Aesthetic Medicine: Art and Techniques

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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M.T. Turk

Table 5.1  Categorization of body mass index (BMI) BMI (kg/m ) <18.5 18.5–24.9 25–29.9 30–34.9 35–39.9 ³40 2

Category Underweight Normal weight Overweight Obese: Class 1 Obese: Class 2 Obese: Class 3

Adapted from National Heart, Lung, and Blood Institute [6]

study in Taiwan of more than 36,000 adults age 40 and older found that for every unit increase in BMI, from 25 kg/m2 and higher, a 9% increase in all-cause mortality risk was noted [10]. Thus, the Western Pacific Regional Office of the WHO in conjunction with the International Association for the Study of Obesity and the International Obesity Task Force recommend that the BMI cut point for obesity be lowered to 25.0 kg/m2 and to 23.0–24.9 kg/m2 for overweight among Asian populations [11]. Differences between specific Asian groups suggest the need for BMI cut points that are specific to the Asian country and ethnicity [12].

5.2.2 Waist Circumference Because central or abdominal obesity is associated with visceral fat around the abdominal organs, measurement and monitoring of waist circumference is an important part of the complete clinical assessment. Abdominal obesity has in fact been found to have a strong relationship with risk for coronary heart disease and metabolic disorders like impaired glucose functioning or diabetes mellitus [13, 14]. Specifically, intra-abdominal adiposity is a more sensitive predictor of obesity-related morbidity and mortality than BMI [15, 16], and a large waist is associated with an increased risk of heart failure, myocardial infarction, and all-cause mortality in patients with cardiovascular disease [17]. Even among normalweight patients, an elevated waist circumference is associated with increased risk of disease [18, 19]. The National Heart, Lung, and Blood Institute’s evidence report on the evaluation and treatment of overweight and obesity [1] advises measurement of waist circumference as a suitable technique for assessing the patient’s visceral adiposity (Table  5.2). Cutpoints by gender have been determined as a basis for pinpointing relative risk to develop obesity-associated health problems. High risk for the development of

Table 5.2  Process for waist circumference measurement • With the patient wearing an examining gown, stand to the right of the patient and palpate the right iliac crest • Draw a horizontal line just above the edge of the iliac crest and cross the horizontal line with a vertical line at the midaxillary position • With the measuring tape horizontal to the floor and snuggly against the skin without pressure, circle the abdomen at the level of the marked location • Measure the circumference at the end of the patient’s normal exhalation Adapted from National Heart, Lung, and Blood Institute [6]

morbidities related to obesity (dyslipidemia, cardiovascular disease, and type 2 diabetes) is associated with a waist circumference of 102 cm (40 in.) for men and 88  cm (35  in.) for women [20]. As with BMI, increased risk is seen at a lower waist circumference for Asian populations compared to those of European descent. Because of this, recommended waist circumference cut-points have been designated at 90  cm (35.5 in.) for Asian men and 80 cm (31.5 in.) for Asian women [11]. Further investigations of the relationship between waist circumference and disease risk have noted differences among Asian groups, and subsequent recommendations include an 80–85 cm waist circumference for men and a 70–75 cm waist for Asian women [21, 22]. See Table 5.2 for the description of how to accurately measure waist circumference.

5.2.3 Assessment of Knowledge and Motivation Ascertaining the patient’s underlying knowledge of nutrition, physical activity, and the consequences of obesity along with the patient’s motivation to enact lifestyle change is an important initial step in treating patients with excess weight. Assessment of current eating patterns and the interest in changing eating habits can be accomplished using a brief questionnaire [23] that can assist in identifying particular problem areas for calorie intake, e.g. high-calorie snacks or sugar-sweetened beverages. This assessment may also be accomplished by asking the patient to complete a 3-day food diary, which would include documenting all food intake on two working days and one leisure day; the patient should be directed as to how to complete the diary and the specifics to include (e.g., precise amount of food consumed and actual food labels

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if the item is uncommon) [24]. Evaluation of current physical activity patterns is essential to determine the patient’s energy expenditure, and brief assessment tools are available that ask the patient to report the duration and frequency of vigorous activity and moderate activity (like walking) in a typical week [25]. Furthermore, patients may not have an understanding of the health consequences of obesity or realize the effects of excess body weight (EBW) on physical and mental health. Younger patients may need to be educated about the effects of elevated glucose or cholesterol levels, while older patients already experiencing the comorbidities associated with obesity may not realize that some are reversible with weight loss. Patient goals and motivation for change play a critical role in weight loss success. Providers need to evaluate factors like the patient’s attitude related to weight loss, history of weight loss attempts, readiness to begin lifestyle changes [1], and self-efficacy for [26] and barriers to weight loss [27]. Patient goals and expectations for weight loss are often 2–3 times higher than the 8–15% weight loss typically seen; patients are then dissatisfied when they do not reach these goals [6]. Clinicians should help patients be realistic about weight loss goals and reinforce the value of losing 5–10% of one’s body weight, a loss that is associated with an improvement in the metabolic profile and decrease in heart disease risk factors [28]. The initial goal for weight loss should be 10% of current weight at a rate of 1–2 lb (0.5–0.9 kg) per week with the maintenance of that lower body weight long-term [6]. Decisions about goals for weight loss should be arrived at jointly between the clinician and the patient. Evidence suggests that an adverse health episode is a motivating event for a patient to initiate weight loss and actually relates to higher weight loss and less weight regain [29], which indicates that these episodes could be used by clinicians to initiate the discussion about weight loss with the patient. For patients who are ambivalent about weight loss, the clinician should discuss the health risks of EBW along with the benefits of losing weight and how the clinician will assist the patient with the process. Motivational interviewing, a patient-centered style of counseling aimed at bringing about behavior change by increasing intrinsic motivation and assisting patients to examine and reconcile ambivalence [30], can be an effective method to encourage behavior change and weight loss [31], even in the format of a brief 15-min appointment [32].

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5.3 Treatment Approaches Lifestyle modification for weight loss includes three chief components – dietary treatment, increased physical activity, and behavioral therapy [6]. Behaviors resulting in a reduction in caloric intake and an increase in energy expenditure are promoted and reinforced by strategies learned through standard behavioral weight loss treatment [33]. Pharmacotherapy and surgical intervention are second-line treatment approaches considered adjunctive to lifestyle modification. The addition of pharmacotherapy is reserved for individuals with a BMI ³ 30 kg/m2 or those with a BMI ³ 27 kg/m2 and comorbid weight-related diseases or risk factors. Surgical intervention is considered for individuals with extreme obesity (BMI ³ 40 kg/m2) or a BMI ³ 35 kg/m2 if comorbid conditions exist [1]. The following paragraphs discuss the elements of lifestyle modification as well as pharmacotherapy and surgical treatment for weight loss.

5.3.1 Dietary Treatment A negative energy balance is the feature component of successful weight loss and the extent of this deficit is the greatest determining factor for how quickly and how much weight is lost [34]. A reduction in daily caloric intake is the main characteristic of dietary ­therapy, and patients should reduce total calories ­consumed by 500–1,000 kcal/day to achieve a 1–2 lb/ week weight loss. This low-calorie diet typically results in patients consuming 1,000–1,600 calories per day and has been associated with an 8% weight loss after 6  months [6]. In addition to reducing calories, patients should be counseled to decrease fat intake to 20–30% of total daily calories in order to address risk factors like elevated blood cholesterol and hypertension. Nutritional education is also incorporated in dietary therapy. For example, patients are instructed about the energy content of foods (4 calories in a gram of carbohydrate or protein, 9 calories in a gram of fat, and 7 calories in a gram of alcohol), how to read and evaluate food labels, food preparation techniques to reduce fat and calorie content, limiting consumption of high-calorie foods, and reducing portion sizes. See Table 5.3 for the Low-Calorie Step I diet suggested by the National Heart, Lung, and Blood Institute [6].

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Table 5.3  Low-calorie step 1 diet Nutrient Calories Total fat Saturated fatty acids Monounsaturated fatty acids Polyunsaturated fatty acids Cholesterol Protein Carbohydrate Sodium chloride

Calcium Fiber

Recommended consumption Reduction of 500–1,000 kcal/ day from typical intake Maximum of 30% of total calories 8–10% of total calories Up to 15% of total calories Up to 10% of total calories Less than 300 mg/day About 15% of total calories 55% of total calories Maximum of 100 mmol/day (about 2.4 g of sodium or 6 g of sodium chloride) 1,000–1,500 mg/day 20–30 g/day

Adapted from National Heart, Lung, and Blood Institute [6]

Much attention has recently been given to the use of low-carbohydrate diets for weight loss. When consuming a very-low-carbohydrate diet (e.g., <20  g/day), ketones are generated to maintain fuel utilization in the brain, which some short-term evidence suggests may help with dietary adherence through decreased hunger [35]. Although larger weight losses have been seen with a low-carbohydrate diet in the short term [36], long-term data are still lacking regarding the benefits of this diet for weight loss maintenance. A large, multisite trial found that diets with a reduction in calories resulted in similar 2-year weight losses no matter which macronutrient was emphasized [37]. Similar results were noted by Vetter et al. [38] after 36 months, although their results showed a larger weight regain after 12  months in the low-carbohydrate group compared to the low-fat group. A trial that compared the popular diets of Atkins, Zone, Weight Watchers, and Ornish found that adherence to the dietary plan was more important for 1-year weight loss than the type of diet [39]. Of concern regarding the low-carbohydrate diet is the high-fat and high-protein intake that often accompanies this diet and the subsequent effect on heart disease risk factors. Benefits and disadvantages to the low-carbohydrate diet regarding the effect on the lipid profile compared to a low-fat diet have been reported. Greater decreases in triglycerides and increases in HDL-cholesterol have been associated with following a low-carbohydrate diet, but increases in LDL-cholesterol and total cholesterol have also been noted [40, 41]. A recent study examining the

effect of these diets on endothelial function suggests that diets that are very low in carbohydrate intake and high in fat intake may result in decreased flow-mediated dilatation and have negative long-term effects on vascular function [42]. Additional aspects of dietary treatment that must be considered by practitioners as they provide guidance to patients about weight loss include counseling on food portion sizes along with frequency and timing of meals [43]. The ubiquity of large portion sizes in our environment has led to a perception that these portions of food and beverages, which are commonly at least two times the size of a standard serving size [44], are appropriate amounts to consume in one eating session. This distortion of portion sizes is supported by serving utensils, plates, glasses, and silverware that have grown in size as well [45]. Portion control is an important contributor to an energy deficit that should be emphasized with dietary treatment. Strategies for informing patients about how to control portion sizes include education on the appearance and calorie content of commonly eaten foods (e.g., ½ cup of cereal vs. 1 bowl of cereal), the use of prepackaged foods (e.g., caloriecontrolled frozen or snack foods), and portion control dinnerware that partitions the plate into specified sections for proteins, carbohydrates, cheese, sauces, and vegetables [43, 46, 47]. Although the evidence on the weight-loss benefits of a specific frequency for eating and timing of meals, like consuming a breakfast, is cross-sectional in nature, the American Dietetic Association advocates that total energy intake be dispersed throughout the day consisting of 4–5 meals and snacks (including breakfast); consuming a greater proportion of calories earlier in the day may be more desirable than evening consumption [43].

5.3.2 Physical Activity The incorporation of physical activity as a component of weight loss treatment and maintenance is fundamental to successful outcomes. For health maintenance and prevention of chronic diseases, current recommendations from the American College of Sports Medicine (ACSM) and the American Heart Association (AHA) state that persons between age 18 and 65 should take part in moderate-intensity aerobic physical activity, like walking at 3.5–4.0 mph, for a minimum of 30 min on 5 days of each week or vigorous intensity aerobic

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activity, like jogging or bike riding at 10 mph, for at least 20  min on 3  days of each week. Moderateintensity activity results in a noticeably elevated heart rate, e.g., brisk walking; vigorous activity results in rapid breathing and a significant elevation in heart rate. The 2007 guidelines from the ACSM and AHA also include recommendations for muscle strength training at least twice each week performing 8–10 exercises using the major muscles with 8–12 repetitions [48]. The quantity of physical activity needed to prevent weight gain, lose weight, and prevent weight regain after weight loss is higher than the amount of physical activity needed for health maintenance. In order to prevent weight gain through adulthood, one should partake in 60  min of moderate-to-vigorous physical activity a day on most days of the week. A decrease of 3,500 kcal from usual intake is necessary to lose one pound of body weight in a week [1], and physical activity provides a tool for tipping energy balance in the negative direction. Because physical activity alone as a weight loss intervention has only been associated with a 3% weight loss [49], caloric restriction is also necessary for individuals who need to lose a larger amount of weight. Physical activity combined with reduced caloric intake results in significantly greater weight loss than dietary restriction alone [50]. For an average weight loss of approximately 2–3  kg (4.4– 6.6 lb), physical activity of moderate intensity in the amount of at least 150  min/week is recommended. Moderate-intensity activity between 225 and 420 min each week results in a 5–7.5  kg (11–16.5  lb) weight loss, and a dose–effect relationship for physical ­activity and weight loss appears to exist [49]. Among individuals who were formerly obese, 60–90 min of moderateintensity activity each day is necessary to maintain weight loss and prevent regain [48]. These sizeable amounts of activity can be quite daunting for many individuals. Fortunately, evidence indicates that physical activity can be accumulated in multiple 10-min intervals throughout the day and remain beneficial for weight loss [51, 52]. To facilitate engagement in physical activity, practitioners should encourage their patients to develop a specific plan for physical activity at the start of each week, make the time in their schedule to carry it out, and write down in a diary the duration and intensity of their exercise activities [6]. Although there has been a slight decrease from 2000 to 2008 in the proportion of US adults reporting no leisure-time physical activity (27.8–25.1%) [53],

33 Table 5.4  Varying-intensity activities for patient teaching Intensity Very light Light Moderate High

Activity Painting a room, yard work, ironing Walking slowly, child care, golf Brisk walking, gardening, tennis Jogging (10 min/mile), basketball

Adapted from National Heart, Lung, and Blood Institute [6]

most individuals are sedentary and not particularly motivated to increase their activity level [6]. Various approaches are available for persons beginning to exercise and should be introduced and increased gradually for the obese patient. Pedometers have recently become popular for motivating people to do more walking. A systematic review of 26 studies examining the use of pedometers to increase physical activity found that pedometer use was significantly associated with increased physical activity and decreased BMI and blood pressure. Having a goal for number of steps taken, like 10,000 steps/day was predictive of increased activity [54]. Daily lifestyle activity is an additional means of augmenting weight loss efforts. Encouraging patients to include activities in each day that result in increased energy expenditure (e.g., using the stairs instead of elevator and parking further from entrances) and discouraging the amount of sedentary activities (i.e., television viewing or Internet use) can help to shift overall daily calories toward an energy deficit. See Table 5.4 for examples of very light to high-intensity activities for patient teaching.

5.3.3 Behavioral Therapy Cognitive behavioral therapy (CBT), as applied to weight loss treatment, seeks to influence eating, activity, and thinking behaviors that affect the overweight or obese patient’s weight [33]. Behavioral therapy for weight loss stems from the principle of classical conditioning, which indicates that certain stimuli repeatedly present before or with a particular behavior (e.g., eating) will become linked to that behavior. For example, snacking on junk food is often linked to watching television; the more frequently these two activities are coupled, the stronger the relationship between them becomes [55]. Through participation in CBT for weight loss, patients learn to identify antecedent events or cues for eating or inactivity and then develop new reactions

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that are more congruent with their weight loss goals. The consequences of behaviors are also examined, and reinforcement of new, more appropriate eating and activity behaviors is emphasized. Internal thoughts and ideas about oneself also impact behavior, and patients are taught to restructure negative thoughts about weight management to more positive thinking, when these thoughts do not match identified weight loss behaviors or goals [56]. The three defining characteristics of behavioral treatment are that it is goal-focused, process-oriented, and encourages small instead of large changes in behavior [33]. Specific, measurable goals (e.g., a number of calories to consume each day or a number of steps to register on the pedometer) are defined that enable a clear assessment of goal attainment. Process orientation is focused on assisting patients to decide what they wish to accomplish and how they will go about identifying and carrying out the behaviors to accomplish their goal. It advocates a skill-building perspective that weight loss involves a set of skills and strategies one can learn. Lastly, behavioral treatment promotes small behavior changes over large ones, which is derived from the learning principle of successive approximation or behavior shaping, where a patient has a chance to be successful at small changes and can build on these successes to obtain more difficult goals [33]. Behavioral therapy is typically structured as a group format with a planned curriculum where individuals meet weekly for the initial 4–6  months and then the frequency of meetings is gradually decreased to biweekly for an additional few months and then monthly until treatment is complete. Treatment sessions for hospital or university-based programs are typically provided to groups of about 10–20 patients and are approximately an hour in duration. Sessions are led by professionals from multiple disciplines that may include psychologists, registered dieticians, exercise physiologists, or physicians, and the group structure allows for social support as well as a friendly competitive atmosphere. A weigh-in with each session provides motivation for patients to stay on track with their goals. Various behavioral strategies to facilitate behavior change for weight loss are covered in the group meetings, and rather than simply lecturing on the topic being covered, group leaders encourage patients to discuss their progress, problem solve, and ask questions. A set of behavioral strategies is common to standard behavioral therapy [33]:

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1. In goal setting, patients are allotted goals to help them achieve their desired weight loss. These goals must be outcome-specific, short-term, and achievable for the patient. In most situations according to goal setting theory, establishing specific goals leads to enhanced performance compared with no goals or unclear goals [57]. Daily goals are assigned for total calories and fat grams (based on a percent of calories from fat, e.g., 25%); weekly goals are given for energy expenditure through exercise [56]. Goals should focus on the patient’s change in behavior, (e.g., selecting a piece of fruit for a snack instead of a candy bar), rather than on physiologic results, (e.g., lower serum cholesterol level), since behaviors are under a patient’s direct influence and many factors can impact physiologic outcomes. Goals that are incremental in nature allow the patient to experience small achievements; yet, the patient will not take seriously goals that are too simplistic and will not make an attempt at those that are too difficult. Regular feedback from the practitioner regarding goal attainment will instill in the patient a sense of mastery and accomplishment [58]. 2. Self-monitoring, recording one’s eating and activity behaviors, is one of the true hallmarks of behavioral therapy and includes a detailed, daily description of the type, amount, caloric content, and fat gram content of all foods consumed as well as the type and duration of physical activity. Selfmonitoring may also incorporate information on places and feelings related to eating. The intent of self-monitoring is to enhance individuals’ awareness of their existing eating and activity behaviors and the related circumstances that would benefit from behavior change [33]. Patients become aware of patterns of behavior and may express surprise at seeing their excessive food intake in writing [59]. While self-monitoring has traditionally been performed in a paper diary and patients were required to look up in a reference booklet the calorie and fat gram content of foods, technological advances have provided additional methods for recording food intake and activity. Internet sites, like www.sparkpeople.com, www.FitDay.com, and www.caloriecount. about.com, are accessible as a mechanism for online self-­monitoring. Additionally, software for personal ­digital assistants now exists and contains a comprehensive database of foods and physical activities, removing the necessity of searching for the

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nutrient composition of foods in a booklet [60]. The body of literature continues to grow in support of the observation that self-monitoring dietary intake and physical activity is a critical element for success in weight loss [61–63]. 3. Problem solving is a behavioral strategy whereby the patient identifies the problematic circumstance associated with poor food and/or activity behaviors, formulates solutions, chooses a solution, tests that solution, and evaluates the solution’s effect on the problem [64]. It is preferable that the practitioner allow the patient to formulate possible solutions to the problem situation him/herself, and have the patient practice a few of the identified solutions. For example, the patient could role play how he/she might respond to a host who is adamant about serving the patient a second helping of the dinner foods. 4. Stimulus control is based on the notion that environmental triggers influence behaviors, and stimulus control strategies assist the patient to handle triggers related to eating and activity behaviors that do not support the weight loss goals. Avoiding high-risk situations and changing environmental cues to positive cues for appropriate eating and exercise behaviors results in actions that are congruent with goals. For example, patients are instructed to avoid all-you-can-eat restaurants or unhealthy grocery store aisles, to reduce exposure to poor food choices by avoiding the workplace vending machine and packing ready-to-eat fruits as an afternoon snack, to store food out of one’s sight, and to remove serving plates from the table to avoid overeating during meals [33]. 5. In cognitive restructuring, patients are taught how negative thoughts, self-critical perceptions, all-ornone thinking, and comparisons with others foil the patient’s weight loss efforts. For example, a patient who envisions having a piece of cake as “sabotaging the diet,” may continue with this catastrophic perspective and despair that overeating for the rest of the day is inevitable. With the cognitive restructuring strategy, patients learn to alter their inappropriate ideas to include positive, rational thoughts about their behaviors and themselves [33]. 6. Relapse prevention involves patients learning that lapses in weight control behaviors are a normal occurrence. These lapses need to be expected in certain occasions (like vacations, parties, special

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events) and planned for by using strategies to cope with the circumstances, thereby preventing relapses [65]. Practitioners can discuss these potential problem situations in advance and help patients to problem solve and plan appropriate methods of coping with the temptations they face. 7. Other behavioral strategies include recruiting social support from friends and family to assist with and reinforce lifestyle changes, incorporating contingency management and rewards associated with meeting an incremental goal, and including stress management to reduce the use of inappropriate eating as a coping mechanism [66]. In order to promote adherence to the eating and activity changes, evidence suggests that ongoing contact and the frequency with which patients interact with the health care provider is an important contributor to successful weight control [6]. This contact may take the form of interaction with the office staff or nurse, in the interim between physician visits, and need not be restricted to in-person contact. Empirical findings support the use of telephone contact [67] as well as e-mail and Internet behavioral counseling [68] as a beneficial means of continuing to support patients in their weight loss efforts. The most promising results for treatment success are attained through a combination of behavioral treatment, dietary treatment, and increased activity, and multi-center trials using these techniques have demonstrated not only a 5–10% loss of body weight but also a decrease or even the prevention of obesity-related comorbid conditions like diabetes and hypertension [69–71]. Importantly, obesity must be recognized as a chronic disease that requires long-term, continued treatment in order to achieve long-term weight management success [72].

5.3.4 Pharmacotherapy Despite the inherent appeal of pharmacologic treatment of obesity, the multi-faceted nature of this disease with its genetic [73], metabolic [74], and behavioral influences [75] has eliminated the reality of a single, “silver bullet” pharmacotherapy. Lifestyle modification that includes dietary, activity, and behavioral therapy remains the first tier of treatment with pharmacotherapy being considered as a second tier used in combination with lifestyle change for those

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who are unsuccessful at standard interventions. Pharmacotherapy is reserved for individuals with no serious contraindications to using the medication(s) who have a of BMI > 30 kg/m2 or > 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

M.T. Turk

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.

M.T. Turk

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

M.T. Turk

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.

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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

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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.

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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.

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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

193

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 <5 mm superficial burn [4, 6, 32]. In the senior author’s experience, these are self-limited and can be treated with topical antibiotic ointment. The treatment tip has built in sensors which continuously monitor temperature and surface pressure. RF energy delivery is aborted if measurements are outside a safe threshold, making significant skin burns unlikely. The complication of greatest concern with capacitive RF treatment is localized over tightening of subcutaneous collagen-based fibrous septae or possible fat atrophy resulting in skin surface irregularity [22]. This complication was more common initially when single pass high energy regimens were being followed, often with the patient under profound anesthesia [4, 22, 32]. The senior author has found in two patients with this complication, the indentations

195

improved over the course of a few months without any additional intervention, most likely as a result of new collagen formation. Other treatments including autologous fat transfer have been advocated [22]. With current lower energy multiple pass treatment algorithms and in experienced hands, complications in general are rare.

16.8 Conclusions Capacitive RF skin treatment provides an additional avenue of skin rejuvenation, especially for patients not interested in invasive surgical options. Candidates for treatment must be made aware of the limitations of the procedure and the gradual nature of the changes seen. Patients with significant skin laxity or underlying structural ptosis should be counseled that capacitive RF treatment does not currently achieve the dramatic changes provided by traditional surgery, although there is a theoretical antiaging benefit to stimulating collagen formation in the skin. Combining RF treatment with other nonsurgical or minimally invasive procedures can achieve a more significant result. Future developments and refinement of RF technology will undoubtedly expand the role of capacitive RF treatments for facial and body rejuvenation.

References 1. Zelickson BD, Kist D, Bernstein E et al (2004) Histological and ultrastructural evaluation of the effects of a radiofrequency-based non-ablative dermal remodeling device: a pilot study. Arch Dermatol 140(2):204–209 2. Abraham M, Chiang S, Keller G, Rawnsley J, Blackwell K, Elashoff D (2004) Clinical evaluation of non-ablative radiofrequency facial rejuvenation. J Cosmet Laser Ther 6(3):136–144 3. Koch RJ (2004) Radiofrequency non-ablative tissue tightening. Facial Plast Surg Clin North Am 12(3):339–346 4. Abraham MT, Ross EV (2005) Current concepts in nonablative radiofrequency rejuvenation of the lower face and neck. Facial Plast Surg 21(1):65–73 5. Narins DJ, Narins RS (2003) Non-surgical radiofrequency facelift. J Drugs Dermatol 2(5):495–500 6. Fitzpatrick R, Geronemus R, Goldberg D, Kaminer M, Kilmer S, Ruiz-Esparza J (2003) Multicenter study of noninvasive radiofrequency for peri-orbital tissue tightening. Lasers Surg Med 33(4):232–242 7. Nahm WK, Su TT, Rotunda AM, Moy RL (2004) Objective changes in brow position, superior palpebral crease, peak angle of the eyebrow, and jowl surface area after volumetric

196 radiofrequency treatments to half of the face. Dermatol Surg 30(6):922–928 8. Fritz M, Counters JT, Zelickson BD (2004) Radiofrequency treatment for middle and lower face laxity. Arch Facial Plast Surg 6(6):370–373 9. Alster TS, Tanzi E (2004) Improvement of neck and cheek laxity with a non-ablative radiofrequency device: a lifting experience. Dermatol Surg 30(4 Pt 1):503–507, Hughes P, comment in Dermatol Surg 2004;30(11):1430 10. Bassichis BA, Dayan S, Thomas JR (2004) Use of a non-ablative radiofrequency device to rejuvenate the upper one-third of the face. Otolaryngol Head Neck Surg 130(5): 397–406 11. Jacobson LG, Alexiades-Armenakas M, Bernstein L, Geronemus RG (2003) Treatment of nasolabial fold and jowls with a noninvasive radiofrequency device. Arch Dermatol 139(10):1371–1372 12. Ruiz-Esparza J (2004) Noninvasive lower eyelid blepharoplasty: a new technique using nonablative radiofrequency on periorbital skin. Dermatol Surg 30(2 Pt 1):125–129 13. Ruiz-Esparza J, Gomez JB (2003) The medical face lift: a noninvasive, nonsurgical approach to tissue tightening in facial skin using nonablative radiofrequency. Dermatol Surg 29(4):325–332 14. Hsu TS, Kaminer MS (2003) The use of non-ablative radio­ frequency technology to tighten the lower face and neck. Semin Cutan Med Surg 22(2):115–123 15. Iyer S, Suthamjariya K, Fitzpatrick RE (2003) Using a radiofrequency energy device to treat the lower face: a treatment paradigm for a nonsurgical facelift. Cosmet Dermatol 16:37–40 16. Ruiz-Esparza J, Gomez JB (2003) Nonablative radio­ frequency for active acne vulgaris: the use of deep dermal heat in the treatment of moderate to severe active acne vulgaris (thermotherapy): a report of 22 patients. Dermatol Surg 29(4):333–339 17. Fisher GH, Jacobson LG, Bernstein LJ, Kim KH, Geronemus RG (2005) Nonablative radiofrequency treatment of facial laxity. Dermatol Surg 31(9 Pt 2):1237–1241 18. Finzi E, Spangler A (2005) Multipass vector (mpave) technique with nonablative radiofrequency to treat facial and neck laxity. Dermatol Surg 31(8 Pt 1):916–922 19. Meshkinpour A, Ghasri P, Pope K, Lyubovitsky JG, Risteli J, Krasieva TB, Kelly KM (2005) Treatment of hypertrophic scars and keloids with a radiofrequency device: a study of collagen effects. Lasers Surg Med 37(5):343–349 20. England LJ, Tan MH, Shumaker PR, Egbert BM, Pittelko K, Orentreich D, Pope K (2005) Effect of mono-polar radiofrequency treatment over soft-tissue fillers in an animal model. Lasers Surg Med 37(5):356–365 21. Shumaker PR, England LJ, Dover JS, Ross EV, Harford R, Derienzo D, Bogle M, Uebelhoer N, Jacoby M, Pope K (2006) Effect of mono-polar radiofrequency treatment over soft-tissue fillers in an animal model: part 2. Lasers Surg Med 38(3):211–217 22. Narins RS, Tope WD, Pope K, Ross CE (2006) Overtreatment effects associated with a radiofrequency tissue-tightening device: rare, preventable, and correctable with subcision and autologous fat transfer. Dermatol Surg 32(1):115–124

M.T. Abraham and J.J. Rousso 23. Kushikata N, Negishi K, Tezuka Y, Takeuchi K, Wakamatsu S (2005) Is topical anesthesia useful in noninvasive tightening using radiofrequency? Dermatol Surg 31(5):526–533 24. Kushikata N, Negishi K, Tezuka Y, Takeuchi K, Wakamatsu S (2005) Non-ablative skin tightening with radiofrequency in Asian skin. Lasers Surg Med 36(2):92–97 25. Lack EB, Rachel JD, D’Andrea L, Corres J (2005) Relationship of energy settings and impedance in different anatomic areas using a radiofrequency device. Dermatol Surg 31(12):1668–1670 26. Sadick N, Sorhaindo L (2005) The radiofrequency frontier: a review of radiofrequency and combined radiofrequency pulsed-light technology in aesthetic medicine. Facial Plast Surg 21(2):131–138 27. Hodgkinson DJ (2009) Clinical applications of radiofrequency nonsurgical skin tightening. Clin Plast Surg 36(2): 261–268 28. Sukal SA, Geronemus RG (2008) Thermage: the nonablative radiofrequency for rejuvenation. Clin Dermatol 26(6): 602–607 29. Abraham MT, Mashkevich G (2007) Monopolar radiofrequency skin tightening. Facial Plast Surg Clin North Am 15(2):169–177 30. Suh DH, Chang KY, Son HC, Ryu JH, Lee SJ, Song KY (2007) Radiofrequency and 585-nm pulsed dye laser treatment of striae distensae: a report of 37 Asian patients. Dermatol Surg 33(1):29–34 31. Wu WT (2007) Achieving optimal results with thermage using mesoanesthesia and revised treatment parameters. Aesthet Surg J 27(1):93–99 32. Weiss RA, Weiss MA, Munavalli G, Beasley KL (2006) Monopolar radiofrequency facial tightening: a retrospective analysis of efficacy and safety in over 600 treatments. J Drugs Dermatol 5(8):707–712 33. Alam M, Levy R, Pajvani U, Ramierez JA, Guitart J, Veen H, Gladstone HB (2006) Safety of radiofrequency treatment over human skin previously injected with medium-term injectable soft-tissue augmentation materials: a controlled pilot trial. Lasers Surg Med 38(3):205–210 34. Dover JS, Zelickson B, 14-Physician Multispecialty Consensus Panel (2007) Results of a survey of 5,700 patient monopolar radiofrequency facial skin tightening treatments: assessment of low-energy multiple-pass technique leading to a clinical end point algorithm. Dermatol Surg 33(8): 900–907 35. Carruthers J, Carruthers A (2007) Shrinking upper and lower eyelid skin with a novel radiofrequency tip. Dermatol Surg 33(7):802–809 36. Biesman BS, Pope K (2007) Monopolar radiofrequency treatment of the eyelids: a safety evaluation. Dermatol Surg 33(7):794–801 37. Bogle MA, Ubelhoer N, Weiss RA, Mayoral F, Kaminer MS (2007) Evaluation of the multiple pass, low fluence algorithm for radiofrequency tightening of the lower face. Lasers Surg Med 39(3):210–217 38. Anolik R, Chapas AM, Brightman LA, Geronemus RG (2009) Radiofrequency devices for body shaping: a review and study of 12 patients. Semin Cutan Med Surg 28(4): 236–243

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

17

Bruce M. Freedman and Toral P. Balakrishnan

17.1 Introduction Intense pulsed light (IPL) has become a widely accepted and reliable technique for the nonablative treatment of several undesirable skin problems including telangectasias, photoaging, and unwanted hair. This success can be attributed to its versatility in treating this wide array of dermatologic conditions rapidly, cost-effectively, and with minimal recovery. IPL systems utilize high-intensity flashlamps that emit pulses of polychromatic light in a broad wavelength spectrum between 500 and 1,200 nm. The light energy is attracted to target structures or chromophores in the skin according to their intrinsic lightabsorbing capacity. For example, hemoglobin has a primary absorption peak at 580 nm and IPL effectively treats vascular problems when the device is set to emit this wavelength. Through the mechanism of selective photothermolysis, the light energy is converted to heat and the anatomic structures are affected correspondingly. When dealing with unwanted hair, the melanin in the follicle bulbs absorbs the light and the hair-producing cells are damaged by the transmitted heat energy. Likewise, in pigmented tissue the melanosomes are inactivated by the energy absorbed by the resident melanin. In vascular conditions such as rosacea and telangectasias, the intimal linings of the involved small vessels are seared by the heat radiating from the energized hemoglobin. This results in small vessel collapse and subsequent improvement of the

B.M. Freedman (*) • T.P. Balakrishnan Plastic Surgery Associates of Northern Virginia, 8180 Greensboro Drive, Suite 1015, McLean, VA 22102, USA e-mail: [email protected], [email protected] e-mail: [email protected]

condition. In the correction of photoaging, the thermal effects in the dermis initiate a cascade of metabolic events including fibroblast proliferation and collagen expression [1]. This allows for diminished fine lines and improved skin texture. Generational advances in IPL technology have led to simpler treatment protocols, devices with default settings, and reproducible energy delivery. These factors have conveyed greater efficacy and patient satisfaction with less discomfort. To optimize outcome, it is important to be familiar with the technical parameters associated with IPL. An IPL can be configured for different emission spectra by adjusting the filter, pulse duration and interval, and energy setting [2]. IPL devices use dichroic filters, which are stacks of dielectric materials wedged between sapphire plates, to transmit a defined wavelength spectrum during use. Different filters allow for the treatment of blood vessels of various size and depth, pigmented structures, rhytids, and hair follicles. Depending on the manufacturer, the filters can either be changed manually or internally rotated by changing settings on the control panel. Active cooling using recirculating cold water or cryogen spray protects the epidermis resulting in less erythema and blistering. Most devices allow for an adjustment of the circulating cold water temperature between 5°C and 25°C. Lower temperatures allow for higher fluences with less potential side effects, especially in patients with darker skin types. Less patient discomfort has also been noted with active cooling. Current IPL devices employ a wide range of available pulse durations (0.5–90 ms). This allows for the selected pulse duration to be less than the thermal relaxation time of the target chromophore, limiting tissue damage. These longer pulse durations have allowed for the safer

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_17, © Springer-Verlag Berlin Heidelberg 2011

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B.M. Freedman and T.P. Balakrishnan

198 Table 17.1  Treatment parameters for pigmented lesions with 515-nm filter Skin type I–II III–IV V VI

Fluence (J/cm2) 12 9 7 n/a

Pulse width (ms) 10 20 30 n/a

Filter (nm) 515 515 515 n/a

Cooling (°C) 10–25 10–25 10–25 n/a

Taken from Broad Based Light (BBL) Treatment Manual, Sciton Corporation (Palo Alto, CA) Recommended energy guidelines for Sciton BBL Table 17.2  Treatment parameters for vascular improvement with 560-nm filter Skin type I–II III–IV V VI

Fluence (J/cm2) 20 14 10 n/a

Pulse width (ms) 20 14 10 n/a

Filter (nm) 560 560 560 n/a

Cooling (°C) 25 20 15 n/a

Taken from Broad Based Light (BBL) Treatment Manual, Sciton Corporation (Palo Alto, CA) Recommended energy guidelines for Sciton BBL Table 17.3  Treatment parameters for hair reduction Skin type I–II III–IV V VI

Dark hair fluence (J/cm2) 5–10 5–10 5–12 n/a

Medium hair fluence (J/cm2) 7–15 7–15 7–18 n/a

Light hair fluence (J/cm2) 10–20 10–20 n/a n/a

Pulse width (ms)

Filter (nm)

15–20 20–30 30–50 n/a

590 640 695 n/a

Taken from Broad Based Light (BBL) Treatment Manual, Sciton Corporation (Palo Alto, CA) Recommended energy guidelines for Sciton BBL

treatment of darker skin types. The interval between pulses, known as the interpulse delay, can be set at values between 1 and 300 ms. In selected cases, the longer delay allows the epidermal elements to cool down lessening adverse effects. Also, the larger IPL handpiece creates a sizable footprint that permits rapid treatment of most anatomic areas, minimizing operator fatigue and treatment time. The available energy for light-based technology is characterized as fluence and quantified in joules (J) delivered to an area. This is analogous to energy “pressure,” since it reflects an energy force applied to a specified area. In the case of IPL it is J/cm2. Energy settings are dependent upon the flashlamp type, manufacturer, and the skin problem being treated. There are complex relationships between fluence and pulse duration and the manufacturers have compiled data that take these factors into account when treating different skin types and levels of pigmentation. Tables  17.1–17.3 provide manufacturer-provided guidelines for a particular IPL device (Sciton BBL) [3].

17.2 Clinical Results The best outcomes for facial skin rejuvenation result from a series of 4–6 IPL treatments spaced at 3–4 week intervals. Bitter [4] reported that 69% of his patients noted much or very much overall improvement; 88% were satisfied with their treatment. By using relatively short pulses of 2.4–4.7  ms with interpulse delays of 10–60 ms, fluence of 30–50 J/cm2 and a 570-nm cutoff filter, Bitter was able to effectively treat all elements of facial photoaging including skin texture, irregular pigmentation, and telangectasias. He coined the term “photofacial” to describe this photodynamic treatment of photoaging. Figure 17.1 demonstrates the results of a series of IPL treatments in a 47-year-old woman. Recently, Dover et al. [5] promoted the adjunctive use of the photosensitizing agent 5-aminolevulinic acid with IPL treatments to enhance the therapeutic effects of IPL on photoaging. The compound is applied to the face 1 h prior to the IPL treatment to allow for

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

a

199

b

Fig. 17.1  (a) Pretreatment photograph of a 47-year-old woman with signs of photoaging. (b) After a series of IPL treatments

adequate penetration. IPL activation of the levulinic acid results in greater heat exchange and a more exuberant reaction. Afterward, strict sun avoidance for 36 h and careful sun protection are critical to minimize persistent redness and blistering. In carefully selected patients, the “activated photofacial” can produce more profound results than IPL alone. However, there is increased cost, risk, and recovery. Dover used pulse durations of 2.4–4.0 ms, interpulse delay of 15 ms, and fluence between 24 and 28 J/cm2 to obtain significant improvements in his patients. He opined that a series of three of these photodynamic rejuvenation procedures produced the same results as five or six plain IPL treatments. Figure 17.2 illustrates the improvement in photoaging in a 52-year-old woman observed after two activated IPL treatments. In general, the best outcomes for the treatment of unwanted hair result from a series of 4–8 IPL treatments spaced at 6–8  week intervals. Troillus [6] reported an 80% reduction in hair counts after 4 IPL treatments in

the bikini line. A pulse duration of 44.5 ms with 1.5 ms interpulse delay, a mean fluence of 18.3  J/cm2 and a 600 nm cutoff filter were used to obtain these results. Likewise, Sadick [7] reported an 83% hair reduction following an average of 3.9 IPL treatments for excessive body hair. Certain body areas require more treatments than others due to skin type, hair density, hair depth, and hormonal considerations. Figure 17.3 shows before and after pictures of a woman treated with a series of IPL treatments for unwanted hair. Numerous vascular lesions have been treated with IPL. The essential telangectasias on the nose and cheeks appear most conducive to this therapy. Angermeier [8] noted small vessel clearance rates of 75–100% in patients treated with up to 4 IPL sessions. Pulse durations of 10–30 ms, interpulse delay of 10 ms, fluence of 10–20 J/cm2, and a 560-nm filter are suitable initial parameters. Leg telangectasias or spider veins can also be treated with IPL. However, additional considerations must be taken into account. First, the existence of underlying varicosities must be ruled out

B.M. Freedman and T.P. Balakrishnan

200

a

b

Fig. 17.2  (a) Pretreatment photograph of a 52-year-old woman with signs of photoaging. (b) After two “activated photofacial” IPL and levulinic acid treatments

a

b

Fig. 17.3  (a) Pretreatment photograph of a 32-year-old woman with unwanted facial hair. (b) After four IPL treatments

as the presence of perforating vessels will preclude ­successful treatment. Second, vessels >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

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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

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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

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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.

