Aesthetic Medicine: Art and Techniques

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Aesthetic Medicine

 

Peter M. Prendergast • Melvin A. Shiffman Editors

Aesthetic Medicine Art and Techniques

Editors Dr. Peter M. Prendergast, M.B., B.Ch., MRCSI. Venus Medical Heritage House Dundrum Office Park Dublin 14 Ireland [email protected]

Dr. Melvin A. Shiffman, M.D., J.D. Surgery Section Newport Specialty Hospital 17501 Chatham Drive Tustin, CA 92780-2302 USA [email protected]

ISBN 978-3-642-20112-7     e-ISBN 978-3-642-20113-4 DOI 10.1007/978-3-642-20113-4 Springer Heidelberg Dordrecht London New York Library of Congress Control Number: 2011928412 © Springer-Verlag Berlin Heidelberg 2011 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer. Violations are liable to prosecution under the German Copyright Law. The use of general descriptive names, registered names, trademarks, 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. Product liability: The publisher can give no guarantee for information about drug dosage and application thereof contained in this book. In every individual case the respective user must check its accuracy by consulting other pharmaceutical literature. Cover design: eStudioCalamar, Figueres/Berlin Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com)

This book is dedicated to my beautiful children, Ciara and Niall, and to my wife and dearest love, Pyn. Peter M. Prendergast, M.B., B.Ch., MRCSI.

 

Foreword

In 1973 in Paris the words medicine and aesthetic appeared alongside each other. The combination of these two words gave rise to a new concept of correcting various aspects of the human body. Cosmetic surgery for years has created transformations, and aesthetic medicine can achieve similar results using a lighter technique. From 1973 until the early 1980s, aesthetic medicine spread from France to the Mediterranean, and then on to America, maintaining and using all the medicine and physiotherapy that make aesthetic improvements to the body. The reason for this wide and rapid spread was the desire for changes in people’s ways of life in a more modern society. In fact, the most important aspect had become ‘time.’ People had less time and more things to think about in this increasingly competitive way of living. Therefore, the time needed for two people to meet was insufficient to really get to know each other, which meant that people began to find ways of improving themselves: how they dress, their way of speaking, their body language, and last but not least their appearance. The old saying “Clothes don’t make the man” could be seen as incorrect and actually the exact opposite is true: first impressions count. To dwell on how much this transformation is or is not true would just stray from the point. The reality is that people request the expertise of surgeons and doctors to better their aesthetic appearance to conform with what is seen as the ideal in society today. Corrective treatments should not be seen as negative. In fact, improving the aesthetic appearance allows individuals to like themselves more and feel more balanced psychologically. This not only improves the psyche, but also the metabolism. Today a new science called psycho-neuro-endocrino-immunology studies the positive and negative effects our psyche, equilibrium, anxiousness, stress, and depression can have on our endocrine system, interfering with the metabolism and immune system, which defends us against infection and cancer. Helping someone to see him/ herself in a better light not only improves ‘beauty,’ but also health, having a positive effect on the nervous, immune, and endocrine systems. Therefore today, aesthetic medicine should be seen as an important branch of medicine improving the quality of people’s lives. It is important to have correct scientific information for those doctors who wish to enter into the field of aesthetic medicine All scientific information originates from study and should communicate the reasoning behind and technical operation of aesthetic medicine. Peter Prendergast and Melvin A. Shiffman are doctors with great skills and experience in aesthetic medicine and cosmetic surgery who have put together a text that includes all the theoretical and practical information needed to operate in this area. A staff of international specialists, expert in particular areas, have

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been selected to compile chapters in a way that gives students the best knowledge and know-how regarding aesthetic treatment. The book starts by looking at aesthetic medicine and its ethics, and continues on to other clinical aspects relating to this branch of medicine, going into useful techniques for improving the patients’ body. Also new to this area are techniques like mesotherapy, always respecting science and medical and surgical guidelines. The title of this book, “Aesthetic Medicine: Art and Techniques,” means that we can ultimately understand that this area appears simple, but in fact is not only a science but also an art. Furthermore, the maintenance and improvement of aethestic harmony in our patients not only require scientific knowledge and technical skills, but also, and arguably more importantly, artistic inspiration and taste. This book represents up-to-date advances in the aesthetic medicine sector, and can be used as a base and reference for all who wish to advance in the field of aesthetic medicine. Rome, Italy  

Maurizio Ceccareli, M.D., Sc.D., Cl.Path.S.

Preface

Aesthetic medicine is a rapidly growing specialty that is largely procedure-oriented. Non-surgical and minimally invasive techniques for enhancing the face and body are now possible without the need even for sedation. These include facial rejuvenation with lasers, lights, and tissue tightening technologies, augmentation with fillers and autologous fat, chemodenervation, and thread lift techniques. Breast augmentation with fat or fillers is performed under local anesthesia, as is body contouring using the tumescent technique. Although procedures in aesthetic medicine certainly do not replace those in cosmetic surgery, patients frequently request rejuvenation that is minimally invasive and requires little or no downtime. This demand has steadily increased over the last decade and has been the driving force in the evolution of aesthetic medicine into a discipline practiced by surgeons and physicians alike. Indeed, many of the techniques described in this book, such as facial volumizing and skin resurfacing, are ideal adjuncts to a plan of surgical facial rejuvenation. The pace of growth in aesthetic medicine, coupled with the explosion in the number of new devices and treatment modalities for rejuvenation, precludes any exhaustive text on the subject. However, we have endeavored to include topics of interest for the beginning and advanced practitioner in aesthetic medicine, including advanced applications of the most common procedures such as botulinum toxins and fillers. Separate chapters detail the latest techniques in suture face lifts, stem cell-enriched fat transfer, mesotherapy, carboxytherapy, thermolysis, Vaser lipoplasty, and treatments for cellulite, varicose veins, and telangiectasias. This book is intended as a manual. The emphasis is on protocols, parameters, instruments, materials, and descriptions of techniques. Our aim is not only to facilitate an understanding of the principles of aesthetic medicine, but also to allow the reader to incorporate the various techniques described into their practice. The book will also serve as a valuable resource for physicians and surgeons of any specialty undergoing formal instructional courses or workshops in aesthetic medicine. The contributors, all international authorities in their fields, share their advice, tips, and experience using clear explanations, illustrations, and step-by-step photographs. We hope that, by describing and showing the techniques in detail, the reader will both appreciate the artistic element of aesthetic medicine and gain a practical knowledge for immediate application. Dublin, Ireland Tustin, California, USA

Peter M. Prendergast, M.B., B.Ch., MRCSI. Melvin A. Shiffman, M.D., J.D.

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Contents

Part I  Aesthetic Medicine   1 Defining Aesthetic Medicine. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Peter M. Prendergast

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  2 Ethical Aspects of Aesthetic Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . Urban Wiesing

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Part II  Preoperative   3 Medical History. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Melvin A. Shiffman   4 Clinical Assessment of Facial Aging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 Melvin A. Shiffman   5 Assessment and Treatment of Excess Weight. . . . . . . . . . . . . . . . . . . . . . 29 Melanie T. Turk   6 Phytonutrient and Phytotherapy for Improving Health. . . . . . . . . . . . . 47 Jian Zhao   7 Skin Imaging in Aesthetic Medicine. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59 Peter M. Prendergast   8 Cosmeceutical Treatment of the Aging Face . . . . . . . . . . . . . . . . . . . . . . 69 Jennifer Linder Part III  Cutaneous Procedures   9 Local Regional Anesthesia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 Peter M. Prendergast 10 Botulinum Toxins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103 Peter M. Prendergast 11 Biostimulation and Biorestructuring of the Skin. . . . . . . . . . . . . . . . . . . 131 Maurizio Ceccarelli 12 Microdermabrasion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145 Preeti H. Savardekar 13 Aesthetic Cryotherapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151 Michael H. Swann xi

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14 Facial Peels. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157 Niti Khunger 15 Fractional Laser Resurfacing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179 Vic A. Narurkar 16 Capacitive Radiofrequency Skin Rejuvenation. . . . . . . . . . . . . . . . . . . . 187 Manoj T. Abraham and Joseph J. Rousso 17 The Use of Intense Pulsed Light (IPL) in Aesthetic Medicine . . . . . . . . 197 Bruce M. Freedman and Toral P. Balakrishnan 18 Thermolysis in Aesthetic Medicine: 3D Rejuvenation . . . . . . . . . . . . . . 205 Nassim Tabatabai and Neil S. Sadick 19 Neodym-Yag-Laser Treatment for Hemangiomas and Vascular Malformations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213 Thomas Hintringer 20 Foam Sclerotherapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221 Marcondes Figueiredo 21 Facial Laser Hair Removal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235 Benjamin A. Bassichis 22 Laser Treatment of Telangiectasias. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241 Alia S. Brown and David J. Goldberg 23 Mesotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 249 Narmada Bharia 24 Mesotherapy Solutions for Inducing Lipolysis and Treating Cellulite. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255 Benje Gutierrez and Frank L. Greenway 25 Cellulite: Etiology, Classification, Pathology, and Treatment. . . . . . . . . 265 Melvin A. Shiffman 26 Dermaroller: The Transepidermal Delivery System. . . . . . . . . . . . . . . . 273 Madhuri Agarwal 27 Scar Management. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277 George John Bitar, Priscilla Patel, and Lauren Craig 28 Arnica montana. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 289 Melvin A. Shiffman Part IV  Shaping Face and Body 29 Augmentation with Injectable Fillers. . . . . . . . . . . . . . . . . . . . . . . . . . . . 297 Peter M. Prendergast 30 Potential Risks and Complications of Injectable Alloplastic Facial Fillers. . . . . . . . . . . . . . . . . . . . . . . . . . . . 337 Melvin A. Shiffman

Contents

Contents

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31 Facial Augmentation with Autologous Fat. . . . . . . . . . . . . . . . . . . . . . . . 347 Melvin A. Shiffman 32 Face and Neck Remodeling with Ultrasound-Assisted Lipoplasty (Vaser). . . . . . . . . . . . . . . . . . . . . . . . . . 357 Alberto Di Giuseppe and George Commons 33 Injection/Filler Rhinoplasty. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 371 George John Bitar, Olalesi Osunsade, and Anuradha Devabhaktuni 34 Suture Lifting Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391 Peter M. Prendergast 35 Breast Augmentation with Hyaluronic Acid Filler . . . . . . . . . . . . . . . . . 427 Peter M. Prendergast 36 Cell-Assisted Lipotransfer for Breast Augmentation . . . . . . . . . . . . . . . 445 Kotaro Yoshimura, Yuko Asano, Noriyuki Aoi 37 Penile Enhancement Using Fillers. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 459 Hassan Abbas Khawaja and Enrique Hernandez-Perez 38 Body Contouring with Ultrasound-Assisted Lipoplasty (VASER). . . . . 465 Peter M. Prendergast 39 The Use of Low-Level Laser Therapy for Noninvasive Body Contouring. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509 Robert F. Jackson and Ryan Maloney 40 Ultrasound-Assisted Lipoplasty: Basic Physics, Tissue Interactions, and Related Results/Complications . . . . . . . . . . . . 519 William W. Cimino 41 Medical Management Options for Hair Loss . . . . . . . . . . . . . . . . . . . . . 529 Samuel M. Lam, Brian R. Hempstead, and Edwin F. WilliamsIII 42 Hair Removal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 537 Afshin Sadighha and Gita Meshkat Razavi 43 Carboxytherapy in Aesthetic Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . 547 Nina Koutná 44 Emerging Technologies: Chemical Peels. . . . . . . . . . . . . . . . . . . . . . . . . . 577 Basil M. Hantash and Vishal Banthia 45 Emerging Technologies: Laser Skin Resurfacing . . . . . . . . . . . . . . . . . . 587 Basil M. Hantash and Vishal Banthia 46 Emerging Technologies: Nonablative Lasers and Lights . . . . . . . . . . . . 605 Basil M. Hantash and Vishal Banthia 47 Emerging Technologies in Aesthetic Medicine: Nonablative Skin Tightening. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 617 Basil M. Hantash Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 627

 

Part I Aesthetic Medicine

 

1

Defining Aesthetic Medicine Peter M. Prendergast

1.1 Introduction Aesthetic medicine is an art and a science. It is an emerging branch of medicine that relies on procedures and techniques to improve and enhance the ­appearance, texture, and contours of the skin, face, and body. Although some degree of overlap exists between ­aesthetic medicine and aesthetic surgery, for the most part, aesthetic medicine employs techniques and technologies that are either noninvasive or minimally invasive and performed without general anesthesia. Invasive surgical procedures that require significant tissue undermining, dissection, or skin excision, such as rhytidectomy, brachioplasty, and abdominoplasty remain the exclusive domain of aesthetic surgery, and are mostly performed in the hospital setting under general anesthesia. Typically, “invasive” procedures in aesthetic medicine require only dermal or subcutaneous injections, punctures, or small incisions. These include botulinum toxins, temporary fillers, fat transfer, suture lifts, and various forms of lipoplasty. These topics are covered in detail in this book. The rapid growth in aesthetic medicine internationally is partly due to an increased patient demand for rejuvenating procedures that do not involve surgery. Patients request procedures not because they are unwell but because they want to look and feel better. This patient profile is unique to aesthetic medicine and surgery, in contrast to most other medical specialties where the focus is on the diagnosis and treatment of

P.M. Prendergast Venus Medical, Heritage House, Dundrum Office Park, Dublin 14, Ireland e-mail: [email protected]

pathologies and illnesses. With the advent of botulinum toxins, hyaluronic acid fillers, and other nonsurgical procedures, patients can look and feel better quickly and discretely, with virtually no downtime. There is a natural enthusiasm for therapies that are quick, relatively painless, offer natural-looking but measurable results and cause little interruption to normal activities. Although aesthetic medicine has been embraced for this reason, it does not serve to replace aesthetic surgery. The relationship between the two disciplines is synergistic. Occasionally, less invasive techniques can be used in place of surgery for similar indications in patients who request them or where it is considered more appropriate (Table 1.1).

1.2 Origins of Aesthetic Medicine Aesthetic medicine as it is practiced today has evolved from the pioneering efforts, inventions, and discoveries of individuals from a variety of medical and surgical specialties. Jean Carruthers, an ophthalmologist, discovered the remarkable aesthetic application of botulinum toxin [1]. Chemodenervation with botulinum toxins is the most commonly performed procedure in aesthetic medicine [2]. Jeffrey Klein, a dermatologist, developed tumescent anesthesia, making lipoplasty a safe and effective possibility in the office-based setting without sedation or general anesthesia [3]. Fischer, Ilouz, and Fournier, with backgrounds in gynecology, plastic and general surgery, pioneered liposuction techniques in the 1980s [4]. Although fillers have been used for decades, the development and approval of safe, cross-linked hyaluronic acid fillers has revolutionized the practice of soft tissue augmentation for the

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Table 1.1  A comparison of options in aesthetic surgery and aesthetic medicine Indication Face lift Neck lift

Aesthetic surgery Rhytidectomy, MACS lift Neck lift, platysmaplasty

Brow lift Lip enhancement Gummy smile Cheek or chin enhancement Nose reshaping Skin laxity Breast augmentation

Foreheadplasty, endoscopic brow lift Surgical, mucosal advancement Surgical lip lengthening Surgical implants Rhinoplasty Resection, e.g., abdominoplasty Silicone/saline implants

Aesthetic medicine Suture lift Suture lift, tissue tightening, chemodenervation of platysma bands Botulinum toxin, suture brow lift Hyaluronic acid fillers Botulinum toxin Augmentation with injectable fillers Injectable fillers Tissue tightening, e.g., radiofrequency Injectable hyaluronic acid or fat

MACS minimal access cranial suspension

treatment of wrinkles, as well as contouring the face and body. Laser medicine and dermatology developed following the original description of selective photothermolysis by Anderson and Parrish in 1983 [5]. Carbon dioxide laser skin resurfacing became popular in the early 1990s but has largely been replaced by safer, nonablative, or fractional resurfacing devices. Dermatologists, such as Goldberg, have made significant contributions to the dissemination of knowledge on the aesthetic applications of lasers and lights. Shiffman, a general, cosmetic, and oncologic surgeon, has further defined aesthetic medicine by writing and editing numerous books on topics such as liposuction, facial rejuvenation, and body contouring. Aesthetic medicine is therefore characterized by an eclectic ­collection of techniques, developed or derived from several disciplines, including dermatology, plastic and reconstructive surgery, laser medicine, and various other surgical subspecialties.

1.3 Procedures Procedures in aesthetic medicine address most aging signs including abnormal skin pigmentation, skin laxity, ptosis, rhytids, fat loss, and contour irregularities such as the tear trough deformity. In addition, contouring of the face and body using fillers or lipoplasty is achieved to improve facial and lip volume, define the cheekbones, or remove unwanted fat. A summary of the most common procedures in aesthetic medicine is provided in Table 1.2.

1.4 Training Many of the procedures in aesthetic medicine have been performed for decades, including mesotherapy, ­lipoplasty, and chemodenervation with botulinum toxins. More recently, aesthetic medicine has emerged as a discipline that integrates established techniques with newer ones such as hyaluronic acid fillers, skin tightening, fractional resurfacing, third generation ultrasound-assisted lipoplasty, and advanced skin imaging. Implementing techniques in aesthetic medicine safely requires appropriate theoretical and practical training in anatomy, aging, patient assessment and selection, anesthesia, technique, potential side effects, and complications and their management. In addition, a thorough knowledge of the materials, products, and devices used in aesthetic medicine should be attained. These include botulinum toxins, temporary, long-lasting, and permanent fillers, volume stimulators, lasers, lights, radiofrequency systems, peeling agents, suture devices, and cosmeceuticals. Several accredited training programs in aesthetic medicine are available worldwide that offer instruction and hands-on training for physicians and surgeons with varying levels of experience [6].

1.5 Future Directions The most defining landmark in the evolution of modern aesthetic medicine was the aesthetic application of botulinum toxin type A. Its use for the treatment of hyperdynamic lines remains the most widely performed cosmetic procedure [2]. Aesthetic applications have

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Table 1.2  Procedures in aesthetic medicine Indication Hyperdynamic rhytids Lower face rhytids

Treatment modality Chemodenervation STA with fillers

Facial contouring Photoaging Acne scarring Textural irregularities Dyschromias Telangiectasias, varicose veins Ptosis jowls, brow, cheeks, neck Skin laxity Breast augmentation Lipoplasty Striae

STA with fillers, fat Skin resurfacing Micro-needling Microdermabrasion Selective photothermolysis Sclerotherapy Suture lifting techniques Radiofrequency, infrared STA with fillers Ultrasound-assisted lipoplasty Carboxytherapy

Example products/devices Botox, Dysport, Xeomin Restylane, Teosyal global action, Juvederm SubQ, Teosyal ultimate, Radiesse Fractional CO2 lasers, chemical peels Genuine dermaroller SilkPeel Intense pulsed light Fibro-vein, sclerofoam Silhouette sutures, Anchorage sutures KonturMD, titan Macrolane VRF 20/30 VASER Carboxypen, RioBlush

STA soft tissue augmentation

been expanded to include use in the lower face and neck, as well as hands, axillae, and feet for hyperhidrosis. The future of botulinum toxins will include the addition of new brands, and further refinement in techniques to enhance results. Similarly, novel filler agents will be brought to market with the hope of competing with the main hyaluronic acid brands. The concept of volume restoration with fillers and stimulating agents for facial rejuvenation will continue to play a central role in aesthetic medicine and compliment procedures in aesthetic surgery. Cell-assisted lipotransfer (CAL) and stem cell-enriched fat transfer are novel approaches to autologous fat transfer that promise to improve graft cell survival after grafting to the face or breasts [7, 8]. The role of sutures for facial rejuvenation continues to interest the world of aesthetic medicine. The goal is to improve further upon current suture designs and techniques to enhance results and increase the longevity of visible benefits. It is certain that lasers, ultrasound, and radiofrequency technologies will play a prominent role in the future of aesthetic medicine. Emerging techno­ logies include fractional lasers, focused ultrasound devices, and multipolar radiofrequency technology for fat reduction and skin tightening [9]. For the same reasons that aesthetic medicine has become widely practiced, antiaging medicine has become one of the fastest growing medical fields today. Put simply, more and more people want to feel good and look good. It behooves the aesthetic physician and surgeon to pay attention to the world of antiaging, preventive, and regenerative medicine as it relates to his own

practice and the patients they treat. Optimizing skin health with nutritional supplements, hormone replacement, or phytotherapy exemplify the synergy between aesthetics and antiaging.

References 1. Carruthers JD, Carruthers JA (1992) Treatment of glabellar frown lines with C: botulinum A exotoxin. J Dermatol Surg Oncol 18(1):17–21 2. The American Society for Aesthetic Plastic Surgery: Cosmetic surgery national databank statistics (2009); Available at: ASAPS website www.surgery.org 3. Prendergast PM (2010) Liposculpture of the abdomen in an office-based practice. In: Shiffman MA, Di Giuseppe A (eds) Body contouring: art, science and clinical practice. Springer, Berlin, pp 219–237 4. Flynn TC (2006) The history of liposuction. In: Shiffman MA, Di Giuseppe A (eds) Liposuction, principles and ­practice. Springer, Berlin, pp 3–6 5. Anderson RR, Parrish JA (1983) Selective photothermolysis: precise microsurgery by selective absorption of pulsed ­radiation. Science 220(4596):524–527 6. The European College of Aesthetic Medicine. Available at: ECAM website www.ecamedicine.com 7. Yoshimura K, Sato K, Aoi N, Kurita M, Inoue K, Suga H, Eto H, Kato H, Hirohi T, Harii K (2008) Cell-assisted lipotransfer for facial lipoatrophy: efficacy of clinical use of adiposederived stem cells. Dermatol Surg 34(9):1178–1185 8. Yoshimura K, Sato K, Aoi N, Kurita M, Hirohi T, Harii K (2008) Cell-assisted lipotransfer for cosmetic breast augmentation: supportive use of adipose-derived stem/stromal cells. Aesthetic Plast Surg 32(1):48–55 9. Fatemi A (2009) High-intensity focused ultrasound effectively reduces adipose tissue. Semin Cutan Med Surg 28(4):257–262

 

2

Ethical Aspects of Aesthetic Medicine Urban Wiesing

2.1 Introduction When physicians concern themselves with the ­aesthetic aspects of their patients, public opinion varies on the topic. On the one hand, certain measures are required in order to improve the aesthetic appearance of a person. They are a normal part of the medical profession. For example, to reconstruct the deformed face of a caraccident victim or to give a patient with a serious skin disease the most “normal” appearance possible undoubtedly belongs to the art of medicine. On the other hand, there are several medical procedures that are concerned with the aesthetics of their patients being criticized. For example, one could mention television programs in which physicians help participants to look more like celebrities (“I want a famous face,” MTV). Furthermore, there are cases in which physicians performed aesthetic operations obviously too frequently and with harm to the patient or did not do so in accordance with safety standards [1]. Here the question arose whether physicians’ participation is ethically acceptable. The doubts were supported by the fact that medicine is expanding with the growing number of aesthetic measures to a field that frequently does not have anything to do with the treatment of illness anymore and goes beyond the traditional core of medicine.

U. Wiesing  Institut für Ethik und Geschichte der Medizin, Eberhard-Karls-Universität Tübingen, Gartenstrasse 47, 72074 Tübingen, Germany e-mail: [email protected]

At this point, it should be addressed whether and – if so – under what conditions physicians should perform aesthetic interventions on their patients. This question cannot be answered without reference to the medical profession and its characteristics. Furthermore, one must systematize the various medical efforts for the aesthetics of the patient. Only then, it can be clarified to what extent certain measures are in accordance with the ethos of the medical profession and what responsibility physicians have. Aesthetic operations on children and adolescents as a special case should be examined as well. At this point, the question concerning the participation of the medical profession in certain measures should be discussed. It should not be asked whether a person should have an aesthetic operation or not, but whether physicians should perform it.

2.2 Preliminary Remarks 1. The only measures to be addressed here are those that exclusively serve aesthetic purposes. If measures are carried out for medically functional reasons, then there are usually enough reasons to consider them medically necessary and ethically acceptable (the patient’s consent as a requirement). Furthermore, if medically functional measures happen to be aesthetically beneficial as well, like frequently in dentistry, then this additional characteristic does not provide a reason to doubt its ethical acceptability. 2. Actions for the sake of one’s own aesthetic ­improvement belong to the basic behavior of human beings. To consciously form the body beyond pure

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naturalness under aesthetic aspects distinguishes human beings from the animal world. They do this in many ways, be it clothes, cosmetics, care, or sport. It would therefore not be the activity itself, but the measures – the medical, especially surgical intervention – which give rise to a special investigation.

2.3 Moral Construction of the Medical Profession Why should one ask the question whether physicians are allowed to take part in this genuinely human action with all their knowledge and capability? There are people who wish for better looks and physicians who can make this wish come true. What should be problematic about it – it could be asked. In other professions, expansion does not usually raise critical questions. So, why in the medical profession? The medical profession is a unique profession, and whoever doubts it, can take a look in the “Declaration of Geneva of the World Medical Association”. There, the medical profession is committed to one particular goal, namely to the health of the patients: “The health of my patient will be my first consideration” [2]. This goal shapes physicians’ behavior, and for this reason, the medical profession is a profession and not a business. What does this mean? What makes the medical profession so unique? Professions have established themselves in all developed industrial nations and possess the following traits [3]: They primarily aim for a worthwhile goal and not – like a business – primarily for the realization of profit. (That, of course, does not exclude that the members of certain professions earn their livelihood through their job.) However, professions are primarily committed to a socially deemed and important task. The task of medicine is clear: It is supposed to maintain and re-establish health, ease suffering and help sick people. The professions are geared toward the interests of their clients or – in medicine – their patients. For this, a high ethos is expected from the members, an ethos that puts the patient in the center of the considerations and actions. Or, as the World Medical Association International Code of Medical Ethics describes it: “A physician shall be dedicated to providing competent medical service in full professional and moral independence, with compassion and respect for human dignity” [2]. In professions, the services frequently have to be locally based and be personally delivered. They cannot be delegated,

with the exception of assistant physicians. Advertising is only allowed within limits – at least in numerous countries – as to not induce demand. Why is this orientation so important for physicians, why is a high ethos from the members of the medical profession demanded, why do they have to work in a patient-oriented fashion? If one puts oneself in the situation of a patient, then an answer can be found: people experience various difficulties in the course of their lives such as health problems, and it proved to be beneficial as an answer to these contingencies for sick people that the members of certain professions (in this case the medical profession) dedicate themselves to the patients’ problems, are competent and act patient-oriented. Sick people must expect that the members of the medical profession know exactly what they are doing, have a command of their duties and simultaneously use these abilities to the benefit of the patient. Patients must trust that physicians possess a certain ethos, a work-related, humane disposition. Physicians cannot guarantee the success of a medical measure, but they can guarantee that they possess abilities and take a certain moral stance. Since the patients cannot verify the stance of each and every member of the profession in advance, they have to rely on the fact that just because someone is a member of the profession, certain capabilities and moral stances can be expected. It is in the sense of professionalism, of a binding professional ethos, because it makes the so-called system of anticipatory trust possible [4]. A working party on “Doctors and Society Medical professionalism in a changing world” of the Royal College of Physicians defined in 2005 medical professionalism “as a set of values, behaviours, and relationships that underpin the trust the public has in doctors” [5]. The patient can expect certain behavior simply because of the membership in the medical profession. The system of medicine entitles one to the expectation. This confidence is certainly not to be understood as a nostalgically glorifying adjunct to a service relationship, but is essential in the doctor– patient relationship. With that, the profession agrees to a contract with society. “Professionalism is the basis of medicine’s contract with society. It demands placing the interests of patients above those of the physician, setting and maintaining standard of competence and integrity” [6]. This should also be considered if one wants to answer the question to what extent physicians should

2  Ethical Aspects of Aesthetic Medicine

be devoted to the aesthetics of their patients. Then, one should study the measures taken to change the aesthetics of a person to determine whether they threaten the constitutive element of medicine, namely the “system of anticipatory trust.”

2.4 Classification of Aesthetic Interventions First, the undisputed cases are discussed that were already mentioned above: there is no doubt that several aesthetic interventions are compatible with the medical ethos. As a profession, physicians are committed to health. When they treat the ill, thereby correcting the aesthetic drawbacks of a disease, there is no contradiction with the medical ethos. However, with that the whole area of aesthetic interventions is not covered for the following two reasons: 1. The concept of disease is fuzzy around the edges; it also has changed historically. For many symptoms, it can be difficult to say whether they should be regarded as a disease or not. The best-known examples are the symptoms of aging: Are they diseases or the physiological course of events? 2. Certain aesthetic interventions to correct conditions are beyond what – despite all the uncertainty – is widely seen as a disease. How should physicians face up to that? In order to assess these aesthetic interventions ethically, a subdivision is proposed here that is oriented to the attention of events. Medical interventions for the purpose of altering the aesthetic appearance can 1. diminish undesired, excluding or negatively perceived attention from other people, 2. increase positively perceived attention from other people. We must realistically concede that this distinction is not clear-cut for all cases. There could be cases in which both aspects are touched upon. However, this distinction proves to be helpful for the issue discussed here.

2.5 Medical Ethos and Aesthetic Activities The first group: This includes, for example, medical treatment of disfigurements or of characteristics that act stigmatizing and often but not always have a ­disease reference, which often but not always differs widely

9

from the average. The treatments are reconstructive in many cases, inasmuch as they want to restore a “normal” state as much as possible. With these treatments, people should get the chance to lead a life free of excessive, unwanted negatively perceived attention, a life free of stigmas. Basically, one wants to help them get to that “normal” level of attention as much as possible and avoid stigmatization and exclusion. These measures can be justified by considerations of justice: It’s about giving people chances for a good life, or, as the “Central Ethics Commission at the German Medical Association” recently formulated it, as a maxim for allocating resources in health care, making it possible for humans to “participate in social life” [7]. There is no doubt that measures to prevent stigmatization – within the scope of good medical treatment – are compatible with the medical ethos and do not ­compromise the medical profession in any way, provided that they are carried out lege artis. This is also true when it is a matter of aesthetic, not functional corrections. The other group of aesthetic measures, including operations, however, intends to increase desired, positively perceived attention from others through physical changes. In addition, the changed appearance is supposed to contribute to the attractiveness in comparison with others. Frequently, these operations are supposed to correct the symptoms of old age or effects of excess weight. There is usually no sign of disease and no “medical” indication. The patient’s desire and money decide on the measure. What happens in the relationship between physician and patient in this case? There is no medical indication and therefore the physician is not responsible for an indication. The physician is only responsible for proposing a method by which the patient’s goal should be achieved and for proper performance. Therefore, the physician’s responsibility has changed dramatically. Since it has nothing to do with the health of a patient, the physician is not obligated to perform such measures. But are physicians not allowed to perform for this reason? And if they do it, if physicians offer purely cosmetic measures, even operations, will the medical profession be compromised? Simply because of the lacking reference to illness, trust in the medical profession is not necessarily compromised when it comes to purely aesthetic measures. For example, physicians are already working in areas beyond illness, whether it be abortion, contraception, improvement of performance through training in

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sports, etc. However, what needs to be guaranteed to ensure that the “system of anticipatory trust” is not compromised? 1. Measures that the patient wants but cannot really help the patient in any way should not be performed. For example, if the patient’s desire for a change in appearance is caused by a serious mental disorder, a medically obtained change in appearance will probably not relieve the suffering of the patient. Here, it is the physician’s duty to recognize this and suggest other helpful measures such as further discussions or psychotherapy. The International Code of Medical Ethics of the WMA states: “A physician shall act in the patient’s best interest when providing medical care” [2]. 2. The consultation must also be geared toward the goal of assisting the patient and searching for an appropriate approach for him or her. The consultation shall not serve the purpose of “selling” a particular measure. “Placing the interests of patients above those of the physician” [6] is one of the fundamental principles of professionalism. 3. The patients also have to be thoroughly informed that there is no medical indication to be found. They have to be informed in detail about the measure and must give their free informed consent. 4. The high standards of avoiding harm must be maintained. Medical measures generally bear risks, but the avoidable ones should be avoided, especially those that come with voluntary operations. Otherwise, it would go against the basic principle of “setting and maintaining a standard of competence of professionalism” [6]. 5. Advertising should be limited to factual information as not to induce demand. These conditions must be met in order to exclude that a measure, which is most likely not helpful, is implemented, that the patient is forced to do it, is not sufficiently informed and that preventable damage occurs. All this would jeopardize the “system of anticipatory trust” in the medical profession. But, if this is largely excluded, then the answer to the central question of how aesthetic actions jeopardize the medical profession is: This is not the case, provided that the orientation towards the patient and the high quality of consultation and implementation are guaranteed. Cosmetic medicine and particularly cosmetic surgery expand what medicine has to offer, but they do not demonstrate any unknown, new dimension of

U. Wiesing

medical practice. It would certainly give cause for concern if physicians displayed in their traditional area (the treatment of diseases) even some of the attitude from aesthetic medicine, namely that only the will and financial power of the customer can make something happen. However, provided that this is not the case for the main medical duty – the prevention, treatment or alleviation of disease – the medical profession would with certain cases of cosmetic interventions, in particular of purely cosmetic surgery, only expand their services. If the medical profession makes this expansion recognizable, and a high standard of quality in aesthetic medicine and patient orientation is guaranteed, there is no reason for a threat to the “system of anticipatory trust” and the medical profession to be seen.

2.6 Aesthetic Measures for Children and Adolescents? The suggested distinction between “reducing undesired attention” and “increasing desired attention” is also supportive for assessing the situation of children and adolescents. Of course, a clear-cut line cannot always be found even in these cases. Nevertheless, one can divide the interventions according to the previously noted distinction concerning attention to events into two groups: How should aesthetic medical interventions, even operations on children and adolescents be assessed, that are supposed to reduce undesired, exclusionary, negatively perceived attention from other people and those intended to increase positively perceived attention? In the first group, for example, could be operations on injuries that caused disfigurement or characteristics that can have a stigmatizing effect. A good example would be bat ears. Their correction carried out on children and adolescents can be justified insofar as one would like to provide the child or adolescent with the chance of an unencumbered childhood or adolescence without frequent, undesired, negatively perceived attention, without a stigma. Exclusion and teasing should be prevented. At this particular period in life, social contacts and confidence are extremely important because they facilitate opportunities for a further good life. Orientations on a concept of illness in the process are not helpful and are not even mentioned, for example, at the surgery on bat ears.

2  Ethical Aspects of Aesthetic Medicine

The assessment looks completely different for operations or measures that only serve the purpose of drawing desired, positively perceived attention from others onto oneself through physical change. With such operations or measures, children or adolescents enter a contest for additional attention. The contest is present anyway and is largely unavoidable, especially in youth. However, this raises the question as to whether this contest should be exacerbated by the possibilities of medicine. There are convincing reasons to speak against it, especially when it comes to aesthetic operations. First, the medical risks should be mentioned: In addition to the usual medical risks, the results of operations during childhood or adolescence are more difficult to be predicted because of their growth. The possibility of an unwanted result is increased in case of some surgical procedures. Furthermore, cosmetic operations and other medical measures confirm and strengthen the competition for desired, positively perceived attention through physical appearance just by being yet another available tool. The pursuit of altering the aesthetic appearance (that does not stop at surgery) is problematic in two senses: It suggests that we must be beautiful on the one hand and must be willing to have cosmetic surgery for beauty on the other. This could induce increased suffering, while simultaneously offering services for the reduction of suffering. It would be more desirable to not dictate new standards and suggest new measures for rule compliance, but to provide an unencumbered ­childhood and adolescence without additional aesthetic pressures. These arguments speak for a restriction of aesthetic measures and operations on children and adolescents that only serve the purpose of increasing the desired attention. Nevertheless, there are ­convincing arguments for the avoidance of stigmatization of children and adolescents through medical interventions.

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2.7 Conclusions Medical interventions that are only supposed to increase the desired, positively perceived attention from others are not necessary according to medical ethos. However, they do not go against them, provided that high quality requirements are guaranteed. The measures have to be deemed beneficial to the patient in advance, a patient must be informed and the avoidance of harm must be guaranteed. Aesthetic measures, especially operations, which only serve the purpose of increasing desired, positively perceived attention, should not be performed on children and adolescents. Nevertheless, there are convincing arguments for an avoidance of stigmatization of children and adolescents, even through medically aesthetic measures.

References 1. Mercer N (2009) Clinical risk in aesthetic surgery. Clin Risk 15:215–217 2. http://www.wma.net/en/30publications/10policies/c8/index. html 3. Taupitz J (1991) Die Standesordnungen der freien Berufe, Geschichtliche Entwicklung, Funktionen, Stellung im Rechtssystem. De Gruyter, Berlin 4. Schluchter W (1980) Rationalismus der Weltbeherrschung, Studien zu Max Weber. Suhrkamp, Frankfurt am Main, p 191 5. http://www.rcplondon.ac.uk/pubs/books/docinsoc/docinsoc. pdf 6. ABIM Foundation. American Board of Internal Medicine, ACP-ASIM Foundation. American College of PhysiciansAmerican Society of Internal Medicine, European Federation of Internal Medicine (2002) Medical professionalism in the new millennium: a physician charter. Ann Intern Med 136(3):243–246 7. Stellungnahme der Zentralen Kommission zur Wahrung ethischer Grundsätze in der Medizin und ihren Grenzgebieten (Zentrale Ethikkommission) bei der Bundesärztekammer. Priorisierung medizinischer Leistungen im System der Gesetzlichen Krankenversicherung (GKV). Deutsches Ärzteblatt (2007) 104:A1–5, A2

 

Part II Preoperative

 

3

Medical History Melvin A. Shiffman

3.1 Introduction With any patient who is first seen by the physician, a proper history should be obtained. Not only the patient complaints but a proper complete medical history should be taken. In aesthetic medicine, as with many medical specialties, there is a tendency to shortcut the history with the idea that it is not important to learn everything about the patient. In medical malpractice litigation, the medical record is the best defense.

3.2 Content of the History 3.2.1 Format of a Proper Medical History Some of the worst and consistent problems this author has encountered in examining records for medical legal problems are the lack of enough information to make a diagnosis and decide on treatment and the extraordinary lack of readable handwriting. If the record cannot be read by another person, it is useless. The physician with poor hand writing must understand that the record must then be printed or typed out, whatever the cost. The record should contain the present complaints, list of allergies, past medical history, prior surgical

M.A. Shiffman  Surgery Section, Newport Specialty Hospital, 17501 Chatham Drive, Tustin, CA 92780-2302, USA e-mail: [email protected]

procedures, family history, and review of systems. This is taught in medical school and should be followed consistently. Many of these aspects of the history can be filled out by the patient if there is a standard form.

3.2.2 Present Complaints The first aspect of a proper history is to find out what the patient is complaining about. Have the patient explain what he/she is concerned about, why he/she is bothered by the perceived deficit, and what he/she wishes to have done. Cover all the possible aesthetic problems with the patient. Have the patient point out the exact areas of the face or body to be sure what is being complained about.

3.2.3 Allergies A standard form (Table 3.1) with a request to list allergies may not be enough. Some injectable fillers with a known propensity for allergies should be listed, such as collagen, porcine products, and hyaluronic acid. Charriere et al. [1] reported a positive skin test in 3.8% of patients and adverse reactions in 2.3% of patients with negative skin testing. Allergic reaction to hyaluronic acid complications has occurred [2]. Lidocaine is in some injectable fillers and should be specifically listed since allergy can be present. There should be a question as to whether the patient has had any reaction, especially allergic, to any subdermal filler.

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_3, © Springer-Verlag Berlin Heidelberg 2011

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16 Table 3.1  Allergies 1. Please list any allergies especially to foods and medications _________________________________________________ _________________________________________________ _________________________________________________ 2. Have you ever had a reaction to (please circle):    a. Iodine    b. Seafood    c. Collagen injections    d. Porcine (pig) products    e. Hyaluronic acid injections    f. Any dermal fillers    g. Any local anesthetic including lidocaine

For safety purposes, the list of allergies should be placed on the front of the patient’s chart.

3.2.4 Present Medications A list of all present medications should be obtained (Table 3.2). A standard form requesting the information can be used. Present medications may give an indication of disorders being treated that were not recalled by the patient. Ask if the patient has had steroids within the prior 6 months.

M.A. Shiffman Table 3.2  Present medications Please list all medications you are presently taking: _________________________________________________ _________________________________________________ _________________________________________________ _________________________________________________ Are you taking any medications with aspirin? _______________ Are you taking any nonsteroidal anti-inflammatory drugs? _____________ Are you taking any medications for or are you on a diet for diabetes? ____________ Do you take any herbal medications? ________________

3.2.6 Past Surgical History The past surgical history can be in the form of a questionnaire (Table  3.4). The past surgical history may not seem important for an aesthetic medicine physician, but any surgical procedure that had been performed in the area you intend to treat may portend problems if not known about. Be especially aware of prior cancer having been treated surgically. The area of treatment may have residual or recurrent cancer or there may be metastatic disease. Sometimes it may be prudent to send for the surgical records from prior surgery.

3.2.5 Past Medical History The past medical history can be a questionnaire filled out by the patient (Table 3.3). Some specific questions should be asked about autoimmune diseases, including dermatomyositis, lupus erythematosis, or rheumatoid arthritis, since collagen should not be injected into such patients. All prior medical aesthetic procedures should be in the questionnaire including the exact place of each area that was treated and with what method. If fillers have been used, then the exact kind of filler should be determined. If the patient does not know, a release for medical records should be signed and the records retrieved from the treating physician. Most of the time, it is best to send for the records since there may be more to the prior treatment than the patient remembers.

3.2.7 Family History The family history can be in a standard questionnaire form (Table 3.5). Ask specific questions of the important body systems that may be related to hereditary problems to be sure nothing is missed.

3.2.8 Review of Systems Review of systems is usually in a standard questionnaire form including each system (Table 3.6). Be especially aware of heart and/or lung problems, if deep sedation or general anesthesia is contemplated.

3  Medical History Table 3.3  Past medical history Please list all chronic or serious diseases that you have had treated: _________________________________________________ _________________________________________________ _________________________________________________ Have you ever had (please circle):   1. Hypertension (high blood pressure), heart or lung disease   2. Diabetes   3. Kidney or urinary tract disease   4. Autoimmune disease such as lupus erythematosis, dermatomyositis, rheumatoid arthritis   5. Thrombosis or pulmonary embolism   6. Cancer   7. Liver disease   8. HIV or AIDS Have you ever been hospitalized for any disorder? If yes, please explain _________________________________________________ _________________________________________________ Have you had a recent infection (within the past 30 days)?

17 Table 3.5  Family history Please circle any of the disorders below that have occurred in any of your family members including children, parents, aunts and uncles, and grandparents:   1. Cancer   2. Heart disease   3. Autoimmune disease such as lupus erythematosis, dermatomyositis, rheumatoid arthritis   4. Glaucoma Table 3.6  Review of systems Have you had within the past 6 months any disorders involving (please circle):   1. Eyes, ears, nose, or throat   2. Heart or lungs   3. Kidney or urinary tract   4. Sex organs   5. Joints or bones including the back   6. Muscles   7. Stomach or bowel   8. Skin

3.3 Conclusions

Table 3.4  Past surgical history Please list all the cosmetic or aesthetic procedures that you have ever had including the dates if possible: [Please include injections of dermal or skin fillers and botulinum toxin] _________________________________________________ _________________________________________________ _________________________________________________ _________________________________________________ Please list all surgeries that you have had (include the dates if possible): _________________________________________________ _________________________________________________ _________________________________________________ _________________________________________________

A proper history is the essence of the practice of medicine. Even with limited medical aesthetic procedures to be proposed, there is a need to evaluate the patient properly and thoroughly. It is relatively simple for patients to fill out the necessary forms before being seen by the physician.

References   1. Charriere G, Bejot M, Schnitzler L, Ville G, Hartmann DJ (1987) Reactions to a bovine collagen implant. Clinical and immunologic study in 705 patients. J Am Acad Dermatol 21(6):1203–1208   2. http://www.ukcosmeticsurgery.info;hylaform. Accessed 23 Dec 2009

 

4

Clinical Assessment of Facial Aging Melvin A. Shiffman

4.1 Introduction The purpose of classifying facial aging is to have a clinical method to determine the severity of the aging process in the face. This allows an estimate as to the types of procedures that the patient would need to have the best results. Procedures that are presently used for facial rejuvenation include laser, chemical peels, suture lifts, fillers, neck left, brow lift, blepharoplasty, rhinoplasty, otoplasty, suture facelift, modified facelift, and full facelift. All of these procedures have modifications and variations. The physician is already using his best judgment to determine which procedure would be best for any particular patient. This classification may help to refine these decisions.

4.2 Clinical Classification The clinical classification utilizes different areas of the face that are affected by the aging process (Table 4.1). The appearance of a tear trough depression is one of the first manifestations of facial aging. This is followed by extension of the tear trough and

loss of cheek fat, prominence of the jowls, and then deepening of the various facial folds. The most prominent fold is the nasolabial fold followed in time by the marionette lines. The use of neck manifestations such as loose skin, platysmal bands, and transverse folds is variable since a heavy neck would hide these changes (Fig. 4.1) and a thin neck may show the changes earlier. These bands and skin looseness may require neck lift and resection of the platysmal bands. Rhytids (wrinkles) generally are a result of heredity, skin aging from sun damage, overuse of facial expression muscles, sleep pressure, and skin laxity (Fig.  4.2). Rhytids can be treated with chemical peel or laser resurfacing. Laxity of eyelid skin and appearance of eyelid fat pads occur with aging but the skin laxity may be associated with heredity and sun damage. Treatment would consist of blepharoplasty. Ears can be prominent and distressing to the patient and this is corrected with otoplasty. The nose may have features that are noticeable and bothersome to the patient that would require some form of rhinoplasty.

4.3 Use of the Clinical Classification M.A. Shiffman  Surgery Section, Newport Specialty Hospital, 17501 Chatham Drive, Tustin, CA 92780-2302, USA e-mail: [email protected]

The clinical classification for rapid evaluation of a patient concerns mainly the midface. The first change of aging from Stage 0 (no changes noted) to Stage 1 is the appearance of a deepening in the tear trough and a very

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_4, © Springer-Verlag Berlin Heidelberg 2011

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Table 4.1  Clinical classification of facial aging [1]

a

M.A. Shiffman Stage 0 1 2 3 4

Tear trough depth None Slight: to cheek fat Mild: into cheek fat Moderate Severe

Cheek fat loss No loss No loss Slight loss medially Moderate Severe: flattening of cheek prominence

b

c

Fig. 4.1  Morbid obesity leaves the neck fat, hanging, and a challenge to treat

Nasolabial fold depth None Slight Mild Moderate Severe

Jowl prominence None None Slight Moderate Severe

4  Clinical Assessment of Facial Aging

a

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b

Fig. 4.2  (a) A face with no aging. (b) The same face when submitted to rhytids, skin damage with hyperpigmentations, deep nasolabial folds, neck platysma bands, and flattening of the cheeks

slight appearance of the nasolabial fold depth (Figs. 4.3 and 4.4). This is followed by extension of the tear trough with slight loss of cheek fat medially, mild nasolabial fold deepening, and the appearance of the jowl prominence in Stage 2 (Fig.  4.5). Stage 3 (Fig.  4.6) has a slightly more prominent tear trough depth than in Stage 2, moderate loss of total cheek fat, moderate depth of the nasolabial fold, and mild to moderate prominence of the jowls. Stage 4 has severe changes in all of the areas being examined (Fig.  4.7). Not every patient presents with these changes at the same time or in the same order. The most prominent category of change is in the extent of the tear trough and loss of cheek fat. Classification should take this into account when deciding the type of procedure for any particular patient.

4.4 Treatment Stage 0 ordinarily needs no treatment, whereas Stage 1 would improve with a filler such as autologous fat to the tear trough. Stage 2 would be improved with fillers to the tear trough and cheeks while suture lifts can be attempted to improve the jowl prominence (possibly with minimal liposuction) and nasolabial fold. Stage 3 would be treated with fillers in the defect areas, liposuction of the prominent jowls, as well as possibly a modified facelift if there were sufficient skin laxity. Stage 4 would benefit by fillers and possibly a full facelift. As the skin gets more sun damage and more rhytids appear, consideration should be given to the use of chemical peels and laser. Suture lift of the neck for mild

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a

M.A. Shiffman

b

c

Fig. 4.3  Stage 0. No loss of fat in the cheeks or evidence of nasolabial trough

4  Clinical Assessment of Facial Aging

a

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b

c

Fig. 4.4  Stage 1. No loss of cheek fat but slight tear trough depression

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a

M.A. Shiffman

b

c

Fig. 4.5  Stage 2. Slight loss of cheek fat with mild tear trough depression

4  Clinical Assessment of Facial Aging

a

25

b

c

Fig. 4.6  Stage 3. Moderate loss of cheek fat with tear trough depression into the cheek

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a

M.A. Shiffman

b

c

Fig. 4.7  Stage 4. Severe loss of cheek fat and tear trough extending into cheek

4  Clinical Assessment of Facial Aging

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loose skin does not work very well. Neck lift surgery should be considered for moderate laxity of the neck skin and transection of platysmal bands would help.

shape of the ears and nose. Classifying these problems helps to determine the possible treatment that may be required.

4.5 Conclusions

Reference

Evaluation of the face and neck includes all aspects of the skin including looseness, wrinkles, scarring, and depressions; fat accumulations or loss; bone loss; and

  1. Shiffman MA (2007) Facial aging: a clinical classification. Indian J Plast Surg 40(2):178–180

 

5

Assessment and Treatment of Excess Weight Melanie T. Turk

5.1 Introduction Overweight (a body mass index [BMI] between 25.0 and 29.9 kg/m2) and obesity (a BMI of 30 kg/m2 or more) [1] are wide-spread, global health problems [2]. In fact, obesity has surpassed undernutrition and infectious disease as the most substantial contribution to poor health and mortality worldwide [3]. The latest prevalence statistics for the United States from 2007 to 2008 show that 68.3% of adults age 20 and older are either overweight or obese, with 33.9% of this group considered obese [4]. Recent predictions indicate that as many as 47.5% of US adults will be obese by 2018, and $344 billion or 21% of US direct health care dollars will be spent on obesity-related illnesses [5]. Clearly, extensive weight loss treatment strategies are needed to abate this epidemic. Primary methods for the treatment of overweight and obesity have included a number of approaches. Behavioral modification of lifestyle in combination with reduced energy intake and increased energy expenditure continues to be the cornerstone of obesity treatment. Additional modalities of treatment, including pharmacotherapy and bariatric surgical approaches, have shown some success in assisting with weight loss, but potential side effects or complications are an unfortunate reality of these interventions. Ongoing adherence to lifestyle change is often difficult for many patients though, making successful long-term management of weight

M.T. Turk  Duquesne University School of Nursing, 524 Fisher Hall, 600 Forbes Avenue, Pittsburgh, PA 15282, USA e-mail: [email protected]

problematic, but some strategies have been shown to improve weight loss maintenance. This chapter presents techniques for the treatment of overweight and obesity based on empirical findings and evidence-based clinical guidelines and will include (1) assessment and evaluation of the overweight or obese patient; (2) treatment strategies including lifestyle modification (dietary intake, physical activity, behavioral modification), pharmacotherapy, and surgical therapy; and (3) weight loss maintenance strategies.

5.2 Assessment 5.2.1 Body Mass Index Evaluation of the patient should begin with assessment of BMI, which can be calculated as the weight in kilograms divided by the height in meters squared or weight in pounds multiplied by 704.5 then divided by the height in inches squared [6]. See Table 5.1 for the categorization of overweight and obesity according to BMI. Increased risk for chronic health problems is seen as BMI rises; even within the normal range, an increased risk is noted from a BMI of 21 kg/m2 [7]. An evidence-based review centered upon the primary care clinician’s role in diagnosing and treating overweight and obese patients concluded that BMI should be another vital sign used to screen for and determine treatment options for these patients [8]. Information ascertained by a scientific review of the World Health Organization (WHO) indicates that different relationships between BMI, percentage of body fat percentage, and health risks exist for Asian patients compared to patients of European descent [9]. A prospective

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_5, © Springer-Verlag Berlin Heidelberg, 2011

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Table 5.1  Categorization of body mass index (BMI) BMI (kg/m )  27 kg/m2 if significant co-morbidities are present [1]. Individual response to medication use varies greatly between patients with 2–5% experiencing a better than average weight loss and a large proportion exhibiting little to no weight loss [76]. Medications that have been utilized have resulted in an increase in the average amount of weight lost in 1–2 years by approximately 4–6% [77, 78] but also undesirable or even harmful side effects, some of which have necessitated removing the medication from the market, e.g., cardiac valvulopathy associated with fenfluramine [76]. US Food and Drug Administrationapproved (FDA) medications indicated for the treatment of obesity are discussed here. Phentermine is an adrenergic reuptake inhibitor that enhances adrenergic signals in peripheral tissue and the brain; it is thought to augment weight loss by decreasing food intake and increasing resting energy expenditure through sympathetic nervous system activation [76]. Phentermine was previously used in combination with fenfluramine until detrimental effects on cardiac valves were identified, but phentermine was not associated with valvulopathy as fenfluramine was [79, 80]. Because of its adrenergic effects, however, in addition to constipation and xerostomia, side effects may include tachycardia and hypertension, and phentermine should be cautiously used in patients with known cardiovascular disease or uncontrolled hypertension. Usual dosing is 18.75–37.5 mg/day for phentermine-HCl and 15–30 mg/day for phentermine resin; usage for 3  months is approved by the FDA [76]. Among six placebo-controlled randomized clinical trials, the average weight loss for phentermine was 3.6 kg greater than placebo [81]. Orlistat, a pancreatic and intestinal lipase inhibitor, stops the breakdown of consumed triglycerides and the absorption of monoacylglycerols and fatty acids resulting in up to 30% non-absorption of dietary fat [82, 83]. Among 22 studies reporting 1-year results, participants using orlistat lost 2.9 kg more weight than participants taking placebo [43]. Usual dosing is 120 mg three times daily with meals and requires dietary counseling to encourage decreased consumption of high-fat foods. Over-the counter dosing is now available at 60 mg three times daily and has been associated with a 50% greater weight loss after 4  months compared to placebo, for

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individuals with a BMI between 25 and 28 kg/m2 following a reduced-calorie and reduced-fat diet [84]. Treatment with orlistat is associated with gastrointestinal side effects including steatorrhea, flatulence, diarrhea, fecal incontinence, and anal discharge [76]. Of particular concern is the potential for fat-soluble vitamin deficiencies (vitamins A, D, E, and K) that may occur due to the malabsorption associated with orlistat. Patients treated with this weight loss medication should take a daily supplement of these vitamins at least 2 h prior to or after every orlistat dose [82]. In particular due to the higher prevalence of vitamin D deficiency among obese individuals, vitamin D levels should be measured prior to initiating orlistat therapy and intermittently throughout treatment to ensure a serum 1,25-OH-vitamin D level of at least 30 IU/mL [76]. Sibutramine is a monoamine reuptake inhibitor and suppresses appetite by inhibiting the reuptake of serotonin and norepinephrine [85]. Although pharmacologically similar to fenfluramine, the use of sibutramine has not been associated with cardiac valvulopathy and seems to result in a mean weight loss of 3–4% (~4.5 kg) over placebo during the first year of treatment [76, 86]. Sibutramine is approved by the FDA for up to 1 year of use, but extending treatment beyond 1 year may result in less weight regain [87], and some clinicians continue to prescribe it for individuals who are responding to the medication and not regaining weight. Typical dosing is 10–15  mg/day with 10  mg/day as the preferred initial dose, and patients who lose ³4 lb each month for 3 months are considered to have an appropriate clinical response to continue with treatment [76]. Doses above 15 mg/day have not been associated with greater efficacy and are not recommended [88]. Major side effects, hypertension and tachycardia, are attributed to the adrenergic effects of sibutramine with 10–15% of patients experiencing hypertension that is controlled by anti-hypertensive medication or discontinuation of sibutramine. Fewer patients experience tachycardia, but an increase of 4.9 beats per minute has been noted among patients receiving sibutramine compared to placebo [89]. Due to the higher risk of serotonin syndrome, (e.g., hypotension, diarrhea, flushing), the use of sibutramine is typically contraindicated for patients taking serotonin-selective reuptake inhibitors (SSRI) [76]. In support of the notion that pharmacotherapy should be combined with a treatment plan that includes dietary, physical activity, and behavioral therapy,

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Wadden et  al. [63] found the greatest 1-year weight loss was experienced by the treatment group that received sibutramine plus lifestyle modification with group meetings. The other three treatment arms were sibutramine alone, lifestyle modification alone, and sibutramine with brief primary care provider visits. Of note, the group that received sibutramine plus brief primary care provider visits (8 brief, 10–15 min sessions over the course of a year) experienced the second highest weight loss among the four groups. These findings support that practitioners play an valuable role in counseling for weight loss; the provider visits combined with sibutramine therapy were superior to medication alone or lifestyle modification alone [63]. Currently only two medications are FDA-approved for weight loss treatment beyond 3 months and both have been associated with modest results as well as weight regain when medications are discontinued [90]. Obesity is a disease with complex metabolic and behavioral components that may be amenable to medication therapy, but these pharmacotherapeutic agents with an acceptable side effect profile have not yet been identified and approved for use. Because of this complexity, it is improbable that any one drug with a single mechanism of action will be the weight-loss answer for the obese patient. With increased understanding of the physiologic mechanisms that affect body weight regulation, new targets for treating obesity have been identified and over 80 medications are currently in development [76]. Long-term weight control may in the future be managed by multiple medications with various mechanisms of action, but current pharmacotherapy is limited and must be combined with lifestyle modification that includes nutritional planning, increased physical activity, and behavioral treatment.

5.3.5 Surgical Treatment Bariatric surgery is another treatment option for severely obese individuals who have been unsuccessful at other methods of weight loss. Because of the inherent anatomical changes, surgery has the advantage of promoting long-term weight loss. Guidelines for determining which patients are candidates for surgical intervention were developed in 1991 by the NIH Consensus Conference for Bariatric Surgery and are still utilized today [91]. These criteria indicate that patients have Class 3 obesity (BMI ³ 40  kg/m2) or Class 2 obesity

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(BMI 35–39.9  kg/m2) with significant obesity-related health conditions like type 2 diabetes mellitus, sleep apnea, hypertension, or cardiomyopathy. Other surgical criteria include an age range of 18–60 years, failure at other more conservative treatment, and acceptable operative risk (e.g., adequate ­cardiac function, myocardial perfusion, pulmonary function, normal gastrointestinal anatomy) [92]. Updated ­recommendations added by the American Society for Bariatric Surgery Consensus Conference in 2004 include that bariatric surgery in an experienced center be ­considered for adolescents with Class 3 obesity, and ­surgery may be warranted for Class 1 obesity (BMI 30–34.9 kg/m2) if the patient’s obesityrelated co-­morbidity could be substantially improved or cured by significant, lasting weight loss. Furthermore, a multidisciplinary approach to the care of bariatric patients is essential for long-term successful outcomes, including an internist, dietician, nurse, and other necessary specialists (e.g., cardiologist, psychologist) in addition to the surgeon and anesthesiologist [91]. Although both open and laparoscopic procedures are effective modalities [92], bariatric surgeries should be performed laparoscopically when possible [93]. Procedures that are minimally invasive and circumvent an open abdomen with a sizeable abdominal incision are particularly suited to these patients because of the negative interaction of obesity and the inflammatory physiological responses [94]. Additional benefits of the laparoscopic technique are decreased length of hospitalization and postoperative pain, fewer wound complications, and more rapid normalization of bowel function [95, 96], even though this technique also has an increased intra-abdominal complication rate when compared with the open technique [91]. Other surgeryrelated factors associated with better outcomes include the volume of bariatric patients treated at the medical center along with surgeon experience and skill [43]. Specific bariatric “Centers of Excellence” have been designated by the American College of Surgeons and the American Society for Metabolic and Bariatric Surgery based on surgical outcomes and medical-center patient volume. Centers that reported over 100 cases annually had lower mortality rates, fewer complications, shorter length of stay, and lower costs compared to facilities with fewer than 50 cases annually [97]. Weight loss outcomes for bariatric surgeries are measured in terms of percent of excess body weight (EBW) that is lost, where excess body weight is calculated by subtracting ideal weight from the patient’s actual

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weight; ideal weight is based on the 1983 Metropolitan Life Insurance height and weight tables’ determination of the weight associated with the longest life expectancy [98]. Three main categories of bariatric surgery exist – malabsorptive, restrictive, and combined restrictive and malabsorptive procedures [99]. Malabsorptive surgeries cause a reduced absorption of calories and nutrients by decreasing the functional amount of small intestine involved in digestion. Resultant weight loss from malabsorptive techniques often comes with nutritional deficits including protein, vitamin, and mineral insufficiencies that must be medically managed longterm. Restrictive surgeries decrease the size and capacity of the stomach to store food, thereby inducing satiety earlier in the meal, which results in reduced energy intake. Because procedures that are solely restrictive do not affect small bowel anatomy, they infrequently result in metabolic complications but are associated with an increased risk of dumping syndrome and some nutritional deficiencies (particularly calcium, iron, and vitamin B12) [100]. Some procedures incorporate both restrictive and malabsorptive techniques to induce weight loss. Four currently recommended surgical options – biliopancreatic diversion with/without duodenal switch, vertical banded gastroplasty, laparoscopic adjustable gastric banding, and gastric bypass – are used worldwide. The biliopancreatic diversion with/without duodenal switch is the least commonly performed bariatric procedure among the four [101] and is considered a malabsorptive approach. It involves performing a gastrectomy of approximately 80% of the distal stomach, preserving a 100–150  mL gastric compartment, and creating a Roux-en-Y construction with an alimentary limb, a biliopancreatic limb, and a common limb. While the alimentary and biliopancreatic limbs are approximately the same length, the degree of malabsorption is controlled by the length of the common limb. With the duodenal switch, the pylorus is preserved using a vertical-sleeve gastrectomy, and a duodeno-ileostomy is created. Weight loss after this surgery is typically approximately 70% of EBW [91]. Long-term complications are those associated with malabsorptive procedures. The vertical banded gastroplasty and laparoscopic adjustable gastric banding are restrictive techniques where a small upper gastric compartment is constructed to limit the capacity of the stomach to hold food.

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Restrictive techniques are generally less difficult to perform than malabsorptive techniques with fewer long-term complications but may result in less weight loss [99]. Typically an open procedure, the vertical banded gastroplasty is performed by stapling off the fundus parallel to the lesser curvature and applying a band to narrow the distal opening of this small compartment (~50 mL) into the body of the stomach. Usual percent of EBW lost is 50% [91]. For the laparoscopic adjustable gastric banding procedure, the upper 5% of the stomach is partitioned off using an inflatable, silicone band. A gastric pouch of approximately 20 mL is created by inflating the band using a subcutaneous port. This band can be adjusted by the physician at office visits to accommodate the needs of the patient, and periodic adjustments may be necessary up to six times a year for appropriate outcomes. This procedure is associated with a loss of about 50% of EBW [91]. Common side effects of these restrictive procedures include vomiting as a result of over consumption, eating too quickly, not chewing food well, or drinking fluids right after eating [94]. Gastric bypass is the most commonly performed bariatric surgery worldwide [91] and has both restrictive and malabsorptive features. In the restrictive component, a 15–25 mL gastric pouch is divided from the distal stomach with four rows of staples or completely separated. Continuity of the pouch with the jejunum is re-established using a Roux-Y limb, incorporating a malabsorptive element as the distal stomach, duodenum and part of the proximal jejunum are bypassed. The Roux-en-Y technique is the preferred approach, and variations of this approach include using a long Roux limb or a very long limb to affect more substantial weight loss in individuals with a BMI ³ 50 kg/m2. After the standard Roux-en-Y bypass, weight loss outcomes of approximately 65–70% of EBW are achieved [91]. Empirical evidence suggests that this surgery results in decreased plasma levels of the hormone ghrelin [102, 103], mainly secreted in the fundus of the stomach and known to stimulate appetite [104], which may be an additional mechanism contributing to the sustained weight loss observed after gastric bypass surgery. Surgical treatment of obesity results in substantial weight loss that is largely maintained by patients and leads to amelioration or even resolution of co-morbidities [100] as well as decreased mortality [105]. The Swedish Obesity Study is a large, prospective trial that

5  Assessment and Treatment of Excess Weight

compared bariatric surgery patients with matched, obese control patients. At 2 and 10 years, this study showed that recovery from diabetes mellitus, hypertriglyceridemia, hypertension, a low HDL cholesterol level, and hyperuricemia was more frequent in the surgical patients than in the control patients. Although weight loss peaked at 1–2 years, long-term weight loss outcomes from bariatric surgeries at 15  years were 27 ± 12%, 18 ± 11%, and 13 ± 14%, for gastric bypass, vertical banded gastroplasty, and gastric banding, respectively; the mean 15-year weight change among the control group was ±2% [106]. Lifelong adjustments in eating behaviors and medical supervision are essential following these surgical procedures, however, and patients need to be counseled about the lifestyle changes necessary to reduce complications and maintain weight loss.

5.4 Weight Loss Maintenance Long-term maintenance of lost weight has remained the Achilles heel of weight loss treatment as approximately one third of weight lost among patients treated with lifestyle modification is regained by the first year after treatment [107]. Average 4-year weight losses approximate 1.8  kg or an unremarkable 4  lb [108]. Some have suggested that the behaviors necessary for weight loss differ from those required in weight loss maintenance in that the goal of maintenance is to undo small weight gains before they become large ones where as the goal for weight loss is to lose substantial amounts of weight after an extended period of gain. While active weight loss treatment is time restricted, weight loss maintenance is long-term and continued. Weight loss is tangibly rewarding and individuals often receive positive feedback and reinforcement from significant others and health care practitioners about their new appearance or improved health status, whereas in maintenance ongoing reinforcement tends to lapse [109]. The greatest challenge in obesity treatment for health care professionals is not only assisting patients in their weight loss efforts but also helping them to sustain the weight loss they have achieved. Much of what is known about the behaviors related to successful weight loss maintenance comes from a large registry of individuals who have successfully lost 13.6 kg (30 lb) and maintained that loss for a minimum of 1 year with the average weight loss being 30.4 kg

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(67  lb) that has been maintained for 5.7  years [110, 111]. Many descriptive studies of this National Weight Control Registry (NWCR) have reported on behavioral strategies used by these successful weight loss maintainers – increasing physical activity, consuming a diet low in fat, regularly self-monitoring weight and food intake [112], limiting the variety of foods eaten [113], eating breakfast [114], and restricting time spent watching television [115]. Factors associated with weight regain in this group have included a greater initial weight loss, shorter period of time in weight maintenance and psychological factors like depressive symptoms, increases in disinhibition (vulnerability to loss of control over eating), and decreases in eating restraint (conscious control of eating) [111, 115, 116]. These findings from the NWCR have been corroborated by other cross-sectional [117] and prospective studies [118] and provide information about areas of weight maintenance that providers can address when counseling patients. Two elements of weight loss treatment have been noted as particularly beneficial for weight loss maintenance – pharmacotherapy and physical activity. Both sibutramine and orlistat, combined with dietary modification and caloric deficit, have been repeatedly shown to be efficacious in promoting longterm maintenance [87]. A 3-year randomized controlled trial (RCT) of weight loss maintenance using orlistat or placebo found that patients who received orlistat maintained a 2.4  kg greater weight loss than those who received a placebo [119]. In a 1-year RCT examining sibutramine versus placebo for weight maintenance, Apfelbaum and colleagues found that 75% of the sibutramine patients maintained at least 100% of their lost weight compared to 42% of placebo patients who achieved this level of maintenance [120]. There is some evidence that sibutramine might be effectively used intermittently for weight loss maintenance. One maintenance RCT found a similar amount of weight change over 44  weeks for the participants that received 15 mg of the drug continuously (−3.8 kg) compared to those receiving sibutramine intermittently (−3.3 kg). The intermittent sibutramine group received a placebo for two 6-week periods, after week 12 and week 30 of the trial [121]. These medications may play an important role in weight loss maintenance, but they are currently FDA-approved for 1–2 years of continued use only [78], and dietary and behavioral modification must be emphasized and sustained.

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Physical activity has been frequently highlighted as an essential component of successful weight loss maintenance in both descriptive [122, 123] and intervention studies [124–126] with patients engaging in higher amounts of activity regaining less weight [124, 126]. A contributing factor to the need for physical activity has been labeled the energy gap [127]. This gap, approximated at 8 kcal/day for each pound of weight lost, is created after weight loss because one’s total energy expenditure decreases as a result of a drop in resting metabolic rate and less energy needed to move and support less total body weight. For example, a patient who had lost 50 lb would need to continually maintain a 400 kcal/day deficit in total caloric intake below his/ her pre-weight loss intake. Some experts believe that, in the current obesogenic environment promoting lessthan-healthful foods in large portions, increasing energy expenditure through physical activity is an easier way to fill this energy gap [127]. The ideal amount of physical activity for maintenance of weight loss remains somewhat unclear however, because most evidence does not come from randomized controlled trials [49]. Jakicic et  al. [128] recently reported that among individuals who had lost at least 10% of their original weight and maintained that loss for 24 months, physical activity levels were 275  min per week; others have noted similar findings with this level of activity at 2 years after a very-low-calorie diet [129]. Recommendations for maintaining lost weight in adults include partaking in at least 60–90 min of moderate-intensity activity daily [48], and the recent position stand from ACSM reinforces that avoiding a weight change of more than 3% likely requires approximately 60  min of daily, moderate-intensity physical activity, like brisk walking for 4 miles [49]. Although these levels of physical activity may be challenging for many patients to maintain, they seem to be associated with the best weight maintenance outcomes. With weight loss typically peaking at 6 months after initiation of a behavioral lifestyle treatment plan [130], a weight maintenance plan should be introduced at this time. Maintenance plans that include a schedule of sustained, frequent contact with the health care practitioner who provides ongoing support, instruction, and health monitoring are recommended to promote longterm weight loss maintenance [1]. These visits might be handled via an office nurse, allowing patients to stop in to be weighed, have their food diaries reviewed, receive feedback on a problem area, or receive words

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of encouragement for motivation and support [131]. Empirical evidence suggests that providing patient contact by telephone is even efficacious for promoting weight loss maintenance [132], provided the contact is made by an individual who is known to the patient [133]. Additionally, a practitioner could suggest that a patient join a self-help (e.g., Taking Off Pounds Sensibly) or commercial group (e.g., Weight Watchers) as a means of providing ongoing support for adhering to the behaviors necessary to maintain weight loss.

5.5 Conclusions Obesity and overweight are chronic conditions with numerous adverse health effects that require direct, ongoing attention by the health care provider. The goals of weight loss treatment are improved overall health and decreased morbidity. Current first-line treatment consists of lifestyle modification that includes dietary, physical activity, and behavioral therapy, with pharmacotherapy and bariatric surgery as subsequent weight loss modalities when indicated. The treatment of this chronic disorder requires a multidisciplinary approach including health professionals with expertise in nutrition, exercise, and possibly clinical psychology as members of the comprehensive, weight management health care team [3]. Similar to treating other chronic conditions like hypertension and diabetes, providers should instruct patients about self-management strategies for prolonged weight loss maintenance because the positive effects on risk-factor reduction do not remain unless weight loss is sustained [134]. Health care providers have a major part in helping this ever-increasing subgroup of patients successfully lose and maintain weight so that patients can continue to benefit from the physical and psychological effects of a lower body weight.

