentiation and are 
technically considered to be dead [2, 3]. The 
physical and biochemical properties of cells in the 
cornified layer vary in accordance with position in 
order to promote desquamation, with the cells 
moving outward. For instance, cells in the middle 
layers have a much higher capacity for water 
binding than those in the deeper layers because of 
the high concentration of free amino acids found 
in the cytoplasm of middle-layer cells. The deep-
layer cells also are more densely compact and dis-
play a greater array of intercellular attachments 
than the more superficial layers. Desmosomes 
undergo proteolytic degradation as the cells prog-
ress outward, thus contributing to the shedding of 
corneocytes during desquamation [4].
26.3 Melanocytes
With a neural crest origin, the melanocyte is a 
dendritic, pigment-synthesizing cell confined pre-
dominantly to the basal layer and the hair bulb in 
the skin [3]. Melanocytes come into contact with 
keratinocytes but do not form cellular junctions. 
The function of melanocytes is the production of 
the pigment melanin and its transfer to keratino-
cytes. The ratio of melanocytes to basal cells is 
1:4–1:9 and varies with anatomic location on the 
body. Melanin varies in color from yellow to 
brown or black and accounts for the various skin 
colors within and among races. It is produced in a 
rounded, membrane-bound organelle known as 
the melanosome. Melanin is thought to protect the 
mitotically active basal epidermal cells from the 
damaging effects of ultraviolet light. Increased 
ultraviolet light exposure stimulates an increase in 
melanogenesis and a corresponding increase in 
melanosomes, which are transported through the 
dendritic processes of the melanocytes and trans-
ferred to the keratinocytes. This response, which 
results in the tanning of the skin, increases the 
ability of the cell to absorb light and thus protect 
genetic information in the nucleus from harmful 
radiation (Figs. 26.1 and 26.2).
Fig. 26.1 Histology of 
the normal epidermis 
and dermis (arm skin). 
(H&E 4x)
26 Tip Chapter: Histology and Physiology of the Skin
182
26.4 Langerhans Cells
Langerhans cells are intraepidermal antigen- 
processing cells involved in a variety of T-cell- 
mediated immunoreactions. Derived from the 
bone marrow, these cells are distributed among 
the squamous and granular layers with fewer 
cells in the basal layer. They are found in other 
squamous epithelia in addition to the epider-
mis, including the oral cavity, esophagus, and 
vagina, as well as in lymphoid organs and in 
the normal dermis. Langerhans cells are char-
acterized by their dendritic processes, which 
extend between the keratinocytes extending 
from the granular cell layer to the dermal-epi-
dermal junction. The cells do not form cellular 
junctions with neighboring cells given the 
absence of desmosomes and tonofilaments. 
Langerhans cells recognize and process solu-
ble antigens found in the epidermal tissue and 
participate in delayed hypersensitivity and 
skin allograft reactions. In addition to mediat-
ing T-cell responses, Langerhans cells also 
appear to play a role in extrathymic 
T-lymphocyte maturation and intraepidermal 
differentiation [7].
26.5 Merkel Cells
Merkel cells are oval-shaped, slow-adapting, 
type I mechanoreceptors located in the basal 
layer of the epidermis, hair follicular epithelium, 
and mucous membranes. Their precise origin 
remains unknown; however, they appear to repre-
sent a modified keratinocyte with neuroendocrine 
features. They are present in sites of high tactile 
sensitivity such as digits, palms, lips, hard palate, 
proximal nail folds, and dorsum of the feet. 
Merkel cells have been shown to increase in 
number in sun-damaged skin. In addition to their 
mechanoreceptor function, Merkel cells may 
play a primary role in the induction of subepider-
mal and perifollicular nerve plexuses.
26.6 Dermoepidermal Interface
The interface between the epidermis and dermis 
is formed by a porous basement membrane zone. 
It consists of a glycoprotein matrix consisting of 
collagen, reticulin, and fine elastic fibers, which 
is highlighted by a periodic acid-Schiff (PAS) 
stain. The basement membrane zone continues 
Fig. 26.2 Histology of 
acral skin showing 
thickened stratum 
corneum 
(hyperkeratosis) and 
thickened stratum 
granulosum 
(hypergranulosis). (H&E 
10x)
R. Joffe et al.
183
around all the epidermal appendages. This layer 
allows the exchange of cells and fluid and holds 
the two layers together [1]. It has been divided 
into four zones:
Cytoskeleton Hemidesmosomes and plasma 
membrane of basal keratinocytes that 
compose the upper border of the 
interface
Lamina 
lucida
Layer synthesized by basal cells of the 
epidermis consisting mainly of type IV 
collagen as well as anchoring fibrils and 
dermal microfibrils
Lamina 
densa
Layer situated below the lamina lucida 
and above the papillary dermis
Sublamina 
densa
Located immediately below the lamina 
densa and consisting of the uppermost 
portion of the papillary dermis
Structural components of these four zones 
are responsible for binding the epidermis to the 
dermis. The dermal-epidermal junction not only 
acts as a support for the epidermis but also 
establishes cell polarity and direction of growth, 
directs the organization of the cytoskeleton in 
basal cells, provides developmental signals, and 
functions as a semipermeable barrier between 
layers [8].
26.7 Hair Follicles
Hair follicles are found on all body surfaces 
except the palms and soles. Although the most 
important roles of the hair are providing pro-
tection from the elements and distributing 
sweat gland products, it has a prominent psy-
chosocial role in social interactions. Variation 
in size, shape, number, and distribution of hair 
follicles across the body is dependent on ana-
tomic location, race, and sex. Deep-seated ana-
gen hairs are noted in the scalp of both sexes as 
well as the beard region of men. In areas such 
as extremities and trunk, the follicles are more 
superficially located with decreased density of 
hair. In addition, variation exists in rate of 
growth and response to stimuli such as sex hor-
mones. Eyebrows and eyelashes, for example, 
are not stimulated by sex hormones, whereas 
during puberty, the hairs of the axilla, face, and 
pubic area are highly affected by such hor-
mones. The number of hair follicles is deter-
mined during fetal development as are the 
phenotype and distribution of the follicles. 
During embryogenesis, the basophilic cells of 
the epidermis, located within the basal layer, 
undergo induction to eventually develop into a 
mature follicle [2]. The melanosome distribu-
tion determines the hair color of an individual. 
These melanosomes are located within the hair 
bulb. Larger melanosomes are found in indi-
viduals of African descent and smaller ones in 
Caucasians. As individuals age, there is a 
decrease/loss of these melanosomes, which 
results in gray hair [1].
The hair follicle is composed of three regions:
• The upper segment (infundibulum) which 
extends from