218

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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)

220

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

221

222

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

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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

228

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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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.

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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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A.S. Brown and D.J. Goldberg

242 Fig. 22.1  Hemoglobin absorption curve

10,000

Absorption coefficient (cm−1)

418 1,000 542 577 100

10

1 300

400

500

600

700

800

900

1,000

Wavelength (nm)

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

a

243

b

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

a

b

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

A.S. Brown and D.J. Goldberg

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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.

a

b

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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a

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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.

A.S. Brown and D.J. Goldberg

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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 <50% clearance in 12.6% patients. Poor results were correlated with anatomical location on the nasal alae and nasal tip and also with vessel size. They concluded that the copper bromide laser is a safe and effective modality for the treatment of the majority of facial telangiectasias. It is less effective in treating very small vessels and diffuse erythema. In conclusion, there are a variety of lasers and light sources that may be employed for the treatment of facial ectasias and they all have unique individual features. Currently, there is no one device or light source made to treat all types of telangiectasias. Laser medicine has continued to evolve to allow for the treatment of facial telangiectasias with a low risk side effect profile. IPL devices and KTP lasers have become the gold standard for the treatment of facial telangiectasias due to their ease of use, minimal side effects, and greater lesion clearance than other laser systems.

References 1. Goldman L, Blaney DJ, Kindel DJ Jr, Franke EK (1963) Effect of the laser beam on the skin. Preliminary report. J Invest Dermatol 40:121–122 2. Anderson RR, Parrish JA (1983) Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 220(4596):424–427 3. Ross EV, Smirnov M, Pankratov M, Altshuler G (2005) Intense pulse light and laser treatment of facial telangiectasias and dyspigmentation: some theoretical and ­practical complications. Dermatol Surg 31(9 Pt 2): 1188–1198 4. Jorgensen GF, Hedelund L, Haedersdal M (2008) Long pulse dye laser versus intense pulsed light for photodamaged skin a randomized split face trial with blinded response evaluation. Lasers Surg Med 40(5):293–299 5. Silver BE, Livshots YL (1997) Preliminary experience with the KTP/532 nm laser in the treatment of facial telangiectasia. Cosmet Dermatol 9:61–64 6. Tierney E, Hanke CW (2009) Randomized controlled trial: comparative efficacy for the treatment of facial telangiectasia with 532 nm versus 940 nm diode laser. Lasers Surg Med 41(8):555–562

22  Laser Treatment of Telangiectasias 7. Uebelhoer NS, Bogle MA, Stewart B, Arndt KA, Dover JS (2007) A split-face comparison study of pulsed 532-nm KTP laser and 595-nm pulsed dye laser in the treatment of facial telangiectasias and diffuse telangiectatic facial erythema. Dermatol Surg 33(4):441–448 8. Cassuto D, Ancona D, Emanuelli G (2000) Treatment of facial telangiectasias with a diode-pumped Nd:YAG laser at 532 nm. J Cutan Laser Ther 2(3):141–146 9. Aamic M, Troilius A, Adatto M, Drosner M, Dahmane R (2007) Vascular lasers and IPLS: guideline for care from the European Society for Laser Dermatology (ESLD). J Cosmet Laser Ther 9(2):113–124 10. Tanghetti E, Sherr E (2003) Treatment of telangiectasia using the multi-pass technique with the extended pulse width, pulsed dye laser (Cynosure V-Star). J Cosmet Laser Ther 5(2):71–75 11. Goldberg DJ, Meine J (1999) A comparison of four frequency-doubled Nd:YAG (532 nm) laser systems for the treatment of facial telangiectasias. Dermatol Surg 25(6): 463–467 12. Dover JS, Arndt KA (2000) New approaches to the treatment of vascular lesions. Lasers Surg Med 26(2): 158–163

247 13. Travelute Ammirati C, Carniol PJ, Hruza GJ (2001) Laser treatment of facial vascular lesions. Facial Plast Surg 17(3):193–201 14. Bevin AA, Parlette EC, Domankevitz Y, Ross EV (2006) Variable-pulse Nd:YAG laser in the treatment of facial telangiectasias. Dermatol Surg 32(1):7–12 15. Major A, Brazzini B, Campolmi P, Bonan P, Mavilia L, Ghersetich I, Hercogova J, Lottit T (2001) Nd:Yag 1064 nm laser in the treatment of facial and leg telangiectasias. J Eur Acad Dermatol Venereol 15(6):559–565 16. Alam M, Dover JS, Arndt KA (2003) Treatment of facial telangiectasias with variable-pulse high-fluence pulsed-dye laser: comparison of efficacy with fluencies immediately above and below the purpura threshold. Dermatol Surg 29(7):681–684 17. Dover JS, Sadick N, Goldman M (1999) The role of lasers and light sources in the treatment of leg veins. Dermatol Surg 25(4):328–336 18. Dover JS (2000) New approaches to the laser treatment of vascular lesions. Australas J Dermatol 41(1):14–18 19. McCoy SE (1997) Copper bromide laser treatment of facial telangiectasias: results of patients treated over five years. Lasers Surg Med 21(4):329–340

 

23

Mesotherapy Narmada Bharia

23.1 Introduction Pioneered by the French physician Dr. Michel Pistor in 1952, mesotherapy is a minimally invasive procedure that is widely used in Europe and elsewhere to treat various injuries and medical conditions. Multinational research in intradermal therapy culminated with Pistor’s work from 1948 to 1952 in human mesotherapy treatments. The French press coined the term mesotherapy in 1958. The French Academy of Medicine recognized mesotherapy as a Specialty of Medicine in 1987. Popular throughout European countries and South America, mesotherapy is practiced by approximately 18,000 physicians worldwide. This medical specialty targets problem areas with microinjections of conventional or homeopathic medicines, vitamins, minerals, and amino acids. Tiny “medicinal bullets” are delivered directly into the mesoderm (middle layer of skin) that is highly specific to the condition being treated. Among its many applications, mesotherapy can be used for the following: aging, sagging, and wrinkling of the skin, accumulation of fat; loss of skin elasticity, and excessive free radical damage. Infusing potent antioxidants and amino acids by mesotherapy into the dermis at the level of the cellular matrix can reverse

N. Bharia  Medical Operations, 1st Floor, C 10, Dalia Industrial Estate, Off New Link Road, Andheri (W), Mumbai 400058, India e-mail: [email protected]

free radical damage, and tighten loose skin. It rejuvenates and revitalizes the skin of the face and neck with a natural result and with minimal downtime or recovery. Patients who have had mesotherapy for rejuvenation describe their skin as radiant, youthful, and glowing. Mesotherapy is usually performed in an initial series of 2–4 treatments spaced a week apart. Results are maintained by sessions done once a month or as and when required. Mesotherapy skin rejuvenation is a wonderful complement to other skin treatments including photorejuvenation, chemical peels, BOTOX®, and dermal fillers. But it also stands on its own as a powerful antiaging therapy.

23.2 Indications for Mesotherapy in Dermatology 1. Mesotherapy to provide rejuvenation and antiaging benefits 2. Mesotherapy to promote weight loss 3. Mesotherapy for cellulite reduction 4. Mesotherapy to eliminate localized fat deposits Other potential uses in dermatology include 1. Melasma 2. Hair loss 3. Fat deposits – buffalo neck/double chin/lipomas/ xanthelasma 4. Stretch marks 5. Keloids 6. Smokers’ skin 7. Sebum production regulation 8. Psoriasis 9. Body contouring 10. Under eye dark circle and under eye puffiness

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The benefits of mesotherapy include skin rejuvenation, skin tightening, enhanced blood flow and lymphatic drainage, and the breakdown of sclerotic tissue. These effects also improve the appearance of cellulite. Meso­ therapy is a nonsurgical procedure, performed using tiny 4 mm needles. As such, downtime is minimal. Mesotherapy protocols for rejuvenation require the injection of a combination of drugs that have different mechanisms of action. These work synergistically to improve skin clarity and complexion, skin tone, hydrate the skin, and ameliorate unwanted pigmentation and periorbital dark circles. Results vary from person to person and younger patients respond better as compared to older patients. Indications for mesotherapy for rejuvenation include dull skin, irregular skin texture, and uneven skin tone.

23.3 Mechanism of Action The various drugs used have multiple benefits that include the following properties: 1. Antioxidant 2. Detoxification 3. Antipigmention – decrease tyrosinase activity 4. Vasoprotective effect 5. Collagen synthesis 6. Photo protective effect There are a number of mesotherapy drugs and compounds that are used worldwide; these drugs are used in various combinations to obtain the desired benefit. The following substances can be used: 1. DMlift – DMAE 2. Silorgamine – DMAE + organic silicium 3. Hyalift – non-reticulated hyaluronic acid 4. GSH – glutathione 5. Purascorbol – ascorbic acid 6. Dermastabilon – phosphatidylcholine + deoxycholate 7. Taurinox – taurine 8. Silorg – organic silicium 9. Centellasial – ivy/sea weed extracts 10. Puretinol – retinoic acid 11. Melirutol – coumarin 12. L-carnitrans – L carnitine (amino acid) 13. Pyrustim – sodium pyruvate 14. Dexenol – Dexpanthenol 15. Biovita-H – biotin¨botulinum toxin 16. Bilobin-G – Ginkgo¨Biloba 17. Mixture of vitamins A, C, E, K 18. Mixture of minerals Zn, Cu, Se, Cr, Mn

N. Bharia

Mesotherapy is useful for: Nutrition: polyvitamins, hyaluronic acid, micro trace elements, etc. Metabolic stimulation: glycolic acid and retinoic acid. Enzymatic enhancement: collagenase and hyaluronidase. Fat dissolution: phosphatidylcholine and/or deoxycholate. Myofibrillar relaxation: Dimetylaminoethanol (DMAE).

23.4 Vitamins The vitamins provide an antideficiency function. Vitamin A acts on the flexibility of the skin by regulating the growth of epidermal cells. By acting on the keratinization process, it favors cicatrization and partially corrects the thinning of the dermis due to skin aging. Vitamin E is an antioxidant due to its major antiradical properties. It maintains the integrity of ­tissue by fighting the formation of toxic peroxides. Vitamin C helps stimulate the synthesis of collagen and inhibit the synthesis of melanin. Vitamin D is required for the homeostasis of calcium. Vitamin B and its sub-groups are excellent antideficiency substances and are essential for the healthy functioning of the skin. Vitamin K plays a major role in the regulation of the microcirculation. The amino acids allow better protein construction, minerals guarantee the ionic balance of the medium, coenzymes activate the biochemical reactions.

23.5 Drugs for Various Skin Treatments For rejuvenation DMlift – DMAE (dimethylethanalomine) Silorgamine – DMAE + organic silicium Hyalift – non-reticulated hyaluronic acid GSH – glutathione Purascorbol – ascorbic acid¨Taurinox-taurine Silorg – organic silicium Centellasial – ivy/sea weed extracts Puretinol – retinoic acid¨Pyrustim – sodium pyruvate Botox Glycolic acid

23  Mesotherapy

Mixture of minerals Zn, Cu, Se, Cr, Mn Mixture of vitamins A, C, E, K Skin tightening/lift DMlift – DMAE Silorgamine – DMAE + organic silicium Hyalift – non-reticulated hyaluronic acid GSH – glutathione Purascorbol – ascorbic acid Taurinox – taurine Puretinol – retinoic acid Silorg – organic silicium Botox – botulinum toxin Bilobin-G – Ginkgo biloba Glycolic acid Drugs for cellulite treatment Dermastabilon – phosphatidylcholine + deoxycholate Silorg – organic silicium Centellasial – ivy/sea weed extracts Melirutol – coumarin L-carnitrans – L carnitine (amino acid) Pyrustim – sodium pyruvate Drugs for lipolysis Dermastabilon L-carnitrans Silorg Silorgamine Drugs for melasma GSH – glutathione Purascorbol – ascorbic acid Dexenol Pyrustim Drugs for hair loss Minoderma – minoxidil Final hair – finasteride Dexenol Bilobine-G Biovita-H

23.6 Products Used for Mesotherapy for Rejuvenation 23.6.1 GSH: 5 mL vial – 100 mg Content: Glutathione Mechanism of Action Antioxidant. Detoxifying agent – glutathione S-transferase is involved in detoxification and protection against degeneration.

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Depigmenting agent – direct inactivation of tyrosinase quenching free radicals and peroxides that contribute to tyrosinase activity, modulation of depigmenting abilities of melanocytotoxic agents. Indications: melasma, antiaging, rejuvenation. Side effects: none reported.

23.6.2 Purascorbol: 5 mL vial – 1 g Content: Ascorbic Acid Mechanism of Action Stimulates collagen synthesis, healing, and wound repair. For psoriasis and atopic dermatitis, replenish vitamin C concentration. Photoprotective action – rescue keratinocytes from UV-mediated cytotoxicity. Inhibition of melanogenesis – antityrosinase, antioxidant indications: glow and pigmentation, antiaging, melasma, psoriasis, atopic dermatitis, hair loss, skin healing enhancement.

23.6.3 Silorgamine: 5 mL ampoule Content: 1 mL − 5% DMAE and 4 mL 0.5% Organic Silicium DMAE: Dimethylethanalomine is a precursor of acetylcholine a neuromediator which plays an important role in dermis and epidermis.

23.6.3.1 Actions Keratinocytes, fibroblasts, myofibroblasts, sweat glands, and endothelial cells have membrane receptors responding to acetylcholine. The tensile effect of DMAE may result in a cholinergic stimulation of membrane receptors of fibroblasts and simulate progressive contraction of myofilaments. DMAE also has antiradical and antilipofuscin thus repairing collagen and elastin damage. This results in the tensing effect on the skin which can be instantaneous and noticed by the patient immediately after the procedure. Indications: Antiaging skin tightening. Also used in mixtures for tensing face and body (arms, legs, abdomen) skin. Toxicity: Allergic contact dermatitis but only with prolonged contact with very large doses. Organic silicium: silicium induces longer and wider fibril synthesis by fibrillogenesis.

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23.6.3.2 Organic Silicium Content Monomethyl trisilanol salicylate actions: silicium induces longer and wider collagen fibril synthesis by fibrillogenesis. Indications: Antiaging, wound healing, alopecia, lypolysis. Toxicity: No toxicology or side effects have been reported.

23.6.4 Taurinox: 8 mL vial – 50 mg Content Taurine which is a semi-essential sulfur ­containing beta amino acid found in all tissues. Mechanism of action: with aging, hepatic taurine production falls producing aging-related diseases. Involved in keratinocyte volume hemostasis and hydration in the dermis. Increases hydroxyproline  dermal concentration resulting in increased collagenogenesis. Antioxidant effect – free radical scavenger and restores GSH and catalase cellular content after oxidative stress. Anti-inflammatory. Vasoprotective – prevents progression of atherosclerosis. Indications: antiaging, smokers skin, skin rejuvenation toxicity: it is a non-toxic endogenous antioxidant.

23.7 Techniques of Injections Mesotherapy involves injecting microquantities of medicine in the right place, using one of the following techniques. Intra-epidermal technique involves placing small quantities of the medicine within the epidermis. It is simple, painless, and there is no bleeding. This ­technique is useful for patients with low pain threshold and is ideal for facial rejuvenation. Papular technique involves injecting the medicine at the dermoepidermal junction. It is useful for the treatment of wrinkles and alopecia. This is the technique used for mesobotox. Nappage – Here injections are given at a depth of 2–4 mm at an angle of 30–60°. It is used mainly on scalp and in the treatment of cellulite. Point by point – This is a precise single injection into the deep dermis. It is used mainly for fat reduction.

N. Bharia

Adverse effects of mesotherapy for face ­rejuvenation are uncommon and depend on the product used. Bruising may occur especially in the periorbital area and on curvatures but is mild and subsides in a few days. Itching and burning sensation may occur. Pain especially on the forehead. Pinpoint papules/minimal erythema may occur and subside in an hour or two. Skin necrosis with phosphatidylcholine can occur due to the irritant effect on dermis and epidermis. Liver toxicity, vasovagal attack, and demyelination of nerves have been reported with large doses of phosphatidylcholine. Atypical mycobacterial infections are a rare side effect. Following mesotherapy there have been reports of atypical mycobacterial infections at sites of injections necessitating antimycobacterial therapy.

23.8 Alternative to Mesotherapy: Needleless Mesotherapy This is a newer technique which delivers the mesotherapy products by using ultrasound and/or iontophoresis. Although it is less traumatic and painless, the efficacy of this treatment does not compare to traditional mesotherapy. It may be an option if patients insist on a painless procedure. Dermoelectroporation, electroporation, or electropermeabilization causes significant increase in the electrical conductivity and permeability of the cell plasma membrane by an externally applied electrical field. It is usually used in molecular biology as a way of introducing some substance into a cell, such as loading it with a molecular probe, a drug that can change the cell’s function or a piece of coding DNA. Pores are formed when the voltage across a plasma membrane exceeds its dielectric strength. If the strength of the applied electrical field and/or duration of exposure to it are properly chosen, the pores formed by the electrical pulse reseal after a short period of time, during which extracellular compounds have a chance to enter into the cell. This system is a powered drug-delivery system that has been FDA approved for the “local administration of ionic drug solutions into the body for medical purposes and can be used as an alternative to injections”. Dermoelectroporation® technology utilizes the skin’s water-based “channels” to allow ionic drug solutions to penetrate due to ­controlled “electroporation-like”

23  Mesotherapy

continuous reversed polarity electrical pulses delivery. These pulses increase the skin permeability and allow transdermal delivery of drugs as occurs in traditional iontophoresis, even if the average current value on the patient is zero. Due to this either micromolecules or macromolecules (greater than 800 Kdalton in size, such as hyaluronic acid, vitamins, amino acids, and heparin) are safely delivered into the body without either modification of the ionic drug solutions pH or electrolysis effect of the ionic solution itself. This was not possible with traditional iontophoresis systems before both positive and negative ions of the drug are transdermally delivered, which means that the technology works like

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an injection and it is not invasive. When combined with ­microdermabrasion it allows for a very efficient transdermal delivery of products. Microdermabrasion enables a standardization of the skin characteristics, so the drug delivery rate is reproducible. This was one of the drawbacks with the classical iontophoresis. This new technique is used to provide the following: 1. Skin biorevitalization treatments 2. Cellulite treatments 3. Needles free mesotherapy applications 4. Pre-laser treatments 5. Skin resurfacing 6. Botox for axillary hyperhidrosis

 

Mesotherapy Solutions for Inducing Lipolysis and Treating Cellulite

24

Benje Gutierrez and Frank L. Greenway

24.1 Background The way that mesotherapy is practiced is a result of the way in which it came into being, so a review of the history is appropriate. Michael Pistor, a physician in France, injected a man suffering from asthma with procaine during the 1950s. The man’s asthma did not improve, but his deafness improved temporarily. Thus, mesotherapy was born and was given that name by Dr. Pistor because he injected into the tissue derived from mesoderm, skin, and subcutaneous tissue [1]. Mesotherapy became increasingly popular in France, and the injection of procaine was used for a variety of diseases. Dr. Pistor developed a syringe with multiple needles to assist in speeding the injection process, and mesotherapy has even been taught in French medical schools. A smooth appearance to the skin is felt to be beautiful, but the structure of the subcutaneous adipose tissue in women includes fibrous connective tissue septae that surround fat cells and attach to the underside of the skin. As fat cells increase in size, the septa are stretched and pull down on the underside of the skin making dimples. This orange-peel appearance to the thighs is felt by women to be cosmetically unappealing and was given the term “cellulite” by Ronsard in her popular book

B. Gutierrez ATI College of Health, Miami, FL 33169, USA F.L. Greenway (*) Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA e-mail: [email protected]

written in the early 1970s [2]. Although she suggested a therapy to rid women of cellulite, no experimental evidence has been published to support her suggestions. Mesotherapy has become popular in the United States as a treatment for cellulite and to reduce local accumulations of fat. Mesotherapy can be divided into two general types. One type involves the injection of phosphatidylcholine and deoxycholate to destroy the fat cells, and the second is based on increasing lipolysis locally to reduce fat cell size. Deoxycholate is a detergent that destroys cell membranes. The injection of deoxycholate or phosphati­ dylcholine with deoxycholate results in immediate burning, erythema, transient urticaria, and variable amounts of itching. Biopsies taken one and two weeks following the procedure demonstrate a panniculitis with lymphocytic and macrophage infiltration. The macrophages consist of foam cells and multinucleated fat-containing giant cells. The inflammation was associated with serious atrophy and microcyst formation [3]. Complications of this form of therapy have been reported, including benign neuromas, permanent scarring, skin deformation, and painful subcutaneous knots [4]. A warning about the unapproved nature of this therapy was issued by the FDA in 2010. Although the injection of phosphatidylcholine and deoxycholate has been considered mesotherapy, the rest of this chapter will consider nonablative treatments for cellulite and local fat reduction due to their greater safety and the cloud overhanging ablative fat therapy due to the attention focused upon it by the FDA. Mesotherapy based on stimulating lipolysis evolved from Pistor’s experience and some of the physicians who brought the practice to the United States studied under Pistor. Pistor started mesotherapy with the injection

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Fig. 24.1  Lipolysis fold induction compared to assay buffer. Iso isoproterenol, Amin aminophylline, Yoh yohimbine

Lipolysis fold induction compared to assay buffer 3.5

Glycerol fold induction

3 2.5 2 1.5 1 0.5 0

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of procaine, and since it is a local anesthetic that should reduce any pain associated with injections, it has traditionally been included in mesotherapy injections to stimulate lipolysis. Although many of the solutions used to stimulate lipolysis and reduce cellulite are known to stimulate lipolysis, they are often used in combination on the presumption that they will work better together, and homeopathic remedies that have not been tested for their lipolytic potential have been used as well. Since these lipolytic combinations and some of the homeopathic remedies have not been tested for their potential to stimulate lipolysis we attempted to fill that knowledge gap.

24.2 Lipolytic Mesotherapy Solutions The authors discussed mesotherapy lipolytic solutions with a physician who practices mesotherapy. On the basis of that discussion it was chosen to test isoproterenol, aminophylline, and yohimbine, three compounds that have been demonstrated to stimulate lipolysis. They were tested alone and in combination to determine whether combining them gives superior lipolysis. Melilotus, an extract of sweet clover, was chosen to test as an example of a compound that has been used empirically to stimulate lipolysis. Since there is evidence in the literature to suggest that local anesthetics can inhibit lipolysis, we also tested the effect of ­including lidocaine in the lipolytic mixture [5].

Iso

Amin

Yoh

The mesotherapy solutions were tested in a human fat cell assay. The differentiated human adipocytes in 96-well plates generate glycerol into the media in proportion to the amount of lipolysis. The results of the assay are a comparison of the fold induction of glycerol induced by the compound being tested compared to the buffer. Isoproterenol and/or isobutylmethylxanthine (IBMX) were used in the assay as positive controls. The incubation time in the assay was 5 h and the glycerol was measured by adding a glycerol reagent that could be read in a colorimetric assay using a spectrophotometer at 540 nm and compared to a standard curve. The concentration of the mesotherapy solutions tested was chosen through consultation with the ­physician mesotherapist who gave us the concentrations to test that were used in patients undergoing mesotherapy. As expected, isoproterenol, aminophylline, and yohimbine all stimulated lipolysis significantly and between 2 and 3 times the values in the buffer control (Fig. 24.1). Melilotus was shown to stimulate lipolysis significantly compared to control, and lipolysis was further stimulated to a significant degree over melilotus alone with the addition of aminophylline (Fig.  24.2). Isoproterenol stimulated lipolysis significantly compared to control, and the addition of aminophylline stimulated lipolysis to a significant degree over isoproterenol alone (Fig.  24.3). When lidocaine was added to isoproterenol and aminophylline, lipolysis was inhibited to a level no different than control (Fig.  24.4). The combination of

24  Mesotherapy Solutions for Inducing Lipolysis and Treating Cellulite Fig.  24.2  Lipolysis fold induction compared to assay buffer. Mel/Amin melilotus and aminophylline, Mel melilotus

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Lipolysis fold induction compared to assay buffer 3

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Lipolysis fold induction compared to assay buffer

4 Glycerol fold induction

3.5 3 2.5 2 1.5 1 0.5

Fig. 24.3  Lipolysis fold induction compared to assay buffer. Iso isoproterenol, IA isoproterenol and aminophylline

0

4.5

Buffer

Iso

IA

Lipolysis fold induction compared to assay buffer

4 Glycerol fold induction

3.5

Fig. 24.4  Lipolysis fold induction compared to assay buffer. IA Isoproterenol and Aminophylline, IA-L isoproterenol, aminophylline, and lidocaine

3 2.5 2 1.5 1 0.5 0

Buffer

IA

IA-L

258

B. Guiterrez and F.L. Greenway Lipolysis fold induction compared to assay buffer

3 2.5 Glycerol fold induction

Fig. 24.5  Lipolysis fold induction compared to assay buffer. IAY Isoproterenol, Aminophylline, and Yohimbine, IAY-L isoproterenol, aminophylline, yohimbine, and lidocaine

2 1.5 1 0.5 0

Buffer

IAY

IAY-L

Table 24.1  Stimulation of lipolysis by compounds used in mesotherapy Fold induction Components IBMX control Assay buffer Aminophylline Isoproterenol Yohimbine Melilotus Melilotus Aminophylline Aminophylline Isoproterenol Aminophylline Isoproterenol Yohimbine Aminophylline Isoproterenol Lidocaine Aminophylline Isoproterenol Yohimbine Lidocaine

Concentration (SEM) 1.0 × 10−4 M full strength 1.0 × 10−4 M 1.0 × 10−7 M 1.0 × 10−7 M 0.02% 0.02% 1.0 × 10−4 M 1.0 × 10−4 M 1.0 × 10−7 M 1.0 × 10−4 M 1.0 × 10−7 M 1.0 × 10−7 M 1.0 × 10−4 M 1.0 × 10−7 M 1.0 × 10−5 M 1.0 × 10−4 M 1.0 × 10−7 M 1.0 × 10−7 M 1.0 × 10−5 M

Observations (wells) n = 3 n = 5 n = 3 n = 3 n = 3 n = 3 n = 3

2.5 ± 0.12

p-value p < 0.01 control p < 0.00004 p < 0.002 p < 0.001 p < 0.01 p < 0.001 vs. control p < 0.001 vs. melilotus p < 0.001 vs. control p < 0.01 vs. isoproterenol p < 0.0007 vs. control

1.5 ± 0.41

p = NS vs. control

n = 21

1.4 ± 0.04

p < 0.05 vs. control

n = 3

2.3 ± 0.24 1.0 2.5 ± 0.57 2.7 ± 0.06 2.0 ± 0.19 2.2 ± 0.33 2.7 ± 0.05 3.6 ± 0.42

i­ soproterenol, aminophylline, and yohimbine stimulated lipolysis to a significant 2.5-fold above the control. When lidocaine was added to isoproterenol, aminophylline, and yohimbine, the fold induction dropped to less than 1.5 times control, but the stimulation was still statistically different from control at p < 0.05 (Fig. 24.5). These studies confirmed the known stimulation of lipolysis by isoproterenol, aminophylline, and yohim-

n = 20 n = 3

bine alone. In addition, they demonstrated that ­combining these lipolytic stimulators gave additive lipolytic stimulation. Melilotus was shown to stimulate lipolysis and aminophylline was shown to give additive lipolysis in combination with melilotus. As suggested by prior studies showing the lipolytic inhibition of local anesthetics, lidocaine dramatically inhibited the lipolysis of lipolytic stimulator combinations (Table 24.1).

24  Mesotherapy Solutions for Inducing Lipolysis and Treating Cellulite

There are several messages that can be derived from these studies. First, it is important to confirm that the products used to stimulate lipolysis in the mesotherapy practice actually do stimulate lipolysis. Products like lidocaine which are now routinely included in mesotherapy solutions and inhibit lipolysis should be eliminated from mesotherapy solutions in the future. Lipolytic inhibition has been confirmed for procaine [6] and others have shown that procaine uncouples adenylate cyclase from activating hormone-sensitive lipase, the lipolytic enzyme in fat cells [7]. The inhibition of lipolysis by procaine is shared by lidocaine [8], and since another topical anesthetic, prilocaine, also inhibits lipolysis, this inhibition of lipolysis seems to be a class effect of local anesthetics that inhibit sodium channels [9]. Secondly, although melilotus was confirmed to be a lipolytic stimulator and adds to the stimulation of lipolysis by aminophylline, other herbal or homeopathic ingredients without data being used by mesotherapists to stimulate lipolysis should be studied in the same way as we studied melilotus to insure that all the products included in mesotherapy solutions stimulate, and do not inhibit, lipolysis. Thirdly, the contention by mesotherapists that different lipolytic stimulators give additive stimulation of lipolysis was confirmed for isoproterenol, aminophylline, and yohimbine as well as for melilotus and aminophylline. It is well known that isoproterenol stimulates the betaadrenergic receptor, aminophylline inhibits phosphodiesterase and the adenosine receptor, and that yohimbine is an alpha-2 adrenergic inhibitor. Thus, all three of these compounds work through a different mechanism and might be predicted to give additive lipolytic stimulation. Other herbal products used in mesotherapy solutions may not have been tested. In addition, even if they are found to be stimulators like melilotus, the mechanism of action in stimulating lipolysis may be unknown. Thus, although some lipolytic stimulators are clearly additive, additivity should be tested as we did with the combinations we studied in the assay. Without doing so, one could easily combine two lipolytic stimulators that work by the same mechanism will not increase lipolysis when used together and might add to potential adverse events.

24.3 Lipolysis in Humans During fat loss following bariatric surgery, it was noted that the thigh fat was lost more slowly than fat from the abdominal region in women [10, 11]. Lipolysis can be

259

Lipolysis Beta V

Adenosine V

Gs G1

Alpha 2 Gs

Adenylate Cyclase

Phosphodiesterase

Cyclic AMP

V G1 5′AMP

Adenylate cyclase A-kinase Hormone sensitive lipase

Glycerol & fatty acids

Fat cell

Fig. 24.6  Fat cell with the simulatory beta-adrenergic receptor working through a stimulatory G-protein, adenosine and alpha-2 adrenergic inhibitory receptors working through inhibitory G proteins. Stimulation of adenylate cyclase stimulates hormone sensitive lipase through generation cyclic AMP which activated adenylate cyclase A kinase. Phosphodiesterase is the enzyme that breaks down cyclic AMP. The stimulation of hormone sensitive lipase results in the lipolysis with the release of glycerol and free fatty acids

influenced in several ways. Isoproterenol directly stimulates the beta-adrenergic receptor which increases cyclic AMP inside the fat cell leading to stimulation of hormone-sensitive lipase and release of fatty acids and glycerol. Methylxanthines inhibit phosphodiesterase, the enzyme that breaks down cyclic AMP. Thus, ­methylxanthines amplify the cyclic AMP signal inside the fat cell and increase lipolysis. In addition, methylxanthines inhibit the adenosine receptor on fat cells. The adenosine receptor inhibits the beta receptor through an inhibitory G-protein, and inhibiting the adenosine receptor increases lipolysis by releasing the beta receptor from adenosine-mediated inhibition. Yohimbine, on the other hand, is an alpha-2 adrenergic inhibitor. The alpha-2 receptor also stimulates an inhibitory G-protein that reduces the activity of the beta-adrenergic receptor. Inhibiting the alpha-2 ­adrenergic receptor on the fat cell stimulates lipolysis by releasing the beta-adrenergic receptor from alpha-2 inhibition (Fig. 24.6). Women have more alpha-2 adrenergic receptors on the fat cells of their hips and thighs due to the influence of estrogen [12]. This is the reason that women have larger hips and thighs than men and why they develop more of an abdominal fat pattern as their estrogen falls at menopause. The reason for the fat distribution on the hips and thighs of women in the reproductive age group has been attributed to the need for women to store fat

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for pregnancy and lactation. The fat is ­distributed on a person’s body according to the ­lipolytic threshold in the fat cells at different body sites. The lipolytic threshold is high in the female thigh due to the estrogen-mediated increase in alpha-2 adrenergic receptor numbers in that site. Women with lower body obesity tend to have smaller breasts and desire larger breasts with smaller thighs. Unfortunately, due to the differential lipolytic thresholds, lower body obese women lose weight from their breasts while their thighs remain large. In addition to the size of their hips and thighs, women are concerned about the skin appearance as well. There are connective tissue strands that attach to the underside of the skin and to deeper structures within the fat tissue. As the fat cells enlarge, they put tension on these connective tissue strands creating a downward pull on the underside of the skin. This downward pull creates dimples that have been termed cellulite on the thighs. The connective tissue strands are oriented at right angles to the skin surface in women and have a more diagonal orientation in men making women more susceptible to the appearance of cellulite than men [13].

24.4 Treating Cellulite and Local Fat Deposits with Mesotherapy The authors have used isoproterenol as the lipolytic agent in the injection studies to explore fat physiology [14]. In the first study, the effect of isoproterenol on thigh girth was evaluated. Since the lipolytic response to isoproterenol peaks at around 10−6  M and then declines slowly at higher doses, 10−5 M was chosen for the first experiment in mesotherapy thinking that the concentration might be diluted somewhat in the tissues [15]. Since isoproterenol has a vasodialation effect, it was possible to observe a circular red spot on the thighs of light skinned individuals after injection. By knowing the length of the insulin needle when injecting 0.2  mL of isoproterenol and the size of the red spot, the authors were able to determine that the isoproterenol diffused in a sphere with a radius of 2 cm. Thus, the circumference of the thigh was injected with 0.2  mL of isoproterenol every 4  cm. The thigh was measured 2/3 of the distance from the knee to the greater trochanter with the women supporting their weight on the measured thigh to keep muscle tension uniform in the thigh for measurement. Five women

B. Guiterrez and F.L. Greenway

participated in this study with body weights ranging from 53 to 130  kg. They were asked to follow a 600 kcal/d diet to reduce the lipolytic threshold, and they lost between 0 and 2 kg over the 4-week treatment period. The injections of isoproterenol were given daily 5 days per week on one thigh, and saline injections on the other thigh served as a control. The subjects and the person administering the injections were blind to the thigh assigned to isoproterenol or control. All subjects except one, the subject who lost no weight, lost more girth from the treated than from the untreated thigh. The subject who did not lose weight had no differential thigh girth loss. The average thigh girth loss over the 4 weeks was 1.5 cm, which was statistically significant (p < 0.05) [14]. The next study was to evaluate stimulation of lipolysis in lipomas as a potential nonsurgical treatment. Lipomas are benign subcutaneous fatty tumors that grow slightly faster than the surrounding fat tissue. Although maximal stimulated lipolysis in lipomas has been reported to be normal, the ability to regulate lipolysis has been reported to be impaired in lipomas due to a lack of feedback inhibition on phosphofructokinase by citrate [16]. The standard treatment for lipomas is surgery, but this treatment is limited by poor aesthetic outcomes due to deformation and scarring. Ablative measures to treat lipomas with deoxycholate and phosphatidylcholine gave less than a 50% reduction in size and created a painful inflammatory response that lasted 3 days [17]. Isoproterenol is a beta-2 adrenergic agonist approved for injection in humans. Glucocorticoids have been demonstrated to increase the appearance of beta-2 receptors on murine fat cells at low concentrations (2.5 nM to 10 mM) [18]. The prevention of beta-2 adrenergic receptor down-regulation by low doses of corticosteroids has been confirmed in human subcutaneous fat cells [19]. Since prednisolone is a glucocorticoid that is approved for injection in humans, the authors tested the potential of injected isoproterenol with prednisolone to act as a nonsurgical therapy for lipomas. The authors first tested the concentration of isoproterenol that has been shown to maximally stimulate lipolysis, 10−6 M, with a dose range of prednisolone to determine the optimal lipolytic concentration. Maximal lipolysis was seen in a human fat cell assay using glycerol generation as a readout at a prednisolone concentration of 10−6  M with isoproterenol 10−6  M. The lipolysis in a lipoma was compared to the lipolysis in

24  Mesotherapy Solutions for Inducing Lipolysis and Treating Cellulite

subcutaneous fat in the same person, using 5 healthy volunteers with subcutaneous lipomas. The lipomas responded with less lipolysis to isoproterenol than subcutaneous fat during mirodialysis in  vivo. During microdialysis, prednisolone increased lipolysis in both lipomas and subcutaneous fat. The 5 microdialysis subjects and 5 additional subjects with subcutaneous lipomas were treated 5 times a week for 4 weeks with injections of 0.2 mL of prednisolone 10−6 M and isoproterenol 10−6 M into the lipoma in a 4 cm grid. The lipomas decreased an average of 50% in volume and the 2 subjects who did not have surgery had a slow increase in volume with return to baseline volume over the ensuing year. To evaluate the satisfaction of subjects with the therapy, those who desired surgery after the month of injections had their lipoma removed at the expense of the study. Eight of 10 subjects elected for surgery to remove the lipoma. The subjects who did not request surgery had lipomas of less than 3 cm in diameter which responded to the treatment with a 70% reduction in volume. Thus, if there is a subset of patients with lipomas who might be candidates for this treatment, it would appear to be those with lipomas of less than 3  cm in diameter. There were no adverse reactions to the treatment and urinary free cortisol remained normal, confirming that the glucocorticoid did not have a systemic effect [20].

24.5 Noninvasive Treatments for Cellulite and Local Fat Reduction Although mesotherapy has been increasing in popu­ larity and other injectable cosmetic therapies like ­botulinum toxin have flourished, it only seems logical that a safe and effective noninjection therapy for ­cellulite would be even more acceptable to patients. We ­demonstrated that cream containing forskolin (a beta-adrenergic stimulator) and a cream containing aminophylline (a phosphodiesterase and alpha-2 adrenergic receptor inhibitor) each gave safe and effective girth loss from the treated thigh compared to a vehicle treated control thigh. The girth reduction was greatest with aminophylline, so aminophylline cream was used for the rest of our experimentation. Through a series of clinical trials, the authors were able to demonstrate that aminophylline 0.5% cream was more effective than higher concentrations. This observation is consistent with the dose response of lipolysis that

261

falls off at higher and lower concentrations compared to the concentration that gives maximal lipolysis [15]. Treatment with 0.5% aminophylline cream applied once a day 5 days a week for 4 weeks in weight stable women gave a 2.5 cm greater reduction in girth compared to the thigh treated with vehicle control which was highly significant statistically. The women noted a smoothing of the skin and improvement in the appearance of cellulite by the 2-week point in the study. Aminophylline is a reactive molecule and the cream base needs to stabilized so that the ethylene diamine joining the two theophylline molecules of aminophylline does not react with the cream base. If the aminophylline is not stabilized the ethylene diamine will react with the cream base, causes the cream to turn from white to yellow, and inactivate its ability to give girth loss and cause rashes [21]. The fat distribution of the body is controlled by the local lipolytic thresholds of subcutaneous fat cells. Therefore, it should be possible to reduce the lipolytic threshold in an area from which one wants to lose fat and direct the location where the fat will disappear with weight loss. Reducing a local lipolytic threshold will also direct where the fat will be mobilized during the night as the body uses its fat stores until breakfast when a person is weight stable. Our studies with aminophylline cream on the thigh demonstrated girth loss without weight loss [21]. We demonstrated direction of weight loss from the waist in 50 centrally obese men and women who went on a dietary weight loss program and were randomized to aminophylline 0.5% cream to the waist (25 subjects) or no cream treatment (25 subjects) for 12  weeks [22]. Both groups lost exactly the same amount of weight, but the group using the aminophylline cream lost 11 cm from waist girth compared to only 5 cm in the control group, a difference which was highly significant. Another promising noninvasive treatment for cellulite and local fat reduction is low-level laser treatment. This minimal risk device has been shown to create pores in fat cells using scanning electron microscopy. These pores allow the fat to escape into the interstitial space and be taken away by the lymphatics [23]. It was demonstrated that 2 low level laser treatments per week over 4  weeks to the waist gave a 2.15  cm girth loss that was statistically significant. It was also demonstrated that the low level laser released triglycerides from the fat cells into the lymphatic space without any inflammation or cell death [24].