References 1. National Institutes of Health (1998) Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults-the evidence report. Obes Res 6(suppl 2):51S–209S 2. Roth J, Qiang X, Marban SL, Redelt H, Lowell BC (2004) The obesity pandemic: Where have we been and where are we going? Obes Res 12(suppl 2):88S–101S 3. Lau DC, Douketis JD, Morrison KM, Hramiak IM, Sharma AM, Ur E, Obesity Canada Clinical Practice Guidelines Expert Panel (2007) 2006 Canadian clinical practice

5  Assessment and Treatment of Excess Weight guidelines on the management and prevention of obesity in adults and children [summary]. CMAJ 176(8):S1–S13 4. Flegal KM, Carroll MD, Ogden CL, Curtin LR (2010) Prevalence and trends in obesity among US adults, 1999– 2008. J Am Med Assoc 303(3):235–241 5. United Health Foundation, The American Public Health Association (2009) Partnership for Prevention: The future costs of obesity: national and state estimates of the impact of obesity on direct health care expenses. Retrieved from http:// www.nccor.org/downloads/CostofObesityReport-FINAL.pdf 6. National Heart Lung and Blood Institute, North American Association for the Study of Obesity (2000) Practical guide to the identification, evaluation, and treatment of overweight and obesity in adults. Available via http://www. nhlbi.nih.gov/guidelines/obesity/prctgd_c.pdf. Accessed 19 May 2010 7. World Health Organization (2006) Obesity and overweight: What are overweight and obesity? Retrieved from http:// www.who.int/mediacentre/factsheets/fs311/en/index.html 8. Orzano JA, Scott JG (2004) Diagnosis and treatment of obesity in adults: an applied evidence-based review. J Am Board Fam Pract 17(5):359–369 9. WHO Expert Consultation (2004) Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. Lancet 363(9403):157–163 10. Wen CP, David CTY, Tsai SP, Chan HT, Hsu HL, Hsu CC, Eriksen MP (2009) Are Asians at greater mortality risks for being overweight than Caucasians? Redefining obesity for Asians. Public Health Nutr 12(4):497–506 11. World Health Organization, International Association for the Study of Obesity & International Obesity Task Force (2000) The Asia-Pacific perspective: redefining obesity and its treatment. Retrieved from http://www.wpro.who.int/ internet/resources.ashx/NUT/Redefining+obesity.pdf 12. Low S, Chin MC, Ma S, Heng D, Deurenberg-Yap M (2009) Rationale for redefining obesity in Asians. Ann Acad Med Singapore 38(1):66–69 13. Mosca L, Edelman D, Mochari H, Chrisian AH, Paultre F, Pollin I (2006) Waist circumference predicts cardiometabolic and global Framingham risk among women screened during National Woman’s Heart Day. J Women’s Health Larchmt 15(1):24–34 14. Canoy D, Boekholdt SM, Wareham N, Luben R, Welch A, Bingham S, Buchan I, Day N, Khaw KT (2007) Body fat distribution and risk of coronary heart disease in men and women in the European Prospective Investigation Into Cancer and Nutrition in Norfolk cohort: a population-based prospective study. Circulation 116(25):2933–2943 15. Kuk JL, Katzmarzyk PT, Nichaman MZ, Church TS, Blair SN, Ross R (2006) Visceral fat is an independent predictor of all-cause mortality in men. Obesity 14(2):336–341 16. Zhu S, Heymsfield SB, Toyoshima H, Wang Z, Pietrobelli A, Heshka S (2005) Race-ethnicity-specific waist circumference cutoffs for identifying cardiovascular disease risk factors. Am J Clin Nutr 81(2):409–415 17. Dagenais GR, Yi Q, Mann JF, Bosch J, Pogue J, Yusuf S (2005) Prognostic impact of body weight and abdominal obesity in women and men with cardiovascular disease. Am Heart J 149(1):54–60 18. Chen Y, Rennie D, Cormier YF, Dosman J (2007) Waist circumference is associated with pulmonary function in

41 normal-weight, overweight, and obese subjects. Am J Clin Nutr 85(1):35–39 19. Balkau B, Deanfield JE, Despres JP, Bassand JP, Fox KA, Smith SC Jr, Barter P, Tan CE, Van Gaal L, Wittchen HU, Massien C, Haffner SM (2007) International Day for the Evaluation of Abdominal Obesity (IDEA): a study of waist circumference, cardiovascular disease, and diabetes mellitus in 168 000 primary care patients in 63 countries. Circulation 116(17):1942–1951 20. Grundy SM, Cleeman JI, Merz CN, Brewer HB Jr, Clark LT, Hunninghake DB, Pasternak RC, Smith SC Jr, Stone NJ, Coordinating Committee of the National Cholesterol Education Program (2004) Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. J Am Coll Cardiol 44:720–732 21. Pan W-H, Flegal KM, Chang H-Y, Yeh W-T, Yeh C-J, Lee W-C (2004) Body mass index and obesity-related metabolic disorders in Taiwanese and US whites and blacks: implications for definitions of overweight and obesity for Asians. Am J Clin Nutr 79(1):31–39 22. Wildman RP, Gu D, Reynolds K, Duan X, He J (2004) Appropriate body mass index and waist circumference cutoffs for categorization of overweight and central adiposity among Chinese adults. Am J Clin Nutr 80(5):1129–1136 23. Kushner RF, Kushner N (2003) Dr. Kushner’s personality type diet. St. Martin’s, New York 24. Krall EA, Dwyer JT (1987) Validity of a food frequency questionnaire and a food diary in a short-term recall situation. J Am Diet Assoc 87(10):1374–1377 25. Marshall AL, Smith BJ, Bauman AE, Kaur S (2005) Reliability and validity of a brief physical activity assessment for use by family doctors. Br J Sports Med 39(5): 294–297 26. Warziski MT, Sereika SM, Styn MA, Music E, Burke LE (2008) Changes in self-efficacy and dietary adherence: the impact on weight loss in the PREFER study. J Behav Med 31:81–92 27. Burke LE, Styn MA, Elci OU, Music E, Warziski M (2007) How do barriers to healthy eating impact weight loss? Circulation 115(suppl 8):55 28. Klein S, Burke LE, Bray GA, Blair S, Allison DB, Pi-Sunyer X, Hong Y, Eckel RH, American Heart Association Council on Nutrition, Physical Activity, and Metabolism (2004) Clinical implications of obesity with specific focus on cardiovascular disease. A statement for professionals from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism: endorsed by the American College of Cardiology Foundation. Circulation 110(18):2952–2967 29. Gorin AA, Phelan S, Hill JO, Wing RR (2004) Medical triggers are associated with better short- and long-term weight loss outcomes. Prev Med 39(3):612–616 30. Miller WR, Rollnick S (1991) Motivational interviewing preparing people to change addictive behavior. The Guildford, New York 31. West DS, DiLillo V, Bursac Z, Gore SA, Greene PG (2007) Motivational interviewing improves weight loss in women with type 2 diabetes. Diabetes Care 30(5):1081–1087 32. Rubak S, Sandbaek A, Lauritzen T, Christensen B (2005) Motivational interviewing: a systematic review and metaanalysis. Br J Gen Pract 55(513):305–312

42 33. Wadden TA, Crerand CE, Brock J (2005) Behavioral treatment of obesity. Psychiatr Clin North Am 28(1):151–170 34. Jakicic JM, Otto AD (2005) Physical activity recommendations in the treatment of obesity. Psychiatr Clin North Am 28(1):141–150 35. Johnstone AM, Horgan GW, Murison SD, Bremner DM, Lobley GE (2008) Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum. Am J Clin Nutr 87(1):44–55 36. Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L (2003) A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 348(21):2074–2081 37. Sacks FM, Bray GA, Carey VJ, Smith SR, Ryan DH, Anton SD, McManus K, Champagne CM, Bishop LM, Laranjo N, Leboff MS, Rood JC, de Jonge L, Greenway FL, Loria CM, Obarzanek E, Williamson DA (2009) Comparison of weightloss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med 360:859–873 38. Vetter ML, Iqbal N, Dalton-Bakes C, Volger S, Wadden TA (2010) Long-term effects of low-carbohydrate versus lowfat diets in obese persons. Ann Intern Med 152(5): 334–335 39. Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ (2005) Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. J Am Med Assoc 293(1):43–53 40. Nordmann AJ, Nordmann A, Briel M, Keller U, Yancy WS Jr, Brehm BJ, Bucher HC (2006) Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials. Arch Intern Med 166(3):285–293 41. Brinkworth GD, Noakes M, Buckley JD, Keogh JB, Clifton PM (2009) Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo. Am J Clin Nutr 90(1):23–32 42. Wycherley TP, Brinkworth GD, Keogh JB, Noakes M, Buckley JD, Clifton PM (2010) Long-term effects of weight loss with a very low carbohydrate and low fat diet on vascular function in overweight and obese patients. J Intern Med 267(5):452–461 43. Seagle HM, Strain GW, Makris A, Reeves RS, American Dietetic Association (2009) Position of the American Dietetic Association: weight management. J Am Diet Assoc 109(2):330–346 44. Young LR, Nestle M (2003) Expanding portion sizes in the US marketplace: implications for nutrition counseling. J Am Diet Assoc 103(2):231–234 45. Wansink B, van Ittersum K (2007) Portion size me: downsizing our consumption norms. J Am Diet Assoc 107(7):1103–1106 46. Pedersen SD, Kang J, Kline GA (2007) Portion control plate for weight loss in obese patients with type 2 diabetes mellitus: a controlled clinical trial. Arch Intern Med 167:1277–1283 47. The Diet Plate. Portion control made easy. Retrieved from http://www.thedietplate.com/ 48. Haskell WL, Lee IM, Pate RR, Powell KE, Blair SN, Franklin BA, Macera CA, Heath GW, Thompson PD, Bauman A (2007) Physical activity and public health: updated recommendation for adults from the American

M.T. Turk College of Sports Medicine and the American Heart Association. Circulation 116(9):1081–1093 49. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK, American College of Sports Medicine Position Stand (2009) Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 41(2):459–471 50. Curioni CC, Lourenco PM (2005) Long-term weight loss after diet and exercise: a systematic review. Int J Obes Lond 29:1168–1174 51. Jakicic JM, Winters C, Lang W, Wing RR (1999) Effects of intermittent exercise and use of home exercise equipment on adherence, weight loss, and fitness in overweight women: a randomized trial. J Am Med Assoc 282(16):1554–1560 52. Jakicic JM, Wing RR, Butler BA, Robertson RJ (1995) Prescribing exercise in multiple short bouts versus one continuous bout: effects on adherence, cardiorespiratory fitness, and weight loss in overweight women. Int J Obes Lond 19:893–901 53. Centers for Disease Control and Prevention (2010) Physical activity statistics, 1988–2008 no-leisure time physical activity trend chart. Retrieved 12 May 2010 from http://www. cdc.gov/nccdphp/dnpa/physical/stats/leisure_time.htm 54. Bravata DM, Smith-Spangler C, Sundaram V, Gienger AL, Lin N, Lewis R, Stave CD, Olkin I, Sirard JR (2007) Using pedometers to increase physical activity and improve health: a systematic review. J Am Med Assoc 298(19):2296–2304 55. Stuart RB (1967) Behavioral control of overeating. Behav Ther 5:357–365 56. Wing RR (2002) Behavioral weight control. In: Wadden T, Stunkard AJ (eds) Handbook of obesity treatment. Guilford, New York, pp 301–316 57. Rothman AJ, Baldwin AS, Hertel AW (2004) Self-regulation and behavior change: disentangling behavioral initiation and behavioral maintenance. In: Vohs KD, Baumeister RF (eds) The handbook of self-regulation: research, theory, and applications. Guilford, New York, pp 130–148 58. Strecher VJ, Seijits GH, Kok GJ, Latham GP, Glasgow R, DeVellis B, Meertens RM, Bulger DW (1995) Goal setting as a strategy for health behavior change. Health Educ Q 22(2):190–200 59. Burke LE, Swigart V, Turk MW, Derro N, Ewing LJ (2009) Experiences of self-monitoring: successes and struggles during treatment for weight loss. Qual Health Res 19(6):815–828 60. Burke LE, Warziski M, Starrett T, Choo J, Music E, Sereika S, Stark S, Sevick MA (2005) Self-monitoring dietary intake: current and future practices. J Ren Nutr 15(3): 281–290 61. Acharya SD, Elci OU, Sereika SM, Music E, Styn MA, Turk MW, Burke LE (2009) Adherence to a behavioral weight loss treatment program enhances weight loss and improvements in biomarkers. Patient Prefer Adherence 3:151–160 62. Tate DF, Wing RR, Winett RA (2001) Using Internet technology to deliver a behavioral weight loss program. J Am Med Assoc 285(9):1172–1177 63. Wadden TA, Berkowitz RI, Womble LG, Sarwer DB, Phelan S, Cato RK, Hesson LA, Osei SY, Kaplan R, Stunkard AJ (2005) Randomized trial of lifestyle modification and pharmacotherapy for obesity. N Engl J Med 353(20): 2111–2120

5  Assessment and Treatment of Excess Weight 64. D’Zurilla TJ, Goldfried MR (1971) Problem solving and behavior modification. J Abnorm Psychol 78(1):107–126 65. Marlatt GA, Gordon JR (1980) Determinants of relapse: implications for the maintenance of behavior change. In: Davidson PO, Davidson SM (eds) Behavioral medicine: changing health lifestyles. Brunner/Mazel, New York, pp 410–452 66. Wing RR (2004) Behavioral approaches to the treatment of obesity. In: Bray GA, Bourchard C, James WPT (eds) Handbook of obesity: clinical applications, 2nd edn. Marcel Dekker, New York, pp 147–167 67. Jeffery RW, Sherwood NE, Brelje K, Pronk NP, Boyle R, Boucher JL, Hase K (2003) Mail and phone interventions for weight loss in a managed-care setting: weigh-to-be oneyear outcomes. Int J Obes Lond 27(12):1584–1592 68. Tate DF, Jackvony EH, Wing RR (2003) Effects of Internet behavioral counseling on weight loss in adults at risk for type 2 diabetes: a randomized trial. J Am Med Assoc 289(14):1833–1836 69. Svetkey LP, Erlinger TP, Vollmer WM, Feldstein A, Cooper LS, Appel LJ, Ard JD, Elmer PJ, Harsha D, Stevens VJ (2005) Effect of lifestyle modifications on blood pressure by race, sex, hypertension status, and age. J Hum Hypertens 19(1):21–31 70. The Look AHEAD Research Group (2007) Reduction in weight and cardiovascular disease risk factors in individuals with type 2 diabetes: one-year results of the Look AHEAD trial. Diabetes Care 30(6):1374–1383 71. Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemiö K, Hämäläinen H, Härkönen P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Paturi M, Sundvall J, Valle TT, Uusitupa M, Tuomilehto J, Finnish Diabetes Prevention Study Group (2006) Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study. Lancet 368(9548):1673–1679 72. Hill JO (1998) Dealing with obesity as a chronic disease. Obes Res 6(suppl 1):S34–S38 73. Loos RJF, Bouchard C (2003) Obesity – Is it a genetic disorder? J Intern Med 254(5):401–425 74. Chitwood LF, Brown SP, Lundy MJ, Dupper MA (1996) Metabolic propensity toward obesity in black vs white females: responses during rest, exercise and recovery. Int J Obes Lond 20(5):455–462 75. Kayman S, Bruvold W, Stem JS (1990) Maintenance and relapse after weight loss in women: behavioral aspects. Am J Clin Nutr 52(5):800–807 76. Kaplan LM (2010) Pharmacologic therapies for obesity. Gastroenterol Clin North Am 39(1):69–79 77. Bray GA (2008) Lifestyle and pharmacological approaches to weight loss: efficacy and safety. J Clin Endocrinol Metab 93(11 suppl 1):s81–s88 78. Padwal R, Li SK, Lau DC (2003) Long-term pharmacotherapy for overweight and obesity: a systematic review and meta-analysis of randomized controlled trials. Int J Obes 27(12):1437–1446 79. Connolly HM, Crary JL, McGoon MD, Hensrud DD, Edwards BS, Edwards WD, Schaff HV (1997) Valvular heart disease associated with fenfluramine-phentermine. N Engl J Med 337(9):581–588 80. Centers for Disease Control and Prevention (CDC) (1997) Cardiac valvulopathy associated with exposure to fenflu-

43 ramine or dexfenfluramine: U.S. Department of Health and Human Services interim public health recommendations. MMWR Morb Mortal Wkly Rep 46:1061–1066 81. Stafford RS, Radley DC (2003) National trends in antiobesity medication use. Arch Intern Med 163(9):1046–1050 82. Leung WYS, Neil TG, Chan JCN, Tomlinson B (2003) Weight management and current options in pharmacotherapy: orlistat and sibutramine. Clin Ther 25(1):58–80 83. Sjöström L, Rissanen A, Andersen T, Boldrin M, Golay A, Koppeschaar HP, Krempf M (1998) Randomised placebocontrolled trial of orlistat for weight loss and prevention of weight regain in obese patients. Lancet 352(9123):167–172 84. Anderson JW, Schwartz SM, Hauptman J, Boldrin M, Rossi M, Bansal V, Hale CA (2006) Low-dose orlistat effects on body weight of mildly to moderately overweight individuals: a 16 week, double-blind, placebo-controlled trial. Ann Pharmacother 40(10):1717–1723 85. McNeely W, Goa KL (1998) Sibutramine. A review of its contribution to the management of obesity. Drugs 56(6): 1093–1124 86. Li Z, Maglione M, Tu W, Mojica W, Arterburn D, Shugarman LR, Hilton L, Suttorp M, Solomon V, Shekelle PG, Morton SC (2005) Meta-analysis: pharmacologic treatment of obesity. Ann Intern Med 142(7):532–546 87. Turk MW, Yang K, Hravnak MH, Sereika SM, Ewing LJ, Burke LE (2009) Randomized clinical trials of weight loss maintenance: a review. J Cardiovasc Nurs 24(1):58–80 88. Bray GA, Ryan DH (2007) Drug treatment of the overweight patient. Gastroenterology 132(6):2239–2252 89. McMahon FG, Fujioka K, Singh BN, Mendel CM, Rowe E, Rolston K, Johnson F, Mooradian AD (2000) Efficacy and safety of sibutramine in obese white and African American patients with hypertension: a 1-year, double-blind, placebo-controlled, multicenter trial. Arch Intern Med 160(14):2185–2191 90. Klein S (2004) Long-term pharmacotherapy for obesity. Obes Res 12(suppl):S163–S166 91. Buchwald H, Consensus Conference Panel (2005) Consensus conference statement bariatric surgery for morbid obesity: health implications for patients, health professionals, and third-party payers. Surg Obes Relat Dis 1(3):371–381 92. NIH Consensus Conference Statement Online (1991) Gastrointestinal surgery for severe obesity. Obesity 9(1):1–20. http://www.ncbi.nlm.nih.gov/books/NBK15123/. Accessed 24 May 2010 93. Kral JG, Naslund E (2007) Surgical treatment of obesity. Nat Clin Pract Endocrinol Metab 3(8):574–583 94. Kral JG (2006) ABC of obesity management: part III– surgery. Br Med J 333(7574):900–903 95. El Shobary H, Christou N, Beckman SB, Gvocdic B, Schricker T (2006) Effect of laparoscopic versus open gastric bypass surgery on postoperative pain and bowel function. Obes Surg 16:437–442 96. Samplis JS, Liberman M, Auger S, Christou N (2004) The impact of weight reduction surgery on health-care costs in morbidly obese patients. Obes Surg 14:939–947 97. Nguyen NT, Paya M, Mavandadi S, Zainabadi K, Wilson SE (2004) The relationship between hospital volume and outcome in bariatric surgery at academic medical centers. Ann Surg 240:586–593 98. Deitel M, Greenstein RJ (2003) Recommendations for reporting weight loss. Obes Surg 13:159–160

44 99. Bult MJF, van Dalen T, Muller AF (2008) Surgical treatment of obesity. Eur J Endocrinol 158(2):135–145 100. Schneider BE, Mun EC (2005) Surgical management of morbid obesity. Diabetes Care 28:475–480 101. Buchwald H, Williams SE (2004) Bariatric surgery worldwide 2003. Obes Surg 14:1157–1164 102. Tritos NA, Mun E, Bertkau A, Grayson R, Maratos-Flier E, Goldfine A (2003) Serum ghrelin levels in response to glucose load in obese subjects post-gastric bypass surgery. Obesity 11(8):919–924 103. Cummings DE, Weigle DS, Frayo RS, Breen PA, Ma MK, Dellinger EP, Purnell JQ (2002) Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med 346(21):1623–1630 104. Cummings DE, Purnell JQ, Frayo RS, Schmidova K, Wisse BE, Weigle DS (2001) A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans. Diabetes 50(8):1714–1719 105. Sjostrom L, Narbro K, Sjostrom CD, Karason K, Larsson B, Wedel H, Lystig T, Sullivan M, Bouchard C, Carlsson B, Bengtsson C, Dahlgren S, Gummesson A, Jacobson P, Karlsson J, Lindroos AK, Lönroth H, Näslund I, Olbers T, Stenlöf K, Torgerson J, Agren G, Carlsson LM, Swedish Obese Subjects Study (2007) Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med 357(8):741–752 106. Sjostrom L, Lindroos A, Peltonen M, Torgerson J, Bouchard C, Carlsson B, Dahlgren S, Larsson B, Narbro K, Sjöström CD, Sullivan M, Wedel H, Swedish Obese Subjects Study Scientific Group (2004) Lifestyle, diabetes, and cardiovascular risk factors 10  years after bariatric surgery. N Engl J Med 351(26):2683–2753 107. Wadden TA, Butryn ML, Byrne KJ (2004) Efficacy of lifestyle modification for long-term weight control. Obes Res 12(suppl):S151–S162 108. Perri MG, Foreyt JP (2004) Preventing weight regain after weight loss. In: Bray GA, Bouchard C (eds) Handbook of obesity: clinical applications, 2nd edn. Marcel Dekker, New York, pp 185–199 109. Wadden TA (1995) What characterizes successful weight maintainers? In: Allison DB, Pi-Sunyer F (eds) Obesity treatment: establishing goals, improving outcomes, and reviewing the research Agenda. Plenum Publishing Corp, New York, pp 103–111 110. Klem ML, Wing RR, McGuire MT, Seagle HM, Hill JO (1997) A descriptive study of individuals successful at long-term maintenance of substantial weight loss. Am J Clin Nutr 66(2):239–246 111. Butryn ML, Phelan S, Hill JO, Wing RR (2007) Consistent self-monitoring of weight: a key component of successful weight loss maintenance. Obesity 15(12):3091–3096 112. Wing RR, Hill JO (2001) Successful weight loss maintenance. Annu Rev Nutr 21:323–341 113. Raynor HA, Jeffery RW, Phelan S, Hill JO, Wing RR (2005) Amount of food group variety consumed in the diet and long-term weight loss maintenance. Obes Res 13(5): 883–890 114. Wyatt HR, Grunwald GK, Mosca CL, Klem ML, Wing RR, Hill JO (2002) Long-term weight loss and breakfast in subjects in the National Weight Control Registry. Obes Res 10(2):78–82

M.T. Turk 115. Raynor DA, Phelan S, Hill JO, Wing RR (2006) Television viewing and long-term weight maintenance: results from the National Weight Control Registry. Obesity 14(10): 1816–1824 116. McGuire MT, Wing RR, Klem ML, Lang W, Hill JO (1999) What predicts weight regain in a group of successful weight losers? J Consult Clin Psychol 67(2):177–185 117. Weiss EC, Galuska DA, Khan LK, Gillespie C, Serdula MK (2007) Weight regain in U.S. adults who experienced substantial weight loss, 1999–2002. Am J Prev Med 33(1):34–40 118. Wing RR, Papandonatos G, Fava JL, Gorin AA, Phelan S, McCaffery J, Tate DF (2008) Maintaining large weight losses: the role of behavioral and psychological factors. J Consult Clin Psychol 76(6):1015–1021 119. Richelsen B, Tonstad S, Rossner S, Toubro S, Niskanen L, Madsbad S, Mustajoki P, Rissanen A (2007) Effect of orlistat on weight regain and cardiovascular risk factors following a very-low-energy diet in abdominally obese patients: a 3-year randomized, placebo-controlled study. Diabetes Care 30(1):27–32 120. Apfelbaum M, Vague P, Ziegler O, Hanotin C, Thomas F, Leutenegger E (1999) Long-term maintenance of weight loss after a very-low-calorie diet: a randomized blinded trial of the efficacy and tolerability of sibutramine. Am J Med 106(2):179–184 121. Wirth A, Krause J (2001) Long-term weight loss with sibutramine: a randomized controlled trial. J Am Med Assoc 286(11):1331–1339 122. Kruger J, Blanck HM, Gillespie C (2008) Dietary practices, dining out behavior, and physical activity correlates of weight loss maintenance. Prev Chronic Dis 5(1):1–14 123. McGuire MT, Wing RR, Klem ML, Seagle HM, Hill JO (1998) Long-term maintenance of weight loss: Do people who lose weight through various weight loss methods use different behaviors to maintain their weight? Int J Obes Lond 22(6):572–577 124. Tate DF, Jeffery RW, Sherwood NE, Wing RR (2007) Long-term weight losses associated with prescription of higher physical activity goals. Are higher levels of physical activity protective against weight regain? Am J Clin Nutr 85(4):954–959 125. Villanova N, Pasqui F, Burzacchini S et al (2006) A physical activity program to reinforce weight maintenance following a behavior program in overweight/obese subjects. Int J Obes Lond 30(4):697–703 126. Jeffery RW, Wing RR, Sherwood NE, Tate DF (2003) Physical activity and weight loss: Does prescribing higher physical activity goals improve outcome? Am J Clin Nutr 78(4):684–689 127. Hill JO, Thompson H, Wyatt H (2005) Weight maintenance: What’s missing? J Am Diet Assoc 105(5):63–66 128. Jakicic JM, Marcus BH, Lang W, Janney C (2008) Effect of exercise on 24-month weight loss maintenance in overweight women. Arch Intern Med 168(14):1550–1559 129. Ewbank PP, Darga LL, Lucas CP (1995) Physical activity as a predictor of weight maintenance in previously obese subjects. Obes Res 3(3):257–263 130. Jeffery RW, Drewnowski A, Epstein LH, Stunkard AJ, Wilson GT, Wing RR, Hill DR (2000) Long-term maintenance of weight loss: current status. Health Psychol 19(1 suppl):5–16

5  Assessment and Treatment of Excess Weight 131. Anderson DA, Wadden TA (1999) Treating the obese patient. Suggestions for primary care practice. Arch Fam Med 8(2):156–167 132. Perri MG, McAdoo WG, Spevak PA, Newlin DB (1984) Effect of a multicomponent maintenance program on longterm weight loss. J Consult Clin Psychol 52(3):480–481 133. Wing RR, Jeffery RW, Hellerstedt WL, Burton LR (1996) Effect of frequent phone contacts and optional food provi-

45 sion on maintenance of weight loss. Ann Behav Med 18(3):172–176 134. Wadden TA, Anderson DA, Foster GD (1999) Two-year changes in lipids and lipoproteins associated with the maintenance of a 5% to 10% reduction in initial weight: some findings and some questions. Obes Res 7(2): 170–178

 

6

Phytonutrient and Phytotherapy for Improving Health Jian Zhao

6.1 Introduction Advancing scientific research and increasing knowledge on medicine and food nutrition has dramatically changed the concepts about food, medicine, and healthcare and brought in a revolution on them in past decades. What people eat or drink has become the major cause of various diseases and health problems, besides infections or epidermal diseases. Nowadays people pay extensive attentions to what they eat, including foods and medicines, which largely determine one’s health in the life. In addition to staple foods, fruits, and vegetables, strong recommendations by nutrition or clinical professionals to consume nutraceuticals and phytonutrients have become progressively popular [1]. Alternative therapeutics based on nutraceutical therapy and phytotherapy have emerged as new healing systems and quickly and widely spread [1, 2]. It is generally believed that plant nutrients and bioactive natural products (here all together called phytonutrients) in plant-derived diets, herbs and botanicals hold great promise in benefiting human health due to their potentials to promote overall health, prevent some diseases, reduce side effects associated with chemotherapy or radiotherapy, reduce the health care cost, or to even improve drug effectiveness by various mechanisms [1, 3]. A large population in all over the

J. Zhao  Plant Biology Division, The Samuel Roberts Noble Foundation, 2510 Sam Noble Parkway, Ardmore, OK 73401, USA e-mail: [email protected], [email protected]

world, including two-thirds of Americans, regularly take certain kinds of nutraceuticals or herbs for various health purposes. Correspondingly, manufacturing and marketing of nutraceuticals and phytonutrients and related therapeutic and professional practices are rapidly growing. While concerns on the use, quality control, safety, efficacy, or standardization of phytonutrients and phytotherapy remain as major issues, legislations on these foods and healthcare products are yet to be completed [1]. The information regarding these phytonutrients and their related alternative therapies from media such as Internet, TVs, printed publications, and even in research data is either limited or confusing or sometime controversial. This chapter attempts to display and remark on phytonutrients and phytonutrientbased therapeutics, phytotherapy, and to give a more comprehensive but clear view of these. It introduces phytonutrients and phytotherapy from their scientific concepts, scientific research- or evidence-based facts, clinical trials, and epidemiological studies, to their roles with beauty and cosmetic surgery. It can lead to a complete understanding of the most aspects of phytonutrients and phytotherapy.

6.2 Plant Food, Medicine, Natural Product, and Phytonutrients Plant natural products provide humans with huge sources for foods, medicines, flavors, colors, fine chemicals, and other agricultural and industrial materials. Human beings once and now still extensively rely on plant resources and environments. Plant-derived foods, such as grains, fruits, and vegetables, provide humans a major portion of dietary nutrients, such as ­carbohydrates,

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_6, © Springer-Verlag Berlin Heidelberg, 2011

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lipids, proteins, vitamins, minerals, and dietary fibers. Food chemistry and nutrition studies have revealed that humans actually benefit from plant foods all the time from numerous aspects because of their rich and diverse natural products. Plant foods provide rich and ideal phytonutrients combinations for human beings, such as whole sets of different types of vitamins, essential amino acids, essential fatty acids, macro- and micro-minerals, and plant-specific proteins, lipids, and carbohydrates. Although many of them can also be taken up from animal-derived foods, the presence of other nonhealthy or even potentially harmful ingredients such as high levels of cholesterol, saturated fatty acids, and disease infection and contaminations makes animal-derived foods less desirable. Even fish and other sea foods that are popularly regarded as the top omega-3-containing healthy foods is often inevitably contaminated with heavy metals such as mercury or other toxic organic chemicals. Therefore, plant foods, particularly raw organic plant foods such as grains, fresh vegetables and fruits, nuts, with high phytonutrient values, are strongly recommended for human health benefit. Epidemiological and prospective studies indicate that comprehensive lifestyle changes may modify the progression of prostate cancer [4]. Similarly, dietary habits and changes could significantly affect overall health status and lifespan [5], although the molecular mechanisms by which improvements in diet and lifestyle might affect the prostate microenvironment are poorly understood. Recent studies have suggested that dietary choices may have an effect on epigenetic of individual genome, providing a profound insight into our understanding of relationships between diet and human health [6]. Human beings rely on plants not only due to foods for relief of starvation, but also for their medicine effects and healthcare function. From ancient time, human beings have been using some medicinal plants to diagnose and treat various diseases, or to enhance health and increase longevity of their lives. Extensive use of plants for healthcare and disease treatment have led to numerous discoveries of diverse important plant natural products from medicinal plants and crops, and accumulated invaluable therapeutic experiences. The heritages of folk medicine or traditional medicine and their therapies benefit human health for thousands of years and now continue to serve humans [7]. The modern pharmaceutical industry is born from folks or traditional plant medicine. Many important drugs used in chemotherapy are originally derived

J. Zhao

from plant natural products such as aspirin originating from salicin, a natural product in Salix alba plants. Some drugs now still heavily rely on extraction from medicinal plant: anti-lymphoma and histiocytosis drugs vinblastine/vincristine from Madagascar periwinkle (Catharanthus roseus); anticancer drug Taxol (paclitaxel) from the pacific yew tree; antimalaria drugs derived from natural lead artemisinin in a Chinese tradition medicinal plant wormwood (Artemisia annua); anticancer drug (ovarian and small cell lung cancers) topotecan synthesized from its natural analogue podophyllotoxin in Mayapple (Podophyllum peltatum); anticholinergic medicine atropine from Atropa belladonna, etc. Although synthetic drugs and modern drug discovery based on them have become standard and mainstream for many years, plant-derived folk medicines, herbs or botanicals, continue to be used or developed into effective therapies [7]. For example, Chinese traditional medicines, a long-history therapy system and multi-component herb medicines, have been main pharmaceuticals in China and now are gradually recognized as an important complementary healing system and new drug discovery resources by western countries [8]. On the other hand, many synthetic drugs have been reported regarding of their toxicity and/or serious side-effects, together with their almost unaffordable expensive costs, and failures to treat many common degenerative diseases, drive people to look for alternative therapies, including phytonutrients- and phytotherapies. Such return back to plant functional foods and phytotherapy is also due to greater-than-expect performances of many phytonutrients and phytotherapy.

6.3 Clearance of Concepts and Terms Because of long history of using medicinal plants by humans, the similar concepts with phytonutrient and phytotherapy have been given different names in different regions, nations, or at development stages and by different producers or providers [1, 7]. These cause a lot of confusing and misunderstanding. For examples, herbs, herbal medicines, botanical medicines, medicinal plants, phytonutrients, phytomedicines, herbalism, herbology, herbal therapy, and phytotherapy appeared in different types of media actually refer to concepts with the similar meanings: plants or plant extracts with proved health benefits, and therapeutics

6  Phytonutrient and Phytotherapy for Improving Health

based on such materials. Clarifying these concepts are of particular importance to avoid any misunderstanding or misleading of patients, professionals, researchers, other interested parties. Herbs, herbal medicine, medicinal plants, botanicals, folk medicines, or phytomedicine refer to plants or parts of plants and their extracts with certain biological activities and can be used for promote health, prevent or treat human disease. Health benefits of these plant materials or plant-derived materials are either proved by a long history of using and their treatment evidence in folks, or by modern scientific research on their bioactive components with biological activity against health problems. However, usually an herb contains multiple bioactive components, which makes their overall therapeutic effects more complicated and research on them difficult. Their major ingredients may show similar and synergistic effects or different and even antagonist effects because of their targets on similar or different biochemical pathways or cellular processes. Herbal remedy, or herbalism, medical herbalism, and herbology are old names for phytomedicine-based belief or theory, studying subjective or healing and disease treatment system. All of them believe that medicinal plants contain necessary medicines for solving most human health problems. However, due to the lack of strict practical protocols, supporting evidence from scientific study, standardization of quality and quantity of herbs regarding of their bioactive components, and thereby reliable clinical effects, many old herbal remedies have been discarded or changed for modern medicine study, if they are still believed valuable. Phytonutrients refer to plant-derived all natural products with particular biological activities in supporting human health. The concept covers the common food nutrients derived from agricultural plants, but also covers plant natural products with biological activity. Unlike phytochemicals that generally refers to all plantderived chemicals regardless of their biological activity, also different from phytomedicine that only includes plant natural products that show potent biological activity and can potentially be developed into drugs, phytonutrient focuses on plant derived bioactive products with health benefits. Therefore, phytonutrients here include all nutrients derived from plants, not only function-known vitamins, proteins, lipids, and carbon essential minerals, but also unknown health-promoting plant natural products including primary and secondary metabolites. Such broad definition on phytonutrient is

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based on (1) plants are born to be an important part of human beings’ life. All natural products in plant foods and medicinal plants are significantly involved in the evolution of humans. (2) “Let food be thy medicine and medicine be thy food” is still the wisdom prediction of the relationship between appropriate foods for health and their therapeutic benefits and the final goal of food nutrition and medical sciences. (3) Our understanding of plant natural bioactive products continues expending with advancing scientific research on phytochemistry, nutrition, and medical sciences. New beneficial effects of plant natural products on human health are being revealed, and therefore, the concept phytonutrient evolves. Phytonutrients play positive roles in maintaining well being, enhancing health, and modulating immune function to prevent specific diseases. Under proper management, phytonutrient hold great promise in clinical therapy due to their potential to improve health conditions of humans in a more natural way, to cure diseases without side effects and affordable cost, to complement the shortages of current chemotherapy or radiotherapy by reducing side effects associated with chemotherapy or radiotherapy and significantly reducing the healthcare cost [4]. Phytotherapy presents an alternative healing system with long histories using whole or parts of medicinal plants or herbals or their effective extracts to improve health conditions, prevent or treat diseases. Compared with herbal remedy, phytotherapy is an evolved concept and its methodology is based on modern phytochemistry, nutrition, and medicine research, although most phytotherapeutics are developed from herbal remedy that uses folk medicines to promote health and treat diseases. However, compared to herbal remedy, phytotherapy is based on modern scientific researches and most often are through various types of clinical trials. The phytonutrients have been and are continuously being improved for their safety, bioactivity, and quality and quantity control. Advancing studies on their photochemical principles and biological activities, and clinical trials on feeding protocols pave a solid base for patient practice. Phytotherapy relies on diverse bioactive phytonutrients that make plant foods cannot only relief hunger, but also modify health status, aid in medical practices such as drug delivery. The plant primary and secondary metabolites include several classes such as essential amino acids, essential fatty acids,

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unique carbohydrates, and many potent bioactive secondary metabolites such as terpenoids, phenolics, alkaloids, and others. They provide humans with numerous biologically active products, which have been used extensively as food additives, flavors, ­colors, drugs, fragrances, and other fine chemicals. Exploration of new phytonutrients and their biological activities has led and continue to make more discoveries for improving phytotherapies.

6.4 Health Benefits of Phytonutrients and Phytotherapy 6.4.1 Dietary Fibers Plant dietary fiber can reduce cholesterol level and risk of cardiovascular diseases, maintain healthy weight, therefore has promising benefits to obesity and diabetic patients [9]. FDA for the first time approved the claim about solid functions of soluble fiber from plant foods. Plant foods rich in dietary fibers include wheat bran (rich in insoluble fiber with benefit of reducing risk of breast or colon cancer), psyllium and oat and barley mails (rich in soluble fiber and beta-glucan, well known for lowering low density lipoprotein (LDL) and total cholesterol and reducing risk of cardiovascular disease and some cancers).

6.4.2 Phenolic and Polyphenolic Compounds Chlorogenic acid is marketed under the trademark Svetol in Norway and the United Kingdom as a food active ingredient used in coffee, chewing gum, and mints to promote weight reduction. Resveratrol found in nuts and red wine has strong antioxidant, antithrombotic, anti-inflammatory, and anti-carcinogenesis activities. Hydroxytyrosol from olives and olive oil is a potent antioxidant. Curcumin from Indian spice turmeric shows strong antioxidant, anti-inflammatory, and anticancer activity [10]. Plant lignans are contained in plants-derived foods and have multiple biological activities, such as antimitotic, antifungal, antioxidant, and antiviral activity. The most famous lignan is podophyllotoxin, which has potent anticancer activity and its derivatives have been developed into drugs for chemotherapy against different

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types of cancers. Secoisolariciresinol and matairesinol were the first plant lignans identified in foods. The main dietary lignans in our daily foods might be pinoresinol and lariciresinol, which contribute about 75% to the total lignan intake whereas secoisolariciresinol and matairesinol contribute only about 25% [11]. Flax seed and sesame seed are rich in lignans, such as secoisolariciresinol diglucoside. Other sources of lignans include cereals (rye, wheat, oat and barley), pumpkin seeds, soybeans, broccoli, beans, and some berries. Flavonoids such as anthocyanins, flavonols, isoflavones, proanthocyanidins (also known as tannins) are most abundant dietary plant secondary metabolites, and widely contented in plant foods. OPC (oligomeric proanthocyanidins) are combined proanthocyanidin extract (mainly from grape seeds). OPC has been marketed for many years as a phytonutrients in phytotherapy with strong antioxidant and anti-aging agents, recently the active components oligomeric proanthocyanidins from grape seeds are shown to delay Alzheimer’s disease [12]. Proanthocyanidins can improve urinary tract health by preventing urinary tract infection and reducing risk of cardiovascular disease through their strong antioxidant activity. A positive correlation between dietary flavonoid (such as myricetin, quercetin, and isoflavones) intake and decreased mortality from coronary heart disease, partly due to the inhibition of LDL oxidation and reduced platelet aggregability by flavonoids [13–16]. Dietary intake of flavonoids ranges between 23 mg/day estimated in The Netherlands (mainly green tea, onions, apples, and red wine) and 170 mg/day estimated in the USA. The consumption of 30–50  mg/day of soy isoflavones in the traditional eastern diet may help lower the incidence of breast cancer. The soy isoflavone phytoestrogens, genistein and daidzein, and a daidzein metabolite equol produced by intestinal microflora have potent antioxidant activity. Particularly, equol is an inhibitor of LDL oxidation taking place in the arterial intima. Therefore, intake of soy-derived phytoestrogens provides protection against oxidative modification of LDL, and helps to reduce the risk of atherosclerosis, ­cardiovascular disease, and cancer [17]. A randomized, ­double-blind, placebo-controlled, cross-over study with 30 healthy postmenopausal women indicated that 8 weeks consumption of cereal bars enriched with 50 mg soy isoflavones/d increased plasma nitrite and nitrate concentrations and improved endothelium-independent vasodilatation in healthy postmenopausal women [17]. There are continuously increasing numbers of breast

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cancer patients in Western societies, which are higher than these in eastern Asian countries, mainly because Asian women eat more soy and other plant-derived foods such as tofu, vegetables, and raw cereals that contain phytoestrogens, lignans, and fibers [1, 17].

6.4.3 Terpenoids Plant terpenoids are an important group of phytonutrients, including pre-vitamin A carotenoid, zeaxanthin, and vitamin E, Coenzyme Q10, and bioactive monoterpene, sesquiterpenes, diterpenoids. Coenzyme Q is a lipid-soluble antioxidant and a very popular food supplement. carotenoid lycopene. Epidemiological studies have clearly shown the great benefits of consumption of tomato to human health due to tomato carotenoids, mainly lycopene, b-carotene, and lutein [18]. Lycopene from tomatoes and other fruits is a potent antioxidant carotenoid protective against prostate and other cancers and inhibiting tumor cell growth in animals [18]. b-Carotene from carrots, fruits and other vegetables not only are pre-vitamin A, but also have potent antioxidant activity by neutralizing free radicals, which are regarded as one of the major causes of aging and various cancers. Humans benefit from eating dietary carotenoid-rich plants and various vegetables containing vitamin E, lycopene, lutein, zeaxanthin through their strong antioxidant and anti-aging activity. Monoterpenes in citrus fruits, cherries, peppermint, and herbs have anticarcinogenic actions, as well as cardioprotective effects in experimental models. Sesquiterpenes from plants usually have strong antibacterial, antiviral, antifungal, and insecticidal activities, and are used to treat infectionrelated diseases. The unique monoterpene derivatives thujaplicins from trees are widely used as antifungal medicine in clinic, cosmetic products, and wood preservation [19]. The most well-known sesquiterpenes such as artemisinin and their derivatives are dominant antimalarial drugs [20]. Many plant diterpenes are medicines such as famous anticancer drugs Taxol and derivatives. Another important class of terpenoid phytosterols, such as stigmasterol, sitosterol, campesterol, are natural components of many plant foods. Because of their similar structures with cholesterols from meats, phytosterols competitively inhibit human cholesterol absorption by the gut [21, 22]. FDA approved the claim “Foods containing at least 0.4 gram per serving of plant sterols, eaten twice a day with meals for a daily total intake of at

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least 0.8 gram, as part of a diet low in saturated fat and cholesterol, may reduce the risk of heart disease.”

6.4.4 Fatty Acids and Lipids Fat occupies nearly 60% of human brains and determines brain’s integrity and performance. Clinical studies have associated the imbalanced dietary intake of essential fatty acids including alpha-linolenic acid (an omega-3 fatty acid) and linoleic acid (an omega-6 fatty acid) with impaired brain development, performance, and diseases [23]. They are essential for human body to make many important molecules affecting neurofunction, cellular function, inflammation, mood, and behavior. Dietary long-chain polyunsaturated fatty acids, such as arachidonic acid, eicosapentaenoic acid (EPA), and decosahexaenoic acid (DHA) are also helpful for proper function of the retina and visual cortex [24]. People now take extra omega-3 fatty acids from fish oils, flaxseeds, or nutraceutical products. However, correct intake in terms of EFA form, dosage, and time for optimal wellness is still speculative. Plant foods such as flaxseed, soya oil, canola oil, Oliver oil, pumpkin seeds, sunflower seeds, leafy vegetables, and walnuts contain different levels of omega-3 fatty acids. Although the ideal and higher ratio of omega-3 to omega-6 fatty acids varies largely in these foods. A plenty of scientific evidence shows that substitution of dietary saturated fat by oleic acid and/or polyunsaturated omega-3 fatty acids benefit cardiovascular health by reducing blood cholesterol, LDL-cholesterol and triglycerides [25]. Recent studies show that medium-chain fatty acids or triglycerides also have benefits to human health [26]. Unlike long- or very-long-chain fatty acids, these fatty acids passively diffuse into the portal system without requirements of modification and digestion. Therefore, malnutrition or malabsorption patients are treated with these medium-chain fatty acids (MCFAs) and triglycerides (MCTs). Metabolic syndromes, such as abdominal obesity, dyslipidemia, hypertension and impaired fasting glucose, contribute to increased cardiovascular morbidity and mortality. Medium-chain fatty acids and medium-chain triglycerides suppress fat deposition through enhanced thermogenesis and fat oxidation in animal and human subjects [27]. Several reports suggest that MCFAs/MCTs offer the therapeutic advantage of preserving insulin sensitivity in ­animal

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models and patients with type 2 diabetes [27]. Coconut oil is composed of approximately 66% medium-chain triglycerides.

6.4.5 Essential Amino Acids Eight essential amino acids are so called because mammals cannot synthesize them by themselves but have to take up from plant foods or meat sources. Taking up adequate essential amino acids are very important for health since they are building blocks of proteins, which carried functions of human body [1, 28]. Tryptophan is used for synthesis of neurotransmitter serotonin and relief of depression; flaxseeds have high tryptophan levels. Tyrosine is for dopamine, norepinephrine and adrenaline synthesis for normal neurosystem activity and enhances positive mood. Isoleucine is necessary for the synthesis of hemoglobin in red blood cells. Leucine has beneficial effects for skin, bone and tissue wound healing, and promotes growth hormone synthesis. Lysine and valine are essential for muscle proteins, as well as the synthesis hormones and l-carathine which is essential for healthy nervous system function. Methionine is essential for all protein synthesis and helps in breakdown of fats and reduces muscle degeneration. All these essential amino acids can be found in plant foods such as cereals, soybean, flaxseeds, nuts, and peas [29]. Phenylalanine is beneficial for healthy nervous system and boosts memory and learning. Phenylalanine may be useful against depression and suppressing appetite. In addition, l-Arginine is a conditional essential amino acid for infants and growing children, as well as for pregnant women. Glutamine is considered a conditionally essential amino acid in metabolic stress.

6.4.6 Phytoestrogen Various phytoestrogens are diverse nonsteroidal plant secondary metabolites with similar structure with hormone estradiol and thus with ability to cause estrogenic or/and antiestrogenic effects. Many of them are contained in our daily diets, such as soybean and cabbage, nuts, and oilseeds, therefore also called “dietary estrogens.” These phytonutrients such as coumarins, prenylated flavonoids, and isoflavones can act as antioxidants, estrogen agonists, and antagonists with multiple effects [30]. An optimal “estrogen balance” has implications

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for cancer prevention and successful aging in both women and men. They protect against heart disease, anticancer activity against some cancers such as breast cancer, lower LDL, and total cholesterol [18]. Soybean products, cruciferous vegetables such as cabbage, cauliflower, and broccoli possess unique phytochemicals able to modify the metabolism of estrogen or to enhance the beneficial action and safety of estrogen. Several large-scale investigations suggest that the likely contributory factor to dramatic difference between Asian women who have significantly lower levels of breast cancer and women in western countries may be that Asian women take a vegetarian diet with higher intake of legumes and other plant foods containing a variety of lignans, dietary fibers, and isoflavonoid phytoestrogens, which act as nature’s sex hormone modulators and provide estrogenic effects and an anti-estrogenic competitive effect [16, 17, 31]. Epidemiological studies demonstrated that l-arginine, chlorogenic acid, fermented milk, garlic, onion, tea, soybean, ginger, hawthorn, and fish oil have beneficial effects on prevention, improvement, or treatment of patient’s elevated blood pressure [32].

6.5 Herbs and Multi-Component Herbal Formulations Phytotherapy strategies using herbal drug combinations with superior efficacy and lesser side effects in comparison with single isolated constituents of plant extracts has been repeatedly assessed clinically as well as pharmacologically [1]. A multicomponent herbal preparation, STW5, has been clinically proved effective for the treatment of patients with functional dyspepsia and irritable bowel syndrome [33]. Like other Chinese herbal medicines combined with various herbs containing different bioactive substances, STW5 is a combination of nine plant extracts with different active constituents [34]. Except for nutraceuticals such as glucosamine and chondroitin, many herbs have been tried for treatment of osteoarthritis and rheumatoid arthritis diseases [1, 35]. Other degenerative diseases and immunosystem problems that could not be effectively treated by current synthetic drugs become targets of herbs, nutraceuticals, and phytotherapies. Allergic rhinitis is the most frequently occurring immunological disorder. A traditional Chinese formulation Aller-7 comprising seven herbal extracts was shown well tolerated and ­efficacious

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in patients with allergic rhinitis without serious adverse effect [36]. Similarly, another formulation was also studied in clinical trial and appears to offer symptomatic relief and improvement of quality of life for some patients with seasonal allergic rhinitis [37]. The efficacy and safety of the butterbur leaf extract Ze 339 were to be safe and efficacious in the treatment of patients with seasonal allergic rhinitis [38]. All these studies clearly suggest that multi-component traditional herbals can offer a very efficacious and better therapeutic option to patients in many diseases. However, a lack of information on the phytochemistry and pharmacological section of phytochemicals, or the synergistic effects of phytotherapies may threaten and damage the customers and market [39]. Clinical trials and epidemiological studies are commonly used methods to investigate effects of phytonutrients and herbs on various health targets. However, strict clinical trials and epidemiological studies, particularly latter, require not only rationale designs, proper controls, a long time period for feeding, observation and physiological measurements, data collection, but also a large population of patients willing to cooperatively participate in the study, as well as final systematic analysis. This is largely because effects of phytonutrients are usually marginal, long-term, and individually differential. Also, other factors also can significantly affect the outcome of clinical trials and epidemiological studies, for instance, quality and quantity of herbs or phytonutrients, absorption and metabolism of phytonutrient, and drug–herbs or drug–phytonutrient interaction. Therefore, it is uneasy to obtain reliable results from clinical trial and epidemiological study on phytonutrients. For example, as one of the widely commercialized example of phytotherapeutics, Saw palmetto (Serenoa repens) combined with others is widely used for the treatment of lower urinary tract symptoms and benign prostatic hyperplasia. Although the majority of adverse events of using saw palmetto are mild, results of many different clinical trials are complicated and controversial [40, 41]. However, highquality clinical trials and epidemiological studies on phytonutrients and physiotherapies provide most close-to-realty and reliable evaluation of their biological effects on human health, and they are essential and highly needed to evaluate phytonutrients and phytotherapies for continuous and healthy development of natural resources and healing system.

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The rapidly increasing number of such proof-of-concept studies strongly support success of some phytonutrients and their phytotherapies on improvement of health or even solve health problems.

6.6 Phytonutrients for Beauty: Weight Loss, Facial Aging, and Cosmetic Surgery An increasing prevalence of overweight and obesity has reached global proportions. Overweight and obesity generate a major risk of chronic diseases such as type 2 diabetes, cardiovascular disease, hypertension, stroke, and cancers. Overweight and obesity are dietrelated health problems, their patients, however, may not be simply and easily recovered by reducing diet consumption because overweight and obesity have changed many physiological and psychological processes to patients. Some synthetic drugs have been developed, yet their side effects and potential risks are nor ignoble. With strong belief on the potential health benefits of phytonutrients people look for herbs and phytonutrients that are effective in weight loss and diet control. Actually, plants-based foods have low saturated fats and sugar, high levels of diet fibers, and more balanced minerals and vitamins, and be eaten against many health-problems including weight and obesity [42]. Moreover, some phytonutrients from plant foods or medicinal plants have potent effects on prevention and treatment of overweight and obesity. For example, clinical studies have demonstrated that plant-derived sterols, phytosterols, can repeatedly lower bad LDL cholesterol in the blood, which is a major risk factor for coronary heart disease [43]. Hydroxycitric acid (HCA) from Garcinia cambogia is a main bioactive component in several popular Hydroxycut weight management formulation products [44]. Herbs and phytonutrients are also believed to delay facial aging, improve facial rejuvenation and facial beauty because of their rich amino acids, vitamins, antioxidants and other phytonutrients with antibacterial, antifungal, and anti-inflammatory activity that are helpful for the skin. Nowadays use of phytonutrients or herbs, effective cosmetics (many of them also contain phytonutrients), aesthetic plastic and cosmetic surgery, or combinations of them are widespread among people for various levels of beauty purposes [45, 46]. There are many claims that

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certain herbs or phytonutrients have potent effects on reduction of weight, obesity, diabetes, facial aging and rejuvenation, or other degenerative diseases, and nutritional deficiencies, or improvement of overall health and beauty [47, 48]. However, there are also warns of negative effects on uses of herbs and natural products, particularly perioperative use of herbs and phytonutrient supplements regarding aesthetic plastic, and cosmetic surgery because these health problems on patients have a significant impact on surgical outcome and complications [49]. Although phytonutrients have beneficial effects on some aesthetic plastic and cosmetic surgeries [47, 49], some raw herbs are more complex due to multiple-components, limited information on their phytochemical, medical/toxical, or clinical researches; perioperative taking of these herbs by patients who are undergoing surgery may have unexpected influences on any surgical outcome. Many plastic or cosmetic patients are taking herbal medications or supplements, and a descriptive “top-10” list of such herbs and preoperative recommendations was compiled for the plastic surgeon [50]. Chondroitin (used to treat osteoarthritis in conjunction with glucosamine), ephedra (Ephedra sinica, used to promote weight loss, to treat respiratory tract conditions, but it has been banned by the FDA because of potential and serious side effects, active ingredients ephedrine and pseudoephedrine), echinacea (Echinacea purpurea, used for chronic wounds, immune stimulant and arthritis, active component: phenolic compounds), Ginkgo biloba (improve blood circulation and mental function, active component: ginkgoflavoneglycosides), goldenseal (Hydrastis canadensis, used for strong antibacterial regent, active ingredient: berberine), milk thistle (Silybum marianum, used for liver problems like liver cirrhosis, chronic hepatitis, etc., active ingredient: silymarin), ginseng (used to revitalize and boost energy and reduce stress and fatigue, active component: ginsenosides), kava (Piper methysticum, promotes relaxation and antidepressant, active component: kavalactones) and garlic (used to maintain healthy cholesterol and anticoagulant, or antibiotic regent, active ingredient: sulfur compound allicin), black cohosh (Cimicifuga racemosa, estrogenic activity to treat gynecological and other age-related disorders, active component: triterpenoid glycosides), valerian (Valeriana officinalis, used as mild sedative to treat insomnia and anxiety, active ingredients: sesquiterpenes and valepotriates), Saw palmetto (Serenoa repens, used for improvement of urinary

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symptoms and benign prostatic hyperplasia, bioactive ingredients fatty acids and phytosterols), arnica Montana (used as anti-inflammatory and antibiotic regent, active ingredient: helenalin), St. John’s Wort (Hypericum perforatum, used for mild and moderate mood disorders or depression, active ingredient hypericin), bromelain (pineapple stem, anti-inflammatory, antibacterial, and proteolytic activity), thunder god vine (Tripterygium wilfordii, root extracts used to treat rheumatoid arthritis, bioactive component: triptolide). However, some of these herbs may have negative effects on surgical procedure or recovery, such as bleeding (ginger, ginseng, Ginkgo biloba, and garlic), immunosuppression (Echinacea), inflammation (garlic, ginkgo), wound healing (Echinacea and garlic), blood pressure and/or heart rate (Ephedra, garlic, ginseng, and goldenseal), increase anesthesia effects (Kava, St. John’s Wort, Valerian) and unexpected hormone-like effects (Saw palmetto). However, just as biological activities of these herbs remain to be confirmed by more phytochemical, clinical trials, and epidemiological studies, the potential negative effects of these commonly used herbs on aesthetic plastic and cosmetic surgeries are also not well confirmed scientifically. It is still responsible and helpful for surgeons or professionals to learn the potential effects of phytonutrients that patients take and communicate well with patients to incorporate nutritional and supplementation management into their preoperative office for optimizing surgical outcome.

6.7 Absorption and Metabolism of Phytonutrients and Their Interaction with Drugs Although we take great benefits from eating plant foods and their bioactive phytonutrients, our understanding of absorption and metabolism of phytonutrients is limited. Now it is generally accepted that the bottleneck for the alleviating nutrient deficiencies may be largely due to the limited absorption of nutrients from diets. Although exact percent absorption of most phytonutrients has yet to be determined, recent studies suggest that many important phytonutrient, such as vitamins, minerals (Ca2+, Fe2+, and Zn2+), and bioactive plant products, are not fully absorbed in the human body. Unlike a synthetic drug, phytonutrients in plant foods, or a herb or its extract, normally contain low levels of bioactive ingredients, which cause difficulties

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to trace their absorption and metabolism in gut intestine system. Moreover, some phytonutrients may be metabolized by microbial organisms lived in the gut systems [51]. The human gut is populated by an array of bacterial species that develop important metabolic and immune functions and markedly affect the nutritional and health status of the host. Phytonutrients from diets and their metabolic products may also affect, either positively like prebiotics or negatively, the gastrointestinal gut microbiota. The reciprocal interactions between the gut microbiota and phytonutrients influence their effects on human health. The gut microbiota transforms dietary compounds into different bioactive metabolites in  vivo and, in turn, plant food bioactive compounds might influence the gut microbiota composition and its physiological effects on mammalian tissues [52]. The most extensively studied plant natural products on their absorption and metabolism by mammalian models might be flavonoids. Anthocyanins and proanthocyanidins are most abundant ones in plant diets. These flavonoids most often are found to be glucuronylated or methylated in blood plasma after ingestion [53]. However, it is not clear where (intestine cells, liver, or other organs) these flavonoids are glucuronylated or methylated which could pass blood-brain barrier. Studies are designed to investigate why anthocyanins or proanthocyanidins are modified, for uptake or physiological function? The majority of the dietary anthocyanins and proanthocyanidins were catabolized into phenolic acids. It is proposed that most likely these glucuronylated or methylated flavonoids circulated in the blood and brains may exert physiological functions [54]. Many drugs are metabolized by human Cytochrome P450 class enzymes, one of the well-studied targets on phytonutrients–drug or herb–drug interaction is how phytonutrients affect P450 enzyme activity. Gurley et al. evaluated effects of several herbs, including milk thistle, black cohosh, kava, goldenseal, St. John’s Wort, Echinacea on P450 CYP2D6 activity in vivo and found only goldenseal shows significant inhibition on drug urinary recovery [55]. By searching effective research literatures, Brazier and Levine [56] identified about 50 possible drug–herb interaction pairs. Among them, 22 drug–herb pairs were supported by randomized clinical trials, case–control studies, cohort studies, case series, or case studies. Warfarin was the most common drug and St. John’s Wort was the most common herbal product reported in drug–herb interactions. Another types of

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targets of plant natural products in mammalians are transporters in intestine walls or throughout the gastrointestinal tract, liver, and kidney, that are responsible for drug absorption into body and their metabolism in liver and release through urinary system. Dietary flavonoids have been reported to exert mostly inhibitory effects on mammalian ABC transporters, and therefore affect drug absorption, metabolism and release [57]. A recent survey reports that about 49% of American elderly community with ages 57 through 85 used dietary supplements on a regular basis, and about 25% of them are at risk for a major drug–drug interaction [58].

6.8 Regulation, Manufacture, Consumer, Market, and Outlooks The governmental administration of food and drugs all has strict regulations on food and drugs in terms of manufacturing, servicing, and marketing, and usage. But they do not have a complete regulation on nutraceuticals, phytonutrients, functional foods, and their related therapeutic practices; such situation, however, is changing as market volume dramatically increases, in particularly nutraceutical, phytonutrients and phytotherapy. Due to increasing demands and relatively loose regulations, there exist many problems in manufacturing, marketing, and consumption of herbs and phytonutrients, as well as misled phytotherapy practices with various reasons. For examples, some commercially available herbs or herbal products are being marketed in the United States with little or no publicly available scientific validation of efficacy or consistency [59]. Not only variations in clinical trials of herbs or phytonutrients confuse patients or consumers, a significant limiting factor to our understanding of the use and effectiveness of phytotherapy may also be the lack of standardization of herbs and phytonutrient products. The bioactive components and composition of herbs can change over time of growth, collection, and storage. Measurement of herbs with their dry weight rather than bioactive components can generate huge variations. Furthermore, effectiveness of many herbs may not depend on only one chemical composition but a multi-component effect. There is growing evidence from clinical trials that phytotherapeutic agents may lead to subjective and objective symptom improvement beyond a placebo effect. Therefore, more researches on chemical compositions of herbs and

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phytonutrients, their dynamic changes during growth, collection and storage, as well as their biological activity are very necessary for herb quality and quantity control and standardization. More regulations are being worked out through consultations with expert panels on these products and practices, Good Manufacturing Practice (GMP) compliance, Generally recognized as safe (GRAS) status, analytical methods and validation. All claims and labels on products of phytonutrients and herbs should be accurate and substantiated by scientific evidence and should not lead to misunderstanding. While advanced education and training is also necessary, professionals, patients or consumers can contribute to knowledge discovery, translation, and outreach to improve the phytonutrients and phytotherapy development and health of populations. The safety assessment of herbs and phytonutrients is complicated and involve chemical identification of bioactive composition, quantification of the material, quality control, bioactivity and toxicity tests (including acute, subacute, subchronic, chronic and long-term toxicity studies, reproductive toxicology). In addition, although phytonutrients and phytotherapy have attracted extensive attentions and are rapidly developed, still a large portion of claims on effectiveness of herbs and phytonutrients need to be tested [60]. Using advanced technologies such as mass spectrometry for identification of chemical components of herbs and metabolism of phytonutrients in human body [61], proteomics technology for testing direct targets of phytonutrients or herbs on mammalian models or human body, and transcriptomics – the global gene expression detected by using microarray technology to probe the safety and efficacy of phytonutrients or herbs, will provide more profound and precise insights into how phytonutrients or herbs affect human health [62]. These high-throughput technologies will greatly fasten various processes such as evaluation of validity, safety, effectiveness, and mechanism of phytonutrients and herbs, even though with many challenges ahead [63]. Integration of these strategies and technologies into nutrition study, also called functional nutrition genomics, which study how food nutrients or bioactive chemicals affect the expression of genetic information in an individual and how an individual’s genetic metabolizes and responds to nutrients and bioactive compounds, now emerges as a fast-­g rowing

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and critical research area. Many hopes and great expectations on development of phytonutrients and phytotherapies might rely on functional nutrition genomics study.

References 1. Zhao J (2007) Nutraceuticals, nutritional therapy, phytonutrients, and phytotherapy for improvement of human health: a perspective on plant biotechnology application. Recent Pat Biotechnol 1(1):74–97 2. Bland JS (1996) Phytonutrition, phytotherapy, and phytopharmacology. Altern Ther Health Med 2(6):73–76 3. Eussen S, Klungel O, Garssen J, Verhagen H, van Kranen H, van Loveren H, Rompelberg C (2010) Support of drug therapy using functional foods and dietary supplements: focus on statin therapy. Br J Nutr 103(9):1260–1277 4. Ornish D, Weidner G, Fair WR, Marlin R, Pettengill EB, Raisin CJ, Dunn-Emke S, Crutchfield L, Jacobs FN, Barnard RJ, Aronson WJ, McCormac P, McKnight DJ, Fein JD, Dnistrian AM, Weinstein J, Ngo TH, Mendell NR, Carroll PR (2005) Intensive lifestyle changes may affect the progression of prostate cancer. J Urol 174(3):1065–1069 5. Chan JM, Holick CN, Leitzmann MF, Rimm EB, Willett WC, Stampfer MJ, Giovannucci EL (2006) Diet after diagnosis and the risk of prostate cancer progression, recurrence, and death (United States). Cancer Causes Control 17(2):199–208 6. Ornish D, Magbanua MJ, Weidner G, Weinberg V, Kemp C, Green C, Mattie MD, Marlin R, Simko J, Shinohara K, Haqq CM, Carroll PR (2008) Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proc Natl Acad Sci USA 105(24):8369–8374 7. Schmidt B, Ribnicky DM, Poulev A, Logendra S, Cefalu WT, Raskin I (2008) A natural history of botanical therapeutics. Metabolism 57(7 suppl 1):S3–S9 8. Graziose R, Lila MA, Raskin I (2010) Merging traditional Chinese medicine with modern drug discovery technologies to find novel drugs and functional foods. Curr Drug Discov Technol 7(1):2–12 9. Grunberger G, Jen KL, Artiss JD (2007) The benefits of early intervention in obese diabetic patients with FBCx: a new dietary fibre. Diabetes Metab Res Rev 23(1):56–62 10. Mancuso C, Barone E (2009) Curcumin in clinical practice: myth or reality? Trends Pharmacol Sci 30(7):333–334 11. Milder IE, Arts IC, van de Putte B, Venema DP, Hollman PC (2005) Lignan contents of Dutch plant foods: a database including lariciresinol, pinoresinol, secoisolariciresinol and matairesinol. Br J Nutr 93(3):393–402 12. Pasinetti GM, Ho L (2010) Role of grape seed polyphenols in Alzheimer’s disease neuropathology. Nutr Diet Suppl 2:97–103 13. Plosch T, Kruit JK, Bloks VW, Huijkman NC, Havinga R, Duchateau GS, Lin Y, Kuipers F (2006) Reduction of cholesterol absorption by dietary plant sterols and stanols in mice is independent of the Abcg5/8 transporter. J Nutr 136(8):2135–2140 14. Kris-Etherton PM, Hecker KD, Bonanome A, Coval SM, Binkoski AE, Hilpert KF, Griel AE, Etherton TD (2002) Bioactive compounds in foods: their role in the prevention

6  Phytonutrient and Phytotherapy for Improving Health of cardiovascular disease and cancer. Am J Med 113(suppl 9B):71S–88S 15. Nöthlings U, Murphy SP, Wilkens LR, Henderson BE, Kolonel LN (2007) Flavonols and pancreatic cancer risk: the multiethnic cohort study. Am J Epidemiol 166(8):924–931 16. Duncan JL, Aleman TS, Gardner LM, De Castro E, Marks DA, Emmons JM, Bieber ML, Steinberg JD, Bennett J, Stone EM, MacDonald IM, Cideciyan AV, Maguire MG, Jacobson SG (2002) Macular pigment and lutein supplementation in choroideremia. Exp Eye Res 74(3):371–381 17. Hallund J, Bugel S, Tholstrup T, Ferrari M, Talbot D, Hall WL, Reimann M, Williams CM, Wiinberg N (2006) Soya isoflavone-enriched cereal bars affect markers of endothelial function in postmenopausal women. Br J Nutr 95(6):1120–1126 18. Kong KW, Khoo HE, Prasad KN, Ismail A, Tan CP, Rajab NF (2010) Revealing the power of the natural red pigment lycopene. Molecules 15(2):959–987 19. Zhao J (2007) Plant troponoids: chemistry, biological activity, and biosynthesis. Curr Med Chem 14(24):2597–2621 20. Balint GA (2001) Artemisinin and its derivatives: an important new class of antimalarial agents. Pharmacol Ther 90(2–3):261–265 21. Marangoni F, Poli A (2010) Phytosterols and cardiovascular health. Pharmacol Res 61(3):193–199 22. Rideout TC, Harding SV, Jones PJ (2010) Consumption of plant sterols reduces plasma and hepatic triglycerides and modulates the expression of lipid regulatory genes and de novo lipogenesis in C57BL/6 J mice. Mol Nutr Food Res 54(suppl 1):S7–S13 23. Heinrichs SC (2010) Dietary omega-3 fatty acid supplementation for optimizing neuronal structure and function. Mol Nutr Food Res 54(4):447–456 24. Lopez-Huertas E (2010) Health effects of oleic acid and long chain omega-3 fatty acids (EPA and DHA) enriched milks. A review of intervention studies. Pharmacol Res 61(3):200–207 25. Psota TL, Gebauer SK, Kris-Etherton P (2006) Dietary omega-3 fatty acid intake and cardiovascular risk. Am J Cardiol 98(4A):3i–8i 26. Nagao K, Yanagita T (2010) Medium-chain fatty acids: functional lipids for the prevention and treatment of the metabolic syndrome. Pharmacol Res 61(3):208–212 27. Martena B, Pfeuffer M, Schrezenmeir J (2006) Mediumchain triglycerides. Int Dairy J 16:1374–1382 28. Fürst P, Stehle P (2004) What are the essential elements needed for the determination of amino acid requirements in humans? J Nutr 134(6 suppl):1558S–1565S 29. McDougall J (2002) Plant foods have a complete amino acid composition. Circulation 105(25):e197 30. Bhathena SJ, Velasquez MT (2002) Beneficial role of dietary phytoestrogens in obesity and diabetes. Am J Clin Nutr 76(6):1191–1201 31. Lotito SB, Frei B (2006) Consumption of flavonoid-rich foods and increased plasma antioxidant capacity in humans: cause, consequence, or epiphenomenon? Free Radic Biol Med 41(12):1727–1746 32. Chen ZY, Peng C, Jiao R, Wong YM, Yang N, Huang Y (2009) Anti-hypertensive nutraceuticals and functional foods. J Agric Food Chem 57(11):4485–4499 33. Rosch W, Liebregts T, Gundermann KJ, Vinson B, Holtmann G (2006) Phytotherapy for functional dyspepsia: a review of

57 the clinical evidence for the herbal preparation STW5. Phytomedicine 13(suppl 5):114–121 34. Hijikata Y, Yasuhara A, Yoshida Y, Sento S (2006) Traditional Chinese medicine treatment of epilepsy. J Altern Complement Med 12(7):673–677 35. Rosenbaum CC, O’Mathúna DP, Chavez M, Shields K (2010) Antioxidants and antiinflammatory dietary supplements for osteoarthritis and rheumatoid arthritis. Altern Ther Health Med 16(2):32–40 36. Saxena VS, Venkateshwarlu K, Nadig P, Barbhaiya HC, Bhatia N, Borkar DM, Gill RS, Jain RK, Katiyar SK, Nagendra Prasad KV, Nalinesha KM, Nasiruddin K, Rishi JP, Roy Chowdhury J, Saharia PS, Thomas B, Bagchi D (2004) Multicenter clinical trials on a novel polyherbal formulation in allergic rhinitis. Int J Clin Pharmacol Res 24(2–4):79–94 37. Xue CC, Thien FC, Zhang JJ, Da Costa C, Li CG (2003) Treatment for seasonal allergic rhinitis by Chinese herbal medicine: a randomized placebo controlled trial. Altern Ther Health Med 9(5):80–87 38. Kaufeler R, Polasek W, Brattstrom A, Koetter U (2006) Efficacy and safety of butterbur herbal extract Ze 339 in seasonal allergic rhinitis: postmarketing surveillance study. Adv Ther 23(2):373–384 39. Wagner H (2006) Multitarget therapy – the future of treatment for more than just functional dyspepsia. Phytomedicine 13(suppl 5):122–129 40. Agbabiaka TB, Pittler MH, Wider B, Ernst E (2009) Serenoa repens (saw palmetto): a systematic review of adverse events. Drug Saf 32(8):637–647 41. Tacklind J, MacDonald R, Rutks I, Wilt TJ. (2009) Serenoa repens for benign prostatic hyperplasia. Cochrane Database Syst Rev 2:CD001423 42. Roy S, Rink C, Khanna S, Phillips C, Bagchi D, Bagchi M, Sen CK (2004) Body weight and abdominal fat gene expression profile in response to a novel hydroxycitric acid-based dietary supplement. Gene Expr 11(5–6):251–262 43. Demonty I, Ras RT, van der Knaap HC, Duchateau GS, Meijer L, Zock PL, Geleijnse JM, Trautwein EA (2009) Continuous dose-response relationship of the LDLcholesterol-lowering effect of phytosterol intake. J Nutr 139(2):271–284 44. Stohs SJ, Preuss HG, Ohia SE, Kaats GR, Keen CL, Williams LD, Burdock GA (2009) No evidence demonstrating hepatotoxicity associated with hydroxycitric acid. World J Gastroenterol 15(14):4087–4089 45. Shiffman MA (2001) Warning about herbals in plastic and cosmetic surgery. Plast Reconstr Surg 108(7):2180–2181 46. Shiffman MA (2007) Facial aging: a clinical classification. Indian J Plast Surg 40(2):178–180 47. Rahm D (2005) Perioperative nutrition and nutritional supplements. Plast Surg Nurs 25(1):21–28 48. Ang-Lee MK, Moss J, Yuan CS (2001) Herbal medicines and perioperative care. J Am Med Assoc 286(2):208–216 49. Rowe DJ, Baker AC (2009) Perioperative risks and benefits of herbal supplements in aesthetic surgery. Aesthet Surg J 29(2):150–157 50. Heller J, Gabbay JS, Ghadjar K, Jourabchi M, O’Hara C, Heller M, Bradley JP (2006) Top-10 list of herbal and supplemental medicines used by cosmetic patients: what the plastic surgeon needs to know. Plast Reconstr Surg 117(2):436–445

58 51. Manach C, Williamson G, Morand C, Scalbert A, Rémésy C (2005) Bioavailability and bioefficacy of polyphenols in humans. I. Review of 97 bioavailability studies. Am J Clin Nutr 81(1 suppl):230S–242S 52. Laparra JM, Sanz Y (2010) Interactions of gut microbiota with functional food components and nutraceuticals. Pharmacol Res 61(3):219–225 53. Spencer JP, Schroeter H, Kuhnle G, Srai SK, Tyrrell RM, Hahn U, Rice-Evans C (2001) Epicatechin and its in  vivo metabolite, 3’-O-methyl epicatechin, protect human fibroblasts from oxidative-stress-induced cell death involving caspase-3 activation. Biochem J 354(Pt 3):493–500 54. McGhie TK, Walton MC (2007) The bioavailability and absorption of anthocyanins: towards a better understanding. Mol Nutr Food Res 51(6):702–713 55. Gurley BJ, Swain A, Hubbard MA, Williams DK, Barone G, Hartsfield F, Tong Y, Carrier DJ, Cheboyina S, Battu SK (2008) Clinical assessment of CYP2D6-mediated herb-drug interactions in humans: effects of milk thistle, black cohosh, goldenseal, kava kava, St John’s Wort, and Echinacea. Mol Nutr Food Res 52(7):755–763 56. Brazier NC, Levine MA (2003) Drug-herb interaction among commonly used conventional medicines: a compendium for health care professionals. Am J Ther 10(3): 163–169 57. Brand W, Schutte ME, Williamson G, van Zanden JJ, Cnubben NH, Groten JP, van Bladeren PJ, Rietjens IM

J. Zhao (2006) Flavonoid-mediated inhibition of intestinal ABC transporters may affect the oral bioavailability of drugs, food-borne toxic compounds and bioactive ingredients. Biomed Pharmacother 60(9):508–519 58. Qato DM, Alexander GC, Conti RM, Johnson M, Schumm P, Lindau ST (2008) Use of prescription and over-the-counter medications and dietary supplements among older adults in the United States. J Am Med Assoc 300(24):2867–2878 59. Ribnicky DM, Poulev A, Schmidt B, Cefalu WT, Raskin I (2008) Evaluation of botanicals for improving human health. Am J Clin Nutr 87(2):472S–475S 60. Blundell J (2010) Making claims: functional foods for managing appetite and weight. Nat Rev Endocrinol 6(1):53–56 61. Bino RJ, Hall RD, Fiehn O, Kopka J, Saito K, Draper J, Nikolau BJ, Mendes P, Roessner-Tunali U, Beale MH, Trethewey RN, Lange BM, Wurtele ES, Sumner LW (2004) Potential of metabolomics as a functional genomics tool. Trends Plant Sci 9(9):418–425 62. Gibney MJ, Walsh M, Brennan L, Roche HM, German B, van Ommen B (2005) Metabolomics in human nutrition: opportunities and challenges. Am J Clin Nutr 82(3): 497–503 63. Astle J, Ferguson JT, German JB, Harrigan GG, Kelleher NL, Kodadek T, Parks BA, Roth MJ, Singletary KW, Wenger CD, Mahady GB (2007) Characterization of proteomic and metabolomic responses to dietary factors and supplements. J Nutr 137(12):2787–2793

7

Skin Imaging in Aesthetic Medicine Peter M. Prendergast

7.1 Introduction Several procedures in aesthetic medical practice focus on improving the appearance and texture of the skin. Homogeneity of skin texture and color play an important role in facial attractiveness [1]. Intense pulsed light devices and certain lasers target brown and red chromophores to clear the skin by reducing unwanted melanin and hemoglobin, respectively. Resurfacing chemical peels and lasers ablate epidermal and dermal layers, improving skin texture and clarity. Recently, nonablative laser rejuvenation and tissue tightening using light and radiofrequency have emerged as useful treatment modalities that heat the dermis and improve skin texture by remodeling and increasing collagen [2, 3]. These less aggressive methods usually require multiple treatments and show gradual, subtle improvement. Although “naked eye” assessment and color photography of the skin remain important for skin examination and documenting changes before and after aesthetic procedures, they do not highlight individual chromophores or provide quantitative information and are prone to significant interobserver variability [4]. Skin imaging devices that visualize and display information on epidermal and dermal chromophores, skin texture, and wrinkles have emerged as valuable tools for skin analysis in aesthetic medicine [5]. Using cross-polarized diffuse reflectance imaging and appropriate algorithmic computer software, quantitative assessments of hemoglobin and melanin can be made [6]. P.M. Prendergast  Venus Medical, Heritage House, Dundrum Office Park, Dublin 14, Ireland e-mail: [email protected]

Images define the nature and extent of the problem being treated, document before-and-after comparisons, and facilitate the monitoring of skin changes over time. They also have a role as evidence in medical legal scenarios. Newer skin imaging devices produce excellent threedimensional images and provide quantitative information on melanin, hemoglobin, skin roughness, and wrinkle depth. Novel devices that perform quantitative analyses are likely to play an increasingly important role in research and in studies that compare treatment modalities or devices in aesthetic medicine. A comparison of skin imaging devices useful in aesthetic medicine is provided in Table 7.1.