262

24.6 Discussion Mesotherapy is a process of injection into the skin and subcutaneous tissues. Although deoxycholate and phosphatidylcholine have been used to ablate fat cells, this form of mesotherapy is associated with inflammation, pain edema, and scarring. Mesotherapy that injects lipolytic substances has the potential to be safer, but mesotherapy has developed in an empirical manner with few studies to confirm its efficacy. In fact, local anesthetics that block lipolysis have been routinely included in many mesotherapy solutions, a practice that should be discouraged. Mesotherapists have empirically included many untested, but potentially lipolytic, substances in mesotherapy combinations. Although mesotherapy combinations can give additive lipolysis, and some lipolytic compounds like melilotus appear to be safe and effective, others like triiodothyroacetic acid have been reported to give adverse events like thyrotoxicosis [25]. It is imperative that mesotherapy solutions and their components be tested to confirm lipolytic activity prior to use in mesotherapy treatments. Reduction in the lipolytic threshold can direct where fat is lost during a weight loss program or cause a redistribution of fat from the site of the lowered threshold when weight is stable. The same principle could be applied to lipomas or other abnormal fat collections, but large lipomas are not reduced sufficiently in volume to avoid surgical treatment. Not only can local fat loss be engendered by injections, but lipolytic creams have been demonstrated to be safe and effective. New low-energy laser treatment also shows promise and seems to work by creating pores in the fat cells which empty their triglycerides into the interstitial space to be removed by the lymph system.

24.7 Conclusions Lipolytic mesotherapy solutions are often combined. Some combinations are effective for increasing lipolysis more than the individual components, but the components and combinations should be tested in an in vitro human fat cell assay for lipolytic activity prior to their empiric use. Some previously untested herbal ingredients like melilotus do give active lipolysis, but lidocaine, which has been routinely included in ­lipolytic solutions, blocks lipolysis and should be avoided. Although

B. Guiterrez and F.L. Greenway

mesotherapy appears to be an effective cosmetic procedure, other noninvasive treatments like lipolytic creams and low-level laser treatment hold promise as noninvasive cosmetic treatments that may be safer.

References 1. Pistor M (1964) Mesotherapy. Librairie Maloine S.A, Paris 2. Ronsard N (1973) Those lumps, bumps and bulges you couldn’t lose before. Beauty and Health Publishing Co., New York 3. Rose PT, Morgan M (2005) Histological changes associated with mesotherapy for fat dissolution. J Cosmet Laser Ther 7:17–19 4. Nabavi CB, Minckler DS, Tao JP (2009) Histologic features of mesotherapy-induced orbital fat inflammation. Ophthal Plast Reconstr Surg 25:69–70 5. Caruso MK, Roberts AT, Bissoon L, Self KS, Guillot TS, Greenway FL (2008) An evaluation of mesotherapy solutions for inducing lipolysis and treating cellulite. J Plast Reconstr Aesthet Surg 61:1321–1324 6. Mersmann HJ (1983) Effect of anesthetic or analgesic drugs on lipogenic and lipolytic adipose tissue activities. Proc Soc Exp Biol Med 172:375–378 7. D’Costa MA, Asico W, Angel A (1979) Inhibition of rat and human adipocyte adenylate cyclase in the antilipolytic action of insulin, clofibrate, and nicotinic acid. Can J Biochem 57:1058–1063 8. Komabayashi T, Sakamoto S, Tsuboi M (1978) Effects of various drugs on the lipolytic actions caused by catecholamines and methylxanthine derivatives in white adipose tissues. 1. Effects of procaine and xylocaine. Nippon Yakurigaku Zasshi 74:459–466 9. Arner P, Arner O, Ostman J (1973) The effect of local anaesthetic agents on lipolysis by human adipose tissue. Life Sci 13:161–169 10. Kral JG, Bjorntorp P, Schersten T, Sjostrom L (1977) Body composition and adipose tissue cellularity before and after jejuno-ileostomy in severely obese subjects. Eur J Clin Invest 7:413–419 11. Smith U, Hammersten J, Bjorntorp P, Kral JG (1979) Regional differences and effect of weight reduction on human fat cell metabolism. Eur J Clin Invest 9:327–332 12. Lafontan M, Berlan M (1993) Fat cell adrenergic receptors and the control of white and brown fat cell function. J Lipid Res 34:1057–1091 13. Pierard GE, Nizet JL, Pierard-Franchimont C (2000) Cellulite: from standing fat herniation to hypodermal stretch marks. Am J Dermatopathol 22:34–37 14. Greenway FL, Bray GA (1987) Regional fat loss from the thigh in obese women after adrenergic modulation. Clin Ther 9:663–669 15. Crampes F, Beauville M, Riviere D, Garrigues M (1986) Effect of physical training in humans on the response of isolated fat cells to epinephrine. J Appl Physiol 61:25–29 16. Atkinson JN, Galton DJ, Gilbert C (1974) Regulatory defect of glycolysis in human lipoma. Br Med J 1:101–102

24  Mesotherapy Solutions for Inducing Lipolysis and Treating Cellulite 17. Bechara FG, Sand M, Sand D et al (2006) Lipolysis of ­lipomas in patients with familial multiple lipomatosis: an ultrasonography-controlled trial. J Cutan Med Surg 10:155–159 18. Lai E, Rosen OM, Rubin CS (1982) Dexamethasone regulates the beta-adrenergic receptor subtype expressed by 3 T3 L1 preadipocytes and adipocytes. J Biol Chem 257:6691–6696 19. Lacasa D, Agli B, Giudicelli Y (1988) Permissive action of glucocorticoids on catecholamine-induced lipolysis: direct “in vitro” effects on the fat cell beta-adrenoreceptor-­coupledadenylate cyclase system. Biochem Biophys Res Commun 153:489–497 20. Redman LM, Moro C, Dobak J, Yu Y, Guillot TS, Greenway FL (2011) Association of beta-2 adrenergic agonist and corticosteroid injection in the treatment of lipomas. Diabetes Obes Metab 13(6):517–522

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21. Greenway FL, Bray GA, Heber D (1995) Topical fat reduction. Obes Res 3(Suppl 4):561S–568S 22. Caruso MK, Pekarovic S, Raum WJ, Greenway F (2007) Topical fat reduction from the waist. Diabetes Obes Metab 9:300–303 23. Neira R, Toledo L, Arroyave J et al (2006) Low-level laserassisted liposuction: the Neira 4 L technique. Clin Plast Surg 33:117–127 24. Caruso-Davis MK, Guillot TS, Podichetty VK, et al (2011) Efficacy of Low-Level Laser Therapy for Body Contouring and Spot Fat Reduction. Obes Surg 21:722–729 25. Danilovic DL, Bloise W, Knobel M, Marui S (2008) Factitious thyrotoxicosis induced by mesotherapy: a case report. Thyroid 18:655–657

 

Cellulite: Etiology, Classification, Pathology, and Treatment

25

Melvin A. Shiffman

25.1 Introduction Cellulite refers to the popular description of the uneven, bumpy, “orange peel,” or “cottage cheese” appearance of the thighs, buttocks, and breasts of postpubertal women. Cellulite reflects a variety of conditions such as adiposis edematosa, dermatopanniculosis deformans, and status potrusus cutis [1]. Synonyms include cellullalgie, infiltrats cellulalgiques, fibrositis, weichteilrheumatismus, pannikulose, pannikulitis, cellulitis, gynoid lipodystrophy, and zellulitis [2].

Subjective complaints include feeling of tightness, heaviness, and tenderness or diffuse, spontaneous pain [2].

25.3 Grades Draelos and Marenus [1] proposed four grades of cellulite with increased degree of surface irregularity with increasing grade.

25.2 Clinical Manifestations

25.4 Stages

Piérard-Franchimont [3] stated that “Incipient cellulite is recognized by the mattress phenomenon upon pinching of the skin and moderate fat lobule enlargement with reactive focal fibrosclerotic hyperplasia of connective tissue strands partitioning the subcutis. Women who do not put on excess bodyweight rarely develop the severe, full-blown cellulite.” Cellulite is often combined with obesity and a family tendency that does not require inheritance [4, 5]. It can occur in men with deficiencies of androgens (Kleinfelter’s syndrome, primary secondary hypogonadism, mumps orchitis, estrogen therapy for prostate cancer, and chemical castration with cyproteronacetate).

Nürnberger and Müller [6] described four stages of cellulite: Stage O: Skin on thighs and buttocks is smooth surface with patient standing or lying. Pinch test throws the skin into folds and furrows. Stage I (or one plus): Skin surface is smooth while patient stands or lies. Pinch test clearly positive for mattress phenomenon. Stage II (or two plus): Skin surface is smooth while lying down. Mattress phenomenon (dermo-panniculosis deformans) when standing. Stage III (or plus three): Mattress phenomenon (dermo-panniculosis deformans) positive in both lying and standing positions (Fig. 25.1). Elson [7] has proposed the following classification for cellulite (patent pending): GRADE I: The skin of the thighs and buttocks appears normal, but reveals a “peau d’orange” or orange peel effect when the skin of the affected area is pinched.

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

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_25, © Springer-Verlag Berlin Heidelberg 2011

265

266

Fig.  25.1  Stage III cellulite (Nürnberger and Müller classi­ fication)

M.A. Shiffman

Fig.  25.2  Stage II cellulite (Elson classification) (Used with permission)

GRADE II: Orange peel appearance present without manipulation of the affected area (Fig. 25.2). GRADE III: Horizontal indentations and/or ripples without compartmentalization (Fig. 25.3). GRADE IV: Compartmentalization appears in addition to the indentation and/or ripples with appearance of fibrous bands surrounding islands of fat (Fig. 25.4). GRADE V: Overlapping skin appears in addition to the fibrous bands surrounding islands of trapped fatty tissue and rippling (Fig. 25.5).

25.4.1 Pinch Test (Mattress Phenomenon) In the female there are fat cell conglomerations of the upper part of the subcutis (standing fat chambers) and papillae adiposae [7] that protrude upon the overlying cutis that produces deformation and pits while in the male only folds and furrows are produced (Fig. 25.6) [8].

25.5 Etiology There are sex-typical differences of the inner structure of the skin and subcutaneous tissue of the thigh and hip region [6]. Septae of connective tissue (retinacula cutis) in the male are a network of criss-crossing septae dividing the chambers into small polygonal units and in the female there are “standing fat-cell chambers” that are

Fig. 25.3  Stage III cellulite (Elson classification) (Used with permission)

separated by septae of connective tissue (retinacula cutis) (Fig. 25.7). Orientation of the subcutaneous fibers in the female is vertical whereas in the male they are angled and this predisposes the female to develop ­extrusion of adipose tissue into the dermis that is

25  Cellulite: Etiology, Classification, Pathology, and Treatment

267

a

Fig. 25.4  Stage IV cellulite (Elson classification) (Used with permission)

b

Fig. 25.6  Pinch Test. (a) In the female there are fat cell conglomerations in the upper part of the subcutis (standing fat chambers) and papillae adiposae. (b) In the male there are only folds and furrows produced Fig.  25.5  Stage V cellulite (Elson classification) (Used with permission)

c­ haracteristic of cellulite [9]. The presence of androgens determines the male subcutaneous fibrous structure. Piérard and Piérard-Franchimont [10] viewed cellulite as the result of an imbalance between moderate but chronic excess in fat lobule pressure and less than perfect reactive processes taking place in the hypodermal fibrous strands. “The cellulite-prone condition is due to a moderate increase in fat deposits within clustered hypodermal lobules encased by focally thickened

and fibrosclerotic strands containing a few myofibroblasts. As such clusters of fat lobules are not compressible, but can change in shape, they are squeezed upward upon pinching the skin while their fibrosclerotic strands act like belts and shrouds bound to the deepest fascia. The mattress phenomenon is the result of such fat outpouching restricted by a tethering fibrosclerotic network. In time and with further accumulation of fat,  intrahypodermal pressure increases pushing the fibrous strands under excessive tension. Stretch marks ensue inside the connective tissue of the subcutis.

268

a

b

Fig. 25.7  (a) Septae of connective tissue (retinacula cutis) in the male are a network of criss-crossing septae dividing the chambers into small polygonal units and (b) in the female there are “standing fat-cell chambers” that are separated by septae of connective tissue (retinacula cutis)

The  lumpy-bumpy aspect of the skin occurs, the ­outward protrusions corresponding to the most altered portions of the hypodermis.” Some authors have suggested the cause of cellulitis include endogenous factors like hormonal, metabolic, nervous, enzymatic, and hemodynamic disorders while others presume abnormalities of the skeleton, allergies, acute and chronic infections, and intoxications [11–18]. There are authors who claim exogenous factors are a cause of cellulite, such as gross and minor trauma, scarring, sensitivity to cold, and constriction by clothing [11, 19, 20]. However, there is no experimental evidence for these hypotheses.

25.6 Pathology Pathologically there are projections of subcutaneous fat into the reticular and papillary dermis [1].

M.A. Shiffman

Incipient cellulitis, “status potrusus cutis,” is identified by the “mattress” phenomenon. Full blown cellulite has dimpled skin. Spontaneous appearance of pitting, bulging, and deformation is called dermo-panniculosis deformans [21]. The standing lobules, papillae adiposae, rise into pits and dells on the undersurface of the dermis. Cellulite-prone skin is characterized by the uneven thickness of the hypodermal fibrous strands. PiérardFranchimont et al. [3] did not observe inflammation. Piérard-Franchimont et al. [3] stated that “There is no proven link of causality between upward position of the fat compartments beneath the dermis and cellulite.” The “size of these papillae adiposae is much smaller than the uneven bumpy aspect of the skin surface. The lack of correlation between the extent in dermo-hypodermal waviness and the severity of cellulite points to the irrelevance of evaluating therapeutic effects on cellulite through such a microanatomical presentation.” It has been stated that inflammation or hampered lymph and blood circulation may play a prominent or pathogenic role in the development of cellulite [1, 22]. Rosenbaum et al. [9] found no evidence of any primary differences between affected and unaffected areas of the thigh in adipose physiology, blood flow, or biochemistry that would account for cellulite. Maes and Marenus [23] stated that “it is possible that the gaps in dermal structures are the consequence of subclinical inflammatory processes that can result in the constant activation of proteinases, such as collagenase and elastase… The activation of these enzymes is a normal part of the inflammatory response in order to allow for the efficient migration of immune cells to the site of activity.” Scherwitz and Braun-Falco [2] reported pathologic changes that were slight edema, distended lymphatics in the corium, slight perivascular infiltrates, and slight degenerative changes in the musculi arrectores pilorum. There was a conspicuous increase in the volume of fat cells in the subcutis. Collagen fibers in upper layers of the dermis appeared slightly edematous (artifact of local anesthesia?) and elastic fibers were occasionally decreased in the subepidermal plexus and showed tendency to fragmentation or conglomeration in the deeper layers of the dermis (possible artifact of fixation or sectioning). Nürnberger et al. [24, 25] were of the opinion that adiposis edematosa and the fine structure of the skin of women is influenced by the level of testosterone and on the amount of fat deposits.

25  Cellulite: Etiology, Classification, Pathology, and Treatment

Ehlers [26] described alterations in the collagen fibers, particularly swelling or homogenization, and localized necrobiosis of the corium with swelling, loss of form, and vacuoles of different sizes. The development of cellulite starts with repeated episodes of edema and lymphatic stasis followed by serous exudate occurring between the meshes of the subcutaneous fat and connective tissue [11–13, 27]. This is followed by increased polymerization of acid glycosaminoglycans (Lotti et al. [28] reported dermal glycosaminoglycans in cellulite affected areas) and a rise in the amount of water retained. The formation of new or more framework of collagen fibers causes scarlike fibrosis or sclerosis. Histochemically an increased degree of polymerization was not demonstrated [29] and there is no experimental evidence pointing to a change in chemical composition or to metabolic disorder of the skin [26, 30, 31]. Rosenbaum et al. [9] reported a diffuse pattern of extrusion of underlying adipose tissue into the reticular dermis in affected individuals and a diffuse pattern of irregular and discontinuous connective tissue immediately below the dermis. There were no significant differences in subcutaneous adipose tissue morphology, lipolytic responsiveness, or regional blood flow between affected and unaffected sites within individuals.

25.7 Treatment Weight loss is probably the most frequently employed treatment since decreasing the subcutaneous fat may reduce the dimpled appearance of the skin [1]. Rosenbaum et  al. [9] suggested therapeutic attempts be directed at the connective tissue with chemical agents or physical manipulation, including surgery, that weaken radially oriented connective tissue between adipose tissue and the dermis that may, theoretically, lead to reduction or elimination of cellulite. Early stage care suggested by Piérard-Franchimont et al. [3] includes: 1. Reduce estrogen-related regional fat accumulation. 2. Use continuous external compression therapy. 3. Boost and modulate the connective tissue metabolism to prevent the occurrence of hypodermal stretch marks.

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Physical activity, bodyweight reduction, and massage [1, 32, 33] and liposuction [34, 35] are measures that currently purport to be more effective than ­placebo in cellulite care. Coleman et al. [36] felt that liposuction is relatively unsuccessful and may even worsen the dimpled skin appearance. However, Lieberman et  al. [37] had success in treating cellulite with liposuction. Many purported cosmetic and medical treatments show little effect in improving cellulite, and certainly none cause its complete disappearance [1, 32–34, 38, 39].

25.7.1 Topical Agents 25.7.1.1 Methylxanthines (Caffeine, Aminophylline, Theophylline) Methylxanthines are biological phosphodiesterase inhibitors providing beta-adrenergic receptor stimulation that induces hydrolysis of fat stored as triglycerides into free fatty acids and glycerol [38]. This must be in the subcutaneous tissues in sufficient concentration and for a sufficient time to demonstrate an in vivo effect. Toxicity can be demonstrated with aminophylline and theophylline. 25.7.1.2 Retinoids Retinoids improve the denseness of the epidermis and stimulate angiogenesis when applied to facial skin over a period of years [1]. Both of these effects would be beneficial in cellulite treatment since it is thought that cellulite is partly due to decreased firmness and elasticity of the skin allowing herniation of the subcutaneous tissues into the dermis. Piérard-Franchimont et al. [3] reported that topical retinol may reduce the severity of cellulite by improving the tensile properties of skin. 25.7.1.3 Lactic Acid There are no reports demonstrating effectiveness of lactic acid, other alpha hydroxy acids, or beta hydroxy acids in the treatment of cellulite. Lactic acid perhaps might lessen the appearance of cellulite by improving the condition of the stratum corneum [1]. 25.7.1.4 Herbals There are many herbals marketed for the treatment of herbals (Table 25.1).

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Table  25.1  Herbals marketed for topical use in cellulite treatment Botanical name Aloysia triphylla Camellia japonica Citrus limonum Cola acuminate Foeniculum officinale Fucus vesiculosus Hedera helix Hordeum Mitchella repens Origanum vulgare Trifolium subterraneum

Common name Verbena Japanese green tea Lemon Kola nut Fenel Algae Ivy Barley Strawberry Marjoran Sweet clover Caffeine Horse chestnut Bladderwick Butcherbroom Soy

Modified from Draelos and Marenus [1]

Substances such as sweet clover, ivy, and barley may improve the peripheral microcirculation thereby facilitating lymphatic drainage that is thought to be decreased in patients with cellulite [1]. Bascaglia et al. [40] utilized a cream containing caffeine, horse chestnut, ivy, algae, bladderwick, thermal plankton, butcherbroom, and soy protein that was applied for 30 days. Ultrasound demonstrated a decrease of the subcutaneous fat thickness that returned to normal when the cream was stopped. They theorized that the cream broke bonds between the adipocytes allowing the fat to become more compact. It was unknown if the effect on the adipocytes could be maintained.

25.7.1.5 Exothermic Herbal Packs Exothermic herbal packs are a combination of heat, botanical extracts, and massage. Herbal pastes applied to upper thighs and buttocks followed by lymphatic drainage massage, sometimes application of heating pads or warm towels. 25.7.1.6 Enzymes, Iontophoresis, “Rice” Treatment Nürnberger et al. [4] and Ries [5] stated that thiomucase enzyme in salves, suppositories, or injection, iontophoresis or “rice” (rest, ice, compress, elevate) treatment (Nemectron, Alec Eden-Slendertone) are no more effective than placebos.

25.7.2 Massage Vigorous lymphatic massage in the direction of blood flow is designed to encourage removal of extravascular fluid and can reduce thigh diameter in individuals with decreased venous return [1]. The dimpled appearance may be improved as tissue edema is reduced.

25.7.3 Manipulation Skin kneading, Endermologie (LPG, Fort Lauderdale, FL), involves rubbing of the skin with electrically powered rollers. There are claims of efficacy due to improved circulation, reducing tissue congestion, and removing waste products [41]. This is sometimes combined with massage. It only reduces the appearance of cellulite.

25.7.4 Recent Reports Sasaki et al. [42] used a phosphatidylcholine-based gel with a light emitting diode (LED) twice weekly for 12 weeks on grade II–III cellulite. At 3 months, eight of nine thighs were downgraded to a lower cellulite grade. At 18 months, five of those reverted back to the original cellulite grading. This indicates a need for maintenance treatment. Sadick and Magro [43] utilized radiofrequency energy, infrared light, and manipulation of the skin and fat (VelaSmooth system) on 16 subjects for 6 weeks. Thigh circumference decreased in 72% of the treated legs with visual improvement of skin texture and cellulite. There was only one follow-up visit with 50% of subjects showing 25% improvement. Fink et al. [44] studied the response of cellulite to intense pulsed light with and without a retinyl-based cream. The appearance of cellulite was improved in 67% of 12 subjects at 8 month phone follow-up. Manuskiatti et  al. [45] performed a pilot study to determine the safety of TriPollar radiofrequency in the treatment of cellulite. Thirty nine female patients received 8 weekly treatments with TriPollar radiotherapy on cellulite of the abdomen, arms, buttocks, and thighs. By 4 weeks after the treatment there was 50% improvement in cellulite of the abdomen and thighs but not of the buttocks and arms.

25  Cellulite: Etiology, Classification, Pathology, and Treatment

Mesotherapy with phosphatidylcholine and other drugs has been a potentially popular method of fat reduction and secondarily for reduction of cellulite.

25.8 Conclusions Cellulite appears to be the result of excess fat in females and androgenic deficient males that protrude into the dermis while the connective tissue bands hold the skin down. The connective tissue bands differ in direction in the female and in the male and therefore the female is more likely to be affected. There are other unproven theories concerning inflammation, fibrosis, and sclerosis as the cause but these need further and more definitive research. There have been studies with radiofrequency energy, infrared light, intense pulsed light, and phosphatidylcholine cream without complete resolution of cellulite. In general, topical applications of a variety of “medications,” popular in European and South American countries, are not effective in completely resolving cellulite. Lifetime maintenance therapy is necessary. The best methods of treatment are weight loss, exercise, and properly performed liposuction (to break up the subcutaneous fibrous strands), but even that only improves but does not cure cellulite.

References 1. Draelos ZD, Marenus KD (1997) Cellulite etiology and purported treatment. Dermatol Surg 23(12):1177–1181 2. Scherwitz C, Braun-Falco O (1978) So-called cellulite. J Dermatol Surg Oncol 4(3):230–234 3. Piérard-Franchimont C, Piérard GE, Henry F, Vroome V, Cauwenbergh G (2000) A randomized, placebo-controlled trial of topical retinol in the treatment of cellulite. Am J Clin Dermatol 1(6):369–374 4. Nürnberger F, Müller G (1974) Subkutis und haut im alter. Z Gerontologie 7:410–421 5. Ries W (1976) Fettsucht. Johann Ambrosius Barth-Verlag, Berlin 6. Nürnberger F, Müller G (1978) So-called cellulite: an invented disease. J Dermatol Surg Oncol 4(3):221–229 7. Elson M. (2007) Cellulite: etiology and treatment. Austral­ asian J Cosm Surg. Asia Pacific Aesthetic Mag 1:16–19 8. Müller G, Nürnberger F (1974) Das relief der lederhautunterseite des menschen. Kosmetologie 4:124–129 9. Rosenbaum M, Prieto V, Hellmer J, Boschmann M, Krueger J, Leibel RL, Ship AG (1998) An exploratory investigation of the morphology and biochemistry of cellulite. Plast Reconstr Surg 101(7):1934–1939

271 10. Piérard GE, Piérard-Franchimont C (2000) Cellulite: from standing fat herniation to hypodermal stretch marks. Am J Dermatopathol 22(1):34–37 11. Bassas-Grau E, Bassas-Grau M (1966) Klinische, ätiologische, pathologische und therapeutische uüberlegungen zur zelllulitis (pannikulose). Munch Med Wochenschr (Spanische Ausgabe) 106:431–456 12. Bonnet GF (1960) Traitement des cellulites localisées. Rev Med Francs 5:367–369 13. Merlen JF (1958) La cellulite. Entite clinique et mecanisme pathogenique. Concours Méd 80(19):2311–2317 14. Paviot J (1926) Les cellulites. Leur rapports avec troubles hepatodigestifs. Leurs terrains. J Méd Lyon 7:347–358 15. Decormeille G (1961) La cellulite. Syndrome allergic? Concours Méd 83:4833–4836 16. Freytag A (1968) Zellulitis-zellulalge. Ärztl Prax 20: 367–381 17. Kermorgant Y (1960) La notion des altérations du serum et des reactions du tissue conjunctif conduisent a une conception nouvelle de la pathogénie de l’obésité. Bull Acad Natl Méd 144:105–106 18. Monteil-Seurin J (1960) Cellulite et function ovarienne. Sem Hôp Ther 40:88–90 19. Dammann J (1964) Die pannikulose. Dtsch Gesundheitswesen 19:170–174 20. Wilde H (1970) “Zellulitis”? Ein beitrag zur korperverformung durch die mode. Hautarzt 21(8):379 21. Piérard GE, Nizet JL, Piérard-Franchimont C (2000) From standing fat herniation to hypodermal stretch marks. Am J Dermatopathol 22(1):34–37 22. Curri SB, Bombardelli E (1994) Local lipodystrophy and districtual micro-circulation. Cosmet Toilet 109:51–56 23. Maes D, Marenus K (1998) Modulation of inflammatory reactions in skin. In: Baran R, Malbach HI (eds) Textbook of cosmetic dermatology, 2nd edn. Dunitz, London 24. Nürnberger F, Neumann F, Müller G (1976) Hautstruktur und Sexual hormone. Hautarzt (Suppl I): Springer, Berlin, 164–168 25. Nürnberger F, Hasan SH, Müller G (1959) Sexualhormone und unterhautstruktur bei morbus Klinefelter. Vortrag I, Jahrestagung der Arbeitsgemeinschaft. Dermatologische Forschung, Dusseldorf, 24–25 November 1959 26. Ehlers G (1972) The so-called panniculosis with special reference to histological and histochemical examinations. Verh Dtsch Ges Rheumatol 2(Suppl 2):207–214 27. Kermorgant Y (1960) De la cellulite-évolution de la question après trois ans d’espérience. Concours Méd 82: 1371–1376 28. Lotti T, Ghersetich MD, Grappone C, Dini G (1990) Proteoglycans in so-called cellulite. Int J Dermatol 29(4): 272–274 29. Kreysel HW, Kammerer B (1974) Die sogenannte zellulitis im brennpunkt moderner untersuchungsverfahren. Morphologie, biochemie, klinik, therapie und ihre nebenwirkungen. Med Welt 25(15):625–635 30. Braun-Falco O, Scherwitz C (1972) Zur histopathologie der sogenannten cellulitis. Hautarzt 23(2):71–75 31. Braun-Falco O, Scherwitz C (1971) Zellulitis. Med Klin 66(24):827–832 32. Kligman AM (1997) Cellulite: facts and fiction. J Geriatr Dermatol 5:136–139

272 33. Lucassen GW, van der Sluys WLN, van Herk JJ et al (1997) The effectiveness of massage treatment on cellulite as monitored by ultrasound imaging. Skin Res Technol 3:154–160 34. Igra H, Satur NM (1997) Tumescent liposuction versus internal ultrasonic-assisted liposuction. A side-to-side comparison. Dermatol Surg 23(12):1213–1218 35. Piérard-Franchimont C, Damseaux M, Melotte P, Pierard GE (1988) The fate of hypodermis after liposuction surgery. J Am Acad Dermatol 19(4):723–728 36. Coleman WP, Hanke CW, Alt TH, Asken S (1991) Cosmetic surgery of the skin: principles and practice. In: Liposuction. BC Decker Inc, Philadelphia, pp 213–238 37. Lieberman CL, Cohen JA, Rosenstock R (2006) Liposuction treatment of cellulite. In: Shiffman MA, Di Giuseppe A (eds) Liposuction: principles and practice. Springer, Berlin, pp 539–541 38. DiSalvo RM (1995) Controlling the appearance of cellulite. Cosmet Toilet 110:50–59 39. Smith WP (1995) Cellulite treatments: snake oils or skin science. Cosmet Toilet 110:61–70 40. Bascaglia DA, Conte ET, McCain W, Frideman S (1996) The treatment of cellulite with methylxanthine and herbal

M.A. Shiffman extract based cream: an ultrasonographic analysis. Cosmet Dermatol 8:30–40 41. Vergereau R (1995) Use of mechanical skin fold rolling in cosmetic medicine. J Cosmet Med Dermatol Surg 85: 49–53 42. Sasaki GH, Oberg K, Tucker B, Gaston M (2007) The effectiveness and safety of topical PhotoActif phosphatidylcholinebased anti-cellulite gel and LED (red and near infra-red) light on Grade II-III thigh cellulite: a randomized doubleblind study. J Cosmet Laser Ther 9(2):87–96 43. Sadick N, Magro C (2007) A study evaluating the safety and efficacy of the VelaSmooth system in the treatment of cellulite. J Cosmet Laser Ther 9(1):15–20 44. Fink JS, Mermelstein H, Thomas A, Trow R (2006) Use of intense pulsed light and a retinyl-based cream as a potential treatment for cellulite: a pilot study. J Cosmet Dermatol 5(3):254–262 45. Manuskiatti W, Wachirakaphan C, Lektrakul N, Varothai S (2009) Circumferential reduction and cellulite treatment with a TriPollar radiofrequency device: a pilot study. J Eur Acad Dermatol Venereol 23(7):820–827

Dermaroller: The Transepidermal Delivery System

26

Madhuri Agarwal

26.1 Introduction

26.3 Principle and Mechanism of Action

In the arena of cosmetic dermatology, Dermaroller or skin roller is rapidly gaining popularity for treatment of acne scars, wrinkles, and skin rejuvenation. The treatment is also known as collagen induction treatment, microneedling, or skin roller. It is a convenient system easily accessible to dermatologist with minimal training.

The normal human skin has a thickness of 1.5  mm and comprises of three layers, i.e., epidermis, dermis, and subcutis. Epidermis, the outer layer of skin, is a mechanical barrier and prevents water loss and permeation of external agents from environment. The infiltration of the epidermal layer by topical medications is essential to enable action of these drugs. In recent times, Dermaroller has emerged as novel device facilitating transepidermal delivery of such topical drugs. The fine needles in Dermaroller aid by promoting new collagen through release of growth factors and enhance absorption and penetration of active ­ingredients through microchannels created by Dermaroller. Today we know very well that wound healing and epithelial disrupters are controlled by electrical signals when a needle penetrates skin layers. The fine, but sharp needles perforate the vertical and horizontal scar edges and induce new collagen formation. This new formation fills the scar (crater) with new tissue from bottom to top. At the same time, the needles break down the old and hardened collagen scar strands and allow new capillaries to supply the former scar tissue with more blood. This revascularization and better blood supply will change the pigmentation of the tissue around the (former) scar. All these are natural physiological processes (Fig. 26.1). Therefore, a subcision is not necessary as the needles will also break down the collagen fibers that connect the scar to the fascia. In any case it is recommended to perform collagen induction therapy (CIT) first before a subcision is considered [5].

26.2 History A brief synopsis of the life cycle of Dermaroller is as follows: 1. 1995 – Orentreich and Orentreich [1] described subcision or dermal needling for scars. 2. 1997 – Camirand and Doucet [2] described needle dermabrasion using a “tattoo pistol” to treat scars. 3. 2006 – Fernandes [3] developed percutaneous collagen induction therapy (CIT) with the Dermaroller. Dermaroller is a drum-shaped instrument dotted with 192 fine microneedles in eight rows, 0.5–1.5 mm in length and 0.1 mm in diameter. The microneedles are synthesized by reactive ion etching techniques on silicon or medical grade stainless steel. The instrument is presterilized by gamma irradiation [4]. All Dermarollers are advocated for single use only.

M. Agarwal  The Skin Clinic, 230, Hallmark, Vasant Oscar Layout, L.B.S. Marg, Mulund West, Mumbai 400080, India e-mail: [email protected]

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Fig. 26.1  Mechanism of action of Dermaroller (courtesy Dermaroller S.A.R.L.). After scar perforation, venous and arterial capillaries, as well as new fibroblasts, migrate through the former scar tissue

New collagen fibers

Venous capillaries

Ideal perforation of the crater-like acne scar

Arterial capillaries

Fibroblasts

After several treatments (3 − 4) the depressed scar will be filled by new collagen formation(s)

26.4 Indications 1 . Acne scars 2. Aging skin and wrinkles 3. Large pores 4. Stretch marks 5. Pigmentation 6. Hair loss

26.5 Contraindications 1 . Pregnancy and lactation 2. Active acne 3. Photosensitive disorders 4. Recent treatment with photosensitive drugs 5. Active bacterial or viral infections

26.6 Procedure Dermaroller is an office procedure. Three to four treatments are required for moderate to deep scars. The treatments are done at intervals of 6–8  weeks for optimum results.

Pre- and posttreatment photos should be taken after patient consent for personal evaluation and to demonstrate to the patient efficacy of results. Precise recording of session dates should also be maintained. The area to be treated is anesthetized by topical anesthesia for 45 min to 1 h and prepared with disinfectants. The rolling is done 15–20 times in a starshaped manner (Fig.  26.2). Pin point bleeding is expected and easily controlled. The treatment takes an average of 15–20  min. After the procedure, the treated area is dabbed with saline or cold compresses.

26.7 Posttreatment The patient may experience redness and swelling for 1–2  days posttherapy. Local antibiotics can be prescribed and strict photo protection should be advised. There are no other significant adverse effects seen. Dermaroller can be combined with other treatments like microdermabrasion, chemical peels, subcision, or fractional lasers but with a suitable time interval of 3–4 weeks between them.

26  Dermaroller: The Transepidermal Delivery System

Fig. 26.2  Method of rolling conducted on patient skin

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2. Pinpoint bleeding is expected. However, Dermaroller should be used with a gentle hand just sufficient to produce pricks for collagen induction. 3. The passes should be limited to 12–15 passes per area. 4. The new collagen formation and maturation takes time hence the interval between two sessions must be minimum 6–8 weeks. A decrease in time interval will not yield optimum results. 5. Dermaroller is a single use device and must not be reused. 6. Approved and the best quality rollers must be preferred as poor quality devices may lead to breakage of needles in skin.

26.8 Dermaroller Products There are a variety of Dermaroller products available in the cosmetic market: Different manufacturers commonly provide rollers with 0.5–1.5  mm length and 1  mm diameter, 192 microneedles. Miniature versions of Dermaroller, 0 known as Dermastamps, are also available. They are 2 mm in length and 1 mm diameter and used for localized scars such as nasal scars, varicella scars, etc. Home care delivery systems less than 2 mm in length are available for transepidermal delivery of substances like lipopeptides and antiaging products. They can be used twice a week for up to 100 times. After use the rollers can be cleaned in hot tap water and shaken dry. Peptide-based roller cleaners are also available [4].

26.9 Practical Tips 1. Recent or new scars are reported to respond better as compared to older scars.

26.10 Conclusions Dermaroller is a cost effective, easily accessible, and user friendly instrument delivering satisfactory results with negligible downtime. The plethora of indications are on a rise with use of rollers in burn scars, keloids, hair loss, skin rejuvenation, and many more.

References 1. Orentreich DS, Orentreich N (1995) Subcutaneous incisionless (subcision) surgery for the correction of depressed scars and wrinkles. Dermatol Surg 21:6543–6549 2. Camirand A, Doucet J (1997) Needle dermabrasion. Aesthet Plast Surg 21(1):48–51 3. Fernandes D (2005) Minimally invasive percutaneous collagen induction. Oral Maxillofac Surg Clin North Am 17(1):51–63 4. Doddaballapur S (2009) Microneedling with dermaroller. J Cutan Aesthet Surg 2:110–111 5. Training Manual. Dermaroller S.A.R.L., Germany. www. dermaroller.de

 

Scar Management

27

George John Bitar, Priscilla Patel, and Lauren Craig

27.1 Introduction Scar management is one of the most important elements that both plastic surgeons and patients alike focus on after an aesthetic procedure. As current surgical techniques become more standardized and results more predictable, a fine scar may be the deciding factor between acceptable and unacceptable aesthetic results. A visible scar may be the necessary and inevitable end to the healing process, how the scar heals can vary on the protocol taken to achieving beneficial wound healing. With each scar management approach itself is a multitude of nuances and variations among plastic surgeons. There is no such thing as the perfect scar management program; thus the task of which approach to use could be an arduous one. Current ­literature

G.J. Bitar (*) GWU School of Medicine, Bitar Cosmetic Surgery Institute, 3023 Hamaker Court, Suite 109, Fairfax, VA 22031, USA e-mail: [email protected] P. Patel George Washington University School of Medicine and Health Sciences, 1111 Army Navy Drive Appartment 1421, Arlington, VA 22202, USA e-mail: [email protected] L. Craig George Washington University School of Medicine and Health Sciences, 10661 Oakton Ridge Ct., Oakton, VA 22124, USA e-mail: [email protected]

suggests the evolution of a variety of techniques for managing scars such as: the Alpha Centella tape and cream system, laser therapy, compression pressure, silicone therapy, and massage therapy. The authors believe that both the Alpha Centella tape and cream system marketed as ScarScience™ as well as Laser therapy are two approaches of which yield a high level of satisfaction in both appearance and texture; as well as a low rate of adverse effects. This chapter will go beneath the surface and explore how the surgeon and patient alike can work in a symbiotic relationship with the natural process of scar formation to achieve the best results possible. The authors will begin with a general overview of scar formation, different types of scars, and the various elements that affect scar outcome. This will then lead to a discussion of the different modalities of scar management commonly used. Lastly, a thorough discussion will be provided of the Alpha Centella (ScarScience™) Scar Management Program and Laser Therapy, both of which have clinically and experimentally been proven effective for improving the aesthetic appearance of abnormal scars.

27.2 Scar Formation A wound is a break in the skin due to cuts or scrapes. To remedy this, the normal wound healing process is initiated in response to such injury. The sequence of events that follow share the common goal of minimizing two factors: infection and scarring. The scar (result) is simply collagen beneath the skin that develops from the wound healing process [1]. The goal is to facilitate proper wound healing that will result in an invisible

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scar. This is done by working with the three phases to scar formation: the inflammatory phase, the proliferative phase, and the remodeling or maturation phase [2]. The inflammatory phase is initiated first with a duration being between 2 and 6 days [2]. During this phase, white blood cells fight bacterial infections, bleeding halts, and collagen formation begins [1–3]. The collagen is the component holding wounds together. The proliferative phase follows a few days after the inflammatory phase with a duration being 3–4 weeks [2]. Collagen production continues with a slow progression of pulling the wound together by the edges. During healing, new capillaries are formed. Wound thickening of the edges of the skin ensues, granulation tissue forms in the wound as it shrinks [3]. The final phase of scar formation, the maturation phase, has a duration of many weeks to many years [2]. As a slow process, more collagen forms to strengthen the wound. Scar “remodeling” to break down excess collagen in the scar follows. This phase transforms the thick, red, raised scar to a thin, flat, white scar [3]. After the first month, tissue scaffolding is transformed into a pale, avascular scar, composed of spindle-shaped fibroblasts, dense collagen, and fragments of elastic tissue. Even after completed scar formation, the scar tissue is not comprised of the same materials found in undamaged skin. The two most important differences are the lack of dermal appendages and the altered collagen composition. The dermal appendages, or protein anchors found in the dermis, are destroyed in the line of the incision or wound and do not regenerate [4]. In addition, scar tissue is roughly 80% type III collagen and 20% type I collagen, while older scars and undamaged skin have the opposite composition (20% type III and 80% type I) [4]. These are the primary reasons why scared areas look and feel different from normal skin.

G.J. Bitar et al.

27.3.1 Hypertrophic Scars Hypertrophic scars occur when the body’s natural healing mechanism overproduces collagen. Hypertrophic scars often develop after thermal or traumatic injury and usually involve the deep layers of the dermis. The collagen found in scar formation is produced by myofibroblasts, which proliferate in the wounded area through the autocrine production of TGF-b, and the establishment of focal adhesions [4]. Although the collagen found in these scars is not unlike collagen in a normally healing scar, the appearance of the scar is raised, nodular and red in color. These types of scars can occur all over the body, especially in areas that are constantly under pressure or movement. These scars usually develop within a month of the initial injury. Hypertrophic scars are distinguished from keloid scars by their lack of growth beyond the boarders of the original wound [6]. All keloid scars are hypertrophic but not all hypertrophic scars are classified as a keloid.

27.3.2 Keloid Scars Keloids are often reddish-purple in color, appearing in papules or nodules. Patients at high risk of keloids are usually younger than 30  years and have darker skin pigmentation [5].This type of scaring is comprised of thickened bundles of hyalanized acellular collagen arranged in a chaotic tangle with increased hyaluranidase. They result when the body overcompensates for dermal injuries including but not limited to surgery, acne or piercings. A keloid can form weeks or even years after the initial injury and they have also been known to form spontaneously. Although they are a noncancerous growth, they can be itchy or painful in some individuals. They are often extremely unsightly and are removed for cosmetic reasons. Keloids are most commonly found on the upper earlobe, chest, upper back, and anterior shoulder [5].

27.3 Different Types of Scars 27.3.3 Atrophic Scars Upon completion of scar formation, three different types of scars can result: atrophic, hypertrophic, and keloidal [5]. Apart from appearance, the location and orientation of scars is something to be of concern when determining scar type.

Atrophic scars have a “sunken” or “pitted” appearance in the skin. They result after an acute inflammation destroys the underlying structures supporting the skin, such as collagen and elastin. This type of scarring is

27  Scar Management

often associated with cystic acne or varicella. Atrophic scaring can also occur after certain diseases, surgeries, or accidents. They often become hypopigmented and fibrous overtime [6].

27.4 Elements That Affect Scar Outcome In repairing or regenerating damaged tissue, wounds can vary immensely in healing duration due to a wide variety of elements. The cosmetic surgeon must provide an optimum surrounding to support the cellular activities involved for proper wound healing. To do this, the surgeon attempts to remove or protect the wound from various factors that may have the potential to obstruct the healing process. Such factors that could affect the cosmetic appearance of a scar fall into two categories: intrinsic factors and extrinsic factors. Intrinsic factors include the following: a hereditary predisposition for scar formation, health status, age factors, body build, race, age, anatomical location of the burn, and depth of burn. Extrinsic factors include the following: mechanical stress, temperature, infection, medications, alcohol abuse, smoking, and psychological stress [7–10].

27.4.1 Intrinsic Factors Chronic conditions like autoimmune diseases, circulatory conditions, and anemias influence the healing process. In addition, any condition associated with hypotension, hypovolemia, edema, and anemia, as well as other common diseases like diabetes, arteriosclerosis, peripheral vascular disease (PVD), chronic obstructive pulmonary disease (COPD), and heart disease will influence the wound healing process [9]. A chronic circulatory condition, for example, can reduce blood flow thereby decreasing the oxygen available for normal tissue activity and replacement. This can be seen in sickle cell anemia patients whose circulatory system develops a reduced oxygen delivery of which parallels a decrease in the ability to support wound healing [8]. Diabetes, the disease in which blood glucose (sugar) levels can swing out of control shows that high levels of sugar in the blood impair healing. In addition, the physical stress of surgery can cause a deviation from the norm in blood sugar levels [8].

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Age also plays an influential role in healing process. In comparison to younger individuals, an older person will exhibit a slower healing time, as well as a more fragile structure of the healed wound [8, 9]. This is due to the structural changes in the skin of an elderly person such as flattening of the dermal–epidermal junction that leads to skin tears, reduced padding over bony prominences [8] (e.g., tibial tuberosity and medial/lateral malleolus), reduced quality and quantity of collagen, and reduction in the intensity of the immune response. On the contrary, younger patients tend to form thicker scars because their youthful bodies are very good at building collagen. The build of an individual can also affect the availability of oxygen and nutrients to the wound site. For example, an underweight individual will have reduced delivery of energy as well as small protein reserves; both of which are crucial for wound healing. On the contrary, overweight individuals may experience an increased risk of a spontaneous rupture of a wound, hernia formation, and infection [7]. Overall, the supply of nutrients (proteins, fats, vitamins/minerals, and adequate fluid intake) plays a vital role in the cellular activity. For instance, sufficient calorie intake ensures that there will be adequate protein and fat supplies for scar formation. Protein plays a role in tissue replacement and repair; therefore protein deficiencies correlate with poor revascularization, decreased fibroblast proliferation, reduced collagen formation, and immune system deficiencies [7]. For example, vitamin C is required for collagen synthesis, immune response, and fibroblast functions. Vitamin B complex is needed for WBC and antibody formation and vitamin A helps in macrophage mobility and epithelialization. Iron is required for the synthesis of hemoglobin, and copper/zinc is essential for collagen synthesis.

27.4.2 Extrinsic Factors Pressure, friction, and shear are three forms of mechanical stress that can play a role in wound healing. Immobile pressure (e.g., bed bound patient) or local pressure (e.g., cast) under suitable duration can compromise proper blood flow and therefore wound healing. Friction can also cause wound healing difficulties by wearing down newly formed epithelium, thereby reversing the scar formation [8–10] back to the

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i­nflammatory phase. Shear mechanical stress has the potential to occlude blood vessels or disrupt/damage granulation tissue. Temperature can also play a role in wound healing because it plays a role in the activation/deactivation of chemical and enzymatic processes as well as the metabolism of cells and tissues engaged in the repair process. In regards to dressings, those that promote a cooling effect may not aid in wound repair [8]. Sun exposure can cause darkening and thickening of scars for up to a year after surgery. Therefore, the surgeon’s incisions or wounds should be covered during the day and blocked from UV light to prevent this preventable complication [9]. Infection can also be a factor that hinders wound healing. It does this by halting the scar formation process in the inflammatory phase. The clinical signs of a wound infection are the following: erythema, heat, local swelling, and pain. This is when the pathogenic microbes are competing with the immune system [11]. Medications have been shown to effect the phases of scar formation. Systemic steroids commonly used to treat inflammation, pain, asthma, or allergies can significantly slow healing and thin the skin. Chemo­ therapeutic agents can also affect scar formation via the suppression of protein synthesis, inhibiting cell reproduction or the inflammatory response. Also, immu­ no­suppressive drugs will naturally reduce inflammatory activities, thereby increasing the susceptibility of a wound infection [9, 10]. Alcohol and smoking will also affect wound healing. Alcohol and smoking thins the blood, slows healing, and increases bruising. The surgeon should advise a patient to stop drinking at least 1 week before surgery [9]. Stress is also shown to affect a patient’s ability to heal. Optimistic, positive personalities heal more rapidly than those depressed and/or anxious individuals. Stress, sleep, and hormone levels can also contribute to a patient’s mood and healing potential [9, 10].

27.5 Various Modalities of Scar Management

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scientific evidence published over the past 25  years. A stretched scar initiated by neutrophils leads to tension in one axis [12, 13]. On the other hand, a multi-directional or intermittent tension on a scar initiates lymphocytes. This could result in a hypertrophic scar [12, 14, 15]. The common initiating factor is the tension on the scar, and the critical element needed to counteract this tension is scar support. A number of approaches have become the standard of care for hypertrophic scar control – both prevention and treatment. Keloids in general respond minimally to these approaches [12]. This section will introduce the commonly used scar management programs of which consist of the Alpha Centella Cream System, Laser Therapy, Compres­sion Pressure, Silicone Gel sheeting, and Massage Therapy.

27.5.2 Alpha Centella Scar Management Program Microporous tape has been proven clinically to be a reliable method of scar support. Secondly, hydration has a beneficial effect on scar control and is the basis of silicone gel sheeting [12, 16]. The Alpha Centella cream consists of two main components: an extract from the plant Bulbine frutescens. This plant extract leaves a layer of fatty vesicles of glycoprotein on the skin surface, thereby increasing hydration under the tape. Apart from hydration, the Bulbine frutescens also has antibacterial properties. The second component of the Alpha Centella Cream is the principal terpenoids extracted from the Centella asiatica plant which includes Asiatic acid, madecassic acid, and asiaticoside. The most beneficial effect of Centella asiatica appears to be the stimulation of maturation of the scar by the production of type I collagen [4, 17] and the resulting decrease in the inflammatory reaction and myofibroblast production. Thus these components have been incorporated into a formulation used in my office called the Alpha Centella (ScarScience™) Scar Management Program.

27.5.1 Overview

27.5.3 Laser Therapy

Various scar management modalities have been adopted based upon wound support, hydration, and hastened maturity. These factors have stemmed from

Laser therapy is a scar management approach used to tackle both hypertrophic scars and keloids. The mechanism of action is via a laser beam to cause a thermal tissue

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reaction. This will thereby heat the injury or coagulate specific tissues. For instance, the flash lamp-pumped pulsed dye laser selectively decreases scar blood flow with a demonstrated improvement of more than 50% in over 50% of cases. Based upon clinical evidence results have been proven beneficial: a more pliable, less pruritic, and less erythematous scar resides [6, 17, 18].

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function of deep massaging is to stretch fresh scars and thereby break down the cement or matrix holding the scar contracted. Massaging also stimulates fibroblast synthesis of collagen, therefore this approach is combined with an anticollagen synthesis approach [19–23].

27.6 Alpha Centella (ScarScience™) Scar Management Program 27.5.4 Compression Pressure Compression therapy for scar management is via the use of fitted elastic garments to generate about 24 mmHg on the hypertrophic scar. Applying pressure (18–24 h a day for at least 6 months) has been clinically proven to have at least partial success in producing a thinner, more mature/pliable scar. The compres­sion garments are used as soon as the wound has closed thereby decreasing scar blood flow, protein deposition, edema, and chondroitin sulfate while increasing lysis and mast cell stability. In addition, the tight garment weave increases the scar tissue temperature. This increased temperature, even by 1°C, will increase collagenolysis and scar maturation, thus providing heat as a treatment modality [19–23].

27.5.5 Silicone Therapy Silicone therapy of scar management is by the use of form-fitted silicone gel sheets. The sheets are held in place by elastics for minimum 18 h a day for several months. This form of scar therapy has been clinically proven to increase scar maturation and decrease hypertrophy. Although initially it was thought that silicone therapy was due to pressure or increased temperature, the mechanism of action has not been proven. Current evidence suggests that maintaining scar hydration is the common element, although the effect of hydration on decreasing scar is unclear [19–23]. The fitted sheet does take tension off the wound, a known stimulant of scar. For silicone therapy, its early use has proven to yield the best results [19–23].

27.5.6 Massage Therapy Massage therapy is an approach commonly combined with several other scar management modalities. The

Our institution uses the Alpha Centella tape and cream system marketed as Scar Science™, since it addresses the most fundamental elements that affect scar outcome (Figs. 27.1 and 27.2). ScarScience™ combination of gel formula and microporous tape fulfills the following four criteria for an effective cosmetic scar management system: Physical support (3 M microporous tape), Hydration (viscosity-modulated dimethicone), Collagen maturation (triterpenic fraction of Centella asiatica), Modulation of inflammation (oleuropein, a pure phenolic derivative of olive leaves), and an elegant, neutral, proprietary base [12, 13, 24].

27.6.1 Physical Support One of the components of ScarScience™ is system to provide tension on the wound. Many research studies have indicated that tension on a scar from different directions is the trigger and initiating factor in hypertrophic scar formation. Tension causes a prolongation of the inflammatory process and causes increased fibroblast activity, producing excess collagen and overabundant extracellular matrix, which is what constitutes a scar [12, 24]. If there is little tension across a scar, a narrow scar results and the scar collagen that has formed remains aligned along the scar; however, if the tension across the scar is great, the collagen fibers separate and instead of the fibers aligning along the scar, new and more collagen is laid down randomly which characterizes hypertrophic scars [11]. The period where the scar is most vulnerable to collagen aligning haphazardly due to tension occurs during the first 1–3 weeks as the strength of the scar after 3 weeks is only 20% of that of the intact tissue [15]. Thus scar support and minimizing tension forces is especially critical in this early period of scar formation. Since tension is the initiating factor of a hypertrophic scar, the significant element that can offset this

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integral component of the ScarScience™ scar management system.

27.6.2 Hydration

Fig. 27.1  Applications of tape to incision

Fig. 27.2  Application of ScarScience™ cream on tape

tension is scar support. Clinical evidence has indicated that a highly reliable way to support a scar is by using microporous tape. Therefore, ScarScience™ utilizes a long-term microporous tape system in order to minimize this tension and provide scar support as a significant element to prevent hypertrophic scar formation. The efficacy of microporous tape has been supported and confirmed by many clinical research studies. These studies have corroborated that applying an adhesive microporous paper tape to surgical incisions along the line of the scar for several weeks after surgery has proven beneficial in minimizing scar enlargement by eliminating the stretch forces on the scar [14, 15]. Thus, taping is clinically recognized as an effective method of wound support and controlled scar formation. It is an

Another component of ScarScience™ is that the cream maintains the scar well hydrated, the second critical factor in minimizing scarring. The stratum corneum, the most superficial layer of the skin, controls water vapor loss. A cut to the skin disrupts this layer resulting in dehydration [24]. Dehydration of the skin causes excess fibroblast collagen and glycosaminoglycan production, therefore maintaining a hydrated environment will reduce water loss and restores homeostasis to the scar. Thereby, the result will cause a reduction in collagen deposition and hypertrophic scar formation [4]. In order to maintain a hydrated environment, the most consistently used agent in scar management has been silicone in sheeting or in its topical application with dimethicone as a main ingredient. Unfortunately, it has proved to be both awkward and difficult to keep in place and has been associated with “discomfort, maceration and even fungal infection” making patient compliance difficult [17]. Although silicone gel has proved as an effective hydrating agent, a natural substitute that would avoid the above-mentioned adverse effects would be better. One of the ingredients of the ScarScience™ tape/cream system is an extract from the leaf sap from Bulbine frutescens. This extract is widely used for the treatment of wounds, burns, itches, rashes cracked lips, etc. [12, 13, 24]. Not only does it have beneficial antibacterial properties, but also the healing effect is likely due mainly to the glycoprotein in the leaf gel. The fatty vesicles of this glycoprotein are not absorbed but remain on the skin surface together with the  tape, providing an ideal hydration and occlusion ­envi­ronment of the wound [12, 13, 24]. Therefore, the ScarScience™ management uses the extract from Bulbine frutescens as one of its ingredients in the formula to reduce water vapor loss and also uses its adhesive microporous tape that not only helps reduce the tension of the scar, but also helps maintain this well-hydrated environment.

27.6.3 Scar Maturity and Collagen Production Another important factor in scar management is scar maturity and collagen production. During the

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p­ roliferative phase of normal wound healing, initial type III collagen fibers are replaced by more closely woven type I fibers which are more stable [4]. Thus, in normal scarring there is a time-dependent change in the cross-linking pattern of type III and then type I collagen. In hypertrophic scars, it has been demonstrated that there is a prolonged presence and overabundant deposition of type III collagen [4]. The ScarScience™ cream thus counteracts this over-deposition of type III collagen through its promotion of scar maturation via collagen homeostasis by using Centella asiatica as its main ingredient. The Centella extract stimulated scar maturation by the production of type I collagen which reduces inflammation and myofibroblast production [12, 13, 24].

27.7 Laser Therapy

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skin tone and pigmentation plays a large role in how he or she will respond to the various laser treatments. For example, a patient with increased skin pigmentation (III, IV, or higher on the Fitzpatrick scale) has pigment that will interrupt the targeted hemoglobin’s absorption of the specific laser energy emitted by vascular lasers. This limits the effectiveness of the treatment. Patients with darker skin are also at a greater risk for skin dyspigmentation because of undesired melanin destruction. Due to these complications, patients with darker skin pigmentation are typically treated with reduced energy densities. The consequences of reduced fluency include decreased treatment efficacy and the need for more treatments. Patients who naturally have lighter pigmented skin, but who have been acquired a suntan or burn should avoid laser treatment until their pigmentation has normalized [6].

27.7.1 Preoperative Considerations

27.7.3 Infection

When deciding if a patient is a good candidate for laser treatment, the scar, surrounding tissue, medications, number of previous treatments and patient’s expectations must all be evaluated [6]. Primarily, the scar must be assessed for color, location, and texture. For instance, darker scars require lower energy densities compared to lighter pigmented scars. Secondly, the skin must be evaluated for ongoing infections or inflammation. If either of these exists, then treatment should be postponed or the infected area should be avoided. Thirdly, a patient should stop any medications that could worsen the treatment’s effectiveness or lengthen recovery time. For example, patients should discontinue taking anticoagulants [6]. Prior treatments should also be taken into consideration and dyspigmentation around the scar should be assessed. Finally, the patient needs to have their expectations evaluated and adjusted so that they will understand the procedure and its capabilities. These considerations will allow for optimal laser efficacy.

Any patient undergoing laser treatment should have a full physical and history taken to identify any past or ongoing infections. If a patient has an existing autoimmune disorder or an inflammatory skin disorder, laser treatment could exacerbate these conditions, leading to a worsened clinical outcome. Pati­­ents with currently inflamed acne may receive treatment, but the physician should use caution while treating. In addition to detecting prior infections, the physician must inform the patient that laser treatments may cause inflections such as herpes simplex and impetigo [6].

27.7.2 Skin Phototype The color of the scar should be evaluated before any laser treatment. In addition, the ethnic background of the patient is also of importance. A patient’s overall

27.7.4 Medications Some medications can interfere with laser treatment; therefore a patient must tell their physician what they are taking before any procedure is performed. For example, Isotretionin, which is often used to treat patients with chronic acne, can also lead to the development of hypertrophic scaring. It is advised that laser treatment be postponed until 6  months after isotertinoin treatments have been stopped [6]. Anticoagulants and antiplatelet medications should be stopped 1 week before any laser procedure. Medications that increase bleeding should be stopped a week before and a week after any laser procedure.

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27.8 Laser Treatment of Hypertrophic and Keloid Scars 27.8.1 Overview The PDL or pulsed dye laser is the treatment of choice for both hypertrophic and keloid type scaring. There have been numerous studies all aimed at determining which laser best treats hypertrophic scars and keloids. It has been discovered that the 1060-nm neodymium: yttrium–aluminum–garnet (Nd:YAG) lasers decreased collagen production, after attempting to radiate fibroblasts. Once it was discovered that lasers could manage collagen metabolism, argon and CO2 lasers were studied. Both of these lasers were effective in treating hypertrophic and keloid scars, but recurrences were noted in follow-up [18]. Next, pulsed dye lasers (PDLs) were tested and were found to improve scar texture, color, size, and pliability [25]. Further studies have been conducted to explore the range of PDLs. Recently, Nouri et al. showed that the 585-nm PDL can be used to improve the quality and cosmetic appearance of a surgical scar drastically if treatment is given on the day of suture removal.

27.8.2 PDL Mechanism of Action This laser is vascular-specific and uses a 585-nm energy beam. It has been shown to prevent the overproduction of collagen seen in hypertrophic and keloid scaring and to re-structure the body’s normal healing mechanisms through a variety of mechanisms. A study performed by Kuo et al. [26] showed that PDL treatments reduced the transformation of TGF-B1 expression, fibroblast replication, and collagen type III deposition. These factors all contribute to the laser’s ability to control over-scaring. In addition, the PDL aids in correcting scaring by selective photothermolysis of vasculature, releasing mast cell signaling agents, such as histamine and interleukins, both of which can affect collagen metabolism. The laser also heats the collagen directly, which can break the sulfide bonds holding the scar’s tertiary structure together giving the collagen an opportunity to rearrange into a more compact and organized matrix. It has also been hypothesized that laser treatment may induce keloid regression through the induction of apoptosis and the upregulation of extracellular signal-regulated kinase and p38 mitogen-activated protein (MAP) kinase activity [6].

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27.8.3 PDL Treatment PDL treatment is normally performed in an outpatient setting without the use of anesthesia. Often times, a local anesthetic such as a lidocaine cream is applied 30–60 min before the procedure to minimize discomfort. The area of skin being lased should be washed to remove any residue or makeup that could interfere with the laser’s efficacy. Hair should also be secured so that it will not be singed during laser treatment. Ethanol and other flammable substances should not be used during prep or during the treatment itself. All individuals, including the patient, must wear protective eyewear capable of filtering 585 nm light. This is done to avoid retinal damage potentially caused by the laser. During the treatment, the PDL is used in adjacent, nonoverlapping pulses. The energy densities chosen are based on the nature of the scar, the number of previous treatments, and the skin phototype of the patient. If there is any uncertainty about a patient’s responsiveness or sensitivity to the treatment, a test spot should be treated to observe the outcome prior to starting full treatments. Hypertrophic and keloid scars are treated with the lowest energy density ranging from 6 to 7.5 J/ cm2 when using a skin surface size of 5–7  mm. If a larger pulse size (10 mm) is being used, a lower energy density is typically used (4.5–5.5 J/cm2). Pulse durations should be approximately 0.45–1.5  ms. For patients with darker skin or when treating fragile areas (such as the neck or back of the hand), a lower energy density is used (normally a 0.5  J/cm2 reduction). In general, PDL treatments start at a lower energy density and then increase with subsequent visits. When an energy density no longer yields results, the fluency can be increased. Treatments are typically performed every 6–8 months [6]. If adverse side effects arise such as oozing, crusting or vascularization, then the energy density must be decreased on future visits and the treatments must be postponed until any abrasion has completely healed. If treatments are performed with no improvements, then the patient has the option of trying intralesional corticosteroids (10–20  mg) or 5-fluorceil, an antimetabolite. These two drugs have been shown to make additional improvements for patients with hypertrophic or keloid scaring. These can also be used in conjunction with the PDL for a maximal benefit. It has been suggested that higher corticosteroid concentrations potentially yield better results, but this would also increase the risk of unwanted side-effects, such as skin atrophy and telangiectasias [27].

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Fig. 27.4  Scar result after ScarScience™ treatment Fig.  27.3  Tape and cream system enhance scar healing over ensuing weeks

27.8.4 Complications and Side Effects of PDL Treatment Several side effects are known to occur with PDL treatment, although many adverse reactions can be avoided with a comprehensive pre-treatment screening. The most common side effect is postoperative purpura, or the appearance of red or purple spots on the skin. Purpura is caused by bleeding under the skin and usually forms in 0.3–1  cm spots lasting 7–10  days after treatment. Edema may also occur after PDL treatment, but this usually subsides after 48  h. Post treatment, patients should avoid the sun and keep the treated area clean and moist. Patients must not develop a suntan because doing so will lead to increased skin pigmentation. PDL treatments are less effective when performed on hyperpigmented skin and therefore, future treatments will be suspended until the pigmentation returns to normal. If sun exposure does occur, bleaching agents such as hydroquinone usually reduce hyperpigmentations [6].

t­itanyl phosphate) or a CO2 laser can be used for treatment. Furthermore, CO2 lasers have had particular success on keloids located on the earlobe and the posterior neck, although keloids in these areas have been known to re-grow after treatment (Figs. 27.3 and 27.4) [6].

27.9 Laser Treatment of Atrophic Scars 27.9.1 Overview CO2 lasers and Er:YAG (erbium:yttrium–aluminum– garnet) have proven to be the best choice in tackling most atrophic scars. In recent years, the CO2 laser has become the standard in skin resurfacing. The CO2 laser has been shown to tighten the skin while simultaneously improving facial irregularities with minimal down time. Another laser developed for resurfacing is the erbium:yttrium–aluminum–garnet (Er:YAG) laser. This laser was introduced as a bone-cutting tool but is now used for cosmetic resurfacing. The Er:YAG laser allows for more superficial tissue ablation with finer control, but it requires more treatments to yield similar results to that of the CO2 laser.

27.8.5 Results of PDL Treatment Most hypertrophic scars will improve by 50% after two PDL treatments according to a data gathered by Dr. Alster and Dr. Zaulyanov-Scanlon. In contrast, keloid scaring has proven more difficult to treat. Some improvement is seen after multiple PDL sessions, but keloids are not always responsive to laser treatment. If scaring does not respond after multiple PDL treatments, other lasers such as a KTP laser (potassium

27.9.2 Mechanism of Action Both the CO2 and the Er:YAG lasers function by emitting a particular wavelength that gets absorbed by a chromophore contained within the scared tissue in the skin. The surrounding tissue does not absorb this wavelength to the same degree, thereby treating only the scared areas. The carbon dioxide laser is mostly

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transformed into thermomechanical energy that disrupts the dermal blood vessels and the tissue proteins. The Er:YAG laser differs by involving a photomechanical reaction which desiccates tissue, creating a characteristic snapping sound. Since the Er:YAG laser turns the laser energy into primarily mechanical energy, there will be less thermal energy remaining to cause damage to the surrounding tissue. This means a lower risk of damaging the tissue and a less intense treatment. The CO2 laser has been shown to contract collagen by approximately 15–25% [6]. This allows for more compact and organized collagen formations. This collagen contraction can also lead to some of the initial bruising and swelling seen after treatment. During laser treatment, char forms in the wounds and must be cleared from the area before passing over for a second or third time. The Er:YAG laser operates more superficially compared with the CO2 laser. The collagen contraction achieved after Er:YAG lasing is only 1–2% during lasing, but can reach 14% over time [6]. Char does not form with this laser; instead the depressions in the skin turn white. Subsequent passes are required for maximal results because once the Er:YAG laser hit the dermal vessels, they dilate and cause transudation of fluid. This increases the water content with allows for more ablation. The carbon dioxide laser is a more effective option for deeper tissue ablation than the Er:YAG laser because the Er: YAG laser does not promote blood clotting as well as the CO2 laser. When bloods fill in the dermal crevices, the physician cannot make as many passes over the scared area. The CO2 laser not only promotes better hemostasis, it also requires less passes to give an optimal result. Some newer Er:YAG lasers (500 mm) with longer, more variable pulses have allowed for deeper tissue ablation by creating more thermal necrosis. This leads to more collagen contraction, nearing the effectiveness of the CO2 laser. These longer-wavelength Er:YAG lasers result in more postoperative erythema, but they are still not as harsh as the CO2 laser [6].

27.9.3 Additional Approaches to Treatment The Nd:YAG laser is another nonablative laser and is used on patients with darker or more sensitive skin. These lasers cool the surface of the epithelium while also penetrating the deeper layers of the skin with infrared wavelengths. These wavelengths target the

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underlying water and collagen without disrupting the epidermal layer. The Nd:YAG laser requires more sessions (3–5 treatments per month for several months), but a patient can expect to see a 40–50% improvement in the quality of their scaring. Fraxel lasers offer another option when dealing with atrophic scaring. This laser combines ablative and nonablative technique to achieve re-contouring, [6].

27.9.4 Atrophic Scar Treatment Laser treatment of atrophic scarring is generally a quick outpatient procedure focused on reducing the depressions in the skin making them less noticeable. This is achieved by reducing the depth of the boarders of the depression and filling in the center by regenerating collagen. It is recommended that the physician handle atrophic scaring by treating “cosmetic units.” Although one can target the laser to a specific atrophic scar, it is advisable to treat the whole area surrounding the scar to minimize the chances of discoloration after treatment. This will also increase skin tightening making the scar shallower. Most scars require at least two passes of the laser per treatment. During treatment there will most likely be some char formation. This signals that the skin has become too hot and indicates that there may be thermal damage. After treatment, the skin appears red and swollen. The patient can expect to have large amounts of serous discharge, bleeding, and an overall worsening of the skin appearance 4–7 days after the treatment. After these initial stages, the patient’s skin will begin to re-epithelialize. During this time, the patient needs to be monitored closely to make sure they do not develop dermatitis. The patient can prevent against an infection by keeping the skin damp with medical barrier cream. The patients should also use cooling masks. Patients electing for large areas of treatment should take an oral antibiotic to reduce the risk of infection. Postoperative erythma typically lasts 4–6  weeks after the Er:YAG laser and 3–4 months after the CO2 laser.

27.9.5 Results of Treatment The clinical outcome of laser treatment depends on the quality of the patient’s skin and its ability to heal itself. Lasing disrupts the disorganized epidermal cells and

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allows the body to replace it with normal elastin and compact collagen. This creates a more youthful and favorable contour. Patients with the best healing capabilities will show a 50% improvement in wrinkles and skin lesions. CO2 laser patients can see continued improvement for up to 18  months after treatment, whereas Er:YAG laser patients will typically have their final results before 12 months [6].

27.9.6 Complications of CO2 and Er:YAG Lasers Complications for the CO2 and Er:YAG laser ­treatments include infection, hyperpigmentation, hyper­trophic scarring, and ectropion formation. Hyper­pig­mentation can be corrected though the use of a hydroquinone cream. Hypopigmentation is generally not observed after CO2 and Er:YAG treatments. Hypertro­phic scarring and ectropion formation are both the result of overly aggressive lasing or undiagnosed suprainfections [6].

27.10 Conclusions In our constant quest for superior results in cosmetic surgery, we have entered an era in which multiple attempts at “scarless” surgery have been presented. To achieve satisfaction amongst both surgeon and patient, an optimal scar management program is vital. Choo­ sing the optimal scar management program is the medical challenge all practitioners face and nowhere is this truer than in the realm of aesthetic surgery. This chapter provided an overview of scar formation, the external and internal factors that hinder wound healing, and the various modalities currently used for scar management. Extensive attention was given to the Alpha Centella tape and cream system and laser therapy, both being clinically and experimentally proven beneficial approaches to scar management. The Alpha Centella (ScarScience™) Scar Management Program has provided evidence of its clinical efficacy within research, as well as within our institute. It has proven to yield high patient satisfaction with low adverse effects. In addition, current laser technology offers many options for treating the various types of scaring: proper identification of the scar and determin­ing which laser treatment is crucial to maximal ­improvement.

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Based on current data, the 585-nm PDL is the best choice in treating hypertrophic scars and keloids, while the pulsed carbon dioxide and Er:YAG laser treatments are used for atrophic scar resurfacing. We hope that in the next few years, lasers will be widely used to treat scarring and that with more trials, physicians will be able to combine, mix and match the various lasers to achieve the best results on a patientby-patient basis.

References 1. Singer AJ, Clark RA (1999) Cutaneous wound healing. N Engl J Med 341(10):738–746 2. Irion Glenn (2010) Normal wound healing. In: Compre­ hensive wound management, 2nd edn. SLACK Inc., Thorofare, pp 15–24 3. Kirsner RS, Bogensberger G (2002) The normal process of healing. In: Kloth LC, McCulloch JM (eds) Wound healing alternatives in management, 3rd edn. F.A. Davis Company, Philadelphia, pp 3–28 4. Kumar V (2009) Healing by repair, scar formation and fibrosis. In: Abbas AK, Aster J, Fausto N, Kumar V (eds) Robbins and Cotran pathologic basis of disease, professional edition, 8th edn. W.B. Saunders, Philadelphia. http://emedicine. medscape.com/article/1120673-overview. Accessed 5 July 2010 5. Hartman-Adams J (2009) Management of keloid and hypertrophic scars. Am Fam Physician 80(3):253–256 6. Alster T, Zaulyanov L (2007) Laser scar revision: a review. Dermatol Surg 33:131–140 7. Lewis B (2002) Nutrition and wound healing. In: McCulloch JM, Kloth LC, Feeder JA (eds) Wound healing: alternatives in management, 2nd edn. F.A. Davis Company, Philadelphia, pp 35–62 8. Ennis W, Meneses P (2002) Factors impeding wound healing. In: McCulloch JM, Kloth LC, Feeder JA (eds) Wound healing: alternatives in management, 2nd edn. F.A. Davis Company, Philadelphia, pp 68–91 9. Guo S, Dipietro LA (2010) Factors affecting wound healing. J Dent Res 89(3):219–229 10. Arem AJ, Madden JW (1976) Effects of stress on healing wounds: I. intermittent non cyclic tension. J Surg Res 20(2):93–102 11. Irion G (2010) Abnormal wound healing. In: Irion G (ed) Comprehensive wound management, 2nd edn. Slack Inc., Thorofare, pp 15–24 12. Widgerow AD, Chait LA, Stals R, Stals PJ (2000) New innovations in scar management. Aesthet Plast Surg 24(3):227–234 13. Widgerow AD, Chait LA, Stals PJ, Stals R, Candy G (2009) Multimodalities in scar management. Aesthet Plast Surg 33(4):533–543 14. Burgess LP, Morin GV, Rand M, Vossoughi J, Hollinger JO (1990) Wound healing. Relationship of wound closing tension to scar width in rats. Arch Otolaryngol Head Neck Surg 116(7):798–802

288 15. Meyer M, McGrouther DA (1991) A study relating wound tension to scar morphology in the pre-sternal scar using Langer’s technique. Br J Plast Surg 44(4):291–294 16. Reiffel RS (1996) Prevention of hypertrophic scars by longterm paper tape application. Plast Reconstr Surg 96(7): 1715–1718 17. McCraw JB, McCraw JA, McMellin A, Bettencourt N (1999) Prevention of unfavorable scars using early pulse dye laser treatments: a preliminary report. Ann Plast Surg 42(1):7–14 18. Henderson DL, Cromwell TA, Mes LG (1984) Argon and carbon dioxide laser treatment of hypertrophic and keloid scars. Lasers Surg Med 3(4):271–277 19. Berman B, Bieley N (1996) Adjunct therapies to surgical management of keloids. Dermatol Surg 22(2):126–130 20. Carr-Collins J (1992) Pressure techniques for the prevention of hypertrophic scar. Clin Plast Surg 19(3):733–740 21. Fulton J (1995) Silicone gel sheeting for the prevention and management of evolving hypertrophic and keloid scars. Dermatol Surg 21:945–951

G.J. Bitar et al. 22. Sawada Y, Sone K (1992) Hydration and occlusive therapy for hypertrophic scars and keloids. Br J Plast Surg 45(8):599–603 23. Shamberger R, Tabbot T, Tripton H, Thibault LE, Brennan MF (1981) The effect of ultrasonic and thermal treatment on wounds. Plast Reconstr Surg 68(6):860–870 24. Tudhope L, Naude L, Widgerow AD, Mulder M, Smart H, Sibbald RG (2008) Africa’s pride: creating a culture of collaboration in South Africa. Adv Skin Wound Care 21(10):466–468 25. Cohen J, Dregelmann R (1977) The biology of keloid and hypertrophic scar and the influence of corticosteroids. Clin Plast Surg 4(2):297–299 26. Kuo YR, Wu WS, Jeng SF, Huang HC, Yang KD, Sacks JM, Wang FS (2005) Activation of ERK and p38 kinase mediated keloid fibroblast apoptosis after flashlamp pulsed-dye laser treatment. Lasers Surg Med 36(1):31–37 27. Chan HH, Wong DSY, Ho WS (2004) The use of pulsed dye laser for the prevention and treatment of hypertrophic scars in Chinese persons. Dermatol Surg 30(7):987–994

28

Arnica montana Melvin A. Shiffman

28.1 Introduction

28.3 Components

There are many herbal remedies still being used in medicine. Arnica montana is used mainly postoperatively in cosmetic surgery to reduce bruising. Information on Arnica montana is hard to find in one source and, therefore, is the subject of this chapter.

28.3.1 Sesquiterpene, Flavonoids, Caffeic Acid Derivatives Spitaler et al. [1] found secondary metabolites in flowering heads of Arnica montana that were sesquiterpene, flavonoids, and caffeic acid derivatives (1-methox­ yoxaloyl-3,5-dicaffeoylquinic acid).

28.2 Arnica 28.3.2 Sesquiterpene Lactones Arnica is any plant of the genus Arnica that are yellowflowered perennials of the family asteraceae (aster family), native to the north temperate and arctic regions. There are at least 32 species, other the Arnica montana, that are known. Arnica montana (also known as leopard’s bane, wolfs bane, European Arnica, mountain tobacco, Arnica flowers, arnica root, Arnica flos, common arnica, mountain arnica, mountain snuff, sneezewort, Arnica cordifolia, fleurs d’arnica, Arnica sororia, Arnica fulgens, Wundkraut, Bergwohlverieih, Arnikabluten, Kraftwurz, and tumbler’s cure all) (Fig. 28.1) is indigenous to Siberia and Central Europe, from southern Iberia to southern Scandinavia and the  Carpathians. Both roots and flowers are used medicinally.

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

Schröder et  al. [2] noted two sesquiterpene lactones from Arnica montana, helenalin and 11alpha, 13dihydrohelenalin, inhibited collagen-induced platelet ­aggregation, thromboxane, and 5-hydroxytryptamine secretion. These reduced the number of acid-soluble sulfhydryl groups in platelets, by up to 78% at antiaggregatory concentrations. The substances inhibit platelet function via interaction with platelet sulfhydryl groups, probably associated with reduced phospholipase A2 activity.

28.3.3 Flavonoid Glycosides Merfort [3] found betuletol, a methylated flavonoid, in Arnica montana and in 1985 [4] isolated seven flavonoid aglycones from Arnica montana. Five flavonoid glycosides were identified from flowers of Arnica montana by Merfort and Wendisch [5]. These include hispidulin 7-O-beta-glucoside, isorhamnetin 3-O-beta-glucoside, 3-O-beta-d-glucopyranosides of spina­cetin, 6-methoxykaempferol, 6-methoxykaempferol,

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_28, © Springer-Verlag Berlin Heidelberg 2011

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Fig. 28.1  Arnica montana

and patulin and querectin 3-O-(6¢¢-O-acetyl)-beta-dglucopyranoside.

28.3.4 Other Substances Among the biologically active ingredients in the flower heads of the plant are sesquiterpenes, flavonoids, and phenolic acids [6]. Fatty acids of the essential oil was obtained from Arnica montana by Willuhn [7] and Vanhaelen [8] identified carotenoids in Arnica montana. Thirteen helenanolides were isolated from Arnica montana by Willuhn et  al. [9] including 11,13-dihydrohelenalin, helenalin, and their ester derivatives 6-O-isobutyryl-, 6-O-tigloyl-, 6-Oisovaleryl-, and 6-O-(2-methyl)butyrylhelenalin were also reported. In 1984, Willuhn et  al. [10] isolated helenanolides 6-O-isobutyryo-

tetraahydrohelenalin and 2beta-ethoxy-6-O-isobutyryl-2,3hydrohelenalin from Arnica montana. Malarz et  al. [11] detected sesquiterpene lactones, helenalin, and 11,13-dihydrohelenalin esters in green organs only of Arnica montana and not in the roots. New extracts that were found by Kos et al. [12] were 1,5-trans-guaianolides consisting of 11alpha,13-dihydro-2-O-tigloylflorilenalin and 2-O-isovaleryl. Schmidt et al. [13] reported that the in vitro cultivation content of sesquiterpene lactones, helenalin, and 11alpha,13-dihydrohelenalin esters was correlated with tissue differentiation above the ground. In proving field the young plants accumulated mainly helenalin derivatives, the content of which decreases almost to zero within about 6  weeks from the beginning of leaf formation, while the formation of dihydrohelenalin type compounds increases at the same rate and remains constant for a longer period of time.