7.2 Digital Photography Digital photography has largely replaced film photography in medical and skin imaging since the development of single lens reflex (SLR) cameras (Fig. 7.1). Although they are more bulky than compact cameras, SLR cameras are capable of producing exquisite images, and allow the user customize image capturing with different lenses, auxiliary flashes, and by optimizing settings such as optical zoom and white balance [7]. For detailed imaging of the skin’s surface, a macro lens with a focal length of 60–100 mm is appropriate, whereas a focal length of about 18–55 mm is sufficient for full-face imaging. All beforeand-after photographs in aesthetic medicine should be taken with consistent positioning and lighting to ensure comparisons are accurate. Although flash photography provides excellent lighting consistency, a point flash rather than ring flash should be used so that some shadowing is possible. Shadows improve the perception of the skin’s surface texture, and depth of wrinkles and folds.

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_7, © Springer-Verlag Berlin Heidelberg 2011

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P.M. Prendergast

Table 7.1  Comparison of devices for skin imaging in aesthetic medicine

Portable Data collection Full facial imaging Hemoglobin visualization Hemoglobin measurement Melanin visualization Melanin measurement Collagen visualization Rhytid measurement Independent of lighting conditions 3D capabilities Easy report printing

FotoFinder Dermoscope Yes Yes No No

PRIMOS 3D

VISIA

3D Lifeviz Aesthetic

Clarity Pro Advanced

Antera 3D

Yes Yes No No

No Yes Yes Yes

Yes Yes Yes No

No Yes Yes Yes

Yes No Yes Yes

No

No

No

No

Yes

Yes

Yes

No

Yes

No

Yes

Yes

No

No

No

No

Yes

Yes

No

No

No

No

No

No

No Yes

Yes Yes

Yes No

Yes No

Yes No

Yes Yes

No Yes

Yes Yes

No Yes

Yes Yes

No Yes

Yes Yes

and cross-polarized viewers enable clear visualization of pigmentation, pigment structure, vascular pattern, and the border of lesions under scrutiny. Dermoscopy is particularly useful for the differentiation of benign and malignant skin lesions and to monitor pigmented lesions for the early detection of skin cancer. Several dermoscopes are available including the FotoFinder Dermoscope (FotoFinder Systems, Inc., Columbia, MD, USA) and the LiteScope (Quantificare S.A., Cedex, France).

7.3.2 Spectrophotometric Intracutaneous Analysis (SIA)

Fig. 7.1  Single lens reflex (SLR) camera for high-quality photographic documentation before and after aesthetic procedures

The SIAscope delivers harmless radiation at wavelengths of 400–950  nm into the skin. The reflected light is measured, analyzed, and displayed as a graphical representation of the amount of melanin, hemoglobin, and collagen in the epidermis or papillary dermis. The SIAscope is portable and easy to use and is used with various software applications, such as MoleMate and MoleView to aid in the diagnosis of melanoma and nonmelanoma skin cancers [8, 9].

7.3 Skin Imaging Modalities 7.3.1 Dermoscopy

7.3.3 Optical Profilometry

Dermoscopy, or epiluminescence microscopy, is useful for the evaluation of cutaneous lesions by imaging surface and subsurface structures using polarized light. Magnification

This technique is used to measure the roughness of skin or size of fine lines and wrinkles. A silicone or rubber dental impression material is used to make a cast of the

7  Skin Imaging in Aesthetic Medicine

skin’s surface. Then tangential lighting is cast across the replica such that the shadows created reveal the microtopography of the skin. A digital camera, scanner, or stereomicroscope captures the shadows and changes the negative appearance of the replica into a positive one [10]. Although this method of measuring wrinkle size and depth is accurate, the technique can take up to an hour and has largely been replaced by more efficient methods, such as 3D computerized imaging.

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coupled device (CCD) chip of a high-resolution ­camera [14]. It is used to measure skin topography and provide quantitative analysis of wrinkles and roughness [15]. Although the PRIMOS device is regarded as more accurate than the commonly used silicon replica technique [16], it does not measure chromophores in the skin and therefore its use in aesthetic medicine is limited.

7.4.2 Visia 7.3.4 Reflectance Confocal Microscopy Reflectance confocal microscopy and confocal laser scanning microscopy allow detailed high-resolution images of the skin to be taken noninvasively. The Vivascope 1500 (Lucid, Rochester, NY, USA) uses a diode laser with an 830-nm wavelength to image epidermal and dermal structures. In practice, this allows accurate characterization of pigmented and nonpigmented skin lesions, greatly assisting diagnosis. The near histologic resolution of reflectance confocal microscopy also identifies features associated with aging and UV damage, including spongiosus, sunburn cells, micro-vesicles, and vascular dilatation [11].

The Visia Complexion Analysis system (Canfield Scientific Inc., NJ, USA) utilizes photography and imaging software to provide full facial visualization of hemoglobin and melanin, and a quantitative analysis of skin texture and facial wrinkles. Canfield systems are designed to produce consistently positioned beforeand-after images by using chin and forehead rests as well as a guide light. The VISIA system has multiple applications in aesthetic medicine including the evaluation of outcomes following skin rejuvenation with lasers [17, 18].

7.4.3 3D Lifeviz Aesthetic 7.3.5 High Frequency Ultrasound High frequency ultrasound can be used to image the topography and intradermal structures of sliced or in vivo skin using ultrasound impedance imaging and 3D ultrasound imaging, respectively [12]. In aesthetic medicine, skin-targeted ultrasound represents a noninvasive means of imaging pores, surface irregularities, and age-related dermal changes [13]. Features associated with photoaging, such as a subepidermal low-echogenic band, can be monitored before and after aesthetic medical procedures to determine their efficacy.

7.4 Optical Imaging Devices 7.4.1 PRIMOS PRIMOSlite (GFMesstechnik GmbH, Berlin, Germany) is a 32 × 32 mm microtopography imaging system that projects light onto the surface of the skin with a Digital Micromirror Device (DMD; Texas Instruments, Irving, TX, USA) and records the image on the charged

3D Lifeviz Aesthetic (Quantificare S.A., Cedex, France) uses plain photography, stereovision technology, and patented DermaPix® software to produce full facial 3D images for comparison of volume, contours, and wrinkles before and after aesthetic procedures. A newer product produced by Quantificare, 3D Lifeviz Micro, is a portable system for the visualization and measurement of wrinkles, scars, and roughness in localized regions. This technology provides no information on melanin or hemoglobin.

7.4.4 Clarity Pro Advanced This system provides full facial imaging in front, left, and right profile positions using multi-spectral lighting to produce white light and blue light images. As well as providing visualization and quantitative information on rhytids, redness, UV damage, and pigmentation, fluorescence spectroscopy is utilized to identify porphyrins produced by Propionibacterium acnes in oily and acne prone skin. Clarity Pro Advanced is a product of Brigh Tex Bio-Photonics (BTBP), located in California, USA.

62 Fig. 7.2  (a) Antera 3D portable hand-held imaging device. (b) Images are captured instantly and displayed on a computer monitor or laptop

P.M. Prendergast

a

b

7.4.5 Antera 3D The Antera 3D skin imaging system (Miravex, Dublin, Ireland) uses a hand-held, portable camera and software with complex algorithms to convert light reflected from the skin’s surface into digital images that display topography, hemoglobin, and melanin (Fig. 7.2). The camera uses various light-emitting diodes and polarizers to illuminate a 60 × 60 mm area of the face and capture reflected light independent of surrounding lighting conditions (Fig.  7.3). Once captured, the

image can be manipulated in several ways using the user-friendly interface (Fig.  7.4). The image is first selected as either flat or 3D. The contour of the captured area is visualized by selecting the Contour tab and filtering for small, medium, or large wrinkles (Fig. 7.5). The roughness of skin or size of individual wrinkles and folds is measured using clickable tools that allow selection of any area of the image (Fig. 7.6). Melanin and hemoglobin are visualized and measured in a similar way. The imaging serves to highlight the nature and extent of skin surface and pigment irregularities and guide treatment accordingly (Fig. 7.7).

7  Skin Imaging in Aesthetic Medicine

63

a

b

c

d

Fig. 7.3  (a–d) Images displayed independent of surrounding lighting conditions. A directional light tool allows light and shadows to be changed and manipulated

A matching tool incorporated into the Antera 3D interface allows accurate before-and-after comparisons. Improvement in facial redness, roughness, and melanin homogeneity is measured following resurfacing, collagen stimulating, and laser vascular therapies (Fig. 7.8). Using the report tool, comparisons between images are presented in a graphic format.

7.5 Conclusions Skin imaging technologies have become more sophisticated in recent years. Multiphoton microscopy has emerged as a sophisticated method of imaging the detailed morphology of epithelial and dermal structures [19]. In aesthetic medical practice, however, hand-held, portable devices are likely to be more useful [20].

64

P.M. Prendergast

a

a

b

b

c

c

d Fig. 7.4  The user-friendly Antera 3D interface. (a) Filters for small, medium, and large wrinkles. (b) Main selection panel for normal color image, contour (topography), melanin, and hemoglobin. (c) Directional light tool. (d) Main controls for selecting an area for quantitative evaluation, matching before-and-after images, creating a report, and saving an image

Fig. 7.5  Filters for contour analysis. (a) Small wrinkles. This highlights superficial rhytids and skin texture as well as pores and acne scarring. (b) Medium wrinkles. This filter is useful to show deeper lines such as nasolabial folds. (c) The large wrinkle filter is more appropriate to visualize facial contours and volume loss

7  Skin Imaging in Aesthetic Medicine

a

65

c

b

Fig. 7.6  Quantitative skin analysis. (a) Individual wrinkles are selected to measure the overall size, width, and depth of the line. (b) Any area can be measured using a rectangular selection tool.

The selection in the after image is automatically matched using the anchor tool. (c) A circular selection tool is also available

By analyzing the wavelengths of light reflected from the skin’s surface using detailed algorithmic software, quantitative information on surface and subsurface structures is obtained. By measuring the topography of the skin, melanin distribution and content, and extent of hemoglobin, a plan of targeted skin rejuvenation can be implemented with definite goals in mind. Moreover,

measuring changes with serial imaging guides ­treatment programs and helps determine the efficacy of different procedures and different technologies. Providing patients with quantitative reports that illustrate the beneficial effects of treatments encourages them to continue with maintenance programs that improve results further over time.

66

P.M. Prendergast

a

b

c

d

Fig. 7.7  3D skin imaging of an area of active acne and acne scarring. (a) Color image. (b) Contour image showing the topography of the skin with deeper scars represented in purple. (c)

Melanin view showing areas of hypopigmentation within scars. (d) Hemoglobin view with increased vascularity in area of inflammation

7  Skin Imaging in Aesthetic Medicine

67

a

b

c

d

Fig.  7.8  (a) Melanin view before. (b) Two weeks after fractional CO2 laser skin resurfacing. (c) Contour view before. (d) After fractional CO2 laser skin resurfacing. Using the Antera 3D

system, quantitative analysis is possible so that an absolute and percentage improvement can be shown following treatments

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References 1. Fink B, Grammer K, Thornhill R (2001) Human (Homo sapiens) facial attractiveness in relation to skin texture and color. J Comp Psychol 115(1):92–99 2. Kaplan H, Gat A (2009) Clinical and histopathological results following TriPollar radiofrequency skin treatments. J Cosmet Laser Ther 11(2):78–84 3. Dierickx CC (2006) The role of deep heating for noninvasive skin rejuvenation. Lasers Surg Med 38(9):799–807 4. Stefanowska J, Zakowiecki D, Cal K (2010) Magnetic resonance imaging of the skin. J Eur Acad Dermatol Venereol 24(8):875–880 5. Bargo PR, Kollias N (2010) Measurement of skin texture through polarization imaging. Br J Dermatol 162(4):724–731 6. Jung B, Choi B, Durkin AJ, Kelly KM, Nelson JS (2004) Characterization of port wine stain skin erythema and melanin content using cross-polarized diffuse reflectance imaging. Lasers Surg Med 34(2):174–181 7. Bhatia AC, Molenda MA, Heffernan MP, Roach D (2009) Imaging. In: Kaminer MS, Arndt KA, Dover JS, Rohrer TE, Zachary CB (eds) Atlas of cosmetic surgery. Saunders Elsevier, Philadelphia, p 46 8. Moncrieff M, Cotton S, Claridge E, Hall P (2002) Spectrophotometric intracutaneous analysis: a new technique for imaging pigmented skin lesions. Br J Dermatol 146(3):448–457 9. Tehrani H, Walls J, Price G, Cotton S, Sassoon E, Hall P (2006) A novel imaging technique as an adjunct to the in vivo diagnosis of nonmelanoma skin cancer. Br J Dermatol 155(6):1177–1183 10. Hatzis J (2004) The wrinkle and its measurement—a skin surface profilometric method. Micron 35(3):201–219 11. Ulrich M, Rüter C, Astner S, Sterry W, Lange-Asschenfeldt B, Stockfleth E, Röwert-Huber J (2009) Comparison of

P.M. Prendergast UV-induced skin changes in sun exposed vs. sun-protected skin—preliminary evaluation by reflectance confocal microscopy. Br J Dermatol 161(suppl 3):46–53 12. Saijo Y, Kobayashi K, Okada N, Hozumi N, Hagiwara Y, Tanaka A, Iwamoto T (2008) High frequency ultrasound imaging of surface and subsurface structures of fingerprints. Conf Proc IEEE Eng Med Biol Soc 2008:2173–2176 13. Lacarrubba F, Tedeschi A, Nardone B, Micali G (2008) Mesotherapy for skin rejuvenation: assessment of the subepidermal low-echogenic band by ultrasound evaluation with cross-sectional B-mode scanning. Dermatol Ther 21(suppl 3):S1–5 14. Friedman PM, Skover GR, Payonk G, Geronemus RG (2002) Quantitative evaluation of nonablative laser technology. Semin Cutan Med Surg 21(4):266–273 15. Hsu J, Skover G, Goldman MP (2007) Evaluating the efficacy in improving facial photodamage with a mixture of topical antioxidants. J Drugs Dermatol 6(11):1141–1148 16. Gold MH, Goldman MP, Biron J (2007) Human growth factor and cytokine skin cream for facial skin rejuvenation as assessed by 3D in  vivo optical skin imaging. J Drugs Dermatol 6(10):1018–1023 17. Lee MC, Hu S, Chen MC, Shih YC, Huang YL, Lee SH (2009) Skin rejuvenation with 1,064-nm Q-switched Nd:YAG laser in Asian patients. Dermatol Surg 35(6):929–932 18. Kulick MI, Gajjar NA (2007) Analysis of histologic and clinical changes associated with Polaris WR treatment of facial wrinkles. Aesthet Surg J 27(1):32–46 19. Lin SJ, Jee SH, Dong CY (2007) Multiphoton microscopy: a new paradigm in dermatological imaging. Eur J Dermatol 17(5):361–366 20. Fisk NA, Jensen K, Knaggs H, Ferguson S (2010) The clinical utility of a hand-held computerized optical imaging system at assessing skin discoloration. J Cosmet Dermatol 9(2):103–107

8

Cosmeceutical Treatment of the Aging Face Jennifer Linder

8.1 Introduction The increased consumer interest in skin health and appearance combined with a confusing and expansive cosmetic marketplace has led patients to seek educated product recommendations from their physicians. To effectively and ethically deliver on this patient expectation, physicians must understand the intricacies of the skin’s aging process and be aware of the topical ingredients currently available, their mechanisms of action and their efficacy. Clinically proven topical therapies can work to correct many of the visible signs of aging skin and support and enhance the outcomes of more invasive procedures.

8.2 Common Presentations of Visible Aging Structural breakdown of the skin occurs as a result of both intrinsic and extrinsic aging and involves multiple pathological processes. Topical cosmeceuticals are typically formulated to address specific agerelated cutaneous challenges. Identifying the most effective and proven ingredient blends allows the physician to provide patients with topical solutions to correct and prevent the foremost causes of visible facial aging. This can be accomplished by addressing extracellular matrix degradation, textural variances,

J. Linder  6710 Camelback Road, Suite 230, Scottsdale, AZ 85251, USA e-mail: [email protected]

and dyschromias. This chapter will review these ­common causes of visible aging and the proven cosmeceuticals for their correction. The primary cause of cutaneous aging is a result of matrix degradation, which presents as sagging, laxity, rhytids, atrophy, and enlarged pores. Effective therapies are usually designed to protect the existing matrix with sunscreens, antioxidants, and matrix metalloproteinase inhibitors (MMPi) while triggering new matrix production with collagen-building ingredients like retinoids, vitamin C, and peptides. Another common feature of aging skin is textural variances, which present as dryness, dehydration, and coarsening of the skin. These can be reversed with alpha hydroxy acids (AHA), mechanical exfoliators, humectants, and occlusives. The dyschromias typically seen as a result of aging can be effectively addressed with the use of melanogenesis inhibitors. All of these presentations of aging and their possible treatments must be considered when evaluating a patient and making specific recommendations for skin care.

8.3 Matrix Degradation The majority of a healthy dermis is the extracellular matrix (ECM), which is a complex framework of bio­ molecules designed to support and protect the dermal cells. The structural proteins (collagen and elastin), adhesive proteins (laminins and fibronectin), glycosa­ minoglycans (GAG), and proteoglycans that comprise the ECM degrade naturally due to chronological intrinsic aging. Degradation is accelerated by the exogenous causes of extrinsic aging – primarily UV exposure and the resultant oxidative stress and matrix

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_8, © Springer-Verlag Berlin Heidelberg 2011

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­ etalloproteinase (MMP) upregulation [1]. MMP m enzymes, such as collagenase, elastase and hyaluronidase are responsible for the natural recycling and destroying of the ECM’s components that are no longer useful. MMP also play a role in tumorigenesis [2]. Although a small amount of these enzymes are necessary for healthy skin, an overproduction occurs in response to external damaging factors – particularly UV radiation – accelerating matrix breakdown. The expression of MMP is increased with as little as 0.1 minimal erythema dose (MED) (1/10 of the dose of UV exposure required to develop erythema) [3]. It has been demonstrated that the degeneration of dermal collagen fiber bundles (DCFB) is more acute and severe in photodamaged skin [4]. Aged skin as a result of ECM degradation presents with varying degrees of visible sagging and laxity, rhytids, epidermal and dermal atrophy, and enlargement of pores.

8.4 Sagging and Laxity Many factors contribute to the lax appearance of aged skin. Over time, the effects of gravity certainly play a role [5], yet loss of facial volume [6, 7] as a result of the resorption of facial bones [8] and the atrophy of adipose tissue [9], compounded by the degradation of the critical structural components of the dermis, plays a larger role. This occurs due to chronological aging; however, it is exacerbated dramatically by extrinsic factors, particularly UV exposure. The structural and elastic components of the dermis provide youthful skin with support, volume and the ability to stretch and return to its original form. This well-organized framework develops a decreased functionality in aged skin. Sun-protected dermal skin typically decreases in thickness by about 20% after 80 years of age. Sun-exposed skin, in contrast, thins significantly earlier [10, 11]. This strongly supports the daily use of broad-spectrum UV protection as a critical step to preserving a youthful facial appearance. Photodamage is a clear and well-documented cause of premature skin aging and matrix degradation [1, 12, 13]. This can be attributed to an increase of UVB-induced radicals as well as an intensification of MMP activity [14, 15]. Radicals are highly reactive species due to unpaired electrons in their outer shell. There are many types of free radicals, yet reactive oxygen species (ROS) are widely studied due to their damaging effects in the skin. ROS include hydroxyl radicals, nitric oxide,

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peroxynitrite, superoxide anions, peroxide, triplet ­oxygen, and singlet oxygen. An increase of MMP-1 causes collagen fibrils to cleave. Collagen is then increasingly weakened by MMP-3 and MMP-9 activity. These degenerated collagen fibrils are re-stabilized through the formation of intermolecular crosslinks [1]. In addition to crosslinks between collagen fibrils, it has been demonstrated that while the collagen fibers develop indistinct outlines and a smaller diameter with age, the elastic fibers become shorter and thicker, resulting in a general loss of dermal integrity [4]. Additionally, the increase of the MMP elastase negatively affects the elastic fibers’ ability to maintain youthful facial turgor.

8.5 Rhytids: Fine Lines and Deeper Wrinkling Estrogen contributes in the skin as a modulator of connective tissue components, namely collagen and hyaluronic acid (HA). As estrogen production diminishes with age, collagen and HA are not replaced as readily as in young skin [16], making wrinkling a common visible presentation of aging skin. Superficial rhytids begin to form due to this slowing of collagen production [17]. The reduction of HA production results in skin dehydration that further exacerbates the appearance of fine lines [18]. Decreased estrogen levels with advancing age also slow cell regeneration and the production of ECM components. This degeneration of the skin’s matrix is, as stated previously, exacerbated by UV exposure over a patient’s lifetime. More advanced, deeper wrinkling is primarily a result of overexposure to extrinsic factors. UVA-induced breakdown and crosslinking of collagen has been ­well-demonstrated, as is the escalated degeneration of collagen and elastic fibers due to an increase in elastase and collagenase expression [17, 19]. In addition, the repeated muscular contractions demonstrated in facial expressions lead to dynamic wrinkling, including lines in the glabella, forehead and crows’ feet as well as perioral vertical lines due to aging and smoking [20, 21].

8.6 Epidermal and Dermal Atrophy The loss of facial volume that contributes to an aged appearance is compounded by the atrophy of both the epidermis and the dermis. As mentioned, the

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age-dependent drop in estrogen levels during perimenopause and menopause slows the production of matrix components [16, 22, 23]. It is also evident that UV exposure not only degrades mature collagen but also impedes the formation of new collagen by downregulating both type I and type II procollagen gene expression [24]. This dermal atrophy contributes substantially to visible facial aging. Age-related degeneration of the epidermis includes: enlarged corneocyte surface area, flattening and reduced adherence of the keratinocytes, and an overall slowing of cell turnover [25–27]. Additionally, the flattening of the rete ridges leads to an epidermis that appears thin and fragile and is nourished less effectively [5].

8.7 Enlarged Pores Another common visible characteristic of aged skin is enlarged pores. This is due to a disorganized and degenerated collagen and elastin network providing reduced support to the follicle walls [28]. In advanced age, and with cumulative ultraviolet exposure, these enlarged pores can progress to solar comedones [29].

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8.9 Broad-Spectrum UV Protection Because sunscreens can limit UV-induced skin damage and MMP production, they are accepted as the most active and beneficial of the anti-aging products [30]. Understanding the variety of ingredients available and their individual advantages and disadvantages will allow a physician to make more informed recommendations regarding the use of sunscreens. Sunscreens can have either chemical or physical ingredients or a combination of both. It is critical for skin health and age-controlling benefits that the product protects against both UVB and UVA wavelengths, as UVA has the ability to penetrate into the dermis and breakdown the ECM due to its longer wavelength. Unfortunately, only four of the ingredients currently approved by the FDA ­provide true broad-UVA-spectrum protection. For this reason, a broad-spectrum sunscreen should include one of the following: avobenzone, ecamsule, zinc oxide, or titanium dioxide. A blend of multiple ingredients is typically necessary to provide “ideal” sunscreen protection. Sunscreen ingredient regulations differ around the world. Refer to Table 8.1 for a list of FDA-approved sunscreen ingredients and their corresponding wavelength-absorbing/reflecting capabilities.

8.8 Topical Therapies for Collagen and Matrix Protection

8.10 Chemical Sunscreen Agents

One must consider that each patient’s skin represents a unique combination of their DNA, environment, lifestyle choices, and product usage. Patients that exhibit dramatic degeneration of critical matrix components, due to overexposure to UV rays, smoking and other exogenous offenders, may require more invasive therapies to ameliorate their visible facial degradation. That said, even patients with advanced matrix breakdown can benefit from the use of proven topicals to impede further destruction. The most efficacious treatment plans for aging skin typically combine potent protection of the existing matrix in addition to the use of topical therapies to promote the deposition of new matrix components. A combination of broad-spectrum sunscreens, MMPi and a range of proven antioxidants provide the skin with excellent matrix-protecting benefits. When used with collagen-building ingredients like vitamin C, retinoids and peptides, dramatic improvements in the ECM can be demonstrated. The final outcome is healthier and more attractive skin.

A chemical sunscreen is an organic substance that penetrates the corneocytes and absorbs UV rays before they affect the skin. Although some patients avoid chemical sunscreens out of concern for skin sensitivities, these concerns are typically misdirected, as most reactions are due to a product’s base rather than its OTC active ingredients [31, 32]. Para-aminobenzoic acid (PABA) was among the first chemical sunscreens to be approved by the FDA. While it is an effective UVB absorber, PABA has become nearly extinct in current sunscreen preparations due to photoallergy concerns [33]. Octyl dimethyl PABA, or Padimate O, is an aminobenzoic acid derivative that was introduced as a less sensitizing alternative to PABA. Other PABA derivatives, such as glyceryl PABA (glyceryl aminobenzoate) and padimate A (amyldimethyl PABA) are available in other countries but are not FDA-approved [34]. PABA-free marketing claims have ultimately led to decreased use of PABA derivatives throughout the industry.

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Table 8.1  UV attenuation of commonly used FDA-approved sunscreen agents. Adapted from [176] UVA

UVB

400

390

380

370

360

350

340

330

320

310

300

290

Ensulizole Octisalate Homosalate Octyldimethyl PABA Octinoxate Octocrylene Oxybenzone Meradimate Titanium dioxide Zinc oxide Ecamsule Avobenzone Attenuated UV Peak absorbency

Cinnamates are the most widely used chemical sunscreen agents on the market [35]. This category of sunscreens encompasses UVB shielding ingredients octinoxate (octyl methoxycinnamate) and cinoxate. Allergic reactions are uncommon with cinnamates, which has led to their popularity; however, they typically must be used in conjunction with other UVB absorbers in order to provide adequate protection [36]. Octocrylene (2-ethylhexyl-2-cyano-3,3 diphenylacrylate) offers weak UVB-absorbency yet has impressive stability. Octocrylene is often used to prolong the activity of other sunscreen agents and also to improve water resistance [34, 35]. Salicylates include octisalate (octyl salicylate) and homosalate (homomenthyl salicylate). These agents offer UVB protection and are considered nonsensitizing sunscreens [37]. Salicylates are often referred to as weak sunscreen agents; however, their excellent safety profile contributes to their sustained use in the industry [38]. Like cinnamates, salicylates are most often used in conjunction with other UV filters. Phenylbenzimidazole sulfonic acid is typically referred to as ensulizole. The use of ensulizole in topical preparations is relatively rare despite a decent safety record and a light feel [39]. Ensulizole is one of many UVB absorbing agents and it offers virtually no UVA attenuation, which may explain the rarity of its use [40]. Benzophenones are unique in that they offer UVB absorbency as well as weak UVA protection. Several benzophenones are available, including oxybenzone, dioxybenzone and sulisobenzone. Benzophenones are now considered the most sensitizing of the chemical sunscreens, although reactions are still relatively

rare [41]. While these agents do expand narrowly into the UVA spectrum, products containing benzophenones should not be considered truly broadspectrum [42]. Anthranilates are salts or esters of anthranilic acid. Meradimate (menthyl anthranilate) is the only FDAapproved anthranilate. It maintains a high safety and stability profile; however, an unappealing texture limits its use in cosmetic preparations [43]. Camphor derivative ecamsule (terephthalylidene dicamphor sulfonic acid) was the most recent sunscreen agent to receive FDA approval. Ecamsule’s absorbency peak is in the short-end of the UVA spectrum [44]. While it is effective and photostable, ecamsule must be formulated in conjunction with other sunscreening agents, such as avobenzone and titanium dioxide, in order to provide optimal protection. Oil-soluble forms of camphor derivatives are also available in countries outside of the United States [43]. Dibenzoylmethanes are a group of UVA-absorbing sunscreens. Avobenzone (butyl methoxydibenzoylmethane) is the only dibenzoylmethane used in the United States. While it is an effective UVA screening agent, photo-instability has raised concerns in the industry [45]. Formulary considerations, such as the addition of salicylates, benzophenones, octocrylene, bemotrizinol or ecamsule, can be made to prolong the activity of avobenzone [36, 46]. Certain products employ 2-6 diethylexhyl naphthalate as a means to stabilize avobenzone. Although concerns with the potential carcinogenicity of phthalates have surfaced within recent years, more research is necessary in order to conclude whether this is a valid concern [47].

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Tinosorbs include methylene-bis-benzotriazolyl tetramethylbutylphenol (Tinosorb M or Bemotrizinol) and bis-ethylhexyloxyphenol methoxyphenoltriazine (Tinosorb S or Bemotrizinol). Although neither of these ingredients has received FDA-approval as of 2010, they are widely used throughout Europe. Tinosorb M and S are unique in that they are said to offer the reflective and absorbent benefits of both physical and chemical sunscreens [36]. Both ingredients have been found to provide UVA and UVB protection, with Tinosorb M being a water-soluble form and Tinsorb S oil-soluble. Their safety profiles combined with their photostability makes them good options for sunscreen formulations [48].

8.11 Physical Sunscreen Agents A physical sunscreen agent is comprised of inorganic molecules that sit on the surface of the skin and reflect or scatter UV radiation before it can induce cellular damage. In the past, although physical sun protection was effective, it was often associated with thicker product consistency and a white appearance on the skin. Proper formulation and smaller particle sizes can alleviate these concerns, leading to a lighter, more appealing product feel. Zinc oxide offers broad-spectrum protective benefits with a high safety and stability profile. It is considered the more cosmetically elegant of the physical sunscreens, as zinc formulas typically cause less of a white appearance on the skin compared to titanium dioxide formulas when micronized [49]. Zinc is naturally anti-inflammatory, which gives it additional benefits when used to prevent the erythema of sun exposure [50]. Titanium dioxide is an inert sunscreen ingredient with no record of photosensitization. The large particle sizes of titanium dioxide can leave a white hue on the skin when applied, limiting their use in darker-skinned patients. Titanium dioxide, like zinc oxide, is often formulated with micronized particles to overcome this cosmetic concern [51]. Zinc oxide and titanium dioxide, as well as nearly all of the chemical sunscreen ingredients may induce cellular oxidation in response to UV radiation [52, 53]. Certain physical sunscreen products use a stabilized, coated particle to overcome this potentially damaging effect [54]. Additional means of counteracting this

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type of reaction include formulating sunscreens with supportive antioxidants and/or incorporating topical antioxidant serums into a patients’ morning skin care routine along with sunscreen products [37, 55].

8.12 Antioxidants Although the body has its own endogenous free radical-quenching mechanisms, daily application of topical antioxidants provides significantly heightened protection against matrix breakdown and the visible signs of facial aging [56, 57]. Antioxidants function in three ways: primary antioxidants, or electron donors; secondary antioxidants, which chelate metal ions; and co-antioxidants, which facilitate other antioxidants. Many offer multiple protective benefits [58]. The following are some of the most effective and accepted antioxidants. Resveratrol is a natural constituent of certain colored berries, grapes, red wine, and parts of the peanut plant. It is a potent polyphenolic compound that exhibits both primary and secondary antioxidant benefits. Topical application prior to UVB exposure has been shown to suppress the production of hydrogen peroxide radicals and lipid peroxidation [59, 60]. Resveratrol has also demonstrated antiproliferative and preventative effects on tumorigenesis within the skin [61]. Silymarin is a powerful flavanoid antioxidant found in milk thistle whose most active component is the primary and secondary antioxidant, silybin. Research suggests that silymarin inhibits lipid peroxidation, nitric oxide and hydrogen peroxide production, and increases the amount of the skin’s natural glutathione [62, 63]. Protection against UV-induced immunosuppression, carcinogenesis and cellular degradation has also been attributed to topical application of silymarin [64–66]. Caffeine is believed to play a significant role in the antioxidant behavior of several potent antioxidants, including coffea Arabica and green tea [67–69]. Studies comparing caffeinated and decaffeinated beverages demonstrate a clear increase in the antioxidant activity of those containing caffeine [67]. Caffeine is considered a primary and secondary antioxidant that is capable of scavenging hydroxyl radicals, hydrogen peroxide, peroxyl radicals, and singlet oxygen [70]. Research also suggests that topical application of caffeine can reduce UV-induced carcinogenesis by inducing cellular apoptosis in UV-exposed keratinocytes [68, 70].

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Coffea Arabica extract is a polyphenol that has demonstrated a clear quenching of free radicals in vitro. The exact antioxidant mechanism has not been clearly elucidated, although it could be attributed to its coantioxidant capability to increase endogenous glutathione reductase, superoxide dismutase, and catalase content [71–73]. Ergothioneine is newer to the cosmeceutical market. Research indicates strong primary antioxidant, free radical scavenging capabilities [74].1 Scientific studies suggest that ­ergothioneine reduces several forms of ROS, including hydrogen ­peroxide, hydroxyl radicals, singlet oxygen, peroxynitrite, lipid peroxides, and nitric oxides [74–77]. Chemopreventive benefits have also been demonstrated with topical ergothioneine use [74]. Ferulic acid is a polyphenol whose mechanisms of action include prevention of nitric oxide production and lipid peroxidation [78]. Ferulic acid is a primary antioxidant that is also able to absorb UV radiation, although it is not considered a sunscreen agent [79]. Comparative studies suggest that while ferulic acid surpasses idebenone in photoprotection, its scavenging effects are not as potent as green tea polyphenols [80, 81]. Green tea is the source of several potent polyphenol antioxidants. Epigallocatechin gallate (EGCG) is found in abundance in camellia sinensis and is thought to provide green tea’s primary antioxidant, antiinflammatory, and chemoprotective benefits [82]. EGCG has been shown to inhibit lipid peroxidation and prevent the formation of nitric oxide, hydroxyl radicals, and singlet oxygen [82, 83]. Research also indicates that topically applied EGCG is able to reverse the immunosuppressive effects of UV rays [84] and induce degradation of cutaneous carcinogenic cells [85]. Idebenone is an engineered analog of coenzyme Q-10 that serves as a potent primary antioxidant. Clinical trials preformed on the topical benefits of idebenone suggest an impressively well-rounded radical scavenging capacity when compared to traditional antioxidant agents such as alpha lipoic acid, kinetin, tocopherol, and ascorbic acid [86]. In vivo tests showed a decrease in lipid peroxidation and an inhibition of UVB-induced DNA damage and erythema [86]. Further research, however, indicates a lack of photoprotection when compared to other topical antioxidants [81, 87].

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Genistein is an isoflavone derivative of soybeans that increases the activity of the skin’s endogenous antioxidants [88]. Studies suggest that genistein prevents lipid peroxidation and hydrogen peroxide production. Genistein also interferes with UV-induced DNA damage and mutation [58, 89]. In vivo studies involving genistein indicate short- and long-term UV damage prevention, including erythema, skin cancer, and visible photoaging [90]. l-Ascorbic acid is the only true bioavailable form of vitamin C, and it is the only ingredient to provide all of vitamin C’s topical benefits. Topically applied ­l-ascorbic acid serves as a primary, secondary, and coantioxidant that effectively quenches ROS in the aqueous environment of the skin [91]. Because vitamin C is easily oxidized, products must be stabled by one of three methods. Products with an aqueous base should have a pH of 3.5 or lower [92]. An impressively stable, and therefore effective, method of protecting the l-ascorbic acid molecule is to use encapsulation and an anhydrous product base [93]. Esterification is another method of stabilization; however, ester versions of vitamin C, such as ascorbyl palmitate and magnesium ascorbyl phosphate, have been shown in clinical studies to provide only the antioxidant capabilities of vitamin C and they do not offer the collagen synthesis, anti-inflammatory, and photoprotective activities [94]. Therefore, esterification is not the preferred method of stabilization. Glutathione is part of the body’s endogenous antioxidant systems. Many of the most commonly used topical antioxidants work by regenerating this essential protective component. Research indicates that glutathione provides primary antioxidant capabilities by neutralizing current and preventing future oxidation [95]. In addition, glutathione serves as a co-antioxidant that supports l-ascorbic acid and vitamin E [96]. Studies also indicate that topically applied glutathione reduces UV-induced erythema to a higher degree than superoxide dismutase, ascorbyl palmitate, and tocopherol [97].

8.13 Matrix Metalloproteinase Inhibitors (MMPi) While the term MMP inhibitor has recently seen increased use in the marketing of cosmeceuticals, most MMPi ingredients have been used for decades throughout the industry.

8  Cosmeceutical Treatment of the Aging Face

Retinoids describe all members of the vitamin A family, including retinoic acid and its analogues and derivatives (e.g., adapalene, tazarotene, retinol). Cosmeceutical vitamin A products containing retinol or retinaldehyde are successfully converted into retinoic acid within the skin [98]. Retinoids are responsible for multiple matrix-­protecting actions within the skin, including decreasing collagenase and elastase levels [99]. Vitamin E ingredients include tocopherol, tocotrienols, and tocopheryl acetate. Research shows that tocopherol inhibits the activity of fibroblastic protein kinase C and the production of collagenase [100]. Studies have also found that tocotrienols are capable of decreasing nuclear factor-kB activation, which is responsible for the production of several MMP enzymes [101]. Aloe vera has been used topically for centuries, and its anti-inflammatory effects are well-documented [9, 102, 103]. Research on the individual constituents of aloe found that aloin effectively downregulates collagenase levels as well as granulocyte MMP [104]. Soy extracts are used throughout the industry. The most topically active components, though, have shown to be soy-derived isoflavones, such as genistein and daidzein. They are typically used as antioxidants, although research on the effects of oral soy isoflavones demonstrated a decrease in UV-induced MMP production [105, 106]. Further studies are needed to verify whether these effects are also achieved through topical application. Resveratrol is a powerful antioxidant, and research indicates that resveratrol effectively decreases UV-induced MMP production and downregulates nuclear factor-kB activity [59, 79, 107]. Beta-carotene is a carotenoid found in yellow/ orange fruits and vegetables and some dark leafy greens. When beta-carotene is applied topically, this vitamin A precursor inhibits MMP expression in both UV-exposed and un-irradiated tissue [108]. Epigallocatechin gallate (EGCG) is a green and black tea polyphenol responsible for multiple protective benefits. Studies show that EGCG reduces the production of various MMP enzymes and the activation of nuclear factor-Kb [109, 110]. l-Ascorbic acid is bioavailable vitamin C. Rather than directly inhibiting the expression of a particular MMP, vitamin C upregulates levels of the endogenous tissue inhibitor of matrix metalloproteinase-1 [111].

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8.14 Collagen and Matrix Producers Gradual breakdown of the skin’s structural components is inevitable for most patients, particularly those with excessive UV exposure. Once degradation occurs, use of clinically proven topical ingredients works to trigger the synthesis of such matrix proteins as collagen and elastin to improve the health and appearance of the skin. l-Ascorbic acid, bioavailable vitamin C, is a cofactor for collagen-stabilizing enzymes prolyl and lysyl hydroxylase and activates transcription of and stabilizes procollagen mRNA [91, 111, 112]. Although esters such as ascorbyl palmitate and magnesium ascorbyl phosphate are beneficial when administered orally, the acids in the skin are not strong enough to cleave the ester’s covalent bonds to free the l-ascorbic acid. Therefore topically, l-ascorbic acid is preferred to maximize collagen production. Retinoids encompass retinol, retinaldehyde, vitamin A esters, retinoic acid, and its analogues. While retinoic acid is the biologically active and most potent retinoid, it is potentially irritating to some patients. Retinol effectively binds with cellular retinol binding protein (CRBP) and is ultimately converted to retinoic acid in the skin [113]. Retinol, retinaldehyde, and retinoic acid are proven to stimulate dermal fibroblast production, increase mRNAs for types I and III collagen and trigger glycosaminoglycan production when applied topically [99, 114]. In addition, retinoids are thought to be one of the only topical methods for encouraging proliferation of elastin [115]. Peptides are the key building blocks of nearly all living tissues. Peptides encompass a large category of topical ingredients; however, very few have been legitimized in scientific studies. The topical use of peptides is still relatively new to the industry and, as of now, while many are being marketed, the most substantiated agents are used in the treatment of aging skin. Neurotransmitter-affecting peptides, carrier peptides, and signal peptides work in different ways to improve the integrity of matrix proteins.

8.15 Neurotransmitter-Affecting Peptides Acetyl hexapeptide-8 is a chain of six amino acids that inhibits soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) complex. In

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vivo studies found that twice daily application of acetyl hexapeptide-8 for 30 days resulted in a 30% decrease in the depth of dynamic rhytids [116].

8.16 Carrier Peptides Copper peptides are considered carrier peptides, as they increase the uptake of copper by the cells when paired with a tripeptide (glycyl-I-histidyl-l-lysine). Copper is used due to its involvement in collagen deposition through the activation of lysyl oxidase. Research suggests that the copper peptide increases collagen, gylcosaminoglycan, and adhesive protein production [117].

8.17 Signal Peptides Signal peptides are used to initiate specific responses within the skin. Several age-control signal peptides are currently available yet only a few are backed by legitimate studies. Palmitoyl pentapeptide-4 refers to lysine-therinetherine-lysine-serine paired with palmitic acid. In vitro studies show a stimulation of types I and III collagen as well as enhanced production of fibronectin [118]. Palmitoyl oligopeptide is a combination of valineglycine-valine-alanine-proline-glycine and palmitic acid. Studies suggest that this long-chain peptide stimulates the production of multiple dermal fibroblasts [119]. Palmitoyl oligopeptide can be used alone or in conjunction with other peptides.

8.18 Textural Variances The texture of the skin’s surface is another key indicator of a patient’s age and lifestyle choices. Varying degrees of dryness, dehydration, coarsening, and epidermal keratinization are hallmarks of aged skin.

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highly compacted, leading to a flaky, dull, and rough appearance. These factors in conjunction with a natural slowing in the production of moisture-binding glycosaminoglycans, and the UV-induced increase in the MMP hyaluronidase, leads to intensified dryness and dehydration [5, 120, 121]. Many patients experiment with topical products in an attempt to minimize the visual signs of their age. Aggressive topicals, improper cleansing habits, and insufficient moisturization often compound age-related and UV-exacerbated dryness [122].

8.18.2 Coarsening The time it takes a keratinocyte to travel from the basal layer to the stratum corneum increases from about 20  days in young skin to approximately 30 in aged skin [123]. This extended cellular lifespan, in addition to aged keratinocytes being more resistant to apoptosis [79], leads to skin that is more prone to DNA damage and oncogenesis. Additionally, the process of desquamation slows with time and with exposure to the elements, leaving the flattened corneocytes to build up, making the skin appear dry, flaky, and coarse [121]. In addition, patients who have experienced extended actinic exposure over their lifetime may present with solar elastosis, which clinically appears as a thickening of the skin that can lead to a yellow tone and a “leather-like” appearance [124]. Histologically, solar elastosis is a result of deposition of large amounts of abnormal elastic material that replaces the more normal collagen-rich ECM. It is triggered by UV radiation or free radicals that activate elastin promoters, which in turn elevate elastin mRNAs resulting in solar elastosis [125, 126]. In cases of advanced extrinsic aging with extensive textural changes, cosmeceuticals are typically used in tandem with more invasive procedures to work toward improvement.

8.19 Cosmeceutical Ingredients for Texture Improvement 8.18.1 Dryness and Dehydration An age-related decrease in the stratum corneum’s natural moisturizing factor (NMF) reduces barrier function, increases transepidermal water loss (TEWL), and contributes to slowed desquamation. As a result the corneocytes flatten and the stratum corneum becomes more

The textural changes associated with visible skin aging can be addressed in multiple fashions. Regular exfoliation and maintaining optimal skin hydration levels with humectants and occlusive agents can significantly decrease the appearance of coarsening, xerosis, and fine lines.

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8.19.1 Exfoliation with Alpha Hydroxy Acids (AHA) AHA are a class of water-soluble carboxylic acids that can be naturally derived or synthetically produced for topical use. They have the ability to break down intracellular desmosomal bonds to allow for easier exfoliation of impacted cells. Although the exact mechanism of action is not fully elucidated, this may be a result of chelation of calcium ions [127]. AHAs are also thought to stimulate fibroblasts to produce collagen and elastin to strengthen the matrix and firm the skin. AHAs can either be used as active ingredients in daily skin care products like washes, moisturizers and serums or they can be used in medical treatments such as superficial chemical peels. There are multiple AHA; however, only glycolic acid, lactic acid, and citric acid have significant research regarding their topical use. Each of these acids offers unique secondary and tertiary benefits. Glycolic acid has a very low molecular weight, which allows for hastened penetration and epidermolysis [128]. The fast penetration often induces higher instances of inflammation and stimulation than is associated with other AHA. Glycolic acid also has demonstrated pigment reducing benefits and has strong degreasing properties, making it ideal for oily, acneic skin but potentially dehydrating for drier skin types [129]. Lactic acid is a relatively larger molecule in comparison to glycolic acid, which allows it to penetrate into the skin slowly [128], reducing the chances of irritation and inflammation. Lactic acid has been shown to reduce bacteria [130], act as a humectant [131] and suppress the formation of tyrosinase. Lower concentrations (up to 5%) are recommended for daily use to promote cellular exfoliation of the corneocytes without causing sensitization or visible flaking [132]. Citric acid has demonstrated an ability to increase the thickness of viable epidermal cells. In addition, testing also showed topical use increased epidermal and dermal hyaluronic acid levels [133].

8.19.2 Mechanical Exfoliants Mechanical exfoliation is a method of physically removing skin cells through friction and abrasive media. This type of exfoliation can be utilized in-office with microdermabrasion or in cosmeceuticals, such as

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granular exfoliation products. While these can be effective in smoothing the skin’s surface, over-use by the patient often leads to sensitization. Gentle products with rounded beads as the exfoliating media may reduce the occurrence of over-treatment.

8.19.3 Humectants Humectants are used to increase hydration of the stratum corneum by drawing water from the dermis and, in locales with high humidity levels, the air. Enhancing topical hydration helps to improve the appearance of the skin’s texture and may also temporarily decrease the depth of rhytids. Humectants should not be used alone in topical preparations, as not occluding the area may increase surface dehydration [134]. Hyaluronic acid is a naturally occurring glycosaminoglycan used topically for its impressive moisture-attracting capabilities. Although hyaluronic acid does not penetrate intact skin, it moisturizes the epidermis by holding up to 1,000 times its molecular weight in water [135]. Sodium PCA is the salt of pyrrolidone carboxylic acid and is part of the skin’s NMF. When applied topically, sodium PCA showed greater hygroscopic activity than glycerin and sorbitol [136]. Sorbitol is often used as a more cost-effective alternative to sodium PCA and hyaluronic acid. Sorbitol is a unique humectant in that it is also able to chelate metal ions, allowing for potential antioxidant capabilities [137]. Honey has exhibited humectant properties in multiple wound-healing studies. In addition to being hygroscopic, honey also offers antibacterial and antiinflammatory benefits [138, 139]. Glycerin is one of the most effective humectants, as it is able to hydrate on many levels. Glycerin has been shown to penetrate through intercellular aquaporins, thereby enhancing surface and intercellular skin hydration [140]. Glycerin also has optimal sustainability and repeated application increases its moisture-binding benefits [141]. Urea is often used for its keratolytic benefits [142] as well as its hygroscopic properties. Like glycerin, urea is capable of entering and hydrating the skin cells by way of aquaporin-3 [141]. The exfoliation and hydration provided by urea make it especially effective for moderate to severe xerosis and keratinization [142].

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8.19.4 Occlusive Agents Occlusive agents’ function is to create an invisible barrier on the skin to maintain moisture levels. When used alone, occlusive agents merely retain hydration, rather than significantly increasing moisture levels in the skin. Moisturizing products that employ both humectants to draw water from the dermis to the epidermis and occlusive ingredients to trap it within can heighten moisture content throughout the epidermis [143]. Petrolatum is considered the most effective occlusive agent available [144]. Many find petrolatum-based products to have an unappealing, greasy texture and studies indicate possible comedogenicity [145]. Petrolatum products are often used immediately following deeper chemical peels or laser resurfacing treatments, as they serve as an effective barrier replacement during re-epithelialization [146]. Lanolin acts as an effective occlusive agent derived from the sebaceous glands of sheep [145]. Although lanolin is considered safe, research has indicated that lanolin alcohols are potential allergens and contributors to various types of dermatitis [147, 148]. Silicones, such as dimethicone and cyclomethicone, are polymers that provide occlusion with a light, powder-like texture. Silicones are often used in hydrating products designed for daily use on any skin type, including acne and oily skin. This group of occlusive ingredients is not associated with comedogenicity or allergenicity [149]. Shea butter, or butyrospermum parkii, has been used in cosmetic products for decades due to its occlusive capabilities. Its rich texture typically makes shea butter more appropriate for drier skin types. Studies on wound healing suggest that shea butter also may decrease the risk of infection and accelerate healing time [150]. Niacinamide, also referred to as nicotinamide, serves as an occlusive agent, based on its ability to increase the skin’s natural barrier components. Research indicates that topical niacinamide triggers the production of epidermal free fatty acids, ceramides, and cholesterol [151]. Plant oils, such as squalane, vegetable oils and jojoba oil provide mild occlusion as well. In addition, certain plant oils, specifically rosehip seed, borage and evening primrose, among others, may also provide secondary skin health benefits because of their content of essential fatty acids (EFA). EFA have been shown to

J. Linder

be beneficial in the inhibition of inflammatory skin conditions [152]. A reduction of inflammation may also decelerate the extrinsic aging process.

8.20 Dyschromias An easily apparent and common sign of aged skin is a visibly mottled and uneven skin tone. These dyschromias are due to a degeneration of the vascular system and melanogenesis. Both blood and melanin-related dyschromias are intensified by ultraviolet exposure and are more apparent in highly photodamaged patients due to the thinning of skin [153, 154]. Although there is a lessening in the dermal vascularity of intrinsically aged skin, UV exposure and cigarette smoke are both known to stimulate angiogenesis [155]. Telangiectasias can develop due to congenital factors, but much of the facial telangiectasias that are seen in older skin are due to environmental causes. Exposure to UVA rays causes necrosis of endothelial cells leading to dermal blood cell damage [79]. UVBinduced free radical formation causes a dilation of capillaries [153, 154]. Additionally, as the skin thins with age, this vascularity is more readily visible [154]; therefore, telangiectasias and increased vascularity are frequent presentations of aging. Poikiloderma of Civatte, which presents as reticulated hyperpigmented patches associated with telangiectasias and mild atrophy on the lateral aspects of the neck on fair skinned people, is a classic example of the changes seen in chronically photodamaged skin. Cosmeceuticals can assist with vascular dyschromias by protecting and promoting the collagen around damaged vessels and by limiting inflammation and dilation. Sun avoidance and daily broad-spectrum protection are critical and they can also help to mitigate vascular changes, but once facial telangiectasias have developed, there are no great cosmeceutical options for their resolution. Use of laser therapy for their removal is recommended. Hyperpigmentation is one of the most common skin concerns world-wide. Hyperpigmentation is deposited in the skin as a result of UV exposure, hormonal stimuli, or inflammation [156, 157]. In general, the density of melanocytes should decrease as a result of intrinsic aging [157, 158]. However, the hormonal shifts that occur as a result of menopause can cause an increase in the number and activity level of the melanocytes [159].

8  Cosmeceutical Treatment of the Aging Face

Actinic damage, pregnancy, and menopause will increase the number of melanocytes and increase pigment deposits in the keratinocytes [157, 158]. As with all visible signs of facial aging discussed, hypermelanosis is exacerbated in photoaged skin. The process of melanogenesis is comprised of many interconnected reactions, providing the physician with multiple opportunities to interrupt melanin production through the use of a variety of proven OTC and cosmeceutical ingredients. The use of several topical pigment-reducing ingredients with different mechanisms of action typically leads to accelerated results compared with the use of a single tyrosinase inhibitor.

8.21 Melanogenisis Inhibitors Hydroquinone (HQ) is the most prescribed skin-lightening agent world-wide [160]. HQ inhibits tyrosinase activity by suppressing the binding of copper and tyrosinase. In addition, studies show that HQ decreases the formation and promotes the degradation of melanosomes and induces melanocyte-specific cytotoxicity [156, 161, 162]. HQ is the most potent option of the melanogenesis inhibitors. Cosmeceuticals can contain up to 2% of HQ. These lower concentrations assist in the avoidance of inflammation and potential postinflammatory hyperpigmentation (PIH) that can be experienced as a result of irritation from higher percentages of HQ. Further, one study comparing the efficacy of 2% and 5% HQ found that there was no significant difference in lightening benefits; however, there was an increased risk of sensitivities with the higher percentage preparation [163]. Due to the potential of irritation, patch tests should be considered to determine patient tolerance prior to product use. Kojic acid acts by chelating the copper bound to the tyrosinase [156, 162, 164]. In addition, kojic acid decreases the number of melanosomes and melanocytic dendrites [165] while inhibiting nuclear factorkappa B (NF-kB) activation in keratinocytes, mitigating the inflammatory response [166]. There is a potential for contact dermatitis following kojic acid application; therefore, highly sensitive patients should be patchtested to ensure no undue inflammation is caused during treatment [166]. Lactic acid is a hydrophilic AHA that increases exfoliation of melanin-filled keratinocytes, ultimately fading dyschromias. In addition, lactic acid suppresses

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the formation of tyrosinase, contributing to the ­inhibition of melanogenesis [156, 167]. l-Ascorbic acid is able to convert dopaquinone back to l-DOPA during melanogenesis, preventing melanin formation [161, 168]. l-Ascorbic acid’s antioxidant, anti-inflammatory, and photoprotective capabilities may also help to avert the stimulation of melanogenesis. Retinoids, such as retinoic acid, retinol and retinaldehyde, assist in the reduction and hindrance of hyperpigmentation by inhibiting tyrosinase, enhancing cell turnover, and limiting melanosomal phagocytosis [114, 156, 168]. Retinol is typically used in cosmeceutical preparations, as it is successfully converted to retinoic acid within the skin [98]. Similar results may be achieved with retinol without the heightened irritant risk commonly associated with retinoic acid [113]. Azelaic acid provides melanocyte-specific antiproliferative and cytotoxic effects while also inhibiting tyrosinase activity. Further, azelaic acid is thought to be able to reduce DNA synthesis and mitochondrial activity in hyperactive and abnormal melanocytes [156, 169]. Arbutin is a natural b-d-glucopyranoside derivative of HQ that allows controlled release of HQ [156, 170]. Arbutin also suppresses the activity of tyrosinase, inhibits melanosome maturation, and provides antioxidant protection [161, 168]. Resorcinol derivatives, such as phenylethyl resorcinol and 4-n-butylresorcinol have demonstrated inhibition of the conversion of tyrosinase to l-DOPA [171, 172] during the melanogenesis process. Resorcinol derivatives have also demonstrated antioxidant benefits. Undecylenoyl phenylalanine is thought to prevent the synthesis of the melanocyte-stimulating hormone (MSH) and, as a result, prevent the formation of tyrosinase, melanin, and melanosome transfer [173–175].

8.22 Conclusions An understanding of the primary visible signs of aging skin, including matrix degradation, textural variances and dyschromias, and their individual causes allows the physician to make informed product choices for their patients. With the plethora of new anti-aging cosmeceuticals available to the physician, and the consumer, product recommendations based on science, not marketing, are what patients need. This overview is intended to provide the physician with the information necessary for selecting the best topical therapies

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for their patients working to prevent and reverse the visible signs of aging. Physicians may also develop cosmeceutical strategies to support more invasive procedures for patients with advanced dermal degradation.

References 1. Fisher G, Kang S, Varani J, Bata-Csorgo Z, Wan Y, Datta S, Voorhees JJ (2002) Mechanisms of photoaging and chronological skin aging. Arch Dermatol 138(11):1462–1470 2. Kerkelä E, Saarialho-Kere U (2003) Matrix metalloproteinases in tumor progression: focus on basal and squamous cell skin cancer. Exp Dermatol 12(2):109–125 3. Fisher GJ, Datta SC, Talwar HS, Wang ZQ, Varani J, Kang S, Voorhees JJ (1996) Molecular basis of sun-induced premature skin aging and retinoid antagonism. Nature 379(6563): 335–339 4. Nishimori Y, Edwards C, Pearse A, Matsumoto K, Kawai M, Marks R (2001) Degenerative alterations of dermal collagen fiber Bundles in photodamaged human skin and UV-irradiated hairless mouse skin: possible effect on decreasing skin mechanical properties and appearance of wrinkles. J Invest Dermatol 117(6):1458–1463 5. Herschthal J, Kaufman K (2007) Cutaneous aging: a review of the process and topical therapies. Expert Rev Dermatol 2:753–761 6. Coleman S, Grover R (2006) The anatomy of the aging face: volume loss and changes in 3-dimensional topography. Aesthet Surg J 26(1S):S4–S9 7. Donath AS, Glasgold RA, Glasgold MJ (2007) Volume loss versus gravity: new concepts in facial aging. Curr Opin Otolaryngol Head Neck Surg 15(4):238–243 8. Ramirez OM, Robertson KM (2001) Comprehensive approach to rejuvenation of the neck. Facial Plast Surg 17(2):129–140 9. Thakur ND, Batheja P, Kaushik D, Michniak B (2008) Structural and biochemical changes in aging skin and their impact on skin permeability barrier. In: Dayan N (ed) Skin aging handbook: an integrated approach to biochemistry and product. William Andrew Inc., Norwich, NY, pp 55–90. 10. de Rigal J, Escoffier C, Querleux B, Faivre B, Agache P, Lévêque JL (1989) Assessment of aging of the human skin by in  vivo ultrasonic imaging. J Investig Dermatol 93(5): 621–625 11. El-Domyati M, Attia S, Saleh F, Brown D, Birk DE, Gasparro F, Ahmad H, Uitto J (2002) Intrinsic aging vs. photoaging: a comparative histopathological, immunohistochemical, and ultrastructural study of the skin. Exp Dermatol 11(5):398–405 12. Stoebner PE, Meunier L (2008) Photoaging of face. Ann Dermatol Venereol 135(1 Pt 2):1S21–1S26 13. Kang S, Fisher GJ, Voorhees JJ (2001) Photoaging: pathogenesis, prevention, and treatment. Clin Geriatr Med 17(4):643–659 14. Murphy G, Cockett M, Ward RV, Docherty AJ (1991) Matrix metalloproteinase degradation of elastin, type IV collagen

J. Linder and proteoglycan: a quantitative comparison of the activities of 95 kDa and 72 kDa gelatinases, stromelysins-1 and -2 and punctuated metalloproteinase (PUMP). Biochem J 277 (Pt 1):277–279 15. Fuchs J (1992) Oxidative injury in dermopathology. Springer, Berlin, p 360 16. Gendimenico G, Mack V, Siock PA, Mezick JA (2002) Topical estrogens: their effects on connective tissue synthesis in hairless mouse skin. Arch Dermatol Res 294(5):231–236 17. Lochner K, Gaemlich A, Südel KM, Venzke K, Moll I, Knott A, Stäb F, Wenck H, Döring O, Böttger M, Gallinat S (2007) Expression of decorin and collagens I and III in different layers of human skin in vivo: a laser capture microdissection study. Biogerontology 8(3):269–282 18. Wilhelm KP, Cua AB, Maibach HI (1991) Skin aging: effect on transepidermal water loss, stratum corneum hydration, skin surface pH, and casual sebum content. Arch Dermatol 127(12):1806–1809 19. Brenneisen P, Briviba K, Wlaschek M, Wenk J, ScharffetterKochanek K (1997) Hydrogen peroxide (H2O2) increases the steady-state mRNA levels of collagenase/MMP-1 in human dermal fibroblasts. Free Radical Biol Med 22(3):515–524 20. Koh JS, Kang H, Choi SW, Kim HO (2002) Cigarette smoking associated with premature facial wrinkling: image analysis of facial skin replicas. Int J Dermatol 41(1):21–27 21. Fagien S (1999) Botox for the treatment of dynamic and hyperkinetic facial lines and furrows: adjunctive use in facial aesthetic surgery. Plast Reconstr Surg 103(2):701–713 22. Soldano S, Montagna P, Brizzolara R, Sulli A, Parodi A, Seriolo B, Paolino S, Villaggio B, Cutolo M (2010) Effects of estrogens on extracellular matrix synthesis in cultures of human normal and scleroderma skin fibroblasts. Ann NY Acad Sci 1193(1):25–29 23. Shah MG, Maibach HI (2001) Estrogen and skin: an overview. Am J Clin Dermatol 2(3):143–150 24. Fisher GJ, Datta S, Wang Z, Li XY, Quan T, Chung JH, Kang S, Voorhees JJ (2000) c-Jun dependent inhibition of cutaneous procollagen transcription following ultraviolet irradiation is reversed by all-trans retinoic acid. J Clin Invest 106(5):663–670 25. Kligman AM (1979) Perspectives and problems in cutaneous gerontology. J Invest Dermatol 73(1):L39–L46 26. Neerken S, Lucassen GW, Bisschop MA, Lenderink E, Nuijs TA (2004) Characterization of age-related effects in human skin: a comparative study that applies confocal laser scanning microscopy and optical coherence tomography. J Biomed Opt 9(2):274–281 27. Guinot C, Malvy D, Ambroisine L, Latreille J, Mauger E, Tenenhaus M, Morizot F, Lopez S, Le Fur I, Tschachler E (2002) Relative contribution of intrinsic vs extrinsic factors to skin aging as determined by a validated skin age score. Arch Dermatol 138(11):1454–1460 28. Zouboulis CC, Boschnakow A (2001) Chronological ageing and photoageing of the human sebaceous gland. Clin Exp Dermatol 26(7):600–607 29. Patterson WM, Fox M, Schwartz RA (2004) FavreRacouchot disease. Int J Dermatol 43(3):167–169 30. Draelos ZD (2010) Active agents in common skin care products. Plast Reconstr Surg 125(2):719–724 31. Nixon RL, Frowen KE, Lewis AE (1997) Skin reactions to sunscreens. Australas J Dermatol 38(suppl 1):S83–S85

8  Cosmeceutical Treatment of the Aging Face 32. Ortiz KJ, Yiannias JA (2004) Contact dermatitis to cosmetics, fragrances, and botanicals. Dermatol Ther 17(3): 264–271 33. Gasparro FP, Mitchnick M, Nash JF (1998) A review of sunscreen safety and efficacy. Photochem Photobiol 68(3): 243–256 34. Levy SB (2009) UV filters. In: Barel AO, Paye M, Maibach HI (eds) Handbook of cosmetic science and technology, 3rd edn. Informa Healthcare, New York, pp 311–322 35. Lim HW, Thomas L et al (2004) Photoprotection. In: Rigal DS, Weiss RA, Lim HW, Dover JS (eds) Photoaging. Marcel Dekker, New York, pp 73–88 36. Kullavanijaya P, Lim HWJ (2005) Photoprotection. J Am Acad Dermatol 52(6):937–958 37. Baumann L, Avashia N, Castanedo-Tardan MP (2009) Sunscreens. In: Baumann L (ed) Cosmetic dermatology principals and practice, 2nd edn. McGraw Hill Companies Inc., Columbus, OH, pp 245–255 38. Fisher AA (1992) Sunscreen dermatitis: part IV – the salicylates, the anthranilates, and physical agents. Cutis 50(6): 397–398 39. Levy SB (1997) Sunscreens for photoprotection. Dermatol Ther 4:59–71 40. Rai R, Srinivas CR (2007) Photoprotection. Indian J Dermatol Venereol Leprol 73(2):73–79 41. Darvay A, White IR, Rycroft RJ, Jones AB, Hawk JL, McFadden JP et al (2001) Photoallergic contact dermatitis is uncommon. Br J Dermatol 145(4):597–601 42. Lim H, Draelos Z, Rigel DS, Ruenger TM (2006) Shedding light on complete UV protection. J Cosmet Dermatol 19:3–8 43. Draelos ZD (2007) Cosmeceuticals. In: Goldberg DJ (ed) Facial rejuvenation: a total approach. Springer, Berlin, p 172 44. Jancin B (2009) Two UVA sunscreen filters are better than one. Skin & Allergy News 19 45. Schwack W, Rudolph T (1995) Photochemistry of dibenzoyl methane UVA filters part 1. J Photochem Photobiol B Biol 28:229–234 46. Chatelain E, Gabard B (2001) Photostabilization of butyl methoxydibenzoylmethane (avobenzone) and ethylhexyl methoxycinnamate by bis-ethylhexyloxyphenol methoxyphenyl triazine (tinosorb S), a new UV broadband filter. Photochem Photobiol 74(3):401–406 47. David RM, Gans G (2003) Summary of mammalian toxicology and health effects of phthalate esters. In: Staples CA (ed) Phthalate esters. Springer, Berlin, pp 299–316 48. Reisch MS (2005) New-wave sunscreen. Chem Eng News 83:18–22 49. Pinnell SR, Fairhurst D, Gillies R, Mitchnick MA, Kollias N (2000) Microfine zinc oxide is a superior sunscreen ingredient to microfine titanium dioxide. Dermatol Surg 26(4): 309–314 50. Agren MS (1990) Studies on zinc in wound healing. Acta Derm Venereol Suppl 154:1–36 51. DeBuys HV, Levy SB, Murray JC, Madey DL, Pinnell SR (2000) Modern approaches to photoprotection. Dermatol Clin 18(4):577–590 52. Brezova V, Gabčová S, Dvoranová D, Stasko A (2005) Reactive oxygen species produced upon photoexcitation of sunscreens containing titanium dioxide (an EPR study). J Photochem Photobiol B 79(2):121–134

81 53. Hansen KM, Gratton E, Bardeen CJ (2006) Sunscreen enhancement of UV-induced reactive oxygen species in the skin. Free Radic Biol Med 41:1205–1212 54. González S, Fernández-Lorente M, Gilaberte-Calzada Y (2008) The latest on skin photoprotection. Clin Dermatol 26(6):614–626 55. Edlich RF, Winters KL, Lim HW, Cox MJ, Becker DG, Horowitz JH, Nichter LS, Britt LD, Long WB (2004) Photoprotection by sunscreens with topical antioxidants and systemic antioxidants to reduce sun exposure. J Long Term Eff Med Implants 14:317–340 56. Dreher F, Maibach H (2001) Protective effects of topical antioxidants in humans. Curr Probl Dermatol 29:157–164 57. Burke KE (2004) Photodamage of the skin: protection and reversal with topical antioxidants. J Cosmet Dermatol 3(3):149–155 58. Pinnell SR (2003) Cutaneous photodamage, oxidative stress, and topical antioxidant protection. J Am Acad Dermatol 48(1):1–19 59. Baxter R (2008) Anti-aging properties of resveratrol: review and report of a potent new antioxidant skin care formulation. J Cosmet Dermatol 7(1):2–7 60. Jang M, Cai L, Udeani GO, Slowing KV, Thomas CF, Beecher CW, Fong HH, Farnsworth NR, Kinghorn AD, Mehta RG, Moon RC, Pezzuto JM (1997) Cancer chemopreventive activity of resveratrol, a natural product derived from grapes. Science 275(5297):218–220 61. Aziz MH, Reagan-Shaw S, Wu J, Longley BJ, Ahmad N (2005) Chemoprevention of skin cancer by grape constituent resveratrol: Relevance to human disease? FASEB J 19(9): 1193–1195 62. Katiyar SK (2005) Silymarin and skin cancer prevention: anti-inflammatory, antioxidant and immunomodulatory effects. Int J Oncol 26(1):1213–1222 63. Kaur M, Agarwal R (2007) Silymarin and epithelial cancer chemoprevention: How close we are to bedside? Toxicol Appl Pharmacol 224(3):350–359 64. Katiyar SK (2002) Treatment of silymarin, a plant flavonoid, prevents ultraviolet light-induced immune suppression and oxidative stress in mouse skin. Int J Oncol 21(6): 1213–1222 65. Singh RP, Agarwal R (2002) Flavonoid antioxidant silymarin and skin cancer. Antioxid Redox Signal 4(4): 655–663 66. Li LH, Wu LJ, Zhou B, Wu Z, Tashiro S, Onodera S, Uchiumi F, Ikejima T (2004) Silymarin prevents UV irradiation-induced A375-S2 cell apoptosis. Biol Pharm Bull 27(7):1031–1036 67. Huang MT, Xie JG, Wang ZY, Ho CT, Lou YR, Wang CX, Hard GC, Conney AH (1997) Effects of tea, decaffeinated tea, and caffeine on UVB light-induced complete carcinogenesis in SKH-1 mice: demonstration of caffeine as a biologically important constituent of tea. Cancer Res 57(13): 2623–2629 68. Richelle M, Tavazzi I, Offord E (2001) Comparison of the antioxidant activity of commonly consumed polyphenolic beverages (coffee, cocoa, and tea) prepared per cup serving. J Agric Food Chem 49(7):3438–3442 69. Devasagayam TPA, Kamat JP, Mohan H, Kesavan PC (1996) Caffeine as an antioxidant: inhibition of lipid peroxidation induced by reactive oxygen species. Biochim Biophys Acta 1282(1):63–70