28  Arnica montana

Delayed flower harvesting of Arnica montana until the flower petals had withered greatly improved the sesquiterpene lactone concentration of the drug [14]. Spitaler et al. [15] noted that the proportion of flavonoids and caffeic acid derivatives increased with altitude, increasing the antioxidant effect. The study suggests that enhanced UV-B radiation and decreased temperature trigger the augmented biosynthesis. Diffe­ ring proportions of helenalin and dihydrohelenalin esters of Arnica montana were found in 16 different places in Spain varying from heath lands, peat bogs, and meadows [16]. Albert et al. [17] reported that there were pronounced differences in phenolics of Arnica montana with altitude changes. The phenolics increased with altitude increasing their antioxidative capacity presumable from temperature changes rather than the UV-B radiation. Cornu et al. [18] noted that there were variations in some of the sesquiterpene lactones due to climatic factors. Pietta et al. [19] showed that Arnica montana drugs are often adulterated by blending them with heterotheca inuloides flowers

28.4 Composition of Extracts Arnica montana extract is used in almost 100 cosmetic formulations and Arnica montana in only one [20]. The extract includes fatty acids (especially palmitic, linoleic, myristic, and linolenic acids), essential oil, triterpenic alcohols, sesquiterpene lactones, sugars, phytosterols, phenol acids, tannins, choline, inulin, phulin, arnicin, flavonoids, arotenoids, coumarins, and heavy metals.

28.5 Effects of Arnica montana Ganzera et al. [6] found that Arnica montana preparations have been used in Europe for centuries to treat skin disorders. Arnica montana was approved by the German Commission E, an advisory panel on herbal medicines, for external use as an anti-inflammatory, analgesic, and antiseptic. It is used widely for bruises, aches, sprains, and inflammation in the USA [21]. Tekko et  al. [22] described that after 12  h on the skin the first components of Arnica montana, 11,13dihydrohelenalin (analogs methacrylate and tiglate

291

esters), were detected. When the sesquiterpene lactone extract tincture was concentrated tenfold, the same components were detected within 3  h of application. Maeda et al. [23] described an inhibitor of melanin in melanoma cells that was composed of traxastanetype triterpene (3beta,16beta-dihydroxy-21alpha-hydro­ peroxy-20(3)-tataxastene). The mechanism of action was considered to involve inhibition of transcriptional factor MITF-M (melanocyte-isoform of microphthalmia-associated transcription factor) that would lead to a decrease of tyrosinase and related genes. Hofmeyer et  al. [24] noted that the sesquiterpene lactones, helenalin and 11alpha,13-dihydrohelenalin inhibit platelet function via interaction with platelet sulfhydryl groups, probably associated with reduced phopholipase A2 activity. Puhlmann et al. [25] reported that they found polysaccharides from Arnica montana cell cultures. The fucogalactoxyloglucan shows a pronounced enhancement of phagocytosis in  vivo and arabino-3,6-galactan-protein displays a strong anticomplementary effect and stimulates macrophages to excrete the tumor necrosis factor alpha. Baillargeon et al. [26] showed that Arnica montana significantly decreased bleeding time. However, Kotlus et al. [27] showed that there was no statistically significant difference in the area of ecchymosis or the severity of ecchymosis for 3–7  days after treatment with homeopathic doses of A. montana versus placebo. In a study by Koo et al. [28], the Arnica extract did not demonstrate significant antimicrobial activity and showing only slight inhibition of adherence of growing cells of Strep. mutans and Strep. sobrinus and of waterinsoluble glucan formation. According to Karow et  al. [29], Arnica D4 and diclofenac were equivalent in wound redness, swelling, heat (calor), and patient mobility. With respect to pain, Arnica D4 was inferior to diclofenac. There was no evidence of effects of A. montana and Bryonis alba combination on bleeding, inflammation, pain, or myocardial ischemia in a study by Belon et al. [30].

28.5.1 Analgesia In a report by Kaziro [31], after removal of impacted wisdom teeth, metronidazole was found to be more effective than Arnica montana in pain control,

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p­ revention of swelling, and promoting of healing. Arnica montana appeared to give rise to greater pain and caused more swelling than the placebo. Robertson et  al. [32] described treatment for post-tonsillectomy analgesia had small but statistically significant decrease in pain compared to placebo.

28.5.2 Anti-inflammatory In a study of histamine-induced increase of vascular permeability in the rat, Macedo et al. [33] pretreatment with Arnica montana blocked the action of histamine in increasing vascular permeability.

28.5.3 Blood Coagulation Baillargeon et al. [26] noted that Arnica montana did not have a significant impact on various parameters of blood coagulation in the period immediately following administration.

28.5.4 Osteoarthritis Topical application of Arnica montana gel for 6 weeks for pain, stiffness, and function in moderate osteoarthritis of the knee was an effective treatment [34].

28.5.5 Postpartum Bleeding Oberbaum et al. [35] concluded that Arnica montana may reduce postpartum blood loss as compared to placebo.

28.5.6 Traumatic Injuries Lüdtke and Hacke [36] found significant effectiveness of Arnica montana in traumatic injuries in a prospective trial. Studies from Medline-listed journals and high-quality studies are less likely to report positive results.

M.A. Shiffman

Testing so far is insufficient to support the safety of these ingredients in cosmetic formulations [20].

28.6 Complications Arnica is generally safe when used externally or topically, and in homeopathic doses [38]. However, prolonged use of arnica (3  weeks or more) can lead to skin irritations and other possible side effects. It is recommended for use to relieve pains, bruises and trauma, but it is most effective and safe when taken with caution and guidance from a professional [38]. Arnica has been seen to be safe when used in diluted or homeopathic doses for a maximum of 2  weeks under constant supervision of a doctor or healthcare professional [38]. However, at extremely higher doses, Arnica montana can lead to very serious side effects and even death. Possible side effects of high arnica dosage include stomach discomfort, nausea and vomiting, as well as liver and kidney damage and organ failure. Skin rashes, lesions of the mouth, and eczema might occur in some people as a result of allergies [38]. Topical arnica should never be used on open wounds or anywhere near the eyes and mouth. There have also been reported cases of mouth ulcers caused by arnicacontaining mouthwash. Other less probable side effects of increased arnica doses taken orally include irregular heart rhythm, high blood pressure, rapid heartbeat, and heat failure. Theoretically, arnica can increase the possibility of bleeding. The use of arnica during pregnancy is not highly recommended [38]. Though homeopathic arnica can be beneficial for minimizing some pregnancy discomfort, large arnica doses have the ability to stimulate the uterus and spontaneously cause miscarriage or a possible premature delivery. Ingestion of Arnica montana products has induced gastroenteritis, nervousness, accelerated heart rate, muscular weakness, and death [20]. An extract of Arnica montana was found to be mutagenic possibly related to the flavenoid content [34].

28.6.1 Allergic Reactions 28.5.7 Cosmetic Procedures In a study by Seeley et al. [37], Arnica montana exhibited less ecchymosis than placebo in facelift patients.

In a study by Reider et al. [39], it was found that out of 443 patients, five patients (1.13%) reacted to Arnica montana with an allergic reaction. Patch testing was

28  Arnica montana

recommended. Knuesel et al. [34] reported one allergic reaction in their study. Allergy to the flowers may be caused by the sesquiterpene lactones [20]. The authors in Reider et  al. [39] concluded that Compositae allergy contributes significantly to the epidemiology of contact dermatitis. As extracts of these plants are frequently used in occupational and cosmetic products, patch testing with additional plant extracts or adjustment of the commercial Compositae mix to regional conditions is recommended.

28.7 Discussion Arnica montana contains many metabolites and esthers, the majority of which are sesquiterpene lactones, phenolics, and flavenoids [6]. The content of the drug varies according to the flower maturity, temperature during growth, and region of growth [15–18]. The effects of Arnica montana include inhibitions of platelet function [24], enhanced phagocytosis with macrophages excreting tumor necrosis factor alpha [25], and decreased bleeding time [26]. However, it has been reported [27] that there was no significant decrease in ecchymosis or blood coagulation although one report [37] showed less ecchymosis following facelift. There was no significant antimicrobial activity [28], poor pain relief [31, 32] except for tonsillectomy [32] and for osteoarthritis [34]. Arnica montana is generally safe when used externally in homeopathic doses but dangerous in extremely high doses [38]. Allergies have been reported [34, 38, 39]. It is not recommended during pregnancy because in large doses it may stimulate miscarriage or premature delivery [38]. There is a possible mutagenic effect [34], and side effects in high doses may include gastroenteritis, nervousness, tachycardia, muscle weakness, and death [20]. Arnica montana drugs are often adulterated by blending them with heterotheca inuloides flowers [19]. According to Murray and Pizzorno [40], “In traditional Chinese Medicine the typical daily dosage of prescribed crude herbal material is approximately 20 grams…” whereas the “…average amount of the herbal material recommended in the British herbal pharmaopoeia…” is less than 1  g. This contributes to  the popularity of herbal medicine in China. In  the  USA, there has been an “…influx of highquality standardized extracts into the marketplace.

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Developments in cultivation, extraction, and concentration processes led to the successful commercial development of these herbal products. Better clinical results were achieved with these herbal medicines because they were able to deliver an effective dosage of active constituents.”

References 1. Spitaler R, Schlorhaufer PD, Ellmerer EP, Merfort I, Bortenschlager S, Stuppner H, Zidorn C (2006) Altitudinal variation of secondary metabolite profiles in flowering heads of Arnica montana cv. ARBO. Phytochemistry 67(4):409–417 2. Schröder H, Losche W, Ströbach H, Leven W, Willuhn G, Till U, Schör K (1990) Helenalin and 11 alpha, 13dihydrohelenalin, two constituents from Arnica montana L., inhibit platelet function via thiol-dependent pathways. Thromb Res 15:839–845 3. Merfort I (1984) Methylated flavonoids from Arnica montana and Arnica chamissonis. Planta Med 50(1):107–108 4. Merfort I (1985) Flavonoids from Arnica montana and Arnica chamissonis. Planta Med 51(2):136–138 5. Merfort I, Wendisch D (1987) Flavonoid glycosides from Arnica montana and Arnica chamissonis. Planta Med 53(5):434–437 6. Ganzera M, Egger C, Zidorn C, Stuppner H (2008) Quantitative analysis of flavonoids and phenolic acids in Arnica montana L. micellar electrokinetic capillary chromatography. Anal Chim Acta 614(2):195–200 7. Willuhn G (1972) Fatty acids of the essential oil form leaves of Arnica montana and Arnica longifolia. Z Naturforsch B 27(6):728 8. Vanhaelen M (1973) Identification of carotenoids in Arnica montana. Planta Med 23(4):308–311 9. Wulluhn G, Rottger PM, Matthiesen U (1983) Helanalinand 11,13-dihydrohelenalinester from flowers of Arnica montana. Planta Med 49(112):226–231 10. Willuhn G, Rottger PM, Wendisch D (1984) 6-isobutyryltetrahydrohelenalin from the flowers of Arnica montana. Planta Med 50(1):35–37 11. Malarz J, Stojakowska A, Dohnal B, Kisiel W (1993) Helenalin acetate in in-vitro propagated plants of Arnica montana. Planta Med 59(1):51–53 12. Kos O, Lindermeyer MT, Tubaro A, Sosa S, Merfort I (2005) New sesquiterpine lactones from Arnica tincture prepared form fresh flower heads of Arnica montana. Planta Med 71(11):1044–1052 13. Schmidt TJ, Bomme U, Alfermann AW (1998) Sesquiterpene lactone content in leaves of in  vitro and field cultivated Arnica montana. Planta Med 64(3):268–270 14. Douglas JA, Smallfield BM, Burgess EJ, Perry NB, Anderson RE, Douglas MH, Glennie VL (2004) Sesquiterpene lactones in Arnica montana: a rapid analytical method and the effects of flower maturity and simulated mechanical harvesting on quality and yield. Planta Med 70(2):166–170 15. Spitaler R, Winkler A, Lina I, Yanar S, Stuppner H, Zidorn C (2008) Altitudinal variation on the phenolic contents in flowering heads of Arnica montana cv. ARBO: a 3-year comparison. J Chem Ecol 34(3):369–375

294 16. Perry NB, Burgess EJ, Rodriguwz Guitián MA, Romero Franco R, López Morquero E, Smallfield BM, Joyce NI, Litrtlejohn RP (2009) Sesquiterpene lactones in Arnica montana helenalin and dihydrohelenalin chemotypes in Spain. Planta Med 75(6):660–666 17. Albert A, Sareedenchai V, Heller W, Seidlitz HK, Zidorn C (2009) Temperature is the key to altitudinal variations of phenolics in Arnica montana L. cv. ARBO. Oecologia 169(1):1–8 18. Cornu C, Joseph P, Gaillard S, Bauer C, Vedrinne C, Bissery A, Melot G, Bossard N, Seeman A, Wallner T, Poschlod P, Heilmann J (2010) Variations of sesquiterpene lactone contents in different Arnica montana populations: influence of ecological parameters. Planta Med 76(8):837–842 19. Pietta PG, MAuri PL, Bruno A, Merfort I (1994) MEKC as an improved method to detect falsifications in the flowers of Arnica montana and A. chamissonis. Planta Med 60(4): 368–372 20. Final report on the safety assessment of Arnica montana extract and Arnica montana. Int J Toxicol 20(Suppl 2):1–11 (2001) 21. http://www.answers.com/topic/arnica?cat=health. Accessed 1/10/08 22. Tekko IA, Bonner MC, Bowen RD, Williamsw AC (2006) Permeations of bioactive constituents of Arnica montana preparations through human skin in vitro. J Pharm Pharmacol 58(9):1167–1176 23. Maeda K, Naitou T, Umishio K, Fukuhara T, Motoyama A (2007) A novel melanin inhibitor: hydroperoxy traxastanetype triterpene from flowers. Biol Pharm Bull 30(5): 873–879 24. Hofmeyr GJ, Piccioni V, Blauhof P (1990) Postpartum homeopathic Arnica montana: a potency-finding pilot study. Br J Clin Pract 44(12):619–621 25. Puhlmann J, Zenk MH, Wagner H (1991) Immunologically active polysaccharides of Arnica montana cell cultures. Phytochemistry 30(4):1141–1145 26. Baillargeon L, Drouin J, Desjardins L, Leroux D, Audet D (1993) The effects of Arnica montana on blood coagula­ tion.  Randomized control trial. Can Fam Physician 39: 2362–2367 27. Kotlus BS, Heringer DM, Dryden RM (2010) Evaluation of homeopathic Arnica montana for ecchymosis after upper blepharoplasty. Ophthal Plast Reconstr Surg (published ahead of print) 28. Koo H, Gomes BP, Ambrosano GM, Park YK, Cury JA (2000) In vitro antimicrobial activity of propolis and Arnica

M.A. Shiffman montana against oral pathogens. Arch Oral Biol 45(2):141–148 29. Karow JH, Abt HP, Fröling M, Ackerman H (2008) Efficacy of Arnica montana D4 for healing of wounds after hallux valgus surgery compared to diclofenac. J Altern Complement Med 14(1):17–25 30. Belon P, Lehot JJ (2010) No effect of homeopathic combination of Arnica montana and Bryonis alba on bleeding, inflammation, and ischaemia after aortic valve replacement. Br J Clin Pharmacol 69(2):136–142 31. Kaziro GS (1984) Metronidazole (Flagyl) and Arnica montana in the prevention of post-surgical complications, a comparative placebo controlled clinical trial. Br J Oral Maxillofac Surg 22(1):42–49 32. Robertson A, Suryanarayanan R, Banerjee A (2007) Homeopathic Arnica montana for post-tonsillectomy analgesia: a randomized placebo control trial. Homeopathy 96(1):17–21 33. Macedo SB, Ferreira LR, Perazzo FF, Carvalho JC (2004) Anti-inflammatory activity of Arnica montana 6cH: preclinical study in animals. Homeopathy 93(2):84–87 34. Knuesel O, Weber M, Suter A (2002) Arnica montana gel in osteoarthritis of the knee: an open, multicenter clinical trial. Adv Ther 19(5):209–218 35. Oberbaum M, Galoyan N, Lerner-Geva L, Singer SR, Grisaru S, Shashar D, Samueloff A (2005) The effect of the homeopathic remedies Arnica montana and Bellis perennis on mild postpartum bleeding—a randomized, double-blind, placebo-controlled study—preliminary results. Complement Ther Med 13(2):87–90 36. Lüdtke R, Hacke D (2005) On the effectiveness of the homeopathic remedy Arnica montana. Wien Med Wochenschr 155(21–22):482–490 37. Seeley BM, Denton AB, Ahn MS, Maas CS (2006) Effect of homeopathic Arnica montana on bruising in face-lifts: results of a randomized, double-blind, placebo-controlled clinical trial. Arch Facial Plast Surg 8(1):54–59 38. http://www.nutritional-supplement-health-guide.com/sideeffects-of-arnica-montana.html. Accessed 9/5/10 39. Reider N, Komericki P, Hausen BM, Fritsch P, Aberer W (2001) The seamy side of natural medicines: contact sensitization to arnica (Arnica montana L.) and marigold (Calendula officinalis L.). Contact Dermat 45(5):269–272 40. Murray MT, Pizzorno JE Jr (2006) Botanical medicine – a modern perspective. In: Pizzorno JE Jr, Murray MT (eds) Textbook of natural medicine, 3rd edn. Churchill Livingstone – Elsevier, Philadelphia, pp 327–337

Part IV Shaping Face and Body

 

Augmentation with Injectable Fillers

29

Peter M. Prendergast

29.1 Introduction The development of biocompatible, temporary, and long-lasting fillers for soft tissue augmentation has transformed the practice of aesthetic medicine. Injec­ table fillers reduce and soften wrinkles, enhance features, and provide facial volume and contouring in procedures that are usually performed under local anesthesia in a matter of minutes. In recent years, there has been a paradigm shift in aesthetic medicine and surgery from a focus on lifting and excisional techniques to one on procedures that add and restore volume to the face. This change in practice reflects our better understanding of facial aging and the significance of volume loss, both as a result of fat atrophy and bony resorption [1, 2]. The asynchronous volume loss in the different superficial and deep fat compartments of the face leads to contour irregularities and folds that define the signs of aging [3]. The midface flattens, tear trough hollows under the eyes appear, nasolabial folds deepen, and oral commissures give the mouth a downturned appearance (Fig. 29.1). With appropriate use of fillers, either in the skin, subcu­taneous, or supraperiosteal plane, all of the effects of aging due to volume loss are improved or corrected, without the need for invasive surgery. When surgical procedures such as rhytidectomy are

appropriate, the ­complementary use of fillers provides a third dimension to facial rejuvenation with superior, more natural-looking results than lifting alone [4]. Most fillers are presented in prefilled syringes for injection at various depths in the skin and subcutaneous tissues depending on the filler used and specific indication (Fig. 29.2). Lines and wrinkles require dermal injections, whereas facial volumizing and contouring require deeper injections, either in the subcutaneous tissues or supraperiosteal plane. Temporary and permanent fillers can be further classified depending on their origin or source: xenogenic, allogenic, bacterial, synthetic, or combination fillers (Table  29.1). This chapter provides a summary of these fillers, and describes the techniques for facial rejuvenation using temporary hyaluronic acid fillers and long-lasting calcium hydroxylapatite. Rejuvenation of the hands is also described. It is the author’s view that permanent synthetic fillers may be useful in selected individuals who request long-lasting results and understand the potential sequelae following complications with permanent fillers, but should not be used as first-line treatments for aesthetic purposes. Volume enhancement using autologous fat is described in a separate chapter.

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

The practice of soft tissue augmentation began at the end of the nineteenth century when Neuber harvested blocks of free fat from the upper arms and transferred them to concave defects in the face [5]. At the turn of the century, Gersvny used paraffin as an injectable

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Fig. 29.1  Signs of facial aging Orbitopalpebral sulcus Tear trough Bony resorption Nasojugal groove Flattened cheek

Nasolabial fold

Perioral lines

Oral commisure Lip atrophy

Fig. 29.2  Injectable fillers for soft tissue augmentation

filler for cosmetic enhancement [1]. Paraffin was ­initially embraced as a safe, inexpensive, and effective way to rejuvenate the face. As experience increased, significant complications such as paraffinomas and product migration were encountered, and the use of paraffin dwindled quickly [6]. In 1911, Bruning first reported the use of autologous fat injections to fill a postrhinoplasty deformity [7]. With the introduction of liposuction in 1975, several authors reported their experience using aspirated fat as a filler for soft tissue augmentation with promising

results [8]. Although autologous fat transfer has been widely accepted as a viable method of augmentation in aesthetic medicine, disadvantages include the need for harvesting, operator-dependence on graft survival, and the significant downtime associated with the use of blunt cannulae for injection of small ­parcels of fat throughout the face. The early deve­ lopment of a bovine collagen gel in the 1960s by Gross and Kirk led, in 1981, to the Food and Drug  Administration (FDA) approval of Zyderm I (INAMED Aesthetics, CA), an injectable bovine

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Table 29.1  Classification of temporary and permanent injectable fillers Xenogenic Bovine collagen (temporary) Hyaluronic acid derived from cockerel combs (avian) (temporary) Allogenic Bioengineered human collagen (temporary) Bacterial Hyaluronic acid derived from streptococcus equi (temporary)

Synthetic Calcium hydroxylapatite (long-lasting) Polyacrylamide (permanent) Polyalkylimide (permanent) Purified polydimethylsiloxane (permanent) Combination Polymethylmethacrylate + bovine collagen (long-lasting) Hyaluronic acid + dextranomeres (long-lasting)

Zyderm I, Zyderm II, Zyplast (Allergan, Irvine, CA, USA) Hylaform, Hylaform Fineline, Hylaform Plus (no longer marketed in USA) Cosmoderm, Cosmoplast (Allergan, Irvine, CA, USA) Restylane, Restylane Fine Lines, Restylane Lipp, Perlane, Sub-Q (Q-Med, Uppsala, Sweden); Teosyal Fine Lines, Teosyal Global Action, Teosyal Deep Lines, Teosyal Ultra, Teosyal Ultimate (Teoxane, Geneva, Switzerland); Juvederm Ultra, Juvederm Ultra Plus, Juvederm Voluma, Juvederm Smile (Allergan, Irvine, CA, USA); Elevess (Anika Therapeutics, MA, USA); Prevelle Silk, Puragen (Mentor Corp., Santa Barbara, CA, USA); Belotero (Merz, Germany) Radiesse (Bioform Medical, San Mateo, CA, USA) Aquamid (Contura Int., Soeborg, Denmark) Bio-Alcamid (Polymekon, Italy) Silikon-1000 (Alcon Laboratories, Fort Worth TX, USA) Artefill (Artes, San Diego, CA, USA) crm-DEX, crm-DX (Biopolymer GmbH & Co. KG, Montabaur, Germany)

c­ ollagen filler. Zyderm II, a similar product with a higher concentration of ­collagen, was introduced in 1983 and Zyplast, a bovine collagen cross-linked with glutaraldehyde to increase longevity, received FDA approval in 1985. About 20 years following the approval of bovine collagen in the USA, a bio­ engineered human collagen was developed to obviate the need for skin testing and reduce the incidence of hypersensitivity reactions. Cosmoderm and Cosmo­ plast received FDA approval in 2003. Hyaluronic acid, a naturally occurring biopolymer, was first identified as a viable dermal filler in 1989 by Balazs who noted its biocompatibility and lack of immunogenicity [9]. In 1998, the first efficacy studies of nonanimal stabilized hyaluronic acid (Restylane, Q-Med, Uppsala, Sweden) were performed. In 1999, the product was purified further to reduce immunogenicity and hypersensitivity reactions. In 2003, after 4  years of use in Europe, Restylane was approved in the United States by the FDA and has maintained a large share of the hyaluronic acid filler market since. Other FDA-approved hyaluronic acid fillers include Restylane Perlane, Juvederm, Elevess, and Prevelle Silk. In Europe, many more hyaluronic acid and other fillers are available for soft tissue

a­ ugmentation [10]. Although testing of fillers by the FDA delays approval in the USA, it is likely that many of the fillers currently available in Europe will become available for use in the USA in the near future [11].

29.3 Types of Fillers 29.3.1 Collagens The first FDA-approved dermal fillers were a group of collagen products derived from the hides of a closed herd of cattle in the USA. The three products within the group, Zyderm I, Zyderm II, and Zyplast, were used extensively for over two decades for treating facial wrinkles and folds, until hyaluronic acid fillers received FDA approval in 2003 and became more popular. The bovine collagens consist of 95–98% type I collagen and up to 5% type III collagen presented in 0.5–2.5  mL syringes and suspended in phosphate buffered saline with 0.3% lidocaine. Zyderm I contains 35  mg/mL of bovine collagen for superficial injection in the papillary dermis to correct fine lines. Since saline absorbs soon

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Table 29.2  Comparison of hyaluronic acid fillers Source

HA concentration mg/mL

Particle size (mm)

Cross-linking agent

Degree of cross-linking (%)

Restylane

Streptococcus equi

20

300

BDDE

1.2

Elastic modulus (G¢) (Pa) 660

Juvederm Ultra Prevelle Silk Hylaform Plusa

Streptococcus equi Streptococcus equi Cockerel combs

24 5.5 5.5

300 350 700

BDDE DVS DVS

2 12 12

105 230–260 140–220

BDDE 1,4-butanediol diglycidyl ether, DVS divinyl sulfone Hylaform is no longer promoted in the USA

a

after injection, overcorrection by up to 200% is required to achieve satisfactory results that last up to 3 months. Zyderm II contains 65 mg/mL of collagen for deeper injection in the papillary dermis to correct deeper lines. Some overcorrection is required with Zyderm II to achieve satisfactory final results. Zyplast, the most robust in this family of bovine collagens, contains 35 mg/mL of collagen cross-linked with gluteraldehyde. Zyplast is suitable for nasolabial folds, marionette lines, and to define the vermilion border of the lip. No overcorrection is required, and results last 3–4 months. About 3% of the population are allergic to bovine collagen. As such, double skin testing is required prior to treatment with these products. About 0.1 mL of Zyderm I is injected into the dermis of the forearm and inspected for erythema, swelling, pain and pruritis. Up to 1–2% of those with  negative initial skin tests prove to be allergic to bovine collagen. Therefore, a second test 2  weeks after the initial one should be performed. The inconvenience and delay in treatment with skin testing prompted the search for a collagen-based filler that is nonimmunogenic. A bioengineered collagen, derived from human tissue, received FDA approval for soft tissue augmentation in 2003. Cosmoderm I contains 35 mg/mL of collagen that is purified and screened for viral and bacterial pathogens. Like Zyderm I, Cosmoderm I is injected in the superficial dermis for fine lines. Cosmoplast, like Zyplast, is cross-linked with gluteraldehyde and injected in the deep dermis and lips for deep wrinkles and lip enhancement. Despite the evolution in collagen products in terms of immunogenicity, shortcomings include the need to overcorrect, the relatively short residence times in tissues, and the potential for serious adverse effects such as vascular occlusion or compression [12].

29.3.2 Hyaluronic Acid Fillers Hyaluronic acid (HA) is a naturally occurring polysaccharide that is ubiquitous in the extracellular matrix of all animal tissues and consists of regularly repeating units of d-glucuronic acid and N-acetyl-d-glucosamine [13]. It provides structural support to tissues by attracting up to 1,000 times its weight in water. The HA biopolymer shows no tissue or species specificity, a feature that has led to the development of hyaluronic acid ­fillers for human injection from both avian and bacterial sources. In its natural state, noncross-linked hyaluronic acid has a half-life of approximately 24 h before it is broken down in the skin by hyaluronidase and free radicals into carbon dioxide and water [14]. Although there are only a small number of FDAapproved hyaluronic acid fillers marketed in the USA, there are many more in use in Europe and some of these are likely to become available in the USA in the future. The important differences between currently available HA fillers include the source of HA, concentration of HA in each syringe, agent used for crosslinking HA polymers, degree of modification and cross-linking, amount of free unmodified HA present, and whether the product is monophasic (cohesive gel) or biphasic (particulate). In addition, the elastic modulus (G¢) of a gel is a measure of its firmness and resistance to deformation when a force is applied [15]. A comparison of HA fillers is shown in Table 29.2. Most currently marketed HA fillers are derived from the biofermentation of Streptococcus equi bacteria and are presented in prefilled syringes with volumes ranging from 0.5 to 3.0 mL. Monophasic products such as the Juvederm and Teosyal range are viscoelastic gels that are not sliced or sized into particles during the manufacturing process. Biphasic particulate gels, such as the Restylane group of products, are passed through

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301

subcutaneous plane through 27- or 28-gauge needles. Compared to hyaluronic acid fillers, Radiesse feels firm following injection, although this softens somewhat over a few days. Superficial injections, injections in the mucosa, and lip injections with Radiesse should be avoided to prevent lumps or nodules. Typically, the  results following soft tissue augmentation with Radiesse last about 12–18 months [17].

29.3.4 Permanent Fillers Fig. 29.3  Particulate hyaluronic acid filler

screens during the manufacturing process, so that Restylane Fine Lines has 200,000 particles per milliliter of product, Restylane has 100,000 particles, Perlane has 10,000, and Restylane Sub-Q is thicker with just 1,000 particles per milliliter (Fig. 29.3). Products with a higher concentration of cross-linked HA or larger particle sizes are generally indicated for deeper injection in the dermis and subcutaneous tissues to correct deep folds or for facial contouring and may have higher tissue residence times compared to products with lower concentrations of cross-linked HA or smaller particle sizes.

29.3.3 Calcium Hydroxylapatite Radiesse (Bioform Medical, San Mateo, CA, USA) is a long-lasting filler consisting of calcium hydroxylapatite microspheres of 25–45 mm diameter suspended in a carboxymethylcellulose gel carrier. The calcium hydroxylapatite found in Radiesse is identical to that found in the matrix of bone. Radiesse is biocompatible and provides long-lasting correction of deep wrinkles and folds and contouring of facial features such as cheekbones and the nasal dorsum. Following injection, the microspheres undergo fibrous encapsulation and provide a network of scaffolding for collagen ingrowth from surrounding tissue. Although the gel carrier absorbs over about 2 months, tissue ingrowth provides long-lasting results until the calcium hydroxylapatite microspheres degrade over several months to years [16]. Radiesse is an opaque, white, viscous product presented in 0.3 mL, 0.8 mL, and 1.5 mL syringes for injection in the dermal–subcutaneous junction or

The concept of permanently correcting an imperfection with an injectable procedure or providing ­aesthetic enhancement with permanent results is attractive. However, it must be remembered that facial aging is a dynamic process. A filler implant that corrects volume loss or improves facial contours in a 35-year-old patient may look out of place 10  years later when overlying skin and surrounding tissues have become thin, involuted, or ptotic. More importantly, complications associated with permanent injectable fillers are generally more difficult to treat than the transient side-effects typical of temporary fillers such as hyaluronic acid [18]. Nevertheless, several permanent fillers are available, most of which are synthetic polymers or combination materials. Table 29.3 provides a summary of the most common permanent fillers available today. Artefill (Artes Medical, San Diego, CA, USA) is currently the only FDA-approved permanent filler, indicated to treat nasolabial folds.

29.4 Choosing the Right Filler The decision to choose one filler over another for soft tissue augmentation depends on a number of factors, including the particular indication, injector experience, patient expectations, and local restrictions and availability. Hyaluronic acid fillers have become the gold standard for temporary soft tissue augmentation in most countries, and now supersede bovine and human collagen in the USA as the most popular choice. In general, finer, less viscous products are indicated for superficial wrinkles and lines, such as those above the lip, in the skin of the cheeks, and around the eyes. Thicker hyaluronic acid fillers with larger gel particle sizes, higher elastic moduli, and a greater degree of modi­ fication and cross-linking are appropriate for deep,

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Table 29.3  Summary of permanent fillers Product Artefill (Antes, San Mateo, CA, USA)

Aquamid (Contura A/S, Soeborg, Denmark) Bio-Alcamid (Polymekon, Italy)

Composition Polymethylmethacrylate microspheres (20–40 mm) in 3.5% bovine collagen + 0.3% lidocaine 2.5% hydrophilic polyacrylamide gel in 97.5% water 97% hydrophilic polyalkylimide gel

Silikon-1000 (Alcon Int., Fort Worth, TX, USA)

Polydimethylsiloxane oil (1,000 cSt)

Evolution (ProCytech, France)

Polyvinyl microspheres (40 mm) suspended in polyacrylamide gel

Indications Deep wrinkles and folds

Complications Granulomas, palpable nodules

Facial contouring

Migration, granuloma, infection, delayed inflammatory reactions Facial contouring, treatment Palpable nodules, implant of lipoatrophy migration, infection, delayed inflammatory reactions Wrinkles, lipoatrophy, acne Granulomas, migration, palpable nodules scarring (microdroplet technique) Moderate to deep wrinkles Inflammatory reactions and folds

Table 29.4  Author’s choice of filler for facial rejuvenation Indication Nasolabial folds (superficial) Nasolabial folds (deep) Oral commissures Lip enhancement Perioral (smoker’s) lines Tear trough hollows Upper eyelids Anterior cheek Cheekbones Nasal dorsum Glabellar linesa

Filler Teosyal Global Action, Restylane Teosyal Deep Lines, Perlane, Radiesse Teosyal Deep Lines, Perlane Teosyal Kiss, Restylane Lipp Restylane, Teosyal Global Action Restylane, Perlane Restylane Teosyal Ultimate, Restylane Sub-Q Radiesse Radiesse Restylane, Teosyal Global Action

Needle/cannula choice 30 G × ½" needle 27 G × ¾" needle 27 G × ½" needle 27 G × ½" or 28 G × ¾ “needle 30 G × ½" needle 30 G × ½" or 27 G × ½" needle 30 G × ½" needle 21 G × 2" or 18 G × 3" cannula 27 G × 1¼" needle 27 G × ½" needle 30 G × ½" needle

First-line treatment for the glabella is botulinum toxin type A

a

s­ ubcutaneous or supraperiosteal placement during facial contouring. Thicker gels placed superficially may create unsightly ridges or palpable lumpiness, whereas finer gels placed deeply below the dermis provide in­sufficient projection of tissues and absorb quickly. Manufacturers endeavor to cater for all indications by providing a selection of products with varying viscosity, particle size, and HA concentration (Table  29.4). Some fillers, such as Radiesse, are too viscous and firm for superficial placement and should only be placed at the dermis–subcutaneous junction or subdermal plane. The firmness of Radiesse provides excellent structural support, making it ideal for deep nasolabial folds, cheekbone enhancement, and ­nonsurgical nose reshaping [19, 20]. Injections of Radiesse in the superficial dermis or lips have a propensity for nodule formation [21]. Soft fillers should be used to augment naturally

soft facial compartments, such as the buccal and malar fat pads. As such, large volume hyaluronic acid fillers such as Restylane SubQ, Juvederm Voluma, and Teosyal Ultimate are ideally suited to provide smooth anterior projection of the cheeks lateral to the nasolabial folds. For tear trough hollows in the medial infraorbital area, conservative volumes of a small particle hyaluronic acid filler should be placed below the orbicularis oculi muscle on the periosteum to avoid visible and palpable lumpiness. Several HA fillers designed for lip enhancement have been introduced that are soft enough to provide natural results but robust enough to optimize longevity in this dynamic area. These include Teosyal Kiss, Restylane Lipp, and Juvederm Ultra Smile. Although collagens such as Zyplast and Cosmoplast do not provide lasting results, they provide crisp definition rather than just volume to the vermillion border of the

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Table 29.5  Areas amenable to treatment with injectable fillers Common Nasolabial folds Lip border Lip body Oral commissures Vertical lip lines Fine lines Zygomatic arch Malar fat pad Acne scars

a

Less common Tear trough Upper eyelid Nasal dorsum Columella of nose Philtrum of lip Jawline Brow Chin Hands Glabella, crow’s feet, and forehead linesa

First-line treatment is botulinum toxin type A

lip. When starting the practice of injectable fillers, the author recommends using hyaluronic acid products only as they tend to be more forgiving than long-lasting fillers and, although rarely necessary, can be reversed using hyaluronidase [22].

29.5 Pretreatment Considerations 29.5.1 Patient Selection There are several basic and advanced indications for injectable fillers in facial rejuvenation (Table  29.5) (Fig. 29.4). Basic indications are commonly performed and technically simple. Advanced techniques require more precision, are less forgiving, or involve contouring of features rather than just filling lines. With all filler treatments, patients should have realistic expectations and understand that the aim is to soften folds and lines or improve features and proportions, rather than eliminate lines altogether or create perfection. The value of combining soft tissue augmentation with other aesthetic medical procedures such as botulinum toxins and skin resurfacing should be emphasized, particularly if the patient seeks more dramatic results. Facial assessment begins during the consultation while the patient is speaking by observing the activity of the muscles acting on the mouth. Often, there is a discrepancy in the activity of the right and left levator labii muscles during animation, resulting in asymmetry of nasolabial fold depth that is resistant to correction using fillers alone. Any asymmetry should be brought to the attention of the patient before treatment, and documented with photography. The face is inspected

Fig.  29.4  Indications for injectable fillers. Blue basic techniques, green advanced techniques

from the front and side profiles to determine the presence and extent of tear trough hollows, nasojugal grooves, malar flattening, nasolabial folds, marionette lines, lip height and projection, chin projection, nose shape, and perioral and cheek lines. Effacing the nasolabial fold with gentle lateral traction on the skin of the cheek indicates that fillers are likely to soften the fold satisfactorily (Fig.  29.5). Similarly, if skin traction above the lip softens vertical rhtyids, fillers in this area are likely to be of benefit. Minimal or no improvement in the lines with this maneuver is common with “etched in” lines that require more aggressive measures such as CO2 laser skin resurfacing. Rejuvenation of the infraorbital area with fillers alone can be challenging, particularly when there is  skin laxity or prominent infraorbital fat pads. Nevertheless, appropriate use of fillers in the right candidate can produce dramatic results, sometimes obviating the need for surgery. The value of soft tissue augmentation in this area is appreciated when one studies the lid–cheek complex [23]. The aim of injectable fillers under the eye is to create a smooth lid– cheek junction, so that the lid blends seamlessly with

304

a

P.M. Prendergast

b

Fig. 29.5  (a) Assessing the nasolabial fold. (b) Folds that soften with gentle lateral traction are treated successfully with fillers

a

b

Fig. 29.6  (a) Pretreatment. (b) After hyaluronic acid fillers. The nasojugal groove has been effaced, improving the smooth convexity of the lid–cheek complex

the cheek, without a groove or depression between them (Fig. 29.6). Atrophy of midface volume results in a cheek that “falls away” from the lid, giving the appearance of a longer lower eyelid and “bags” under the eyes. Restoring a smooth lid–cheek junction is achieved by placing filler along the tear trough groove, and often complementing this with volume in the malar area anteriorly, to lift the cheek and efface the nasojugal groove that runs further laterally from the tear trough (Fig. 29.7). Botulinum toxin type A is the treatment of choice for hyperdynamic lines in the upper third of the face: glabellar lines, horizontal forehead lines, and periorbital lines. For “etched in” lines or deep glabellar lines that remain despite chemodenervation, dermal fillers

should be considered. Fillers injected in very dynamic areas such as the glabella without chemodenervation first may lead to migration and premature absorption. Adverse effects associated with fillers in the upper face include vascular compromise in the glabellar area and palpable lumps in the thin skin around the eye [24].

29.5.2 Contraindications Contraindications to treatment with fillers include a known allergy to any ingredient within the product, active inflammation or infection in the treatment area, anticoagulation, and unrealistic expectations. For medico

29  Augmentation with Injectable Fillers

a

305

b

Fig. 29.7  (a) Pretreatment. (b) After 1  mL hyaluronic acid filler (Teosyal Deep Lines) in each tear trough and 2  mL (Teosyal Ultimate) in each malar area to improve volume and smooth contour irregularities

legal reasons, the author also defers treatment for anyone who is pregnant or breastfeeding. Patients on antiplatelet therapy such as aspirin should be advised that bruising is likely if they wish to proceed.

29.6 Preparation In order to minimize post-treatment ecchymosis, patients are advised to stop aspirin, anti-inflammatory medication, and nutritional and herbal supplements such as fish oils, vitamin E, ginger, garlic, Ginkgo biloba, and St. John’s Wort at least 7 days before the treatment. Patients should be warned that swelling, transient erythema, and bruising are possible, and should plan their social activities accordingly. Herpes simplex prophylaxis with an antiviral such as valaciclovir (500 mg/day) can be commenced 2 days prior to

treatment in patients susceptible to cold sores, particularly for lip enhancement. A consent form describing the procedure in detail, after-effects, risks, benefits, potential complications, and alternatives to treatment should be provided and signed by the patient before treatment. Finally, good quality photographs should be taken from frontal, oblique, and side views using a digital camera.