82 70. Heffernan TP, Kawasumi M, Blasina A, Anderes K, Conney AH, Nghiem P (2009) ATR-CHK1 pathway inhibition promotes apoptosis after UV treatment in primary human keratinocytes: potential basis for the UV protective effects of caffeine. J Invest Dermatol 129(7):1805–1815 71. Farris P (2007) Idebenone, green tea, and Coffeeberry® extract: new and innovative antioxidants. Dermatol Ther 20(5):322–329 72. Baumann LS (2007) Less-known botanical cosmeceuticals. Dermatol Ther 20:330–342 73. Gomes RA, Moldes CA, Delite FS, Gratäo PL, Mazzafera P, Lea PJ, Azevedo RA (2006) Nickel elicits a fast antioxidant response in coffea arabica cells. Plant Physiol Biochem 44:420–429 74. Asmus KD, Bensasso RV, Bernier JL, Houssin R, Land EJ (1996) One-electron oxidation of ergothioneine and analogues investigated by pulse radiolysis: redox reaction involving ergothioneine and vitamin C. Biochem J 315(Pt 2):625–629 75. Chaudieá Re J, Ferrari-Iliou R (1999) Intracellular antioxidants: from chemical to biochemical mechanisms. Food Chem Toxicol 37(9–10):949–962 76. Akanmu D, Cecchini R, Aruoma OI, Halliwell B (1991) The antioxidant action of ergothioneine. Arch Biochem Biophys 288(1):10–16 77. Aruoma OI, Spencer JPE, Mahmood N (1999) Protection against oxidative damage and cell death by the natural ­antioxidant ergothioneine. Food Chem Toxicol 37(11): 1043–1053 78. Saija A, Tomaino A, Lo Cascio R, Trombetta D, Proteggente A, De Pasquale A, Uccella N, Bonina F (1999) Ferulic and caffeic acids as potential protective agents against photooxidative skin damage. J Sci Food Agric 79:476–480 79. Svobodová A, Psotová J, Walterová D (2003) Natural phenolics in the prevention of UV-induced skin damage. a review. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 147(2):137–145 80. Scott BC, Butler J, Halliwell B, Aruoma OI (1993) Evaluation of the antioxidant actions of ferulic acid and catechins. Free Radic Res Commun 19(4):241–253 81. Tournas JA, Lin FH, Burch JA, Selim MA, Monteiro-Riviere NA, Zielinski JE, Pinnell SR (2006) Ubiquinone, idebenone, and kinetin provide ineffective photoprotection to skin when compared to a topical antioxidant combination of vitamins C and E with ferulic acid. J Invest Dermatol 126(5): 1185–1187 82. Afaq F, Mukhtar H (2006) Botanical antioxidants in the prevention of photocarcinogenesis and photoaging. Exp Dermatol 15(9):678–684 83. F’guyer S, Afaq F, Mukhtar H (2003) Photochemoprevention of skin cancer by botanical agents. Photodermatol Photo­ immunol Photomed 19(2):56–72 84. Katiyar SK, Challa A, McCormick TS, Cooper KD, Mukhtar H (1999) Prevention of UVB-induced immunosuppression in mice by the green tea polyphenol (−)-epigallocatechin-3-gallate may be associated with alterations in IL-10 and IL-12 production. Carcinogenesis 20(11): 2117–2124 85. Lu YP, Lou YR, Xie JG, Peng QY, Liao J, Yang CS, Huang MT, Conney AH (2002) Topical applications of caffeine or (−)-epigallocatechin gallate (EGCG) inhibit carcinogenesis

J. Linder and selectively increase apoptosis in UVB-induced skin tumors in mice. Proc Natl Acad Sci 99(19):12455–12460 86. McDaniel DH, Neudecker BA, DiNardo JC, Lewis JA 2nd, Maibach HI (2005) Idebenone: a new antioxidant – part I. Relative assessment of oxidative stress protection capacity compared to commonly known antioxidants. J Cosmet Dermatol 4(1):10–17 87. Huang C, Miller T (2007) The truth about over-the-counter topical anti-aging products: a comprehensive review. Aesthet Surg J 27(4):402–412 88. Cai Q, Wei H (1996) Effect of dietary genistein on antioxidant enzyme activities in SENCAR mice. Nutr Cancer 25(1):1–7 89. Salvi M, Brunati AM, Clari G, Toninello A (2002) Interaction of genistein with the mitochondrial electron transport chain results in opening of the membrane transition pore. Biochim Biophys Acta 1556(2–3):187–196 90. Burke KE (2005) Nutritional antioxidants. In: Draelos ZD (ed) Procedures in cosmetic dermatology series: cosmeceuticals, 1st edn. Elsevier, Philadelphia, PA, pp 125–132 91. Farris PK (2005) Topical vitamin C: a useful agent for treating photoaging and other dermatologic conditions. Dermatol Surg 31(7 Pt 2):814–818 92. Pinnell SR, Yang HS, Omar M, Omar M, Monteiro-Riviere N, DeBuys HV, Walker LC, Wang Y, Levine M (2001) Topical L-ascorbic acid: percutaneous absorption studies. Dermatol Surg 27(2):137–142 93. Heber GK, Markovic B, Hayes A (2006) An immunohistological study of anhydrous topical ascorbic acid compositions on ex vivo human skin. J Cosmet Dermatol 5(2): 150–156 94. Traikovich SS (1999) Use of topical ascorbic acid and its effects on photodamaged skin topography. Arch Otolaryngol Head Neck Surg 125(10):1091–1098 95. Glutathione, reduced (GSH) (2001) Monograph. Altern Med Rev 6(6):601–607 96. Chan AC (1993) Partners in defense, vitamin E and vitamin C. Can J Physiol Pharmacol 71(9):725–731   97. Montenegro L, Bonina F, Rigano L, Giogilli S, Sirigu S (2007) Protective effect evaluation of free radical scavengers on UVB induced human cutaneous erythema by skin reflectance spectrophotometry. Int J Cosmet Sci 17:91–103   98. Kang S (2005) Mechanism of action of retinol. J Cosmet Dermatol 18:6–8   99. Varani J, Warner RL, Gharaee-Kermani M, Phan SH, Kang S, Chung J, Wang Z, Datta SC, Fisher GJ, Voorhees JJ (2000) Vitamin A antagonizes decreased cell growth and elevated collagen-degrading matrix metalloproteinases and stimulates collagen accumulation in naturally aged human skin. J Invest Dermatol 114:480–486 100. Riwcciarelli R, Maroni P, Ozer N, Zingg JM, Azzi A (1999) Age-dependent increase of collagenase expression can be reduced by a-tocopherol via protein kinase C inhibition. Free Radic Biol Med 27(7–8):729–737 101. Ahn KS, Sethi G, Krishnan K, Aggarwal BB (2007) Gamma-tocotrienol inhibits nuclear factor-kB signaling pathway through inhibition of receptor-interacting protein and TAK1 leading to suppression of antiapoptotic gene products and potentiation of apoptosis. J Biol Chem 282(1):809–820

8  Cosmeceutical Treatment of the Aging Face 102. Davis RH, Rosenthal KY, Cesario LR, Rouw GA (1989) Processed Aloe vera administered topically inhibits inflammation. J Am Podiatr Med Assoc 79(8):395–397 103. Klein AD, Penneys NS (1988) Aloe vera. J Am Acad Dermatol 18(4 Pt 1):714–720 104. Barrantes E, Guinea M (2003) Inhibition of collagenase and metalloproteinases by aloins and aloe gel. Life Sci 72(7):843–850 105. Kim SY, Kim SJ, Lee JY, Kim WG, Park WS, Sim YC, Lee SJ (2004) Protective effects of dietary soy isoflavones against UV-induced skin-aging in hairless mouse model. J Am Coll Nutr 23(2):157–162 106. Shao ZM, Wu J, Shen ZZ, Barsky SH (1998) Genistein exerts multiple suppressive effects on human breast carcinoma cells. Cancer Res 58(21):4851–4857 107. Woo JH, Lim JH, Kim YH, Suh SI, Min DS, Chang JS, Lee YH, Park JW, Kwon TK (2004) Resveratrol inhibits phorbol myristate acetate-induced matrix metalloproteinase-9 expression by inhibiting JNK and PKC signal transduction. Oncogene 23(10):1845–1853 108. Wertz K, Hunziker PB, Seifert N, Riss G, Neeb M, Steiner G, Hunziker W, Goralczyk R (2005) Beta-Carotene interferes with ultraviolet light a-induced gene expression by multiple pathways. J Invest Dermatol 124(2):428–434 109. Ahmed S, Wang N, Lalonde M, Goldberg VM, Haqqi TM (2004) Green tea polyphenol epigallocatechin-3-gallate (EGCG) differentially inhibits interleukin-1-induced expression of matrix metalloproteinase-1 and -13 in human chondrocytes. J Pharmacol Exp Ther 308(2):767–773 110. Song XZ, Xia JP, Bi ZG (2004) Effects of (−)-epigallocatechin-3-gallate on expression of matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 in fibroblasts irradiated with ultraviolet A. Chin Med J 117(12):1838–1841 111. Nusgens BV, Humbert P, Rougier A, Colige AC, Haftek M, Lambert CA, Richard A, Creidi P, Lapière CM (2001) Topically applied vitamin C enhances the mRNA level of collagens I and III, their processing enzymes and tissue inhibitor of matrix metalloproteinase 1 in the human dermis. J Invest Dermatol 116(6):853–859 112. Dreher F, Denig N, Gabard B, Schwindt DA, Maibach HI (1999) Effect of topical antioxidants on UV-induced erythema formation when administered after exposure. Dermatology 198(1):52–55 113. Kang S, Duell EA, Fisher GJ, Datta SC, Wang ZQ, Reddy AP, Tavakkol A, Yi JY, Griffiths CE, Elder JT et al (1995) Application of retinol to human skin In vivo induces epidermal hyperplasia and cellular retinoid binding proteins characteristic of retinoic acid but without measurable retinoic acid levels or irritation. J Invest Darmatol 105(4):549–556 114. Draelos ZD (2005) Retinoids in cosmetics. J Cosmet Dermatol 18:3–5 115. Stratigos AJ, Katsambas AD (2005) The role of topical retinoids in the treatment of photoaging. Drugs 65(8): 1061–1072 116. Blanes-Mira C, Clemente J, Jodas G, Gil A, FernándezBallester G, Ponsati B, Gutierrez L, Pérez-Payá E, FerrerMontiel A (2002) A synthetic hexapeptide (argireline) with antiwrinkle activity. Int J Cosmet Sci 24(5):303–310 117. Lupo MP, Cole AL (2007) Cosmeceutical peptides. Dermatol Ther 20(5):343–349

83 118. Katayama K, Armendariz-Borunda J, Raghow R, Kang AH, Seyer JM (1993) A pentapeptide from type I procollagen promotes extracellular matrix production. J Biol Chem 268(14):9941–9944 119. Robinet A, Fahem A, Cauchard JH, Huet E, Vincent L, Lorimier S, Antonicelli F, Soria C, Crepin M, Hornebeck W, Bellon G (2005) Elastin-derived peptides enhance angiogenesis by promoting endothelial cell migration and tubulogenesis through upregulation of MT1-MMP. J Cell Sci 118(pt 2):343–356 120. Ghersetich I, Lotti T, Campanile G, Grappone C, Dini G (1994) Hyaluronic acid in cutaneous intrinsic aging. Int J Dermatol 33(2):119–122 121. Grove GL, Klingman AM (1983) Age-associated changes in human epidermal cell renewal. J Gerontol 38(2):137–142 122. Grunewald AM, Gloor M, Gehring W, Kleesz P (1995) Damage to the skin by repetitive washing. Contact Dermat 32(4):225–232 123. Kligman AM (1979) Perspectives and problems in cutaneous gerontology. J Invest Dermatol 73(1):39–46 124. Moloney SJ, Edmonds SH, Giddens LD, Learn DB (1992) The hairless mouse model of photoaging: evaluation of the relationship between dermal elastin, collagen, skin thickness and wrinkles. Photochem Photobiol 56(4):505–511 125. Kligman LH (1989) Photoaging: manifestations, prevention, and treatment. Clin Geriatr Med 5(1):235–251 126. Bernstein EF, Chen YQ, Tamai K, Tamai K, Shepley KJ, Resnik KS, Zhang H, Tuan R, Mauviel A, Uitto J (1994) Enhanced elastin and fibrillin gene expression in chronically photoaged skin. J Invest Dermatol 103(2):182–186 127. Wang X (1999) A theory for the mechanism of action of the a-hydroxy acids applied to the skin. Med Hypotheses 53(5):380–382 128. Brody HJ (1992) Superficial peeling. In: Brody HJ (ed) Chemical peeling and resurfacing, 2nd edn. Mosby-Year Book, Inc., St. Louis, pp 73–108 129. Effendy I, Kwangsukstith C, Lee JY, Maibach HI (1995) Functional changes in human stratum corneum induced by topical glycolic acid: comparison with all-trans retinoic acid. Acta Derm Venereol 75(6):455–458 130. Orth DS, Kabara JJ, Denyer Stephen P, Tan SK (2005) Cosmetic and drug microbiology. Informa Healthcare, New York, pp 163–184 131. Leyden JJ, Rawlings AV (2002) Skin moisturization. Marcel Dekker, Inc, New York, pp 323–352 132. Helms RA, Quan DJ (2006) Textbook of therapeutics: drug and disease management, 8th edn. Lippincott Williams & Wilkins, Philadelphia, pp 203–256 133. Bernstein EF, Underhill CB, Lakkakorpi J, Ditre CM, Uitto J, Yu RJ, Scott EV (1997) Citric acid increases viable epidermal thickness and glycosaminoglycan content of sun-damaged skin. Dermatol Surg 23(8):659–694 134. Draelos ZD (2000) Therapeutic moisturizers. Dermatol Clin 18(4):597–607 135. Bhat SV, Nagasampagi BA, Suvakumar M (2005) Mucopolysaccharides. In: Bhat SV, Nagasampagi BA, Suvakumar M (eds) Chemistry of natural products. Narosa Publishing House, New Delhi, pp 523–524 136. Takahashi M, Yamada M, Machida Y (1984) A new method to evaluate the softening effect of cosmetic ingredients on the skin. J Soc Cosmet Chem 35:171–181

84 137. Gesslein B (1999) Humectants in personal care formulation: a practical guide. In: Schueller R, Romanowski P (eds) Conditioning agents for hair and skin, vol 21, Cosmetic science and technology series. Marcel Dekker, Inc, New York, NY, pp 95–110 138. Marshall C (2002) The use of honey in wound care: a review article. Br J Podiatry 5:47–49 139. Biswal BM, Zakaria A, Ahmad NM (2003) Topical application of honey in the management of radiation mucositis. a preliminary study. Support Care Cancer 11(4): 242–248 140. Hara-Chikuma M, Verkman AS (2005) Aquaporin-3 functions as a glycerol transporter in mammalian skin. Biol Cell 97(7):479–496 141. Draelos ZD (2008) New channels for old cosmeceuticals: aquaporin modulation. J Cosmet Derm 7(2):83 142. Fluhr JW, Cavallotti C, Berardesca E (2008) Emollients, moisturizers, and keratolytic agents in psoriasis. Clin Dermatol 26(4):380–386 143. Kraft JN, Lynde CW (2005) Moisturizers: what they are and a practical approach to product selection. Skin Ther Lett 10(5):1–8 144. Krivda MS (2004) Making the choice. Skin & Aging 12(6). http://www.skinandaging.com/article/2766. Accessed 6/11/10 145. Fluhr J, Holleran WM, Berardesca E (2002) Clinical effects of emollients on skin. In: Leyden JJ, Rawlings AV (eds) Cosmetic science and technology series: skin moisturization. Marcel Dekker, Inc., New York, pp 223–243 146. Eaglstein WH (2001) Moist wound healing with occlusive dressings: a clinical focus. Dermatol Surg 27(2): 175–182 147. Schlossman ML, McCarthy JP (1979) Lanolin and derivatives chemistry: relationship to allergic contact dermatitis. Contact Dermat 5(2):65–72 148. Giorgini S, Melli MC, Sertoli A (1983) Comments on the allergenic activity of lanolin. Contact Dermat 9(5):425–426 149. Draelos ZK (1995) Patient compliance: enhancing clinician abilities and strategies. J Am Acad Dermatol 32(5 Pt 3):S42–S48 150. Ezema DO, Ozoiko ZO (1992) Butyrospermum lipids as an ointment base. Pharm Biol 30:117–123 151. Gehring W (2004) Nicotinic acid/niacinamide and the skin. J Cosmet Dermatol 3(2):88–93 152. Horrobin DF (1989) Essential fatty acids in clinical dermatology. J Am Acad Dermatol 20(6):1045–1053 153. Takema Y, Yorimoto Y, Kawai M, Imokawa G (1994) Agerelated changes in the elastic properties and thickness of human facial skin. Br J Dermatol 131(5):641–648 154. Glogau RG (1997) Physiologic and structural changes associated with aging skin. Dermatol Clin 15(4): 555–559 155. Chung JH, Eun HC (2007) Angiogenesis in skin aging and photoaging. J Dermatol 34(9):593–600 156. Lotti T, Thiers BH (2007) Dermatologic clinics. Pigmentary disorders, vol 25(3). Elsevier Saunders, Philadelphia 157. Ortonne J, Bissett DL (2008) Latest insights into skin hyperpigmentation. J Investig Dermatol Symp Proc 13(1):10–14 158. Whiteman DC, Parsons PG, Green AC (1999) Determinants of melanocyte density in adult human skin. Arch Dermatol Res 291(9):511–516

J. Linder 159. Tadokoro T, Itami S, Hosokawa K, Terashi H, Takayasu S (1997) Human genital melanocytes as androgen target cells. J Invest Dermatol 109(4):513–517 160. Picardo M, Carrera M (2007) New and experimental treatments of cloasma and other hypermelanoses. Dermatol Clin 25(3):353–362 161. Badreshia-Bansal S, Draelos ZD (2007) Insight into skin lightening cosmeceuticals for women of color. J Drugs Dermatol 6(1):32–39 162. Bennett S, Chaudhuri RK, Closs B, Draelos ZD, Loiseau A, Maibach HI et al (2006) Anti-aging: physiology to formulation. Allured Publishing Corporation, IL 163. Arndt KA, Fitzpatrick TB (1965) Topical use of hydroquinone as a depigmenting agent. J Am Med Assoc 194(9):965–967 164. Kim YM, Yun J, Lee CK, Lee H, Min KR, Kim Y (2002) Oxyresveratrol and hydroxystilbene compounds: inhibitory effect on tyrosinase and mechanism of action. J Biol Chem 277(18):16340–16344 165. James AJ (2006) “Skin Lightening and Depigmenting Agents” emedicine from WebMD. http://www.emedicine. com/derm/topic528.htm 166. Zhu WY, Zhang RZ (2006) Skin care skin lightening agents. In: Draelos ZD, Thaman L (eds) Cosmetic formulation of products. Taylor and Francis Group LLC, New York, pp 205–218 167. Ando S, Suemoto Y, Mishima Y, Suemoto Y, Mishima Y (1993) Tyrosinase gene transcription and its control by melanogenic inhibitors. J Invest Dermatol 100(2 suppl): 150s–155s 168. Rendon MI, Gaviria JI (2005) Review of skin lightening agents. Dermatol Surg 31(7 Pt 2):886–890 169. Fitton A, Goa KL (1991) Azelaic acid. a review of its pharmacological properties and therapeutic efficacy in acne and hyperpigmentary disorders. Drugs 41(5):780–798 170. Maeda K, Fukuda M (1996) Arbutin: mechanism of its depigmenting action in human melanocyte culture. J Pharmacol Exp Ther 276(2):265–269 171. SymRise AG (2007) Symwhite product information. Frankfurt, Germany 172. Katagtri T, Okubo T, Oyobikawa M, Futaki K, Shaku M, Kawai M (1998) Novel melanogenic enzymes inhibitor for controlling hyperpigmentation. 20th IFSCC International Congress 1:1–11 173. Seppic SA (2003) Sepiwhite product information. Paris, France 174. Katoulis AC, Alevizou A, Bozi E, Makris M, Zafeiraki A, Mantas N, Kousta F, Mistidou M, Kanelleas A, Stavrianeas NG (2009) A randomized double-blind vehicle-controlled study of a preparation containing undecylenoyl phenylalanine 2% in the treatment of solar lentigines. Clin Exp Dermatol 4:69–72 175. Bissett DL, Robinson LR, Raleigh PS, Miyamoto K, Hakozaki T, Li J, Kelm GR (2009) Reduction in the appearance of facial hyperpigmentation by topical N-undecyl-10enoyl-L-phenylalanine and its combination with niacinamide. J Cosmet Dermatol 8(4):260–266 176. Diffey BL, Tanner PR, Matts PJ, Nash JF. In vitro assessment of the broad-spectrum ultraviolet protection of sunscreen products. J Am Acad Dermatol. 2000;43: 1024–1035

Part III Cutaneous Procedures

 

9

Local Regional Anesthesia Peter M. Prendergast

9.1 Introduction As less invasive, ambulatory aesthetic procedures have become more popular over the last decade, so too has the use of local and regional anesthesia. Using nerve blocks, procedures such as injectable lip enhancement, facial contouring, laser skin resurfacing, chemical peels, suture lifts, and autologous fat transfer can be performed painlessly without general anesthesia, oral, or intravenous sedation. As well as obvious benefits to the patient by avoiding unnecessary general anesthesia or sedation, nerve blocks are quick, reliable, and safe, and may obviate the need for extensive infiltrative anesthesia. The learning curve for basic nerve block techniques is short. Once mastered, they afford the physician and surgeon the opportunity to provide a comprehensive range of facial procedures in an officebased setting. The first step in performing accurate nerve block technique is to study the anatomy of the sensory nerves, the foramina from which they arise, and their relationship to surrounding and underlying structures (Fig. 9.1). The sensory innervation of the face is via the three divisions of the trigeminal nerve: ophthalmic, maxillary, and mandibular nerves (Fig. 9.2). Regional anesthesia in the face is achieved by blocking these nerves and their branches and allows most injectable, minimally invasive, and laser resurfacing procedures to be performed easily and without pain or discomfort for

P.M. Prendergast  Venus Medical, Heritage House, Dundrum Office Park, Dublin 14, Ireland e-mail: [email protected]

the patient. There are several advantages for using nerve blocks in aesthetic medicine (Table  9.1). They allow large areas to be anesthetized without infiltrating the entire treatment area. This is particularly relevant for full-face treatments such as laser skin resurfacing. Regional nerve blocks typically require less anesthetic solution and produce less local distortion of tissues than local infiltrative anesthesia and are preferred for soft tissue augmentation using fillers where a careful assessment of the volume and architecture of the tissues is required during the procedure. Injecting smaller volumes of anesthetic around main nerve branches, compared to local infiltrative anesthesia using larger volumes, may reduce the chance of lignocaine toxicity, particularly if epinephrine is used. This chapter describes nerve block techniques for the commonly performed procedures in aesthetic medicine described in this book. These include blocks of the sensory nerves of the face, wrist block, and ankle block. Although the techniques are straightforward, a thorough knowledge of the anatomy of the nerves and their location in relation to bony landmarks is essential. It is important also to keep in mind that anatomic variations exist, such as the presence of multiple foramina for a single named nerve [1]. In the face, the ophthalmic nerve supplies the forehead, upper eyelid, and dorsum of the nose via the supraorbital, supratrochlear, infratrochlear, and external nasal nerves. The maxillary nerve supplies the lower eyelid, cheek, upper lip, ala of the nose, and part of the temple through the infraorbital, zygomaticofacial, and zygomaticotemporal nerves. The sensory fibers of the mandibular nerve supply the skin over the mandible, lower cheek, part of the temple and ear, and the lower lip through the buccal and auriculotemporal nerves. The greater auricular

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a

b

Fig. 9.2  Sensory innervation of the face. The trigeminal nerve (Cranial nerve V) has three main branches: ophthalmic division (V1), maxillary division (V2), and mandibular division (V3)

nerve, derived from the primary rami of the second and third cervical nerves, innervates the angle of the mandible. Nerve blocks of the median, ulnar, and radial nerves anesthetize the skin of the hand and allow injectable procedures to be performed on the sensitive palmar surface without pain. An ankle block allows similar injections on the plantar surface of the foot. Nerve blocks can also be used in conjunction with infiltrative local anesthesia where procedures are more vigorous or extensive such as suture facelift techniques or autologous fat grafting.

9.2 Indications Fig.  9.1  (a) Frontal view. (b) Lateral view of skull showing foramina and location of sensory nerves where they are blocked: (1) Supraorbital notch. (2) Supratrochlear notch. (3) Infratrochlear notch. (4) Site of dorsal nasal nerve. (5) Infraorbital foramen. (6) Zygomaticofacial foramen. (7) Mental foramen. (8) Separate foramen of deep branch of supraorbital nerve. (9) Site of zygomaticotemporal nerve. (10) Mandibular nerve posterior to lateral pterygoid plate (marked X)

There are numerous indications for regional nerve blocks in the face in aesthetic medicine (Table 9.2). An infraorbital nerve block allows painless injection of filler below the eye in the tear trough area and along the nasolabial fold. To anesthetize the malar and anterior cheek area, a combined infraorbital and zygomaticofacial nerve block is used. In the authors view, lip enhancement with

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Table 9.1  Advantages of nerve blocks in aesthetic medicine Small volumes sufficient to anesthetize large areas Injection sites distant to treatment areas avoid tissue distortion Anesthesia of the entire face is achieved using multiple facial blocks Avoid general anesthesia and sedation where invasive treatments are performed Quick onset of local anesthesia (5–10 min) Safe and reliable with correct technique Table 9.2  Indications for nerve blocks in aesthetic medicine Indication Lip enhancement Cheek enhancement Nose contouring Augmentation of tear trough Laser skin resurfacing (full face)

Chin enhancement Botulinum toxin for palmar hyperhidrosis Botulinum toxin for plantar hyperhidrosis

Nerve block Infraorbital, mental Infraorbital, zygomaticofacial Infraorbital, dorsal nasal Infraorbital, zygomaticofacial Supraorbital, supratrochlear, infratrochlear, infraorbital, zygomaticofacial, zygomaticotemporal, mandibular, mental Mental plus mylohyoid augmentation Median, ulnar, radial Posterior tibial, sural, saphenous

hyaluronic acid injections into the vermilion border and body of the lip should not be performed without nerve blocks. Topical anesthesia only for the lips provides insufficient pain relief, whereas infiltrative local anesthesia can distort the tissues and interfere with the assessment of a satisfactory aesthetic outcome. Infraorbital and mental nerve blocks allow painless injections into the lips within seconds. Complementary injections into the frenulum of the upper and lower lips are sometimes required to ensure complete anesthesia of the central portion of the lips. Occasionally, fillers are used to define or shape the tip of the nose. Blocking the dorsal nasal nerve makes these otherwise painful injections completely tolerable. Collagen stimulating and panfacial volumizing procedures such as those using poly-L-lactic acid are best performed following multiple nerve blocks, including infraorbital, mental, zygomaticofacial, zygomaticotemporal, buccal, and auriculotemporal nerve blocks. For laser skin resurfacing, these blocks, as well  as blocks to the supraorbital, supratrochlear, and

infratrochlear nerves, provide anesthesia to the entire face. Augmentation of facial features using autologous fat employs similar anesthesia with multiple regional nerve blocks. The injection of botulinum toxin into the palms of the hands for palmar hyperhidrosis is a painful procedure unless a wrist block is performed. For plantar hyperhidrosis, an ankle block allows injections of botulinum toxin into the sole of the foot without the need for additional anesthesia.

9.3 Materials In current practice, the amide local anesthetics are most commonly used because they are stable in solution and rarely produce hypersensitivity reactions. They include lignocaine, prilocaine, mepivacaine, and bupivacaine, and act by blocking sodium channels in the nerve cell membrane (Table 9.3). This depolarization prevents the development of an action potential and blocks nerve impulses. Although equal success can be achieved with most of these agents [2], the author uses lignocaine, with or without epinephrine, almost exclusively. Lignocaine is excellent for minor nerve blockade and is presented as a dilute solution in 0.5, 1.0, 1.5, and 2% concentrations. The addition of epinephrine results in local vasoconstriction that reduces the systemic absorption of the anesthetic, improves the quality of the block, and prolongs the duration of anesthesia. A sufficient epinephrine concentration to achieve these effects is 5  mg/mL, or a concentration in solution of 1:200,000 [3]. Although guidelines exist for the maximum recommended dosages of local anesthetic agents, both with and without epinephrine, the evidence to support the guidelines is lacking [4]. Calculating maximum dosages of local anesthesia should take into account the location of the nerve block, age of the patient, medications, and any concurrent illness. The rate of absorption and peak plasma concentration of local anesthetic depends on the location of the block and especially on the vascularity of the tissues [5]. A reduction in 10–20% should be made for the maximum dosage in elderly patients or those with renal, hepatic, or cardiac dysfunction. Local anesthetic with epinephrine should never be used for blocks where there are end-arteries, such as the nose, fingers, or penis, where intense vasoconstriction could compromise perfusion and lead to ischemia or necrosis. For the nerve blocks described in this chapter, the following materials are required (Fig. 9.3):

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Table 9.3  Properties and dosage guidelines of amide local anesthetic agents Agent Lignocaine

Duration of actiona (min) 30–60

Prilocaine

30–90

Mepivacaine Bupivacaine

50–90 120–240

Maximum dosageb 4.5 mg/kg without epinephrine or max 300 mg 7 mg/kg with epinephrine 500 mg without epinephrine 600 mg with epinephrine 7 mg/kg or max 400 mg 2.5 mg/kg or max 175 mg without epinephrine 225 mg with epinephrine

Duration of action without epinephrine Dosage should be reduced in presence of chronic or acute illness, in the elderly and pediatric population, and in patients with renal, liver, and cardiovascular disease

a

b

Fig. 9.3  Materials required for minor nerve blocks

1 . Syringes: 3 mL and 5 mL 2. Needles: 30 gauge, 27 gauge, 25 gauge 3. Needle: 22 gauge spinal 4. Lignocaine 1–2% plain 5. Lignocaine 1–2% with 1:200,000 epinephrine 6. Sodium chloride for injection (for dilution if necessary) 7. Sterile gauze 8. Isopropyl alcohol pads

9.4 Anatomy and Technique 9.4.1 Infraorbital Nerve (Fig. 9.4) The infraorbital nerve is the largest cutaneous branch of the maxillary nerve. It emerges onto the face at the infraorbital foramen, along a vertical line between the pupil and medial limbus, about 7 and 6  mm below the inferior orbital rim in men and women, respectively. The foramen

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opens downward and medially, so the most accurate nerve block approach is from below and medially, either intraorally or percutaneously [6]. For the intraoral approach, a 27- or 30-gauge needle is passed through the vestibule between the canine and first premolar, aiming the needle toward the infraorbital foramen. The index finger of the non-injecting hand rests on the inferior orbital rim to prevent inadvertent passage of the needle beyond the rim. About 1.5 mL of anesthetic is injected around the foramen. The anesthetized area includes the lower eyelid, side of the nose, medial cheek, and upper lip. Alternatively, the nerve can be approached through the skin by injecting between the ala of the nose and the upper part of the nasolabial fold, directing the needle toward the infraorbital foramen.

9.4.2 Dorsal Nasal Nerve (Fig. 9.5)

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This nerve represents one or more dorsal branches of the ethmoid nerve. It passes under the nasal bone about 6 to 9  mm from the midline and passes under the nasalis muscle toward the tip of the nose [7]. The dorsal nasal nerve supplies sensory innervation to the tip of the nose via its 1–3 branches. The block is made at the level of the periosteum at the junction of the nasal and cartilaginous parts of the nose on either side of the midline.

9.4.3 Mental Nerve (Fig. 9.6)

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The mental nerve arises from the inferior alveolar nerve, a branch of the mandibular nerve, and exits the mental foramen between the apices of the lower premolar teeth, usually in line vertically with the infraorbital foramen, although it is sometimes slightly anterior or posterior to this position [8]. It usually exists as several fascicles that are visible or palpable through stretched oral mucosa. The mental nerve supplies skin over the lower lip and

Fig. 9.4  Infraorbital nerve block. (a) The nerve (dot) emerges below the inferior orbital rim and supplies the shaded area. (b) Percutaneous approach to the nerve from below and medially. The entry point is between the ala of the nose and the nasolabial fold. Note the finger protecting the orbit along the orbital rim. (c) More commonly performed intraoral approach. The needle enters the vestibule between the canine and first premolar (red dot) and aims toward the infraorbital foramen

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Fig. 9.5  Dorsal nasal nerve block. (a) Location of nerve (dot) on either side of the midline as it emerges from underneath the nasalis muscle and supplies the tip of the nose (shaded). (b) The nerve block is performed by injecting at the junction of the nasal bone and cartilage on either side of the midline

chin. Occasionally, a branch of the mylohyoid nerve innervates the central chin pad. To block the mental nerve, 1 ml of anesthetic is injected just under the mucosa between the premolars or around the nerve fibers if they are visible. Reaching the nerve percutaneously is also

Fig.  9.6  Mental nerve block. (a) Nerve location (dot) as it emerges from its foramen on the mandible and area of the chin and lower lip it innervates (shaded). (b) The nerve is approached intraorally by injecting under the mucosa at the root of the second premolar tooth

9  Local Regional Anesthesia

possible but is not frequently performed and may be more painful [9]. To anesthetize the central part of the chin, this block is augmented by injecting a further 2–3  mL preperitoneally over the mental protuberance using a 27-gauge 1.5-in. needle.

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9.4.4 Supraorbital, Supratrochlear, Infratrochlear Nerves (Fig. 9.7) The supraorbital nerve emerges from the orbit at the supraorbital notch (or foramen) 2.3–2.7  cm from the midline in men and 2.2–2.5  cm from the midline in women [10]. The nerve has superficial and deep branches. The superficial branch passes through the corrugator and frontalis muscles to innervate most of the forehead over the eyebrows and the anterior scalp. Sometimes the deep branch arises from a separate foramen up to 1 cm above the orbital rim and as far as 3–4 cm lateral to the medial branch. The deep branch usually runs superiorly between the galea and the periosteum of the forehead 0.5–1.5 cm medial to the superior temporal crest line. The supratrochlear nerve arises about 1 cm medial to the supraorbital nerve at the orbital rim and branches to supply the skin over the medial lower forehead and medial eyelid. The infratrochlear nerve arises medial and inferior to the supratrochlear nerve and supplies a small area of skin on the medial aspect of the upper eyelid and bridge of the nose. All three nerves can be blocked together. A 1.5-in. needle is passed from a point just lateral to the midline in the brow, along the orbital rim until the needle touches the nasal bone medially. The index finger of the noninjecting hand protects the globe. About 2 mL of local anesthetic is injected as the needle is withdrawn. Immediately after the needle exits, firm pressure is placed over the orbital rim with gauze to minimize bleeding and ecchymosis. A second horizontal injection is made under the frontalis muscle about 1 cm above the orbital rim to block a separate deep branch of the supraorbital nerve.

Fig. 9.7  Supraorbital, supratrochlear, and infratrochlear nerve blocks. (a) The sites of the foramina or notches from which the nerves appear on the face are represented by dots along the brow. From medial to lateral, the infratrochlear, supratrochlear, and supraorbital nerves innervate the shaded area. (b) The three nerves are blocked by passing the needle along the rim from the middle of the brow as far as the nasal bone and injecting on the way out. Note the finger protects the globe. (c) A second injection is made under the frontalis 1  cm above the brow to block an aberrant deep branch of the supraorbital nerve

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9.4.5 Zygomaticofacial Nerve (Fig. 9.8)

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The zygomaticofacial nerve exits its foramen just below and lateral to the junction of the inferior and lateral orbital rim. It provides sensory innervation to the skin over the malar eminence. The nerve is blocked by injecting 1–2 mL of anesthetic on the periosteum at the estimated location of the foramen just inferolateral to the bony rim.

9.4.6 Zygomaticotemporal Nerve (Fig. 9.9) The zygomaticotemporal nerve arises from its foramen behind the posterior aspect of the lateral orbital rim just above the point where the zygomatic arch meets the lateral orbital rim. It innervates the temple area. To block this nerve, the needle enters the skin behind the lateral orbital rim about 10–12  mm behind and just below the palpable zygomaticofrontal suture and passes deeply until it hits the posterior part of the orbital rim. The needle is slid down the posterior part of the rim to a point about 1 cm below the level of the lateral canthus near the zygomatic arch. On withdrawal, 2 mL are injected behind the lateral orbital rim where the nerve arises from its foramen [11]. b

9.4.7 Mandibular Nerve (Fig. 9.10) For procedures requiring anesthesia of the entire face, blocking the mandibular nerve proximally is beneficial because the buccal and auriculotemporal nerves innervate parts of the cheek and temple not covered by the nerves described above. The mandibular nerve passes about 1  cm posterior to the pterygoid plate, deep to the lateral pterygoid muscle. To block the nerve, first mark the location of the sigmoid notch, the depression below the zygomatic arch between the coronoid process and condyle of the mandible. Pass a 1.5-in. 27-gauge needle perpendicularly to infiltrate the skin first, and then continue through the fascia and masseter until the needle hits the lateral pterygoid plate. Remove the needle and pass a 22-gauge spinal needle attached to a 5 mL syringe in the same

Fig. 9.8  Zygomaticofacial nerve block. (a) The position of the zygomaticofacial nerve (dot) is shown just inferolateral to the lateral part of the inferior orbital rim. It innervates the skin over the zygomatic bone and arch (shaded). (b) The nerve block is easily performed by injecting on the periosteum over the foramen, while the non-injecting hand feels for the rim

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way until it tips the pterygoid plate. Use the plastic guard on the needle to mark the depth of the needle in this location. Then withdraw the needle partly and redirect it about 1 cm posteriorly until it reaches the depth marked on the needle. Advance the needle a few millimeters further, aspirate, and inject about 4 mL of anesthetic. This blocks the buccal and auriculotemporal nerves and anesthetizes the lateral part of the face and temple.

9.4.8 Greater Auricular Nerve (Fig. 9.11)

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The greater auricular nerve arises from the anterior primary rami of the second and third cervical nerves. It pierces the deep cervical fascia at the posterior border of sternocleidomastoid and runs on the muscle toward the angle of the jaw. Below the ear it divides into anterior and posterior branches and innervates the skin of the inferior part of the ear, the area below the ear, and the angle of the jaw. The nerve can be blocked at its location 6.5 cm inferior to the external acoustic meatus, midway between the anterior and posterior borders of sternocleidomastoid. About 2  mL of anesthetic is injected on the muscle at this point.

9.4.9 Wrist Block (Fig. 9.12)

Fig.  9.9  Zygomaticotemporal nerve block. (a) The nerve (shown as dot) arises from behind the posterior aspect of the lateral orbital rim near the zygomatic arch and supplies the skin over the temple (shaded). (b) The needle enters just behind and below the zygomaticofrontal suture and passes behind the posterior lateral orbital rim toward the zygomatic arch. Just below the level of the lateral canthus (and behind the lateral orbital rim) 2  mL of local anesthetic are injected as the needle is slowly withdrawn

Nerve blocks to the hand, especially the palmar surface, facilitate the injection of botulinum toxin into the dermis to treat palmar hyperhidrosis. Topical anesthesia only is usually insufficient as injections into the sensitive dermis of the palms are painful. To anesthetize the palmar surface of the hand, the median nerve, ulnar nerve, and radial nerves are blocked. The sensory innervation to the palm of the hand is shown in Fig. 9.12. The median nerve lies just deep to the palmaris longus tendon proximal to the wrist crease and continues under the flexor retinaculum to innervate the palmar surface of the radial three and a half digits and part of the thenar eminence. In about 10% of individuals the palmaris longus tendon is absent. A palmar cutaneous branch of the median nerve arises up to 10  cm proximal to the wrist crease, passes superficially over the retinaculum,

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Fig.  9.10  Mandibular nerve block. (a) The mandibular nerve (green) lies just posterior to the lateral pterygoid plate (black shaded). The auriculotemporal and buccal branches of the mandibular nerve innervate the skin over the side of the face (yellow shaded). The distribution of the mental nerve is not depicted here. (b) The sigmoid notch is marked between the mandibular condyle and coronoid process which are palpable below the zygomatic arch.

(c) A 1.5-in. 27-gauge needle passed perpendicularly through the center of the notch will reach the lateral pterygoid plate (shaded). Local anesthetic is infiltrated along this tract. (d) A 22-gauge spinal needle is then passed along the same course to the pterygoid plate. The depth on the needle is noted and it is then redirected 1 cm posteriorly to the same depth. In this position, the tip of the needle lies close to the nerve. After aspirating, 4 mL of anesthetic are injected

and innervates the central and proximal part of the palm of the hand. To block the median nerve, a 27-gauge needle is passed under the palmaris longus tendon 3 cm proximal to the distal wrist crease. At a depth of about 1  cm, 3–5  mL of anesthetic without epinephrine is injected slowly, after aspiration to avoid intravascular injection. With all nerve blocks at the wrist, advise the patient to report any “electric shock”-type sensations along the distribution of the nerves. If this occurs, withdraw the needle a few millimeters to avoid intraneural injection. As the needle is withdrawn, inject a further 2  mL subcutaneously to block the palmar branch.

Massage this bleb of anesthetic medially and laterally over the tendon to ensure the nerve is not missed. If the palmaris longus tendon is not present, simply inject deep to the fascia medial to the flexor carpi radialis tendon. If present, the palmaris longus is clearly visible when the thumb is opposed against the little finger and the wrist slightly flexed. The ulnar nerve lies deep and a little to the radial side of the flexor carpi ulnaris tendon. On the palmar surface it supplies sensory innervation to the ulnar one and a half fingers and the hypothenar eminence. To block the nerve, pass the needle just deep to the tendon

9  Local Regional Anesthesia

Fig.  9.11  Greater auricular nerve block. The nerve is found 6.5 cm below the external acoustic meatus in the midpart of sternocleidomastoid. It innervates the lower part of the ear, behind and below the ear, and the angle of the jaw (shaded area). The nerve is blocked by injecting on the fascia of the muscle at its predicted location (dot)

about 3  cm from the distal wrist crease and inject 3–5  mL. If the needle passes into the substance of the tendon, tough resistance will be felt and the needle should be partially withdrawn and redirected. The radial nerve supplies sensation to a small area on the thenar eminence through its superficial branches. It courses alongside the cephalic vein proximal to the anatomical snuff box on the radial side of the forearm and can be felt or rolled on the underlying fascia and bone. To block the radial nerve, a small area around the nerve is isolated with the non-injecting hand and 2–3 mL of anesthetic is injected onto the fascia adjacent to the cephalic vein. The trapped solution bathes the nerve to ensure adequate blockade.

9.4.10 Plantar Block (Fig. 9.13) Blocking the sensory innervation to the sole of the foot is indicated before injections of botulinum toxin for plantar hyperhidrosis. Without nerve blocks, the patient does not easily tolerate the procedure. This technique requires nerve blocks to the posterior tibial, sural, and saphenous nerves. The sensory supply to the sole of the foot is shown in Fig. 9.13. The posterior tibial nerve is found between the medial malleolus and Achilles

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tendon where it is related to the posterior tibial artery before it divides to form the lateral and medial plantar nerves. To block the posterior tibial nerve, a 25-gauge needle is passed on the medial side of the Achilles tendon at the level of the superior border of the medial malleolus. The needle is advanced until it touches the posterior border of the tibia, then withdrawn 5 mm, and 5 mL of plain lignocaine is injected. The nerve lies just posterior to the posterior tibial artery in this location. The sural nerve runs behind the lateral malleolus to innervate skin over the lateral aspect of the ankle, lateral foot, and a small area on the lateral plantar surface. An injection is made at the level of the superior malleolus on the lateral aspect of the Achilles tendon. The needle is advanced until it reaches the fibula, withdrawn 5 mm, and 5 mL is injected around the nerve. The saphenous nerve runs with the great saphenous vein on the anterior aspect of the medial malleolus. It innervates the medial ankle and a small area on the medial plantar surface of the foot. To block the nerve, injections are made just medial and lateral to the great saphenous vein anterior to the medial malleolus.

9.5 Complications Immediate complications following the injection of local anesthesia include pain, bleeding, hematoma, edema, nerve damage, and adverse drug reactions due to overdosage or allergy [12]. Vasoconstriction occurs when local anesthetic agents with epinephrine are inadvertently injected intravascularly, leading to a range of phenomena from local blanching of tissues and necrosis to transient loss of vision, diplopia, and amaurosis [13–16]. The positive chronotropic effects of epinephrine also result in transient tachycardia that may be uncomfortable for some patients. Systemic toxicity from local anesthesia following nerve blocks is possible if an excessive dosage is used, if the injection site is particularly vascular, or if the threshold for toxicity is lower due to advanced age or a comorbid condition. Systemic toxicity ­manifests first as central nervous system signs and symptoms, including tremor, twitching, dizziness, circumoral paresthesia, tinnitus, blurred vision, and progresses to convulsions and coma in severe cases. At higher plasma concentrations, cardiovascular toxicity occurs, leading to bradycardia, vasodilatation and

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Fig.  9.12  Wrist block. This requires blocks of the radial, median, and ulnar nerves. (a) Area on the palm innervated by the radial nerve. (b) The radial nerve (green) lies adjacent to the cephalic vein (blue) on the radial side of the forearm and can sometimes be felt if it is rolled against the underlying bone. (c) The non-injecting hand traps the nerve between two fingers proximal to the anatomical snuff box as the injection is made on the fascia. (d) Palmar surface innervated by the median nerve. (e) The visible flexor carpi radialis proximal to the wrist crease (marked) as the wrist is flexed against resistance. The palmaris longus tendon is absent in this patient (as it is in 10% of the population). When present, the median nerve is located deep to the palmaris longus tendon. If the tendon is absent, the nerve can be predicted to lie on the ulnar side of the flexor carpi radialis.

f

(f) The block is made 3  cm proximal to the wrist crease by injecting 1 cm deep, after aspirating. (g) In this patient, the palmaris longus tendon is clearly visible when the thumb is opposed. In 90% of the population, where the tendon is present, the median nerve is found deep to the tendon 3 cm proximal to the wrist crease where it can be blocked by passing a needle at 45° about 1 cm under the tendon. (h) A palmar cutaneous branch of the median nerve (green) arises up to 10 cm proximal to the wrist crease and supplies an area on the proximal part of the palm (shaded). This nerve is blocked by injecting 3 mL subcutaneously over the site of the median nerve. (i) Sensory innervation of the ulnar nerve on the palm. (j) The nerve is blocked by injecting 3 cm proximal to the wrist crease, deep to and slightly radial to the flexor carpi ulnaris tendon

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Fig. 9.12  (continued)

hypotension, arrhythmias and even asystole. Severe acute toxicity secondary to local anesthetics is rare if recommended dosages are used. Toxicity should be managed according to the clinical scenario. The airway should be maintained and oxygen delivered as required. Intravenous atropine is appropriate for bradyarrhythmias although volume expansion with colloid may be required if there is hypotension secondary to vasodilatation. In severe cases, epinephrine may be necessary, or cardioversion for cases of ventricular fibrillation.

9.6 Conclusions Nerve block techniques are simple to learn and invaluable to the practitioner of aesthetic medicine. Small or large areas of the face can be anesthetized in

a few minutes allowing most non-surgical and ­minimally invasive procedures to be performed without the need for adjuvant anesthesia. Successful nerve block requires that a sufficient volume and concentration of local anesthetic surround the regional nerve at its origin or at a site proximal to the area it innervates. However, the maximum dosage should not be exceeded to avoid the risk of toxicity. Complications secondary to nerve blocks are uncommon but can occur if the maximum dosage is exceeded or if the solution is injected intravascularly. Simple measures to ensure safe technique and maximum comfort for the patient include aspiration prior to injection, slow injection of solution at room temperature, use of plain anesthetic without epinephrine for extremities, and protecting the orbit with the non-injecting hand for blocks around the eye.

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Fig. 9.13  Plantar block. (a) The plantar surface of the foot receives innervation from the posterior tibial nerve, sural nerve, and saphenous nerve: (blue dash) calcaneal branches of posterior tibial nerve; (black dots) medial plantar nerve; (black dash) lateral plantar nerve; (red dash) sural nerve; (green dash) saphenous nerve. (b) Ankle showing the medial malleolus (M), posterior tibial artery and nerve

posterior to the malleolus. (c) The sural nerve is blocked by injecting the needle at the superior level of the lateral malleolus (M), advancing toward the fibula until it is reached. About 5 mL local anesthetic is injected slowly as the needle is withdrawn. (d) The saphenous nerve is blocked by injecting just anterior to the medial malleolus alongside the great saphenous vein

9  Local Regional Anesthesia

References 1. Loukas M, Owens DG, Tubbs RS, Spentzouris G, Elochukwu A, Jordan R (2008) Zygomaticofacial, zygomaticoorbital and zygomaticotemporal foramina: anatomical study. Anat Sci Int 83(2):77–82 2. McClean C, Reader A, Beck M, Meryers WJ (1993) An evaluation of 4% prilocaine and 3% mepivacaine compared with 2% lidocaine (1:100,000 epinephrine) for inferior alveolar nerve block. J Endod 19(3):146–150 3. Scott DB, Jebson PJR, Braid DP, Oertengren B, Frisch P (1972) Factors affecting plasma levels of lignocaine and prilocaine. Br J Anaesth 44(10):1040–1049 4. Rosenberg PH, Veering BT, Urmey WF (2004) Maximum recommended doses of local anesthetics: a multifactorial concept. Reg Anesth Pain Med 29(6):564–575 5. Tucker GT, Mather LE (1988) Absorption and disposition of local anesthetics: pharmacokinetics. In: Cousins MJ, Bridenbaugh PO (eds) Neural blockade in clinical anesthesia and management of pain. Williams & Wilkins, Baltimore, pp 61–63 6. Lynch MT, Syverud SA, Schwab RA, Jenkins JM, Edlich R (1994) Comparison of intraoral and percutaneous approaches for infraorbital nerve block. Acad Emerg Med 1(6): 514–519 7. Zide BM (2006) Nerve blocks 101. In: Zide BM, Jelks GW (eds) Surgical anatomy around the orbit. The system of zones. Lippincott Williams & Wilkins, Philadelphia, p 116

101 8. Haribhakti VV (1996) The dentate adult human mandible: an anatomic basis for surgical decision-making. Plast Reconstr Surg 97(3):536–541 9. Syrverud SA, Jenkins JM, Schwab RA, Lynch MT, Knoop K, Trott A (1994) A comparative study of the percutaneous versus intraoral technique for mental nerve block. Acad Emerg Med 1(6):509–513 10. Zide BM (2006) Supraorbital nerve. Nuances/dissections from above. In: Zide BM, Jelks GW (eds) Surgical anatomy around the orbit. The system of zones. Lippincott Williams & Wilkins, Philadelphia, p 77 11. Zide BM, Swift R (1998) How to block and tackle the face. Plast Reconstr Surg 101(3):840–851 12. Lustig JP, Zusman SP (1999) Immediate complications of local anesthetic administered to 1007 consecutive patients. J Am Dent Assoc 130(4):496–499 13. Blaxter P, Britten M (1967) Transient amaurosis after mandibular nerve block. Br Med J 1(5541):681 14. Webber B, Orlansky H, Lipton C, Stevens M (2001) Complications of an intra-arterial injection from an inferior alveolar nerve block. J Am Dent Assoc 132(12):1702–1704 15. Torrente-Castells E, Gargallo-Albiol J, Rodriguez-Baeza A, Berini-Aytes L, Gay-Escoda C (2008) Necrosis of the skin of the chin: a possible complication of inferior alveolar nerve block injection. J Am Dent Assoc 139(12):1625–1630 16. Choi EH, Seo JY, Jung BY, Park W (2009) Diplopia after inferior alveolar nerve block anesthesia: report of 2 cases and literature review. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 107(6):e21–e24

 

Botulinum Toxins

10

Peter M. Prendergast

10.1 Introduction

10.2 History

Botulinum toxin (BTX) is a powerful, naturally occurring exotoxin produced by the anaerobic, spore-forming bacterium, Clostridium botulinum. Although there are seven distinct serotypes (A–G), BTX type A is the most potent in humans and is the most widely used botulinum toxin in clinical and aesthetic medicine. In minute doses, purified BTX-A injected into facial muscles causes temporary chemodenervation. Partial or complete paralysis of selected muscles of facial expression reduces hyperdynamic wrinkles, improves the position or shape of the brow and mouth, and even contours the face. The explosion in popularity of BTX-A treatments over the last two decades is a testament to its safety and efficacy. In the USA, chemodenervation with BTX-A was the number one non-surgical procedure every year since 2000, with a 3,824% increase in the number of BTX-A treatments from 1997 to 2009 [1]. Although the treatment of glabellar frown lines is currently the only approved cosmetic indication for certain preparations of BTX-A, off-label use in muscle groups in the upper face, lower face, and neck yield excellent results with minimal complications in experienced hands. This chapter describes the most effective and appropriate use of botulinum toxin type A in aesthetic medicine for face and neck rejuvenation, and its use in the treatment of hyperhidrosis.

Botulism, derived from “botulus,” the Latin word for sausage, is an intoxication from food poisoning with visual disturbance, nausea, vomiting, dizziness that progresses to a symmetric descending neuroparalysis. Justinus Kerner, a German physician, originally described the symptoms of botulism between 1817 and 1822 but did not identify the pathogen [2]. In 1895, an outbreak of botulism in Ellezelles, Belgium, associated with contaminated smoked ham left 34 people ill and three dead. Van Ermengem at the University of Ghent identified the bacterium responsible as bacillus botulinus. This was later renamed Clostridium botulinum. His studies revealed that the toxin produced by the bacteria is heat-sensitive but quite resistant to alcohol, certain enzymes, and acidic environments [3]. Sommer and Snipe purified the toxin in the early 1920s [4]. In 1946, Shantz identified and isolated botulinum toxin type A, the most potent of the serotypes in humans. Burgen et al. [5] elucidated the physiology and mechanism of action of botulinum toxin. Scott [6] was the first to use the toxin experimentally in animals and showed that it effectively weakened extraocular muscles in monkeys. In 1977, the toxin was used in humans for the same purpose. From this work, protocols were developed for the use of botulinum toxin for the treatment of strabismus. This led to the approval of BTX-A by the Food and Drug Administration (FDA) for the treatment of strabismus in 1989, and for blepharospasm in 1989 [7]. In 1987, Carruthers made the serendipitous discovery that BTX-A injections improve the appearance of frown lines. She was using BTX-A to treat patients with benign essential blepharospasm and noticed that spread

P.M. Prendergast  Venus Medical, Heritage House, Dundrum Office Park, Dublin 14, Ireland e-mail: [email protected]

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_10, © Springer-Verlag Berlin Heidelberg 2011

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Fig. 10.1  Commonly used botulinum toxins

of some of the toxins into the adjacent glabellar muscles improved hyperdynamic wrinkles in this area. Although Clark and Berris published a paper on the use of BTX-A to treat facial asymmetry in 1989 [8], it was Carruthers’ landmark paper in 1992 [9] describing its efficacy in treating frown lines that heralded the modern era of botulinum toxin in aesthetic medicine. In 2003, the FDA approved Botox® (Allergan, CA, USA) for the treatment of glabellar lines. In 2009, FDA approval was also granted for Dysport® (Ipsen, Berkshire, UK), another type A botulinum toxin, for the treatment of glabellar folds.

10.3 Available Botulinum Toxins Several botulinum toxin type A products are available from the USA, the UK, Germany, Korea, and China. Botox and Dysport are the market leaders worldwide and currently the only two type A botulinum toxins approved by the FDA. Their aestheticindication counterparts are Botox Cosmetic and Azzalure, respectively. These products are produced from cultures of Clostridium botulinum that yield the neurotoxin itself surrounded by a protective protein complex. Although the complexes, consisting mostly of hemagglutinins, may vary in mass between products, the neurotoxin itself is identical, consisting of a light chain and a heavy chain (HC) joined by a disulfide bond. The compound is prepared with excipients that include human albumin, then vacuum freeze dried and presented as a white powder in vials for reconstitution with sterile saline before use (Fig. 10.1). Botox and Dysport should be stored at 2–8°C and ideally used within 48  h following reconstitution,

although potency is probably preserved for up to 2 weeks [10]. Botox is presented in vials of 100 U and Dysport in vials of 500 U or 300 U. It is important to understand that the units of Botox and Dysport are not interchangeable [11]. One biological unit (U) of Botox or Dysport is the dose required (LD50) to kill 50% of 20  g Swiss-Webster (CFW®) mice when injected intraperitoneally. However, the effects on mice cannot be extrapolated to other species, so 1 U Botox does not exhibit the same effect in humans as 1 U Dysport. The literature on dose equivalence between Dysport and Botox is confusing, with different authors concluding ratio conversions from 4:1 to 2:1 [12]. In the author’s experience, a conversion of 1 U Botox to 2.5 U Dysport is appropriate for most aesthetic indications. However, if a physician chooses to use both products, experience dictates dosage requirements for satisfactory outcomes rather than simply converting from one to another using a simple and largely unsubstantiated ratio. 1. Azzalure® is adapted from Dysport and branded and marketed by Galderma (Lausanne, Switzerland). The two products are identical in activity and the units are interchangeable. Azzalure is presented in vials of 125 U and approved for glabellar lines. 2. Xeomin® (Merz, Frankfurt, Germany) was introduced to the market in 2005 and is now available throughout Europe presented as 100 U vials. It differs in structure to the other BTX-A products by consisting of the 150 kDa neurotoxin only without the surrounding protein complex [13]. For practical purposes, a conversion ratio of 1:1 between Xeomin and Botox is considered appropriate. 3. Bocouture® is Xeomin’s sister toxin, presented in 50 U vials and licensed for aesthetic use. Inactive

10  Botulinum Toxins

ingredients also differ between products; Botox/ Botox Cosmetic contains sodium chloride. 4. Dysport/Azzalure contains lactose, and Xeomin/ Bocouture contains sucrose. Other products include Neuronox® (Medy-Tox, Seoul, South Korea) and Prosigne® (Lanzhou Institute of Biological Products, China). Although these products are presented as 100 U vials of lyophilized botulinum toxin type A complex and reportedly have 1:1 conversion rates to Botox®, efficacy and safety studies and trials are lacking compared to the market leading products [14].

10.4 Mechanism of Action Botulinum toxin causes a flaccid paralysis of striated muscle by blocking the release of the neurotransmitter acetylcholine at the neuromuscular junction. Normally, an action potential along a nerve terminal stimulates fusion of acetylcholine-containing vesicles with the cell membrane at the synaptic cleft, releasing acetylcholine to act on ­cholinergic receptors in striated muscle. This fusion is mediated by two groups of SNARE (soluble N-ethylmale­ imide-sensitive factor attachment protein receptors) proteins: synaptobrevin on the acetylcholine-containing vesicle; syntaxin 1A and SNAP-25 on the plasma membrane at the neuromuscular junction (Fig. 10.2). Any interference with one or more of these proteins prevents formation of the so-called synaptic fusion complex and blocks release of acetylcholine [15]. Most botulinum toxin A products consist of the neurotoxin surrounded by a protective protein complex. The complex is resistant to acidic environments and protects the toxin from the harsh environment of the digestive tract. In tissues with a higher pH, such as subcutaneous, intramuscular, or intravascular compartments, the covalent bonds binding the complex quickly dissociate, releasing the neurotoxin. After injection, the neurotoxin is probably released in less than a minute [16]. BTX-A consists of three 50  kDa segments, designated L, HN, and HC [17]. The HC binds to the cholinergic nerve cell membrane, leading to endocytosis of the toxin into the intracellular compartment. The intermediate chain (HN) facilitates the translocation of the light chain (L) from the vesicle into the cytosol of the nerve. The light chain of BTX-A cleaves the SNAP25 protein at the neuromuscular junction and blocks the neuroexocytosis of acetylcholine into the synaptic cleft (Fig. 10.2). Botulinum toxin type B (Myobloc®)

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cleaves the vesicle-associated membrane protein (VAMP), synaptobrevin, rather than SNAP-25, but both type A and type B toxins ultimately block the release of acetylcholine leading to temporary paralysis of striated muscle. Clinically, the effects of botulinum toxin injections begin 2–3 days following treatment and are maximal at 10–14 days. After approximately 1 month, new unmyelinated nerve “sprouts” begin to grow from the nerve endings to re-establish functional connections within the motor units. Normal muscular activity slowly returns within 3–4 months. Following repeated injections over several years of treatment, disuse atrophy of denervated muscle may prolong the effects of subsequent treatments, to 6 months or longer in some cases. The release of sweat from eccrine sweat glands is also mediated by acetylcholine. Intradermal injections of BTX-A block this release through the same mechanisms described above and effectively reduce unwanted sweating. This application has led to the treatment of axillary, palmar, and plantar hyperhidrosis with anhidrosis typically lasting longer than the effect of acetylcholine blockade in striated muscle.

10.5 Clinical Effects When botulinum toxin is injected subcutaneously or intramuscularly, it exhibits effects at the injection site and over an area 1–2 cm in diameter around the point of injection. The spread of toxin in the tissues is termed the “action halo.” A number of factors may influence the size of the action halo: manipulation or manual spreading following injection, volume of solution injected, dose, and type of toxin used [18]. Even without forceful or deliberate contraction, the mimetic muscles of the face have a resting tone that determines the position of the tissues they act upon (Fig. 10.3). Frontalis, a brow elevator, works in opposition to the brow depressors, which include procerus, corrugators, and fibers of orbicularis oculi. Unopposed activity of the elevators will therefore elevate the brow (Fig.  10.4). To achieve this, the brow depressors are treated with BTX, whilst preserving frontalis. Similarly, unopposed action of the depressors will drop the brow and forehead. For this reason, treating frontalis alone without the depressors will result in a heavy ptotic brow and should never be ­performed. Around the mouth, denervating depressor anguli oris results in reduced

106 Fig. 10.2  Mechanism of action of botulinum toxin A. (Left) Normal release of acetylcholine. (Right) Botulinum toxin blocks neuromuscular transmission by cleaving the SNAP-25 component of the synaptic fusion complex. HC heavy chain, LC light chain, Ach acetylcholine

P.M. Prendergast HC

LC

Nerve cell receptor

Endocytosis of botulinum toxin

Translocation of LC

ACh-containing vesicle

Synaptobrevin

SNAP-25 Syntaxin-1A

opposition to the lateral lip elevators (Fig.  10.5). Denervating one part of a muscle with BTX and preserving other fibers of the same muscle also increases the activity of the preserved fibers. For example, treatment of the medial part of frontalis with preservation of the lateral part increases the activity of lateral frontalis and creates a lateral brow lift. An understanding of the dynamics and behavior of the mimetic muscles and their response to chemodenervation allows them to be manipulated to achieve a variety of aesthetic results.

Cleavage

10.6 Anatomy A thorough knowledge of facial anatomy and musculature is necessary for injectable treatment with BTXA. Imprecise injections will at best lead to suboptimal results and at worst to complications such as brow or lid ptosis, mouth asymmetries, or even visual disturbance. The muscles of facial expression are thin, flat muscles that act either as sphincters of facial orifices, as dilators, or as elevators and depressors of the

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Fig. 10.3  Superior and inferior vectors on the brow and mouth produced by normal resting tone and activity of the facial muscles

Fig.  10.5  Selective denervation of depressor anguli oris produces a reduced opposition to the mouth corner elevators. This activity lifts the mouth corners

Fig.  10.4  Brow elevation is produced by denervating the depressors and sparing the frontalis

e­ yebrows and mouth (Table 10.1). Many of these muscles are intimately related to or mingle with fibers of the muscles around them. Inadvertent injection or spread of botulinum toxin into the “wrong” muscle can lead to complications. Frontalis, corrugator supercilii, depressor supercilii, procerus, and orbicularis oculi represent the periorbital facial muscles. The perioral muscles include the levator muscles, zygomaticus major and minor, risorius, orbicularis oris, depressor anguli oris, depressor labii, and mentalis. The nasal group includes compressor naris, dilator naris, and depressor septi. In the neck, the platysma muscle lies superficially and extends into the lower face (Fig. 10.6). Frontalis represents the anterior belly of the occipitofrontalis muscle and is the main elevator of the brows. It arises from the epicranial aponeurosis and passes forwards over the forehead to insert into fibers of orbicularis oculi, corrugators, and dermis over the brows. Contraction raises the eyebrows and creates horizontal furrows across the forehead. Orbicularis oculi acts as a sphincter around the eye. It consists of three parts, the orbital, preseptal, and pretarsal parts. The orbital part arises from the nasal part of the frontal

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Table 10.1  Mimetic facial muscles Brow elevator Brow depressors

Lower lid elevator Mouth and lip elevators

Mouth and lip depressors

Nose

Neck

Frontalis Procerus Corrugator supercilii Depressor supercilii Orbicularis oculi (orbital part) Orbicularis oculi (pretarsal part) Levator labii Levator anguli oris Levator labii superioris alaeque nasi Zygomaticus major and minor Mentalis (lower lip) Depressor labii Depressor anguli oris Platysma Compressor naris Dilator naris Depressor septi Platysma

Frontalis (medial) Depressor supercilli Levator labii superioris alaeque nasi

bone, the frontal process of the maxilla, and the anterior part of the medial canthal tendon. Its fibers pass in concentric loops around the orbit, well beyond the confines of the orbital rim. Contraction causes the eyes to squeeze closed forcefully. Superior fibers also depress the brow. Preseptal orbicularis oculi arises from the medial canthal tendon, passes over the fibrous orbital septum of the orbital rim, and inserts into the lateral palpebral raphe. The pretarsal portion, involved in blinking, overlies the tarsal plate of the eyelid and has similar origins and insertions to its preseptal counterpart. In some individuals, contraction of the pretarsal part results in fine lines under the eye or bulging of the lid itself. Corrugator supercilii arises from the superomedial aspect of the orbital rim and passes upwards and outwards to insert into the dermis of the middle of the brow. From its origin deep to frontalis, two slips of muscle, one vertical and one transverse, pass through fibers of frontalis to reach the dermis. Corrugator supercilii depresses the brow and pulls it medially, as in frowning. Depressor supercilii is a thin slip of muscle

Frontalis (lateral) Procerus Corrugator Orbicularis oculi:

Zygomatici

Pretarsal part Preseptal part Orbital part Compressor naris Dilator naris

Orbicularis oris

Depressor anguli oris

Depressor septi

Mentalis

Depressor labii Platysma

Fig. 10.6  Anatomy of the facial muscles

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that is difficult to distinguish from the superomedial fibers of orbicularis oculi. It inserts into the medial brow and acts as a depressor. Procerus arises from the nasal bone, passes superiorly, and inserts into the dermis of the glabella between the brows. It depresses the lower forehead skin in the midline to create a horizontal crease at the bridge of the nose. Zygomaticus major and minor are superficial muscles that originate from the body of the zygoma and pass downward to insert into the corner of the mouth and lateral aspect of the upper lip, respectively. Superior fibers of these muscles lie beneath the orbital part of orbicularis oculi where they are prone to denervation with injudicious injections of botulinum toxin below the lateral canthus. Zygomaticus major and minor lift the corners of the mouth. Levator labii superioris alaeque nasi (LLSAN) originates from the frontal process of the maxilla and inserts into the nasal cartilage and upper lip. This thin slip of muscle elevates the upper lip during smiling. Orbicularis oris acts as a sphincter around the mouth and its fibers interlace with all of the other facial muscles that act on the mouth. Contraction of orbicularis oris has various actions including pursing, dilation, and closure of the lips. Smokers who overuse this muscle are prone to vertical rhytids above the lip. Depressor anguli oris arises from the periosteum of the mandible along the oblique line lateral to depressor labii inferioris. Its fibers converge on the modiolus with fibers of orbicularis oris, risorius, and sometimes levator anguli oris. Depressor labii inferioris arises from the oblique line of the mandible in front of the mental foramen, where fibers of depressor anguli oris cover it. It passes upwards and medially to insert into the skin and mucosa of the lower lip and into fibers of orbicularis oris. Mentalis arises from the incisive fossa of the mandible and descends to insert into the dermis of the chin. Contraction elevates and protrudes the lower lip and creates the characteristic “peach-pit” dimpling of the skin over the chin. Nasalis consists of two parts, the transverse part (compressor naris) and alar part (dilator naris). Compressor naris arises from the maxilla over the canine tooth and passes over the dorsum of the nose to interlace with fibers from the contralateral side. It compresses the nasal aperture and contributes to the formation of “bunny lines” over the dorsum of the nose. Dilator naris originates from the maxilla just below and medial to ­compressor

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naris and inserts into the alar cartilage of the nose. It dilates the nostrils during respiration. Depressor septi is a slip of muscle arising from the maxilla above the central incisor, deep to the mucous membrane of the upper lip. It inserts into the cartilaginous nasal septum and pulls the nose tip inferiorly. Platysma is a broad thin sheet of muscle that arises from the fascia of the muscles of the chest and shoulders and passes upwards over the clavicles and neck toward the lower face. Fibers insert into the border of the mandible, perioral muscles, modiolus, and dermis of the cheek. As part of aging, its fibers attenuate or thicken to create platysmal bands. Functionally, platysma depresses the mandible during deep inspiration but is probably more important as a mimetic muscle to express horror or disgust. The action of the facial muscles on the brow and mouth are shown in Table 10.1.

10.7 Indications The skin of the face is adherent to the underlying mimetic muscles through the superficial musculoaponeurotic system (SMAS) and its fibrous septae. Contraction of these facial muscles creates hyperdynamic lines, particularly in the upper face where there is very little subcutaneous fat between the muscles and the dermis. Botulinum toxin improves hyperdynamic lines by inducing a flaccid paralysis in the underlying muscles that cause them. Indications for treatment with botulinum toxin type A in aesthetic medicine are shown in Table 10.2. Although most areas of the face, including the neck, are amenable to treatment with botulinum toxin, chemodenervation in the lower face is less forgiving and should be performed only once the physician has gained experience in treating the upper face. Contraindications to treatment with BTX-A include known allergy to the product or its components, inflammation or infection at a proposed injection site, pregnancy, breast-feeding, and neuromuscular disorders such as myasthenia gravis.

10.8 Consultation It is important to ask the patient what they wish to achieve from the treatment. Some patients prefer a natural look with some movement, whilst others prefer no movement

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Table 10.2  Aesthetic indications for botulinum toxin Indication Frown lines Horizontal forehead lines Brow lift

Lateral orbital lines (crow’s feet) Lower eyelid lines, lid hypertrophy Gingival show (“gummy” smile) Perioral lines (smokers lines) Downturned mouth Dimpled (“peachpit”) chin Platysmal (“turkeyneck”) bands Horizontal (“necklace”) lines Nasal (“bunny”) lines Masseteric hypertrophy (square jaw) Jawline (“Nefertiti”) lifting

Target muscle(s) Procerus, corrugators Frontalis Procerus, corrugators, orbicularis oculi (orbital part), medial frontalis (lateral brow lift) Orbicularis oculi (lateral orbital part) Orbicularis oculi (pretarsal part) Levator labii superioris alaeque nasi Orbicularis oris Depressor anguli oris Mentalis Platysma Platysma (intradermal) Nasalis (compressor part) Masseter Platysma

and a very smooth appearance. The treatment should be tailored accordingly. In female patients, the desired brow shape should be determined. Although a gentle arch in the lateral brow is aesthetically ideal for most women, some women prefer no arch, or a significant “lift.” A horizontal, lower set brow is more appropriate in the male patient (Fig. 10.7).

10.9 Facial Assessment The Glogau classification system for wrinkles and photoaging is useful when considering suitable candidates for BTX-A treatments. Younger patients with no wrinkles (Glogau I) may seek treatment to prevent lines, elevate the brow, treat a gummy smile, or reduce the appearance of a square jaw due to masseteric hypertrophy. Patients who benefit most from BTX-A injections are those who have wrinkles on animation (Glogau II). Older patients with wrinkles at rest (Glogau III) are frequently candidates for BTX-A but usually achieve superior results when chemodenervation is combined with other treatment modalities such

as soft tissue augmentation and skin resurfacing. Before any treatment is performed, a careful assessment of the proposed treatment areas should be made.

10.9.1 Upper Face First, inspect for the presence of excess skin and tissue under the brows (dermatochalasis) (Fig. 10.8). In these patients, even a drop by 1–2 mm of the brow following treatment of frontalis may be enough to cause hooding and a feeling of heaviness that many patients find distressing. Either avoid treating frontalis in these patients or treat it with very conservative doses superiorly in the forehead well away from the brows. The corrugators should also be treated conservatively in these patients as spread of the toxin into medial fibers of frontalis can lead to medial brow ptosis. Some patients with heavy upper lids compensate, often subconsciously, by constantly contracting frontalis to elevate the brows and keep the excess tissue out of the eyes. This frontalis over activity creates deep horizontal forehead lines. Treating frontalis with BTX-A in these patients can be detrimental, as they lose the ability to elevate the brows and develop a brow ptosis. To determine whether the patient is compensating, perform the following simple test: 1. Ask the patient to close their eyes and relax the forehead completely. Gently stroke the forehead downward to make sure frontalis is relaxed. 2. Focus carefully on the horizontal position of the brow. 3. Ask the patient to open their eyes and look at you. Watch the position of the brow. If the brows elevate upon opening the eyes, there is compensation. If the brow remains at the same level when the eyes open and the patient does not feel “heaviness” in this position, treating frontalis is relatively safe. Next, note the strength of the upper facial muscles, the distribution of rhytids, and the nature of the lines. Deep, etched-in lines usually improve with BTX-A treatments but will not disappear. Explain this to the patient so they have realistic expectations. Additional procedures such as dermal fillers in the glabella or laser resurfacing for crow’s feet may be suggested. Male patients typically have stronger facial muscles and require higher doses to achieve satisfactory denervation [19]. If treatment of pretarsal orbicularis oculi is being considered to improve lines in the lower eyelid, or a hypertrophic muscle, first perform the snap test. Gently pull away the lower eyelid from the globe and release. The lid

10  Botulinum Toxins Fig. 10.7  Aesthetically ideal brow shape. (a) Male, the brow should be horizontal and at the level of the supraorbital ridge. (b) Female, a gently arching brow from medial to lateral is ideal

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a

b

10.9.2 Lower Face Inspect the patient carefully during animation at the time of consultation. Some patients habitually pull the corners of the mouth downward during speech. This over activity of depressor anguli oris may contribute to a downturned mouth, even in the resting position. Although patients may request fillers in the chin to make it smoother, chemodenervation of mentalis is usually more appropriate to soften dermal insertions of the muscle. Vertical lip lines are more appropriately treated with BTX-A if they appear primarily during animation but disappear at rest. In older patients and smokers, a combination of fillers for augmentation and BTX-A for denervation usually provides better results than each treatment on its own.