29.7 Anesthesia Adequate pain relief should be provided to patients prior to injectable filler treatments. Topical anesthesia alone using creams containing lidocaine, benzocaine, tetracaine, prilocaine, or mixtures often do not provide adequate anesthesia, particularly for sensitive areas such as the lips. Infiltrating the treatment area with

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P.M. Prendergast

Table 29.6  Guidelines for anesthesia in facial soft tissue augmentation Area Nasolabial folds Top lip, vertical rhytids above lip Bottom lip, chin Oral commissures Anterior malar area Tear trough, infraorbital Cheekbones, zygomatic arch

Anesthesia Infraorbital n. blocks Infraorbital n. blocks + midline frenulum Mental n. blocks + midline frenulum Mental n. blocks Infraorbital n. block + infiltrative anesthesia (with epinephrine) Infraorbital n. (percutaneous approach) Infraorbital n. + zygomaticofacial n. blocks ± topical cold

local anesthesia is simple and effective, but may distort the tissues and interfere with the ability to assess the efficacy and end-point of augmentation. Regional nerve blocks provide excellent anesthesia for soft tissue augmentation procedures and allow large areas to be anesthetized, often at sites distant to the proposed treatment area. These techniques are described in a separate chapter in this book. The author uses plain 2% lidocaine for most regional blocks, providing a rapid-onset anesthesia that lasts less than 1 h. For augmentation of the malar area using a blunt cannula, infiltrative local anesthesia using lidocaine with 1:200,000 epinephrine is useful for two reasons. First, the vasoconstrictive effects of epinephrine serve to limit ecchymosis from blunt trauma in the cheek. Second, the volume of filler required for optimum enhancement is loosely determined by analyzing the effect the local anesthetic alone has on the tissues. If 3  mL of anesthetic produces ­sufficient augmentation, then the same volume of hyaluronic acid can be placed immediately afterwards. The supplementary use of topical ice or cold packs is often helpful, particularly for areas where nerve blocks are less accurate or produce incomplete anesthesia, such as the lateral cheeks, or when superficial vasoconstriction is desirable. For lip enhancement, small volumes of infiltrative anesthesia into the labial frenulum in the midline supplement infraorbital and mental nerve blocks. Table  29.6 provides a list of guidelines for anesthesia in soft tissue augmentation of the face.

29.8 Materials Fillers are available in different volumes in prefilled syringes. Although needles of appropriate gauge are often included within the product packaging, this does not preclude the use of other needles. However, while

Volume per side (mL) 1–2 1–2 1–2 1 2–3 0.5 2–3

it is acceptable to use a larger bore needle, longer needle, or blunt cannula in place of the needle provided, needles of smaller internal diameter than the one provided should not be used. The rheological (flow) properties of the filler as well as gel particle size may not allow adequate expression through needles of smaller internal diameter. Longer needles (1–1¼") are useful for lip and cheek enhancement where single long passes facilitate the procedure with less needle punctures. Blunt cannulas are ideal for facial contouring and cheek enhancement where 3–4 mL of hyaluronic acid is placed in the deep subcutaneous tissues and over the periosteum through a single skin puncture. For hyaluronic acid, the author employs blunt cannulae ranging in size from 22-gauge to 18-gauge of various lengths (Fig.  29.8). Single-use flexible cannulae are now also available, such as the Pix'L microcannula (Thiebaud S.A.S, France). Before injections, the skin is prepared using 70% isopropyl alcohol wipes. Other materials required for augmentation using injectable fillers include local anesthetic, sterile gauze, 3  mL syringes, needles, cold packs, and gloves.

29.9 Indications and Technique 29.9.1 General Technique The following general techniques are used to inject fillers superficially for lines and folds and deeply for facial contouring or volume enhancement (Fig. 29.9): 1. Superficial droplet The tip of the needle (usually 30-gauge) is barely injected into the skin at approximately a 30º angle, as superficially as possible, and tiny droplets (0.005–0.01  mL) are placed. A small wheal-like appearance or localized blanching is acceptable

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307

Fig. 29.8  Blunt cannulae for subcutaneous placement of fillers for facial contouring

because the droplets are so small and settle quickly (Fig. 29.10). This technique is indicated for superficial wrinkles and lines, such as those along the cheeks, lateral to the oral commissures, or in the glabellar area. A series of extremely superficial, quick injections are made at 3–4 mm intervals so that one droplet fuses into the next along the wrinkle. Only less viscous hyaluronic acid fillers should be injected using this technique. The needle should be changed once or twice during the treatment to ensure it remains as sharp as possible. 2. Linear retrograde threading To place filler along a fold or groove, the needle is inserted to the desired depth, advanced, and withdrawn slowly as product is expressed into the cavity created by the needle in front of it. For nasolabial folds, the depth is usually the deep dermis. For vertical lip rhytids, the needle is placed perpendicular to the lines in the superficial dermis. This technique is also used to define the vermilion border or enhance the body of the lips. Although it is difficult to be sure of the precise depth of the needle in the skin, steady resistance is felt when the needle  is advanced through the dermis, whereas the

s­ ubdermal plane offers little resistance to the needle. If the color of the needle is visible through the skin, the needle is too superficial and should be withdrawn and reinserted before placing any product (Fig.  29.11). Hyaluronic acid filler that is injected too superficially using this technique may result in an unsightly bluish tinge or visible “thread” of filler that may take over a year to degrade. To reduce the likelihood of intravascular injection in the periorbital area, the syringe should be aspirated gently before injection, followed by slow retrograde movement of the syringe as the filler is placed. 3. Perpendicular buttress This technique is indicated for deep nasolabial folds that tend to overhang the crease despite placement of filler along its length using the linear retrograde threading technique. After a column of filler is placed into and medial to the crease in the usual way, multiple short threads are placed intradermally perpendicular to the crease to add support and reduce ptosis (Fig.  29.12). A robust filler such as calcium hydroxylapatite (Radiesse) works well using this buttress technique.

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P.M. Prendergast

Fig. 29.9  Techniques for filler injections. (a) Superficial droplet. (b) Linear retrograde threading. (c) Perpendicular buttress. (d) Fanning. (e) Cross-hatching. (f) Depot. (g) Push technique

4. Fanning The needle is inserted, often to the hilt, and filler is injected during withdrawal as in linear retrograde threading. However, before the needle tip exits the skin, it is redirected so that further product is placed next to the first thread. The maneuver is repeated, through the same needle puncture, until a fan or triangular-shaped layer of filler is laid down. The fanning technique is usually employed at the

s­ uperior part of the nasolabial fold beside the nasal alae, at the oral commissures, and in the cheeks. 5. Cross-Hatching A grid-like pattern of filler is placed through multiple injection points so that the first series of threads lie parallel to one another. A second series of threads is then placed perpendicular to the first threads. This technique provides structural support to an anatomic area and builds up volume over features, such

29  Augmentation with Injectable Fillers

309

a

Fig. 29.10  Superficial droplet technique. Small droplets of thin hyaluronic acid filler are placed in the superficial dermis, raising wheals

as the cheeks. It is particularly appropriate for firm, collagen-stimulating fillers such as calcium hydroxylapatite (Radiesse), where a scaffolding of filler is laid down to allow tissue ingrowth over time. 6. Depot A bolus or depot injection of filler is placed deeply to provide volume and project tissues anteriorly. The depot technique should only be performed using blunt cannulae to avoid intravascular injection. For malar enhancement, the author uses a combination of the depot and fanning techniques through a single puncture lateral to the modiolus. 7. Push This novel technique has been described for filling the tear trough [25]. Using a fine blunt cannula, a small depot of filler is placed supraperiosteally in the infraorbital groove. Then this small pool of filler is “pushed” or massaged gently using the thumb along the tear trough deformity medially. The technique avoids multiple punctures with a needle, and could be applied to other facial areas.

29.9.2 Nasolabial Folds The folds are assessed in the upright position to determine the depth and predict the volume of filler required for correction. Deeper folds generally require larger volumes and more viscous fillers such as Radiesse, Perlane, or Teosyal Deep Lines. Fine lines along the fold should be treated with the superficial droplet technique. Fillers are injected at different depths during the same treatment to address both deep folds and superfi-

b

Fig. 29.11  Linear retrograde threading. (a) Needle placed too superficially with color of needle visible. (b) Correct placement in the dermis

cial rhytids. With the patient reclined at a 45° angle, an infraorbital nerve block is performed. The extent of the fold is determined by gently pushing the tissue toward the nasolabial crease. The needle is measured over the skin to determine a puncture site that will allow the needle tip advance to the most cephalad part of the crease. Filler is placed in the deep dermis using both linear retrograde threading and fanning techniques. At first, a sufficient volume of filler should be placed in the triangle beside the ala of the nose (Fig.  29.13). Then, as filler is placed inferiorly along the crease, it is important to stay slightly medial to the fold to create a smooth transition between the skin of the upper lip and the nasolabial fat. At the inferior part of the nasolabial fold, a dimple or tethered area is often encountered where the zygomatici have dermal attachments. Softening the fold here requires superficial placement of small volumes of filler, using the tip of the needle to

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P.M. Prendergast

a

b

c

d

e

f

Fig. 29.12  Perpendicular buttress technique. (a–d) The needle shows the direction and placement of filler along the nasolabial fold and perpendicular to it. (e) Long threads of filler placed in the deep dermis along and just medial to the fold. (f) Short

threads placed in the deep dermis perpendicular to the fold. (g) Pretreatment. (h) After 1.3 mL Radiesse in each nasolabial fold using perpendicular buttress technique

29  Augmentation with Injectable Fillers

g

311

h

Fig. 29.12  (continued)

a

Fig. 29.13  Filling the nasolabial fold. (a) Filler is injected in the deep dermis starting at the superior aspect of the fold. (b) The area adjacent to the nasal ala should be filled to soften the

b

fold superiorly. (c) The fold is effaced using the linear retrograde threading technique inferiorly along toward the mouth

312

c

P.M. Prendergast

a

Fig. 29.13  (continued)

gently subcise or cut the dermal attachments where possible. Results can be appreciated immediately following the procedure, and improve further once erythema and oedema subside (Fig.29.14).

b

29.9.3 Oral Commissures Soft tissue augmentation of the oral commissures lifts the mouth corners and creates a pleasant countenance (Fig.  29.15). Placing a small amount of filler in this area is almost always indicated during lip enhancement. To treat the oral commissures, the extent of the groove can be assessed by gently pushing the jowl toward the chin. The index finger of the noninjecting hand lifts the mouth corner into the desired position. Then the thumb stabilizes the lower lip skin to allow the needle pass easily into the dermis at the correct depth. The needle is measured over the commissure such that the tip reaches into the upper lip when advanced to its hilt. To achieve a successful lift, the needle must be in the superficial dermis with the distal third of the needle immediately adjacent to the vermilion border. Two or three passes may be necessary to place adequate threads using the linear retrograde technique. Injections in this area that are too deep may worsen the oral commissure rather than improve it. Once the lip edge has been lifted, the fanning technique is used to support the mouth corners and fill along the commissure toward the chin.

Fig. 29.14  (a) Before treatment. (b) Immediately after 1 mL Teosyal Deep Lines in each nasolabial fold

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a

b

c

d

Fig. 29.15  Lifting the mouth corners with fillers. (a) The oral commissure is assessed in the resting position. (b) The index finger of the noninjecting hand lifts the mouth corner to the desired position. (c) The thumb stabilizes the lower lip skin. (d) The needle is measured externally to determine the point of entry. The needle tip should reach the upper lip. (e) A thread of

filler is placed in the superficial dermis just lateral to the vermilion border. Further threads should be placed as required until the lip edge remains elevated. (f, g) Filler is placed medial to the oral commissure to support the lift and soften the fold here. (h) After 0.5  mL hyaluronic acid, the mouth corner appears elevated

314

P.M. Prendergast

e

f

g

h

Fig. 29.15  (continued)

29.9.3.1 Lips Both the vermilion border of the lip and the body of the lip can be augmented using fillers (Figs. 29.16–29.18). Although hyaluronic acid is the most commonly used filler, collagen may also be used for the border to provide crisp definition. Fillers with long-lasting microspheres such as calcium hydroxylapatite and permanent fillers should not be used for lip enhancement. For aesthetically pleasing proportions, the bottom lip to top lip height should be approximately 1:0.6, although this sometimes varies according to personal preference. For anesthesia, infraorbital and mental nerve blocks are performed, supplemented with 0.5 mL of anesthesia in the mucosa at the midline around the upper and lower frenulum.

To enhance the vermilion border, the needle is placed at or just above the vermilion border, in the “white roll,” a tube-like structure that gives the lip border its definition. Using the linear retrograde threading technique, small volumes are injected along the length of the border, from the commissure to the midline. Shorter needles may be used near the philtrum for accurate placement along the lip border without ­distorting the angles of Cupid’s bow. Gentle molding in this area is used to maintain sharp definition. For experienced physicians, a thin thread of filler can also be placed along the philtrum ridges from the vermilion to the columella, using the noninjecting hand to feel the needle and hold the thread of filler in place as the

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315

a

b

c

d

e

f

Fig. 29.16  Defining the lip borders. (a) A ¾" or 1" needle is ideal for placing fillers along the border of the lip. (b) A thread of filler is placed all the way to the cupid’s bow, at or just above the vermilion border in the “white roll” of the lip. (c, d) Using the linear retrograde threading technique, filler is placed from the cupid’s bow to a point just short of the lip edge laterally. (e)

Filler should be placed all the way to the midline to enhance the Cupid’s bow. (f) A small bolus can be placed just prior to the needle exiting the skin where the philtrum line meets the lip. (g) Gentle molding enhances the philtrum. (h) To define the lower lip, a thin thread is placed at or just below the vermilion border along the entire length of the lip

316

g

P.M. Prendergast

h

Fig. 29.16  (continued)

a

b

Fig. 29.17  (a) Before treatment. (b) After lip border enhancement and enhancement of the philtrum ridges

needle is withdrawn (Fig. 29.17). Augmentation of the vermilion border improves definition and also reduces vertical lip rhytids in older patients and smokers who experience “bleeding” of lipstick above the lip. To improve overall lip volume and provide some lip eversion, filler is injected into the body of the lip (Fig. 29.18). The lip is everted slightly with the noninjecting finger and a suitable hyaluronic acid is injected

deeply into the lip at the point where the wet mucosa meets the dry epidermis. A continuous sausage-like tube of filler should be placed along the length of the body of the lip, except for the lateral 3–4 mm, where filler may distort the shape of the lip and make the mouth look wider. When the needle is withdrawn each time, the lip should be grasped gently with sterile gauze to prevent bruising and molded so that the

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317

a

b

c

d

Fig. 29.18  Lip volume enhancement. (a) Slight eversion of the lip with the noninjecting hand exposes the mucocutaneous (wet–dry) junction. (b) Filler should be placed from the midline

to a point just medial to the lateral border of the lip. (c) The needle is placed deeply into the body of the lip. (d) A thin “sausage” of filler is placed as the needle is withdrawn

p­ roduct is distributed evenly. Equal volumes should be placed on either side, unless an asymmetry exists before the procedure. Usually, 1  mL is sufficient to provide subtle lip enhancement, or even less if the border only is being treated. Mild swelling is usual and subsides within a few hours.

lifts the tissues and softens the rhytids. Very superficial placement in the upper papillary dermis should be avoided to prevent lumpiness. Comple­mentary use of botulinum toxin to partially denervated orbicularis oris will enhance the results and may prolong the tissue residence of the filler. For lines that do not respond to either of these modalities, deep complete or fractional CO2 laser resurfacing usually works well.

29.9.3.2 Perioral Lines One of the most commonly requested treatment areas is the skin above the lip, where vertical lines radiate from the vermilion border. These perioral lines are particularly common in smokers with hyperdynamic orbicularis oris muscles and poor skin quality. Sun exposure and normal senescent changes due to loss of fat, collagen, and elastin in the skin are also res­ponsible. To reduce perioral lines, a thin sheet of hyaluronic acid filler is placed in parallel threads into the superficial dermis (Fig. 29.19). The threads act as scaffolding that

29.9.3.3 Tear Trough Filling the tear trough hollow in the medial infraorbital area with even small volumes of hyaluronic acid can result in significant rejuvenation (Fig.  29.20). Unfortunately, it is also a less forgiving area prone to swelling, puffiness, and lumpiness with improper technique or poor patient selection. Patients with very lax skin or excessive ­protrusion of orbital fat should not be treated. An ­understanding of the complex anatomy in

318

P.M. Prendergast

a

b

c

d

Fig.  29.19  Perioral rejuvenation using fillers. (a) The depth and distribution of perioral rhytids is determined by gently compressing the skin above the lip. (b) The skin is stabilized. (c)

Thin threads are placed perpendicular to the lines across the upper lip in the superficial dermis. (d) Further compression produces fewer lines once sufficient filler has been placed

this area is essential before addressing it with fillers (Fig. 29.21). When the orbital and zygomatic retaining ligaments attenuate, fat protrudes below the eye, bags begin to form, and the tear trough and nasojugal folds become prominent. Small volumes (<0.5 mL) of lidocaine with epinephrine are injected transcutaneously over the periosteum around the infraorbital nerve. After waiting 10 min, the needle is placed perpendicularly first to reach periosteum, then withdrawn 1 mm and tunneled slowly medially under orbicularis oculi to reach the medial extent of the tear trough. After aspiration, small aliquots of filler are placed under orbicularis oculi and the orbital retaining ligament as the needle is withdrawn. Gentle massage after each

injection ensures the filler is in the correct position behind the muscle. During the procedure, the patient is asked to gaze upwards intermittently to delineate the tear trough, which becomes more pronounced as the orbital fat bulges outwards. It is imperative to protect the globe by placing the fingers of the noninjecting hand along the orbital rim. This technique can also be performed using fine bore blunt cannulae through one or two skin punctures [26]. The skin in the tear trough area is extremely thin, making it important to place the filler deeply under the muscle, either in the prezygomatic space or in the preperiosteal fat. Subdermal injections in this area can only be performed if microdroplets are used [27]. To efface the

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319

a

b

c

d

Fig. 29.20  Augmenting the infraorbital hollows. (a) The needle is placed along the periosteum just below the infraorbital margin. (b) Markings can be made to define the extent of infraorbital volume loss. (c) The needle is measured over the skin first so that the needle tip reaches the medial extent of the hollow, short of the angular vessels. (d) The needle passes deeply first until the tip touches the periosteum. (e) Then the needle is

­ ithdrawn a fraction, redirected toward the medial canthus, and w glides deep to the orbicularis oculi above the periosteum. After gently aspirating on the syringe, small aliquots are placed using linear retrograde threading, releasing pressure on the plunger before the needle is withdrawn superficial to the muscle. (f) These steps are repeated along the extent of the tear trough hollow until adequate correction is achieved

320

e

P.M. Prendergast

f

Fig. 29.20  (continued)

tear trough hollow, the author usually injects 0.4– 0.5 mL hyaluronic acid per side during an initial treatment, with further filler placed 2–3  weeks later at a follow-up visit if required.

29.9.3.4 Malar Fat Pads A youthful midface is characterized by smooth convex curves from the lower lid with full anterior malar fat pads. The anterior cheek should blend seamlessly with the lower lid, nasolabial fat pad, lateral cheek, and tissue over the lateral orbital rim so light is reflected from the smooth contours. The apex or most anteriorly projecting part of the cheek is usually over the zygoma, just below the lateral canthus. Hyaluronic acid fillers are ideal for soft tissue augmentation of the anterior cheek (Fig.  29.22). First, an infraorbital nerve block is performed using the intraoral approach. Then a small bleb of anesthesia is raised using a 30-gauge needle in the dermis just lateral to the modiolus. To make an entry site for an 18-gauge cannula, a 16-gauge needle is used to puncture the skin. A 20-gauge needle and 21-gauge cannula may also be used. Further infiltrative local anesthesia using lidocaine and epinephrine is performed with deep injections into the site of augmentation with a long 27-gauge needle. After waiting 10 min for adequate vasoconstriction, the blunt cannula is used to deposit hyaluronic acid using the depot and fanning technique. In order to create seamless transitions between the contours, filler must be placed close to the orbital rim, deeply in the buccal fat pad, into the sublevator space deep to levator labii near the nose, along the medial part

of the zygomatic arch, and feathered from the most prominent part over the zygoma toward the lower third of the face. The index finger feels for the tip of the cannula at the infraorbital rim where it advances below the orbicularis oculi muscle. The author typically places 2–4  mL of Teosyal Ultimate or Restylane Sub-Q on each side to achieve satisfactory results (Fig. 29.23).

29.9.3.5 Cheekbones Soft tissue augmentation over the zygomatic arch and zygoma provide an attractive youthful appearance characterized by high, defined cheekbones. This technique is usually indicated for patients who are 25–50 years old who have reasonable soft tissue coverage (Fig.  29.24). Filler implants injected in patients who have very thin faces may look excessively prominent and unnatural. The aim is to create subtle definition so that a shadow is cast along the zygomatic area (Fig. 29.25). Firm, robust fillers such as Radiesse are particularly well suited for enhancing and defining bony features such as the cheekbones. The area is marked bilaterally to ensure symmetry. Infraorbital, zygomaticofacial, and zygomaticotemporal nerve blocks can be used for anesthesia, supplemented with topical ice where ­necessary. Most of the filler is placed over the ­zygomatic arch and below the lateral canthus over the zygoma, with feathering into the malar and buccal areas. Threads of filler are placed at the ­dermal–subcutaneous junction using the fanning and cross-hatching techniques. A long needle facilitates place­ment with fewer ­puncture sites. With calcium

29  Augmentation with Injectable Fillers

321

Orbitopalpebral sulcus Tear trough

Nasojugal fold

Orbicularis oculi Retroorbicularis oculi fat (ROOF) Hyaluronic acid filler

Orbital retaining ligament Suborbicularis oculi fat (SOOF) Hyaluronic acid filler Preperiosteal fat Prezygomatic space Zygomatic retaining ligament

Fig. 29.21  Components of periorbital volume loss and correction using hyaluronic acid filler

322

a

d

P.M. Prendergast

b

c

e

Fig.  29.22  Soft tissue augmentation of the midface. (a–c) Filler is placed medially and laterally along the orbital rim and inferior to it, protecting the globe with the finger resting on the orbital rim. (d) The skin is anesthetized by raising a dermal bleb. (e) A puncture is made using a 16 or 18-gauge needle. (f, g)

With the finger on the orbital rim, the cannula is inserted to the periosteum and filler is placed deep to the muscles and in the subcutaneous tissue using the fanning technique. (h) Smooth anterior projection of the cheek following 3 mL hyaluronic acid filler

29  Augmentation with Injectable Fillers

f

323

g

h

Fig. 29.22  (continued)

hydroxylapatite, approximately 1.3–2  mL filler on each side achieves satisfactory enhancement. Once placed, firm molding into place with the fingertips flattens the subcutaneous threads of filler and helps blend the augmented soft tissue with the surrounding area.

29.9.3.6 Nose Even minor alterations to the shape of the nose with temporary fillers can produce immense patient satisfaction. The most common indication is filling the relative concavity between the nasion and rhinion (Fig. 29.26, 29.27). The nasion lies at the root of the nose in the midline and the rhinion is the junction of the bony and cartilaginous dorsum of the nose in the midline. A small amount of plain lidocaine is placed around the infratrochlear nerve to anesthetize this area. Then a viscous filler such as Radiesse is injected along the periosteum, molding gently until the nasal dorsum

appears straight. Asian patients often request a more prominent nasal bridge. To achieve this, filler is placed more proximally, starting at the glabella and blending with the nasal dorsum. Filler should be placed in small volumes deeply on the periosteum to reduce the likelihood of intravascular injection that could lead to skin necrosis in this area. To lift the tip of the nose, a small depot injection of hyaluronic acid is placed in the subnasale at the junction of the columella and the upper cutaneous lip. An injection of botulinum toxin in the depressor septi muscle complements this by alleviating the downward pull on the tip of the nose.

29.9.3.7 Chin To enhance the chin, a depot injection is placed on the anterior aspect of the mentum in the midline. About 2 mL of hyaluronic acid placed on the periosteum is usually sufficient.

324 Fig. 29.23  (a) Flattening of the midface. (b) Improvement after soft tissue augmentation with 3 mL Teosyal Ultimate

P.M. Prendergast

a

29.9.3.8 Supraorbital Elevation and anterior projection of the lateral third of the eyebrow is achieved by injecting about 0.5 mL of filler along the periosteum under the brow (Fig. 29.28). Placing the filler a fraction inferior to the level of the brow has the effect of pushing the hair of the brow superiorly. 29.9.3.9 Eyelids Periorbital volume loss results in deepening of the superior orbitopalpebral sulcus with a visible bony orbital rim (Fig. 29.29). Improving this “sunken eye” appearance with fillers requires carefully placed injections in the retro-orbicularis oculi fat (ROOF) pad behind the eyelid (Fig.  29.21). This is a particularly unforgiving area and should only be performed by those with plenty of experience using fillers. If too much filler is placed, or if the filler is injected in the skin, the eyelid may appear swollen with visible bumps and unevenness. Successful augmentation in this area softens the appearance and provides a more youthful

b

look (Fig. 29.30). The author uses Restylane for periorbital augmentation, injected through a 29- or 30-gauge needle. Even without anesthesia, injections in the eyelid are well tolerated. Topical anesthesia may be used, but infiltrative anesthesia should not be used because of its propensity to cause tissue distortion. After marking the hollows, tiny threads of filler are placed under the dermis and orbicularis oculi and gently massaged against the supraorbital ridge to ensure an even distribution. The orbital septum lies deep to the ROOF. The septum is very thin, and covers the subseptal fat medially and the lacrimal gland laterally. Injections should remain superficial to avoid penetrating the orbital septum. The needle will enter the correct plane by gently pinching up the skin and placing the needle into the tented area. Soft tissue augmentation using hyaluronic acid provides instant results that last about 6–8 months. A similar technique using fat has also been described [28]. For eyelid filling, very small volumes are the key to avoiding unwanted effects. It is better to add filler during a second treatment rather than overfill.

29  Augmentation with Injectable Fillers

325

a

b

c

d

e

f

Fig.  29.24  Cheekbone enhancement using calcium hydroxylapatite. (a) The area to be enhanced is marked carefully. This should be quite high over the zygomatic arch and taper toward the zygoma. (b, c) The fanning technique is used to place filler in the superficial subcutaneous plane. (d) Augmentation contin-

ues through further injections medially over the prominent zygoma. (e, f) Further injections are made from the medial aspect of the zygomatic arch to blend with the previously placed filler and feather over the infrazygomatic area

326

P.M. Prendergast

a

b

Fig. 29.25  (a) Before treatment. (b) After cheekbone enhancement with 1.5 mL Radiesse on each side

a

Fig. 29.26  Nose reshaping using fillers. (a) The soft tissue is lifted upwards and the needle is placed deeply on the periosteum. After aspiration, small volumes are injected. (b) Filler can

b

also be placed from a point just proximal to the rhinion. (c) The filler is molded gently to create the desired degree of augmentation or straightening

29  Augmentation with Injectable Fillers

c

Fig. 29.26  (continued)

a

b

Fig. 29.27  (a) Before treatment. (b) After 0.3 mL Radiesse in the proximal nasal dorsum

29.9.3.10 Hands Hand rejuvenation using microdermabrasion, chemical and laser resurfacing, and selective photothermolysis with intense pulsed lights address skin texture, fine lines, and dyschromias but do not address volume loss [29]. Adding volume to the dorsum of the hands reduces the prominence of the extensor tendons and veins (Fig. 29.31, 29.32). Several techniques have been described to place fillers in the subcutaneous ­tissues of the hand, including the push technique and linear retrograde threading. Fillers such as calcium

327

hydroxylapatite, hyaluronic acid, and collagen are used with good results and minimal complications [30, 31]. In addition, hand rejuvenation with stimulating agents such as poly-l-lactic acid has been repor­ ted  [32]. The author uses calcium hydroxylapatite (Radiesse), admixed with plain lidocaine to reduce pain and improve the flow of the product through the tissues. Usually 1.5  mL of Radiesse with 1.5  mL of lidocaine per hand provides sufficient augmentation. While pinching and tenting the skin, the mixture is injected in 0.3–0.4 mL aliquots under the skin between the wrist joint and metacarpophalangeal joints, taking care to avoid the veins. The lumps that appear immediately on the dorsum of the hands are pushed and massaged evenly over the hand. To make this easier, massage firmly with both thumbs using a lubricant such as Vaseline and have the patient make a clenched fist. The patient should be advised to continue gentle massage for the remainder of the day to ensure the filler is distributed evenly over the hand. As with any injectable treatment, swelling and erythema are normal and transient.

29.10 Combination Approaches Volume loss is only one facet of the aging process. Other aging features, such as hyperdynamic lines, ptosis, and various skin pigmentation and textural irregularities are addressed using injectable, laser, and minimally invasive procedures in combination with the techniques described above. The combination of multiple procedures provides synergy, enhancing overall results without creating an unnatural appearance (Fig. 29.33). In the upper face, botulinum toxin type A is the most appropriate first-line treatment for hyperdynamic lines in the lateral periorbital area, glabella, and forehead. One injection of botulinum toxin in the lower eyelid below the eyelash partially denervates pretarsal orbicularis oculi and softens the appearance of the lid– cheek junction, particularly when fillers are also placed in the tear trough (Fig.  29.30). Carbon dioxide laser skin resurfacing is the gold standard for treating photoaged skin and “etched-in” lines lateral to the orbit and around the mouth. For glabellar frown lines, botulinum toxin is the first-line treatment unless contraindicated, followed 2  weeks later by dermal fillers if deep lines remain despite chemodenervation.

328

P.M. Prendergast

a

b

c

d

Fig. 29.28  Filler enhancement of the lateral brow. (a) An intradermal injection of local anesthetic is made. No other anesthesia is required. (b) Filler is injected along the periosteum using the

linear retrograde threading technique. (c) Before treatment. (d) After enhancement with 0.4 mL Perlane per side

In the midface, suture lifting techniques complement soft tissue augmentation with fillers by elevating the malar fat pad. Superior and superolateral lifting vectors soften the nasolabial fold and improve volume deficiency in the tear trough. Radiofrequency and infrared light devices for tissue tightening may also improve laxity, but the lifting effect of these external technologies is subtle. Fine perioral lines above the lip respond to a combination of ablative resurfacing, dermal fillers, and conservative doses of botulinum toxin. Combined suture lifting of the lower face and filling of the oral commissures provides better results than each procedure can achieve individually. To improve the definition of the jawline, suture lifting of the lower face and soft tissue augmentation of the prejowl sulcus with fillers can be performed together. Softening the chin with botulinum toxin also compliments the use of fillers in the mental crease.

29.11 Aftercare Patients should receive verbal and written instructions following injectable filler treatments. Although patients are advised to massage the face after treatments with stimulating agents such as Sculptra, gentle handling is more appropriate for most other fillers. Manipulating soft, pliable fillers such as hyaluronic acid following a treatment may lead to displacement or lumpiness. Excessive animation, such as laughing or chewing gum, should also be avoided, particularly following filler injections in dynamic areas such as the nasolabial folds. Some swelling, erythema, and bruising are normal after most injectable treatments. The patient should be reassured, and cold packs can be applied as desired for the first few hours. Mineral make-up can be used to camouflage ecchymosis. Although oral steroids are sometimes used for patients who have had fat

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329

a

b

c

d

e

f

Fig. 29.29  Treating the superior orbitopalpebral sulcus (sunken eyelid) with hyaluronic acid. (a) Mark the groove under the brow where there is volume loss. (b) Gently pinch up the eyelid and insert a 30-gauge needle. (c) The needle should be under the dermis or orbicularis oculi in the retro-orbicularis oculi fat (ROOF). (d) Lifting the needle reveals the depth. (e) After each

thread of filler is placed, the lid is gently massaged against the supraorbital rim. (f–h) Injections of tiny aliquots of filler continue medially along the orbitopalpebral sulcus until the groove has been corrected. (i, j) The filler is gently molded against the underlying periosteum to ensure evenness

330

P.M. Prendergast

g

h

i

j

Fig. 29.29  (continued)

a

b

Fig. 29.30  (a) Before treatment. (b) After periorbital rejuvenation with hyaluronic acid and botulinum toxin: 0.2 mL Restylane in each orbitopalpebral sulcus, 0.5 mL Restylane in each tear trough, and 4 IU Dysport in each inferior pretarsal orbicularis oculi

29  Augmentation with Injectable Fillers Fig. 29.31  Hand rejuvenation with injectable fillers. (a) Materials required include 2% plain lidocaine, calcium hydroxylapatite filler (Radiesse), 28-gauge needles, 3 mL syringe, and luer–luer connector. (b) 1.5 mL lidocaine is admixed with 1.5 mL Radiesse by passing it forward and back between the syringes 10–15 times until is homogenous. (c) The skin on the dorsum of the hand is tented up and bolus injections of 0.3–0.4 mL are made. (d) Several injections are made between the wrist joint and metacarpophalangeal joints. (e) The patient makes a fist and the boluses of filler are thoroughly massaged until smooth. (f) No significant lumps should remain following massage

a

b

331

332

P.M. Prendergast

c

e

d

f

Fig. 29.31  (continued)

transfer procedures to reduce swelling, they are rarely necessary following soft tissue augmentation with injectable fillers. Prophylaxis with valaciclovir should be considered in patients who have frequent herpes simplex outbreaks, particularly before injections in or around the lips.

29.12 Complications With the greatly increased use of injectable temporary and permanent fillers for soft tissue augmentation in recent years, there has been an increase in reported complications [33]. Proper training in basic and

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333

Fig. 29.32  The right hand only was treated with 1.5 mL Radiesse. Note the improved volume with reduction in appearance of veins and tendons

a

b

Fig. 29.33  (a) Before treatment. (b) After botulinum toxin for upper face hyperdynamic lines, hyaluronic acid fillers in the nasolabial folds and oral commissures, and a lower face suture suspension lift

334

advanced techniques, a thorough knowledge of soft tissue and facial anatomy, and an understanding of the indications, limitations, and potential side effects with each of the currently used fillers are required to reduce the incidence of unnecessary complications [18]. Using only temporary fillers with high safety profiles such as hyaluronic acid also serves to reduce serious complications [12]. Normal after-effects associated with the use of injectable fillers include transient swelling, erythema, and ecchymosis. The incidence and nature of more serious complications depend on the type of filler used and area injected. Minor complications due to superficial injections include visible or palpable lumpiness. Allergic or inflammatory reactions associated with hyaluronic acid fillers have been documented, but are rare [34]. Granulomatous reactions are more likely with collagen-stimulating synthetic products such as polymethylmethacrylate and poly-l-lactic acid. These may be treated with intralesional steroid injections. Several treatments with small volumes of triamcinolone acetonide injected directly into the granuloma may be required [35]. Some of the most serious complications associated with fillers occur due to inadvertent intravascular injection. In the glabellar tissue, this may lead to skin necrosis. Reports of iatrogenic visual loss due to intravascular injection of collagen and fat in the periorbital area exist [36]. Other significant complications, such as implant migration, infection, and delayed inflammatory reactions, are more likely with permanent fillers [37–40]. Immediate post-treatment swelling and erythema do not require treatment, although topical ice packs may accelerate resolution. In order to minimize bruising, lidocaine with epinephrine can be used for infiltrative local anesthesia, except when treating areas with end-arteries, such as the nose. Although slight lumpiness usually resolves spontaneously, gentle massage is advised to improve resolution of a discrete lump that is bothersome to the patient. Although rarely necessary, hyaluronic fillers may be dissolved quickly using hyaluronidase [41]. The author routinely performs skin testing with hyaluronidase before treatment as hypersensitivity reactions and angioedema can occur [42]. Hyaluronidase (e.g., Hyalase 1,500 IU/amp) is reconstituted with saline and small volumes are injected directly into the lump or area that has been overfilled. Reconstituting 1,500 IU with 10 mL saline produces a 150 IU/mL solution. The volume of this reconstituted

P.M. Prendergast

hyaluronidase solution injected should equate to the volume of HA that requires removal. Breakdown of the filler can be expected within hours.

References 1. Burgess CM (2006) Principles of soft tissue augmentation for the aging face. Clin Interv Aging 1(4):349–355 2. Vleggaar D, Fitzgerald R (2008) Dermatological implications of skeletal aging: a focus on supraperiosteal volu­ misation for perioral rejuvenation. J Drugs Dermatol 7(3):209–220 3. Rohrich RJ, Pessa JE (2007) The fat compartments of the face: anatomy and clinical implications for cosmetic surgery. Plast Reconstr Surg 119(7):2219–2227 4. Lam SM, Glasgold MJ, Glasgold RA (eds) (2007) Aesthetics and aging: a new paradigm. In: Complementary fat grafting. Lippincott Williams & Wilkins, Philadelphia, pp 1–11 5. Ersek RA, Chang P, Salisbury MA (1998) Lipo layering of autologous fat: an improved technique with promising results. Plast Reconstr Surg 101(3):820–826 6. Beer KR, Narins R (2009) Soft tissue augmentation. In: Kaminer MS, Arndt KA, Dover JS, Rohrer TE, Zachary CB (eds) Atlas of cosmetic surgery, 2nd edn. Saunders, Philadelphia 7. Bruning P (1914) Contribution et l’etude des greffes adipeuses. Bull Acad Roy Med Belgique 28:440, Cited by Broeckaert TJ, Steinhaus J 8. Shiffman MA (2010) History of autologous fat transfer. In: Shiffman MA (ed) Autologous fat transfer: art, science, and clinical practice. Springer, Berlin, p 3 9. Matarasso SL, Carruthers JD, Jewell ML (2006) Restylane Consensus Group: consensus recommendations for softissue augmentation with nonanimal stabilised hyaluronic acid (Restylane). Plast Reconstr Surg 117(3 Suppl):3S–34S 10. Ellis DAF, Segall L (2007) Review of non-FDA-approved fillers. Facial Plast Surg Clin N Am 15(2):239–246 11. Jones D (2007) Dermal fillers. In: Goldberg DJ (ed) Facial rejuvenation: a total approach. Springer, Berlin, p 121 12. Alam M, Dover JS (2007) Management of complications and sequelae with temporary injectable fillers. Plast Reconstr Surg 120(6 Suppl):98S–105S 13. Bowman PH, Narins RS (2005) Hylans and soft tissue augmentation. In: Carruthers J, Carruthers A (eds) Procedures in cosmetic dermatology series: soft tissue augmentation. Saunders, Philadelphia, p 34 14. Allemann IB, Baumann L (2008) Hyaluronic acid gel (Juvederm) preparations in the treatment of facial wrinkles and folds. Clin Interv Aging 3(4):629–634 15. Kablik J, Monheit GD, Yu L, Chang G, Gershkovich J (2009) Comparative physical properties of hyaluronic acid dermal fillers. Dermatol Surg 35(Suppl 1):302–312 16. Sukhjit JS, Burgett RA (2006) Dermal filler agents: a practical review. Curr Opin Ophthalmol 17(5):471–479 17. Jacovella PF, Peiretti CB, Cunille D, Salzamendi M, Schechtel SA (2006) Long-lasting results with hydroxylapatite (Radiesse) facial filler. Plast Reconstr Surg 118(3 Suppl):15S–21S

29  Augmentation with Injectable Fillers 18. Duffy DM (2005) Complications of fillers: overview. Dermatol Surg 31(11 Pt 2):1626–1633 19. Siclovan HR, Jomah JA (2009) Injectable calcium hydroxylapatite for correction of nasal bridge deformities. Aesthetic Plast Surg 33(4):544–548 20. Alam M, Yoo SS (2007) Technique for calcium hydroxylapatite injection for correction of nasolabial fold depressions. J Am Acad Dermatol 56(2):285–289 21. Jansen DA, Graivier MH (2006) Evaluation of a calcium hydroxylapatite-based implant (Radiesse) for facial soft-tissue augmentation. Plast Reconstr Surg 118(3 Suppl):22S–30S 22. Smith KC (2008) Reversible vs nonreversible fillers in facial aesthetics: concerns and considerations. Dermatol Online J 14(8):3–14 23. Donofrio LM (2003) Periorbital lipoaugmentation. In: Narins R (ed) Safe liposuction and fat transfer. Marcel Dekker, Basel, p 464 24. Glaich AS, Cohen JL, Goldberg LH (2006) Injection necrosis of the glabella: protocol for prevention and treatment after use of dermal fillers. Dermatol Surg 32(2):276–281 25. Bosniak S, Sadick NS, Cantisano-Zilkha M, Glavas IP, Roy D (2008) The hyaluronic acid push technique for the nasojugal groove. Dermatol Surg 34(1):127–141 26. Hirmand H (2010) Anatomy and non-surgical correction of the tear trough deformity. Plast Reconstr Surg 125(2): 699–708 27. Kane MA (2007) Advanced techniques for using Restylane in the lower eyelids. Aesthet Surg J 27(1):90–92 28. Park DH (2010) Treatment of sunken eyelid. In: Shiffman MA (ed) Autologous fat transfer. Springer, Berlin, p 155 29. Marmur ES, Al Quran H, De Sa Earp AP, Yoo JT (2009) A five-patient satisfaction pilot study of calcium hydroxylapatite injection for treatment of aging hands. Dermatol Surg 35(12):1978–1984 30. Man J, Rao J, Goldman M (2008) A double-blind, comparative study of non-animal stabilised hyaluronic acid versus human collagen for tissue augmentation of the dorsal hands. Dermatol Surg 34(8):1026–1031

335 31. Busso M, Applebaum D (2007) Hand augmentation with Radiesse (calcium hydroxylapatite). Dermatol Ther 20(6):385–387 32. Sadick NS, Anderson D, Werschler WP (2008) Addressing volume loss in hand rejuvenation: a report of clinical experience. J Cosmet Laser Ther 10(4):237–241 33. Hirsch RJ, Stier M (2008) Complications of soft tissue augmentation. J Drugs Dermatol 7(9):841–845 34. Ghislanzoni M, Bianchi F, Barbareschi M, Alessi E (2006) Cutaneous granulomatous reaction to injectable hyaluronic acid gel. Br J Dermatol 154(4):755–758 35. Lemperle G, Romano JJ, Busso M (2003) Soft tissue augmentation with Artecoll: 10-year history, indications, ­techniques, and complications. Dermatol Surg 29(6): 573–587 36. Dreizen NG, Framm L (1989) Sudden unilateral visual loss after autologous fat injection into the glabellar area. Am J Ophthalmol 107(1):85–87 37. Amin SP, Marmur ES, Goldberg DJ (2004) Complications from injectable polyacrylamide gel, a new nonbiode­gradable soft tissue filler. Dermatol Surg 30(12 Pt 2):1507–1509 38. Chrastil-La Towsky B, Wesley NO, MacGregor JL, Kaminer MS, Arndt KA (2009) Delayed inflammatory reaction to bio-alcamid polyacrylamide gel used for soft-tissue augmentation. Arch Dermatol 145(11):1309–1312 39. El-Shafey el SI (2008) Complications from repeated injection or puncture of old polyacrylamide gel implant sites: case reports. Aesthetic Plast Surg 32(1):162–165 40. Jacinto SS (2005) Ten-year experience using injectable silicone oil for soft tissue augmentation in the Philippines. Dermatol Surg 31(11 Pt 2):1550–1554 41. Pierre A, Levy PM (2007) Hyaluronidase offers an efficacious treatment for inaesthetic hyaluronic acid overcorrection. J Cosmet Dermatol 6(3):159–162 42. Andre P, Flechet ML (2008) Angiooedema after ovine hyaluronidase injection for treating hyaluronic acid overcorrection. J Cosmet Dermatol 7(2):136–138

 

Potential Risks and Complications of Injectable Alloplastic Facial Fillers

30

Melvin A. Shiffman

30.1 Introduction All injectable alloplastic facial fillers have potential risks and complications. Indiscriminate use of fillers without knowledge of the possible risks and complications, their diagnosis, and their treatment is a disservice to the patient. Patients should be forewarned of all of the possible risks and complications of any dermal filler being planned to be used. The medical record should mention that the procedure was described, alternatives to the procedure discussed, and material risks and complications explained.

30.2 Calcium Hydroxylapatite Radiesse (Bioform, San Mateo, CA) Radiance (Bioform Medical, San Mateo, CA) Radiance FN (Bioform Medical, San Mateo, CA) Bentkover [1] looked at the relevant biology of facial fillers and stated that calcium hydroxylapatite filler has been shown to stimulate collagen neogenesis. Ridenour and Kontis [2] noted that subdermal injection for correction of defects lasts approximately 1 year.

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

30.2.1 Complications Sklar and White [3] reported five patients with complications after calcium hydroxylapatite treatment. Three patients developed palpable bumps, one had puffiness of the lower eyelid, and one had a pink/white plaque. Tsikas [4] studied 90 patients after calcium hydroxylapatite treatment and noted seven patients who developed persistent visible mucosal lip nodule, four of which required surgical intervention. Georgescu et al. [5] reported two cases of calcium hydroxylapatite-induced skin necrosis after injection in the glabella and nasolabial fold. Patients were given supportive treatment with oral steroids, nitroglycerin paste, and warm compresses approximately 48 h after injection. Both patients underwent microdermabrasion and hydrocortisone ointment to flatten the scar which resulted in a reasonable cosmetic appearance 4 months after the injection. Russo [6] described the mixing of lidocaine with calcium hydroxylapatite for pain reduction. Feeney et al. [7] reported the calcium hydroxylapatite filler is hyperattenuating on computerized tomography (CT), hypermetabolic on FDG-PET imaging, of intermediate signal intensity on magnetic resonance imaging (MRI), and is a potential cause of a false-positive imaging study.

30.3 Collagen of Bovine Origin Resoplast (Rifil Medical International B.V., Breda, The Netherlands) Rhegecoll

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_30, © Springer-Verlag Berlin Heidelberg 2011

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Zyderm 1 (McGhan Medical, Santa Barbara, CA) Zyderm 2 (McGhan Medical, Santa Barbara, CA) Zyplast (McGhan Medical, Santa Barbara, CA) Collagen should not be injected into patients with a history of autoimmune diseases, such as dermatomyositis, lupus erythematosis, or rheumatoid arthritis [8]. Charriere et al. [9] reported a positive skin test in 3.8% of patients and adverse reactions in 2.3% of patients with negative skin testing. Bentkover [1] looked at the relevant biology of facial fillers and found that bovine collagen is the most immunogenic filler. Porcine and bioengineered human collagen implants have very low immunogenicity, but allergic reactions and elevations of IgG are possible. Cross-linking and concentration affect the longevity of collagen fillers.

30.3.1 Complications Most allergic reactions are localized and consist of swelling and redness at the treatment site [10]. Infections, such as recurrent herpes simplex, abscess formation, tissue necrosis, and granulomatous foreign body reactions, were reported infrequently [11]. Cooperman et  al. [12] noted adverse reactions occurred to pretesting of Zyderm I in 3% of patients. In addition, 1.3% of patients experienced adverse reactions despite a negative pretest. Reactions ranged from localized swelling to induration, erythema, and pruritis. Onset ranged from immediate to 3  weeks after implantation. DeLustro et  al. [13] found an estimated 0.4% adverse reactions to bovine collagen after one to seven treatments. Hanke et al. [14] described sterile abscess (may be an atypical form of allergic reaction) being seen more with Zyplast and skin necrosis has occurred in a significant number of patients when Zyplast is injected into the glabellar area. Hanke [15] described the following adverse reactions to bovine collagen: transient erythema, bruising, and needle marks that were temporary. Also noted were local necrosis, infection, surface deformities (beading), intermittent swelling, systemic complaints such as arthralgias, myalgia, headaches, nausea, urticarial rashes, and partial blindness (injection in glabella area). Three percent of patients had positive pretreatment skin tests. Less than 1% of patients with negative pretesting

M.A. Shiffman

demonstrated allergic reactions. Cystic-abscess reactions are rare and occur most commonly with Zyplast treatment and start with pain followed by erythema and swelling. There are tender cysts that develop intermittently for 2 years or more. Incision and drainage relieves the pain and intermittent systemic or intralesional steroids provide relief in some patients. Ashinoff [16] stated that 3–3.5% of patients have localized reaction when tested to bovine collagen. In those patients who have negative skin testing, 1–5% still get an allergic reaction if the implant is then placed in the face, which usually subsides in 4–6 months; however, it can last up to 2 years. Adverse reactions include bruising, reactivation of herpes, bacterial superinfection can occur. Artecoll has shortterm side effects that include swelling, bruising, and sensitivity. Zyderm and Zyplast can have allergic reactions. Intra-arterial injection is suspected in several cases of unilateral blindness because of retinal artery occlusion. Complications of bovine collagen that were des­ cribed by Grossman [8] include bruising that should resolve in several day, temporary swelling, a white bump or raised area from injecting too superficially that may last for several months, necrosis and subsequent scar formation, allergic reactions seen as erythematous papules, streaks, or plaques Homicz and Watson [17] described systemic reactions to bovine collagen consisting of arthralgias and myalgia, fever, and pruritis in less than 5 per 1,000 patients.

30.4 Collagen of Human Origin AlloDerm (LifeCell Corporation, Palo Alto, CA) Autologen (Collagenesis Inc., Beverly, MA) Cosmoderm 1 (Allergan, Santa Barbara, CA) Cosmoderm 2 (Allergan, Santa Barbara, CA) Cosmoplast: (Allergan, Marlow, UK) Cymetra (LifeCell Corporation, Palo Alto, CA) Dermicol (cross-linked collagen of unknown origin) – correction may last 18 months Dermologen (Collagenesis Inc., Beverly, MA) Isolagen (Isolagen Technologies, Paramus, NJ) Rhegacoll (Dermabiol/Kuthra Vital, Lucerne, Switzerland) Autologous cultured fibroblasts serve as injectable protein repair systems for correction of acne scars, rhytids, and other facial scars [18]. The system uses

30  Potential Risks and Complications of Injectable Alloplastic Facial Fillers

the patient’s own cultured fibroblasts to correct contour deformities over time. Cosmoderm and Cosmoplast contain lidocaine and should not be used in patients with severe allergies manifested by a history of anaphylaxis or in patients with known lidocaine hypersensitivity. Longevity 3–6 months. Cymetra is not recommended in patients exhibiting autoimmune connective tissue disease, contraindicated in infected or nonvascular sites. Since Cymetra is supplied in an antibiotic-supplemented medium, it should not be used in patients sensitized to those specific antibiotics. Longevity 3–9 months Dermologen is an aseptically processed suspension of collagen fibers prepared from human donor tissue obtained from US Tissue Banks and lasts 3–6 months but has been know to last 9  months. It takes two to three injection sessions over several months in order to show maximal improvement. Patients over 60 years are not candidates for Isolagen because their skin is not capable of producing vigorous fibroblasts [16]. The cells are alive and cannot be stored so that careful planning and a reliable patient are essential. Correction may take 3–4 months because the fibroblasts take time to produce new collagen [16]. Gradual improvement may be seen over 18 months. Fagien [19] described the problem with Autologen was that the tissue donor was the recipient but noted that in a survey of 100 patients, that 98% would opt to use their own skin. Donor skin of 5 cm2 yields 1 cm3 of collagen. This can be stored refrigerated in BioBank™ for at least 5  years. The skin is processed by Collagenesis Laboratories. (Previously manufactured by Collagenesis (Beverly, Massachusetts) that is very similar to Cymetra.) However, Collagenesis filed Chap. 11 in the US Bankruptcy Court in Boston, #19656. Apesos and Muntzing [20] found only a small subset of patients is willing to donate skin for Autologen.

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Moody and Sengelmann [27] described pretesting with human collagen had reactions of mild, self-limited, and nontender erythema. Apte et  al. [28] reported on cases of choroidal infarction following subcutaneous injection of human collagen in the forehead.

30.5 Collagen of Porcine Origin Fibroquel Permacol Evolence (OrthoNeutrogena, Skillman, NJ) Evolence 30 (OrthoNeutrogena, Skillman, NJ) Ortho Dermatologics, a division of Ortho-McNeilJanssen that is a division of Johnson & Johnson, has discontinued Evolence for economic purposes. Evolence is not to be used in patients that are hypersensitive to any collagen products or porcine products or if there is a history of severe allergies.

30.5.1 Complications Side effects of Evolence include swelling, bruising, erythema, pain, and palpable lumpiness.

30.6 E-Aminocaproic Acid Fibrel (Serona Diagnostics, Inc., Norwell, MA) Fibrel is a lipholized mixture of 100 mg absorbable gelatin powder with 125  mg E-aminocaproic acid (EACA). The EACA enhances collagen synthesis through a blockade of the fibinolytic system [29].

30.6.1 Complications 30.4.1 Complications Cosmoderm and Cosmoplast have adverse reaction including infection, reactivation of herpes simplex, local necrosis (rare), and injection into dermal vessels may cause vascular occlusion, infarction, or embolic phenomena. Lack of permanency from collagen of human origin has been described by a number of authors [21–25]. Hyperpigmentation over injection sites has been reported [26].

Millican et al. [30] showed that 1.9% of 321 patients developed a positive skin test reaction with induration and erythema. None of the patients with negative skin testing developed an adverse allergic reaction. Monheit [31] stated that erythema, inflammation, and induration occur in almost all Fibrel injections. Inflammation and induration last 48–72 h and ­nodulation occasionally may be prolonged for 4–5 days. Bruising and purpura may persist for a week or two. A prolonged

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inflammatory response has occurred in some patients lasting 4–6 weeks. Embolization with cutaneous necrosis has been described.

30.7 Hyaluronic Acid Achya Achyal Captique Fineline (Q-Med, Uppsala, Sweden) (Q-Med, Uppsala, Sweden) Fortélis and Fortélis Extra (Anteis Aesthetics, Geneva, Switzerland) Hyacell Hyaff Hyal-System Hyal 2000 Hylaform (Biomatrix Inc., Ridgefield, NJ; Inamed, Dusseldorf, Germany ) Hylaform Fineline Hylaform Plus Juvederm (Q-Med, Uppsala, Sweden; Corneal, Halber­ gmoos, Germany) Macdermal Matridex (BioPolymer, Siershahn, Germany) Perlane Prevelle (Mentor Corporation, Santa Barbara, CA) Prevelle Plus (Mentor Corporation, Santa Barbara, CA) Puragen (Mentor Corporation, Santa Barbara, CA) Puragen Plus (Mentor Corporation, Santa Barbara, CA) Restylane (Q-Med, Uppsala, Sweden) Reviderm (Rofil, Breda, The Netherlands) Rofilan Hylan Gel Teosyal (Teoxane Laboratories, Geneva, Switzerland) Touchline Hylaform is used for smoothing wrinkles, Hylaform Fineline for delicate lines in the skin including nasolabial folds, glabellar line, and pronounced lines around the mouth, and Hylaform Plus for deeper folds, lip augmentation, and facial contouring. Rzany and Zielke [11] concluded that skin testing is not generally recommended since hyaluronic acid is thought to be less allergenic than bovine collagen. Immunological reactions in the recipient can be caused by residual proteins from the donor (avian or bacterial antigens) or from the cross-linking process.

M.A. Shiffman

30.7.1 Complications Friedman et al. [32] reviewed the data from nonanimal hyaluronic acid from the Restylane family reported to the manufacturer for 1999 and found 0.15% of unwanted effects in 144,000 treatments and for 2000 found 0.06% unwanted effects in 22,000 treatments. Complications include allergic reaction, bleeding, tenderness, pain, and recurrent herpes [33]. Ashinoff [16] described adverse reactions such as erythema, ecchymoses, intermittent swelling, and acneiform dermatitis. Lowe et al. [34] noted an overall incidence of late inflammatory reactions consisting of induration, inflammation/erythema, and abscess formation an average of 8 weeks after injection in 0.42% of 709 patients. Saylan [35] stated that hylauronic acid complication of granulomas was found in 2% of patients. There was resolution after steroid injections. Wolfram et al. [36] reported granuloma with Restylane. Andre [37] evaluated the incidence of adverse reactions with nonanimal hyaluronic acid and noted that out of 12,344 syringes sold and 4,320 patients treated that there were 16 cases of immediate hypersensitivity and 18 cases of delayed reactions. Four cases of sterile abscesses were reported. Rzany and Zielke [11] noted that there are case reports of adverse reactions with the use of hyaluronic acid that consisted of erythema, pruritis, edema, urticaria, and papulocystic nodules. A bluish discoloration may occur that is attributed to injections that were too superficial. This response last in most patients only several weeks. Arterial embolization and exudative granulomatous reaction have been reported after treatment with hyaluronic acid [38–43].

30.8 H  yaluronic Acid and Ethylmethacrylate DermaLive (Dermatech, Paris, France) DermaDeep (Dermatech, Paris, France) Saylan [35] experienced hardening (11%) if injected into muscle, deep mucosa of the lips, or intradermally and granulomas (5.5% at 1  year, 25.5% at 2  years) with Dermalive and Dermadeep.

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Lombardi et al. [44] and Wolfram et al. [36] reported granulomas with Dermalive.

The literature does not have any reports of complications.

30.9 Hydroxyapatite

30.13 Patient Derived Plasma Emulsion

Radiesse (Radiance) Used to augment bone areas. The disadvantages are that they require familiarity with the nuances of the technique and, although amenable to revision, these granules are difficult to remove completely [45].

Plasmagel The literature does not have any reports of complications.

30.10 H  ydroxymethylmethacrylate and Ethylmethacrylate in Hyaluronic Acid Solution Dermadeep (Dermatech SARL, Paris, France) Dermalive (Dermatech SARL, Paris, France; Vivier Oharma, Montreal, Canada)

30.14 P  olioxyethylene Fatty Acid and Elastin Copolymer Gel Kolypolymer 4E (Dermabiol Institute of Kuhra Vital GmbH, Lucerne, Switzerland) The literature does not have any reports of complications.

30.10.1  Complications

30.15 P  olyacrilamide Hydrogel (Unpolymerized Acrilamide Monomer)

Anwar and Sharpe [46] described skin nodules with Dermalive in the nasolabial fold. Weyland and Menke [47] noted granuloma and superinfection with Dermalive. Sidwell et  al. [48] noted localized granulomatous reaction to hyaluronic acid and acrylic gel fillers [48]. There are multiple reports of granulomas with Dermalive [36, 49–54]. Bergeret-Galley [55] published data from the manufacturer of Dermalive and Dermadeep showing the incidence of nodules, swelling, and erythema on average 6 months after injected was 0.012%.

Aquamid (Contura International, Soeborg, Denmark) Amazingel (aka Amazing Gel) (Fuhua Medical Co., Ltd, Shenzhen, China; Aqua Mid, Bexbach, Germany) Argiform Argiriform (Argyriform) (Bioform Russia, Moscow, Russia) Bio-Formacryl (Bioform, Moscow, Russia) Formacryl Outline Polymekon (Brindis, Italy)

30.11 Methacrylate and Acrylate

30.15.1 Complications

Metrex The literature does not have any reports of complications.

Wang et al. [56] described 15 patients with adverse reactions assessed over 2 years and reported 80% nodules, 60% pain, 20% secondary deformity, 13% discomfort, and 6.6% long-lasting swelling. Pathologic examination showed 60% macrophage infiltration, 52.3% capsule formation, and 20% granulomatous reactions. Breiting et al. [57] reported on 104 patients, 49 of whom had undergone breast augmentation and noted palpable lymph nodes in ten patients. Migration of the

30.12 Methacrylate and Copolymer Rhegecoll (Swiss Kuhra Vital Division of the Der­ mabiol Institute)

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gel was demonstrated in three patients who had their nasolabial folds injected. Patrick [58] described infection, granuloma, and migration as complications of polyacrilamide gel injection. Amin et  al. [59] reported a case of inflammatory reaction 1 month after injection of polyacrilamide gel for zygomatic augmentation. Parada et  al. [60] studied granulomas caused by Aquamid, intense necrosis was noted in Aquamid cases. Cheng et al. [61] described 15 patients with migration following injectable polyacrilamide gel. They noted that the injected material had not formed capsules within the muscle and only had thin fibrous tissue capsule in the skin and mammary glands. The authors advised not to inject the gel into muscular or subcutaneous areas with active movement, such as joints and muscles involved in facial expression with thin skin. Kawamura et  al. [62] reported a case of intraoral foreign body reaction resulting from Aquamid application in the nasolabial fold. Parodi et al. [63] had a case of severe scarring from injection of polyacrilamide gel into the penis. Tsvetkov et al. [64] reported a case of necrotic cellulitis after the use of polyacrilamide gel for mammary augmentation. Kalantar-Hormozi et al. [65] reviewed 542 patients who had polyacrilamide gel as a facial soft tissue filler. There was a 7.7% incidence of swelling, abscess formation, lumpiness, change in facial appearance, change in gel location after injection, and sensitivity. El-Shafey el-SI [66] described acute inflammation occurring after repeated punctures of implant sites of polyacrilamide gel.

30.16 P  olyacrilamide Hydrogel with Polyvinyl Microspheres Evolution (PolyCytech, Bourdeaux, France) The literature does not have any reports of complications.

30.17 Polyalkylimide Bio-Alcamid (Bioalcamid)

M.A. Shiffman

Protopapa et al. [67] implanted Bio-Alcamid in 73 patients and described no migration, granuloma, allergic reaction, or intolerance.

30.17.1 Complications Chrastil-LaTowsky et al. [68] noted that Polymekon (Milan, Italy) presented with manifestations of inflammation.

30.18 Polydimethylsiloxane Oil (Silicone) Adatasil 5000 Bioplastique Biopolimero granulomas, migration, necrosis, silicone embolism Biopolymere (possibly polydimethylsiloxane) Bioplastique (suspended by a polyvinylpyrrolidone vector) (Uroplasty BV, The Netherlands) Dermagen (possibly polydimethylsiloxane) Silicex (Antifoam 140): Foam control agent not intended for injection into the human body Silikon 1000 (Alcon Laboratories Inc, Fort Worth, TX) Silskin

30.18.1 Complications Adverse reactions described by Orentreich [69] include pain with needle insertion, edema (usually resolves in several hours to days), ecchymosis, erythema, dyschromia (brownish yellow discoloration of the skin, blue tinge from injecting into thin translucent skin), peau d’orange when injected in excessive amounts or too superficially in the dermis, over­ correction, embolism, granulomatous reactions, and migration. de Maio and Rzany [70] have described local adverse reactions including chronic inflammation, migration, extrusion, ulceration, and granulomas from the literature. Inflammatory reaction surrounding injected silicone is self-limiting. Removal of the injected silicone is quite difficult. There are multiple reports of granulomas from injected silicone [52, 60, 71–75]. Recent reports describe granulomatous reactions, infection, ulceration, and migration [76–78].

30  Potential Risks and Complications of Injectable Alloplastic Facial Fillers

30.19 Polyethylene Microspheres Profill (Profil) The literature does not have any reports of complications.

30.20 Polylactic Acid Sculptra (Sanofi-Aventis, Paris, France) New Fill (European Aesthetics GmbH, Ismaning, Germany) Benthover [1] poly-L-lactic acid fillers have been shown to stimulate collagen neogenesis. Needs to be applied two or three times over a period of 6–8 weeks with touch-up treatment after 4–6 months and results last up to 2 years.

30.20.1 Complications Saylan [35] experienced polylactic acid granulomas (12%), allergic reactions, and infection (5%). Granulomas have been reported with the use of Newfill [36, 44, 60]. Treatment of lipoatrophy in HIV patients with polylactic acid injection have shown granulomatous reactions with palpable, but invisible, subcutaneous micronodules were observed in 44% of patients [79–81].

30.21 Polymethylmethacrylate (PMMA) Artecoll Metacril Benthoven [1] stated that polymethylmethacrylate fillers have been shown to stimulate collagen neogenesis.

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30.22 P  olymethylmethacrylate (PMMA) and Collagen Artecoll (Rifil Medical International B.V., Breda, The Netherlands) has polymethymethacrylate beads renamed ArteFill (Artes Medical, San Diego, CA) Polymethylmethacrylate suspended on bovine collagen (Rifil Medical International B.V., Breda, The Netherlands)

30.22.1 Complications Granulomatous reactions are well known with the combination of polymethylmethacrylate and collagen [44, 49, 84–90]. Lemperle et al. [85] reported swelling, redness, and itching immediately after implantation of PMMA and late reactions of erythema, transparency, unevenness, and dislocation.

30.23 Polyvinyl Alcohol 30.23.1 Complications According to de Maio and Rzany [69], the Berlin register has had acute inflammatory reactions from polyvinyl alcohol reported.

30.24 P  olyvinyl Microspheres Suspended in Polyacrilamide Gel Evolution (ProCytech Labs., Bordeaux, France) Lemperle et al. [88] reported that polyvinyl microspheres in polyacrilamide gel slowly diminishes over 9 months.

30.25 Discussion 30.21.1 Complications Granulomas have been reported with the use of polymethylmethacrylate [35, 36, 44, 52, 60, 82]. Bagal et  al. [83] noted complications including firmness of the lip, increased sensitivity of the lip for 6 months, and lumps in the lips.

Most temporary fillers do not last more than 12 months and, therefore, repeated injections are necessary to maintain volume. Christensen [91] evaluated different gel type fillers as to how they interact with the host tissue and what can go wrong. He concluded that complications

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following homogenous hydrogels are caused by infection with bacteria that have been inserted in the gel during injection. If not treated with relevant antibiotic (but instead steroids or large doses of nonsteroidal anti-inflammatory drugs [NSAIDs]), the bacteria form a biofilm that gives rise to a low-grade chronic infection that is resistant to antibiotics. Bentkover [1] stated that any facial filler can form a granuloma. Bacterial biofilms may play a role in the activation of quiescent granulomas. Sneistrup et al. [92] reported two cases with signs of infection and granulomas seen years after injection of permanent fillers to the lips. Steroid injections are indicated in case of granuloma and antibiotics should be given for infection. Treatment of granulomatous reactions is with injectable steroids. Triamcinolone, either 10  mg/mL or 40 mg/mL can be used. The 40 mg strength may induce severe fat atrophy. The inject should be injected into the granuloma. Using 0.05–0.1 mL performed initially weekly. If the granulomatous tissue reduces subsequent injections can be every 2 weeks. If no response after about eight injections over a 2  month period, 5-fluorouracil (50 mg/mL) can be added to the steroid (1 mg/mL). Steroid fat atrophy should be treated with injecting sterile normal saline to produce tumescence. This can be repeated every 4 weeks. Surgery for granulomas will cause scarring.

30.26 Conclusions The possible risks and complications of dermal fillers include allergic reactions, inflammation, bruising, erythema, pain, swelling, pruritis, unevenness, infection, recurrent herpes simplex, abscess, ulceration, scarring, migration, firmness or induration, lumps, granulomas, necrosis, embolism, overcorrection, and change in facial appearance, Bovine collagen products need skin testing before use but there still may be acute allergic reaction even with a negative skin test. Consider the possibility of blindness when injecting into the glabellar area. Most fillers should not be injected into the dermis. The physician who utilizes dermal fillers must be aware of the possible risks and complications and try to avoid them, recognize the problem in a timely fashion, and treat the problem appropriately.

M.A. Shiffman

References 1. Bentkover SH (2009) The biology of facial fillers. Facial Plast Surg 25(2):73–85 2. Ridenour B, Kontis TC (2009) Injectable calcium hydroxylapatite microspheres (Radiesse). Facial Plast Surg 25(2): 100–105 3. Sklar JA, White SM (2004) Radiance FN: a new soft tissue filler. Dermatol Surg 30(5):764–768 4. Tsikas TL (2004) Evaluation of Radiance FN soft tissue filler for facial soft tissue augmentation. Arch Facial Plast Surg 6(4):234–239 5. Georgescu D, Jones Y, McCann JD, Anderson RL (2009) Skin necrosis after calcium hydroxylapatite injection into the glabellar and nasolabial folds. Ophthal Plast Reconstr Surg 25(6):498–499 6. Russo M (2009) Calcium hydroxylapatite (Radiesse): safety, technique and pain reduction. J Drugs Dermatol 8(10 Suppl):s212–s223 7. Feeney JN, Fox JJ, Akhurst T (2009) Radiologic impact of the use of calcium hydroxylapatite dermal fillers. Clin Radiol 64(9):897–902 8. Grossman KL (2000) Facial scars. Clin Plast Surg 27(4):627–642 9. 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 10. Siegle RJ, McCoy JP, Schade W, Swanson NA (1984) Intradermal implantation of bovine collagen: humoral responses associated with clinical reaction. Arch Dermatol 120(2):183–187 11. Rzany R, Zielke H (2006) Complications. In: de Maio M, Rzany B (eds) Injectable fillers in aesthetic medicine. Springer, Berlin, pp 67–77 12. Cooperman LS, Mackinnon V, Bechler G, Pharrisse BB (1985) Injectable collagen: a six-year clinical investigation. Aesthetic Plast Surg 9(2):145–151 13. DeLustro F, Smith ST, Sundsmo J, Salem G, Kincaid S, Ellingsworth L (1987) Reaction to injectable collagen: results in animal models and clinical use. Plast Reconstr Surg 79(4):581–594 14. Hanke CW, Hingley HR, Jolivette DM, Swanson NA, Stegman SJ (1991) Abscess formation and local necrosis after treatment with Zyderm or Zyplast collagen implant. J Am Acad Dermatol 25(2 Pt 1):319–326 15. Hanke CW (1998) Adverse reactions to bovine collagen. In: Klein AW (ed) Tissue augmentation in clinical practice: procedures and techniques. Marcel Dekker, Inc., New York 16. Ashinoff R (2000) Overview: soft tissue augmentation. Clin Plast Surg 27(4):479–487 17. Homicz MR, Watson D (2004) Review of injectable materials for soft tissue augmentation. Facial Plast Surg 20(1): 21–29, 145–154 18. Boss WK Jr, Usal H, Chernoff G, Keller GS, Lask GP, Fodor PB (2000) Autologous cultured fibroblasts as cellular therapy in plastic surgery. Clin Plast Surg 27(4):613–626 19. Fagien S (1998) Facial soft tissue augmentation with autologous and homologous injectable collagen (Autologen and Dermologen). In: Klein AW (ed) Tissue augmentation in clinical practice: procedures and techniques. Marcel Dekker, Inc., New York, pp 97–124

30  Potential Risks and Complications of Injectable Alloplastic Facial Fillers 20. Apesos J, Muntzing MG II (2000) Autologen. Clin Plast Surg 27(4):507–513 21. Alster T, West T (1998) New options for soft tissue. Skin Aging 7:32 22. Austin H, Weston G (1992) Rejuvenation of the aging mouth. Clin Plast Surg 19(2):511–524 23. Devore D, Hughes E, Scott J (1994) Effectiveness of injectable filler materials for smoothing wrinkle lines and depressed scars. Med Prog Technol 20(3–4):243–250 24. Devore D, Kelman, Fagien S et al (1996) Autologen: autologous injectable dermal collagen. In: Bosniak S (ed) Ophthalmic, Plastic and Reconstructive Surgery. WB Saunders, Philadelphia, pp 671–675 25. Duranti F, Salti G, Bovani B, Calandra M, Rosati ML (2000) Injectable hyaluronic acid gel for soft tissue augmentation. A clinical and histological study. Dermatol Surg 24(12): 1317–1325 26. Elson ML (1999) Soft tissue augmentation techniques: update on available materials. Cosmetic Dermatol 12:13 27. Moody BR, Sengelmann RD (2000) Self-limited adverse reaction to human-derived collagen injectable product. Dermatol Surg 26(10):936–938 28. Apte RS, Solomon SD, Gehibach P (2003) Acute choroidal infarction following subcutaneous injection of micronized dermal matrix in the forehead region. Retina 23(4): 552–554 29. Nilsson IM, Sjoerdsma A, Waldenstron J (1960) Antifibrinolytic activity and metabolism of e-aminocaproic acid in man. Lancet 1(7138):1233–1236 30. Millican L, Rosen T, Monheit G (1987) Treatment of depressed cutaneous scars with gelatin matrix implant: a multicenter study. J Am Acad Dermatol 16(6): 1155–1162 31. Monheit GD (1998) Fibrel: soft tissue augmentation. In: Klein AW (ed) Tissue augmentation in clinical practice: procedures and techniques. Marcel Dekker, Inc., New York, pp 155–171 32. Friedman PM, Mafong EA, Kauver AN, Geronemus RG (2002) Safety data of injectable nonanimal stabilized hyaluronic acid gel for soft tissue augmentation. Dermatol Surg 28(6):491–494 33. http://www.ukcosmeticsurgery.info;hylaform. Accessed 23 Dec 2009 34. Lowe NJ, Maxwell CA, Lowe P, Duick MG, Shah K (2001) Hyaluronic acid skin fillers: adverse reactions and skin testing. J Am Acad Dermatol 45(6):930–933 35. Saylan Z (2003) Facial fillers and their complications. Aesthetic Surg J 23(3):221–224 36. Wolfram D, Tzankov A, Piza-Katzer H (2006) Surgery for foreign body reaction due to injectable fillers. Dermatology 213(4):300–304 37. Andre P (2004) Evaluation of the safety of a nonanimal stabilized hyaluronic acid (NASHA – Q-Medical, Sweden) in European countries: a retrospective study from 1997 to 2000. J Eur Acad Dermatol Venereol 18(4):422–425 38. Lupton JR, Alster TS (2000) Cutaneous hypersensitivity reaction to injectable hyaluronic acid gel. Dermatol Surg 26(2):135–1137 39. Raulin C, Greve B, Hartschuh W, Soegding K (2000) Exudative granulomatous reaction to hyaluronic acid (Hylaform). Contact Dermat 43(3):178–179

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40. Shafir R, Amir A, Gur E (2000) Long-term complications of facial injections with Restylane (injectable hyaluronic acid). Plast Reconstr Surg 106(5):1215–1216 41. Micheels P (2001) Human anti-hyaluronic acid antibodies: is it possible? Dermatol Surg 27(2):135–137 42. Lowe NJ (2003) Arterial embolization caused by injection of hyaluronic acid (Restylane). Br J Dermatol 148(2):379 43. Fernandez-Acenero MJ, Zamora E, Borbujo J (2003) Granulomatous foreign body reaction against hyaluronic acid: report of a case after lip augmentation. Dermatol Surg 29(12):1225–1226 44. Lombardi T, Samson J, Plantier F, Husson C, Küffer R (2004) Orofacial granulomas after injection of cosmetic fillers. Histopathologic and clinical study of 11 cases. J Oral Pathol Med 33(2):115–120 45. Hobat PC, Pantaloni M, Byrd HS (2000) Porous hydroxyapatite for alloplastic enhancement of the facial region. Clin Plast Surg 27(4):557–569 46. Anwar MU, Sharpe DT (2007) Skin nodules after semipermanent cosmetic dermal filler. Aesthetic Plast Surg 31(4):401–402 47. Weyland B, Menke H (2008) Case report: adverse granulomatous reaction (granuloma formation) and pseudomonas superinfection after lip augmentation by the new filler Dermalive®. Eur J Plast Surg 30(6):291–295 48. Sidwell RU, Dhillon AP, Butler PE, Rustin MH (2004) Localized granulomatous reaction to a semi- permanent hyaluronic acid and acrylic hydrogel cosmetic filler. Clin Exp Dermatol 29(6):630–632 49. Requena C, Izquierdo MJ, Navarro M, Martinez A, Vilata JJ, Bottela R et al (2001) Adverse reactions to injectable aesthetic microimplants. Am J Dermatopathol 23(3):197–202 50. Waris E (2003) Alloplastic injectable biomaterials for soft tissue augmentation: a report on two cases with complications associated with a new material (DermaLive) and a review of the literature. Eur J Plast Surg 26:350–355 51. Steenkiste E, Marlen K, van den Oord J (2005) Dermalive granuloma: a lesion with distinctive histologic features. Internet J Dermatol 3(1) http:/www/ispub.com/journal/the_ internet_journal_of_dermatology/volume_3_number_1. Accessed 24 Dec 2009 52. Vargas-Machuca I, González-Guerra E, Angulo J, del Carmen Fariña M, Martín L, Requena L (2006) Facial granulomas secondary to Dermalive microimplants: report of a case with histopathologic differential diagnosis among the granulomas secondary to different injectable permanent filler materials. Am J Dermatopathol 28(2):173–177 53. Angus JE, Affleck AG, Leach IH, Millard LG (2006) Two cases of delayed granulomatous reactions to the cosmetic filler Dermalive, a hyaluronic acid and acrylic hydrogel. Br J Dermatol 154(4):755–758 54. Furmanczyk PS, Wolgamot GM, Zsolte B, Argenyi C, Gilbert SC (2009) Extensive granulomatous reaction occurring 1.5 Years after DermaLive injection. Dermatol Surg 35(Suppl 1):385–388 55. Bergeret-Galley C, Latouche X, Illouz YG (2001) The value of a new filler material in corrective and cosmetic surgery: dermalive and dermadeep. Aesthetic Plast Surg 25(4):45–53 56. Wang YB, Huang JJ, Qiao Q, Zhuang Q, Liu FH (2003) Clinically analyzing the possible side-effects after injecting hydrophilic polyacrilamide gel as a soft-tissue filler. Zhonghua Zheng Xing Wai Za Zhi 19(5):328–330

346 57. Breiting V, Aasted A, Jorgensen A, Opitz P, Rosetzsky A (2004) A study on patients treated with polyacrilamide hydrogel injection for facial corrections. Aesthetic Plast Surg 28(1):45–53 58. Patrick T (2004) Polyacrilamide gel in cosmetic procedures: experience with Aquamid. Semin Cutan Med Surg 23(4): 233–235 59. Amin SP, Marmur ES, Goldberg DJ (2004) Complications from injectable polyacrilamide gel, a new nonbiodegradable soft tissue filler. Dermatol Surg 30(12 Pt 2):1507–1509 60. Parada MB, Michalany NS, Hassun KM, Bagatin E, Talarico S (2005) A histologic study of adverse effects of different cosmetic skin fillers. Skinmed 4(6):345–349 61. Cheng NX, Su SL, Deng H, Ding XB, Zhang XM, Wu DH, Zhong H, Sun ZH (2006) Migration of implants: a problem with injectable polyacrilamide gel in aesthetic plastic surgery. Aesthetic Plast Surg 30(2):215–225 62. Kawamura JY, Domaneschi C, Migliari DA, Sousa SO (2006) Foreign body reaction due to skin filler: a case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 101(4):469–471 63. Parodi PC, Dominici M, Moro U (2006) Penis invalidating cicatricial outcomes in an enlargement phalloplasty case with polyacrilamide gel (Formacryl). Int J Impot Res 18(3):318–321 64. Tsvetkov VO, Kulikova NV, Molchanov VV, Zhdanova AB (2007) Generalized necrotic cellulitis as the complication of mammoplasty with polyacrilamide gel. Khirurgiia (Mosk) 10:60–62 65. Kalantar-Hormozi A, Mozafari N, Rasti M (2008) Adverse effects after use of polyacrilamide gel as a facial soft tissue filler. Aesthetic Surg J 28(2):139–142 66. El-Shafey el-SI (2008) Complications from repeated injection or puncture of old polyacrylamide gel implant sites: case reports. Aesthetic Plast Surg 32(1):162–165 67. Protopapa C, Sito G, Caporale D, Cammarota M (2003) Bio-Alcamid in drug induced lipodystrophy. J Cosmet Laser Ther 5(3–4):226–230 68. Chrastil-LaTowsky B, Wesley NO, MacGregor JL, Kaminer MS, Arndt KA (2009) Delayed inflammatory reaction to bioalcamid polyacrilamide gel used for soft-tissue augmentation. Arch Dermatol 145(11):1309–1312 69. Orentreich DS (2000) Liquid injectable silicone: techniques for soft tissue augmentation. Clin Plast Surg 27(4):595–612 70. de Maio M (2006) Rzany B injectable fillers in aesthetic medicine. Springer, Berlin 71. Winer LH, Sternberg TH, Lehman R, Ashley FL (1964) Tissue reactions to injected silicone liquids: a report of three cases. Arch Dermatol 90:588–593 72. Wilkie TF (1977) Late development of granuloma after liquid silicone injections. Plast Reconstr Surg 60(2):179–188 73. Milojevic B (1982) Complications after silicone injection therapy in aesthetic plastic surgery. Aesthetic Plast Surg 6(4):203–206 74. Kozeny GA, Barbato AL, Bansal VK, Vertuno LL, Hano JE (1984) Hypercalcemia associated with silicone-induced granulomas. N Engl J Med 311(17):1103–1105 75. Duffy DM (1998) Injectable liquid silicone: new perspectives. In: Klein AW (ed) Tissue augmentation in clinical practice: procedures and techniques. Marcel Dekker, New York, pp 237–267

M.A. Shiffman 76. Ersek RA, Gregory SR, Salisbury AC (1997) Bioplastique at 6  years: clinical outcome studies. Plast Reconstr Surg 100(6):1570–1574 77. Ficarra G, Mosqueda-Taylor A, Carlos R (2002) Silicone granuloma of the facial tissues: a report of seven cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 94(1): 65–73 78. Rapaport MJ, Vinnick C, Zarem H (1996) Injectable silicone: cause of facial nodules, cellulitis, ulceration, and migration. Aesthetic Plast Surg 20(3):267–276 79. Cheonis N (2002) New-fill to treat facial wasting. BETA 15(2):10–15 80. Valantin MA, Aubron-Olivier C, Ghosn J, Laglenne E, Pauchard M, Schoen H et al (2003) Polylactic acid implants (New-Fill) to correct facial lipoatrophy in HIV-infected patients: results of the open-label study. AIDS 17(17): 2471–2477 81. Moyle G, Lysakova L, Brown S, Sibtain N, Healy J, Priest C, Mandalia S, Barton SE (2004) A randomized open-label study of immediate versus delayed polylactic acid injections for the cosmetic management of facial lipoatrophy in persons with HIV infections. HIV Med 5(2):82–87 82. Kim KJ, Lee HW, Lee MW, Choi JH, Moon KC, Koh JK (2004) Artecoll granuloma: a rare adverse reaction induced by microimplant in the treatment of neck wrinkles. Dermatol Surg 30(4):545–547 83. Bagal A, Dahiya R, Tsai V, Adamson PA (2007) Clinical experience with polymethylmethacrylate microspheres (Artecoll) for soft-tissue augmentation: a retrospective review. Arch Facial Plast Surg 9(4):275–280 84. Travis WD, Balogh K, Abraham JL (1985) Silicone granulomas: report of three cases and review of the literature. Hum Pathol 16:19–27 85. Lemperle G, Gauthier-Hazan N, Lemperle M (1998) PMMA-Microspheres (Artecoll) for long-lasting correction of wrinkles: refinements and statistical results. Aesthetic Plast Surg 22(5):356–365 86. Hoffman C, Schuller-Petrovic S, Soyer HP, Kedrl H (1999) Adverse reactions after cosmetic lip augmentation with permanent biologically inert implant materials. J Am Acad Dermatol 40(1):100–102 87. Rudolph CM, Soyer HP, Schuller-Petrovic S, Kerl H (1999) Foreign body granulomas due to injectable aesthetic microimplants. Am J Surg Pathol 23(1):113–117 88. Lemperle G, Romano JJ, Busso M (2003) Soft tissue augmentation with artecoll: 10-year history, indications, techniques, and complications. Dermatol Surg 29(6): 573–587 89. Alcalay J, Alkalay R, Gat A, Yorav S (2003) Late-onset granulomatous reaction to Artecoll. Dermatol Surg 29(8):859–862 90. Reisberger EM, Landhaler M, Wiest L, Schröder J, Stolz W (2003) Foreign body granulomas caused by polymethylmethacrylate microspheres: successful treatment with allopurinol. Arch Dermatol 139(1):17–20 91. Christensen LH (2009) Host tissue interaction, fate, and risks of degradable and nondegradable gel fillers. Dermatol Surg 35(Suppl 2):1612–1619 92. Sneistrup C, Hölmich LR, Dahlstrom K (2009) Long-term complications after injection of permanent fillers to the lips. Ugeskr Laeger 171(17):1414

Facial Augmentation with Autologous Fat

31

Melvin A. Shiffman

31.1 Introduction The minimally invasive technique using autologous fat transplantation has become a standard procedure in facial rejuvenation. It is simple, inexpensive, permanent, and effective. Injectable fillers, such as collagen and hyaluronic acid, are only temporary and, therefore, have minimal indication. Gore-Tex, which is a permanent material, may extrude or be palpable. Since 1994, when Adatasil (silicone) was approved by the Federal Drug Administration (FDA) for use in ophthalmic problems, the use of silicone injected into other areas of the body is called an “off-label use” and is considered legal if it is used for a specific patient with a specific product and there is no advertising. Autologous fat can be used to augment facial structures, rejuvenate rhytids, or fill depressed scars or defects of the face. Since the introduction of liposuction in 1975 [1] for body contouring, there has been an easy way to obtain fat for transplantation through very small incisions. The use of the tumescent technique for retrieving large amounts of fat for transfer has reduced the amount of blood loss and made the technique safer [2]. Although some reports have shown that fat transfer had disappointing results in some cases, the success of fat transfer is operator dependent and can be quite successful if attention is paid to the details of the techniques of the procedure. The transfer

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

of fat to the face, where vascularity is excellent, has an excellent chance for fat survival. The only relative drawback has been the resorption of some of the fat graft. With proper technique, approximately 30–70% of the fat is retained. Low speed, short time centrifugation of the fat decreases the fluid in the transplant and reduces the apparent loss of graft by compacting the fat and separating out the excess liquid. Since some of the apparent graft loss is the resorption of fluid from the transplanted fat, there is less fluid in centrifuged fat and, therefore, more mass remains. A newer concept to facilitate graft retention is the use of albumin during the harvesting and transfer phases. Albumin reduces the colloid osmotic pressure (COP) disparity between the low COP of the fat graft with saline, epinephrine, lidocaine, sodium bicarbonate and the interior of the fat cells. The higher difference in COP between the cells and their surrounding fluids, the more fluids that will enter the cells and the more the likelihood of cell destruction. If the COP between the fat cells and the surrounding fluid with albumin are almost equal, the more likely there will be improved fat survival and retention.