10.10 Keys for Success

Fig. 10.8  Patient with dermatochalasis. Treatment of frontalis with botulinum toxin should be conservative or avoided in this patient to avoid brow ptosis

should snap promptly back into place. A sluggish response indicates laxity of the lower lid, and contraindicates denervation of the muscle, which could cause an ectropion.

It should be remembered that the aim of treatment with botulinum toxins is facial rejuvenation and not total paralysis of treated muscles. Careful placement of appropriate doses of botulinum toxin in suitable patients enables satisfactory outcomes with a negligible incidence of complications. Some keys for success include the following: 1. Use conservative doses and accurately placed injections to selectively denervate muscles. This enhances natural-looking results and reduces complica­tions. Adjustments or “top-ups” can be performed at ­follow-up visits. 2. Use low doses in the frontalis to preserve some activity and avoid brow ptosis. 3. Never treat frontalis without treating the brow depressors (corrugators and procerus).

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Fig. 10.9  Insulin syringe with 30-gauge needle used for injection of botulinum toxin

4. Use miniscule doses for injections over the lateral brow where necessary, with additional denervation of the lateral orbicularis oculi in the brow to avoid lateral brow ptosis. 5. Warn the patient of transient weakness around the mouth with perioral injections. 6. Ask the patient to contract the selected muscles before injection to identify the anatomy and improve precision. 7. Increase the dose in male patients and those with stronger muscles as required. 8. Combine treatments with fillers, photorejuvenation, skin resurfacing, and suture lifting techniques for more impressive overall rejuvenation.

a

b

10.11 General Technique The technique using Dysport will be described, although the concepts of chemodenervation can be applied to any of the other botulinum toxins. For practical purposes, 2.5 U Dysport can be considered approximately equal to 1 U Botox or 1 U Xeomin. To reconstitute Dysport, 2.5  mL saline is slowly injected into the vial using a 3 mL syringe and 20-gauge needle. Saline with or without preservative can be used, although there is some evidence that saline with benzyl alcohol is associated with reduced pain on injection [20]. Although reconstitution with less or more volume is possible, a more concentrated solution requires extremely small injection aliquots and a more diluted solution may increase spread and diffusion of the toxin following injection. The 2.5 mL volume produces a solution with 2 U Dysport per 0.01 mL graduation on a 0.5 or 1 mL syringe. For injection, the author prefers a 0.5 mL insulin syringe with attached 30-gauge needle and clear 0.01  mL graduations (Fig.  10.9). Using separate syringe and needles, up to 0.08  mL product remains in the “dead space” of the 30-gauge needle hub and cannot be used. Puncturing the needle through the rubber cap on the vial will cause some blunting and increase the discomfort on injection. As

Fig.  10.10  (a) and (b) Techniques for injecting botulinum toxin. The graduations on the syringe should be clearly visible during injection

such, either the cap and rubber bung should be removed to draw up the solution or several syringes should be used for a single treatment. Before injecting, the syringe should be rotated so the graduations on the barrel are clearly visible. Anesthesia is not required for botulinum toxin injections using 30-gauge needles and is usually well tolerated. The non-injecting hand should have a sterile cotton ball ready to gently compress the injection point

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a

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b

Fig. 10.11  Assessing the glabellar area. (a) Ask the patient to frown and observe the anatomy and strength of the procerus and corrugators. (b) The procerus lies in the midline between the

brows, the belly of the corrugator usually near the medial brow. The lateral insertion should be injected where it inserts into the dermis above the brow

following withdrawal of the needle. This reduces the incidence of ecchymosis. Using the cotton ball, the tissues can also be wiped along the extent of the muscle using 2–3 gentle strokes. This maneuver allows a controlled spread of toxin within the chosen parts of the muscle, or across a broad sheet of muscle such as frontalis. Various general techniques are used to hold the syringe during injection (Fig. 10.10).

is rare if the muscle is injected carefully with conservative doses. The thin fibers of the lateral corrugator are easily denervated, and excessive doses will also denervate frontalis in this area and may create medial brow heaviness. Usually 6–8 U Dysport is sufficient. It is useful to “visualize” the anatomy under the skin and gently wipe the skin with the cotton ball from the medial to lateral injection to spread the toxin along the extent of the muscle. Five injection points should be made to treat the glabella (Fig. 10.12). Two weeks following the treatment, attempted frowning should produce no movement of the glabellar muscles (Fig. 10.13).

10.11.1 Glabella Improving hyperdynamic glabellar frown lines requires chemodenervation of procerus, and medial and lateral parts of corrugators. The patient is asked to frown to determine the strength of the muscles and identify the lateral extent of corrugator where it tethers the dermis (Fig.  10.11). These muscles are brow depressors so their treatment usually produces a subtle brow elevation. The procerus is gently pinched in the midline and an injection is made perpendicularly into the belly of the muscle. Dysport 12–14 U is usually sufficient in a female patient, but up to 20 U may be required in a male patient. To inject the medial part of corrugator, the thumb or finger is placed along the orbital rim to define the belly of the muscle. The author directs the needle along the long axis of the muscle, depositing 8–10 U Dysport in the medial part in a female patient. A perpendicular injection is then made at the lateral insertion of the muscle, deep to frontalis. This is usually at least 1 cm from the orbital margin, but the site of injection is determined by the muscle itself and should not be dictated by bony landmarks here. Ptosis

10.11.2 Forehead Horizontal forehead lines vary in prominence from subtle fine lines to deep furrows depending on the strength of frontalis. If the patient with deep lines actively contracts the muscle during speech and animation, look for dermatochalasis and consider sparing frontalis to avoid brow ptosis and hooding. Similarly, elderly patients with excess skin under the brow should be treated conservatively [21]. In a typical patient, small 4–5 U aliquots of Dysport across the superior aspect of frontalis are sufficient to smooth lines completely without creating an unnatural “plastic-like” appearance (Fig. 10.14). For stronger muscles, or when the muscle fibers extend more superiorly toward the hairline, two rows of injections can be placed (Fig. 10.15). Over the lateral frontalis, even less toxin should be used. The treatment over lateral frontalis

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a

b

c

d

Fig.  10.12  Injection technique for the glabella. (a) The procerus is gently pinched and a perpendicular injection is made into the belly of the muscle. (b) The medial part of corrugator is injected into the belly of the muscle. (c) The lateral part of corrugator is injected where its most lateral fibers are seen to tether

a

the dermis. This injection is made perpendicularly just above the periosteum and deep to frontalis. (d) The thumb or finger is placed along the supraorbital ridge to protect the orbit and define the medial part of corrugator before injection

b

Fig. 10.13  (a) Before. (b) Attempted frowning 2 weeks after chemodenervation of procerus and corrugators with 40 U Dysport

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Fig. 10.14  Typical treatment pattern for patient with average or weak frontalis. To maintain or achieve an arched lateral brow, the lateral frontalis is treated with low doses high in the forehead. When the forehead is treated, the glabella is always treated too to avoid overactivity of the glabellar muscles. Diagram shows units of Dysport at each injection point

depends on the morphology and strength of the muscle in this region. In patients with a very weak frontalis and almost no movement over the lateral brow, the lateral forehead can be avoided completely. By treating the medial frontalis only, resting tone in fibers of the lateral part increases, creating a slight lateral brow lift. When contraction of frontalis produces bunching of skin immediately above the lateral brow, minute doses should be placed in the area of maximal wrinkling to soften the lines and prevent “peaking” above the brow (Fig. 10.16). Although brow ptosis is less likely when extremely small doses are placed immediately above the brow, an additional injection of 3 U should be made in fibers of orbicularis oculi near the tail of the brow to encourage brow elevation in this area. If no injections are placed in a lateral frontalis that is strong, the “Mephisto” or “Spock” appearance is likely (Fig. 10.17). Dysport 2 U placed superiorly near the hairline and 1 U placed lower over the brow will partially denervate the

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Fig. 10.15  Example of injection pattern and doses in a patient with strong frontalis. Two rows of injections are placed. Just 1 U Dysport is placed close to the lateral brow to prevent frontalis activity creating creases or “peaking” here. To maintain a lateral brow lift, a further injection is made in fibers of orbicularis oculi at the temporal crest line near the tail of the brow

Fig. 10.16  Treatment of the lateral forehead. A small dose of botulinum toxin should be placed within the area marked by the circle to soften these lines. An additional injection is placed at the X to prevent lateral brow ptosis

muscle without causing ptosis. The injection in the depressor part of orbicularis oculi serves two purposes. Firstly, it alleviates the depressor action of orbicularis

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a

P.M. Prendergast

b

Fig. 10.17  (a) Patient at rest following chemodenervation of the forehead and frown areas. The physician avoided the area over the lateral brow, presumably to avoid the risk of lateral brow ptosis.

(b) A “Mephisto” brow is evident when the patient attempts to raise the brows. This should be corrected with a small dose injected into the area of maximal wrinkling over the lateral brow

oculi, creating a lift. Secondly, its action-halo affects fibers of frontalis just above the lateral brow, thus softening the “peaking” or wrinkle above the tail of the brow that commonly occurs when frontalis is spared. To determine the best injection point, place the index finger near the tail of the brow where it crosses the temporal crest and ask the patient to raise the eyebrows, and then forcefully shut the eyes. The finger should raise minimally but be pulled down strongly at the correct point. The pattern of injections in the male patient differs, with more aggressive chemodenervation over lateral frontalis to maintain an aesthetically ideal horizontal brow position (Fig.  10.18). Male

patients usually benefit from two rows of injections, with 6 U aliquots of Dysport typically required. Before treatment, asymmetries in the brow and muscle activity should be noted and the treatment should be tailored accordingly (Fig. 10.19). To treat frontalis, the needle is quickly placed through the dermis into the subcutaneous or intramuscular plane. A loss of resistance should be felt as the needle tip traverses the dermal-subcutaneous junction. If the needle tip remains in the dermis, excessive resistance is felt and the solution may leak onto the surface of the skin. If the needle touches the periosteum, the patient may complain of headache after the procedure.

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Fig. 10.18  Typical injection pattern in the male patient. In this example, 114 U Dysport is used for treatment of the frown and forehead. Higher doses may be required, particularly in the glabellar muscles

Every effort should be made to avoid the visible veins in the forehead to avoid bruising. Bleeding should be stemmed immediately with external pressure for 90s to avoid ecchymosis.

10.11.3 Periorbital The crow’s feet or lateral orbital rhytids are commonly treated with 3–4 injections of botulinum toxin achieving excellent periorbital rejuvenation (Fig. 10.20). The patient should understand prior to treatment that the aim is to soften lateral lines, and that some “smile lines” at the upper cheek will remain. Chasing smile

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lines with inferiorly placed injections may result in inadvertent chemodenervation of zygomaticus major or minor with ptosis of the upper lip (Fig.  10.21). Microdroplets of botulinum toxin injected intradermally in the cheeks may improve cheek lines, but the risk of mouth asymmetry still exists [22]. Although rare, lateral injections should be made at least 1  cm from the bony orbital margin to prevent spread into the globe, resulting in extraocular muscle weakness and diplopia [23]. The finger is placed on the rim as injections are made superficially, either in the dermis or subcutaneous plane between the visible blood vessels (Fig. 10.22). As a general rule, 3–4 injections can be made, keeping the inferior injection lateral to an imaginary line dropped vertically from the lateral canthus (Fig.  10.23). Denervating the preseptal portion of orbicularis oculi under the eye may allow the suborbicularis oculi fat (SOOF) pad to bulge anteriorly, worsening undereye bags. Infraorbital injections can be made in the pretarsal portion of orbicularis oculi, however, to reduce lid bulging (Fig. 10.24). One or two injections (e.g., Dysport 4 U) are made tangentially in the lid just below the lashes in the midline, with an additional injection more laterally as required (Fig. 10.25). Medial injections may interfere with the lacrimal apparatus. Before treating the lower eyelid, the snap test should be performed. With the patient gazing forwards, gently retract the lower eyelid inferiorly away from the eye. Upon release, the lid should snap back into place. If it returns sluggishly, avoid treating this area to prevent complications.

10.11.4 Brow Some patients request a brow lift using botulinum toxin. The brow elevates when the depressors are treated and the elevators, or parts of them, are preserved. Subtle elevation of the lateral brow is achieved by denervating the lateral orbicularis oculi under or in the hair of the lateral brow. Further lateral brow elevation occurs when the medial frontalis is treated and fibers of lateral frontalis are preserved (Fig.  10.26). The glabella must also be treated to

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avoid unopposed action of the depressor muscles that act to pull the brow inferiorly. It is preferable to under treat lateral frontalis and allow the brow to lift, rather than over treat, with a risk of brow ptosis. An abnormally elevated lateral brow can easily be adjusted after 2 weeks with a further injection above the most elevated portion.

10.11.5 Nose To treat “bunny lines” over the bridge and lateral part of the nose, the compressor naris portion of nasalis is targeted with about 6 U Dysport injected under the skin on either side of the nose where there is maximal wrinkling. A third injection is placed over the dorsum

a

Fig. 10.19  Tailoring the treatment for each patient. (a) Patient at rest before treatment. The left brow is lower than the right. (b) Patient contracting frontalis. The muscle is relatively strong, with more activity over the right brow compared to the left. (c) Treatment plan. The area over the right brow is treated with one

P.M. Prendergast

to denervate inferior most fibers of procerus (Fig. 10.27). Rarely, dilator naris is injected with 4 U Dysport to reduce the flaring associated with wide nostrils. The tip of the nose can also be made to elevate in patients with active depressor septi muscles. From the side profile, observe the tip of the patient’s nose as they speak. If the tip of the nose tugs inferiorly with movement of the mouth, injecting depressor septi is appropriate. An injection is placed in the midline at the root of the nose near the origin of the muscle where it inserts into the maxilla deep to the mucous membrane of the upper lip. This may also elongate the upper lip and should be avoided in older patients where the upper lip is already lengthened. In these patients, the injection can be made at the insertion point of the muscle under the tip of the nose.

b

unit of Dysport, with 3 U in the lateral brow depressor (orbicularis oculi). Frontalis over the left lateral brow is spared since frontalis does not produce any furrows in this area. (d) The patient attempting to contract frontalis 2 weeks after treatment

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d

Fig. 10.19  (continued)

a

b

Fig. 10.20  (a) Before. (b) After chemodenervation of lateral orbicularis oculi. Complete disappearance of the crow’s feet has been achieved

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Fig. 10.21  An asymmetric smile following treatment of lateral orbital rhytids. The inferiorly placed toxin spread into the lateral lip elevators where they originate over the zygoma

Fig. 10.24  Treating the lower lid bulging and lines. Pretarsal orbicularis oculi is treated by placing the needle tangential to the lid and inserting it superficially in the mid-pupillary line. A small bleb is raised. A second injection can be placed more laterally in the lid, but medial injections close to the lacrimal apparatus should be avoided

10.11.6 Perioral

Fig. 10.22  Injection technique for lateral orbital rhytids. The orbital rim is palpated with the index finger. Superficial injections are made about 1 cm away from the rim. Depending on the distribution of lines, 3–6 injections are placed, avoiding superficial vessels where possible

Fig. 10.23  Injection points for treating lateral orbital rhytids. Injections medial to the red line should be avoided, unless they are in the eyelid in pretarsal orbicularis oculi. The most inferior injection should not be over the zygoma, where denervation of the lip elevators can occur

Although soft tissue augmentation using fillers or autologous fat is usually the first-line treatment for perioral lines and folds, botulinum toxin is appropriate and effective in certain cases. Chemodenervation of muscles that act on the mouth must be precise, with small doses to avoid excessive weakness or asymmetries. To treat “smokers’ lines,” four injections into orbicularis oris are made 5  mm above the vermilion border. Using Dysport, 2 U are placed just under the dermis, two on either side with two further injections in the lower lip if required (Fig.  10.28). The patient should be warned that even with conservative doses a transient subjective feeling of weakness lasting about 1 week can occur. Additional injections can be made after at least 2 weeks if no improvement is observed and the patient reports no weakness. A gummy smile results from excessive activity of the lip elevators, including levator labii and levator labii superioris alaeque nasi (LLSAN). Placing just 4 U Dysport at the superior part of LLSAN, between the nasolabial fold and nasal ala, is sufficient to drop the upper lip and reduce gingival show, even when smiling maximally (Fig. 10.29). The injections should be placed at the same depth bilaterally to avoid asymmetry.

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Fig.  10.25  (a) Before. A hypertrophic pretarsal orbicularis oculi creates bulging of the lower lid. (b) After 4 U Dysport in

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b

the mid-pupillary line just below the eyelash line. Hyaluronic acid filler was also placed in the superior orbitopalpebral sulci

b

Fig. 10.26  (a) Before. (b) After chemodenervation to raise the lateral brow. By preserving fibers of lateral frontalis, and/or treating the lateral brow depressor, the brow elevates

The “peachpit” chin, or cobblestone appearance results from activity of dermal insertions of mentalis (Fig. 10.30). Softening the chin is achieved with two injections into each head of the muscle. Each injection (8–10 U Dysport) is placed deeply into the body of the muscle (Fig. 10.31). The patient should be advised not to rub or massage the chin for up to a week to avoid spread into the adjacent depressor labii muscles. Depressor anguli oris acts to depress the lateral corners of the mouth, giving the mouth a sad or sullen look (Fig. 10.32). To elevate the corners of the mouth, particularly in combination with dermal fillers in the oral commisures, place about 8 U Dysport into the

muscle where it inserts into the periosteum at the border of the mandible. Although the muscle can be felt to contract when the patient is asked to pull the mouth corners downward, if in doubt, place the injection more laterally to avoid inadvertent chemodenervation of depressor labii (Fig. 10.33).

10.11.7 Jawline The “Nefertiti lift” to contour the jawline with botulinum toxin has been documented [24]. The aim is to denervate fibers of platysma along the jawline and

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Fig. 10.27  Contraction or nasalis produces “bunny lines.” An injection is made at either side of the nose into the compressor naris component of the muscle. An additional injection into lower procerus softens the transverse nasal lines near the glabella

P.M. Prendergast

lower face where they insert into the dermis and pull the tissues inferiorly. The lifting achieved is usually subtle. In the author’s view, other techniques such as suture face lifting are more effective and more appropriate to improve jawline definition. A square-jaw appearance may be caused by masseteric hypertrophy, particularly in Asian patients. Botulinum toxin injections into the masseter at the angle of the jaw induces a partial paralysis leading to disuse atrophy. Muscle thickness reduces over time, creating a more oval shape to the face [25]. Three injections into the bulk of the muscle at the angle of the mandible is sufficient (Fig. 10.34). The author usually uses 100 U Dysport per side in equally divided doses, but more may be required depending on the size and strength of the muscle. Treatments are repeated at 3–4 month intervals until atrophy has occurred and facial shape has improved. Once muscle reduction has been achieved, subsequent treatments are less frequent [25]. Complications due to the spread of the toxin into perioral muscles are unusual [26].

10.11.8 Neck

Fig.  10.28  Treatment of perioral lines with botulinum toxin. Injections are placed symmetrically 5 mm above the vermilion border. The lower lip can also be treated. Always start with low doses (Dysport 2 U per site) to avoid excessive weakness or smile asymmetry

a

Fig. 10.29  Treatment of the “gummy” smile. (a) Before. Note the lower lip mouth asymmetry before treatment. (b) After 4 U Dysport in each levator labii superioris alaeque nasi (LLSAN)

Rejuvenation of the aging neck first requires a careful assessment to determine the most appropriate measures. Aging features include skin laxity, lipodystrophy in the submental and jowl areas, submandibular gland ptosis, ptosis of the digastric muscles and platysma, and platysmal hypertrophy and banding [27]. Surgical intervention with skin resection and platysmaplasty is appropriate with advanced signs. Botulinum toxin, injected directly b

muscle lateral to the nasal alae. A subtle but significant drop in the upper lip has been achieved

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a

b Fig. 10.30  The “pebblestone” or “peach-pit” chin. At rest or during animation, dermal insertions of mentalis produce dimpling

Fig. 10.33  (a) The depressor anguli oris is treated by feeling for the muscle over the periosteum and marking the most lateral part of its origin. A slightly laterally placed injection reduces the opportunity for the toxin to affect the depressor labii muscles. (b) After 8 U Dysport in each depressor anguli oris. The mouth corners have elevated

Fig. 10.31  Chemodenervation of mentalis. Two injections are made, one into each head of the muscle

Fig. 10.32  The action of depressor anguli oris. Over activity of this muscle produces a sad or sullen look

Fig. 10.34  Injection points for treatment of masseteric hypertrophy. Three injections are made in the masseter over the angle of the mandible

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into muscular bands, softens the vertical “turkey neck” appearance (Fig. 10.35). Platysmal band asymmetry can also be corrected using botulinum toxin A following rhytidectomy [28]. Although the bands may be visible at rest, asking the patient to forcefully grimace will make them prominent and facilitate marking and injections. Injections of 4 U Dysport at 1.5–2 cm intervals along the band softens the bands without risking spread into deeper muscles. Occasionally, intradermal injections of more diluted botulinum toxin can be made along horizontal “necklace” lines to soften the dermal insertions of platysma along these horizontal creases. Chemodenervation in the neck is also appropriate following lipoplasty when

a

Fig.  10.35  Improvement of platysmal bands with botulinum toxin. (a) Visible bands at rest. (b) Injection points every 1.5–2 cm along each visible band. (c) Injection technique. The

P.M. Prendergast

reduced submental volume postoperatively reveals underlying platysmal bands [29].

10.11.9 Décolleté Superficial, intradermal injections of botulinum toxin along the chest between the lower neck and cleavage provide some improvement to superficial lines where fibers of platysma insert into the dermis [30]. Small intradermal blebs are raised with 2 U aliquots of Dysport at 1 cm intervals (Fig. 10.36). For best results, chemodenervation of the décolleté is combined with

b

band is grasped and the needle is passed directly into the band. (d) Even with contraction, the bands appear softened 3 weeks after treatment

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10.12 Hyperhidrosis The activity of eccrine and apoeccrine sweat glands is under autonomic control, stimulated by release of acetylcholine at postganglionic nerve terminals. Excessive sweating, or hyperhidrosis, may be focal or generalized and primary or secondary [32]. Topical agents such as aluminum salts and aldehyde agents are often ineffective and may cause irritation [33]. Intradermal injections of botulinum toxin represent a novel management option for focal primary hyperhidrosis [34]. Although the only toxin currently approved by the FDA for relief of severe axillary hyperhidrosis is Botox®, the other well-known botulinum toxins are equally effective and commonly used off-label for the treatment of hyperhidrosis [35]. To delineate the area of maximal sweating, the starch-iodine test can be performed. To perform the test, the skin is dried and an iodine solution is applied and left to dry. Then starch is sprinkled over the area. Areas of excessive sweating turn a blue/ black color as iodine reacts with starch. The affected area can be marked to guide placement of injections. In practice, the entire surface of the axilla, palms, or soles of the feet are treated and the test is not essential.

10.13 Axillary Hyperhidrosis

Fig. 10.35  (continued)

other skin rejuvenating procedures including intense pulsed light, laser resurfacing, chemical peels, and rejuvenation mesotherapy with hyaluronic acid and other stimulators [31].

Treating axillary hyperhidrosis with botulinum toxin A requires multiple low-dose intradermal injections throughout the axilla. Injections that are below the dermis in the subcutaneous plane spread too deeply and have little effect on the eccrine sweat glands that are located predominantly in the deep dermis. To inject superficially, the needle is angled at 30° to the skin and small blebs are raised at 1 cm intervals throughout the treatment area (Fig.  10.37). Results are noticeable about 2 weeks following the treatment and provide symptomatic relief from hyperhidrosis for several months. Using Dysport, a 500 U vial is reconstituted with 5 mL physiologic saline to enhance the spread of the solution in the dermis. About 250 U are sufficient to treat each axilla, with 50–70 injections per side

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P.M. Prendergast

b

Fig. 10.36  Botulinum toxin in the décolleté. (a) Immediately after treatment; injections are intradermal. (b) After 1 month

delivering 0.03–0.05  mL each. The treatment is well tolerated and no anesthesia is required.

10.14 Palmar Hyperhidrosis

Fig.  10.37  Treating axillary hyperhidrosis with botulinum toxin. Using Dysport, the 500 U vial is reconstituted with 5 mL saline and 2–2.5  mL are injected in each axilla using equally spaced intradermal injections

The most significant challenge treating palmar hyperhidrosis with botulinum toxin is anesthesia. The palmar surfaces of the hands and fingers are extremely sensitive and patients may not tolerate the procedure unless proper regional anesthesia is performed. Various pain-relief methods are used, including topical anesthetic creams, ice, and topical cooling with forced air or ethyl chloride [36, 37]. However, the author routinely performs bilateral wrist blocks to achieve

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b

Fig. 10.38  (a) Injection points for palmar hyperhidrosis. (b) The medial and lateral aspects and tips of the fingers should not be missed

o­ ptimum analgesia. With proper technique, intradermal injections are well tolerated. The technique for chemodenervation in the palms and fingers is similar to that for axillary hyperhidrosis. To inject the thick dermis of the hands, the needle is angled at about 60° and quickly passed into the dermis. If the tip is too superficial, or if injections are placed perpendicularly, the solution will leak from the puncture [38]. Deep injections should also be avoided to minimize potential denervation of the intrinsic muscles of the hand. Regular needle changes during the procedure facilitate puncture of the dermis. Injections are placed at 1  cm intervals over the palms and fingers, including the sides of the fingers and fingertips (Fig. 10.38). The patient should be warned that transient weakness of the hands might occur but usually resolves in 1–3 weeks. Severe weakness is rare [39]. Typically, a total of 500 U Dysport provides excellent reduction in palmar hyperhidrosis with results lasting 6–8 months.

10.15 Plantar Hyperhidrosis A similar technique to palmar injections is used to treat the relatively larger plantar surfaces of the feet. Pain on injection makes this a challenging treatment unless plantar nerve blocks are accurate and thorough.

Following nerve blocks, 250–400 U Dysport can be injected across the plantar surface of each foot and the toes. The patient should be accompanied for the procedure since transient instability is normal following anesthesia of the feet.

10.16 Complications Injection-related complications following botulinum toxin injections for facial rejuvenation include mild ecchymosis, swelling, and headache [40]. To avoid these problems, visible vessels should be avoided and the needle should be placed either in the belly of the muscle or more superficially, avoiding the periosteum. Brow ptosis occurs with excessive denervation of frontalis, especially in patients with pre-existing dermatochalasis. These patients should be treated conservatively, if at all. Even denervation of the glabellar muscles can lead to medial brow ptosis if there is significant spread to fibers of frontalis in the glabella. Conservative denervation of procerus and corrugators without treating the brow elevators is the best way to avoid potential ptosis in these patients. Eyelid ptosis is rare when botulinum toxin is carefully placed using standard doses. The patient should be advised to ­handle

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the treated area with care for at least 3 days to minimize spread into surrounding muscles. The Mephisto sign or “Spock-eye” is caused by treating the medial frontalis and completely avoiding the lateral frontalis over the lateral brow in a patient with a moderately strong or strong frontalis muscle (Fig.  10.17). In these patients, the lateral frontalis should be treated with 1–2 injections, with reducing doses as the brow is approached. An additional injection in fibers of orbicularis oculi at the brow alleviates the downward pull on the brow here and helps reduce the likelihood of lateral brow ptosis, even when frontalis over the lateral brow has been treated. Chasing smile lines from crow’s feet onto the cheek should be avoided. This can result in paralysis of zygomaticus major or minor with drooping of the upper lip (Fig.  10.21). To address lower crow’s feet and smile lines, injections can continue around the orbit but not beyond an imaginary vertical line dropped from the lateral canthus (Fig. 10.23). The most inferior injections should remain high, close to the lateral canthus and should not be placed over the zygoma. Injections more medial to this for lower lid lines should only be placed in pretarsal orbicularis oculi close to the eyelash in the midline and not lower down over the preseptal part of the muscle. Denervation of preseptal orbicularis oculi can result in protrusion of sub-orbicularis oculi fat (SOOF) and worsen under-eye puffiness. Complications associated with chemodenervation around the mouth include lip weakness, difficulty speaking or eating, and smile asymmetry. In the neck, excessive doses of botulinum toxin have been associated with dysphagia and dysphonia due to spread of toxin into the deeper neck muscles [41].

10.17 Combination Approaches Although chemodenervation with botulinum toxin is the most commonly performed procedure in aesthetic medicine, it should not be considered the answer to all aspects of aging. Botulinum toxin is almost always the first-line choice for treating hyperdynamic lines, but it does not address deeper folds, facial volume loss, and actinic textural and pigmentary changes. For deep lines in the glabella or outside the vermilion border of the lip, a combination of intradermal hyaluronic acid with botulinum toxin achieves better results than each treatment

P.M. Prendergast

individually. Relaxing underlying muscles when fillers are used for augmentation may also increase the longevity of the filler by reducing movement [42]. For “etchedin” lines around the eyes or mouth, laser skin resurfacing combined with botulinum toxin yields excellent results. Botulinum toxin can be combined with almost every aesthetic medical procedure provided there are no contraindications. These procedures include suture lifting techniques, chemical peels, soft tissue augmentation, and photorejuvenation [43]. Botulinum toxins also compliment such cosmetic surgical procedures as brow lift, blepharoplasty, face lift, and platysmaplasty [44].

References 1. The American Society for Aesthetic Plastic Surgery (2009) Cosmetic surgery national databank statistics. ASAPS website, www.surgery.org 2. Erbguth FJ (2004) Historical notes on botulism, Clostridium botulinum, botulinum toxin, and the idea of the therapeutic use of the toxin. Mov Disord 19(Suppl 8):S2–S6 3. Van Ermengem EP (1897) Über einen neuen anaeroben Bacillus und seine Beziehungen zum Botulismus. Z Hyg Infektionskr 26:1–56 4. Snipe PT, Sommer H (1928) Studies on botulinus toxin. Acid precipitation of botulinus toxin. J Infect Dis 43(2): 152–160 5. Burgen AS, Dickens F, Zatman LJ (1949) The action of botulinum toxin on the neuro-muscular junction. J Physiol 109(1–2):10–24 6. Scott AB, Rosenbaum AL, Colins CC (1973) Pharmacologic weakening of extraocular muscles. Invest Ophthalmol 12(12):924–927 7. Rohrer TE, Beer K (2005) Background to botulinum toxin. In: Carruthers A, Carruthers J (eds) Procedures in cosmetic dermatology, Botulinum toxin. Elsevier Saunders, Philadelphia, p 9 8. Clark RP, Berris CE (1989) Botulinum toxin: a treatment for facial asymmetry caused by facial nerve paralysis. Plast Reconstr Surg 84(2):353–355 9. Carruthers JD, Carruthers JA (1992) Treatment of glabellar frown lines with C. Botulinum-A exotoxin. J Dermatol Surg Oncol 18(1):17–21 10. Yang GC, Chiu RJ, Gillman GS (2008) Questioning the need to use Botox within 4 hours of reconstitution: a study of fresh vs 2-week-old Botox. Arch Facial Plast Surg 10(4):273–279 11. Klein AW, Carruthers A, Fagien S, Lowe NJ (2008) Comparisons among botulinum toxins: an evidence-based review. Plast Reconstr Surg 121(6):413e–422e 12. Karsai S, Raulin C (2010) Botox and Dysport: is there a dose conversion ratio in dermatology and aesthetic medicine? J Am Acad Dermatol 62(2):346–347 13. Jost WH, Blümel J, Grafe S (2007) Botulinum neurotoxin type A free of complexing proteins (Xeomin) in focal dystonia. Drugs 67(5):669–683

10  Botulinum Toxins 14. Baumann L, Elsaie ML, Grunebaum L (2009) Botulinum toxin. In: Baumann L (ed) Cosmetic dermatology. McGraw Hill, New York, p 171 15. Koussoulakos S (2009) Botulinum neurotoxin: the ugly duckling. Eur Neurol 61(6):331–342 16. Pickett A (2009) Dysport: pharmacological properties and factors that influence toxin action. Toxicon 54(5):683–689 17. Muraro L, Tosatto S, Motterlini L, Rossetto O, Montecucco C (2009) The N-terminal half of the receptor domain of botulinum neurotoxin A binds to microdomains of the plasma membrane. Biochem Biophys Res Commun 380(1):76–80 18. de Almeida AR Trindade, Marques E, de Almeida J, Cunha T, Boraso R (2007) Pilot study comparing the diffusion of two formulations of botulinum toxin type A in patients with forehead hyperhidrosis. Dermatol Surg 33(1 Spec No):S37–S43 19. Flynn TC (2007) Botox in men. Dermatol Ther 20(6): 407–413 20. Alam M, Dover JS, Arndt KA (2002) Pain associated with injection of botulinum A exotoxin reconstituted using isotonic sodium chloride with and without preservative: a double-blind, randomized controlled trial. Arch Dermatol 138(4):510–514 21. Cheng CM (2007) Cosmetic use of botulinum toxin type A in the elderly. Clin Interv Aging 2(1):81–83 22. De Maio M, Rzany B (2007) Advanced indications and techniques. In: De Maio M, Rzany B (eds) Botulinum toxin in aesthetic medicine. Springer, Berlin, p 117 23. Wutthiphan S, Kowal L, O’Day J, Jones S, Price J (1997) Diplopia following subcutaneous injections of botulinum A toxin for facial spasms. J Pediatr Ophthalmol Strabismus 34(4):229–234 24. Levy PM (2007) The ‘Nefertiti lift’: a new technique for specific recontouring of the jawline. J Cosmet Laser Ther 9(4):249–252 25. Kim NH, Park RH, Park JB (2010) Botulinum toxin type A for the treatment of hypertrophy of the master muscle. Plast Reconstr Surg 125(6):1693–1705 26. Bas B, Ozan B, Muglah M, Celebi N (2010) Treatment of masseteric hypertrophy with botulinum toxin: a report of two cases. Med Oral Patol Oral Cir Bucal 15(4):e649–e652 27. Matarasso A, Matarasso SL (2003) Botulinum A exotoxin for the management of platysma bands. Plast Reconstr Surg 112(5 Suppl):138S–140S 28. Brandt FS, Boker A (2004) Botulinum toxin for the treatment of neck lines and neck bands. Dermatol Clin 22(2):159–166 29. Kane MA (1999) Nonsurgical treatment of platysmal bands with injection of botulinum toxin A. Plast Reconstr Surg 103(2):656–663

129 30. Becker-Wegerich PM, Rauch L, Ruzicka T (2002) Botulinum toxin A: successful décolleté rejuvenation. Dermatol Surg 28(2):168–171 31. Mazzuco R, Hexsel D (2009) Poly-L-lactic acid for neck and chest rejuvenation. Dermatol Surg 35(8):1228–1237 32. Shargall Y, Spratt E, Zeldin RA (2008) Hyperhidrosis: what is it and why does it occur? Thorac Surg Clin 18(2): 125–132 33. Kocyigit P, Bostanci S (2006) Botulinum toxin in the treatment of focal hyperhidrosis. Expert Rev Dermatol 1(2):217–225 34. Arad A, Blitzer A (2004) Botulinum toxin in the treatment of autonomic nervous system disorders. Oper Tech Otolaryngol 15(2):118–121 35. Dressler D (2010) Comparing Botox and Xeomin for axillary hyperhidrosis. J Neural Transm 117(3):317–319 36. Patel R, Halem M, Zaiac M (2009) The combined use of forced cold air and topical anesthetic cream for analgesia during the treatment of palmar hyperhidrosis with botulinum toxin injections. J Drugs Dermatol 8(10): 948–951 37. Richards RN (2009) Ethyl chloride spray for sensory relief for botulinum toxin injections of the hands and feet. J Cutan Med Surg 13(5):253–256 38. Glogau RG (2001) Treatment of palmar hyperhidrosis with botulinum toxin. Semin Cutan Med Surg 20(2):101–108 39. Glass GE, Hussain M, Fleming AN, Powell BW (2009) Atrophy of the intrinsic musculature of the hands associated with the use of botulinum toxin-A injections for hyperhidrosis: a case report and review of the literature. J Plast Reconstr Aesthet Surg 62(8):e274–e276 40. Wollina U, Konrad H (2005) Managing adverse events associated with botulinum toxin type A: a focus on cosmetic procedures. Am J Clin Dermatol 6(3):141–150 41. Carruthers JDA, Glogau RG, Blitzer A, Facial Aesthetics Consensus Group Faculty (2008) Advances in facial rejuvenation: botulinum toxin type A, hyaluronic acid dermal fillers, and combination therapies – consensus recommendations. Plast Reconstr Surg 121(5 Suppl):5S–30S 42. Coleman KR, Carruthers J (2006) Combination therapy with Botox and fillers: the new rejuvenation paradigm. Dermatol Ther 19(3):177–188 43. Flynn TC (2006) Update on botulinum toxin. Semin Cutan Med Surg 25(3):115–121 44. Balikian RV, Zimbler MS (2005) Primary and adjunctive uses of botulinum toxin type A in the periorbital region. Facial Plast Surg Clin North Am 13(4):583–590

 

Biostimulation and Biorestructuring of the Skin

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Maurizio Ceccarelli

11.1 Epidermis The process of differentiation of epidermal skin cells is very complex and regulated by a series of information from the exterior, as well as through complex intercellular enzymatic systems which function as secondary messengers [1]. Among the external informers we must consider the alpha and beta adrenergic mediators that work by stimulating activity of the adenylcyclase and the cholinergic mediators, which work by stimulating the activity of the guanylate cyclase formation of c-GMP. Other factors ruling the keratinocyte differentiation are the Epidermal Growth Factor (EGF) and estrogens. Among the intrinsic regulating factors, the calones (34 KDa glycoprotein), tissue-specific but not very species-specific, blocks the cell cycle in G1 phase, thus preventing S phase [synthetic macromolecular] and then the M phase [mitosis itself]. Has the ability to re-enter the cells in G0 phase and also makes biological agents with power inducer of differentiation. The epidermal G1 calones appear to control the proliferation of adult cells, while the G2 calones set those primitives and are substances with similar hormonal activity and have significant importance. The epidermal calones are produced by keratins in an advanced phase of proliferation and have the function of prohibiting the cellular mitosis of the cells of the basal layer. This regulates skin thickness. The stimulus of the ECP increases the mitosis of the germinative layer; when the thickness reaches its optimal status, the concentration of the calones produced M. Ceccarelli  Corso di Francia, 221, 00191 Roma, Italy e-mail: [email protected]

by the keratinocytes also reaches the necessary level to block the mitosis of the basal layer. When the corneous exfoliation reduces the number of the corneocytes, the concentration of the calones is lowered and the stimulus of the EGF reactivates the mitosis. The correct function of this balance regulates the correct thickness of the skin. In concluding this report on the epidermis functions and bringing it into our aesthetic interventions, we must remember two points: the cholinergic mediators and the calones. This is because treatment with botulinum toxin anticholinergic reduces the effect of this mediator, altering the epidermal function and the peeling treatment exfoliating and reducing the corneocyte layer determines a reduction of the calones with an increase in the mitotic stimulus and epidermal hypertrophy. The quantity and frequency in the use of botulinum toxin and peeling, requires careful attention.

11.2 Dermis Below the epidermis there is the dermis that is formed primarily by collagen and elastic cells or fibers immersed in a colloidal matrix. The cells are represented essentially by fibroblasts. The colloidal matrix is formed by the fundamental substance (glycosaminoglycans (GAGs) and proteoglycans) and by fibrous proteins such as collagen and elastin. Collagen, elastin, and GAGs are produced by fibroblasts and chondrocytes. The physical status of the dermal matrix is important because, depending on its consistency, the metabolic exchanges are either facilitated or inhibited. The state of sol of the colloidal solutions which make up the matrix permits an easier

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metabolic exchange, while the more solid state of the gel impedes this. The colloidal solutions are characterized by solute molecules of considerable dimension, and thus are unable to disperse in the intermolecular spaces of water, but are charged with the same electrical current. Due to gravity the first molecules settle on the bottom but impede others from doing so because the repulsion of the electric charge of the same sign keeps them suspended. If the electric charges of the colloidal molecules are saturated with charges of opposite sign, the repulsion force ceases and the various colloidal molecules become compact, transforming the colloidal solute (sol) into a colloidal gel (gel). In the dermis, the state of sol is maintained by the negative charge present on the surface of the macromolecules of GAG from which they are made. This negative electric charge derives from the dissociation of these macromolecules in the slightly alkaline environment which characterizes the dermis (pH 7.4). This pH value is maintained steady or unchanged by the buffer bicarbonate system. The normal cellular metabolism produces carbon dioxide. This, in a water solution, forms carbonic acid that when dissociating, frees hydrogen ions which acidify the solution. The hydrogen ions, positive, neutralize the negative electric charges of the GAG and determine gasification of the derma with a reduction of the metabolic exchanges. Also the inflammatory processes acidify the dermal matrix with consequent biological damage. Therefore, it is important that any aesthetic interventions does not induce acidification to the derma (inflammation) or a reduction in the buffer bicarbonate systems. The fibroblast is the dermis’ cell capable of producing all the components of GAG, collagens, and elastin. The productive capacity of the fibroblast differs in function; on the age of the cell, on the different stimulated receptors, and on the physicochemical ambiance surrounding it. In particular, we also have to make a distinction regarding the various types of collagen being produced. This is because in various aesthetic interventions we speak of neocollagenogenesis without mentioning the type of collagen being produced and if this neoproduction corresponds to a real biological rejuvenation of the skin. In young skin the relation collagen type III/type I is much higher in adults and that this relation tends to diminish with age. The fibroblast produces an immature collagen, tropocollagen that is assembled in different ways, utilizing portions of carboxy terminal (collagen type I) or

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amino terminals (collagen type III). Collagen type III, reticular, is characteristic of young tissue and maintains the turgidity of the derma. Collagen type I, fibrotic, is characteristic of older and cicatricial tissue and hardens the dermis. Recent studies indicate the capacity of the fibroblast to be activated towards the production of one type or the other of collagen and in particular we can distinguish the fibroblast into two under populations, NF (natural fibroblast) and FF (fibrotic fibroblast) the latter being characterized by inflamed tissues. The NF mainly produces reticular collagen, while the FF mainly produces fibrotic collagen. Considering that the fibrotic collagen is a factor of aging skin, it is important that the neocollagenogenesis induced by our aesthetic treatment do not stimulate the formation, as even if the aesthetic look of the skin could improve, the biological functions are damaged. Neocollagenogenesis treatments of the reticular type is used to improve the skin of young patients, while fibrotic-type neocollagenogenesis for older patients, aware that there is aesthetic improvement even at a cost of damage to the physiology of the skin. A correct biological state of the dermis foresees: 1. Maintenance of the colloidal status of the matrix 2. Activation of the metabolism of the fibroblast 3. Stimulation of the neoformation of collagen and elastic fibers

11.3 Regeneration and Reparation It is important to examine closely the concept of neocollagenogenesis, analyzing the process of regeneration and reparation. Regeneration is a physiologic process at the base of a continuous reconstruction of certain tissues, such as those of the skin. In order to maintain functional tissues and apparatus our organism puts into effect a continuous regeneration process based on a dissolution of the pre-existing tissue and on its own reconstruction. In the skin, there are some particular enzymes called metalloproteinase capable of solubilizing through processes of hydrolysis the macromolecules that form the dermis [2]. The metalloproteinase distinguish themselves with progressive number indicators of the same molecule on which they effect their action: MMPI collagenase, MMP3 gelatinasi, etc. The metalloproteinase is present in the derma in an inactive form with its active site blocked by a residual of cysteine. The

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hydrolysis of this amino acid frees the site containing zinc and permits the action of the enzyme. As in most parts of the biological systems, the dissolution of the matrix is governed by activators and inhibitors of the MMP. The correct balance between the two apparatus permits the maintenance of a healthy and functional derma matrix. Particular receptors on the cellular wall of the fibroblast are being activated by the growth factors or by the lysed components of the dermis and bring the sintering of new molecules. The receptors of the tyrosine–kinase that are activated by the growth factors (fibroblast growth factor), and the CD44 (cluster of differentiation), which are being activated by fragments of hyaluronic lysed acid, determine the hydrolysis of the polyphoinositide of membrane with the liberation of 1–3 of phosphoinositide. This reaches the endoplasmic lysed reticule where joining up with a specific reticule, induces the entry of calcium ions. The calcium ions activate the proteinkinase C with the stimulus of early induction of the Jun and Fos genes and the subsequent start of the protein synthesis. Thus, the neoformation of the components of the dermal matrix and in particular of GAGs of reticular collagen (type III) and of elastin. The reparation is a biological process useful to compensate the loss of part of a tissue as a result of damage. This loss is balanced with the neoformation of a connective tissue called cicatricial tissue. This tissue is richly represented by collagen of type 1. The cell governing the formation of the cicatricial tissue is always the fibroblast. Obviously in this case we have diverse stimuli to induce the construction of new tissue and not the original tissue. If previously there were the fragments freed by the hydrolysis of the normal components of the dermis to activate the regeneration of the skin, now there are the endocellular components freed by the biological damage and the inflammation mediators, consequent to the biological damage, to induce the activation of the reparation process. In particular, there is the activation of the CD39 on behalf of the fragments of the nucleic acid freed by the nucleus of the damaged cell and the activation of the CD40 on the part of the mediators of the inflammation (interleukin 4) to stimulate the formation of the fibrotic tissue rich in collagen of type 1. Is it sufficient to speak in a general way about ­fibroblast activation or do we have to be more precise about which receptors we activate? The stimulation of different receptors could bring biological improvement or aesthetic improvement. Biological improvement is

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useful in all kinds of skins while ­aesthetic ­improvement is useful only in old skins. Therefore, if fibroblastic biostimulation is to be used in a young patient, we have to be sure that the stimulated receptors are only the CD44. While in fibroblastic stimulation of an older  skin, also the stimulus of the CD39 and the CD40, even if inducing a biological damage, can be accepted because of the aesthetic improvement. In stimulating CD44: 1. The proteins derived from the damage of the extracellular matrix stimulate the synthesis of its components. 2. The CD44, cellular receptors of activation of the synthesis of hyaluronic acid, shows the biggest activity in the presence of complexes of 20–38 monomers. While: 1. The extracellular nucleotides stimulate the purinergic receptors of type 2. 2. The adenosine (Purina base) rules the inflammation and the reparation of the tissues. 3. The adenosine receptors play an active role in the pathogenic of the dermal fibrosis. 4. The extracellular nucleotides have been involved as inflammatory mediators in many pathological situations. 5. The stimulation of the purinergic receptors 2 of the CD39 is associated with a chronic inflammatory response. 6. Phlogogen stimulus select the under populations of fibroblasts with an important role in the formation of the fibrosis. 7. The interleukin IL-4 is tied up to the CD40 of the fibroblasts with a profibrotic effect and reduction of the antifibrotic effect of the IFN-range. The stimulus of the CD44 provides biological improvement that is seen also with an aesthetic improvement, while the stimulus of the CD39 and the CD40 determines only an aesthetic improvement consequent to a fibrosis of the dermis and therefore a biological damage.

11.4 Biostimulation The proposals, also medical, present in the field of the biostimulation tell us of the use of: 1. Vitamins 2. Hyaluronic acid

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3 . Fractions of DNA 4. Organic silicon 5. Radiofrequency 6. Laser energy It is important before commencing any of these treatments, to consider the real biological effects of each (as doctors freeing ourselves from the simple economic business and choosing science and conscience). Nowadays the concept of biostimulation has become one of the most requested treatments of aesthetic medicine. Many names are utilized in its definition. 1. Biostimulation 2. Biorestructuring 3. Bioregenaration 4. Biorevitalization The author prefers the use of the term biostimulation to indicate an activation of the biological functions of the skin in order to optimize its physiology and achieve aesthetic improvement. The term biorestructuring is used to indicate an alteration of the normal cutaneous components with damage of the physiology of the skin even if there is an aesthetic improvement. Biostimulation for a young skin is to improve its physiology and the aesthetics, biorestructuring is for an older skin to obtain an aesthetic improvement. The correct biostimulation includes the skin functions being activated through a functional improvement of the epidermal and dermal cells that brings a normalization to the condition of the skin. This foresees a regular epidermal renewal and the optimization of the chemical–physical matrix. Regular epidermal renewal stems from a normalization of the EGF function and of the calones. The chemical–physical optimization of the matrix requires the neoformation of the structural components and the fluidity of its colloidal state. The neoformation of structural components of the matrix requires the physiological stimulation of the fibroblast in the regenerative rather than the reparative sense. The dermal regeneration becomes activated through the growth factor or the fragments of the normal components of the matrix. These work on the CD44 activating the protein synthesis in a regenerative sense and improving the neo formation of reticular collagen, Hyaluronic acid, and elastin. Normalization of the colloidal state of the matrix requires the maintenance of a physiological ph (7.4). This avoids the transformation of the matrix solution from the state of sol to that of gel to maintain free metabolic exchanges.

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The technique of a more physiological biostimulation is today represented by treatment with Growth Factors derived from plasma rich in platelets. This permits the activation of the fibroblast through the use of homologous growth factors and inducing the normal reconstruction of the altered dermal components. The technique by Garcia [3] is histologically verified by its results and is, today, particularly widespread in Spain and is becoming well known in Europe and South America. Born from the clinical use of plasma rich in platelets and of the cellular growth factors connected to them a vast bibliography confirms the importance in ophthalmology, dentistry, neurology, orthopedics, and in branches of aesthetics. The only problem is the lack of legislation able to regulate this type of transplant. The EU is preparing a law on extracting, conservation, and use of any human cell, considering the diffusion of this new type of therapy. In the meantime the use of these off-label-activated platelets remains the responsibility of the physician. Growth factors are small protein fragments, belonging to the group of the cytokines, able to join the receptors of membranes to activate or inhibit the cellular functions. They can be produced by numerous cells and tissues: platelets, fibroblasts, osteoblasts, epidemics cells, liver, kidney, lachrymal glands, etc. The joining of the tyrosine–kinase receptors to the cellular membrane induces the hydrolysis of poliphosphoinositole of the membrane with the liberation of the 1–3 diphosphoinositole. This reaches the endoplasmic smooth reticule where, if joined to a specific receptor, induces the entry of calcium ions: the calcium ions activate the proteinkinase C with the stimulus of the genes at an early induction Jun and Fos and the subsequent start of the protein synthesis. Among the numerous growth factors freed from our cells, the PDGF was chosen for the ease of its finding, for its specific proliferation activity of the fibroblasts, and synthesis of the dermal matrix. The platelets also free other factors (TGF, EGP, VEGF, and IGF) extruded from the big granule alpha after activation. Biologically the activation of the platelets in these cells is by contact with the extravascular connective after a wound (lesion): chemically we obtain this effect with calcium chloride. The platelets, furthermore, also transport proteins useful in the reparation and regeneration of the tissues, whether derived from their precursor cell (megakariocytes) or captured through endocytosis from the plasma.

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The use of the PRP (plasma rich in platelets) in clinics has always been directed towards the improvement of the reparation process. The merit of Garcia and of the studies at Barcelona University is in the verification of the use also in regenerative processes. Histological studies have shown that the introduction of the PRP induces, for a 9-month period, the neoformation of reticular collagen (type III) in the dermis justifying the affirmation of a biological rejuvenation of the skin of the patient. The treatment is carried out on the face, neck, décolleté, and hands in three sessions (the first, then after 3 months and after 6 months). The biological effect is related to the concentration of the platelets, therefore the plasma, before administration, must be enriched. The other certified technique that takes to the use of the PRP is the biostimulation affected with the SKIN-B product. This, a medical device of III level certified CE by the Italian Health Superior Institute, contains: 1. Fragments of hyaluronic acid of 20–38 monomers to activate the CD44 of the fibroblast 2. Amino acid precursor of the components of the matrix 3. Bicarbonate buffer to keep the condition of sol of the matrix Biostimulation with SKIN-B is affected during the intervals of the treatments with PRP. These two treatments represent the base for the biological rejuvenation of the patient’s skin.

11.5 Physical Biostimulation with LED Recently light, and in particular photo stimulation, has been approved by the American FDA for the treatment of wrinkles. The principle is based on the fact that the LED releases photons with a low power but able however to give a positive effect on the cells at a morphological and molecular level. The treatment is today placed at an international level amongst the nonablative technologies and in particular as photo rejuvenation with light emitted by diodes, without thermal effect. The difference between laser light and LED light is that the noncollimation leads to the divergence of rays  with a consequent decrease of intensity at the point of irradiation. While the intensity of the laser is measured in watts, the LED is measured in microwatts. The absorption of the power of incident light is different according to the wavelength and the material met.

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The wavelength between 600 and 900  nm is not absorbed by the biological molecules. In this range (600–900), the longer the wavelength the deeper ­penetration of the skin. But where is the site for action of the photobiostimulation? We know that in nature, whether in the vegetable or the animal world, there are molecules considered photosensitive, they change their functions on the basis of light stimulation. The light activates the photo systems of the vegetable cell by splitting the water and uses the hydro genes to activate the synthesis complex ATP and produce energy necessary for the biological synthesis. Also at an animal level we have some biological structures activated by the light. The most evident example is that given by the rhodopsin contained at a retinal level, the activation of which is at the basis of the mechanism of vision. Also the melanocytes of the skin are cells activated by the light for the production of melanin bodies. The light also develops an important function in the Light Repair of the cellular DNA. The enzyme photoliasis is a flavoprotein that, activated by the light, repairs the portions of the damaged DNA. However, the most interesting point in our discussion is represented by the tetrapyrrollic rings present in the mitochondrial cytochromes. At the mitochondrial level, the Chain of Transport of the Electrons allows the formation of the ATP molecules. The enzymes of the chain are represented by the cythrochroms. The scheme of the electronic transfer foresees the: 1. Transfer of the electrons from NADH to the cytochrome 2. Transfer of the electrons from the FADH to the cytochrome 3. Transfer of the electrons from the cytochrome Q to the cytochrome 4. Transfer of the electrons from the cytochrome c to the oxygen as per action of the cytochromoxidasis Essential in the chain of transport of the electrons is the protonic flux of the hydrogen ions. This flux consents the formation, by way of the ATP-synthetase, of the ATP molecules. The ATP-synthetasis mitochondrial has a particular stereochemical structure equipped with a clockwise and anticlockwise motion on the basis of the protonic flux. The ATP or adenosine– triphosphate is a particular molecule formed by an adenosine nucleus (adenine plus pentose) with three combined phosphoric radicals. The bond of the last phosphoric group is a one with a high energetic ­content,

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the breaking of which gives off a high quantity of energy. We can now understand how the photobiostimulation with LED could be useful in the prevention of the aging process. Scientific studies confirm that the cytochromoxidase is the primary accepter of light between the red and the infrared and this light LED improves the electronic movement in the cytochromoxidase, heart of the formation of the free radicals of oxygen, capable of yielding up to four electrons to the molecule of oxygen. We have to point out the delicacy of this process because the mechanism of oxygen reduction foresees a necessary amount of time for the inversion of the spin of one of the two additional electrons. In fact, oxygen at two electrons with spin parallel in the last orbit and the addition of another two antiparallel spin electrons, must be preceded by an inversion of the spin. If this does not occur at precise times, there can be an escape of the free radicals free from oxygen; the base of cellular aging: 1. The first target is the mitochondrial DNA where only one deletion results in a loss of the function of the whole filament. 2. The damaging of the telomeres in the DNA, results in the nondisjunction of the chromos during the crossing over, with consequent cellular death. 3. The lipoperoxidation of the biological membranes results in a loss of function with cellular death. The loss of double ties of the phospholipids determines a rigidity of the membranes with loss of fluidity and an alteration in the functions of receptor expressions. 4. Liberation of the free radicals free from the oxygen of the cytochromoxidase, results in the activation of the caspasi with induction of the cellular apoptosis and death. The free radicals of the oxygen liberated by the mitochondria join the APAF 1 (protease activating factor 1) which joins the procaspasis 9 with successive aggregation and liberation of activated caspasi 9. This activates the cascade of the caspasi with final cellular apoptosis. Furthermore, the photobiostimulation with LED (red-infrared) results in the activation of the respiratory chain of the mitochondrial with activation of the synthesis of ATP and a functional cellular improvement. The synthesis of ATP is guided by the gradient proton. In fact, the electronic flux moving along the mitochondrial crests is accompanied by a protein flux in the intermembranal space. After the cessation of the electrons to the oxygen the protons pass into the

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ATP synthetase, supplying the force for the formation of the ATP. So we have the passage of a disphosphoric radical in combined to a proton. The radical will join a new proton forming phosphoric acid which terminates its reaction and joins itself to the adenosine– diphosphate, forming ATP. The clockwise rotation consents the synthesis of ATP. The rotation anticlockwise results in the hydrolysis of the ATP. The liberated energy from the ATP is utilized by the cells for the protein synthesis, for the pumps of sodium and calcium and for the synthesis of DNA and RNA. The application times for the photo modulation, per session, range from 15 to 20  min. The number of the sessions can vary from 1 to 2 for a total of 8–10 treatments.

11.6 Heterologous Skin Regeneration Today, medicine, physiology, and aesthetic medicine, in the renewal of treatment for skin aging, are turning to an industry evolving: regenerative medicine [4]. The scientific approach which today must follow the doctor is to regenerate the biological status of skin tissue through autologous or heterologous activities. Skin regeneration, with the goal of inducing regeneration of the dermis and epidermis, which would bring the skin into a youthful state requires the use of autologous patient’s substances [3], such as: 1. Platelet growth factors 2. Plasma rich in platelets 3. Fibrin plasma 4. Support autologous biological tissue The heterologous skin regeneration always involves the activation of regenerative biological processes, however, made by Medical Device certified for this function. The regeneration heterologous replaces the generic term of biostimulation to indicate biological activity useful in functional improvement of skin. The generic term, biostimulation, indicates a generic biological activity, of course included in this term there will be positive and negative results. Undoubtedly the products proposed as biostimulants are accepted by the physician and the patient for a possible hit on the skin. But in reality, all products sold are biostimulants (activators of skin biology), but not all, lead to an improvement of the physiological skin, they often show a positive response on the aesthetic result, but with skin biological damage.

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But what do we mean by physiological improvement of the skin? The physiological normalization of biological functions of the body and thus improve the skin indicates the physiological homeostatic optimization of biochemical reactions that must maintain our functional and trophic skin. To program proper biostimulation, or rather skin regeneration with a Medical Device, we must first understand the biological mechanisms relevant to the biology of the skin. From what we have stated, the dermo-epidermal regeneration obtained with the use of medical devices should lead to the skin: 1. An action of stimulation of receptor tyrosine kinase normally activated by growth factors necessary to enable the growth both of the germinative epidermal layer, and the fibroblast 2. Action mimetic that improves the epidermal cholinergic system 3. Useful buffer action to reduce the states of acidification induced by inflammation and helps to maintain the colloidal state of the matrix 4. Action to stimulate the new formation of matrix components (proteoglycans, elastic fibers and collagen type III) 5. Action to block the activation of metalloproteinase responsible for the dermis catabolization 6. Reduce the processes of skin aging caused by oxidative stress of free radicals of oxygen The pharmaceutical industry, for a long time, has provided a Medical Device Type III certificate for a biostimulation dermo-epidermal. This product contains: 1. Hyaluronic acid fragments of 20–38 monomers capable of activating the CD (Cluster of Differentiation). These receptors, once activated induce a metabolic activation and dermal–epidermal regeneration with multiplication. In particular lead to the synthesis, by the fibroblasts, of the matrix new components and collagen lattice [5]. 2. Amino acids precursors of matrix components, according to the endomodulation principles, trigger biochemical reactions anabolic allowing a growth of the dermis. 3. Amino acid cysteine, zip closing of the active site of metalloproteinases. The excess of this amino acid competes with the removal of the same to level of metalloproteinases, reducing the activation of these and the breakdown of the dermis. 4. Bicarbonate buffer system that inactivates the release of H + ions induced by inflammation of the skin, keeping constant the pH value of 7.4. This allows the

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separation of anionic macromolecules that compose the matrix, keeping the electrostatic repulsion necessary for the maintenance of the matrix. The actions of this second III type device is medically undoubtedly good, omitted, however are two points that are: 1. The mimetic action of epidermal cholinergic system 2. The reduction processes of skin aging caused by oxidation of oxygen-free radicals This forced us to treat these two points with different drugs, not approved for this treatment (glycerate choline and reduced glutathione). Recently, the same pharmaceutical industry has proposed a new type III Medical Device containing the starting material described above with the addition, in one case, of choline, and in the other, antioxidants. The choline is the precursor of the acetyl-choline and, in turn, in its synthesis is stimulated by DMAE (dimethylaminoethanol), already known in cosmetics. Its addition in the Base Medical Device type III takes, according to the Endomodulation principles, an improvement of the acetyl-choline synthesis and an activation of the epidermal cholinergic system. In fact,, Kurzen et al. say, in Hormonal Metabolic Research, February 2007, that the non-neuronal cholinergic system of human skin is involved in basic functions of the skin through ­autocrine, paracrine, and endocrine mechanisms, like keratinocytes proliferation, differentiation, adhesion and migration, epidermal barrier formation, pigment-, sweat- and sebum production, blood circulation, angiogenesis, and a variety of immune reactions. The antioxidants (vitamin C and glutathione) act by inactivating oxygen-free radicals, escaped from the electron transport chain. Vitamin C reactivates with its reversible passage by ascorbic acid to dehydroascorbic acid, vitamin E oxidized in its function block of the superoxide radical. Glutathione converts hydrogen peroxide, formed as a result of SOD (superoxide dismutase) action on the superoxide radical, in water preventing thus the damage of Fenton Reaction.

11.7 Discussion This evolution of the means at our disposal for the biostimulation, allows us to review, for the better, our protocol on the heterologous regeneration, incorporating these two new medical devices. From this, we differentiate our

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protocols on the basis of results of evaluation of our patient’s skin. In particular: 1. In the young patient who does not have excessive skin damage, we keep the classical treatment using the Base Medical Device. The times are those based on each mesotherapy treatment: one session a week for four times, a fortnightly meeting twice, and finally a maintenance session once a month. 2. In the patient with damage of biological aging (photo-aging or chronological-aging) we substitute the Medical Device Base with one with antioxidants, keeping the protocol. 3. In the patient with epidermal damages we replace the Medical Device Base with one with choline, always maintaining the same protocol. Finally, in patients at older ages where they often add up all the needs, the author’s current protocol provides a session with Medical Device Base week for four times. Then one session every fortnight with the Medical Device with choline and one session every fortnight with the Medical Device with antioxidants. Treatment should be maintained over time and supplemented with autologous regeneration.

11.8 Biorestructuring 11.8.1 Macromolecular Hyaluronic Acid Macromolecular hyaluronic acid is a polymer set up by the repetition of monomers formed by the union of hyaluronic acid with acetyl-glucosamine. This union is permitted by the binding of the hyaluronic acid and the uridine-triphosphate. We cannot speak of a biostimulant effect for the macromolecular Hyaluronic acid, because as stated in the scientific literature [6]: 1. The presence of hyaluronic acid does not have effect on the production of endogenous hyaluronic acid. 2. Hyaluronic acid (0.5–1  mmol) limit induce the reduction of the protein synthesis. 3. High concentration of hyaluronic acid limits the formation of extracellular matrix. 4. Hyaluronic acid (1 mg/mL) increases the expression of the metalloproteinase (MMP) and activates those which are latent in the extracellular matrix (MMPs). We speak only of an antioxidant and hydrating effect of the macromolecular hyaluronic acid. Recent reports described antioxidant properties of GAGs.

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Since several have shown that hyaluronic acid (HYA) and chondroitin-4-sulphate (C4S) may act as antioxidant molecules. Hyaluronic acid and chondroitin-4sulphte possess antioxidant properties. Hyaluronan has been assigned various physiological functions in the intercellular matrix, e.g. in water and plasma protein homeostasis. Therefore, there is no stimulation of the fibroblasts and neocollagenogenesis but only a passive hydration and of antioxidant effect.

11.8.2 Fragments of Nucleic Acid Nucleic acid is an intercellular component contained in the nucleus, but present also in the cytoplasm, in the mitochondrions, and in the wrinkled endoplasmic reticule. So the contact of this material with the surface of the fibroblast foresees the cellular rupture due to biological damage. In the derma the fibroblast receives the information of biological damage from the endocellular materials produced by the damage or by the mediators of the inflammation to the damage itself. The joining of fragments of nucleic acid to the CD39, activates the reparative process with formation of a cicatricial tissue. Scientific works with the PDRN tell us of the increase of the fibroblastic activity of 30% with an increase of collagen, fibronectine, and dermal filling. This neocollagenogenesis is relevant to the formation of fibrotic collagen characteristic of a reparative cicatricial tissue. The literature asserts that [7–12]: 1. The extracellular nucleotides (PDRN) stimulate the purinergic receptors of type. 2. The adenosine (Purina basis) regulates the inflammation and the reparation of the tissues. 3. The adenosine receptors play an active role in the pathogen of the dermal fibrosis. 4. The extracellular nucleotides have been involved as inflammatory mediators in many pathological situations. 5. The stimulation of the purinergic receptors 2 of the CD39 is associated with a chronic inflammatory response. 6. Phlogogen stimulus selects some under populations of fibroblast with an important role in the formation of the fibrosis. 7. The interleukin IL-4is tied to the CD40 of the fibroblasts with profibrotic effect and reduction of the antifibrotic effect of the IFN-gamma.

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We do not describe biological rejuvenation but only of the aesthetic, therefore we can only use this technique in older patients.

11.8.3 Radiofrequency in the Aging Skin The best known and publicized radiofrequency tool for the aging skin is thus presented: “It is a safe, clinically proven way to tighten and contour skin, with improvements in tone contour, and texture occurring naturally through the stimulation of your own collagen.” Also in this case we speak of neocollagenogenesis without indicating the type of collagen.

11.8.3.1 Concepts of Radiofrequency Radiofrequency permits the transformation of cold energy at high frequency relevant in heat, with an increase of the internal temperature by way of the Joule effect. All cells of the treated tissue absorb part of this energy, thanks to its grade of resistivity, and is transformed into heat. The law of physics at the base of the effects of radiofrequency, is given by the modification of the electric field of the treated zone with a change of the electrical charge and of the resistance, and to the movement of the ions and molecules which determine heat according to the formula: J = I × R × T, where J = Energy, I = Current (voltage), R = Impedance of the tissue, T = time. Generally the heat produced develops between 3 and 9  mm of depth, according to the tools used, and determines heat up to 55–65°C in homogeneous mode, without thermal diffusion in surrounding areas. The biological effect of the heat produced by the radiofrequency is a denaturation of the collagen fibers (from 5 to 30% of total fibers), with a consequent immediate contraction of the fibers themselves, with a progressive effect in the successive 4–6 months. The protein’s structure is characterized in four classes: primary, secondary, tertiary, and quaternary. The primary formed by a strong covalent bond, units various amino acids; the others formed by weak bonds permit the tridimensionality of the protein and their functions (structure, enzyme, antibody, etc.). The weak bonds break easy with just an increase of the molecular kinetics energy (heat). The covalent bond instead requires an enzymatic process of hydrolysis. The increase in heat beyond the physiological value of 37 °C denatures the protein, leading to a loss in biological functions. If the damage continues, this results in biological damage and

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reparative response. The effects of the RF current are in relation to their frequency and force. Over 1.5 – 2 MHz there is elevated molecular friction which provokes intense heat, enough to induce tissue destruction. Frequencies inferior to 0.3  MHz produce undesirable stimulations in the nervous system. The literature confirms that: 1. Radiofrequency causes movement of charged particles within the tissue, and the resultant molecular motion generates heat. The heat in turn causes collagen shrinkage and new collagen deposition. 2. The physical agents (mechanical, thermal, electrical, radiant, etc.) determine an inflammatory process of varying degrees, on the biological material, resulting in self-damage. 3. Phlogogen stimulus select some under populations of fibroblasts with an important role in the formation of the fibrosis. 4. The interleukin IL-4 is joined to the CD40 of fibroblasts with a profibrotic effect and reduction in the antifibrotic effect of the IFN-range. So, even considering radiofrequency useful for the treatment of the aging skin, this technique must be used only for older skins because the biological effect is harmful and therefore the results are only aesthetic.

11.9 Laser Therapy for Ablative Cutaneous Rejuvenation An argument similar to that for radiofrequency is valid for laser treatment for aging skins. Use is made of a controlled vaporization of thin layers of skin. The light emitted by the laser is so intense that in a very short time (90 ms) it vaporizes and coagulates a thickness of skin between 40 and 60 mm (the thousandth part of a millimeter). Resurfacing with laser will produce very good results and the surface of the skin will regenerate, richer in fibrotic collagen and consequently more compact. A source of energy activates the molecules through a tube containing gas so to determine an atonics excitement followed by a successive release of energy which hits the skin bring about a coagulative or necrotic damage according to the intensity. The protein denaturalization or the coagulation is followed by a reparative process that is evidenced by a deposit of cicatricial tissue containing collagen of Type 1. The literature confirms that:

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1. A 1440-nm inducing no ablative neocollagenesis in the remodeling of scars and rhytids. Histological evidence confirms the micro columnar nature of collagen heating using this microarray. 2. The physical agents (mechanical, thermal, electrical, radiant, etc.) determine the biological material an inflammatory process of varying degrees, with self-damage. 3. Phlogogen stimulus select some under populations of fibroblasts with an important role in the formation of the fibrosis. 4. The interleukin IL-4 is joined to the CD40 of the fibroblasts with a profibrotic effect and reduction of the antifibrotic effect of the IFN-gamma. This confirms the recognition that, although producing biological damage, laser resurfacing results in an aesthetic improvement of the skin, its use therefore is reserved for older patients.

11.10 Polylactic Acid Recently polylactic acid filler has been proposed not only as filler but also as biological stimulus for the rejuvenation of the skin. Polylactic acid is different from other fillers. Simply, its action is based not on the filling of the cutaneous defect, but on the increase in derma’s volume due to the proliferation of neocollagenesis, induced by the stimulus on the fibroblasts provoked by the Polylactic acid itself. This is a correct assessment because a permanent filler induces a fibrotic response from a foreign body. The literature states that: 1. Polylactic and microspheres (New-fill) induces a mild inflammatory response. Host defense mechanisms react differently to the various filler materials. 2. The chemical agents determine an inflammatory process of varying degrees on the biological material with damage of the same. 3. Phlogogen stimulus select some under populations of fibroblasts with an important role in the formation of the fibrosis. 4. The interleukin IL-4 ties itself to the CD40 of the fibroblasts with a profibrotic effect and reduction of the antifibrotic effect of the IFN-gamma. Therefore, the neocollagenogenesis is real but constituted by fibrotic collagen of type I and therefore does not induce a biological rejuvenation but only an aesthetic rejuvenation. The dimensions of the permanent fibrotic capsule which forms can be more or less

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evident. The use of these products should be confined to the deep dermis, avoiding their use on areas of scarce thickness, for example the neck.

11.11 Silanoles A recent proposition has been made on an old product made of silanoles (onometiltrisilanolo orthohydroxybenzoate sodium–silanol salicylate pH:5.7). In this product the organic silicon is connected to the salicylic acid with hydrogen bonds, permitting the product to remain soluble, thus avoiding the polycondensation of the monomethyltrisilanolone. These bonds break once the substance is inserted in the derma. (Caution with those patients allergic to the salicylic acid!). The product is proposed for the treatment of wrinkles, scars, stretch marks, and cellulite, thus proposing the biological effect that silicon makes in the skin. Bridges of silicon among the GAGs and the glycoprotein form the skeleton of the intercellular matrix. In young people the skin is the tissue that, together with the arteries and the thymus, contains more organic silicon. These values decrease progressively with age. This affirmation is real but refers to the silicon introduced in the diet as the literature states: 1. Silicon is one of the important oligoelements for the regular metabolism of some of our tissues and in particular for the bony, cartilaginous and connective tissues. The silicon is being introduced normally in our organism through the diet and it is absorbed at intestinal level as orthosilicic acid. 2. Its principal role is developed in the synthesis of collagen of Type 1 and in the activity of the proline hydroxilasis. 3. Its deficiency is shown with an alteration of the formation of the bony tissue and with a reduced hepatic function of the Ornitina transaminase. 4. The exogenous supplementation of silicon in the diet allows, through the normalization of the concentration of orthosilicic acid, to regulate the formation of the extracellular matrix and the calcium metabolism. 5. The hydroxilate silicon or oxydated forms (silanoles) are utilized in the analytic medical technology (Technologies of selective separation) to stop hydrophilic molecules at high molecular weight, such as the Hyaluronic acid, and tying them up, separate them from other components.

11  Biostimulation and Biorestructuring of the Skin

6. The particles of organic silicon put into the organism induce an inflammatory reaction and a response of fibrotic character. So we cannot credit to an organic silicon put in the derma those actions made by the silicon put in the diet. The silanoles bind themselves to the hydrophilic molecules of the dermis. The silanoles induce an irritative inflammatory stimulation which stimulates a connective response with a neoformation of collagen type 1. The pH of 5.7 saturates the negative bindings of the colloidal solution of the matrix with the gelation and coagulation of it. The salicylic acid regulates the inflammatory process induced by the silanoles thus avoiding excessive damage. The use of the silanoles must be permitted only for the aesthetic rejuvenating of old skins.

11.12 Therapeutic Biostimulation A bridge of biological stimulation between the physiological stimulation and the aesthetic correction is represented from the so-said therapeutic stimulation. This foresees the skin treatment on the basis of the state of the same and has the aim of getting back from an altered state to a normal condition. There are six types of therapeutic biostimulation. The treatment called Sebum Less is needed to reduce the sebaceous secretion in excess in the seborrheic skins and uses the botulinum toxin introduced intradermally with small concentrations. The toxin reacts by blocking, in a reversible way, the liberation of acetylcholine at a neuromuscular level and it is ­useful in the reduction of the mimic face wrinkles. However, the use of this medicine can be enlarged also to other indications. A first use is that of regulating the epidermic growth stimulus, reducing the effect of the epidermal growth  factor. Muscarinic receptors activate a ­metalloproteinase, which liberates surface-associated heparin-binding epidermal growth factor (HB-EGF) and causes transactivation of epidermal growth factor receptors (EGFRs). The use of the toxin after the peeling treatment that by exfoliating the epidermis move the scale EGF/caloni to an access of EGF, can find a usefulness. The toxin has an antioxidant effect. Acetylcholine is required for opening of mitochondrial (ATP) channels with the generation of reactive oxygen species (ROS). This action can be reduced by blocking the acetylcholine.

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The toxin can be used in the seborrheic skins to reduce the production of sebocyte and to narrow the pores and there is a role for Acetylcholine (Ach) in sebum production and as a promoter of sebocyte differentiation. We can utilize the toxin in the couperosic skins to stimulate the vasoconstriction of the skin. Adrenergic neurons release noradrenalin and ATP to reduce cutaneous blood flow while cholinergic neurons release acetylcholine and a co-transmitter to dilate skin blood vessels. The mechanism of formation of the sebum foresees the stimulation of the sebaceous cells on behalf of the dihydrotestosterone, coming from the reduction of the circulating androgens on behalf of the 5-alpha reductase. The dihydrotestosterone reacts at DNA cellular level by stimulating the codification of the RNA necessary for the formation of the sebum. The botulinum toxin, by blocking the secretion of the acetylcholine, reduces the effect of this on the differentiation of the sebocyte and on the liberation of the sebum. It reduces, furthermore the increase of the ematic flux, always induced by the acetylcholine, and consequently to the flux of androgens. For the treatment 10 units of toxin diluted in 3 mL of physiologic solution is needed. Some intradermally injections in those areas with sebaceous hypersecretion. The Hydra Plus treatment utilizes some no crosslinked hyaluronic acid in order to increase the fixation of water at a dermal level. Hyaluronic acid contained in the core of the proteoglycans has the capacity of fixing a high number of molecules of water in the matrix. This is an important function in the keeping of the homeostasis of intradermal water. The intradermal introduction of noncross-linked hyaluronic acid increases the fixation of the water molecules, thus reducing the loss for transpiration and improving the hydration and the turgidity of the dermis. The treatment is repeated one or more times during the month, introducing the product into the dehydrated areas. The treatment called Aging Therapy utilizes the introduction of antioxidants to block the damage from the free radicals of the oxygen. The free radicals of the oxygen are normally produced, in the interior of the mitochondrias, through an enzymatic chain, called chain of transportation of the electrons, as products inbetween of formation of water molecules. The heart of this mechanism is the cytochrome oxidase, an enzyme capable of tying together electrons to the oxygen molecule and put it together later to the atoms of hydrogen in order to form the water molecules. The mechanism

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of reduction of the oxygen foresees a necessary time to the inversion of the spin of one of the two to be added electrons. This can take to the escape of the radical oxygen (with only one electron) before the completion of the orbit. If the escape process exceeds a certain quantity (antioxidant concentration) the free radical of the oxygen can react with many biological structures damaging them. This damage is compensated, up to a certain level, by the antioxidants’ action in vitamin E and vitamin C. Also the enzymatic antioxidants (catalase and glutationperoxidase) develop the blockage function of the lipoperoxidative damage. On this basis it is useful to give intradermally, some Vitamin C and glutathione with the aim of optimizing the skin defenses to the oxidative damage. The treatment is repeated one or more times during a month with intradermal shots. The treatment called Photo Aging Therapy prevents the alterations of the matrix related to the inflammatory process produced by the ultraviolet rays with a special buffer solution. The UV rays hit the skin determining the activation of the cellular phospholipase. This frees from the arachidonic acid membranes reactivating the fall of the ecosanoids with acidification of the dermal matrix. The status of sol of the colloidal solution of the matrix is permitted by the dissociation of the protein macromolecules of which they are made. To the physiological pH of 7.4 the radical acid is dissociated, thus determining a negative charge of the macromolecule. The common negativity of the macromolecules bring to the repulsion of the same by the creation of a colloidal solution to the status of sol, permitting the free metabolic exchange. The inflammatory response induced by the ultraviolet rays brings to an acidification of the matrix with liberation of hydrogen protons. The protons, positives, get together with the carboxylic radical, negative, giving balance to the free charges and transforming the colloidal solution of the matrix from the state of sol to that of gel. The macromolecules of the matrix get compacted due to the loss of the electric repulsion with gelation of the colloidal solution which makes the matrix. The matrix solidifies passing from a status of sol to that of gel and therefore losing its function of metabolic exchange. The treatment foresees one session or more during the month, with the introduction of a bicarbonate buffer with intradermal injections. The treatment called Flabby Less consists of the introduction of a medical device for the restructuring of the derma to reduce tissue looseness. The aim is that

M. Ceccarelli

of increasing the concentration of the fibrotic collagen and of stretching the hypotonic tissue increasing its rigid component. The scheme is one of activating an inflammatory process and the formation of fibrotic collagen. The Medical Device is constituted by a solution of amino acids, acid, and hypertonic. The chemical damage induces a reparative response with the fibrosis of the derma. The treatment is carried out with intradermal injections, one or more times during the month, in the hypotonic areas. The treatment called Choline Therapy foresees the introduction of glycerate choline as an activator of the cholinergic dermo-epidemic system. DMAE, the precursor of the choline, is administered and the direction somministration will anticipate the metabolic passage in the optimization of the concentration of acetylcholine. The treatment is performed with intradermal injections, one or more times a month, in areas where a metabolic improvement is required.

References 1. Ceccarelli M (1992) Invecchiamento generale e cutaneo in medicina estetica. Trimograf, Bologna (Italia) 2. Chang YC, Yang SF, Tai KW, Chou M, Hsieh YS (2002) Increased tissue inhibitor of metalloproteinase-1 expression and inhibition of gelatinase A activity in buccal mucosal fibroblasts by arecoline as possible mechanisms for oral sub mucous fibrosis. Oral Oncol 38(2):195–200 3. Ceccarelli M, García JV (2010) The medical face lifting: regeneration of the face tissues. Physiology Med Lett 1(1):1–9 4. Ceccarelli M, Pelliccia R (2010) Curcio Cl: heterologous skin regeneration. Physiology Med Lett 3(2):1–7 5. Lesley J, Hascall VC, Tammi M, Hyman R (2000) Hyaluronan binding by cell surface CD44. J Biol Chem 275(35):26967–26975 6. Wang Q, Lu K, Yang L (1999) Effects of hyaluronic acidstimulating factor on viability and collagen synthesis of fibroblasts. Zhonghua Zheng Xing Shao Shang Wai Ke Za Zhi 15(2):89–91 7. Denton CP, Abraham DJ (2001) Transforming growth factor-beta and connective tissue growth factor: key cytokines in scleroderma pathogenesis. Curr Opin Rheumatol 13(5):505–511 8. Jelaska A, Strehlow D, Korn JH (1999) Fibroblast heterogeneity in physiological conditions and fibrotic disease. Semin Immunopathol 21(4):385–395 9. Leask A, Holmes A, Abraham DJ (2002) Connective tissue growth factor: a new and important player in the pathogenesis of fibrosis. Curr Rheumatol Rep 4(2):136–142 10. Lu Y, Luo S, Liu J (2001) The influence of transforming growth factor beta 1 (TGF beta 1) on fibroblast proliferation and collagen synthesis. Zhonghua Shao Shang Za Zhi 17(6):345–347

11  Biostimulation and Biorestructuring of the Skin 11. Sato M, Shegogue D, Gore EA, Smith EA, McDermott PJ, Trojanowska M (2002) Role of p38 MAPK in transforming growth factor beta stimulation of collagen production by scleroderma and healthy dermal fibroblasts. J Invest Dermatol 118(4):704–711

143 12. Si Z, Rhanjit B, Rosch R, Rene PM, Klosterhalfen B, Klinge U (2002) Impaired balance of type I and type III procollagen mRNA in cultured fibroblasts of patients with incision hernia. Surgery 131(3):324–331

 

Microdermabrasion

12

Preeti H. Savardekar

12.1 Introduction Microdermabrasion, popularly known as “body polishing,” is a simple and safe, effective cosmetic procedure that has gained popularity. It is an office-based mechanical resurfacing technique in which aluminum oxide crystals or other abrasive substances are blown onto the face, and then vacuumed off, using a single hand piece [1]. This procedure has been widely utilized for a variety of cosmetic objectives, including improvement of photoaging, hyperpigmentation, acne, scars, and stretch marks. Despite its widespread use, little is known about its actual mechanism of action. The few published studies suggest that patients and physicians alike report a mild benefit when microdermabrasion is utilized for photoaging [2]. Aged skin is characterized by rhytids and also epidermal and dermal atrophy, rough skin texture, irregular pigmentation, telangiectasias, and laxity. Using a series of microdermabrasion treatments is an effective, non-invasive method of rejuvenation with minimum risk that improves skin quality [3]. Histologic evaluation reveals little actual abrasion of the skin with the procedure, yet changes are seen in the dermis.

skin would be painful and harmful, and it would result in permanently embedding the tiny grains into the skin. Whether done with a product at home or in a professional setting with a specialized machine, the principle of microdermabrasion is the same. The idea is that if you remove or break up the stratum corneum, the body interprets that as a mild injury and rushes to replace the lost skin with new and healthy cells. In the first hour after treatment, there is mild edema (swelling) and erythema (redness). Depending on the individual, these side effects can last anywhere from an hour to 2 days. With the stratum corneum gone, the skin’s surface is improved. The healing process brings with it newer skin cells that look and feel smoother. Some of the skin’s visible fine lines, post-inflammatory hyperpigmentation, and to some extent, pigmentation due to tanning are removed. Also, without the stratum corneum acting as a barrier, medicinal creams and lotions are more effective because more of their active ingredients and moisture can find their way down to the lower layers of skin. As microdermabrasion temporarily removes some moisture from the skin, it is important to apply moisturizing creams and sunscreen lotions.

12.2 Principles of Microdermabrasion

12.3 Indications and Contraindications

All of the action in microdermabrasion takes place at the level of the stratum corneum. Affecting deeper layers of

Microdermabrasion is used mainly for: 1. Superficial acne scars 2. Post-inflammatory hyperpigmentation 3. Photoaging [3] (fine lines and open pores) Microdermabrasion is not recommended for those with: 1. Active rosacea 2. Fragile capillaries

P.H. Savardekar  Shri Krishna Polyclinic, Kaya Skin Clinic, Krishna Building, J.P. Marg, Opp. Poddar Hospital, Worli, Mumbai 400 018, Maharashtra, India e-mail: [email protected]

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3. Vascular lesions 4. Widespread acne 5. Herpetic lesions 6. Warts 7. Erosions or ulcers 8. Eczema 9. Psoriasis 10. Lupus erythematosus 11. Diabetes mellitus Microdermabrasion should not be used on patients who have taken Isotretinoin in the previous 6 months due to dryness of skin and the possibility of scarring [4].

12.4 Procedure A written and informed consent is mandatory in which the pre- and post-procedure instructions are clearly mentioned. A small crystal sensitivity check is always better to be done prior to starting the treatment on the face. Forearm or inner arm is a common site for the patch test. For darker skin types, priming the skin with lightening agents can be done a few weeks prior to beginning the series of microdermabrasion treatment. After placing the patient in a comfortable position, the area to be treated is cleansed. Normal saline is kept by the side to use as an emergency eyewash in case the crystals irritate the eyes. Protective goggles or eyepads may be used to prevent corneal damage in older or diabetic patients. The technician steadily moves the handpiece, applying even and steady pressure to remove the stratum corneum without affecting the lower skin layers. As the hand holding the handpiece moves smoothly and steadily across the skin, the other hand is used to gently hold taut the skin to achieve a more efficient abrasion. A standard session usually consists of one to three passes with the handpiece with vertical and horizontal orientation. It is best not to leave gaps – overlap to some extent is desirable. The procedure may take anything between 20 and 30  min. More pressure can be applied till pinpoint bleeding is seen in cases of deep acne scars and this is more effective provided the patient is informed of the aftercare and is willing to have a sensitive skin for 2–3 days till healing occurs. The depth of the treatment depends on the strength of

Fig. 12.1  Strokes should follow a standard pattern

flow (speed) of the crystals, the rate of movement of the handpiece against the skin, and the number of passes over the treatment area. Slower movement of the handpiece (allowing longer contact of the abrasive crystals with the skin), higher velocity of crystals, and increased number of passes achieve deeper abrasion [4]. Crystals are available in different sizes like 100, 130 and 180 mm. It is believed by a few that the larger the size of the crystal, deeper is the depth of abrasion [5]. A soft brush can be used in between each pass to clear the powder and skin debris off the skin. The clinical endpoint is mild erythema (flushing). Strokes should follow a standard pattern (Fig.  12.1) starting from the forehead, cheeks, jawline, upper lip and below lower lip, chin and then neck. Finish the first pass on the face with the nose. Treat with extra passes the areas of concern and follow crisscross pattern of strokes on scars. Vacuuming is done at gaps all over the face to complete the treatment.

12  Microdermabrasion

The patients are asked to apply specialized moisturizing lotions and creams to the affected area between sessions. This rehydrates the area and assists in promoting healthier new skin. Immediate improvement in texture and appearance is noticed and the acne scars get more defined and superficial. Makeup and exercise involving sweating are to be avoided for 48–72  h as perspiration contains salt which may cause a stinging and irritated sensation to the skin. Professional microdermabrasion can bruise or discolor the skin if done incorrectly. Tiger stripes are commonly seen for 24–48 h after the procedure on very fair or sensitive skins. The vacuum action tends to cause blemishes if the skin tension is let up or uneven. The lip area is particularly susceptible to bruising, and the eyelids should never be treated with microdermabrasion. Treatment that is too deep or intense can cause permanent discoloration to the skin.

12.5 Techniques of Microdermabrasion Different methods of microdermabrasion include mechanical abrasion from jets of zinc oxide or aluminum oxide crystals, fine organic particles or a roughened surface. Many of the newer microdermabrasion machines offer the facility to use more than one method. When using a crystal machine, abrading crystals and the abraded material are both vacuumed off with the handpiece through which the abrasive particles come. The procedure is not very painful and requires no anesthesia. It is a useful alternative for patients whose skin is too sensitive to use anti-acne drugs like tretinoin.

12.6 Aluminum Oxide Crystal Machines The most commonly used abrasive in microdermabrasion is aluminum oxide (Table 12.1) [6]. It is a good abrasive because of its course, uneven surfaces. It will not cause allergic skin reactions, such as eczema or itching; it is more or less chemically inert and is not absorbed by the skin. It has bactericidal properties, which is an advantage while treating acne, as

147 Table 12.1  Comparison of crystal and non-crystal Crystal MDA Crystal free MDA Efficacy High (deep Moderate (not for acne ablation) scars) Sterility High (disposable Low (not disposable) consumables) Procedure Longer and messy Shorter time Maintenance High Low cost Pain Moderate Low Skin type For thicker skin Thin and sensitive skin Bactericidal Seen in aluminum None property oxide crystals

acne is associated with bacterial proliferation. However, loose abrasive grits are hazardous irritants and are therefore unhealthy not only to the technician (who performs many treatments per day), but also the patient. A mask, along with protective eyewear should be used in order to keep the abrasive out of the eyes, nose or ears.

12.7 Other Crystal Machines Other crystals instead of aluminum oxide can be used for microdermabrasion. These include sodium chloride crystals [7], sodium bicarbonate crystals and magnesium oxide crystals. These media are cheaper, although a bit less effective. Generally these alternative media are not as abrasive as aluminum oxide.

12.8 Crystal Free Instead of crystals, aestheticians and dermatologists alike use diamond-tipped devices that abrade the skin (Table 12.1). These wands have their tips made of diamond chips of varied sizes and coarseness for different types of skin and levels of resurfacing. Dead skin cells are sucked up at the abrasive tip of the wand into a waste filter. The major difference with the crystal-free treatment to the crystal one is the hygiene, and less messy a procedure. Patients have commented that the crystal-free procedure is usually much less painful while not sacrificing results [8].

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12.9 The Vacuum The vacuum action of the machine has the following functions: 1. It pulls and raises a small section of skin to work on. 2. It shoots a stream of crystals across the targeted skin patch. 3. It collects the used crystals and dead skin for disposal. Some tools perform all of these functions with one circuit. The suction process in these devices is called “Venturi suction.” More powerful versions use two circuits, one to shoot the crystals out and another to collect them. If the powder is not cleared away from the face after procedure, itching is experienced by the patient for few hours.

12.10 Histopathologic Studies Volunteers who underwent skin biopsies before and after a treatment series on the dorsal forearms showed that there was statistically significant improvement in roughness, mottled pigmentation, and overall improvement of skin appearance, but not in rhytides [9, 10]. Acne scarring improved, but required deeper ablation. Immediately after the procedure, the stratum corneum was homogenized and focally compacted. There was slight orthokeratosis and flattening of rete ridges and a perivascular mononuclear cell infiltrate, edema, and vascular ectasia in the upper reticular dermis 1 week after completion of the series. Chronically there was epidermal hyperplasia, decreased melanization and some increase in elastin.

P.H. Savardekar

himself/herself with a mask. The crystals may also get into the eyes of the operator or more commonly the patient. Hence, the patient must wear protective eyewear during the procedure. Cross contamination in patients may occur with improper sterilization of the handpiece. Sterilization of the handpiece is necessary before treating the next patient and using disposable distal caps on the handpiece as blood and debris were found on the plateau of the handpiece especially after treating a patient with acne scars [12], since pinpoint bleeding may occur with deep ablation in acne scarring. Each session of microdermabrasion can be repeated every 10–15  days to allow time for healing and see visible changes. Combination with superficial peels alternating with microdermabrasion is claimed to give better results. If used correctly, the microdermabrasion machine can be used for other body parts like back, hands, feet also and gives satisfactory results.

12.12 Important Instructions and Advice Repeated sunscreen application, 3 hourly, is crucial to maintain the results of the procedure. No hot water to be used 24 h after the treatment. Parlor activities like waxing and bleaching should be done after a 3–4 day gap after the treatment. Male patients must shave at least 3–4 h before the treatment. After the procedure, shaving can be done after 12 h. Patients need to stop usage of AHA/Retinol creams 2–3  days before the treatment and the same can be resumed 3–4 days after the procedure.

References 12.11 Side Effects Local side effects are uncommon and transient but include pain, burning, sensitive skin, photosensitivity, tiger stripes or diffuse hyperpigmentation. In case of excessive redness, cold compresses for 10–15  min will reduce the erythema. In case of burning and tiger stripes, mild hydrocortisone (any OTC brand) for 2  days will reduce the irritation. Workers who routinely inhale silica dust (silicosis), asbestos fibers (asbestosis) or hard metal dust are at risk of pulmonary fibrosis [11]. Hence, the operator must protect

1. Spencer JM (2005) Microdermabrasion. Am J Clin Dermatol 6(2):89–92 2. Spencer JM, Kurtz KS (2006) Approaches to document the efficacy and safety of microdermabrasion procedure. Dermatol Surg 32(11):1353–1357 3. Coimbra M, Rohrich RJ, Chao J, Brown SA (2004) A prospective controlled assessment of microdermabrasion for damaged skin and fine rhytides. Plast Reconstr Surg 113(5):1438–1443 4. Whitaker E, Meyers AD (2011) Microdermabrasion. Medscape.com/843957/May 9 5. Monteleone G (2000) Microabrasion of skin with aluminum oxide crystals. Int J Cosmet Surg Aesthet Dermatol 2(3): 181–182

12  Microdermabrasion 6. Karimipour DJ, Kang S, Johnson TM, Orringer JS, Hamilton T, Hammerberg C, Voorhees JJ, Fisher G (2006) Microdermabrasion with and without aluminium oxide crystal abrasion:a comparative molecular analysis of dermal remodeling. J Am Acad Dermatol 54(3):405–410 7. Rajan P, Grimes PE (2002) Skin barrier changes induced by aluminum oxide and sodium chloride microdermabrasion. Dermatol Surg 28(5):390–393 8. Gold MH (2003) Dermabrasion in dermatology. Am J Clin Dermatol 4(7):467–471

149 9. Shim EK, Barnette D, Hughes K, Greenway HT (2001) Microdermabrasion: a clinicopathologic study. Dermatol Surg 27(6):524–530 10. Tan MH, Spencer JM, Pires LM, Ajmeri J, Skover G (2001) The evaluation of aluminum oxide crystal microdermabrasion for photodamage. Dermatol Surg 27(11):943–949 11. Wilson MS, Wynn TA (2009) Pulmonary fibrosis: pathogenesis, etiology and regulation. Mucosal Immunol 2(2):103–121 12. Shelton RM (2003) Prevention of cross- contamination when using microdermabrasion equipment. Cutis 72(4):266–268

 

Aesthetic Cryotherapy

13

Michael H. Swann

13.1 Introduction Cryosurgery, also known as cryotherapy, is the localized freezing of tissue for controlled destruction and removal of unwanted cutaneous lesions. The origin of cold therapy in medicine can be traced back 4,500 years as Egyptians treated injuries and inflammation with cold water. Although ice was the early cryogen, the birth of modern destructive surgery was founded using liquid nitrogen, which readily induced subzero skin temperatures with a low boiling point of −196°C [1]. After becoming commercially available following World War II, liquid nitrogen became the principle modern cryogen, surpassing historic cryogens including liquefied air, solidified carbon dioxide, and liquid oxygen. Significant refinements in the cryosurgical devices during the 1960s brought about the first handheld liquid nitrogen cooled probe in 1967 and subsequently the handheld spray device commonly used today, which became commercially available in 1968 [2]. Liquid nitrogen is readily available in nearly any area with modest industry and advances in modern holding tanks allow liquid nitrogen supplies to be maintained for months without refilling. Along with the development and more widespread use of these sophisticated portable instruments, refinements in techniques of liquid nitrogen have made cryosurgery quite practical in clinical medicine as tissue destruction can be more reliably controlled. This text will primarily

M.H. Swann  Ozarks Dermatology Specialists, 3808 S. Greystone Ct, Springfield, MO 65804, USA e-mail: [email protected]

c­ onsider practical applications of the open spray technique which are founded on this handheld spray device known casually as the “cryo gun” [3]. The use of cryotherapy in clinical medicine is increasing in America along with our aging population and their propensity for these common lesions. The treatment time is quite brief, which is convenient for practitioners and patients, causes minimal pain and no bleeding or odor. Despite preliminary costs of cryosurgical hardware and storage devices, liquid nitrogen is inexpensive and readily available in most communities. Additionally, a conscientious cryosurgeon can offer good aesthetic results. A variety of techniques are available to help the contemporary clinician apply liquid nitrogen to the skin surface, each with distinct advantages and disadvantages. The open spray technique, the chamber technique, and the closed contact or probe technique are all reliable. Some clinicians apply liquid nitrogen by hand using one or more cotton-tipped applicators. This technique is the most unreliable as much of the liquid nitrogen is lost into atmospheric nitrogen gas during transfer to the skin, resulting in unpredictable tissue freezing from an inconsistent cryogen temperature. Although the cotton-tipped applicators do not offer a consistent freeze, use of forceps frozen in liquid nitrogen has been described to offer limited subzero temperature and may be more useful for benign entities in delicate areas [4]. As a practical note, a fine forceps can be submerged into liquid nitrogen to transfer cold to small skin tags or fine seborrheic keratoses on the eyelid. This can be performed without any nitrogen in liquid form, although this procedure, like the cotton-tipped applicator technique, does not elicit the degree of freezing required for thick or resistant skin lesions.

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The open spray method employs a cryosurgical unit, liquid nitrogen, and spray-tip attachments which allow a fine spray of liquid nitrogen at a lesion from a distance of 1–2  cm. This is the most frequently used technique and will be the focus of this practical review. The cryogen canister should be held upright during treatment and the condensation wiped from the top of the canister. With any technique employed, the destruction of keratinocytes and melanocytes as well as ensuing inflammation caused by cryotherapy may cause considerable alterations in skin surface appearance, making recurrences sometimes difficult to identify [5]. The chamber and closed techniques are not commonly used for aesthetic indications, but discussion is included for completeness. In the chamber technique, the cryogen is released into a chamber which is applied with pressure to the skin. The turbulent movement of liquid nitrogen in the chamber lowers the temperature of the cryogen, further magnifying its destructive capabilities. Therefore, this technique must be utilized carefully and is generally limited to treating malignancy and for palliative care. The closed technique uses a metal probe fitted to the size of the lesion. Probes are best for treating lesions on a flat surface and care must be taken to avoid tearing frozen tissue when removing the probe from the skin. It is best to allow complete thawing before attempting to remove the probe. Cryosurgery is a versatile, efficacious, and economical therapy for many benign, premalignant and, in some circumstances, malignant conditions of the skin. The list of benign conditions which have been reported amenable to cryosurgery is extensive and includes acne, adenoma sebaceum, angiokeratoma, chondrodermatitis nodularis helicis, condyloma, ephileds, lentigo simplex, molluscum contagiosum, prurigo nodularis, rosacea, sebaceous hyperplasia, syringomas, venous lake, verruca plana, verruca vulgaris, and more [6]. Although many diagnoses are on this list, cryoablation is often not indicated since other preferred therapies exist. For example, although molluscum contagiosum responds readily to liquid nitrogen, cantheradin is more commonly used. Cantheradin is effective, less irritating, and has no potential for scarring, therefore is preferred to cryotherapy in most cases of molluscum, which are benign and known to remit given enough time. Although sebaceous hyperplasia responds to cryoablation, patients who seek treatment generally are looking for cosmetic improvement, which may be better achieved using other modalities including gentle electrofulguration. Because

M.H. Swann

of the similarity of sebaceous hyperplasia to basal cell carcinoma with respect to both location and morphology, biopsy is indicated before treatment of this entity in all but the most obvious cases. The most common skin lesions for which cryoablation may be considered as first line therapy are verruca (warts), actinic keratoses (premalignant squamous cell carcinoma) and seborrheic keratoses. Like other methods used by a skin specialists such as laser treatments or chemical peeling, safe and effective use requires routine use and a diligent approach with close clinical follow-up. Lentigenes are particularly effectively depigmented by a single 1–2 s freeze– thaw cycle. This is in stark contrast to thicker course seborrheic keratoses which are more likely to be treated with two freeze–thaw cycles at 10–15 s. Thicker seborrheic keratoses are a common complaint and can be a cosmetic priority for women who find their foundation make-up clumps and draws attention at these sites. These thicker lesions can be effectively treated in a single treatment session, but there is risk for persistent hypopigmentation in these thicker plaques. Persistent hypopigmentation is more commonly seen when freeze–thaw times pass 20–30 s. The clinical relevance of the pigmentation varies with the degree of normal skin pigmentation for a patient. The astute cryosurgeon may elect for single session treatment of these in patients with very light skin, where hypopigmentation would not be noticeable, but patient satisfaction is more likely found in planned retreatment in 4–6 weeks and concomitant use of keratolytics such as retinoids or topical lactic or salicylic acid lotion between treatments. Even when a patient is a candidate for photorejuvenation with laser or intense-pulsed light therapy, initial treatment of the thickest lesions will improve the aesthetic result. I often perform a minimal amount of cryotherapy to thick seborrheic keratoses during consultation when patients elect photorejuvenation treatment. Light curettage of the stratum corneum may be helpful before treating thicker lesions as an attempt to bypass the poorly conducting stratum corneum. Cryotherapy is more difficult to use aesthetically in darker pigmented patients because hypopigmentation is readily seen and may persist for 6 months or more. In these patients, caution should be used even after performing test-spots and despite initial treatments in less conspicuous areas using conservative techniques. Although cryotherapy is simple and useful in treating a variety of skin conditions, accurate preoperative

13  Aesthetic Cryotherapy

clinical diagnosis cannot be overemphasized as the dilettante may find benign and malignant skin lesions look quite similar. Therefore, as a rule, cryotherapy should be avoided as empiric treatment when the diagnosis is in doubt. When malignancy is within the clinical differential diagnosis, a simple skin biopsy to establish the diagnosis is appropriate with subsequent treatment recommendations based on histopathology. Actinic and seborrheic keratoses, verruca, and keloids are among the most commonly treated diagnoses. The skin surface interface of frozen and thawed tissue is easily identifiable during cryotherapy treatment and the extent to which the frozen tissue expands is a practical and reliable indicator of the degree of cellular damage. For medical treatments, a margin of frozen tissue extending 1–2  mm beyond the target is effective in benign lesions while aggressive lesions require a longer freeze– thaw time effecting surface ice formation 3–5 mm beyond the lesion. Multiple freeze–thaw cycles, commonly used to treat more aggressive lesions, cause increased cellular destruction and inflammation within the treated area. Cosmetic use of liquid nitrogen calls for more conservative parameters, including no margin beyond the lesion and use of a single 1–2 s freeze–thaw cycle. For best cosmetic outcomes, preference is given to a single cycle in thin lesions, such as lentigenes. Water conducts the temperature difference better than air, which suggests the open spray technique is more effective when concentrating the liquid nitrogen at a single focus. Concentrating the liquid nitrogen on a solitary focus on the skin creates the effect of a three-dimensional “ice ball,” which allows for better depth of penetration. Depth is particularly important when treating raised lesions, as lesion height generally reflects depth, and for actinic keratoses within hair-bearing areas where atypical keratinocytes find sanctuary within deeper follicles. Depth of thermal penetration is limited primarily by the nonviable stratum corneum superficially and deeper by the vertical temperature gradient. These principles of conduction help explain the requirement of more aggressive freeze-to-thaw times for similar therapeutic effect in patients with dry skin, such as diabetic and elderly patients, since a less hydrated stratum corneum is less thermally conducive [7]. Treatment with a high freezing velocity and complete slow thaw between cycles is important for treating aggressive medical indications, but can be avoided when treating lesions such as lentigenes or dyspigmentation. The margin of the frozen epidermis is relentlessly being thawed by the

153 Table 13.1  Practical cryosurgical guidelines for freezing times of various skin lesions Diagnosis Actinic keratosis Cherry angioma Chondrodermatitis Condyloma Keloids Molluscum Sebaceous hyperplasia Seborrheic keratosis Skin tags Verruca plana Verruca vulgaris

Freeze time (s) 5–20 10 20–40 10 30+ 5–10 5–10 8–15 10 5 15–20

These represent practical guidelines which may be useful when using the open spray technique to administer liquid nitrogen. Freeze time determination for an individual lesion should be made clinically and always in conjunction with accurate clinical diagnosis

vertical temperature gradient and by a lesser degree to atmospheric temperature on the skin surface. Compared with a slower freeze, high freezing velocity effects more intracellular ice crystal formation and leads to more consistent cell death. The open spray or probe technique generates much colder (−196°C) skin temperatures than liquid nitrogen applied by cotton tipped applicator (−20°C) or other disposable cryogens available to consumers (−55°C to –70°C) which underscores its more consistent and precise tissue destruction. Ideal cryosurgical freeze times vary according to lesion type, size, depth, and location. “Freeze time” refers to the complete time of tissue ice and is commonly mistaken as the time for which the nitrogen is sprayed. General freeze–thaw time guidelines are useful when learning about cryotherapy, but freeze times for individual lesions should be determined clinically in conjunction with accurate clinical diagnosis (Table 13.1). A thin actinic keratosis can usually be eradicated with 5–10 s of freeze–thaw time using the open spray technique. Depending on the hydration of the skin and canister nosel which controls the volume of liquid sprayed, this may require a single 1–2 s spray of liquid nitrogen. Hypertrophic lesions may require up to 15 s freeze–thaw times and/or a second freeze–thaw cycle. Seborrheic keratoses can be treated with liquid nitrogen alone, but our practice is to combine cryoablation with gentle curettage for thicker lesions. Since verrucas can be quite thick and keratin is a poor cold conductor, it is often quite helpful to debulk the lesion prior to cryotherapy.

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Debulking can be performed with keratolytic substances such as lactic or salicylic acid or by paring with a #15 scalpel blade, which is our preference. If using curettage, it is important to achieve hemostasis prior to initiating cryotherapy as active bleeding increases skin temperatures and limits cryotherapy destruction in these areas. Keloids often pose a very difficult treatment dilemma and require longer freeze times. Cryotherapy may be used alone or in conjunction with other treatment modalities such as intralesional corticosteroids, surgical debulking, and radiation [8]. Malignancies of the skin such as squamous cell carcinoma in situ, superficial basal cell carcinoma, and nodular basal cell carcinomas in low-risk locations may also be treated with cryosurgery. Of course, surgical excision is the gold standard therapy for these cutaneous malignancies and cryosurgery in these tumors should be reserved for practitioners with considerable experience in this area. If cryosurgery is determined to be the optimal therapy, the lesion should be treated until a 5  mm margin of frozen tissue is formed around the lesion which requires approximately 60  s of total freeze time. Malignant tumors are not generally treated by cryotherapy because depth of penetration is a wellknown limitation of this therapy, but in experienced hands the depth of freeze can be monitored by inserting a needle with a thermocouple beneath the tumor. In this practice, –50°C to −60°C is the target temperature [9]. Patients should be aware of expected side effects and potential complications associated with cryotherapy. Postoperative cryosurgical wound care is simple and consists of gentle cleansing and protection by occlusion with ointment for 2–10  days. In aesthetic conditions, blisters should be avoided and patients can utilize Aquaphor ointment to cover the lightly treated lesions for 2 days. Sunscreen should be reinitiated after wound care with ointment has ceased. If intact bullae result from freezing, attempt should be made to protect these “biologic dressings.” Although some patients prefer antibiotic ointments as a part of their wound care regimen, superficial infection of the treatment sites is not as common as the incidence of contact allergy to these antibiotic ointments. Our practice is to use bland petrolatum ointment at least twice daily, which is cheap, safe, and effective. Some patients who complain of post-operative pain may find the immediate application of petrolatum soothing to treated sites. For cosmetically sensitive areas in vigilant patients, results may be optimized with more frequent petrolatum application.

M.H. Swann

When tending to post-operative lesions is difficult because of the anatomical location, such as the back, occlusion with a non-adherent dressing may limit the frequency of ointment application [10]. Expected side effects of treatment using cryotherapy include pain, edema, erythema, bullae formation, exudation, and sloughing. Healing is dependent upon numerous factors including the anatomic location, depth of tissue injury, and the patient’s innate healing response, therefore only generalization can be made about healing times. Benign and premalignant lesions generally heal between 2 and 4 weeks, whereas malignant lesions may take up to 6 weeks or longer to heal. Hypopigmentation is a frequent complication of therapy and, in view of the fact that melanocytes are more sensitive to cold than keratinocytes, difficult to prevent. Melanocytes do not survive at temperatures of −4°C or less, but when total freezing times are limited, the hypopigmentation is often temporary. For that reason, limiting freeze–thaw times no more than 20–30 s is important in cosmetically sensitive areas of all patients, but this hypopigmentation can be especially problematic for darkly pigmented individuals [6]. In these patients, even temporary hypopigmentation may cause more distress than the initial concern treated and other treatment modalities should be considered. Other cryotherapy complications include hypertrophic scarring, delayed bleeding, headache, paresthesias, neuropathy, secondary infection, syncope, nitrogen gas insufflation (nitrogen gas bubbles in skin), milia, hyperpigmentation, alopecia, cartilage necrosis, and pyogenic granuloma. Appropriate patient selection is essential to successful patient outcomes using cryotherapy. There are relatively few contraindications to cryosurgery, but they include patients with a history of cold urticaria, cold intolerance, cryofibrinogenemia, or cryoglobulinemia. Recurrent or aggressive tumors should not be treated with cryosurgery. Caution should also be used when treating lesions at delicate sites and near free margins including the corners of the mouth, alar rim, medial canthi, vermillion lips, eyebrows, and auditory canal as scarring and retraction is possible. In conclusion, cryosurgery is an effective, efficient, and relatively low-risk modality for treating many aesthetic skin lesions. Although useful in other medical fields as well, cryosurgery has become indispensable in most dermatology offices, and in conjunction with accurate diagnosis can be a helpful adjunct to the primary care physician.

13  Aesthetic Cryotherapy

References 1. Gage AA (1998) History of cryosurgery. Semin Surg Oncol 32(2):103–117 2. Zacarian SA (1969) Cryosurgery in skin cancer. Arch Dermatol 100(6):775 3. Kuflik EG, Gage AA, Lubritz RR, Graham GF (2000) Millenium paper: history of dermatologic cryosurgery. Dermatol Surg 26(8):715–722 4. Kuwahara RT, Craig SR, Amonette RA (2001) Forceps and cotton applicator method of freezing benign lesions. Dermatol Surg 27(2):183–184 5. Castro-Ron G, Pasquali P (2005) Cryosurgery. In: Robinson JK, Hanke CW, Sengelmann RD, Siegel DM (eds) Surgery of the skin. Elsevier, Philadelphia, pp 191–202

155 6. Graham GF, Cerveny KA, San Filippo J (2003) Cryosurgery. In: Fitzpatrick TB, Freedberg IM (eds) Fitzpatrick’s dermatology in general medicine, 6th edn. McGraw-Hill, New York, pp 2575–2581 7. Wu KS, van Osdol WW, Dauskardt RH (2006) Mechanical properties of human stratum corneum: effects of temperature, hydration, and chemical treatment. Biomaterials 27(5):785–795 8. Fikrle T, Pizinger K (2005) Cryosurgery in the treatment of earlobe keloids: report of seven cases. Dermatol Surg 31(12):1728–1731 9. Gage AA (1979) What temperature is lethal for cells? J Dermatol Surg Oncol 5(6):459–464 10. Kuflik E (2003) Cryosurgery. In: Bolognia JL, Jorizzo JL, Rapini RP (eds) Dermatology. Elsevier, Philadelphia, pp 177–183

 

14

Facial Peels Niti Khunger

14.1 Introduction Facial peeling with chemicals or chemical peeling is a procedure where a chemical agent or a combination of agents of defined strength is applied to the skin, causing a controlled destruction of the layers of the skin. This is followed by regeneration and remodeling leading to improvement of texture and surface abnormalities. The concept of skin peeling to beautify the skin by the use of chemicals and natural products has been used since the time of Cleopatra. She used sour milk, containing lactic acid, whereas French women used old wine containing tartaric acid for beauty baths. The modern era of chemical peeling began with MacKee [1] who used phenol as a peeling agent to treat facial scars. Peeling procedures attracted wide interest at that time because of the remarkable results they achieved and peeling formulas were closely guarded secrets. Finally, scientific investigations were undertaken and various agents are now being used for chemical peeling with newer agents being added day by day. The objective of chemical peeling is to cause destruction at the required depth without scarring. Chemical peels are divided according to the depth as very superficial, superficial, medium depth, and deep peels. The depth of peeling is controlled by many factors, the most important being the strength and characteristics of the peeling agent. Every physician performing chemical

N. Khunger Department of Dermatology, V.M. Medical College and Safdarjang Hospital, New Delhi 110029, India e-mail: [email protected]

peels should aim to standardize their peeling procedures in order to eliminate the maximum number of variables that can affect the depth of facial peels. The introduction of nonablative lasers and light therapy systems initially led to a decline in the use of chemical peels but lasers are still very expensive to acquire and maintain. Till these newer nonablative light therapies become more predictable, affordable, and widely available, chemical peels continue to be an extremely useful armamentarium in the treatment of common conditions such as skin rejuvenation, photoaging, hyperpigmentation, and acne. Newer, safer, and more effective peeling agents, such as mandelic acid, lactic acid, pyruvic acid, phytic acid, etc., and current peeling options such as combination peels, sequential, segmental, and switch peels have led to resurgence in the use of chemical peels [2]. Sound knowledge of peeling agents, peeling procedures, and experience are still essential to achieve cosmetically pleasing results. Hence chemical peeling is a versatile tool that can help build a good aesthetic practice.

14.2 Basic Principles and Mechanism of Action Chemical peels have a sound scientific, histological, chemical, and toxicological basis. The basic principle of chemical peeling is to cause injury to the skin at the required depth and allow regeneration and remodeling to take place, without causing permanent scarring. Various peeling agents are available. It is essential to understand basic chemistry of these agents, anatomy of the skin, and the skin–chemical interactions in order to optimize treatment [3]. Peeling agents basically act by either of three mechanisms:

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_14, © Springer-Verlag Berlin Heidelberg 2011

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1 . Metabolic 2. Caustic 3. Toxic Alpha hydroxy acids (AHA) are weak acids and include common peeling agents such as glycolic acid, mandelic acid, pyruvic acid, lactic acid, citric acid, etc. They act by metabolic action by interfering with the functioning of enzymes such as kinases, sulfotransferases, and phosphotransferases, which attach sulfate and phosphate molecules to the corneocytes. This causes desquamation of corneocytes, leading to epidermal desiccation and shedding, followed by regeneration. A single light AHA peel can replace the epidermis in 2 weeks [4]. In higher concentrations of free acid, they act as caustic agents that cause epidermolysis or skin necrosis. In the dermis, there is an induction of inflammatory response with deposition of glycosaminoglycans and new collagen formation. Salicylic acid is a beta-hydroxy acid and has keratolytic properties. It causes dissolution of the intercellular cement substance and hence reduces corneocyte adhesion. It is lipophilic and easily penetrates the sebaceous follicles and hence is useful in acne. It also has comedolytic and anti-inflammatory properties. When applied over large areas, it can be absorbed in the systemic circulation and cause salicylism. Trichloroacetic acid (TCA) is a strong acid and has a caustic action. It causes coagulation of proteins, which is seen visually as frosting. TCA causes destruction of cells, the depth depending on the concentration, with stimulation of collagen in the dermis. Regeneration of dermal collagen starts within 2–3  weeks whereas the increase in papillary dermal collagen and the production of elastic fibers continues for 6 months [5]. It is self-neutralizing and is not absorbed into the systemic circulation. Phenol and resorcinol have a toxic action on the cells. They cause enzyme inactivation, protein denaturation, and increased permeability of cell membranes leading to cell death. Resorcinol has a weaker action as compared to phenol. Phenol is absorbed in the systemic circulation and can cause cardiac, renal, and hepatic toxicities. At the same pH and concentration, applying a greater volume of acid on the skin, of course, induces greater necrosis.

N. Khunger

14.3 Histological Classification of Peels and Peeling Depths Chemical peels are divided according to the depth of necrosis as very superficial, superficial, medium depth and deep (Table  14.1). Superficial peels are more frequently used, whereas deep peels have been supplanted by lasers and light devices to a greater extent. There are many variables that can modify the depth of the peel.

14.3.1 Peeling Agent The peeling agent and its concentration is the most important factor in determining the peel depth. Generally, the higher the concentration of the peeling agent, greater is the depth. However, in combination peels, peeling agents can be combined at lower concentrations, to achieve greater depths. In addition, concentration of the peeling agent can vary with different brands and formulations of the same peeling agent. Hence while peeling a patient, one must not interchange the brand of the peeling agent, even if it indicates the same concentration.

14.3.2 Duration of Contact This is important with AHA peels, particularly glycolic acid. Longer the duration of contact, greater is the depth achieved. This is not significant with TCA and salicylic acid, where concentration is important.

14.3.3 Availability of Free Acid The availability of free acid in the formulation is important. The pKa of the solution is the pH at which half of it is in acid form. A lower pKa means that more free acids are available for action. Though many products advertise the acid percentage, the pKa is a more accurate determinant of strength of the peeling agent.

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Table 14.1  Histological classification of chemical peels Type of peel Very superficial

Superficial

Medium

Deep

Histological level Exfoliation of the stratum corneum, without any epidermal necrosis

Necrosis of part or entire epidermis, not below the basal layer

Necrosis of the epidermis, papillary dermis up to the upper one-third of the reticular dermis

Necrosis of the epidermis, papillary dermis up to mid-reticular dermis

14.3.4 Method of Degreasing the Skin Vigorous degreasing of the skin can increase penetration and cause ‘hotspots’ to develop.

Agents Glycolic acid 30–50% applied for 1–2 min TCA 10% applied as one coat Jessner’s solution 1–3 coats Resorcinol 20–30% applied for 5–10 min Glycolic acid 50–70% applied for 2–10 min, depending on the type and thickness of the skin TCA 10–30% Jessner’s solution 4–10 coats Resorcinol 40–50% applied for 30–60 min Glycolic acid 70% applied for 3–15 min, depending on the type and thickness of the skin TCA 35–50% Glycolic acid 70% plus TCA 35% Jessner’s solution plus TCA 35% Phenol 88% Baker Gordon phenol formula

Indications Active acne

Skin brightening

Ephelides

Epidermal melasma

Lentigines

Dermal melasma Superficial acne scars

Superficial wrinkles

of pre-peel priming cause thinning of the stratum ­corneum. This leads to greater penetration of the chemical agent.

14.3.7 Location of Peel 14.3.5 Technique of Application If the peeling agent is rubbed when applying on the skin, it achieves a greater depth than if it is painted on the skin. The number of coats applied as in Jessner’s solution and degree of frosting as with salicyclic acid peel can cause variations in the peel depth.

At the same concentration, a facial peel will have greater depth as compared to a non-facial peel.

14.3.8 Characteristics of Patient’s Skin

If the patient has thick oily skin, penetration is less as compared to thin dry skin. The level of photodamage, actinic damage, and presence of irregular superficial 14.3.6 Priming Agents lesions such as seborrheic keratoses, dermatoses papuThe application of low concentrations of glycolic losa nigra, lentigo all affect penetration of the peeling acid, tretinoin, or salicylic acid during the period­ agent.

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Hence it is essential to standardize the peeling agents used, procedure of priming the patient, cleaning and degreasing the skin and method of application so as to maintain the required depth of the peel.

14.4 Peeling Agents Currently, a wide and often confusing variety of peeling agents are available. For beginners, it is better to start chemical peeling with a few tried and tested products from reputed manufacturers, where the strength of the peeling agent is standardized. The learning curve for aesthetic peels should begin with fewer peels and lower concentrations. Once experience is gained, higher strengths and deeper peels can be more safely and confidently used. It should be remembered that there can be tremendous variability between formulations and brands, even at the same concentration, which can lead to unexpected outcomes and complications. A comparison of the common peeling agents is given in Table 14.2.

14.4.1 Newer Peels and Combination Peels Many newer peels have been introduced that are gentler with lower concentrations and are available singly as well as in combinations. Many of these patented peels have added antioxidants and humectants to make them potent, with improved tolerance and less irritant potential. These newer peels include mandelic acid, lactic acid, pyruvic acid, phytic acid, polyhydroxy acids, citric acid, and malic acid and various agents in combination [6]. Combination peels have the benefit of increased efficacy, without increased risk of complications. The action of individual agents at lower concentrations complements each other, without increasing their concentration. Some of the popular combination peels are: 1. Jessner’s solution: Lactic acid 14 g, salicylic acid 14 g, resorcinol 14 g with ethanol added to make 100 mL. Useful for acne, photoaging, dyschromia. 2. Modified Jessner’s solution: Lactic acid 17%, salicylic acid 17 g, citric acid 8% with ethanol added to make 100  mL. Less toxic as resorcinol is replaced by citric acid. 3. Melaspeel KH® (Sesderma peels, Spain ): Lactic acid 10%, citric acid 10%, kojic acid 5%, hydro-

N. Khunger

quinone 2%, and salicylic acid 2%. Useful for hyperpigmentation. 4. Glicopeel K® (Sesderma peels, Spain): Combination of glycolic acid 33%, citric acid 10%, kojic acid 10%, lactic acid 9%, salicylic acid 5%, willow herb extract and bearberry extract. Useful for hyperpigmentation and photoaging. 5. SM Peel® (Timpac Engineers, India): Salicylic acid 20% and mandelic acid 10% in gel form. Useful in acne. 6. Easy phytic peel® (SkinTech, USA): Slow release AHA combination peel with phytic acid, glycolic acid, lactic acid, and mandelic acid that does need neutralization. Useful for hyperpigmentation, acne, and photoaging. 7. Cosmelan® (Mesoestetic, Spain): Azelaic acid, kojic acid, phytic acid, ascorbic acid, arbutine, titanium dioxide. Useful for hyperpigmentation including melasma. 8. Mandelic acid 15% + lactic acid 15%: A low strength peel for sensitive skin, useful for acne and photoaging. 9. Mandelic acid 30% + lactic acid 40%: Useful for sensitive skin. 10. Fluor-hydroxy® pulse peel: A combination of 5-fluorouracil 5% and glycolic acid 70% lotion (Drogaderma, Brazil). It is useful for actinic keratoses and disseminated actinic porokeratoses.

14.4.2 Choosing the Correct Peel Facial peeling is a useful technique in the treatment of common cosmetic disorders such as photodamage, facial pigmentation including melasma, postinflammatory hyperpigmentation, acne and post-acne scars, mild facial scarring, and for skin rejuvenation (Table 14.3). Some peels are more appropriate for certain conditions and for particular skin types. The choice of the peeling agent should be individualized and a patient may require different peeling agents at different periods of time for maximum benefit. Thus it is important to choose the right peel at the right time for the right patient. The choice of the peeling agent depends on two important factors: the depth of the treating condition and the skin type of the patient. A guide to initial selection of peeling agents is given in Table 14.4.

TCA

Salicylic acid

Agent Alpha hydroxy acids

Plain warts

Freckles Lentigines

Textural changes

Photoaging Skin texture abnormalities Acne scars photoaging

Neutralization not required, washed with water

Use with precaution in darker Concentration, begin with skin types 10–15%, gradually increase concentration Endpoint-frosting

Adequate amounts of water to Neutralization not required, be given after the peel washed with water

Superficial acne scars oily skin enlarged facial pores superficial pigmentation As sequential peels to increase penetration of other peeling agents

Concentration, begin with 20%, gradually increase concentration. EndpointPseudofrosting

Neutralization with sodium bicarbonate 15% or water

Sometimes difficult to judge the end point. Wounds and scarring can occur in higher concentrations Have to be neutralized

Disadvantages Great variability in reactivity and efficacy

No systemic toxicity Peel depth correlates with the intensity of the frost End point is easy to judge No need of neutralization

Stable

Lipophilic Anti-inflammatory Comedolytic Inexpensive

(continued)

Can lose efficacy when repeatedly exposed to air Can cause prolonged PIH Can cause scarring

Highly hydrophilic

Cannot be used in pregnancy and lactation Limited depth of peeling

End point is easy to judge

Causes a pseudofrost

Can be absorbed when applied over large areas and cause salicylism Contraindicated in patients allergic to aspirin

Inexpensive Predictable response

Expensive Can cause PIH in darker skin types Safe in all type of skins I-VI Causes burning when applied

Do not produce systemic toxicity

End point/neutralization Advantages Long shelf life Timing – begin with 3 min and gradually increase time or Well tolerated endpoint erythema

Do not apply over large surface areas to avoid absorption

Grayish discoloration due to Epidermolysis Do not leave the room while doing the peel

Watch out for erythema and hot spots

Precautions Timing is important

Comedonal acne Inflammatory acne Pigmented acne scars

Superficial acne scars

Pigmented acne

Epidermal melasma

Indications Photoaging Skin freshening Fine wrinkling Rough textured skin

Table 14.2  Comparison of the common peeling agents

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Phenol

Agent Retinoic acid

Moderate to severe wrinkles Moderate to severe post-acne scars Adjunct to other aesthetic procedures such as blepharoplasty In darker skin type III–IV, with extreme caution Mild to moderate Dyschromias Mild wrinkles Post-acne scars

Photo ageing

In skin type I-II

Photoaging

Indications Acne hyperpigmentation

Table 14.2  (continued) End point/neutralization

Monitor cardiac activity with Endpoint – frosting pulse oximeter Neutralization not required Give adequate hydration during the procedure to reduce systemic toxicity Peeling is completed in one zone before proceeding to the next, carried out over 90 min

Precautions Do not use in patients with sensitive skin

Requires an OT set-up Presence of anesthetist

Has anesthetic effect

Can cause permanent hypopigmentation in darker skins

Prolonged downtime

Not an office procedure

Can cause systemic toxicitycardiac, renal, hepatic High risk of cardiac arrhythmias

Has to be left on for at least 4 h Can cause excessive peeling

Disadvantages Yellow in color

Deep peel useful for deep wrinkles and post-acne scars Dramatic results with a single peel

Advantages Well tolerated without burning Comedolytic Safe in darker skin types

162 N. Khunger

14  Facial Peels Table  14.3  Indications and contraindications of chemical peeling Indications A. Pigmentary disorders    1. Resistant melasma    2. Post-inflammatory hyperpigmentation (PIH)    3. Pigmented cosmetic dermatitis    4. Lichen planus pigmentosis, ashy dermatosis    5. Freckles    6. Lentigines B. Acne    1. Comedonal acne    2. Macular hyperpigmented post-acne scars    3. Superficial mild post-acne scarring    4. Ice pick scars    5. Acne excoriée C. Cosmetic    1. Photoaging    2. Fine wrinkling    3. Actinic keratoses    4. Seborrheic keratoses    5. Dilated pores Contraindications A. Active infection in the area to be peeled B. Herpes simplex C. Folliculitis, furuncles D. Open wounds E. Pre-existing inflammatory conditions    1. Seborrheic dermatitis    2. Photosensitive dermatitis    3. Atopic dermatitis    4. Contact dermatitis    5. Psoriasis    6. Rosacea F. Drug ingestion    1. History of taking photosensitizing medications G. Patient characteristics    1. Uncooperative patient    2. Patient with unrealistic expectations    3. Patients with body dysmorphophobic disorders    4. Occupations with extensive sun exposure H. Allergy    1. Allergic to contents of peeling agent I. Heavy smoking J. Pregnancy K. For medium depth and deep peels, in addition to the above    1. History of abnormal scarring    2. Keloids    3. Atrophic skin    4. Isotretinoin use in the last 6 months

163

14.5 Patient Management 14.5.1 Counseling Adequate counseling before treatment is very essential to avoid disappointment and potential legal problems at a later stage. Explanation about the nature of treatment, expected outcomes, time taken for recovery of normal skin and the importance of maintenance regimens are essential components of a counseling program. It is always advisable to downplay the degree of improvement expected. Discussion of side effects, likely and unlikely complications, particularly pigmentary changes and alternative treatments available should be done prior to starting facial peeling. If needed, repeated consultations are done utilizing the intervening period for starting home care products. This breathing space also helps in judging the ability of the patient to follow prescribed skin care.

14.5.2 Consent Forms, Documentation, and Photographs Informed consent is a legal document whereby a person gives consent to perform a procedure based upon an understanding of the facts given by the treating physician. The patient should be explained the need for treatment, expected outcomes, duration of the procedure, number of sittings that may be required, approximate cost of treatment, likely complications, consequences of non-treatment, and modes of alternative treatments. Signing the consent form should not be a casual affair like getting signature on a dotted line and should be signed by an informed patient. In the case of teenagers (13–18 years), it is better to take the signatures of both the minor and the parent. The patient should feel free to ask questions and sufficient time should be devoted to expectation alignment between the patient and physician. The patient should also be given written instructions detailing pre- and post-peel care. Photographic records are very important since patients often do not remember the initial condition. Every effort should be made to standardize the photographs, including three views, front, right, and left side, distance, lighting, and background. The progress should be monitored regularly at every peel. Consent for photographs should be incorporated in the consent form. Proper records of the procedure, peeling agent used, concentration, details

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Table 14.4  Selection of peeling agents for common indications and expected response Indication Facial pigmentation Melasma

Depth

Peeling agents

Expected response

SA, MA, combination peels Combination peels SA, MA, TCA TCA Combination peels SA, MA

Good Fair/poor Good Fair Fair/prolonged Good/fair

SA, MA, low strength TCA10,15% MA, combination peels SA, GA, PA, Phytic acid CROSS 50–100% TCA

Good Good Good/fair Good/fair

Upper dermis Upper 1/3 dermis

SA, GA CROSS 50–100% TCA GA, combination peels Phenol

Good Good/fair Good Fair/poor

Epidermal Epidermal

Very carefully SA, MA Fluorouracil

Good/fair Good/fair

Epidermal Dermal/mixed Freckles Epidermal Lentigines Mixed Pigmented cosmetic dermatitis Dermal PIH Epidermal/dermal Acne Comedonal acne Epidermal Pigmented scars Mild atrophic scars Icepick scars Aesthetic Rejuvenation Dilated pores Fine wrinkles Moderate wrinkles Photoaging Dyschromia Actinic/seborrheic keratoses

Epidermal Upper 1/3 dermis Deep dermis Epidermal

GA Glycolic acid, MA Mandelic acid, PA Pyruvic acid SA Salicylic acid

of treatment given pre- and ­post-peel should be maintained. Occurrence of any complications and their treatment should also be recorded.

14.5.3 Patient Evaluation The patient should be thoroughly evaluated at the first visit. It is easier to fill a proforma so that no issues are missed. Occupation, hobbies, and level of sun exposure are important. Patients on photosensitizing drugs or suffering from photosensitive disorders are at higher risk of PIH, particularly in darker skin types. If there is a history of herpes simplex prophylactic acyclovir or valacyclovir should be given to avoid scarring. Conditions that can cause delayed healing such as chronic smoking, immunosuppression, and radiation over the area to be peeled should be ruled out because such patients are at a high risk of complications, particularly with deeper peels. Patients who have undergone recent facelifts or any surgery where extensive undermining of the face has been done that compromises blood supply and delays wound healing should avoid deep chemical peels for at least 6–12 months.

Contraindication of chemical peeling in patients using isotretinoin is controversial. Though there have been reports of abnormal scarring in patients on isotretinoin, following resurfacing procedures, practically it is hardly seen with chemical peels. Precautions may be required when performing deep phenol peels. Assessment of skin phototype, tendency to postinflammatory hyperpigmentation (PIH), thick oily skin, thin dry skin, sensitive skin, wound healing, use of facial scrubs, retinoids, AHAs can all affect penetration of peeling agents and should be asked for.

14.5.4 Pre-Peel Care Pre-peel care is called priming the skin prior to peeling. It is the first step towards performing safe and effective peels. Priming is ideally started at least 2–4  weeks before the peel. The goal of priming the skin is to assist in producing uniform penetration of the peeling agent, accelerate wound healing, and reduce the risk of complications.

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Retinoic acid and alpha-hydroxy acids such as glycolic acid cause thinning of the stratum corneum and help to achieve increased uniform penetration of the peeling agent. Retinoic acid applied for at least 2 weeks prior to peeling has been reported to reduce re-epithelialization time after peeling. In addition, any agent that is likely to be used immediately post-peel or for maintenance therapy should be applied as a priming agent to detect intolerance. This is especially important with regard to sunscreen use and hydroquinone, which can have devastating effects if reactions develop after a peel. In darker skinned patients and in those at risk of PIH, use of hypopigmenting agents such as hydroquinone, kojic acid, arbutin, etc. before the peel greatly reduces the chances of PIH. Priming also helps to enforce patient compliance. Patients who do not follow instructions are at risk for poor results post-peel and should not be taken up for facial peeling. Broad spectrum sunscreens against UVA, UVB, and visible light, with minimum SPF 30 should be given. In patients with sensitive skin, the physical sunscreens containing zinc oxide or titanium dioxide are safer than chemical sunscreens.

14.6 Peeling Technique Chemical peeling is a simple technique that can be performed as an office outpatient procedure, with very few requirements (Table 14.5). However, deep phenol peels should be carried out in a fully equipped surgical suite. The patient should be adequately counseled and primed. A consent form is signed and photographs are taken. Contact eye lenses are removed and the patient is asked to wash the face with soap and water, to remove makeup, dirt, and grime. The hair is pulled back with a hair band or cap. The patient is made to lie down with head elevated to 45° and eyes closed. The skin is inspected for abrasions or inflammation that should be avoided. Sensitive areas where the peeling agent can collect such as the inner canthus of the eye and nasolabial folds are protected with petrolatum or Vaseline®. The skin is cleaned with alcohol and then degreased with acetone, using 2″ × 2″ gauze pieces. The required peeling agent is poured in a glass beaker and neutralizing agent is also kept ready. The label should

165 Table 14.5  Reagents and equipment for facial peels Reagents • Chemical peeling agents with varying concentrations correctly labeled    Glycolic acid – 20%, 35%, 70%,    TCA – 10%, 15%, 25%, 100% (For CROSS technique)    Salicylic acid – 20%, 30%, 50%    Mandelic acid 40%   Combination peels for acne, dyschromia, rejuvenation, according to choice and availability • Neutralizing solutions • Cold water • Syringe filled with normal saline to irrigate the eyes, in case of accidental spillage of reagent in the eyes • Alcohol or spirit for cleansing • Acetone for degreasing Equipment • Cap or headband to pull back the patient’s hair • Glass cups to hold the peeling agent • Cotton tip applicators, ear buds, small brush or fine toothpicks for application • 2″ × 2″ gauze pieces • Timer for glycolic acid peels • Hand held fan for patient comfort • Gloves

be carefully checked. The peeling agent is then applied either with a brush or cotton-tipped applicator without dripping of the agent. The chemical agent is applied quickly on the entire face divided into cosmetic units beginning from the forehead in an upward direction, then the right cheek, nose, left cheek, and chin in that order. The perioral, upper and lower eyelids, if required, are treated last (Fig. 14.1). Feathering strokes are applied at the edges, to blend with surrounding skin and prevent demarcation lines. A hand-held cooling fan helps to reduce burning of the skin. The patient should not be left alone and a strict watch should be kept for redness, hot spots, and epidermolysis. The peel is neutralized as required according to the peeling agent. AHA peels require neutralization with sodium bicarbonate, but can also be washed away with copious amounts of water, while other peels such as TCA peel and salicylic acid peels are self-neutralizing and can be washed away with water. The skin is gently dried with gauze and the patient is asked to wash with cold water till the burning subsides. The patient is then asked to apply a sunscreen, before leaving the clinic, along with post-peel instructions.

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function of the skin is compromised and topical agents can penetrate more easily. This is an advantage and appropriate creams should be applied according to the condition being treated, e.g. in the treatment of melasma, hypopigmenting agents such as hydroquinone, glabridin, arbutin, or kojic acid along with topical ascorbic acid have better permeability. Maintenance treatment is an important component of any peeling regimen and should be continued to maintain results.

14.8 Acne and Post-Acne Scars

Fig. 14.1  Cosmetic units of the face and order of application of a chemical peel

14.7 Post-Peel Care Facial peeling makes the skin very sensitive to sunlight and heat. This can lead to sunburn, erythema, and postinflammatory hyperpigmentation. Hence adequate sun protection is most important in the immediate postpeel period till re-epithelialization is complete. Broad spectrum sunscreens that have been started in the priming period should be applied, ideally every 2 h. Light moisturizers may be used in case of excessive dryness and desquamation. The patient should be warned to avoid picking at the exfoliating lesions, which can lead to excessive erythema and PIH. In darker skinned individuals, who are prone to PIH, hypopigmenting agents should be started as soon as possible. Retinoids and glycolic acid should be started only after complete reepithelialization. In the post-peel period the barrier

Acne is one of the most common skin diseases in clinical practice. Topical and systemic therapy is the mainstay of treatment. Patients frequently have poor self-image, depression, and anxiety due to acne and it can affect the quality of life. Hence, effective management of acne can have a relevant positive impact on the acne patient. Chemical peeling in active acne is an adjuvant therapeutic technique that can help in early resolution of lesions. It is indicated in comedonal acne and mild-to-moderate inflammatory acne. Superficial and ice pick post-acne scars can also be treated with peeling agents. Salicylic acid 20–30% is the peeling agent of choice in acne as it has keratolytic and anti-inflammatory properties. The advantage is that since it is lipophilic in nature and can easily penetrate the pilosebaceous apparatus. It is effective in all grades of active acne because of its comedolytic and anti-inflammatory properties. It is also safer in darker skin phototypes IV-VI. A pseudofrost is formed which is easy to visualize; hence it can be applied evenly, without skip areas (Fig.  14.2). Glycolic acid in low strengths, 20–35%, TCA 10–15%, and Jessner’s solution are other agents that can be used for acne. Newer peeling agents in acne include mandelic acid 30–50%, tretinoin 1–5%, lactic acid 40–90%, and pyruvic acid 40–50%.

14.9 Comedonal Acne If there are many comedones, comedone extraction is done first followed by a 20% salicylic acid peel. This allows better penetration of the peeling agent and hastens improvement. Closed comedones are first pierced with a

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citric acid, and salicylic– mandelic peels repeated every 2  weeks are safer, particularly in darker skin types (Fig. 14.3).

14.12 Superficial Post-Acne Scars Sequential peels with salicylic acid 30% followed by glycolic acid 50–70%, or salicylic acid 20–30% followed by TCA 15–35%, depending on the skin type are effective, but should be used cautiously in patients prone to PIH. Combination peels containing glycolic acid, pyruvic acid, and lactic acid are safer; though they require larger number of sessions [7].

14.13 Ice Pick Acne Scars: CROSS Technique Fig.  14.2  Pseudofrost on application of salicylic acid due to crystallization

No. 26 needle, contents are extracted out with a comedone extractor and then the peel is applied. The peels can be repeated weekly in thick oily skins or every 2–4 weeks in dry skins. Tretinoin peels containing 1–5% retinoic acid are also effective.

14.10 Inflammatory Papulopustular Acne Salicylic acid 20–30% and mandelic acid 40% are the peeling agents of choice. They can also be combined for greater efficacy. The advantage of this combination is that salicylic acid is lipophilic and anti-inflammatory, whereas mandelic acid also has antibacterial properties. Glycolic acid 20–50% and pyruvic acid 40–70% are alternative peeling agents and are useful when there is less inflammation, but more superficial scars.

14.11 Post-Acne Pigmentation For post-acne pigmentation, combination peels are more effective and safer as compared to single agents. Low strength glycolic acid 20%, kojic acid, lactic acid,

Ice pick acne scars are deep and difficult to eradicate, even with lasers. A technique using high strength of the peeling agent, TCA called CROSS technique (Chemical Reconstruction of Skin Scars) has been found to be useful, as a simple office procedure [8]. In this technique 65–100% TCA is applied to the bottom of the icepick scar with a wooden toothpick, which leads to destruction of the epithelial tract. This is followed by collagenization in the healing phase and filling up of the depressed icepick scar. It causes momentary, mild, tolerable burning on application, and no anesthesia is required. After cleaning and degreasing the skin with acetone, the acid is carefully applied up to the depth of the scar, using a fine pointed wooden tip of a toothpick, taking care to avoid spillage on the surrounding skin (Fig. 14.4). The skin is stretched to reach the bottom of the scar. There is immediate blanching with an intense white frost, due to coagulation of epidermal and dermal proteins. A sunscreen is then applied. Within 1–3 days crusts are formed, which fall off in 3–5 days. Collagen formation may take 2–3 weeks and can continue up to 4–6 weeks. A sunscreen is applied in the daytime and 0.05% tretinoin and 5% hydroquinone cream are applied at night for a minimum of 4 weeks to prevent post-inflammatory hyperpigmentation. On an average about 25% improvement of scars takes place with one session. The procedure may be repeated two or three

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Fig. 14.3  (Left) Active acne with persistent pigmented macules. (Right) Following treatment with 40% mandelic acid peels, six peels at 2 weekly intervals

primed adequately with hypopigmenting agents prior to the procedure and these should be continued till improvement [9].

14.14 Facial Pigmentation

Fig. 14.4  Application of 100% TCA by the CROSS technique, by stretching the skin and using a fine wooden toothpick

times, at intervals of 2–4 weeks. The advantage of the CROSS technique is that since the adjacent normal tissue and adnexal structures are spared, healing is more rapid with a lower complication rate than conventional full-face medium to deep chemical resurfacing (Fig.  14.5). However, PIH can commonly occur in patients with darker skins, hence the patient should be

Facial pigmentation can be due to various disorders, which should be identified before treatment so as to select the appropriate peeling agent (Table  14.6). Therapy should be selected according to the etiology and depth of the pigmentation. The primary approach to treatment of facial pigmentation is topical hypopigmenting agents, which inhibit synthesis of melanin and photoprotection with sunscreens that inhibit activity of the melanocyte. Chemical peels are adjuvant measures that remove excess melanin and hasten improvement. The Q-switched Nd:YAG laser causes disruption of melanin and is primarily useful in Nevus of Ota, freckles, lentigines, and epidermal nevi. Melasma is one of the most common causes of facial pigmentation and often recalcitrant to treatment. It requires a combination of agents to improve melasma,

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Fig. 14.5  (Left) Icepick post-acne scars. (Right) After treatment with the CROSS technique using 100% TCA Table 14.6  Common causes of facial pigmentation Epidermal Melasma Freckles Lentigines Post-inflammatory hyperpigmentation Epidermal nevi

Dermal Melasma Post-inflammatory hyperpigmentation Pigmented cosmetic dermatitis Drug-induced melanoses Actinic lichen planus Lichen planus pigmentosus Periocular melanoses Nevus of Ota Pigmentary demarcation lines

along with prolonged maintenance therapy. The mainstay of treatment of facial pigmentation is topical therapy, which should also be used for priming the skin at least 4–6 weeks before chemical peeling. Hydroquinone 2–5% as tolerated is the gold standard for hyperpigmentation. If the pigmentation worsens, the possibility of ochronosis must be kept in mind. A biopsy will confirm the diagnosis, and hydroquinone must be stopped. Ochronosis is seen more commonly with high concentrations like 10% and it is not very common in lower concentrations up to 5%. If hydroquinone causes irritation, alternative agents such as azelaic acid 10–20%, kojic acid 2% and arbutin 5% are alternative agents. Sun protection is very important as it is a common aggravating factor in facial pigmentation and a combination of physical methods such as hats and umbrellas and chemical agents such as broad spectrum sunscreens,

including physical sunscreens should be repeatedly advocated, particularly in patients with outdoor occupations. Glycolic acid 6–12% is also useful as a priming agent in patients with thick uneven skin. Topical retinoids should be used cautiously to avoid retinoid dermatitis and inflammation, which can aggravate pigmentation. Low strengths such as tretinoin 0.025% or adapalene 0.1% applied for short durations initially are preferred. The strength and duration of application of the priming agent should be increased gradually, if the patient has sensitive skin. Facial peeling should also be done cautiously in darker skin types due to the increased risk of PIH. It is always safer to use lower strength of peeling agents either sequentially or in combination to achieve desired results. For example, applying 20% salicylic acid followed by 10–15% TCA or 35% glycolic acid is safer as compared to 70% glycolic acid or 35% TCA used alone. Various combinations of peeling agents are available for facial pigmentation and found to be quite effective for long-term use, even in darker skins (Fig. 14.6). Peels may give variable responses for hyperpigmentation; hence a small test peel may be done in the post-auricular or temple area to detect unpredictable responses. This is particularly common with glycolic acid, TCA, and resorcinol. A low concentration of the peeling agent should be used first and the concentration should be increased gradually, depending on the response. All precautions should be undertaken to avoid excessive inflammation. It is safer to combine peels in lower concentrations to increase depth, rather than increase concentration of a single agent. One can also customize the peel to the individual

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Fig.  14.6  (Left) Pre-treatment persistent melasma. (Right) Three years after treatment with mandelic acid 40%, eight peels at 2 weekly intervals, with maintenance of improvement

Fig. 14.7  (Left) Pre-treatment dermal pigmentation due to lichen planus pigmentosis. (Right) Two years post-treatment with a series of combination peels, 12 combination peels at 2 weekly intervals and maintenance of improvement

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face to get optimum results and vary the peeling agents according to response. Areas with thick, oily, damaged skin may require a deeper peel, while thinner, dry skin zones may only require a superficial peel. Following a peel, the area of hyperpigmentation and scaling can show increased pigmentation initially, that can alarm the patient. The skin may become more sensitive postpeel and lower strengths of retinoids or glycolic acid should be used, if this happens. In a study of 40 Indian patients with melasma, with Fitzpatrick skin types III–V, the group of 20 patients who were treated with serial 30–40% glycolic acid peels along with a modified Kligman’s formula showed a significantly better response as compared to 20 patients who were treated with the modified Kligman’s formula alone [10]. Adverse events were minimal in both the groups, with two patients in the peel group developing PIH. Similar results were observed in another study of recalcitrant melasma treated with serial glycolic acid peels [11]. Focal TCA has also been safely used in benign pigmented facial lesions in darker skin types [12]. Inflammation plays a key role in causing PIH due to the release of cytokines that stimulate the activity of melanocytes. Hence, controlling inflammation with topical and if required, systemic steroids is an essential part of post-peel care when treating hyperpigmentation. Bleaching agents such as hydroquinone, kojic acid or azelaic acid combined with tretinoin or glycolic acid are useful for PIH. Re-peeling with very superficial peels may give good response if PIH persists, in spite of therapy beyond 2–4  weeks [13]. Chemical peels can also improve dermal pigmentation by causing a controlled low-grade inflammation that can stimulate phagocytosis of excess dermal melanin (Fig. 14.7).

14.15 Photoaging and Facial Rejuvenation Photoaging is defined as the superimposed effects of photodamage due to chronic ultraviolet light exposure on intrinsically aging skin. It is characterized by wrinkles, mottled pigmentation, laxity of the skin, sallow complexion, dilated pores, vascular lesions, and texturally rough skin. Ultraviolet light exposure activates matrix degrading metalloproteinase enzymes including collagenase. Cytokines are released from keratinocytes. The cumulative effect of these changes is chronic

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dermal inflammation. The features of photoaging vary with the skin types. In individuals with lighter skin color, Fitzpatrick I–III, wrinkles are more common and appear early along with an increased occurrence of premalignant and malignant skin lesions including actinic keratoses, basal cell carcinoma, squamous cell carcinoma and melanoma. In contrast, in darker skin individuals, there is less wrinkling and reduced incidence of malignancy, whereas pigmentary abnormalities are more common. Topical therapy using broad spectrum sunscreens, retinoids, polyhydroxy acids, salicylic acid along with hypopigmenting agents such as hydroquinone or azelaic acid and cosmeceuticals containing arbutin, licorice, unsaturated fatty acids, soy extracts, idebenone, copper peptides, serine protease inhibitors, resveratrol, etc. are useful for treatment as well as priming the skin [14]. Due to changes in lifestyle and depletion of ozone layer in the atmosphere, the exposure to harmful UV rays of the sun has increased, leading to skin aging becoming more common and evident in younger individuals in their twenties and thirties. Being a regenerative organ, the skin can be stimulated to repair and renew itself. Hence, skin rejuvenation techniques are becoming very popular, with a marked preference for minimally invasive techniques with reduced downtimes. The physician should evaluate the nature of skin and degree of photo damage, techniques available and active cosmeceutical agents that work for skin rejuvenation, before management. Facial peeling is a good technique to hasten response in photoaging. The physician should be aware that mature skin is generally dry, thinner, sensitive, and intolerant to many products and many geriatric patients are on systemic medications that can cause photosensitivity or pigmentation. These factors should be taken into account while selecting patients for chemical peels. Superficial peels are useful for pigmentary changes, whereas medium depth and deeper peels are indicated for wrinkling. If there are any growths like seborrheic keratoses, dermatoses papulosa nigra, these should be treated prior to peeling. Young patients with minimal skin damage often respond best to a series of light superficial peels (lunch time peels) in combination with a good skin care program. The alpha hydroxy acids are particularly good agents for photoaging because of their dermal effects. Glycolic acid 35–70%, pyruvic acid 50%, and lactic acid 90% are peeling agents of choice. Pyruvic acid is an a-keto acid which is converted physiologically to lactic acid. Ghersetich

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et al. [15] treated 20 patients with Glogau’s photoaging types I and II, with pyruvic acid 50% in a series of four peels at monthly intervals. A smoother texture, reduction in fine wrinkles and lightening of areas of hyperpigmentation were observed, with minimal side effects. Salicylic acid has also shown to be effective for photoaging. In a study of 50 women with mild-to-moderate photodamage, salicylic acid reported improvement in pigmented lesions, surface roughness and reduction in fine lines [16]. Medium depth peeling is more useful to treat photodamage, but it should be used cautiously in darker skin types [17]. Combination peels with 70% glycolic acid and 35% TCA are effective. The use of deep phenol peels has declined due to the availability of safer and effective modalities such as fractional ablative and nonablative lasers.

14.16 Customizing Peels and Techniques Various peeling agents with differing mechanisms of action are available, making peeling a very versatile procedure for different skin types and skin conditions. The cosmetic units of the face often differ in the same patient and may have different requirements. Application of the peeling agents can thus be customized to optimize outcomes. Various formulations are available in combination peels and the precise formula may be adjusted to meet each patient’s needs [2]. Patients with oily thick skins and acne will require higher concentrations of salicylic acid, while patients with predominant hyperpigmented lesions benefit from higher concentrations of hydroquinone, kojic acid, and citric acid along with glycolic acid. Patients with sensitive skin can tolerate lactic acid and mandelic acid safely and benefit from lower strength peeling agents in combination. Sequential peels use more than one peeling agent at a time in a sequential manner. They are deeper peels and indicated for conditions that have a dermal component such as mixed melasma, lichenoid pigmentation, and PIH (Fig. 14.8). Facial peeling can also be combined with other techniques to increase the penetration or a complementary effect [18]. Techniques such as microdermabrasion [19], sandabrasion [20, 21], nonablative

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lasers [22], botulinum toxin [23], fillers [23], blepharoplasty, and face lifts can be effectively combined. Each facial concern is customized and addressed individually with the appropriate modality.

14.17 Complications Every physician performing chemical peels must have adequate knowledge about prevention, early detection, and management of complications [24–26].

14.17.1 Prevention The first step in prevention is identifying patients that are at a higher risk of complications. These include skin types III–VI who are at a higher risk of PIH, patients with thin, dry, sensitive skin with a reddish hue, poor wound healing, and those with outdoor occupations, on photosensitizing drugs and a history of sunburn. Peeling should also be performed cautiously in patients who are uncooperative and have unrealistic expectations. Counseling the patient regarding expected results and emphasizing the importance of post-procedure precautions and treatment are essential in preventing complications. The physician should communicate to the patient early warning signs of adverse events as most complications can be minimized when detected early and treated promptly. Prolonged erythema, crusting, vesiculation painful erosions, and pruritus are early signs and should be treated immediately. Prepeel priming regimens should be religiously followed and the patient should avoid scrubs and procedures immediately before peels as it can lead to uneven peeling. Any facial skin disorder such as seborrheic dermatitis, atopic dermatitis, contact dermatitis, etc. should be treated before peeling. The physician should not use too many peels of different manufacturers as peels from different sources, even with the same labeled concentrations, can have varying results. It is better to be familiar with fewer peels on a regular basis and develop safe procedures. When trying out a new peel, or peeling an apprehensive patient, it is preferable do a test peel on the

Fig. 14.8  Dermal melasma after 2 weeks single sequential peel. (a) Before treatment. (b) After salicylic acid peel. (c) Application of glycolic acid, hydroquinone. (d) Two weeks after single sequential peel

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preauricular area, or a small area on the lesion on the forehead or temple area, rather than a full face peel. Ideally one should start with the lowest concentration and gradually titrate upwards. For the beginner, it is better to combine different agents at lower concentrations and use superficial peels, rather than use a high concentration of a single peeling agent or deeper peels. The physician must have a thorough knowledge of selecting the right peeling agent at the right concentration. The label and concentration should be checked before application. The neutralizing agent should be kept ready, in case termination of the peel is required before the scheduled time. To avoid ocular complications, the head must be elevated during the peel. The inner and outer canthi of the eyes must be protected with Vaseline, especially when performing a performing a periocular peel. The peel should never be passed over the eyes, and a syringe filled with saline should be at hand in case of accidental spillage in the eye. If TCA or GA enters the eye it should be flooded with normal saline and for phenolic compounds the eye should be flooded with mineral oil [27]. While applying the peel, vigorous scrubbing should be avoided as it can lead to patchy and deeper peeling than required.

14.17.2 Management The potential complications that can occur are given in Table  14.7. Hyperpigmentation is the most common complication occurring after peels (Fig. 14.9). It can occur any time after the peel and can be persistent, if inadequately treated. It is important to educate the patient about avoiding sun exposure and use of broad spectrum sunscreens before and indefinitely after the peels. Priming the patient with suitable topical hypopigmenting agents such as hydroquinone, kojic acid, and arbutin is an important part of the peeling regimen and should be strictly enforced in the post-peel period. When hyperpigmentation occurs, triple combination creams containing hydroquinone, tretinoin, and steroids are useful. Hypopigmentation is commonly seen immediately after a superficial peel and is due to the removal of excess melanin and sloughing off of the epidermis. In medium depth peels, the hypopigmentation can be more prolonged, till melanocytes migrate from the surrounding skin

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and adnexae. In deep peels, permanent hypopigmentation is common. This may not be noticeable in fair type I and II skins, but can have disastrous consequences in darker skins. In addition, phenol has a direct toxic effect on the melanocytes and can cause a permanent hypopigmentation with a peculiar alabaster look. Hence deep peels are better avoided in darker skin types. Bacterial infection is uncommon, but if it occurs it should be treated aggressively with oral and topical antibiotics to prevent scarring. Herpetic outbreaks present with painful erosions and should be treated with antiviral therapy. Prophylactic antiviral therapy should be given preferably to all patients undergoing medium depth and deep peels and continued till complete re-epithelialization. For superficial peels, it should be given in those patients with a history of herpes simplex. Candidal infection may occur in immunocompromised patients, diabetics and patients with oral thrush. It presents with superficial pustules with a background of erythema and is treated with topical clotrimazole 1% cream and systemic antifungals such as fluconazole 50  mg or ketoconazole 200  mg/day. Post-peel erythema generally fades in 3–5 days, after superficial peels, 15–30 days after medium peels and 60–90 days after deep peels. However, prolonged erythema may be a sign of inadvertent deeper peeling and impending scarring and should be treated promptly with short duration potent topical steroids. Edema in the periocular region can occur and is managed with application of ice. In severe cases, a short course of systemic steroids may be given. Epidermolysis causing vesiculation and blistering may be seen, particularly with AHA peels (Fig. 14.10). Prolonged burning can occur particularly if topical retinoid or glycolic acid is applied immediately after peels or there is prolonged sun exposure. Application of bland emollients and sunscreens are effective and in severe cases, topical steroids such as hydrocortisone or fluticasone may be required. Pruritus may occur after peeling. If it is severe and occurs with the development of papules and erythema, it may be a sign of contact dermatitis to a topical application. It is very important to recognize this and treat as soon as possible, as a delay in treatment can lead to worsening in the outcome of the peel. Hence no new topical agents should be introduced in the maintenance regime after a peel to avoid this complication. Scarring is a dreaded complication and fortunately, very uncommon, after superficial peels, but

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Table 14.7  Complications of chemical peels Topical Pigmentary changes – post-inflammatory hyperpigmentation and hypopigmentation Lines of demarcation Infection – bacterial (Staphylococcus, Streptococcus, Pseudomonas), viral (Herpes Simplex) and fungal (Candida) Persistent erythema Scarring Allergic reactions Milia Acneiform eruptions Textural changes

Systemic Toxicity – resorcinol, salicyclic acid and phenol, when applied over large areas

Ocular Chemical conjunctivitis

Laryngeal edema – it is a rare complication, with symptoms of stridor, hoarseness of voice, and tachypnea developing within 24 h of chemical peeling

Corneal abrasions

Fig. 14.10  Epidermolysis, vesiculation, and edema in the periocular region following 50% glycolic acid peel, without significant erythema

14.18 Systemic Complications

Fig. 14.9  Hyperpigmentation following peeling

can occur with medium depth and deep peels. Patients with a history of poor wound healing, keloid formation, and developing post-peel infection are at a higher risk of scarring. The temple area, mandibular area, upper lips, and the chin are areas prone to developing scars. Abnormal scarring has been reported with patients on isotretinoin. In severe cases, there can be ectropion or eclabion.

Systemic complications are more common with deep phenol peels. When applied over large areas over a short period of time or under-occlusion, phenol can cause systemic toxicity by absorption. The most common adverse effect is cardiotoxicity that presents in the form of arrhythmias [28]. Hence cardiac status must be continuously monitored and intravenous hydration be given along with the peel. Peeling must be done in small segments and completed before moving to the next cosmetic unit, to reduce systemic absorption. If arrhythmia develops, the peel must be stopped and intravenous (IV) lignocaine should be administered. Since phenol is metabolized in the liver and excreted by the kidney, it should not be used in patients with hepatic or renal disease.

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Resorcinol can also produce toxicity, if applied in excess. Diarrhea, vomiting, severe headache, dizziness, drowsiness, bradycardia, dyspnea, and paralysis are presenting features. The best way to avoid resorcinism is to restrict the area of application or limit the concentration of resorcinol. Toxicity with salicylic acid is not observed when it is applied on the face but has been reported when large amounts of 50% salicylic acid paste are applied to 50% or more of the body surface, under occlusion. Salicylism is characterized by tinnitus, dizziness, abdominal cramps, and deafness. Though peels can cause complications, they are uncommon in well-trained hands if done with proper precautions following safety guidelines for different types of skins [29].

14.19 Conclusions There has been a tremendous increase in procedural techniques for skin rejuvenation and the trend is increasingly for procedures that are noninvasive or minimally invasive, requiring little downtime. The majority of chemical peeling procedures fit into this category. The advantage of chemical peeling is that it is flexible, effective, and safe with minimal complications. It is a simple office procedure, requiring no machines, affordable to every physician, and easy to learn and practice. A wide variety of chemical agents are available and treatment can be individualized, according to skin type and requirement of the patient. The downside to peeling is that it is a slower process. Multiple sessions are required with superficial peels to achieve acceptable cosmetic results. Results are not permanent and maintenance peels are often required. Post-peel, pigmentary changes are common in inexperienced hands, especially in darker skins. Facial peeling results in the removal of superficial skin lesions, reducing excess pigmentation, regeneration of new tissue with improvement of the skin texture and long lasting therapeutic and cosmetic benefits. There is a tremendous variability of response to chemical peels; hence physicians must standardize their peeling agents and techniques, in order to maintain results. A patient may require different peeling agents at different concentrations over a period of time and these should be customized and selected accordingly for maximum benefit. The mix and match options and

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customizing techniques give chemical peeling a newer dimension for treating patients optimally, with greater versatility and satisfaction, and enhanced safety at the same time. Hence chemical peeling is a versatile tool that can help build a good aesthetic practice, with minimal investment.

References 1. Brody H (1997) History of chemical peels. In: Baxter S (ed) Chemical peeling and resurfacing, 2nd edn. Mosby Year Book, St. Louis, pp 1–5 2. Khunger N, Arsiwala S (2009) Combination and sequential peels. In: Khunger N (ed) Step by step chemical peels, 1st edn. Jaypee Brothers Medical Publishers Ltd, New Delhi, pp 202–218 3. Dewandre L (2006) The chemistry of peels and a hypothesis of action mechanisms. In: Rubin MG (ed) Chemical peels, 1st edn. Elsevier Inc., Philadelphia, pp 1–12 4. Deprez P (2007) Alpha-hydroxy acids:histology and factors influencing penetration. In: Deprez P (ed) Textbook of chemical peels. Informa Healthcare, New York, pp 53–54 5. McCollough EG, Langsdon PR, Maloney BP (1996) Chemical peel with phenol. In: Roenigk RK, Roenigk HH (eds) Dermatologic surgery, principles and practice, 2nd edn. Marcel Decker Ltd., Oxford, pp 1147–1160 6. Khunger N (2009) Newer peels. In: Khunger N (ed) Step by step chemical peels. Jaypee Brothers Medical Publishers Ltd, New Delhi, pp 160–177 7. Wang CM, Huang CL, Hu CT, Chan HL (1997) The effect of glycolic acid on the treatment of acne in Asian skin. Dermatol Surg 23(1):23–29 8. Lee JB, Chung WG, Kwahck H, Lee KH (2002) Focal treatment of acne scars with trichloroacetic acid: chemical reconstruction of skin scars method. Dermatol Surg 28(11): 1017–1021 9. Bhardwaj D, Khunger N (2010) An assessment of the efficacy and safety of CROSS technique with 100% TCA in the management of ice pick acne scars. J Cutan Aesthet Surg 3(2):93–96 10. Sarkar R, Kaur C, Bhalla M, Kanwar AJ (2002) The combination of glycolic acid peels with a topical regimen in the treatment of melasma in dark-skinned patients: a comparative study. Dermatol Surg 28(9):828–832 11. Erbil H, Sezer E, Taştan B, Arca E, Kurumlu Z (2007) Efficacy and safety of serial glycolic acid peels and a topical regimen in the treatment of recalcitrant melasma. J Dermatol 34(1):25–30 12. Burns RL, Prevost-Blank PL, Lawry MA, Lawry TB, Faria DT, Fivenson DP (1997) Glycolic acid peels for postinflammatory hyperpigmentation in black patients. A comparative study. Dermatol Surg 23(3):171–174 13. Chun EY, Lee JB, Lee KH (2004) Focal trichloroacetic acid peel method for benign pigmented lesions in dark-skinned patients. Dermatol Surg 30(4 Pt 1):512–516 14. Sachdev M (2010) Cosmeceuticals. In: Khunger N, Sachdev M (eds) Practical manual of cosmetic dermatology and surgery, 1st edn. Mehta Publishers, Pune, pp 214–223

14  Facial Peels 15. Ghersetich I, Brazzini B, Peris K, Cotellessa C, Manunta T, Lotti T (2004) Pyruvic acid peels for the treatment of photoaging. Dermatol Surg 30(1):32–36 16. Kligman D, Kligman AM (1998) Salicylic acid peels for the treatment of photoaging. Dermatol Surg 24(3):325–328 17. Kadhim KA, Al-Waiz M (2005) Treatment of periorbital wrinkles by repeated medium-depth chemical peels in darkskinned individuals. J Cosmet Dermatol 4(1):18–22 18. Khunger N (2009) Combination therapies. In: Khunger N (ed) Step by step chemical peels, 1st edn. Jaypee Brothers Medical Publishers Ltd., New Delhi, pp 220–234 19. Briden E, Jacobsen E, Johnson C (2007) Combining superficial glycolic acid (alpha-hydroxy acid) peels with microdermabrasion to maximize treatment results and patient satisfaction. Cutis 79(1 Suppl Combining):13–16 20. Harris DR, Noodleman FR (1994) Combining manual dermasanding with low strength trichloroacetic acid to improve actinically injured skin. J Dermatol Surg Oncol 20(7): 436–442 21. Khunger N (2010) Acne scar revision. In: Khunger N, Sachdev M (eds) Practical manual of cosmetic dermatology and surgery, 1st edn. Mehta Publishers, Pune, pp 230–252 22. Effron C, Briden ME, Green BA (2007) Enhancing cosmetic outcomes by combining superficial glycolic acid

177 (­ alpha-hydroxy acid) peels with nonablative lasers, intense pulsed light, and trichloroacetic acid peels. Cutis 79(1 Suppl Combining):4–8 23. Landau M (2006) Combination of chemical peelings with botulinum toxin injections and dermal fillers. J Cosmet Dermatol 5(2):121–126 24. Khunger N (2009) Complications. In: Khunger N (ed) Step by step chemical peels, 1st edn. Jaypee Brothers Medical Publishers (P) Ltd., New Delhi, pp 280–298 25. Duffy DM (2006) Avoiding complications with chemical peels. In: Rubin MG (ed) Chemical peels: procedures in cosmetic dermatology. Elsevier Inc, Philadelphia, pp 137–170 26. Coleman KM, Coleman WP (2006) Complications of chemical peeling. In: Rubin MG (ed) Chemical peels procedures in cosmetic dermatology. Elsevier Inc, Philadelphia, pp 171–183 27. Fung JF, Sengelmann RD, Kenneally CZ (2002) Chemical injury to the eye from trichloroacetic acid. Dermatol Surg 28(7):609–610 28. Landau M (2007) Cardiac complications in deep chemical peels. Dermatol Surg 33(2):190–193 29. Khunger N (2008) Standard guidelines of care for chemical peels. Indian J Dermatol Venereol Leprol 74(Suppl): S5–S12

 

Fractional Laser Resurfacing

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Vic A. Narurkar

15.1 Introduction Fractional laser resurfacing is rapidly gaining momentum as the treatment of choice for facial and nonfacial skin resurfacing. Traditional ablative laser resurfacing, although effective, is losing popularity due to significant risks such as hypopigmentation, scarring and prolonged erythema and limitation in the treatment of lighter skin types. Fractional laser resurfacing can be divided into nonablative and ablative, and the patient selection, treatment protocols and pre- and postcare vary with these two modalities. This chapter will discuss nonablative fractional laser resurfacing (NFR) and ablative fractional laser resurfacing (AFR) and will enable the physician to develop appropriate treatment protocols for both modalities.

15.2 Principles The basic concept behind fractional laser resurfacing is to employ nonablative and ablative devices with a fractional mode of delivery, leaving a percentage of skin untreated, allowing for more rapid re-epithelialization and recovery. Non ablative (NFR) and ablative fractional

V.A. Narurkar  Bay Area Laser Institute, 2100 Webster Street, Suite 505, San Francisco, CA 94115, USA and Department of Dermatology, California Pacific Medical Center, San Francisco, CA, USA and University of California Davis School of Medicine, Sacramento, CA, USA e-mail: [email protected]

laser (AFR) resurfacing do differ significantly. Non ablative fractional laser resurfacing has an intact stratum corneum, while ablative fractional laser resurfacing does not leave the stratum corneum intact. The times of re-epithelialization also vary, with non ablative fractional laser resurfacing producing a rapid re-epithelialization in less than 24  h, while ablative fractional laser resurfacing producing a more delayed reepithelialization in 3–5  days [1]. Both modalities create thermal zones of injury to the treated tissue, with nonablative fractional devices creating more microthermal zones and ablative fractional laser resurfacing creating macrothermal zones [2]. Both modalities produce a true resurfacing, with extrusion of epidermal contents. Wavelengths employed in NFR include 1,410 nm, 1,440 nm, 1,540 nm and 1,550 nm [3]. The 1,550-nm NFR device is the most widely utilized with the longest clinical experience. Recently, a blended 1,550-nm and 1,927-nm NFR device was introduced to capitalize on superficial and deep components of NFR. Wavelengths employed in ablative AFR include 2,790 nm, 2,940 nm and 10,600 nm, with the 10,600 nm (carbon dioxide) being the most widely utilized and studied wavelength [4]. Table 15.1 lists the different AFR and NFR devices currently available.

15.3 Nonablative Fractional Laser Resurfacing (NFR) 15.3.1 Patient Selection NFR allows the widest group of patients and clinical indications. The author’s main experience with NFR is with the 1,550 nm and 1,927 nm wavelength devices

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Table 15.1  NFR and AFR devices available Type NFR NFR NFR NFR AFR AFR AFR

Wavelength Commercial devices 1,410 Fraxel Refine 1,440 Cynosure Affirm, Palomar Starlux 1440 1,540 Palomar Starlux 1540 1,550 and Fraxel restore and Fraxel restore dual 1,927 (1550/1927) 2,790 Cutera Pearl 2,940 Alma Pixel 2940, Palomar Lux 2940, Sciton Profractional 2940 10,600 Alma Pixel 10600, DEKA SmartXide DOT, Lumenis Activ/Deep FX, Fraxel RePair, Mixto 10600

Table 15.2  Clinical indications for nonablative fractional laser resurfacing Photodamage Dyschromia Acne scars Surgical, traumatic and burn scars Striae distensae Melasma Actinic keratoses Superficial rhytids

(Fraxel Restore and Fraxel Restore Dual, Solta Medical, Hayward, CA), which is also the most widely utilized and studied NFR device in the peer-reviewed literature. Clinical indications of NFR (Table  15.2) include acne scars (1,550 nm), surgical and traumatic scars (1,550 nm), dyschromia of the face and nonfacial skin (1,550 nm/1,927 nm Dual), melasma (1,550 nm and 1,927  nm), striae distensae (1,540  nm and 1,550 nm), moderate rhytides (1,550 nm) and superficial rhytids (1,410  nm, 1,440  nm, 1,540  nm and 1,550 nm) [5]. Skin types I–VI can be safely treated with the 1,550  nm NFR, and skin types I–IV can be safely treated with the combined 1,550 nm/1,927 nm NFR device. All patients with skin types IV–VI should be pretreated with a bleaching cream, preferably 4% hydroquinone, for at least 4 weeks prior to NFR and continued on this regimen post-NFR to prevent postinflammatory hyperpigmentation (PIH). Test sites are also advisable in darker skin types. A test site is

performed on the temporal area for facial skin and on the lateral neck for nonfacial skin. Hypopigmentation has not been an issue with NFR but PIH, especially in East Asian skin, can ensue but is reversible and preventable with a bleaching regimen. Antiviral prophylaxis is started 24 h prior to NFR in patients without a documented history of oral herpes simplex and done 24 h and continued for 3–5 days in patients with a documented history of oral herpes simplex. The author prefers a dose of valacylovir 1  g in morning and 1 g at bedtime the day before NFR treatments. Patients with a history of acne vulgaris should be treated with periprocedure oral antibiotics, as acne flares are very common post-NFR, especially in patients with a history of acne vulgaris. Routine antibiotics are not necessary, as infection is exceedingly rare.

15.3.2 Treatment Protocols NFR treatment protocols are based on the clinical indication, anatomic location and Fitzpatrick skin type of the patient (Table  15.3). Higher energy settings and treatment densities are required in patients with a history of acne scars, surgical and traumatic scars and moderate-todeep rhytids. Lower energy settings and treatment densities are indicated in nonfacial skin resurfacing, melasma and darker skin types. For darker skin types, lower treatment densities are more important than energy settings. Higher incidence of PIH is seen with higher treatment densities. NFR usually requires 2–5 treatment sessions. Acne scars and rhytids usually require more treatment sessions, while dyschromia and melasma usually require fewer treatment sessions. Treatment sessions are generally spaced 4–6  weeks apart but can be performed at longer treatment intervals [6].

15.3.3 Treatment Regimen Topical anesthesia with 7% lidocaine/7% tetracaine for 1  h is our usual protocol. One to two treatment areas are usually advisable per session (e.g., face and neck, neck and chest) to avoid lidocaine toxicity. We occasionally use 23% lidocaine/7% tetracaine or 30%

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Table 15.3  NFR treatment protocols for NFR Fraxel Restore 1550 nm Indication Photoaging face Nonfacial photoaging Acne scars Melasma

Skin types I–III 40–70 J/levels 7–9 20–30 J/levels 5–7 40–70 J/levels 9 to R3 8–10 J/levels 4–6

lidocaine in sensitive areas such as the perioral area, but care must be taken to use these in larger areas to avoid lidocaine toxicity. The area is then wiped clean prior to treatment. A thin coat of gel may be utilized to guide the NFR laser. Most treatments require eight passes with the NFR.

Skin type IV 30–40 J/levels 3–5 10–20 J/levels 3–5 40 J/levels 5–7 6–8 mJ/levels 3–5

Skin types V–VI 20–30 J/levels 3–4 10 J/levels 3–4 40 J/levels 3–5 6 mJ/levels 3–4

patients will begin to notice improvements even after the first treatment, typically at 4–6  weeks. The final results are evident at 9–12 months after the final treatment, with patients noticing continual improvement.

15.3.6 Complications 15.3.4 Posttreatment Care Figure 15.1 shows the sequence of healing with aggressive NFR treatments. Immediately after treatment there is moderate erythema and slight edema and duskiness of the pigmented lesions. Low fluence yellow LED light (Gentlewaves) is performed immediately posttreatment to reduce posttreatment edema and erythema. The edema and erythema become most pronounced at 48–72 h. For more superficial treatments with the 1,927  nm NFR, there is more significant peeling at 72 h. Since the stratum corneum is intact, weeping, crusting and prolonged healing are not evident. Male patients typically tend to heal faster than female patients, and this may be due to more sebaceous activity in male patients. Off face areas will take longer to heal, with the microthermal zone patterns often evident, especially on areas such as the abdomen. Patients can usually wear make up at day 3. A gentle cleanser and sunscreen are recommended. Acne flares are common during the first 2 weeks and if significant, oral antibiotics such as doxycycline 100 mg twice daily can be useful.

15.3.5 Results Figure  15.2 shows a typical pre- and post-NFR 1,550 nm/1,927 nm patient 9 months after two treatments. Even though multiple treatments are necessary,

Long-term complications with NFR are extremely rare. The most common long-term complication is persistent post inflammatory hyperpigmentation (PIH), which is most noted in darker skin types, particularly East Asian skin types (Fig. 15.3). With pre- and postbleaching, this usually resolves. Short-term complications include acne flares, edema, erythema and peeling, all of which resolve. Hypopigmenation has not been reported.

15.4 Ablative Fractional Laser Resurfacing (AFR) 15.4.1 Patient Selection AFR is better suited for a smaller group of patients than NFR. Skin types I–III [7] can be treated safely and there are reports of treating darker skin types, but we do not treat darker skin types with AFR, as there is greater risk of pigmentary changes and these skin types are better treated with the NFR devices. The optimal indications for AFR are deeper rhytids, more exaggerated dyschromia, thicker scars which require debulking and patients who may desire fewer treatments than NFR. While nonfacial areas can be treated safely with AFR devices, the author does not use AFR for nonfacial resurfacing, as it carries significant risks and NFR devices can deliver excellent results with enhanced

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V.A. Narurkar Before 1927 treatment

Immediately post

1 day post

2 days post

3 days post

4 days post

5 days post

1 week post

Fig. 15.1  Sequence of healing after 1,927-nm NFR

safety. Absolute contraindications to AFR are patients with a history of adnexal disease– such as morphea, scleroderma and other connective tissue disorders, postradiation therapy treated skin and recent treatment with oral isotretinoin. All patients should be treated with antiviral prophylaxis, and patients with a history of oral herpes simplex should be kept on oral antiviral until reepithelialization is complete. Treatment with oral antibiotics remains controversial – we routinely treat patients with oral antibiotics in the pre- and posttreatment period, as

unusual infections have been reported. Our antibiotic of choice is azithromycin (Z pack) to start the day before the procedure and continue for 3 days.

15.4.2 Treatment Protocols AFR treatment is best suited for the face. When nonfacial areas such as the neck and chest are treated, extreme caution is advised. Technique is key for all areas, to avoid bulk heating which can produce adverse

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Fig. 15.2  (Left) Pretreatment. (Right) After two treatments of NFR 1,550/1,927 nm laser (Fraxel Dual)

effects such as scarring. Generally, neck treatments should have 20–30% less fluence and treatment densities than facial skin [8]. Full face AFR is recommended for patients with moderate-to-severe rhytids and photoaging. We often perform blended AFR and NFR treatments, with AFR to the moderate-to-deep perioral and periorbital areas and NFR to the rest of the face and nonfacial skin. This has the advantage of faster recovery and fewer complications. Segmental AFR can be done, but can result in hypopigmentation, although much less than traditional ablative laser resurfacing.

15.5 Treatment Regimen The biggest challenge in AFR has been adequate pain control. Segmental AFR is easily done with a combination of topical anesthesia (such as 23% lidocaine/ tetracaine) and nerve blocks. If the periorbital area is to be treated, nonreflective metal eye shields need to be placed. Full face AFR can be done with a combination of topical anesthesia and nerve blocks but is better performed with some sort of sedation, especially if aggressive settings are utilized. Treatment technique is then most critical aspect of AFR. Care must be taken not to

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Fig. 15.4  Complete reepithelialization following AFR

Compared to traditional ablative laser resur­facing, ­healing is considerably accelerated. Aggressive emolliation with petrolatum-based products such as ­aquaphor are recommended until reepithelialization is complete. Figure  15.4 shows a patient following ablative ­fractional resurfacing. Erythema may persist for several weeks after treatment. Strict sun protection is also indicated. Fig. 15.3  PIH in Asian skin after NFR

overlap too aggressively, as bulk heating can ensue. The author’s experience is primarily with the Fraxel Repair 10,600-nm laser, which has a random scanning pattern and a built in smoke evacuator for greater ergonomic comfort. Treatment settings are generally to use 40 mJ, treatment densities of 20–30% on the face, with lower fluencies and treatment densities on the eyelid skin, typically 20  mJ. The author does not perform AFR on the neck and the chest, but if one chooses to do that, fluencies 20–30% less and treatment densities 20–30% are recommended.

15.5.1 Posttreatment Care AFR requires much more aggressive posttreatment care than NFR, as the stratum corneum is compromised.

15.5.2 Results Figure  15.5 shows an example of hypertrophic scar treated with a single treatment with 10,600  nm AFR Fraxel Repair. Fewer treatments are required with AFR compared to NFR, with the general consensus being one to two treatments.

15.6 Complications AFR complications are significantly less than those with traditional ablative laser resurfacing, but much greater than with NFR. Common short-term adverse effects include crusting, weeping, erythema and edema, which generally resolve without long-term sequalae. Long-term complications include infection, hypertrophic scarring and hypopigmentation. This is particularly more evident on the chest and neck (Fig. 15.6).

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Fig. 15.5  (Left) Pretreatment. (Right) After treatment of hypertrophic scar with AFR

15.7 Future Directions and Combination Therapies While both NFR and AFR offer dramatic results for skin resurfacing, they are limited for certain aspects of facial aging such as dynamic rhytids, volume loss and laxity, although there are improvements of laxity. Botulinium toxin A injections and dermal fillers are ideal complements to both AFR and NFR, as they respectively address dynamic rhytids and volume loss. Same day treatments are not advisable. The author generally waits 1 week post-NFR to perform botulinum toxin and fillers and 2–3 weeks after AFR. However, it is safe to perform both AFR and NFR in patient that

already has fillers. Skin laxity can be improved with combining radiofrequency treatments with AFR and NFR. We often do same day treatments with Thermage and Fraxel. If this is done, the Thermage treatment is performed first, followed by Fraxel. The combination approaches allow for synergy of these modalities.

15.8 Conclusions Fractional laser resurfacing is rapidly gaining momentum as the standard of laser resurfacing. Non ablative fractional resurfacing is indicated for the most varied conditions and skin types and affords the highest level

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considerably safer than traditional ablative laser resurfacing and both offer greater recovery and fewer shortand long-term side effects. Combination therapies with botulinum toxins, dermal fillers and radiofrequency complete the picture of fractional laser resurfacing with synergistic effects.

References

Fig. 15.6  Hypertrophic scar after AFR treatment on chest

of safety. Ablative fractional laser resurfacing is indicated for more severe photoaging and best suited for lighter skin types and facial skin. Both modalities are

  1. Laubach H, Tannous Z, Anderson R et  al (2006) Skin responses to fractional photothermolysis. Lasers Surg Med 38(2):142–149   2. Hantash BM, Mahmood MB (2007) Fractional photothermolysis: a novel aesthetic laser surgery modality. Dermatol Surg 33:525–534   3. Narurkar VA (2009) Nonablative fractional laser resurfacing. Dermatol Clin 27(4):473–478   4. Geronemus RG (2006) Fractional photothermolysis: current and future applications. Lasers Surg Med 38:169–176   5. Narurkar VA (2007) Skin rejuvenation with microthermal photothermolysis. Dermatol Ther 20:S10–S13   6. Wanner M, Tanzi E, Alster T (2007) Fractional photothermolysis: treatment of facial and nonfacial cutaneous photodamage using a 1550 nm erbium doped fiber laser. Dermatol Surg 33:23–28   7. Hunzeker CM, Weiss ET, Geronemus RG (2009) Fractionated carbon dioxide laser resurfacing: our experience with more than 2,000 treatments. Aesthet Surg J 29(4):317–322   8. Brightman L, Brauer R, Anolik R et al (2009) Ablative and fractional ablative lasers. Dermatol Clin 27:479–489

Capacitive Radiofrequency Skin Rejuvenation

16

Manoj T. Abraham and Joseph J. Rousso

16.1 Introduction Skin rejuvenation procedures, particularly those that deal with rhytids and skin tightening, are a necessary skill set in the arsenal of the aesthetic clinician. In general, plastic surgical techniques provide the most dramatic improvement. Resurfacing lasers (traditional or fractionated), dermabrasion, deep chemical peels, and coblation are considered standard ablative nonsurgical tools for skin rejuvenating procedures. However, longer duration of recovery, scarring, pigmentary changes, and other complications are more common with surgical and ablative procedures due to the very nature of these treatments. As a result, noninvasive methods have become increasingly popular, and there is significant demand for effective, proven methods of nonablative skin rejuvenation. The senior author (MTA) has found nonablative capacitive radiofrequency (RF) to be a successful and well-received approach for nonsurgical skin tightening in his private practice.

M.T. Abraham (*) Department of Otolaryngology – Head and Neck Surgery, Facial Plastic and Reconstructive Surgery, New York Medical College, Valhalla, NY, USA and Facial Plastic, Reconstructive and Laser Surgery, PLLC, Poughkeepsie, NY 12603, USA e-mail: [email protected] J.J. Rousso Department of Otolaryngology – Head and Neck Surgery, The New York Eye and Ear Infirmary, New York, NY 10003, USA e-mail: [email protected]

Radiofrequency energy is electromagnetic radiation in the range of 3–300 GHz. Solta Medical, Inc. (formerly Thermage, Inc.) based in Hayward, California, has pioneered the aesthetic application of nonablative RF skin tightening. Thermage, Inc. was initially granted FDA regulatory clearance for treatment of periorbital wrinkles and rhytids in November 2002. This was followed by clearance for full face treatment in June 2004. In January of 2006, the FDA expanded its clearance to treatment of all skin surface wrinkles and rhytids. Although there are a growing number of other devices and technologies available for nonablative skin tightening, none of these have the accumulation of published studies reporting efficacy compared to Thermage [1–38]. In addition, Thermage treatment protocols have had time to evolve through several generations, ensuring safety and more consistent and effective results [32, 34, 37]. Thermage systems utilize the company’s proprietary technology incorporating large mono-polar capacitive electrodes to deliver RF energy into the skin while concurrently protecting the skin surface with a cryogen cooling spray. Current flows from the device via the treatment tip, through the skin and out through a grounding pad applied to the patient. This creates a reverse thermal gradient in the skin, with cooling of the epidermis while simultaneously achieving precise volumetric heating of the deeper dermis. As a result, there is partial denaturation of the collagen within the dermis without injury to the skin surface [1, 19]. Initial contraction of the skin collagen network in the dermis occurs immediately as the collagen fibrils reanneal. Tightening continues as a healing response is triggered within the dermis, leading to an overall increase in skin collagen content [12, 30].

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16.2 Indications Nonablative capacitive RF treatment is most appropriate for patients with mild-to-moderate aging and wrinkling of the skin. The treatment is best suited to address deeper rhytids (such as the nasolabial folds and marionette creases in the face), rather than fine, superficial crepe paper type wrinkles along the skin surface. This relates to the epidermis being protected during the treatment (fine skin surface wrinkles and dyschromias are best treated by fractionated or more traditional ablative methods of skin resurfacing). Patients with significant skin laxity or those with noticeable underlying structural ptosis are not ideal candidates for the procedure, but those who are not interested in surgical options for rejuvenation may still obtain a theoretical antiaging benefit from collagen stimulation in the skin. Similarly, patients who have had a surgical lift may benefit from this maintenance effect. It is the senior author’s experience that patients with thinner skin typically achieve a more dramatic result. Patient with thicker, more sebaceous skin may require more than one treatment session. Capacitive RF skin rejuvenation is nonablative and depends on energy delivery based on tissue resistance rather than absorption of laser light energy, and can therefore be used with all Fitzpatrick sunreactive skin types. It follows that since RF energy is not light based, pigmentary dyschromias, hair, and capillary and vascular ectasias are all relatively unaffected by capacitive RF treatment (it is possible that there is some reduction in capillary dilation due to the increased skin collagen content). Nonablative lasers and intense pulsed light systems are more effective for these applications, and can be packaged and performed in conjunction with capacitive RF skin rejuvenation. Thermage treatment can also be combined with other minimally invasive office based or surgical procedures to obtain a cumulative result (Table 16.1) [2–4, 29]. Of note, animal histology studies have shown inflammatory changes associated with tissue fillers in the skin after capacitive RF treatment, but a clinical study by Alam et al. indicated that there was no significant morphological change in the filler material or surrounding tissue when RF treatment was performed in patients 2  weeks after deep dermal injection with hyaluronic acid derivatives or calcium hydroxylapatite [21, 29, 38].

Table 16.1  Minimally invasive procedures that can be combined effectively with capacitive RF skin rejuvenation Surgical procedures   Facial and neck liposuction   Blepharoplasty   Percutaneous suture techniques Nonsurgical treatments   Chemodenervation   Tissue fillers   Intense pulse light and nonablative lasers   Microdermabrasion and superficial chemical peels

It is essential that patients have realistic expectations of the subtle improvements expected with capacitive RF skin rejuvenation. Patients must understand that dramatic surgical or ablative type results are not possible currently with this technology. Patients must also understand that although there is some initial contour change, skin texture and tone will continue to improve gradually for several months after the treatment. Depending on each patient’s individual biology and reaction to the treatment, additional treatments may be necessary. Adequate periprocedure patient counseling is a key component of ensuring patients’ satisfaction with the procedure [4, 10]. When performed alone, there are few contraindications to Thermage treatment (Table 16.2).

16.3 Treatment Considerations 16.3.1 Analgesia Despite newer multiple pass treatment algorithms that require less energy to be delivered at one time, capacitive RF treatment is uncomfortable. There is an initial cooling sensation as the cryogen cooling spray is applied, overcome by a burst of heat as RF energy is delivered, followed by cooling again. The most recent generation of Thermage systems (the CPTTM system) utilizes an enhanced energy delivery algorithm weaving microbursts of RF energy and cryogen cooling within each treatment pulse, combined with a vibrating handpiece to reduce discomfort. According to internal studies by the manufacturer, patients uniformly tolerated treatment better even though the newer treatment tips are four times more effective in heating tissue to the target temperature.

16  Capacitive Radiofrequency Skin Rejuvenation Table 16.2  Contraindications to capacitive RF skin rejuvenation Absolute contraindications   Metallic skin art or tattoo that cannot be removed Implanted medical device   (pacemaker, defibrillator, etc.)   Pregnancy Relative contraindications   Dermatologic conditions   Collagen-vascular or autoimmune diseases   Impaired collagen production (radiation, metabolic, etc.)

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16.3.3 Disposable Costs All Thermage treatment tips are disposable. They are designed for single use per patient, and are electronically programmed to stop firing after a preset number of pulses. Other Thermage system disposable item costs are listed in Table 16.3.

16.4 Technique 16.4.1 Site Preparation

Since a typical full face and upper neck treatment with the 1.5 cm2 tip involves 600 RF pulses and can take an hour to perform, some form of anesthesia can help optimize patient comfort. Most patients with appropriate temperament are able to tolerate treatment using oral narcotic analgesics (oxycodone, hydrocodone, etc.) and short-acting anxiolytics (lorazepam, alprazolam, etc.). Topical anesthetics are counter productive as they numb the epidermis and the cooling sensation, but are not effective in alleviating the discomfort of penetrating RF heat [30]. Local injection anesthetics can alter skin resistance and interfere with proper RF energy delivery [9, 12, 32]. Sedation or general anesthesia should only be utilized by experienced providers, since the additional safety measure of patient feedback is removed.

16.3.2 Tip Selection A variety of Thermage treatment tips are available depending on the treatment site and treatment goals (Fig. 16.1). The appropriate tip is selected based on the size of the treatment tip and the depth of penetration of the RF energy. Face procedures are commonly performed with the 1.5 cm2, medium depth treatment tip, although a 3  cm2 is also available (Table  16.5). For eyelid procedures, the smaller 0.25  cm2, superficial depth treatment tip is appropriate. The much larger, deep tip is suited for large surface area procedures on the body (abdomen, flanks, arms, buttocks, thighs) – this tip has a surface area five times larger than the 1.5 cm2 face tip, and penetrates 79% deeper according to the manufacturer. This uniform, deeper volumetric penetration of the RF energy may help with cellulite treatment.

It is ideal if Thermage treatment is performed in a private procedure room, with the patient positioned on a comfortable adjustable chair or procedure table. The provider is typically seated on a supportive surgeon’s stool. Playing soft music can help the patient relax. Patients are instructed to arrive with the areas to be treated clean and free of any makeup or other skin care product. If hair bearing skin is to be treated, it is best if the hair is shaved or trimmed in advance. The treatment area is exposed and if necessary cleansed with mild soap and water. All metal accoutrements are removed. The grounding pad is applied to an area distant from the treatment site.

16.4.2 Energy Settings Studies by Zelickson et  al. [1] have revealed that multiple treatment passes over the same area using lower energy settings creates more collagen change compared to a single treatment at a higher energy level. Avoiding very high energy settings has the additional benefit of making the treatment more tolerable and decreasing the likelihood of potential complications [1, 34, 37]. Coupling fluid is liberally applied throughout treatment to ensure uniform energy delivery. Complete, even contact of the electrode with the skin surface is necessary to initiate cooling and RF delivery. An initial test pulse is performed prior to beginning treatment to allow the machine to calibrate skin resistance. The patient is asked to provide feedback using a 0–4 point scale (0 – nothing, 1 – warm, 2 – hot, 3 – very hot, 4 – burning), with treatment settings calibrated to a 2–2.5 level. With the 1.5 cm2 tip, this usually translates to a setting of 61–96 J/cm2 in most areas.

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M.T. Abraham and J.J. Rousso

Fig. 16.1  Components of the Thermage CPT™ nonablative RF skin rejuvenation system (Solta Medical, Inc., Hayward, CA). The computer-controlled RF generator unit with integrated cryogen cooling unit is seen on the left, the ergonomic treatment hand

piece which vibrates to provide improved patient comfort is pictured in the middle, and some of the various disposable treatment tips are seen at bottom right. The use of the treatment grid to guide delivery of each treatment pulse is depicted in the inset

Table 16.3  Thermage system disposable costs

16.4.3 Treatment Planning

RF treatment tips Cryogen canisters Grounding pads Coupling fluid Treatment grid

Energy levels are reduced where needed. For instance, when treating the face, lower energy (44–61  J/cm2) is utilized in areas of thinner skin (around the orbital rim and lower neck), over vulnerable superficial fat pads (temporal, malar), and over sensory nerve trunks (greater auricular, supra orbital, infra orbital, mental). Visible tightening, erythema of the skin, and excessive patient discomfort are all subjective clinical endpoints of treatment for each specific area on the skin.

The manufacturer-supplied ink grid is used to guide treatment topography (Fig. 16.1). The grid is useful in knowing exactly where to position the treatment tip for each RF pulse, adjacent to the previous treatment site, without skipping areas or causing undue overlap. After the initial pass of RF treatment has been completed, when making the next pass over the same area, the intersection of the grid lines is used. In this manner, by switching back and forth on the grid on each subsequent pass, an even application of RF energy is ensured throughout. The treatment plan is best visualized in three dimensions (Figs.  16.2–16.4) (Table  16.4). One or two initial passes are performed to cover the entire treatment area to achieve uniform contraction of the collagen skin scaffold in the X-Y plane. Additional

16  Capacitive Radiofrequency Skin Rejuvenation Fig. 16.2  Schematic indicating three-dimensional volumetric tightening of the dermis. Tightening of the fibrous septae in the subcutaneous tissue helps contour in the Z plane (Graphic courtesy of the manufacturer)

191 Volumetric Heating: 3-D Tightening along X, Y, & Z Planes Epidermis Dermis

Y

Fat cells X Z

Septae

Muscle

Visualize tightening in 3 dimensions 1st Two Passes = 80 - 160 REPs *XY Pass = 20 - 40 REPs Total = 100 - 200 REPs

Periorbital Wrinkles ∗Based on using 1.5 cm2 FAST Tip ∗Only one pass over temple region

Fig. 16.3  Computer graphic depicting treatment algorithm for the upper face

Vector Passes

M.T. Abraham and J.J. Rousso

192 1st Two Passes = 300 - 400 REPs XY Pass = 40 - 80 REPs Z Passes = 60 - 120 REPs Total = 400 - 600 REPs

Mid & Lower Face and Neck:

Contour Passes

∗Based on using 1.5 cm2 FAST Tip

Fig. 16.4  Computer graphic depicting treatment algorithm for the mid/lower face. The first two treatment passes (purple) cover all of the areas depicted. The XY treatment pass (red) overlaps

the purple areas, and the Z treatment pass (green) overlaps both the red and purple areas. REP radiofrequency energy pulse (Images courtesy of manufacturer)

Table 16.4  Treatment algorithm to achieve tightening in three dimensions (courtesy of manufacturer) Treatment area (all units in cm2)

1st XY pass

Periorbital/forehead

100

Mid- and lower face and neck Neck alone Full face and neck

Wrinkles Brow effect Nasolabial fold Jawline

240 100 340

Additional XY passes 50 24 50 90 50 120

Final Z passes

Total

N/A N/A 20 20 N/A 40

150 124 310 350 150 500

The numbers shown above are to provide guidance as to the number of firings required for an average size face and should not be taken as absolute Always use as many firings as needed to complete the algorithm

passes are then performed along vectors perpendicular to the relaxed skin tension lines of the skin to achieve maximal lifting and tightening in the direction desired. In the face, superior and lateral vectors are targeted to lift, tighten and stretch the skin around the lips, nasolabial folds and marionette creases, similar to a surgical facelift.

RF energy is known to conduct through collagenbased fibrous septae that surround fat locules in the subcutaneous tissue [11]. Additional shrinkage and definition can be accomplished by targeting the fibrous septae in this 3-dimensional Z plane. This strategy works well in areas of fullness such as the submental and jowl regions. Stacking of treatment pulses on top of each other without

16  Capacitive Radiofrequency Skin Rejuvenation

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Table 16.5  Algorithm rules and clinical premises. Typical number of firings using the 1.5 cm2 tip to treat the face (courtesy of manufacturer) First XY pass

Addl. XY passes

Final Z passes

Rule Cover maximum surface area in a contiguous region of desired tightening/ toning Additional passes along vectors of tightening, similar to facelift vectors. Isolate by physical manipulation of the skin Final passes to correct excessive tissue laxity or contour change due to fat and/or fibrous septae laxity

Clinical premise Every square centimeter treated has 5–20% of collagen volume denatured (setting dependent). More contiguous surface area achieves greater tightening of XY plane Additional passes achieve incremental correction through tightening of the more easily mobilized tissue adjacent to the targeted area of correction

Evidence Published article demonstrating the relationship between collagen volume affected and the treatment setting

Clinical observations led to published histology work showing cumulative collagen damage with multiple passes

Observations of Z-axis contour changes during Tightening in the Z-axis, particularly in the mid- and lower treatment. Pilot histology suggests both fibrous septae and fat involvement face, creates a “narrowing and lifting” effect incremental to XY axis tightening

at least 2 min in between pulses is generally not recommended due to concerns of excessive heat build-up, but can be used effectively in experienced hands to achieve further tissue sculpting in this Z plane [25]. The total number of treatment pulses required for different zones of the face and neck are tabulated in Table 16.5 (Figs. 16.3 and 16.4). It is usually not necessary to treat skin that is densely adherent (over the nasal dorsum, ear, and scalp for instance). Upper lid skin is distracted onto the orbital rim and away from the globe prior to treatment when using the medium depth tip, although the eye lid skin can be treated directly with the superficial depth treatment tip (haptic plastic corneal shields are placed to protect the entire globe) [35].

16.5 Aftercare If other complementary procedures are to be done concurrently (Table 16.2), they should be performed after Thermage treatment is completed [9, 11, 18, 28]. If Thermage is performed alone, aftercare is minimal. Most patients can resume normal activities immediately after the procedure. Routine sun protection is recommended. Patients are instructed to avoid using ice or antiinflammatory medications which may blunt the healing response and impede collagen stimulation.

16.6 Results Initial skin tightening due to thermally mediated collagen tightening is seen as the treatment end point. Results are most impressive in patients with thin skin and moderate laxity. Gradual thickening, toning, and lifting of the skin peaks a few weeks after treatment and continues for 4 months or longer, as a result of increased collagen production in the skin [2–10]. Contour changes seen in the face typically include 2–4 mm of brow elevation, smoothing of the nasolabial folds and marionette creases, and better definition of the jaw line and cervicomental angle (Fig.  16.5) [2–15, 17, 18, 24–27]. Intrinsic characteristics of the skin such as pore size, acne, and tone are also improved [2, 16, 17]. The patient is spared the incisions, complications, and recovery time associated with traditional plastic surgery procedures. Collagen stimulation in the skin may also provide a theoretical antiaging benefit by replenishing collagen lost during aging. A single Thermage treatment is sufficient in most patients, especially those with thinner skin who do not have significant underlying structural ptosis. Additional treatments can provide cumulative results. Results typically last several years in patients who adhere to a healthy lifestyle. The senior author has re-treated patients with Thermage 3–5  years after initial treatment with very

194

Fig. 16.5  (a, b) Typical patient results 9 months after nonablative capacitive RF treatment of the face and neck using a 900 pulse 1.5  cm2 medium depth tip and eyelid treatment with the 225 pulse 0.25  cm2 shallow depth tip with the original

M.T. Abraham and J.J. Rousso

ThermaCool™ system. Lifting and stabilization of the brow, tightening of the eyelid skin, and improvement in the jaw line and mid-face profile are evident. (Left) Pretreatment. (Right) Following treatment

16  Capacitive Radiofrequency Skin Rejuvenation

good patient satisfaction, perhaps because of continually improved technology and treatment algorithms. As with any procedure, setting realistic patient expectations is crucial to achieving patient satisfaction [4, 10].

16.7 Complications Compared to invasive surgical procedures and ablative methods of skin rejuvenation, the incidence of complications following capacitive RF treatment is extremely low [2, 4–10, 13, 18–22, 26, 27, 32]. Clinically noticeable asymmetry is unlikely if treatments are performed uniformly and treatment guidelines are followed. A mild amount of transient erythema and edema is common after the procedure, and resolves within a few days. On rare occasion, low-dose oral steroid therapy may be useful, but is avoided unless necessary since the inflammatory and healing response is what is felt to trigger new collagen formation. There can be some numbness of the skin (in the face and neck often in the distribution of the greater auricular nerve), possibly as a result of perineural inflammation. Numbness may take a few weeks to recover, but permanent nerve injury has not been reported [2–4]. Localized inflammation of superficial muscles like the platysma in the neck can cause temporary ridging or lumping which may take a month or two to dissipate. Anecdotally, patients who have the greatest evidence of inflammation appear to get the most amount of skin tightening. If the treatment tip is not kept completely flat against the skin surface, arcing of RF energy can occasionally cause a small 1.0 mm in diameter and/or are blue in color do not respond well to IPL. Laser therapy or sclerotherapy are recommended when

approaching these vessels. Finally, while certain hemangiomas and port-wine stains have been satisfactorily treated with IPL, pulsed dye and YAG lasers are generally considered the preferred treatment for these lesions.

17  The Use of Intense Pulsed Light (IPL) in Aesthetic Medicine

a

201

b

Fig. 17.4  (a) Pretreatment photograph of a 24-year-old female with a vascular malformation on the left cheek. (b) After four IPL treatments

a

b

Fig. 17.5  (a) Pretreatment photograph of a 36-year-old woman with solar lentigines and ephelides (e.g., freckles). (b) Postprocedure after four IPL treatments

Figure 17.4 illustrates the efficacy of IPL in treating vascular conditions on the face. The spectrum of pigmented problems that are readily treated by IPL includes solar lentigines, melasma, ephelides (freckles), and postinflammatory hyperpigmentation. Significant pigmentary reduction has been observed after the treatment of these particular problems (Fig. 17.5). Pulse durations of 10–30 ms, interpulse delay of 10 ms,

fluence of 9–12 J/cm2, and a 515-nm cutoff filter generally produce effective outcomes. In addition, IPL treatments can be performed in conjunction with other minimally invasive procedures. Botulinum toxin (i.e., Botox, Dysport) injections can be safely administered immediately following an IPL treatment, without concern for altered effect or increased sensitivity. Microdermabrasion type procedures can

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also be performed sequentially with IPL. Freedman [9] demonstrated that the beneficial effects of IPL on photoaging are enhanced when a microdermabrasion technique that included a topical antioxidant application immediately preceded an IPL treatment. The microdermabrasion process activated metabolic pathways that worked in synergy with IPL mechanisms of action; the topically infused antioxidants conferred protective and reparative effects on the skin. However, the use of dermal fillers during an IPL treatment session could be problematic and should be avoided. This is due to the possibility of adverse interactions of IPL energy within the dermis on the filling materials.

B.M. Freedman and T.P. Balakrishnan

17.3.4 Step 4: Set IPL Treatment Parameters Because IPL treatments are performed for a variety of conditions, energy settings must be adjusted accordingly. Treatment guidelines are provided by each manufacturer and should initially be followed. After determining the proper filter for the clinical problem, set the fluence, pulse width, interpulse delay, and cooling temperature. With experience, modifications can be made to accommodate each provider’s style and patient needs.

17.3.5 Step 5: Observe and Complete Treatment

17.3 IPL Treatment Protocol 17.3.1 Step 1: Analyze the Skin Document the Fitzpatrick skin phototype. Note texture irregularities, scarring, areas of redness, broken capillaries, and dyspigmented lesions. Make note of tattoos, especially tattooed eyebrows and lip liner; avoid these areas. Ask the patient about their oral and topical medications so as to avoid treatment while they are taking photosensitizing medications (i.e., tetracycline, Retin-A). Take pretreatment photographs for later outcome assessment. Obtain informed consent (Table 17.4).

17.3.2 Step 2: Cleanse the Skin For all facial treatments, it is important to work with clean, dry skin. Massage a hypo-allergenic, pH neutral cleanser into the skin starting at the décolleté (upper chest) and working upward toward the forehead. Afterward, use moist gauze pads to remove the cleanser in upward strokes starting at the décolleté and finishing with the forehead. Pat the skin dry. Prior to treating nonfacial body areas for unwanted hair or vascular conditions, remove lotions and deodorants. This will optimize IPL energy absorption.

17.3.3 Step 3: Protect Technician and Patient IPL machines are FDA-approved Class 2 devices. It is mandatory to utilize eye protection in order to prevent ocular injury. Place eye shields over the patient’s eyes and assure that the provider dons protective goggles.

Apply a thin layer of colorless ultrasound jelly to the treatment site. This will facilitate heat removal and improve optical coupling and hand piece gliding. Place the hand piece onto the skin with minimal pressure and in full contact with the treatment area. Activate the IPL device; after each pulse cycle, move the hand piece so that there is 20% overlap. During treatment, observe the area for any unwanted reactions. When treating hyperpigmented lesions, the correct energy level will cause the pigmented lesion to darken within 5–10 min. If this is not achieved, consider treating the area again or increasing the fluence at the next treatment. For vascular areas, the treated area should become erythematous within a few minutes. Increase the fluence in small increments until the desired response is achieved. After adjusting the energy accordingly, continue to treat with non-overlapping scans. Thoroughly remove the excess ultrasound jelly from the hand piece and treatment site after treatment is completed.

17.3.6 Step 6: Posttreatment Instructions Erythema and perifollicular edema can be seen for up to 6 h after treatment. Cool compresses or ice packs can provide comfort if the patient complains of “burning pain.” In the event of blistering, the location and extent of injury should be documented. Wound care should be initiated with topical antibacterials, debridement, and appropriate dressings. Retreatment should be scheduled at 3–4 week intervals for pigmented or vascular lesions and at 6–8 week intervals for hair reduction.

17  The Use of Intense Pulsed Light (IPL) in Aesthetic Medicine

203

Table 17.4  IPL patient informed consent Intense pulsed light (IPL) consent form 1. I understand that treatment for pigment, photodamage, vascular lesions, and unwanted hair is being performed with an IPL system that uses electronically controlled high-intensity multi-wavelength light. 2. I understand this procedure may cause discomfort during treatment. Redness and irritation may occur on the skin during and after treatment. This sunburn-like irritation usually subsides in 12–24 h. The pigmented and/or vascular lesions will darken after treatment prior to fading. In some cases side effects may include, but are not limited to, lightening or darkening of the skin, blistering, or skin irregularities. 3. I understand that results vary and that there is a possibility that the procedure will not remove all the pigmented/vascular lesions and/or unwanted hair on my skin. I also understand that in order for the procedure to be effective, the following guidelines must be followed:   a. Multiple treatments are performed until the desired level of pigment and/or vascularity removal is observed. (Usually four (4) to six (6) treatments).   b. Multiple treatments are performed until the desired level of hair reduction is observed. (Usually four (4) to six (6) treatments).   c. Sunscreen must be worn for at least 3 weeks after treatment. 4. I understand that sun exposure 2 weeks prior to treatment and/or 2 weeks after treatment may result in unwanted darkening or lightening side effects of the skin. 5. I understand that other forms of treatment for these conditions may exist. 6. All my questions regarding this procedure have been answered. _________________________ _________________________ Signature of patient Date _________________________ _________________________ Provider signature Witness signature

17.3.7 Step 7: Cleanse and Protect

References

Cleanse the skin. Apply sunblock. Remind patient to avoid any chemical ointments and creams such as glycolic acid or Retin-A for 72 h following treatment.

1. Alam M, Hsu TS, Dover JS, Wrone DA, Arndt KA (2003) Nonablative laser and light treatments: histology and tissue effects – a review. Lasers Surg Med 33(1):30–39 2. Ross EV (2006) Laser versus intense pulse light: competing technologies in dermatology. Lasers Surg Med 38(4): 261–272 3. Sciton Profile Operator Manual (Sciton Corporation, Palo Alto, CA) (2005) Section 7.7 Broad Band Light. 48–58 4. Bitter PH (2000) Noninvasive rejuvenation of photodamaged skin using serial, full-face intense pulsed light treatments. Dermatol Surg 26(9):835–842 5. Dover JS, Bhatia AC, Stewart B, Arndt KA (2005) Topical 5-aminolevulinic acid combined with intense pulsed light in the treatment of photoaging. Arch Dermatol 141(10): 1247–1252 6. Troilius A, Trolius C (1999) Hair Removal with a second generational broad spectrum intense pulsed light source – a long-term follow-up. J Cutan Laser Ther 1(3):173–178 7. Sadick NS, Weiss RA, Shea CR, Nagel H, Nicholson J, Prieto VG (2000) Long-term photoepilation using a broadspectrum intense pulsed light source. Arch Dermatol 136(11):1336–1340 8. Angermeier MC (1999) Treatment of facial vascular lesions with intense pulsed light. J Cutan Laser Ther 1(2):95–100 9. Freedman BM (2009) Topical antioxidant application enhances the effects of intense pulsed light therapy. J Cosmet Dermatol 8(4):254–259 10. Raulin C, Greve B, Grema H (2003) IPL technology: a review. Lasers Surg Med 32(2):78–87

17.4 Conclusions High-intensity pulsed flashlamp systems (IPL) have proven to be a successful and noninvasive means of treating a variety of skin issues. The low rates of adverse effects combined with its efficacy lead to a high rate of patient satisfaction [10]. IPL treatment regimens are effective in improving all aspects of facial photoaging, reducing unwanted facial and body hair, and lessening hyperpigmentation and certain vascular irregularities. Treatments are relatively easy for the patients to tolerate with an average session lasting approximately 20 min. Although a series of treatments is required for optimal results, the lack of downtime and low per treatment cost make IPL an excellent option for most patients. This is especially true at this time when patients are interested in less invasive, less costly procedures for cosmetic enhancement. For these reasons IPL has become a mainstay in the aesthetic medicine practice.

 

Thermolysis in Aesthetic Medicine: 3D Rejuvenation

18

Nassim Tabatabai and Neil S. Sadick

18.1 Introduction The desire to reverse the signs of aging and attain cosmetic enhancement with minimal side effects and rapid recovery has inspired the field of nonsurgical rejuvenation. Since its emergence in the 1980s, laser resurfacing has evolved from ablative lasers such as carbon dioxide (CO2) lasers and erbium: YAG lasers to nonablative laser resurfacing and fractional resurfacing methods [1]. Lasers direct a high-energy beam of light into specific tissues. These beams of light are of specific wavelengths and vary in terms of strength and the type of tissue they target. The fundamental principle behind the use of lasers is based on the theory of selective photothermolysis (photo = light, thermolysis = decomposition by heat) [2, 3]. This theory encompasses the following: optical energy penetrates deep enough to reach the target tissue; optical energy is mostly absorbed by the target although surrounding skin may be heated significantly; and optical energy is strong enough to create thermal damage of the target tissue [4, 5]. In selective photothermolysis, by selecting a specific wavelength and specific duration unique to one target, heat can be delivered rapidly to the target keeping the thermal damage confined to that target. In photorejuvenation, melanin, hemoglobin, and water are the most common molecular targets. This structural approach to photoreju-

N. Tabatabai (*) • N.S. Sadick Department of Dermatology, Weill Medical College of Cornell University, 911 Park Avenue, Suite 1A, New York, NY 10075, USA e-mail: [email protected] e-mail: [email protected], [email protected]

venation is based upon age-related changes in the dermal matrix components including collagen, elastic fibers, glycosaminoglycans, and fibroblasts (Table 18.1) [6]. Photorejuvenation of the skin can be accomplished by utilizing ablative lasers and nonablative resurfacing technologies. The carbon dioxide (CO2) lasers and the erbium: YAG lasers are mainstays of ablative laser treatment. The mechanism involves the delivery of an intense burst of laser energy onto the skin where this energy heats up the water in the skin and causes both the water and tissue to vaporize. In response to the injury and subsequent healing, new layers of collagen are produced. Ablative lasers remove 100% of the epidermis and varying thickness of underlying dermis which results in smoother appearance of the skin and skin tightening due to heat-induced collagen shrinkage [7]. Although ablative lasers produce superior results, they are associated with several unfavorable side effects and prolonged and complex aftercare [1, 8, 9]. Patients can have posttreatment erythema, edema, burning, and crusting. There is an increased risk of infection, scarring, pigment alteration, acne flares, herpes infection/ reactivation, scars, milia and dermatitis. Also, these lasers are limited to the thicker skin of the face and are contraindicated in most other settings [10]. Nonablative laser resurfacing improves structural changes in the skin without disruption of the epidermis. Through selectively targeting specific dermal components, the epidermis is spared while a wound-healing response produces new collagen. The Nd: YAG 1,320-nm laser and the light-emitting diodes (LEDs) are examples of nonablative lasers [11]. Although there is minimal risk and a much reduced to no recovery period, the efficacy of these systems is inferior compared to ablative lasers for the repair of photodamaged skin [12].

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_18, © Springer-Verlag Berlin Heidelberg 2011

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206 Table 18.1  Scientific basis of aging Collagen   Each year, 1% of dermal collagen is lost   Anchoring fibrils are decreased in photoaged skin Elastic fibers  Aging and UVA/UVB increase elastic tissue breakdown by increasing expression of elastin Glycosaminoglycans  Decreases with aging leading to decreased water content, decreased cell adhesion, migration, development, and differentiation Fibroblasts   Number of fibroblasts decrease with age

18.2 Photoaging and Thermolysis Photoaging involves the loss and remodeling of collagen in the dermis, increase in vascular ectasia, and fragmentation of elastin fibers in the dermis [13]. These histological changes are observed clinically as static and dynamic rhytids, pore enlargement, and dyschromia. Dyschromia includes telangiectatic changes of the skin, erythema, solar lentigines, and generalized loss of skin luster [14]. The challenge faced by any photorejuvenation method is to improve the appearance of all the component of photoaging in a safe and effective matter. As compared to ablative resurfacing, nonablative technologies result in faster recovery period and fewer side effects but with mild-to-moderate improvements in photodamaged skin.

18.3 Rejuvenation There are three types of rejuvenation based on the target skin components. In type 1 or epidermal rejuvenation, epidermal turnover, skin toning, and chromophore targeting are the main objectives [6]. Epidermal turnover can be achieved by chemical peels, microdermabrasion, laser micopeels, retinoids, and alpha hydroxy acids (AHAs). Skin toning is usually achieved by LED. Chromophore targeting, which includes both hemoglobin and melanin targeting, is treated with pulsed light with or without radiofrequency (RF) energy, pulsed dye lasers (PDL), or Q-switched lasers. Dermal or type 2 rejuvenation addresses decreased collagen, disorganized elastin, decreased glycosamin-

N. Tabatabai and N.S. Sadick

oglycans, rhytids, and textural changes. The treatment modalities for type 2 rejuvenation include diode lasers, RF technologies, infrared (IR) lasers, Nd:YAG lasers, erbium glass lasers, and fractional technologies. Type 3 rejuvenation involves deep dermal and subcutaneous structures. The treatment modalities include microablative fractional lasers, broad band light, IR lasers, and RF technologies.

18.4 Nonablative Rejuvenation Technologies Nonablative rejuvenation methods improve aging structural changes in the skin without disruption of the epidermis, minimize downtime, and have a low-risk profile. Nonablative laser technologies create skin remodeling by: targeting dermal water, hemoglobin, melanin, or collagen to absorb the light energy, producing a thermal effect on the dermis which results in a wound healing effect via cellular mediators. Furthermore, laser energy applied to dermal microvasculature can cause cytokine-mediated responses that produce collagen [15]. A summary of these technologies is presented in Table 18.2 [6]. Infrared lasers target dermal water to induce collagen production and remodeling, leading to improvements in fine lines and skin texture. Vascular-specific lasers target erythema, flushing, and telangiectasia that occur in photodamaged skin. Pigment-specific lasers can be used to lighten solar lentigines and ephelides that accumulate with ongoing exposure to the sun. Intense pulsed light (IPL) sources have broad wavelengths that can target both vascular and pigmentary alterations in the skin [16]. Radiofrequency devices deliver energy in the form of an electrical current that generates heat. This produces collagen damage and an inflammatory cascade, which results in a tightening effect. Furthermore, combinations of nonablative lasers are often used to achieve optimal rejuvenation results.

18.4.1 Light-Emitting Diodes (LED) Light-emitting diodes (LED) devices are narrow band emitters of low-intensity light ranging from ultraviolent (UV) through visible and into infrared [17]. LED therapy is a nonablative, athermal treatment modality

18  Thermolysis in Aesthetic Medicine: 3D Rejuvenation Table 18.2  Non-ablative rejuvenation technologies Superficial chemical peels Microdermabrasion Botulinum Toxin A, B Retinoids/Alpha hydroxy acids (AHA) Intense pulsed light sources (585–110 nm) Laser technologies   Yellow light    Potassium titanyl phosphate (KTP) laser (532 nm)    CuBr laser (578 nm)    Pulsed dye laser (PDL) (585–600 nm)    N-Lite laser (585 nm)   Broad band light    Intense pulsed light (IPL) (500–1,100 nm)   Infrared lasers    Nd: YAG (1,064 nm)    Cool Touch (1,320 nm)    Smooth beam (1,450-nm diode)    Aramis (1,540-nm erbium glass laser)   Nonlaser modalities    Radiofrequency technologies (Thermage)

that works by effecting photomodulation. The mechanism of light therapy is based around the absorption of specific wavelengths of light by cellular photoreceptors [18]. Several studies have demonstrated that LED technology stimulates collagen deposition and the wound-healing cascade [19]. Omnilux is an LED device which uses a panel of 2,000 diodes to deliver 415-nm blue light, 633-nm red light or 830-nm infrared light. The lights can be used separately or in sequence. Other LED devices include the LIGHTWAVE Professional, Max7 and Medilite.

18.4.2 Pigment-Specific Lasers Pigment-specific lasers are melanin-specific and can be used to lighten or destroy the pigment changes that occur with photoaging including solar lentigines, ephelides, patchy hyperpigmentation, or melasma. These lasers include the high-energy QS laser systems: QS Nd:YAG (532 and 1,064 nm), QS ruby (694 nm), and QS alexandrite (755 nm) [16]. QS laser systems induce thermal necrosis that remains largely confined to the melanosomes with limited spread of coagulative necrosis to surrounding structures [20, 21].

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18.4.3 Vascular-Specific Lasers Vascular-specific lasers target intravascular oxyhemoglobin to treat erythema, flushing, and telangiectasias that commonly occur in photodamaged skin. These lasers also induce collagen remodeling which results in rhytid reduction and improved skin texture. The three primary absorption peaks for oxyhemoglobin are within the visible range of the electromagnetic spectrum at 418, 542, and 577 nm [20]. Vascular-specific lasers include the argon (488–514  nm), APTD (577 and 585 nm), KTP (532 nm), krypton (568 nm), copper vapor/bromide (578  nm), PDL (585–595  nm), and Nd:YAG (532 and 1,064 nm).

18.4.4 Pulsed Dye Lasers PDL selectively target hemoglobin and melanin. For years, physicians who used PDL in the treatment of various vascular lesions noticed significant skin texture improvements in their patients after series of PDL treatment [22]. Histological studies have demonstrated neocollagenesis following PDL treatment. However, the exact role of PDL in collagen remodeling remains controversial. Photorejuvenation with PDL technology is beneficial since it reduces erythema, flushing, and telangiectasias while stimulating collagen remodeling. Hence, PDL improves overall skin tone and color as well as enhancing skin texture and rhytids [16].

18.4.5 Intense Pulsed Light Intense pulsed light (IPL) is a nonlaser broad-spectrum light of multiple wavelengths up to approximately 1,000 nm, with cutoff filters placed to exclude shorter wavelengths, thereby targeting various chromophores. IPL targets both melanin and hemoglobin, and it is commonly used to treat the changes of photoaging including erythema, telangiectasias, and fine textural changes. The term “photorejuvenation” was coined in describing the global improvements in multiple parameters of photoaging that is observed with IPL [1]. This technique is highly sought by patients due to the dramatic improvement of dyspigmentation and vascularity observed. Histological studies show neocollagenesis 6  months after treatment resulting in modest clinical

208

improvement in rhytids [23]. The combination of IPL and aminolevulinic acid photodynamic therapy can increase the efficacy of IPL [16]. IPL has also been combined with RF technology, increasing overall efficacy at lower energies for a safer and more effective treatment.

18.4.6 Infrared Lasers Infrared lasers create thermal energy and stimulate new collagen deposition by targeting dermal water. Infrared lasers used for non-ablative rejuvenation include Nd: YAG (1,320 and 1,064  nm), 1,450-nm diode and the 1,540-nm erbium glass lasers [16]. Cryogen spray or contact cooling cools and protects the epidermis from heat injury. Since infrared lasers specifically target dermal water and the epidermis is preserved, no improvements are seen in dyspigmentation or erythema.

18.4.7 Radiofrequency Radiofrequency (RF) produces a thermal effect when its high-frequency electrical current flows through the skin. Thermal energy contracts, compresses, and thickens the collagen fibers restoring skin laxity and reversing the signs of aging. Unlike lasers in which laser light is converted to heat, RF technology produces an electrical current, which generate heat through resistance in the dermis [6]. RF energy can be applied to tissue between two points on the tip of the probe, bipolar RF energy, or between a single electrode tip and a grounding plate, monopolar RF energy. Thermage and Visage are examples of RF devices [14]. To protect the epidermis, the electrode is cooled before and during the radiofrequency pulse by a cryogen spray device.

18.4.8 Combined RF and Optical Energy Combining RF energy and optical energy produces an electro-optical synergy that can further enhance the clinical outcome of nonablative technologies. Aurora SR system integrates bipolar RF and optical energies. The theory underlying this system is that selective photothermolysis is used to preheat a target tissue, altering its impedance and its susceptibility to a subsequent pulse of RF is increased. The warm tem-

N. Tabatabai and N.S. Sadick

perature of the dermal structures alleviates the directed application of RF energy to dermal chromophores with less impedance. Skin precooling and targeted heating create this optimal condition [15]. Polaris WR uses a combined 900-nm diode laser with an RF energy device. Optical energies are delivered through a bipolar electrode tip with fluences ranging from 10 to 50 J/cm2 and RF energies of 10–100 J/cm3 [15]. While the energies are transferred into the tissue, the RF energy penetrates deep and begins collagen production, addressing superficial rhytids, pigmentation, and vascularity. In addition, the 900-nm diode laser targets intravascular hemoglobin or melanin [24, 25]. RF energy has also been combined with intense pulsed light energy in the same pulse profile, generating electro-optical synergy for enhanced textural changes and skin rejuvenation [26]. The combination increases overall efficacy at lower light energies allowing for safer, more efficient treatments. The theory behind combining the optical and bipolar RF energies is that the combination allows for lower energies with both methods to achieve target heating, thereby increasing safety and reducing discomfort.

18.4.9 Fractional Resurfacing The newest technology to enter the laser arena is fractional resurfacing or fractional photothermolysis [27]. Fractional photothermolysis maintains the short recovery period and favorable risk factor profile of the nonablative systems while increasing the efficacy in treating photoaging [28]. The concept behind this approach is to thermally alter a fraction of the skin, leaving intervening areas of normal skin untouched, which rapidly repopulate the ablated columns of tissue [1]. The 1,550-nm erbium-doped mid-infrared fiber laser, which is mainly absorbed by aqueous tissue, creates a dense pattern of epidermal and dermal microscopic thermal wounds, referred to as microthermal zones (MTZ), sparing islands of viable epidermis and untreated dermis. These islands maintain the skin’s barrier function while speeding reepithelialization [29]. Similar to ablative laser resurfacing, the areas of thermally ablative tissue are repopulated by fibroblast and neocollagenesis and epidermal stem cell reproduction occurs. Fractional photothermolysis increases efficacy compared to nonablative laser resurfacing and has a faster recovery

18  Thermolysis in Aesthetic Medicine: 3D Rejuvenation

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period and minimal side effects as compared to ablative resurfacing. However, neither nonablative laser resurfacing nor fractional resurfacing produces results comparable to ablative laser resurfacing.

Cold packs may be applied immediately after laser treatment to alleviate any further discomfort.

18.5 Nonablative Laser Resurfacing Method

The treatment parameters differ greatly among the various nonablative laser modalities (Table 18.3) [1]. Erythema and minimal edema is the desired clinical endpoint regardless of laser system used and it is correlated directly with optimal clinical outcome. Generally, a minimum of four treatments is required before improvement is seen.

18.5.1 Patient Selection For every patient, the application of the treatment and their skin prototype should be considered. Patients with mild, moderate, and severe rhytids and photodamage are candidates for nonablative technology. Although the downtime and side effects are minimal, the patient’s social context should be considered for any treatment. Dark-skinned and tanned patients should be cautioned for the risk of posttreatment dyspigmentation with the majority of the nonablative laser modalities. Patients should be instructed to avoid the sun and to wear sunscreen after treatment [1]. For any patients with a history of isotretinoin use, it is recommended to wait at least 6 months after the discontinuation of isotretinoin due to reports of impaired wound healing in patients with a history of isotretinoin use [30]. Pregnant women are not treated until after delivery and breastfeeding because of the pain and discomfort during the procedure as well as an increased risk of hyperpigmentation [31].

18.5.2 Preoperative Management Herpes or bacterial prophylaxis is not routinely prescribed before nonablative resurfacing. However, in patients with a history of recurrent herpes infections, a course of oral antivirals, such as acyclovir, staring 1 day before and continuing for 5 days postoperatively is prescribed. For patients with a history of bacterial infections of the facial skin, an oral antibiotic, such as azithromycin, is prescribed [1].

18.5.3 Anesthesia After the skin is thoroughly cleansed and prepped with 70% alcohol, topical anesthesia is applied. Typically lidocaine 30% in a gel base is applied 1 h prior to treatment.

18.5.4 Technique

18.5.5 Postoperative Management There is some mild erythema and edema following treatment, which resolves within several hours. Majority of patients can return to their daily normal activities immediately following treatment.

18.6 Discussion Nonablative rejuvenation technologies have revolutionized the field of cosmetic dermatology, providing safe and effective means for treating the aging skin. A structured approach to utilizing these technologies based on type of rejuvenation that the patient desires is critical to optimize clinical outcome. The spectrum of skin rejuvenation ranges from procedures such as superficial chemical peels and microdermabrasion to laser resurfacing and RF technology. Superficial wavelength rejuvenation technologies are more effective in treating vascular, pigmentary, and pilosebaceous irregularities. Longer wavelength lasers induce more dermal collagen and skin remodeling [6]. The successful approach to photorejuvenation techniques depend heavily on realistic patient expectations and maintenance programs. More thermal energy may be necessary in order to achieve the clinical improvements desired by the individual patient. Serial treatments with these technologies may be necessary in order to achieve improvement associated with neocollagenesis, which can take up to 12 months after the last treatment. Nevertheless, minimally invasive skin rejuvenation techniques will continue to be improved, optimized and technologic advancement and new devices will continue to develop.

N. Tabatabai and N.S. Sadick

210 Table 18.3  Nonablative laser resurfacing systems Laser type Wavelength Vascular Pulsed KTP 532 Pulsed dye 585 LP PDL 595 Infrared Nd: YAG 1,064 1,320 Diode 1,450 Erbium glass 1,540 IPL Quantum SR 515–1,200 Radiofrequency RF, monopolar (Thermacool) RF current bipolar RF current bipolar; RF, bipolar/diode/IPL (Elos, Galaxy, Elite; Syneron) 900 nm; 590–1,200 nm RF current bipolar; RF/red light (ST Refirme; Syneron) 590–1,200 nm RF, unipolar (Accent; Alma RF electromagnetic Laser) radiation RF, bipolar (Accent; Alma RF current bipolar Laser)

Fluence

Pulse duration

Spot size(mm)

15 3 6–8

20 ms 320 mm 6 ms

10 5 10

50 18 8–14 Up to 126

50 ms 200 ms 250 ms 3.3 ms

12 6 6 4

24–28

2.4, 4.0

61.5–63.5 18–100; 20–30; 20–30 100–120 50–250 40–100

References 1. Alexiades-Armenakas MR, Dover JS, Arndt KA (2008) The spectrum of laser skin resurfacing: nonablative, fractional, and ablative laser resurfacing. J Am Acad Dermatol 58(5): 719–723 2. Sukal SA, Geronemus RG (2008) Fractional photothermolysis. J Drugs Dermatol 7(2):118–122 3. Cohen SR, Henssler C, Johnston J (2009) Fractional photothermolysis for skin rejuvenation. Plast Reconstr Surg 124(1):281–290 4. Sadick NS, Makino Y (2004) Selective electro-thermolysis in aesthetic medicine: a review. Lasers Surg Med 34(2): 91–97 5. Anderson RR, Parrish JA (1983) Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 220(4596):524–527 6. Sadick NS (2003) Update on non-ablative light therapy for rejuvenation: a review. Lasers Surg Med 32(2):120–128 7. Fitzpatrick RE, Goldman MP, Satur NM, Tope WD (1996) Pulsed carbon dioxide laser resurfacing of photo-aged facial skin. Arch Dermatol 132(4):395–402 8. Dover JS, Hruza GJ (1996) Laser skin resurfacing. Arch Dermatol 132(4):451–455 9. Waldorf HA, Kauvar AN, Geronemus RG (1995) Skin resurfacing of fine to deep rhytides using a char-free carbon dioxide laser in 47 patients. Dermatol Surg 21(11):940–946 10. Wanner M, Tanzi EL, Alster TS (2007) Fractional photothermolysis: treatment of facial and nonfacial cutaneous

photodamage with a 1,550-nm erbium-doped fiber laser. Dermatol Surg 33(1):23–28 11. Kelly KM, Nelson JS, Lask GP, Geronemus RG, Bernstein LJ (1999) Cryogen spray cooling in combination with nonablative laser treatment of facial rhytides. Arch Dermatol 135(6):691–694 12. Geronemus RG (2006) Fractional photothermolysis: current and future applications. Lasers Surg Med 38(3):169–176 13. Calderone DC, Fenske NA (1995) The clinical spectrum of actinic elastosis. J Am Acad Dermatol 32(6):1016–1124 14. Sukal SA, Geronemus RG (2008) Thermage: the nonablative radiofrequency for rejuvenation. Clin Dermatol 26(6): 602–607 15. Elsaie ML, Choudhary S, Leiva A, Nouri K (2010) Nonablative radiofrequency for skin rejuvenation. Dermatol Surg 36(5):577–589 16. Rostan EF (2005) Laser treatment of photodamaged skin. Facial Plast Surg 21(2):99–109 17. Sauder DN (2010) Light-emitting diodes: their role in skin rejuvenation. Int J Dermatol 49(1):12–16 18. Sadick NS (2008) A study to determine the efficacy of a novel handheld light-emitting diode device in the treatment of photoaged skin. J Cosmet Dermatol 7(4):263–267 19. Weiss RA, McDaniel DH, Geronemus RG, Weiss MA (2005) Clinical trial of a novel non-thermal LED array for reversal of photoaging: clinical, histologic, and surface profilometric results. Lasers Surg Med 36(2):85–91 20. Tanzi EL, Lupton JR, Alster TS (2003) Lasers in dermatology: four decades of progress. J Am Acad Dermatol 49(1):1–31

18  Thermolysis in Aesthetic Medicine: 3D Rejuvenation 21. Kurban AK, Morrison PR, Trainor SW, Tan OT (1992) Pulse duration effects on cutaneous pigment. Lasers Surg Med 12(3):282–287 22. Zelickson BD, Kilmer SL, Bernstein E, Chotzen VA, Dock J, Mehregan D, Coles C (1999) Pulsed dye laser therapy for sun damaged skin. Lasers Surg Med 25(3):229–236 23. Goldberg DJ (2000) New collagen formation after dermal remodeling with an intense pulsed light source. J Cutan Laser Ther 2(2):59–61 24. Jacob CI, Kaminer MS (2005) Skin tightening with radiofrequency. In: Dover JS, Alam M, Goldberg D (eds) Procedures in cosmetic dermatology series: laser skin surgery, vol 2. Elsevier, Philadelphia, pp 43–60 25. Zelickson BD, Kist D, Bernstein E, Brown DB, Ksenzenko S, Burns J, Kilmer S, Mehregan D, Pope K (2004) Histological and ultrastructural evaluation of the effects of a radiofrequency-based nonablative dermal remodeling device: a pilot study. Arch Dermatol 140(2):204–209 26. Sadick NS, Alexiades-Armenakas M, Bitter P Jr, Hruza G, Mulholland RS (2005) Enhanced full-face skin rejuvena-

211 tion using synchronous intense pulsed optical and conducted bipolar radiofrequency energy (ELOS): introducing selective radiophotothermolysis. J Drugs Dermatol 4(2): 181–186 27. Manstein D, Herron GS, Sink RK, Tanner H, Anderson RR (2004) Fractional photothermolysis: a new concept for cutaneous remodeling using microscopic patterns of thermal injury. Lasers Surg Med 34(5):426–438 28. Laubach HJ, Tannous Z, Anderson RR, Manstein D (2006) Skin responses to fractional photothermolysis. Lasers Surg Med 38(2):142–149 29. Hantash BM, Mahmood MB (2007) Fractional photothermolysis: a novel aesthetic laser surgery modality. Dermatol Surg 33(5):525–534 30. Rubenstein R, Roenigk HH Jr, Stegman SJ, Hanke CW (1986) Atypical keloids after dermabrasion of patients taking isotretinoin. J Am Acad Dermatol 15(2 Pt 1): 280–285 31. Tunzi M, Gray GR (2007) Common skin conditions during pregnancy. Am Fam Physician 75(2):211–218

 

Neodym-Yag-Laser Treatment for Hemangiomas and Vascular Malformations

19

Thomas Hintringer

19.1 Introduction Treatment and diagnosis of hemangiomas and vascular malformation is widely discussed and there is no golden standard commonly accepted until now. Various problems in classification exist and lead to misunderstandings or difficulties in an interdisciplinary approach to the problem. Mulliken and Glowacki [1] were the first to propose an accepted classification and differentiated between vascular tumors and vascular malformations. The most common vascular tumor in childhood is hemangioma, which is usually not visible at birth and which starts to grow in the first weeks of life. After a period of proliferation during the first year of life, involution takes place in more than 70% of the hemangiomas within the first decade. Vascular malformations are inborn errors of angiogenesis, which are present at birth and do not have any tendency of regression. A newer classification (ISSVA) includes a more ­differentiated nomenclature, including the vascular flow of the lesion and the origin of tissue. Vascular tumors such as hemangiomas or hemangioendotheliomas are included as well as slow flow and fast flow vascular

T. Hintringer Department of Plastic and Reconstructive Surgery, Hospital of Sisters of Charity, Linz, Austria and Klinische Abteilung für Plastische, Aesthetische und Rekonstruktive Chirurgie, Krankenhaus der Barmherzigen Schwestern Linz Betriebsgesellschaft m. b. H, FN 140108 t Landesgericht Linz Firmensitz Linz, 4010 Linz, Seilerstätte 4, Linz, Austria e-mail: [email protected]

­ alformations. R.I.C.H. (rapidly involuting congenital m hemangiomas) and N.I.C.H. (noninvoluting congenital hemangiomas) seem to be different than normal hemangiomas and are undefined by the ISSVA classification. They are usually fully formed at birth, have a higher flow than hemangiomas, and are GLUT-1 (glucose transporter protein 1) negative whereas the common hemangiomas stain positive to GLUT-1 [2]. A broad spectrum of therapeutic modalities is discussed especially in the treatment of hemangiomas. Some authors recommend only observation of hemangiomas as the first line. Different treatments with corticosteroids, interferon, cryotherapy, compression, or surgical excision have been published. In the last 2 years, propranolol seems to be a new approach to stop the proliferation of hemangiomas and to induce the involution period early after their primary detection. Lasers are well known in the treatment of hemangiomas. The pulsed dye laser is recommended as a golden standard for superficial hemangiomas. KTP, Argon, and Alexandrite lasers are also described as successful options for small and thin lesions. Most of the published articles conclude that laser treatment has no success in treating hemangiomas that are located deep or are thicker than 1 cm. Only a few articles [3–6] suggest using the Neodym-Yag laser for hemangiomas and/or vascular malformations. The intralesional use of Neodym-Yag is described by very few authors [3–7].

19.2 Background Hemangiomas represent the most common type of benign vascular tumors in childhood. A proliferative phase of unknown duration and extent is followed by an

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_19, © Springer-Verlag Berlin Heidelberg 2011

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214 Fig. 19.1  Algorithm of interdisciplinary treatment of hemangiomas and vascular malformations

T. Hintringer

Hemangioma Vasc. MF Growth

Severe

No growth

Minimal

Treatment

Treatment

Observation

Regression or stop

Interdisciplinary (OP at age of 4–6 years)

involutional period that passes into regression in approximately 70% of all cases. Due to the high rate of spontaneous regression, many authors advise not to undertake any treatment. The dilemma of this “wait and see” approach constitute those cases in which sudden and pronounced growth is not followed by complete regression with possible severe aesthetic and functional impairment. To avoid this dilemma, a specific algorithm for the treatment of hemangiomas has been instituted at our department more than 10 years ago, based essentially on early laser treatment when relevant growth is present. A similar algorithm is described by Burns et al. [8]. The author has had experience with the NeodymYag laser for over more than 15 years and has treated over 2,500 patients with hemangiomas or vascular malformations. Laser treatment is one of the many possible options to stop the growth of a proliferating hemangioma or lead to interstitial fibrosis of superficial and deep vascular malformations. To find out the best treatment options for an individual patient an interdisciplinary approach is strongly recommended (Fig.  19.1). Life-threatening lesions such as giant hemangiomas of the airways, mouth or intra-abdominal region as well as arteriovenous

fistulas are contraindications for laser treatment and need a multimodal interdisciplinary treatment using combinations of all known methods. The aim of this chapter is to show the indications and technique of Neodym-Yag lasers in the wide spectrum of different treatment modalities of hemangiomas and vascular lesions. As the treatment is painful, general anesthesia is required in most cases.

19.3 Technique of Neodym-Yag Laser Treatment Neodym-Yag lasers beams have a wavelength of 1,064 nm and can effectively coagulate vessels. Very little laser light is absorbed by melanin. Its depth can reach up to 2 cm due to the intensity of the laser beam. Therefore, a negative side effect is the production of heat, which is why a limit to treatment by direct laser beam is reached when the epidermis is damaged because of scarring. Three different methods of using Neodym-Yad laser for treating hemangiomas or vascular malformations are currently known. As with all medical lasers it is absolutely necessary to comply with safety regulations

19  Neodym-Yag-Laser Treatment for Hemangiomas and Vascular Malformations

as to minimize risks for the patient and the surgeon. Protection of eyes, teeth, and skin as described in operating manuals is imperative. The three different methods are 1. Direct Mode Direct treatment of superficial vascular lesions by using about 7–9 W in pulsed mode will produce small white points on the surface of the hemangioma. The laser beam is focused directly onto the surface of the vascular lesion, setting punctual energy every few millimeters, which has to be instantly followed by cooling. As an alternative, the pulsed dye or KTP laser can be used for superficial parts of vascular lesions with a lower risk of scarring (Fig. 19.2). 2. Transcutaneous Mode This method relates to the extension of the energy of the ND-YAG laser to deeper regions, where other lasers have no effects (1–3 cm), and where it is possible to use higher energy. When using this method it is necessary to protect the epidermis from heat damage. Different cooling devices are available. A very easy and effective method is the use of crystal clear ice cubes placed between the skin and the laser beam. These ice cubes make it easy to focus the laser light to deeper parts of the lesion and cool the surface of the skin simultaneously. It is strongly recommended to use effective cooling and very clear ice cubes, because light has a tendency to be dispersed by air entrapments, making it impossible for focused laser light to reach the depth of the vascular lesion. Pressure on the ice cube and onto the lesion can extend the depth of penetration. This makes it possible to reach parts of the lesion up to 2 or 3 cm of depth. The energy needed by this method is much higher than in direct use (about 30–40 W, continuous mode). It is important to move the ice cube continuously during laser treatment and to replace the ice cube regularly in order to have constant cooling, because the laser beam damages the ice cube very quickly (Fig. 19.3). 3. Intralesional Mode To bring laser light directly into deep vascular lesions, intralesional mode is a good option (Fig. 19.4). The bare fiber of the Neodym-Yag laser is used to puncture the lesion with a small cannula or needle (Fig. 19.5). The tip of the fiber can be visualized easily by sonographic control. It can also be palpated easily by the surgeon. Direct coagulation is performed in a fan-shape movement of the bare fiber with settings of energy of

215

Fig.  19.2  Direct ND-YAG laser treatment of a superficial hemangioma of the upper lid

Fig.  19.3  Transcutaneous mode of ND-YAG laser treatment using crystal clear icecubes for cooling of the surface

216

T. Hintringer

a

b

Bare fibre

Skin Fan shaped Laser therapy

Hemangioma

Fig. 19.4  Schematic drawing of intralesional ND-YAG laser treatment with barefiber (a) and clinical situation (b)

a

b

Fig. 19.5  (a) Barefiber of ND-YAG laser with pilotbeam threaded through a needle for puncturing (b) intralesional ND-YAG with barefiber

19  Neodym-Yag-Laser Treatment for Hemangiomas and Vascular Malformations

217

and vascular malformations. ND-YAG laser treatment can lead to complete disappearance of the lesion but can also be extremely valuable in decreasing the volume of the lesion and improving the quality of the remaining tissue, which can in turn be used for surgical reconstruction.

19.4 Complications The rate of complication is very low, provided that the ND-YAG laser is operated with care and experience. It is strongly recommended to use low energy at the beginning of treatment and to slowly increase the energy until the effect of laser light is visible as small white points in the direct mode, or until decrease of blood flow controlled by duplex sonography is detected in the intralesional mode. Aggressive use of ND-YAG laser has a risk of skin necrosis followed by a visible scar and should be avoided at any time. In the intralesional mode, bleeding from the impact point of the needle can easily be stopped by short coagulation just before removing the bare fiber from the skin surface. When the bare fiber is already removed, compression with cool packs over 5 min will stop bleeding effectively. Ulceration is a very rare complication, which can be caused by aggressive treatment leading to skin necrosis. On the contrary, according to the experience of the author, small preexisting ulcerations of hemangiomas will improve after transcutaneous or intralesional ND-YAG laser treatment.

19.5 Conclusions

Fig.  19.6  Intraoperative songraphic control of intralesional laser therapy (a) preop (b) visualizied barefiber in situ (c) bloodflow immediately after treatment

7–10 W (continuous mode). The decrease of blood flow can be controlled by color-coded duplex sonography immediately after the treatment (Fig. 19.6) [5]. The coagulation effect promotes the involution of hemangiomas and reduces the size of hemangiomas

ND-YAG laser is an effective tool in a multimodal field of various methods dealing with hemangiomas and vascular malformations (Figs.  19.7–19.10). Safety regulations and experience of the surgeon are required to avoid failure. Transcutaneous and intralesional use of ND-YAG enlarge the spectrum of therapy of hemangiomas and vascular malformations and can be used as single treatment as well as in combination with other methods as sclerotherapy, corticosteroids, and others. A multidisciplinary approach for all vascular lesions is strongly recommended to find out the best treatments for every single patient.

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T. Hintringer

a

b

Fig. 19.7  Hemangioma of the nose at the age of 6 months (a) and after 6 ND-YAG laser treatments (transcutaneous and intralesional) at the age of 10 years (b)

a

b

Fig. 19.8  14 year old girl with lymphatic malformation in the neck before (a) and 3 months after a single intralesional ND-YAG laser treatment (b)

19  Neodym-Yag-Laser Treatment for Hemangiomas and Vascular Malformations

a

219

b

Fig. 19.9  Hemangioma of external ear (a) and 3 months after a single ND-YAG laser treatment transcutaneous and direct (b)

a

b

Fig. 19.10  Venous malformation of upperlip and cheek in a 8 months old boy (a) One year after 3 intralesional ND-YAG laser treatments for debulking, followed by surgical resection without any noteworthy blood loss (b)

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References   1. Mulliken JB, Glowacki J (1982) Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg 69(3):412–422   2. Guyuron B, Erikson E, Persing J (2009) Plastic surgery: indications and practice. Saunders Elsevier, Philadelphia, pp 761–777   3. Achauer BM, Celikoz B, VanderKam VM (1998) Intralesional bare fiber laser treatment of hemangioma of infancy. Plast Reconstr Surg 101(5):1212–1217   4. Lippert BM, Godbersen GS (1992) Treatment of hemangioma with the neodymium: ytrium-aluminium-garnet laser (Nd: YAG laser). Laryngorhinootologie 71(8):388–395

T. Hintringer   5. Rosenfeld H, Sherman R (1986) Treatment of cutaneous and deep vascular lesions with the Nd: YAG laser. Lasers Surg Med 6(1):20–23, 50–51   6. Spendel S (2001) Ultrasosund-navigated interstitial ND: Yag Laser coagulation of congenital vascular disorders. Med Laser Appl 16(2):121–127   7. Burns AJ, Navarro JA (2009) Role of laser therapy in pediatric patients. Plast Reconstr Surg 124(1 Suppl): 82e–92e   8. Burns AJ, Navarro JA, Cooner RD (2009) Classification of vascular anomalies and the comprehensive treatment of hemangiomas. Plast Reconstr Surg 124(1 Suppl): 69e–81e

Foam Sclerotherapy

20

Marcondes Figueiredo

20.1 Introduction The word “sclerotherapy” comes from the Greek sklerōsis, meaning “hardening.” Sclerotherapy is a method whereby a sclerosing agent is injected into lower limb varicose veins, damaging the vessel endothelium, obliterating its lumen, and turning the vein into a fibrous cord [1]. Sclerotherapy has been one of the foremost choices of treatment for varicose veins over the past century [2]. Sclerosing agents are available as foam or in liquid form. In 1944, Orbach [3], one of the pioneers of foam sclerotherapy, reported that the introduction of bubbles into the vein displaced blood, improving the therapeutic effect of the sclerosing agent. However, for many years, uncertainty as to the dimensions of the foam bubble and its distribution in the bloodstream limited clinical use of this form of sclerotherapy. In the 1990s, Cabrera [4] introduced a new method of sclerotherapy for truncal varicose veins that consisted of the injection of small bubbles (called a “microfoam” by Cabrera) under vascular ultrasound guidance. Building on this novel approach, authors the world over then began to use foam sclerotherapy in all CEAP classes [5]. This classification was based on clinical manifestation (C), etiologic factors (E), anatomic distribution of disease

M. Figueiredo  Univerisade Federal de Sao Paulo, Sao Paulo, SP, Brazil and Rua Marquez Povoa, 88 CEP 38400–438, Uberlandia, MG, Brazil e-mail: [email protected]

(A), and underlying pathophysiologic findings (P) (Fig. 20.1).

20.2 Mechanism of Action and Foam Preparation When compared with liquid sclerosing agents, foam completely shifted the focus of sclerotherapy, particularly in the treatment of large truncal varicose veins. Foam has several distinctive features: it is solid when within vessels, occupying the space through which displaced blood flowed, and fluid while being injected; it remains within the blood vessel for a substantial amount of time; and minute quantities are able to occupy a large segment of vessel. Two sclerosing agents are currently used in foam sclerotherapy: polidocanol and sodium tetradecyl sulfate. Only the former is approved for use in Brazil (Aethoxysklerol, Kreussler Pharma, Wiesbaden, Germany). Polidocanol is available in several concentrations (0.25%, 0.5%, 1%, and 3%), each more appropriate for a different size of target vein. Polidocanol is considered a detergent-type sclerosing agent. This class of sclerosants works by affecting the surface tension of endothelial cell membranes, denaturing proteins, and inducing cell death. The endothelium is denuded and an iatrogenic thrombus is formed, which ­progresses to definitive sclerosis; the vessel becomes a fibrous cord [2]. Several methods have been described for foam preparation: Monfreaux, double syringe, Turbofoam, Tessari, and the Varisolve® product by Provensis, which has yet to be approved for clinical use. Since 2003, we have used the Tessari method [6] with room air (Fig. 20.2).

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_20, © Springer-Verlag Berlin Heidelberg 2011

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M. Figueiredo

a

b

d

e

c

Fig.  20.1  Types of varicose veins according to the CEAP classification (classification was based on clinical manifestation). (a) CEAP 1. (b) CEAP 2. (c) CEAP 3. (d) CEAP 4 and 5. (e) CEAP 6

20  Foam Sclerotherapy

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Fig. 20.2  Tessari method

20.3 Patient Selection

a

The author uses foam sclerotherapy in varicose veins of all CEAP classes, from spider telangiectasias to large trunk veins.

20.4 Techniques 20.4.1 Telangiectasias For cosmetic reasons, “spider veins” are undoubtedly the most common phlebological complaint in clinical practice. At the present time, the most popular treatment modality in Brazil is liquid sclerotherapy. The author uses 75% glucose to great effect (Fig. 20.3). Polidocanol-based foam sclerotherapy is indicated when liquid sclerotherapy with 75% glucose failed to produce good results or in the presence of concurrent reticular veins, but both methods are combined whenever possible, obliterating the feeder vein with foam and then sclerosing any telangiectasias with 75% glucose in a two-stage procedure (Fig. 20.4). For telangiectasias, the sclerosing foam is prepared with polidocanol 0.25%, using a fluid-to-air ratio of 1:1, i.e., 1 mL of room air is used for every 1 mL of polidocanol. Two syringes (one each 2.5 mL and 5 mL) are connected by a three-way tap, and both plungers are depressed and pulled back vigorously, repeatedly,

b

Fig. 20.3  Patient with spider veins (CEAP class 1). (a) Prior to treatment. (b) After treatment: sclerotherapy with 75% glucose

224

a

M. Figueiredo

b

Fig. 20.4  Patients with reticular veins (CEAP class 2). (a) Before treatment. (b) After foam sclerotherapy

simultaneously, and then in an alternating manner, at least 20 times, pushing the content of one syringe into the other and mixing room air into the fluid to form a froth. After this series of oscillating movements, the stopcock is closed further to restrict the passage of foam and ten more push-pull motions are performed to increase the density of the foam and make bubbles smaller (the target bubble size is 100–150 mm). As the foam must be injected immediately after preparation, strategic points for injection must be chosen and demarcated prior to compounding. Injection must proceed slowly and carefully enough to allow visualization of the foam passing through the entire venous meshwork to be obliterated. A single dressing is placed over the needle puncture to prevent retrograde flow and/or bleeding. Compression bandages are not used in these cases, since inordinately high pressures (>70  mmHg) would be required to compress telangiectasias, which is of course not feasible, particularly in the thigh.

20.4.2 Reticular Veins Alongside telangiectasias, reticular veins are a frequent complaint in clinical practice due to aesthetic considerations. Up until 5 years ago, the author’s only approach to these cases was micropuncture phlebectomy under local anesthesia with adjunctive liquid sclerotherapy (75% glucose). As expertise has improved, foam ­sclerotherapy was adopted in a substantial portion of cases. The procedure follows the same technique used in treatment of telangiectasias, apart from polidocanol concentrations, which may be 0.25% or 0.5% depending on varicosity size; foam preparation also follows the same sequence described above. In these cases, however, transcutaneous phleboscopy is performed before the procedure to guide needle placement (Fig. 20.5), and inelastic bandages (Atadress, Atamed, São Paulo, SP, Brazil) are used to provide compression. Compression pads are occasionally used to

20  Foam Sclerotherapy

225

improve vein collapse and reduce thrombus formation. Treatment is performed over several sessions with 2–5 mL of foam injected during each visit. A follow-up appointment for assessment of possible thrombus formation and drainage is scheduled for 8–10  days postprocedure (Fig.  20.6), and a second follow-up visit is arranged for 4  weeks after sclerotherapy to assess the need for further foam or glucose application. Dated before-and-after photos of all patients are taken for safety purposes and to help patients assess treatment results.

20.4.3 Sclerotherapy of Truncal Varicose Veins (CEAP 3, 4, 5, and 6)

Fig. 20.5  Transcutaneous phleboscopy used to identify reticular veins in the lower limb

Sclerotherapy is appropriate for patients with greater or lesser saphenous trunk involvement. In our practice, the patient is placed in the Trendelenburg position and the great or small saphenous vein is mapped by ultrasound at a distance of 15–20 cm from the saphenofemoral or saphenopopliteal junction. Ultrasound-guided venipuncture is performed with a 20  G × 1.88 in Insyte®

a

b

c

d

Fig. 20.6  (a) Patient with reticular veins (b) 7 days after treatment with foam sclerotherapy – chemical phlebitis. (c) Clinical aspect of chemical phlebitis following thrombus drainage. (d) Long-term posttreatment result

226

M. Figueiredo

Table 20.1  Volume and concentration of polidocanol by target vein Vein Great saphenous vein Small saphenous vein Collaterals Perforators

Volume injected/ visit (mL) 8–10

Polidocanol concentration (%) 3

5

1 or 3

5 1–2

1 1

needle. Access to collateral veins is obtained with a 25 gauge Butterfly® type infusion set, and a 22 gauge × 1¼ in needle is used for insufficient perforating veins, both under ultrasound guidance as well. Foam was prepared as described by Tessari [5], at a polidocanolto-gas ratio of 1:4. An overview of foam volumes and polidocanol 3% concentrations is shown in Table 20.1. Foam is injected in bolus form, under constant vascular ultrasound guidance. No more than 10 mL of foam is injected per visit; depending on patient improvement, up to three further applications may be performed (once every 30 days). Before the procedure, the limb is kept elevated for 15–20 min to empty the superficial venous system of the leg. When perforating veins are present, the patient is asked to keep the ipsilateral foot dorsiflexed so as to avoid the passage of significant amounts of foam into the deep venous system. After the procedure, the limb is wrapped in 12 cm wide inelastic bandages (Atadress, Atamed, São Paulo, SP, Brazil), which are kept on for 3–5 days. After bandage removal, we prescribe 3/4 or 7/8 length 30–40 mmHg elastic compression stockings (Select Comfort, SIGVARIS, Jundiaí, SP, Brazil) to be worn for 3  months. The patient is discharged home with instructions to avoid strenuous activity and no restrictions on ambulation.

20.4.4 Truncal Varicose Veins: CEAP 3 In Brazil, operative treatment of patients with truncal varicose veins is indicated, as local vascular surgeons have acquired outstanding expertise in the management of these cases (Fig. 20.7). In these cases, there is a substantial risk of extensive thrombophlebitis and formation of large hyperpigmented areas, with significant pain and patient discomfort (Fig.  20.8). Foam

sclerotherapy is, therefore, performed in CEAP class three patients with recurrent varicose veins (neovascularizaton in the groin after stripping) and hard-to-reach inferior gluteal or femoropopliteal varicosities, and as adjunctive therapy for residual varicose veins.

20.4.5 Advanced Chronic Venous Insufficiency: CEAP 4, 5, and 6 Foam sclerotherapy is perhaps most appropriate in patients with lipodermatofibrosis of the distal third of the leg, hampering surgical intervention, as “the foam gets where the scalpel doesn’t” [7]. In addition to using saphenous trunk and collateral vein sclerotherapy, a novel approach was developed to treat CEAP class 6 patients: crossectomy and foam. Crossectomy and foam, or foam crossectomy, was developed with a specific population in mind: older patients with chronic leg ulcer, a normal deep venous system, a great saphenous vein diameter of approximately 10  mm near the saphenofemoral junction and a small saphenous vein diameter of >6–7 mm. The procedure is performed under local anesthesia (20 mL of 2% lidocaine without epinephrine diluted to 40  mL with a diluting solution). Even though this procedure can be performed in an outpatient setting, for this study it was carried out in hospital to ensure adequate patient monitoring. Superficial veins were emptied by raising the leg, using a catheter or no. 8 probe inserted cranio-caudally into the great saphenous vein down to the knee and into the small saphenous vein to the mid-calf level. After cannulation, the leg was kept in an elevated position for about 15  min POL foam (Aethoxysclerol, Kreussler, Pharma, Wisbaden, Germany), compounded as described by Tessari et al. [6], was injected in two concentrations: 2 mL of 3% POL and 8 mL of air into the great saphenous vein, and 1 mL of 2% POL and 4 mL of air into the small saphenous vein. The catheter was then withdrawn and the saphenous vein was ligated. The wound was closed in a layered fashion and the leg was wrapped in inelastic bandages (Atadress, Atamed, São Paulo, Brazil). Patients were discharged from the hospital 2 h after the procedure. All were able to walk and resume their normal routine, although physical activity was restricted for 30 days. A follow-up visit was scheduled 7–10 days postprocedure for removal of sutures and routine vascular ultrasound examination to rule out deep vein thrombosis.

20  Foam Sclerotherapy

a

c

Fig. 20.7  (a–c) Patients with truncal varicose veins (CEAP class 3)

227

b

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M. Figueiredo

a

b

c

Fig.  20.8  (a) Hyperpigmentation following treatment of truncal varicose veins with foam sclerotherapy. (b) Pretreatment. (c) Hyperpigmentation 1 year after treatment

Patients also received instructions on wound care: washing with soap and water, applying a polyhexanide agent (Aquasept, Walkmed, Santos, Brazil) to the wound bed, and dressing with gauze. Inelastic bandages were worn for 7–10 days, after which 30–40 mmHg below-knee

graduated elastic compression stockings were prescribed, to be worn until ulcer healing. Patients were also advised to wear below-knee compression stockings (20–30 mmHg or 30–40 mmHg) indefinitely after ulcer healing.

20  Foam Sclerotherapy

a

b

229

Surgery always precedes sclerotherapy: large varicose trunks are excised and a vein stump is cannulated with a catheter no. 8 for foam injection. The leg is then wrapped in traditional inelastic bandages. A word about the contrast between vascular ultrasound results, the clinical status of patients, and ulcer healing is in order. Early in the author’s experience, it was believed that treatment success could only be achieved with complete occlusion. However, over time, it was learned that some patients experience clinical improvement even in the presence of some degree of reflux or of an ulcer that has not healed completely (Fig. 20.11). Geux [8] has made a similar observation regarding healed ulcers in the presence of reflux in the saphenous vein trunk. Therefore, sclerotherapy should only be repeated in cases with significant reflux associated with clinical worsening or reopening of the venous ulcer. It is clear that the proposed treatment is a palliative measure, not a cure for chronic venous disease. However, among the available alternatives, this was a feasible and technically simple method that addressed the needs of this specific group of patients, namely elderly patients with comorbidities.

20.5 Complications Fig. 20.9  (a) Pretreatment patient with CEAP class 6 varicose veins and ulceration. (b) After treatment

Crossectomy and foam was indicated for several reasons: The choice of a diameter ³8–10 mm for the saphenous vein at the saphenofemoral junction is explained in part by the difficulty of producing an effect on a thick-walled, large-caliber vein with foam. Second, ligation itself hinders the passage of foam into the deep venous system. Further advantages include the ability to palpate the catheter and the fact that the vein is easier to empty, which increases the effectiveness of the foam (Fig. 20.9).

20.4.6 Combination Sclerotherapy and Surgical Treatment Sclerotherapy is indicated as an adjunct to surgical treatment in cases of large varicose veins with lipodermatosclerosis (Fig.  20.10). Management of these patients is best approached on a case-by-case basis.

In cases of telangiectasias and reticular veins, the most common complication of foam sclerotherapy has been thrombophlebitis. In such cases, 7–10 days of drainage is used to improve hyperpigmentation and relieve pain (Fig.  20.12). Visual or respiratory disturbances and thromboembolism have not been observed by the author. This low rate of complications may be explained by the small volume of foam injected during each visit (2–5 mL). Obliteration of trunk veins is the most fearsome application of foam sclerotherapy, due to the large volume of foam required and the large diameter of the affected vessels. There is a wealth of literature on the complications of foam sclerotherapy, particularly venous thromboembolism (VTE) [9, 10]. In these studies, the incidence of VTE has been less than 1%. None of the author’s patients has ever experienced severe complications after foam sclerotherapy. The most frequent adverse events have included thrombophlebitis and hyperpigmentation, the former often requiring and improving satisfactorily with micropuncture or needle aspiration drainage. Hyperpigmentation fades over

230 Fig. 20.10  (a, b) Patients with truncal varicose veins associated with dermatofibrosis

M. Figueiredo

a

time and the discoloration improves within 12 months of the procedure (Fig. 20.12). The author has not encountered a case of VTE requiring anticoagulation after foam sclerotherapy. Symptomatic treatment of superficial thrombophlebitis with nonsteroidal anti-inflammatory drugs and application of local heat has sufficed in our practice. The other

b

usual complications of visual disturbance, respiratory difficulty, and allergic reaction have not occurred. Early in the author’s experience, a single case of posttherapy ulceration occurred due to injection of foam prepared with sclerosing agent at a higher concentration than recommended for the target vein. The resulting ulcer healed after 3 months (Fig. 20.13).

20  Foam Sclerotherapy

a

231

b

c

Fig. 20.11  (a) Patient (CEAP class 6) with ulcer pretreatment. (b) Healed ulcer following treatment. (c) Posttreatment vascular ultrasound image showing presence of reflux not affecting clinical results

232

M. Figueiredo

a

a

b

b

c

Fig.  20.13  (a) Pretreatment varicose ulcer. (b) Healed ulcer following foam sclerotherapy and 1 month of clinical treatment

results. In the author’s view, a bright future is in store for this simple, affordable, and accessible treatment.

References

Fig. 20.12  (a–c) Patient with spider varicose veins treated with foam sclerotherapy: hyperpigmentation resolved spontaneously after 12 months of treatment

20.6 Conclusions In its brief history, foam sclerotherapy has proved to be a stellar treatment choice in certain stages of venous insufficiency, providing cost reductions and unprecedented

1. Maffei FH, Lastória S, Yoshida WB, Rollo HA (2002) Doenças vasculares periféricas, 3rd edn. Médica e Científica, Rio de Janeiro 2. Garcia Mingo JG (2003) Escleroterapia: Cómo? Quando? Por qué? Valencia 3. Orbach EJ (1944) Sclerotherapy of varicose veins. Am J Surg 66:362–366 4. Cabrera J, Cabrera A Jr (1995) Nuevo método de esclerosis en las varices tronculares. Patol Vasc 4:55–73 5. Bergan JJ, Eklof B, Kistner RL, Moneta GL, Nicolaides AN, International ad hoc committee of the American Venous Forum (1996) Classification and grading of chronic venous disease in the lower limbs. A consensus statement. Eur J Vasc Endovasc Surg 30:5–11 6. Tessari L, Cavezzi A, Frullini A (2001) Preliminary experience with a new sclerosing foam in the treatment of varicose veins. Dermatol Surg 27(1):58–60

20  Foam Sclerotherapy 7. Figueiredo M, Araújo S, Barros N Jr, Miranda F Jr (2009) Results of surgical treatment compared with ultrasoundguided foam sclerotherapy in patients with varicose veins: a prospective randomized study. Eur J Vasc Endovasc Surg 38(6):758–763 8. Geux JJ (1995) Indications for the sclerosing agent polidocanol: response. Dermatol Surg 21(1):106–107

233 9. Jia X, Mowatt G, Burr JM, Cassar K, Cook J, Fraser C (2007) Systematic review of foam sclerotherapy for varicose veins. Br J Surg 94(8):925–936 10. Guex JJ, Schliephake DE, Otto J, Mako S, Allaert FA (2010) The French polidocanol study on long-term side effects: a survey covering 3,357 patient years. Dermatol Surg 36 (Suppl 2):993–1003

 

Facial Laser Hair Removal

21

Benjamin A. Bassichis

21.1 Introduction As governed by cultural norms, excess hair, especially on the face, is a very common and often embarrassing issue for many patients. In the past century, unwanted hair has been traditionally treated with many different modalities that were slow, tedious, painful, imprac­tical, and resulted in poor long-term efficacy. Conse­quently, there has been a public demand for novel, rapid, reliable, safe, and affordable hair removal techniques. In the last couple of decades, a number of laser and light-based technologies have been developed for hair removal that specifically target hair follicles and allow for the potential treatment of large areas with long-lasting results. The quest for truly permanent photoepilation, the ability to treat white hairs, and dar­ker skinned patients are the current goals for improve­ment in this evolving field. Laser hair removal works by sending a beam of laser light to a group of hair follicles. The light energy causes thermal injury to the follicles. This occurs because laser light is converted into heat as it passes through the skin and is absorbed in the target pigment melanin found in the hair follicle. This process is called selective photothermolysis [1]. It is selective because it targets only the hair and not the skin. The surrounding

B.A. Bassichis  Advanced Facial Plastic Surgery Center, 14755 Preston Road, Suite 110, Dallas, TX 75254, USA and Department of Otolaryngology – Head and Neck Surgery, University of Texas – Southwestern Medical Center, Dallas, TX, USA e-mail: [email protected], www.advancedfacialplastic.com

skin is usually cooled via several methods including gels, cryogenic sprays, or a cooling tip. Hair grows in cycles. Anagen is the active growth phase, catagen is the transition phase, and telogen is the resting phase. The laser is effective only in the active growth or anagen phase, during which time the hair has an abundance of melanin and the hair follicles are easily targeted. When the temperature in a hair follicle reaches a high enough level during its active growth phase, the treated hair structures are disabled, thus inhibiting hair regrowth. The laser beam finds the hair follicles by targeting the melanin pigment that gives skin and hair dark coloration. Therefore, the ideal candidate for laser hair removal has dark hair and light skin. These patients will have more significant photoepilation results in fewer treatments than patients with red, white, gray, or true blond hair. The laser light is also attracted to the melanin in the skin, so individuals with suntans or dark skin types have an increased risk for discoloration of pigment and other side effects with most types of lasers, making this category of patients a treatment challenge. However, new laser technologies, especially the YAG lasers, have made it possible for people with many skin color and hair color combinations to enjoy the benefits of laser hair removal. These newer lasers have been designed to safely treat patients of all skin types [2]. Excess facial hair is a common issue in both men and women for cultural, social, cosmetic, or psychological reasons. Unwanted facial hair can result in feelings of embarrassment or emotional burden that can negatively affect the quality of life for affected individuals. Hirsutism is an excess of thicker darker hairs in a male pattern of distribution where they are normally thin or absent in the female. Often caused by

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_21, © Springer-Verlag Berlin Heidelberg 2011

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B.A. Bassichis

Table 21.1  Fitzpatrick skin types and recommended hair removal devices Skin type I

Skin color White, freckled

Tanning response Always burns, never tans

II

White

III IV

White to olive Brown

Usually burns, tans with difficulty Mild burn, average tan Rarely buns, tans easily

V

Dark brown

VI

Black

Very rarely burns, tans very easily Does not burn, tans very easily

endocrine disorders leading to excessive androgen levels or by hair follicles that are more sensitive to normal levels of androgens, the excess facial hair can be treated by laser hair removal and/or medical antiandrogen therapy. Women frequently experience unwanted facial hair of varying etiologies on the upper lip, chin, sideburn or eyebrow areas. Men often wish to rid themselves of unwanted hair between their eyebrows or on other parts of their face, including areas affected by pseudofolliculitis barbae. There are several laser and laser-like devices currently used for hair removal. These include, but are not limited to: Ruby laser – including the EpiTouch or the Epilaser Alexandrite laser – such as the Candela GentleLase Plus Light-based or intense pulsed light (IPL) devices – for example, the Palomar Starlux Diode laser – such as the Light Sheer Long Pulse Nd: YAG laser – for example, the Candela GentleYAG These are all effective, fast, comfortable, and safe for permanent hair removal. Each hair removal system has a specific set of advantages and disadvantages depending on the skin color and hair color for the particular laser hair removal candidate. A good laser practitioner can achieve excellent results with a wide range of skin types, hair types, and colors. A general paradigm (Table  21.1) to follow for selecting the best laser for your patients would be to treat clients with light hair or thin hair, and Fitzpatrick skin types I–II with radiofrequency technology, 694 nm Ruby lasers or 755  nm Alexandrite lasers. Patients with brown and medium thickness hair, who are

Recommended hair removal device Radiofrequency, Ruby (694 nm), Alexandrite (755 nm) IPL, Radiofrequency, Ruby (694 nm), Alexandrite (755 nm) IPL, Alexandrite (755 nm) IPL, 800 nm diode or the 1,064 nm Nd:YAG Laser Diode (800 nm), Nd:YAG (1,064 nm) Diode (800 nm), Nd:YAG (1,064 nm)

Table 21.2  Variables involved in photoepilation Wavelength Fluence Depth of penetration Pulse duration Spot size (beam characteristics) Pulse interval Cooling

Fitzpatrick types II–IV are best treated with the 755 nm Alexandrite or broad wavelength spectrum 515– 1,200 nm IPL devices. The black hair, coarse texture hair patients with Fitzpatrick Skin Phenotypes IV–VI are optimally treated with 800  nm Diode or the 1,064 nm Nd:YAG Laser [3, 4]. There are also several factors (Table  21.2) that a laser technician can control to customize treatments for efficacy, safety, and comfort: • Pulse length – long pulsed lasers are considered safest • Fluence – selection of energy levels can be varied for skin type • Delay – the time in between pulses of light affects how much the skin and hair follicle are allowed to cool off • Spot size – affects the speed and penetration of the laser. A larger spot penetrates deeper. A good selection of spot sizes helps the technician reach the hair at the depth at which it grows • Cooling – the surrounding skin may be protected by a cooling gel, spray, or cooled tip pressed against the skin Patients who are not ideal candidates for laser hair removal are those with red, white, gray, or very

21  Facial Laser Hair Removal

light blond hair, those who presently or have recently used Accutane or Bactrim, those taking photosensitizing medications, those who are tanned or very dark skinned (except when using a Nd:YAG laser), and those who are pregnant. Anabolic steroids should certainly not be taken unless medically necessary, as these can increase male-pattern hair growth in some cases. Medicines which inhibit hair growth (for example, spironolactone, Diane-35 birth control pills, Euflexxa, Androcur, and Vaniqa cream) might slightly reduce the pigment in hair roots and make laser treatments less efficient, but this seldom interferes with the overall effectiveness of the treatment. Laser hair removal can be while on these medications, at the patients’ request. Even if a patient is not an “ideal candidate” they may still enjoy some of benefits of laser hair removal. Early in the evolution of the procedure, patients with Fitzpatrick skin types V and VI were not candidates for laser hair removal, and even patients with skin types III and IV were considered high risk. However, innovations in laser technology have permitted more effective hair removal in a broader spectrum of patients, including the more challenging suntanned and Fitzpatrick skin phenotypes IV–VI. Long pulse Nd:YAG lasers have been shown to effectively treat darker skin types, including patients of Afro-American, Asian, Hispanic, Mediterranean, Euro­pean, and Middle Eastern heritages. The design of this laser, with deeper penetration and minimal scattering of laser energy, allows treatment of most skin phenotypes up to and including African American skin types and people with tanned skin. If a traditional laser hair removal device is used on darker skin types, it can result in serious burning or loss of skin pigment (hypopigmentation). However, by utilizing a long pulse Nd:YAG, these patients can be treated with confidence. Fitzpatrick skin type VI can be treated with the Nd:YAG lasers. However, there must be a differentiation between the hair and skin colors to proceed safely. The hair color must be darker than the skin color for effective photoepilation. Additionally, caution should be exercised when treating Asian skin, as excess precooling of the skin may cause hyperpigmentation. Because hair that is naturally blonde, light red, gray, or white does not have enough pigment in the roots, it cannot be reliably treated with any type of laser at this time [3, 5].

237

21.2 Technique 21.2.1 Pretreatment Recommendations 1. Avoid the sun, tanning creams, and tanning salon for 4–6 weeks before and after treatment regimen. A tan can interfere with the effectiveness of the treatment and possibly even cause complications. Patients should wear broad spectrum (UVA and UVB) sunblock with an SPF of 25 or higher before, between, and after treatments. 2. When treating patients with darker skin tones, a bleaching cream may be started 4–6 weeks before treatment to optimize results. 3. The area to be treated should be shaved or trimmed the day before or the morning of treatment. Shaving prior to treatment also allows the patient to shape the exact area they desire for treatment – this is sometimes very useful in areas such as the hairline and sideburns, and bikini line. Excess hair above the surface of the skin absorbs and wastes laser energy, and reduces the amount of energy that reaches the hair root, where it is most effective. Excess hair above the surface of the skin also increases the chance of burning or irritating the skin. 4. Electrolysis, tweezing, plucking, threading, sugaring, or waxing hair must be stopped for at least 2–3 weeks prior to treatment. Hair follicles which do not have hair shafts in them to absorb laser energy will not be treated by the laser energy. 5. If a patient has a history of perioral cold sores or genital herpes in the treatment zone, prophylactic pretreatment with antiviral therapy (Acyclovir, Valtrex, or Famvir) should be prescribed. 6. The skin should be thoroughly cleaned and dried, removing any makeup, creams, oils, or topical anesthetics before laser treatments. 7. It may helpful to take Tylenol and/or Advil a couple hours prior to treatment. Some women find they are less sensitive after their menses and should schedule their treatment sessions accordingly. 8. You should engage in a detailed and honest discussion of desired results and expected improvements with each patient. Together you can decide if laser treatment is the best option. 9. The most important step in laser hair removal is the skin patch test. The results of skin patch testing determine the settings for the laser and the safety profile. Perform testing in a low-visibility area with

238

the same skin type as the area intended for ­treatment. If possible, allow at least 3 days before reexamining the site to assess for efficacy and for a reaction. If sufficient energy is delivered and absorbed, a generalized hyperemia reaction with mild focal swelling is visible after 3–5 min. Increase the fluence for the particular skin type, and note the patient’s pain reaction until the hyperemia reaction is observed. For light or thin hair, the reaction may be minimal even at high settings. Note the laser setting for each type of treated area. Patients have described the sensation from laser hair removal as discomfort rather than pain. After the laser hair removal treatment, patients can expect the treated area to be red and feel similar to a sunburn. For some patients, a topical anesthetic may be used prior to treatment. Although it should be mentioned that some research has shown that topical anesthetics may decrease the effectiveness of treatment by decreasing blood flow to the follicles [3]. The number of treatments required depends upon the patient’s skin color and coarseness of the hair. At minimum, 2–3 treatments are required as the process is only effective on hair during the hair growth cycle. Repeat sessions will be necessary to treat these follicles as they re-enter the anagen phase. Most laser practitioners report treatments at 4–8-week intervals or at the first signs of hairs regrowth [6].

21.2.2 Posttreatment Recommendations 1. After the treatment, the patient may have redness or bumps in the treatment area. Cold compresses will alleviate this. 2. Keep skin moisturized. It is not be uncommon for the treated skin to be slightly drier after treatment and to require more moisturizer. 3. Avoid the sun and tanning salon. Do not use tanning creams between treatments. 4. Use sun block of SPF 25 or higher. 5. The only other acceptable hair removal method during the treatment series is shaving, if needed. 6. Tweezing, plucking, threading, waxing, and sugaring should be avoided because they can reduce the effectiveness of subsequent treatments. 7. Hair shafts will be released from hair follicles in the treated area for a week or two after the treatment. Gentle exfoliation or shaving the areas is fine.

B.A. Bassichis

8. Blistering or scaling after laser hair removal is uncommon, but usually resolves over a few days with Polysporin cream or hydrocortisone several times a day. 9. Makeup may be used if needed [7].

21.3 Complications Most complications of laser hair removal are generally temporary. Special considerations are important when lasers are used on darker skin tones to allow for safe and effective therapy. Hyper- and hypopigmentation are the most common side effects, occurring in 10–20% of treated individuals, and usually resolves within 6 months without any intervention. Mild edema lasting for 12–36  h is common posttreatment. Bland emollients and medium-strength topical corticosteroid lotions can be applied in this setting. Blistering is usually superficial and resolves without scarring. The following complications are also possible: pruritis, pain, tingling, or a feeling of numbness, crusting or scab formation on ingrown hairs, bruising, redness, swelling, infection, and temporary hyper- or hypopigmentation. Scarring may also occur, but this is usually only a consequence when treated with improper fluences and inappropriate skin cooling [8]. Caution is advised when treating around the eye as ocular injury can occur even when light is delivered through the intact eyelid and sclera combined. Even the insertion of laser-protective eye shields over the cornea does not provide complete safety because they cover only the anterior surface of the globe. IPL sources do not carry this risk because of the biologic nature of this technology. Laser hair removal has not been studied long enough to permit a full assessment of its long-term health effects. However, short-term data indicate that laser hair removal is a safe procedure when the appropriate precautions are taken.

21.4 Discussion One of the greatest advantages of laser hair removal is speed of treatment in conjunction with long-lasting results. For example, treating the back with laser hair removal only takes about an hour, while a full back with electrolysis usually takes 125  h. Another advantage

21  Facial Laser Hair Removal

a

239

b

Fig. 21.1  (a) A 28-year-old Indian female before treatment. (b) After six treatments with Nd:YAG laser

a

b

Fig. 21.2  (a) A 33-year-old Mediterranean woman before treatment. (b) After six treatments with Nd:YAG laser

of laser hair removal is that if hairs that do grow back, they are typically finer in texture. Photoepilation, when properly used, offers clear advantages when compared with older, traditional techniques. Although an ever-increasing number of published studies have confirmed the safety and shortand long-term efficacy of laser hair removal, the technology still has limits and risks.

While permanent hair removal is the goal of therapy, some patients may experience hair regrowth that is usually finer and lighter in color. In addition, longlasting laser hair removal typically requires multiple treatments, which can make it more costly. Possible adverse side effects, though uncommon, include damage to the surrounding healthy tissue in the form of scars, burns, redness, pigment changes, and ­swelling.

240

Most complications are generally temporary. Special considerations are important when lasers are used on darker skin tones to allow for safe and effective therapy.

21.5 Conclusions The evolution of new technologies has improved the clinical efficacy of laser hair removal (Figs. 21.1 and 21.2) and increased understanding of hair biology. With the recent FDA approval of lasers for tanned and darker skin types, long-term hair removal is now a realistic goal in the majority of individuals. Newer radiofrequency technologies might address the difficult issue of white and light blond hair phenotypes; however, their exact role in the laser hair removal armamentarium remains to be further determined. Until then, current laser treatments provide gratifying and effective results.

B.A. Bassichis

References 1. Anderson RR, Parrish JA (1983) Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 220(4596):524–527 2. Goldberg DJ, Silapunt S (2001) Histologic evaluation of a millisecond Nd: YAG laser for hair removal. Lasers Surg Med 28(2):159–161 3. Sadick NS (2004) Laser hair removal. Facial Plast Surg Clin North Am 12(2):191–200 4. Fitzpatrick TB (1988) The validity and practicality of sunreactive skin types I through VI. Arch Dermatol 124(6):869–871 5. Dierickx C, Alora MB, Dover JS (1999) A clinical overview of hair removal using lasers and light sources. Dermatol Clin 17(2):357–366 6. Wanner M (2005) Laser hair removal. Dermatol Ther 18(3):209–216 7. Dierickx CC (2002) Hair removal by lasers and intense pulsed light sources. Dermatol Clin 20(1):135–146 8. Nanni CA, Alster TS (1999) Laser-assisted hair removal: side effects of Q-switched Nd: YAG, long-pulsed ruby, and alexandrite lasers. J Am Acad Dermatol 41(2 Pt 1): 165–171

Laser Treatment of Telangiectasias

22

Alia S. Brown and David J. Goldberg

22.1 Introduction The advent of lasers began in 1951, followed shortly thereafter was the first medical application by Goldman et al. in 1963 [1]. Now laser medicine has been revolutionized with selective photothermolysis. This occurs when the laser or energy source targets specific chromophores such as melanin, hemoglobin, and water, thus minimizing damage to the surrounding tissues. In the treatment of facial telangiectasias, the chromophore is intravascular hemoglobin and its derivatives methemoglobin and deoxyhemoglobin (Fig.  22.1). Various yellow light lasers have been used over the past decade in an attempt to eradicate facial telangiectasia. These lasers belong to one of two categories that exist at either end of a spectrum – high power, short pulse, and large spot size, or low power, long exposure, and small spot size [2]. Facial telangiectasias are a common aesthetic problem in millions of people worldwide affecting 15% of

A.S. Brown (*) Skin Laser & Surgery Specialists of New York and New Jersey, New York, NY, USA e-mail: [email protected] D.J. Goldberg Skin Laser & Surgery Specialists of New York and New Jersey, New York, NY, USA and Mount Sinai School of Medicine, New York, NY, USA and UMDNJ-New Jersey Medical School, Newark, NJ, USA and Fordham University School of Law, New York, NY, USA

adults and 2% of children. In children they are referred to as spider telangiectasias due to their radial arrangement of vessels from a central feeding arteriole. Primarily they occur in Fitzpatrick skin types I–III. They consist of erythematous to violaceous dilated tiny linear cutaneous vessels measuring 0.1–1.0 mm in diameter [3]. Location is usually the mid face, and may be the result of actinic damage, metabolic or connective diseases, rosacea, oxidative free radicals, hyperestrogen, alcohol, chronic corticosteroid use, trauma, or Hereditary Hemorrhagic Telangiectasia (Osler Weber Randu). The treatment of facial erythema or telangiectasias is one of the most frequent cosmetic requests. When treating facial telangiectasias there are several important factors to consider such as vessel size, depth, location, quantity, and Fitzpatrick skin type. Various forms of treatment have been tried with varying success including electrodessication, cryosurgery, and sclerotherapy. These methods have fallen out of favor due to their unpredictable side effect profile. With the constant advancement of laser therapy, many lasers have been tried over the years. The earliest attempts were tried using CO2 and argon lasers, however abandoned due to scarring and pigmentary alteration. Facial telangiectasias have been successfully treated with a variety of laser wavelengths. Shorter wavelengths (532 nm) are more effective in treating smaller vessels; longer wavelengths (1,064 nm) are more effective in treating larger vessels, however, have a higher complication rate. With the advancement of laser medicine it became possible to isolate the absorption spectrum of ­oxyhemoglobin

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_22, © Springer-Verlag Berlin Heidelberg 2011

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242 Fig. 22.1  Hemoglobin absorption curve

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using it as a target chromophore. Oxyhemoglobin and its derivatives methemoglobin and deoxyhemoglobin are all targeted in treating telangiectasias. Using oxyhemoglobin as the predominant chromophore, energy is transferred to heat and released, causing vessel wall damage. Wavelengths that correspond to the absorption spectrum for hemoglobin are the most effective; however, this absorption spectrum is shared with melanin which can create competition amongst targets. Selective thermolysis may be achieved using a pulse duration equivalent to the thermal relaxation time. A short pulse duration is less efficacious while longer pulsed durations cause surrounding tissue damage. Patients with rosacea, which is dilation of tiny cutaneous vessels or Poikiloderma of Civatte, a combination of dyschromia, atrophy, and telangiectasias, frequently seek treatment of these conditions. Facial telangiectasias respond well to laser and light-based treatment.

22.2 Intense Pulse Light and Broad Band Light Therapy Intense Pulse Light (IPL) therapy may range between 420 and 1,400  nm in single, double, or triple pulses (Fig. 22.2). It is polychromatic broadband light with normal fluences and pulse durations ranging between 10–45 J/cm2 and 2–25 s in duration. IPL devices have a large spot size (150–828 mm2) and may be used to treat

large surface areas. Different manufacturers make the IPL device with subtle differences being hand piece size, the presence of cooling, and filtering plates which can selectively target specific chromophore. No topical anesthetic is required; however, coupling gel is applied to the skin to minimize epidermal damage and to enable the treatment of deeper target tissues. Light devices have various optical filters used to selectively target specific wavelengths of light for a more optimal treatment [3, 4]. Usually more than one treatment session is required and there is virtually no downtime with this procedure, however there may be some expected transient posttreatment erythema. Unwanted side effects and risks include blistering and postinflammatory hyperpigmentation occurring with overzealous fluences and settings. Hyperpigmentation may also be encountered when treating darker skin or very tanned patients, to avoid this, using a filter with a longer wavelength which bypasses the absorption peak for melanin along with a longer pulse duration is more effective. This procedure has easy tolerability and a relatively low side effect profile [4]. In a study by Ross et al. [3], they did a comparison between IPL and traditional laser treatments examining temperature profiles for monochromatic and broadband light sources. In their results, they determined all three (IPL, 532 nm laser, and 595 nm laser) are capable of achieving a reduction in ectasias and hyperpigmented macules, concluding that IPLs and lasers are

22  Laser Treatment of Telangiectasias

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Fig. 22.2  Intense pulse light treatment of telangiectasias. (a) Before. (b) After

comparable in the treatment of vascular and pigmented lesions with respect to treatment efficiency and safety. Jorgensen et  al. [4] performed a randomized split face trial with blinded response evaluation comparing long-pulsed dye laser versus intense pulsed light for photodamaged skin. In this study, they had 20 women volunteers with Fitzpatrick I–III skin types. Symmetrical split-face photodamage was analyzed. Subjects received three treatments at 3-week intervals with half-face LPDL and half-face IPL. Primary end points were telangiectasias, irregular pigmentation, and preferred treatment. Efficacy was evaluated by patient selfassessments and by blinded clinical on-site and photographic evaluations at 1, 3, and 6 months postoperatively. Adverse effects were evaluated by blinded clinical onsite evaluations. Telangiectasia improved from LPDL and IPL treatments with superior vessel clearance from LPDL treatments. Adverse effects included erythema, edema, and transient hyperpigmentation.

22.3 Potassium Titanyl Phosphate (532 nm, Green) Laser The potassium titanyl phosphate (KTP) laser is a ­frequency-doubled Nd:YAG created from placing crystals in the 1,064  nm Nd:YAG laser beams path (Fig. 22.3). The KTP laser emits green light at 532 nm, which is in range of the 542  nm absorption peak of hemoglobin making it ideal for the treatment of facial telangiectasias. The KTP allows for small linear telangiectasias to be traced and is an ideal choice when you can delineate the vessels. It is effective for treatment of vessels less than 1 mm due to its small spot

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Fig.  22.3  KTP laser treatment of telangiectasias. (a) Before. (b) After

size. Fluence depends on the pulse duration. When using pulse duration in the msec ranges typical fluences are between 10 and 30  J/cm2 with repetition rates between 3 and 8 Hz. The aim is to see disappearance or blanching of the vessel without epidermal changes. The vessel is traced with the laser beam and the use of visual magnification helps enhance accuracy. No coupling gel or anesthetic is required. Postlaser erythema is expected and minimized with the use of ice or cooling packs. Immediately after treatment a patient’s vessels may appear bluish in

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color and darker, this is due to thrombus formation and vessel damage. Patients should practice photo protection with appropriate sunscreens with SPF 30 or greater, avoid trauma, and cigarette smoking [5, 6]. Uelbohoer et al. [7] performed a split face comparison of KTP and PDL for the treatment of telangiectasias and facial erythema in 15 subjects. Subjects were evaluated at 3 weeks after three treatments. Both devices were found to improve telangiectasias. However, the 532 nm device was at least as effective or more effective than the 595-nm laser in all subjects. On average, the KTP laser achieved 62% clearing after the first treatment and 85% clearing 3  weeks after the third treatment, compared to 49% and 75% for the PDL, respectively. Another study performed by Cassuto et al. [8] treated facial telangiectasias in 66 patients with a diode pumped Nd:YAG laser at 532. Sixty two of 66 patients achieved 75–100% (93.9%) clearance of all lesions, while two treatments were needed to reach an acceptable clearance in the remaining 4/66 (6.1%) concluding that the diode pumped frequency double Nd:YAG is an effective device in the treatment of facial telangiectasias.

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22.4 Pulse Dye Lasers

Fig.  22.4  Pulsed dye laser treatment of telangiectasias. (a) Before. (b) After

Pulse dye lasers (PDL) were the first lasers used to treat facial ectasias and other vascular lesions (Fig. 22.4). PDL has a wavelength of 585 nm or 595 nm and a pulse duration ranging from.45  msec allowing deeper depth of penetration of larger vessels. In addition to facial ectasias, PDL are useful in the treatment of various vascular lesions such as Port Wine Stains, angiomas, venous lakes, and hemangiomas. PDL has several features that make its use for facial ectasias ideal [4]. Cooling systems increase its safety profile while an elliptical or circular spot size allows for alignment along the vessel. When treating a patient pulses should not be stacked and a lower fluence coupled with a longer pulse duration (6–20 ms) will help reduce the risk of posttreatment purpura. Posttreatment purpura is caused by microvaporization of red blood cells due to vessel rupture and hemorrhage. Posttreatment purpura makes patients discouraged and increases the amount of downtime making PDL less ideal as first-line treatment of facial telangiectasias [4, 9]. In a study performed by Jorgensen et al. [4], they did a split face comparison with blinded response eval-

uation with long pulsed dye laser (LPDL) versus intense pulsed light for photodamaged skin. Twenty female subjects with Fitzpatrick skin types I–III and rhytids I–II were studied. Telangiectasias were improved in from LPDL and IPL treatments with superior vessel clearance in the LPDL. When evaluating dyschromia and skin texture, there was no clinically significant difference in the side-to-side comparisons. In a study by Tanghetti et al. [10], 40 patients presenting with facial or leg telangiectasia were treated with the extended pulse width PDL (595 nm), used in conjunction with refrigerated air-cooling (SmartCool; Cynosure). Treatment was given using a pulse width of 40 ms and fluences at or below the purpuric threshold (less than 16 J/cm2) and with high-flow air cooling at −4°C. Up to three passes were given until vessel disappearance or intravascular coagulation was observed, and a second treatment given where indicated. Patients were evaluated at 4, 8, and 12 weeks after the final treatment. They found 70% of facial and 80% of leg vessels had 75% clearance. After two

22  Laser Treatment of Telangiectasias

treatments, 14/20 leg vessels cleared at 75–100%. In all cases, vessel clearance was associated with transient purpura lasting less than 7  days. Hyperpig­mentation occurred in 5% of facial vessels and 55% of leg veins. Sub-purpuric doses did not provide acceptable singletreatment clearance. They concluded extended pulse width dye lasers significantly increase the threshold for purpura, allowing higher fluences to be employed. For the goal of single treatment vessel clearance, the extended pulse duration provided acceptable, singletreatment improvement but only in the presence of purpura.

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22.5 Neodymium-Doped Yttrium Aluminum Garnet (Nd:YAG Laser) Nd:YAG lasers for the treatment of facial telangiectasias are often overshadowed by KTP lasers and PDL; however it remains an effective option (Fig.  22.5). Nd:YAG’s absorption spectrum targets the lower peaks of oxyhemoglobin, with absorption in the infrared range (700–1,100 nm). Nd:YAG wavelengths can penetrate up to 6  mm making it a better choice for the treatment of deeper vessels. Deeper penetration is associated with an increased side effect profile including pain and scarring. Blistering may be a concern when trying to treat more superficial ectasias due to the need for increased fluence and shorter pulse duration. Postinflammatory hyperpigmentation remains a concern when using lasers in ethnic skin types. When compared to the diode laser, the Nd:YAG laser has a lower coefficient for melanin making it less likely to compete for absorption during the treatment of vascular lesions in darker skin types [11–13]. In a study by Bevin et  al. [14], they investigated the efficacy of variable pulsed Nd:YAG laser using a small spot size in the treatment of facial telangiectasias. Eight male patients underwent a single treatment of telangiectasias ranging from 0.3 to 2  mm, using variable pulsed Nd:YAG laser with a 1.5  mm spot size and epidermal cooling. Three pulse widths were used (3, 20, and 60 ms) with fluencies varying depending on vessel size. They were evaluated at 13 weeks posttreatment. Fluences ranged between 226 and 425 J/cm2, with smaller vessels requiring larger energies, with pulse durations between 20 and 60  ms settings. Longer pulse width achieved superior vessel elimination. Concluding that a small spot size

Fig.  22.5  Nd:YAG laser treatment of telangiectasias. (a) Before. (b) After

Nd:YAG laser using a pulse width of 20 ms or higher appears to be effective in treating facial telangiectasias with a single pass. In another study by Major et al. [15], they examined the efficacy and safety of treating facial veins with the Nd:YAG laser. Twenty five patients with facial telangiectasias underwent a single treatment with a 100  J/cm2, 10  ms, and 2  Hz repetition rate. Thirty subjects were treated for leg telangiectasias with 125–20  J/cm2, 10–30  ms, and 2  Hz repetition rate. All subjects showed visible improvement with 95% clearing of facial telangiectasias. Concluding that treatment with a long pulsed Nd:YAG laser is a safe and effective method.

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22.6 Diode (800 nm, 810 nm, 940 nm, 980 nm, Near Infrared) Lasers Diode lasers target the tertiary hemoglobin peak with longer wavelengths penetrating more deeply. Diode lasers may be used in up to Type IV Fitzpatrick skin and have limited usage in darker skin types. Diode lasers have a well-known usage in the treatment of unwanted hair; however, they may also be effective in the treatment of facial ectasias [6, 12, 16]. In a study by Tierney et al. [6], they performed a randomized blinded split faced trial comparing 532  nm and 940  nm diode laser wavelengths. Side effects ranging from erythema and blistering were assessed. Telangiectasias were assessed at baseline and 2 month after two treatments. Evaluations were done by two nontreating physicians. Pain associated with the laser treatment was rated as significantly less for the 940 nm wavelength relative to the 532 nm wavelength. Erythema posttreatment was significantly less with 940  nm relative to 532  nm. Significant crusting and swelling were only reported with the 532 nm wavelength. The mean percentage improvement with the 940  nm wavelength (63.0%) was greater than that achieved with the 532  nm wavelength (47.8%). On photographic examination of treated subjects they found 940 nm more efficacious. They concluded 940 nm and 532 nm were both effective in treating facial telangiectasias; however, 940 nm was more efficacious and had a more tolerable side effect profile.

22.7 Copper Vapor and Copper Bromide Lasers (CVL) The Copper Vapor and Copper Bromide lasers are heavy metal lasers that use copper as a medium to produce light with a wavelength of 510 and 578 nm. The longer wavelength is absorbed by oxyhemoglobin. CVL pulse duration is in the 20–25  ns and 10,000– 15,000 pulses per second. These lasers are low output devices with a shutter releasing energy in a series of pulses. There is a continuous emission of light pulses and is referred to as quasicontinuous for this reason. CVL is more commonly used to treat Port Wine Stains; however, they have been found effective in the treatment of facial telangiectasias [17–19].

In a study by McCoy et al. [19], they examined a total of 570 patients with facial telangiectasia of different diameters and on different regions of the face were treated with the copper bromide laser one or more times and followed up over 5 years. More than 75% clearance was achieved in 70% patients, 50–75% clearance in 17.4% patients, and