31.2 History of Fat Transfer Since Neuber [3], in 1893, reported that transplanted fat can be used to fill in a depressed area of the face, there have been many reports [4–14] that have shown fat, in pieces, can be transplanted and survive in various areas of the body. Since liposuction was conceived by Fischer in 1974 [15] and put into practice in 1975 [1], the aspirate has been used to fill defects and for

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_31, © Springer-Verlag Berlin Heidelberg 2011

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vascularity. There is evidence that fat cells will survive and that filling of defects is not from the residual collagen following cell destruction. There is some loss of fat after transplant and most surgeons will overfill the recipient site.

31.2.1 Insulin

b

Some physicians have added insulin to the fat in preparation for transplantation [19, 69, 70]. The theory is that insulin inhibits lipolysis. Sidman [71] found that insulin decreases lipolysis. Hiragun et  al. [72] stated that theoretically insulin may induce fibroblasts to pick up the lipid lost and become adipocytes. Chajchir et al. [73] found that the use of insulin did not show any positive effect on adipocyte survival during transplantation compared to fat not prepared with insulin.

31.2.2 Centrifugation

Fig. 31.1  Hematoxylin eosin stain 200×. (a) Central core of fat with 95–100% intact fat cells that was harvested with a 3 mm cannula at –500  mm mercury vacuum. (b) Periphery of core with > 10% fat cell disruption (arrow) when harvested with a 3 mm cannula at –700 mm mercury vacuum

contouring [16–22]. Aspirated fat should be atraumatically washed in physiologic solution to remove the blood, which would allow better fat survival [23]. Certain principles of fat transfer have evolved [20, 24–68] over the years, which include aspiration at lower vacuum rather than at atmospheric pressure (Fig. 31.1). It is essential to avoid desiccation of the fat during transfer. Fat that is present for over 120 days after transfer will survive and grow, and fat grafts survive when there is vascular ingrowth. The survival of free fat used as an autograft is operator-dependent and requires delicate handling of the graft tissue, careful washing of the fat to minimize extraneous blood cells, and installation into a site with adequate

Some physicians centrifuge the adipose tissue to remove blood products and free lipids to improve the quality of the fat to be injected [69–71]. Asken [42] stated that his “method of reducing the material to be injected to practically pure fat is to place the fat-filled syringe with a rubber cap (the plunger having been previously removed and kept in a sterile environment) into a centrifuge. The syringe is then spun for a few seconds at the desired rpm and the serum, blood, and liquefied fat collects in the dependent part of the syringe…” Toledo [74] reported that “for facial injection we spin the full syringes for 1 minute..... in a manual centrifuge (about 2,000 rpm), eject the unwanted solution, and transfer the fat…” Chajchir et al. [73] centrifuged 1 mL of bladder fat pad from mice (both at 1,000  rpm for 5  min and 5,000 rpm for 5 min) and injected this into the subdermis of the malar area. Microscopically, after 1–2 months there were macrophages filled with lipid droplets, giant cells, focal necrosis of adipocytes, and cyst like cavities of irregular size and shapes. After 12 months following injection no recognized adipocytes could be found. Total cellular damage was present in both groups. Brandow and Newman [75] found that centrifugation of harvested fat did not alter the microscopic structured integrity of cells. Spun and unspun samples

31  Facial Augmentation with Autologous Fat

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a blunt typed cannula, with 2.3 mm internal diameter, to inject the fat. Berdeguer [76] used a lipo transplant gun to inject fat into areas to be enhanced. Fulton et al. [68] stated that it is beneficial for a beginning surgeon to use a ratcheted pistol for injection as this gives a more uniform injection volume.

31.3 Albumin in Improving Fat Cell Survival 31.3.1 Oncotic Pressure

Fig.  31.2  Hematoxylin eosin stain 200×. Centrifugation at 3,600 rpm for 1 min showing cell compaction

were examined and were similar. Fulton et  al. [68] noted that centrifuged fat, at 3,400  rpm for 3 min, works well for small volume transfers, but not for large volume transfers into breasts, biceps, or buttocks. Low rpm centrifugation for a short time will compact the fat cells and not destroy them (Fig. 31.2).

31.2.3 Ratchet Gun for Injection Newman and Levin [23] designed a lipo-injector with gear-driven plunger to inject fat tissue evenly into desired sites. Fat injected with excessive pressure in the barrel of a syringe can cause sudden injections of undesired quantities of fat, which will pour into recipient sites. Agris [44] stated that a ratchet-type gun allows controlled accurate deposition of autologous fat. Each time the trigger is pulled, 0.1 mL is deposited. Asaadi and Haramis [55] described the use of a gun with a disposable 10 mL syringe for fat injection. Niechajev and Sevcuk [60] utilized a special pistol and

When a molecule is greater than 10,000 D (Dalton – arbitrary unit of mass equal to the mass of the nuclide of carbon-12 or 1.657 × 10−24 g), it is called a colloid and is capable of generating an oncotic pressure if it is restricted to one side of a semipermeable membrane. Colloid restricted to one side of a semipermeable membrane creates an osmotic gradient measured in millimeters of mercury. Very small molecules and ions such as sodium, potassium, glucose, and urea easily cross a capillary membrane and can increase osmolarity toward isotonicity to prevent red blood cells from taking up water and bursting. Osmolarity is measured by freezing point depression and the greater the number of particles in solution the colder the solution must be before it will freeze.

31.3.2 Colloid Osmotic Pressure In determining the colloid osmotic pressure (COP), the Landis-Pappenheimer equation [77] takes into account that soluble proteins, whether albumin, globulin, or fibrinogen, are highly negatively charged: COP = 2.1(TP) + (0.16 TP2) + 0.009 TP3 COP = Colloid Osmotic Pressure TP = Total Protein Positively charged sodium ions surrounding the core protein attracts and holds water thus accumulating more fluid on one side of the semipermeable membrane. The combination of the oncotic pressure of the protein and the osmotic pressure of the sodium ions

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resulting in an increased pressure gradient is called the colloid osmotic pressure. Albumin is 69,000 D, whereas, globulin is 150,000 D and fibrinogen 400,000 D. Since it is the number of molecules that are held on one side of the semipermeable membrane that creates COP, albumin will create the most pressure because 1 g of albumin has twice as many molecules as globulin and five times the number of molecules as fibrinogen. Starch molecules, found in hetastarch and dextran, should not be used for fat transfer since such molecules are too large to be evacuated through the lymphatics and will cause localized edema in the interstitial space.

31.3.3 Avoiding Hypo-Oncotic Trauma in Fat Transfer When Klein’s solution or any modification is used in harvesting fat, the infranatant of the harvested fat contains 1.1–1.2 g% protein. The normal level is 2.0– 4.0  g%. When one ampule of concentrated human albumin (12.5  g in 50  mL) is added to one liter of tumescent solution or 8.3 mL added to a 60 mL harvesting syringe, the harvested fat contains 2.6  g% protein. Three washes of harvested fat also increase the difference in colloid osmotic pressure and, therefore, it is necessary to add 18.75 g of albumin to each liter of washing solution. Adequate time must be allowed between each wash to allow the fat cells to pack above the infranatant layer. The process can be accelerated by centrifugation. The supranatant oil must be removed before insertion of the fat into the recipient site.

M.A. Shiffman

31.5 Preoperative Consultation The patient is carefully examined in relation to the specific complaint for which the patient has come in for consultation. A description of the physical problem needs to be recorded with appropriate measurements. Pictures should be taken before any procedure is undertaken and postoperative photos taken at an appropriate interval of time when healing is completed. If there are other problems detected by the physician, other than that of which the patient complains of, this must be recorded and possible treatment explained to the patient so that steps may be taken to correct other deficits not previously identified by the patient or so that the patient understands that adequate correction may require other procedures. At the same time the patient must not be talked into procedures that are not really wanted by the patient. An interval of time may be needed for the patient to think about what surgery may be necessary and to seek other consultations. The patient must understand the need for using autologous fat as a filler substance in comparison to other fillers presently available. To conform to the standard of care for informed consent, the patient must have sufficient information to be knowledgeable about the procedure, the possible material risks and complications, and the alternatives and their possible material risks. Someone in the office must take time to explain this information and the physician must at least make sure the patient understands the procedure, risks, and alternatives and answer any questions about the procedure. It is suggested that the physician include in the record the statement that “the surgical procedure was discussed as well as viable alternatives and all material risks and complications.”

31.4 Indications for Fat Transfer There are a variety of indications for fat transfer, which can be distilled down to the following: 1. Fill defects (a) Congenital (b) Traumatic (c) Disease (acne) (d) Iatrogenic 2. Cosmetic (a) Furrows (rhytids, wrinkles) (b) Refill of lost supportive tissue (aging) (c) Enhancement

31.6 Technique Fat survival depends upon the careful handling of fat during harvesting, cleansing, and injecting. Harvesting is performed by liposuction in areas of fat with alpha 2 receptors where the fat responds poorly to diet such as the abdominal or lateral thigh areas (genetic fat) [42]. The fat can be retrieved with liposuction using a 2.0–3.0  mm cannula or blunt needle (14–16 gauge) with syringe (10–60 mL) 10% prefilled with saline and albumin in equal amounts.

31  Facial Augmentation with Autologous Fat Fig. 31.3  (a) Fat retrieval with supranatant fat and infranatant fluid of blood and local tumescent fluid. (b) Fat following washing with sterile saline

a

The fat should be cleansed with a physiologic solution of normal saline or lactated Ringers by gently mixing and decanting the infranatant liquid consisting of tumescent fluid, serum, and blood (Fig. 31.3). Fat can be concentrated with the use of centrifugation at 3,600 rpm for 2 min. This allows less need for as much overfilling (30–50%) as is usually used. Kaminski et al. [78] has proposed the addition of 12.5 g of concentrated human albumin for each 1,000 mL of Klein’s solution used for harvesting and 18.5  g for each 1,000 mL washing fluid in order to maintain the normal extracellular oncotic pressure necessary to prevent the influx of solution into the cells with possible rupture. Alternatively, 8.3  mL of human serum albumin can be added to a 60 mL harvesting syringe.

351

b

Injection of the fat is with a blunt needle (18 gauge) or cannula (1.5–2.0  mm) uniformly distributed into tunnels in multiple layers to fill the defect (Figs. 31.4 and 31.5). With depressed scars, the attachments to the skin should be subcised before fat injection. The use of the ratchet gun for injection does not damage fat cells [79]. The areas of the face that can be enhanced include the cheeks (malar, submalar), lips, and chin (mentum) (Fig. 31.6). The brows may be lifted with fat transfer to the forehead and indentations can be improved in almost any area of the face. Rhytids in the glabella, nasolabial fold, and marionette lines can be improved. If the glabella is to be injected, the patient should be informed of the rare possibility of blindness. Any area

352

a

M.A. Shiffman

b

Fig. 31.4  (a) Fat transferred to 1 mL syringe with small cannula attached. (b) Injecting fat into face with palm of hand pressing on the plunger

a

b

Fig. 31.5  (a) Ratchet gun with 1 mL syringe and cannula. (b) Fat being injected with ratchet gun

of the face can have a depressed scar elevated by subcision and fat transfer.

31.7 Complications There are very few serious complications of autologous fat transfer. Since it is the patient’s own tissue, there is no rejection phenomenon or allergic reaction. The harvesting of large amounts of fat using liposuction is prone to the complications of liposuction in the donor area but facial fat transfer is usually with small

amounts of fat. If small amounts of fat (under 50 mL) are retrieved, then one may expect the possibility of bruising or infection in the donor site. The injection of autologous fat may be associated with the following risks: 1. Loss of fat volume (the most frequent problem) 2. Possible need for repeat injection(s) of fat 3. Bruising, hematoma 4. Swelling (especially with over injection) 5. Asymmetry 6. Prolonged erythema (usually temporary over a short period of time)

31  Facial Augmentation with Autologous Fat

a1

a2

b1

b2

c1

c2

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a3

c3

Fig. 31.6  A 60-year-old female with atrophy of facial fat. (a) Preoperative. (b) Fat transfer markings in submalar area. (c) Four years postoperatively

354

7. Scar that is depressed or thickened (rare except in the area of liposuction) 8. Tenderness, pain 9. Fibrous capsule around fat accumulation (from too much fat injected into one area) 10. Fat cyst (mass) 11. Infection (rare) 12. Microcalcifications (has not been reported in the face) 13. Central nervous system damage and/or loss of sight from retinal artery occlusion (can occur with injection in the glabellar or nasal areas) 14. Plus all of the problems following liposuction if a large amount of fat is removed

31.8 Conclusions Autologous fat transfer has been a very successful filler in the facial area. If care is taken in the transfer process and postoperatively, there will be 40–60% fat survival on the first transfer. At times a second or even third fat transfer (using the patient’s frozen fat) may be necessary to reach the volume best for the patient.

References 1. Fischer G (1975): Surgical treatment of cellulitis. IIIrd Congress International Acad Cosm Surg, Rome, Italy, 31 May 1975 2. Klein JA (1987) The tumescent technique for liposuction surgery. Am J Cosmet Surg 4:263–267 3. Neuber F (1893) Fettransplantation. Chir Kongr Verhandl Dtsch Gesellsch Chir 22:66 4. Czerny M (1895) Plastischer Ersatz der brusterlruse durch ein lipom. Verhandl d Deutscher Ges f Chirurg 2:126 5. Verderame P (1909) Ueber fettransplantation bei adharenten knochennarben am orbitalrand. Klin Monatsbl f Augenh 47:433–442 6. Lexer E (1910) Freie Fettransplantation. Deutsch Med Wochenschr 36:640 7. Bruning P (1914) Cited by Broeckaert T.J., Steinhaus J.: Contribution e l’etude des greffes adipueses. Bull Acad Roy Med Belgique 28:440 8. Tuffier T (1911) Abces gangreneux du pouman ouvert dans les bronches: hemoptysies repetee operation par decollement pleuro-parietal; guerison. Bull et Mem Soc de Chir de Paris 37:134 9. Willi CH (1926) The face and its improvement by aesthetic plastic surgery. MacDonald & Evans Ltd, London, pp 15–41 10. Straatsma CR, Peer LA (1932) Repair of postauricular fistula by means of a free fat graft. Arch Otolaryngol 15:620–621 11. Cotton FJ (1934) Contribution to technique of fat grafts. N Engl J Med 211:1051–1053

M.A. Shiffman 12. Peer LA (1956) The neglected free fat graft. Plast Reconstr Surg 18(4):233–250 13. Peer LA (1950) Loss of weight and volume in human fat grafts. Plast Reconstr Surg 5:217 14. Peer LA (1959) Transplantation of tissues, Transplantation of fat. Williams and Wilkins, Baltimore 15. Fischer G (1997) The evolution of liposculpture. Am J Cosmet Surg 14(3):231–239 16. Fischer G (1976) First surgical treatment for modeling body’s cellulite with three 5  mm incisions. Bull Int Acad Cosm Surg 2:35–37 17. Fischer A, Fischer G (1977) Revised technique for cellulitis fat reduction in riding breeches deformity. Bull Int Acad Cosm Surg 2(4):40–43 18. Bircoll M (1982) Autologous fat transplantation. The Asian Congress of Plastic Surgery, Tokyo, Feb 1982 19. Illouz YG (1986) The fat cell “graft”: a new technique to fill depressions. Plast Reconstr Surg 78(1):122–123 20. Johnson GW (1987) Body contouring by macroinjection of autologous fat. Am J Cosmet Surg 4(2):103–109 21. Bircoll MJ (1984) New frontiers in suction lipectomy. Second Asian Congress of Plastic Surgery, Pattiyua, Thailand, Feb 1984 22. Krulig E (1987) Lipo-injection. Am J Cosmet Surg 4(2):123–129 23. Newman J, Levin J (1987) Facial lipo-transplant surgery. Am J Cosmet Surg 4(2):131–140 24. Verderame P (1909) Ueber fettransplantation bei adharenten knochennarben am orbitalran. Klin Montsbl f Augenh 7:433 25. Lexer E (1911) Ueber freie fettransplantation. Klin Therap Wehnschr 18:53 26. Kanavel AR (1916) The transplantation of free flaps of fat. Surg Gynecol Obstet 23:163–176 27. Davis CB (1917) Free transplantation of the omentum, subcutaneously and within the abdomen. J Am Med Assoc 68:705–706 28. Lexer E (1919) Fatty tissue transplantation. In: Die transplantation, part I. Ferdinand Enke, Stuttgart, pp 265–302 29. Mann FC (1921) The transplantation of fat in the peritoneal cavity. Surg Clin N Am 1:1465–1471 30. Neuhof H (1923) The transplantation of tissues. D. Appleton & Co, New York, p 74 31. Guerney CE (1938) Experimental study of the behavior of free fat transplants. Surgery 3:679–692 32. Hilse A (1928) Histologische ergebuisse der experimentellen freien fettgewebstronsplantation. Beitr 2 Path Anal UZ Allg Path 79:592–624 33. Green JR (1947) Repairing bone defects in cranium and tibia. South Med J 40:289 34. Wertheimer E, Shapiro B (1948) The physiology of adipose tissue. Physiol Rev 28(4):451–464 35. Bames HO (1953) Augmentation mammoplasty by lipotransplant. Plast Reconstr Surg 11(5):404–412 36. Hansberger FX (1995) Quantitative studies on the development of autotransplants of immature adipose tissue of rats. Anat Rec 122:507 37. Schorcher F (1957) Fettgewebsver pflanzung bei zu kneiner. Brust Munchen Med Wochenschr 99(14):489 38. Van RL, Roncari DA (1978) Complete differentiation of adipocyte precursors: a culture system for studying the cellular nature of adipose tissue. Cell Tissue Res 195(2):317–329

31  Facial Augmentation with Autologous Fat 39. Van RL, Roncari DA (1982) Complete differentiation in vivo of implanted cultured adipocyte precursors from adult rats. Cell Tissue Res 225(3):557–566 40. Saunders MC, Keller JT, Dunsker SB, Mayfield FH (1981) Survival of autologous fat grafts in humans and mice. Connect Tissue Res 8(2):85–91 41. Illouz YG (1985) New applications of liposuction. In: Illouz YG (ed) Liposuction: the Franco-American experience. California, Medical Aesthetics, Inc., Beverly Hills, pp 365–414 42. Asken S (1987) Autologous fat transplantation: micro and macro techniques. Am J Cosmet Surg 4:111–121 43. Campbell GL, Laudenslager N, Newman J (1987) The effect of mechanical stress on adipocyte morphology and metabolism. Am J Cosmet Surg 4:89–94 44. Agris J (1987) Autologous fat transplantation: a 3-year study. Am J Cosmet Surg 4(2):95–102 45. Bircoll M (1988) Autologous fat transplantation: an evaluation of microcalcification and fat cell survivability following (AFT) cosmetic breast augmentation. Am J Cosmet Surg 5(4):283–288 46. ASPRS Ad-Hoc Committee on new Procedures: Report on Autologous fat transplantation. September 30, 1987 47. Billings E Jr, May JW (1989) Historical review and present status of free fat graft autotransplantation in plastic and reconstructive surgery. Plast Reconstr Surg 83(2):368–381 48. Markman B (1989) Anatomy and physiology of adipose tissue. Clin Plast Surg 16(2):235–244 49. Illouz YG (1990) Fat injection: a four year clinical trial. In: Hetter GP (ed) Lipoplasty: the theory and practice of blunt suction lipectomy, 2nd edn. Little, Brown and Company, Boston, pp 239–246 50. Hudson DA, Lambert EV, Block CE (1990) Site selection for fat autotransplantation: some observations. Aesthetic Plast Surg 14(3):195–197 51. Nguyen A, Pasyk KA, Bouvier TN, Hassett CA, Argenta LC (1990) Comparative study of survival of autologous adipose tissue taken and transplanted by different techniques. Plast Reconstr Surg 85(3):378–386 52. Kononas TC, Bucky LP, Hurley C, May JW Jr (1993) The fate of suctioned and surgically removed fat after reimplantation for soft-tissue augmentation. A volume and histologic study in the rabbit. Plast Reconstr Surg 91(5):763–768 53. Ersek RA (1991) Transplantation of purified autologous fat: a 3-year follow-up is disappointing. Plast Reconstr Surg 87(2):219–227 54. Courtiss EH, Choucair RJ, Donelan MB (1992) Largevolume suction lipectomy: an analysis of 108 patients. Plast Reconstr Surg 89(6):1068–1079 55. Asaadi M, Haramis HT (1993) Successful autologous fat injection at 5-year follow-up. Plast Reconstr Surg 91(4):755–756 56. Samdal F, Skolleborg KC, Berthelsen N (1992) The effect of preoperative needle abrasion of the recipient on survival of autologous free fat grafts in rats. Scand J Plast Reconstr surg Hand Surg 26(1):33–36 57. Eppley BL, Sidner RA, Plastis JM, Sadove AM (1992) Bioactivation of free-fat transfers: a potential new approach to improving graft survival. Plast Reconstr Surg 90(6): 1022–1030 58. Carpaneda CA, Ribeiro MT (1993) Study of the histologic alterations and viability of the adipose graft in humans. Aesthetic Plast Surg 17(1):43–47

355 59. Carpaneda CA, Ribeiro MT (1994) Percentage of graft viability versus injected volume in adipose autotransplants. Aesthetic Plast Surg 18(1):17–19 60. Niechajev I, Sevchuk O (1994) Long-term results of fat transplantation: clinical and histologic studies. Plast Reconstr Surg 94(3):496–506 61. Chang KN (1994) Surgical correction of postliposuction contour irregularities. Plast Reconstr Surg 94(1):137–138 62. Fagrell D, Enerstrom S, Berggren A, Kniola B (1996) Fat cylinder transplantation: an experimental comparative study of three different kinds of fat transplants. Plast Reconstr Surg 98(1):90–96 63. Jones JK, Lyles ME (1997) The viability of human adipocytes after closed-syringe liposuction harvest. Am J Cosmet Surg 14:275–279 64. Coleman S (1995) Long-term survival of fat transplants: con­­trolled demonstrations. Aesthetic Plast Surg 19(5): 421–425 65. Sattler G, Sommer B (1997) Liporecycling: immediate and delayed. Am J Cosmet Surg 14:311–316 66. Ullmann Y, Hyams M, Ramon Y, Peled IJ, Linderbaum ES (1998) Enhancing the survival of aspirated human fat injected into mice. Plast Reconstr Surg 101(7):1940–1944 67. Fulton JE Jr (1992) Breast contouring by autologous fat transfer. Am J Cosmet Surg 9(3):273–279 68. Fulton JE, Suarez M, Silverton K, Barnes T (1998) Small volume fat transfer. Dermatol Surg 24(8):857–865 69. Ellenbogen R (1986) Free autogenous pearl fat grafts in the face – a preliminary report of a rediscovered technique. Ann Plast Surg 16(3):179–194 70. Newman J (1986) Preliminary report on “fat recycling” – liposuction fat transfer for facial defects. Am J Cosmet Surg 3:67–69 71. Sidman RL (1956) The direct effect of insulin on organ cultures of brown fat. Anat Rec 124(4):723–739 72. Hiragun A, Sato M, Mitsui H (1980) Establishment of a clonal line that differentiated into adipose cells in  vitro. In Vitro 16(8):685–693 73. Chajchir A, Benzaquen I, Moretti E (1993) Comparative experimental study of autologous adipose tissue processed by different techniques. Aesthetic Plast Surg 17(2):113–115 74. Toledo L (1991) Syringe liposculpture: a two-year experience. Aesthetic Plast Surg 15(4):321–326 75. Brandow K, Newman J (1996) Facial multilayered micro lipo-augmentation. Int J Aesthetic Restor Surg 4(2):95–110 76. Berdeguer P (1995) Five years of experience using fat for leg contouring. Am J Cosmet Surg 12(3):221–229 77. Guyton AC (1986) Capillary dynamics and exchange of fluid between the blood and interstitial fluid. In: Guyton AC (ed) Textbook of medical physiology, 7th edn. Philadelphia, Saunders, p 348 78. Kaminski MV Jr, Fulton JE, Wolosewick JJ (2001) New consideration in fat transfer: a possible role for maintaining interstitial protein to reduce shrinkage of transferred volume. In: Shiffman MA (ed) Autologous fat transplantation. Marcel Dekker, Inc., New York, pp 299–309 79. Shiffman MA (2000) Effect of various methods of fat harvesting and reinjection. J Aesthetic Dermatol Cosmet Surg 1(4):231–235

 

Face and Neck Remodeling with Ultrasound-Assisted Lipoplasty (Vaser)

32

Alberto Di Giuseppe and George Commons

32.1 Introduction The author has utilized internal ultrasound solid probe to face and neck since 1996 in order to defat heavy faces or to undermine neck lax skin and possibly achieving skin retraction. At that time sculpture ultrasound device (by SMEI, Italy), with a solid probe of 2.5 mm of diameter and 17 cm long was used [1]. When utilizing the solid probe in the face, the power administrated was 30% of the total potential of the ultrasound tool in order to reduce undesired side effects of ultrasound energy (heat, essentially). The aim of the technique was: 1. To reduce numbers and extension of scars of the face for remodeling procedures of face and neck. 2. To perform under local tumescent anesthesia essentially the majority of facial contouring surgery. 3. To induce skin retraction, in face and neck, even in lax skin, avoiding major open surgery operation, as standard facelift. 4. To undermine and induce skin retraction with a minimal trauma by utilizing a solid probe and the ultrasound energy instead of an open approach and a scalpel. 5. To debulk heavy faces, neck, jowls, with a smooth device, able to emulsify fat in specific target, with a minimal trauma, low energy, and safe surgical planes. A. Di Giuseppe (*) Institute of Plastic and Reconstructive Surgery, School of Medicine, University of Ancona, Via Simeoni 6, 60122, Ancona, Italy e-mail: [email protected] G. Commons 1515 El Camino Real, Suite C, Palo Alto, CA 94306, USA e-mail: [email protected]

6. To contour difficult areas such as the mandible border, the neck line, and the chin. 7. To access to facial surgery even patients who refused major open surgery operations, which normally leads to a longer recovery time. Under those circumstances, what was called the “harmonic lift” was offered as an alternative technique in facial contouring surgery.

32.2 Patient Selection The harmonic lift can be used in young patients with fatty necks and cheeks as well as in older patients with loose skin and wrinkles. Each patient is evaluated as to the aims of surgery such as treatment of crow’s feet, nasolabial and commissural folds, jowls, and waddle neck. The procedure is appropriate in the following type of patients: 1. Face and neck lift in Fitzpatrick type 4–6, thus avoiding keloid formation and postinflammatory hyper pigmentation that may occur with skin rejuvenation with laser or peel. 2. Young patients who require only treatment of chubby cheeks and double chin. 3. To enhance neck definition with chin augmentation. 4. To substitute for endoscopic forehead lift in balding scalps. 5. To achieve dermal stimulation and retraction in the neck beyond areas amenable to laser resurfacing. 6. To release acne scarring of the cheeks. 7. In secondary and tertiary facelifts when partial removal of the skin is a questionable procedure but the central face needs further tightening.

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_32, © Springer-Verlag Berlin Heidelberg 2011

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Fig. 32.1  Incision lines

Other indications include rhytids in the malar area, crow’s feet, frontal, nasolabial, glabella (horizontal and vertical), and neck as well as descent of the cheek fat, ptosis of the lateral eye-brows, laxity of the upper lids, jowls, and diffuse acne scarring of the cheeks and neck.

A. Di Giuseppe and G. Commons

Fig. 32.2  Tension lines of action

each side. A blunt-tipped, 14-gauge cannula is used to infiltrate the subcutaneous tissues of the neck, jowls, cheeks, temple, and brow. Digital pressure aids in directing and expanding the fluid evenly.

32.3.1 Ultrasonic-Assisted Dissection

32.3 Technique of Facial Liposculpture Lines are drawn on the face to show the full area of undermining, the vectors of muscle tension, relaxation creases and folds, and crisscrossing lines of tunneling and dermal stimulation. Incisions are placed at different sites to allow ease of access depending on the target areas (Fig. 32.1). In the forehead incisions are vertical to avoid nerve damage and are at the hairline, midline, or frontal recess. Temporal incisions are parallel to the hairline while submental incisions are at the submental crease. Preauricular incisions are made at the earlobe and upper and lower eyelid incisions are at blepharoplasty sites. The use of the tumescent technique reduces bleeding and bruising and decreases ­surgical time. Modified Klein’s solution [2] used ­contains 1,000  mL of normal saline with 1  mL ­epinephrine (15 mg), and 500 mg lidocaine. Intravenous sedation is generally utilized but when general ­anesthesia is used with lidocaine it is reduced to 200  mg and sodium bicarbonate is eliminated. Approximately 350–500 mL of solution is utilized on

Ultrasonic dissection is performed with a titanium solid probe (Sculpture by SMEI, Italy) that is 15 cm in length [3, 4]. The areas include frontal from the hairline to the brow, glabella, dorsum of the nose, temple, lateral canthal region (crow’s feet), cheeks to nasolabial grooves, chin, jowls, and anterior neck from chin to sternal notch (anterior triangles). The probe is advanced subdermally and the tip of the probe tents the skin while it is withdrawn. Blanching of the skin occurs with treatment and is more noticeable in the patient with ruddy complexion. The skin softens and smoothes following use of the probe. The sequence of dissection starts with the submental area and neck from the submental and earlobe incisions. The probe is then used over the mandible, cheek and temple reaching the nasolabial fold, side of the nose, and the crow’s feet in a radiating fashion through the earlobe incision. An upper eyelid incision allows access to the glabella and central portion of the forehead releasing the cutaneous insertion of the corrugator and procerus muscles without altering skin sensation. The rest of the forehead is dissected through a separate hairline incision (Fig. 32.2).

32  Face and Neck Remodeling with Ultrasound-Assisted Lipoplasty (Vaser)

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The results were ­compa­rable to more extensive, difficult surgeries with higher morbidity, risks, and costs.

32.4 Technique of Vaser (Vibration Amplification of Sound Energy at Resonance) Neck Lipoplasty 32.4.1 Indications

Fig. 32.3  Face supporting garment

The fat emulsion and tumescent fluid is evacuated by gentle massage of the areas. When the incisions are closed with skin sutures and Epifoam is applied to the skin, a chin strap is applied. Ice packs are used on the face and orbital regions are not covered by the foam. A supporting garment is applied for 1 week, and then for 2 weeks more at night time (Fig. 32.3). Any other cosmetic procedure can be performed at the same time including upper and lower blepharoplasty, platysmaplasty, facelift, neck-lift, chin or cheek implants, temporal-lift, forehead-lift, skin rejuvenation with laser or chemical peel, and fat transfer.

32.3.2 Complications Two patients developed postoperative hematomas, which required aspiration, however, both were hypertensive and noncompliant with their medications. Contour deformities of the neck were noted in three patients with two of them improving over 2 months. One patient required surgical release of the subdermal scar and asked for a more extensive surgery, a standard open facelift with SMAS. There were no instances of nerve injury, alopecia, or a vascular necrosis. The ­ultrasonic-assisted facial rejuvenation was safe, ­effective, and reproducible.

Heavy neck and/or chin with moderate to food skin tone and where extra volume is expected to be excess fatty tissue. Patients may seek good predictable aesthetic outcome (contouring of the neck/jowls) with maximum safety, fast recovery, and minimum down-time. The protocol establishes that Vaser-assisted neck contouring should only be performed by surgeons already experienced with the Vaser system for fatty tissue emulsification, which means at least 20 cases of standard liposelection are recommended before moving to application to face and neck. Indicated patients are who is seeking contouring of the neck and jowl areas, who have heavy neck and/or chins with moderate to good skin tone, and where extra volume is expected to be excess fatty tissue.

32.4.2 Marking and Incisions There should be a strategy plan for volume removal and associated marking. Landmarks include the lower border of mandible and thyroid cartilage.

32.4.3 Anesthesia The neck is divided into thirds and local tumescent fluid is infiltrated, about 100 mL in each third. The face and the neck are more vascular and have more innervations than typical fat layers in the body. The concentration of adrenaline should be increased to 1:500.000, the concentration of lidocaine to 0.3–0.5% in order to guarantee enough analgesia and vasoconstriction of the area.

32.4.4 Incisions Incisions are placed under the chin, and in front of or behind ears (bilaterally), earlobe, chin, and lower neck (Fig.  32.2). Possible placement may be bilaterally in

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the neck at the lowest anticipated level of treatment. The surgeon must wait between 8 and 10 min before starting surgery, until the effects of lidocaine and adrenaline begin. It is advisable to infuse with a small diameter blunt infusion cannula (2.0 mm or smaller 14 gauge or smaller). Never use a needle. The infusion should be uniform and into all locations where the Vaser or the suction cannula may be used. The infusion should be slow, 100  mL per minute, with gentle action.

32.4.5 Skin Protection Skin protection should be used in all incisions, utilizing the black skin parts with the orange silicone discs. The discs should be stitched into place (three anchor sutures are necessary) using 3/0 or 4/0 nylon. The surgeon must make sure the knots are tight as the silicon disc tends to cause the knots to unwind. The skin ports protect the incision edges and reduce visible incision scarring. Stretch the incisions and tissues below the incision with a hemostat to ease insertion.

32.4.6 Emulsification Utilize the 2.2 mm diameter (18 cm long) or 2.2 mm (11 cm long) probes, initially with the Vaser mode at 20% or 40% maximum of the power of the system. The 20% amplitude in face and neck works well when the tissues encountered are soft. The 30% amplitude is better for moderate/average fat. The 40% amplitude is indicated if face is fibrous. Never exceed 40% with the 22 mm probes, they may break. Apply Vaser until targeted fat is emulsified, likely 2–3 min total per side depending on volumes, with additional 2–3  min under the chin depending on how the Vaser was applied on the sides. The total Vaser time is 6–10 min depending on patients and infused volumes. The surgeon must try to achieve the targeted 6–10 min of Vaser time to minimize aspiration trauma.

32.4.7 Aspiration/Cleaning Two small stab incisions are sometimes placed in the lateral aspects of the neck at the lowest point of treatment and left open for drainage purposes. A small

A. Di Giuseppe and G. Commons

s­ uction cannula with no vacuum applied and passed through the stab incisions to open channels into the treated areas. At the end, it is advisable to massage and press tissues to express, emulsified tissues and fluids out of incisions. The emulsified fat and fluidscan be massaged out or will drain out of the incisions on its own.

32.4.8 Postoperative The recommended dressing will make a gentle compression to help the skin redraped and settle into position and aid to prevent ripples or folds in the skin. The options include cotton pads with elastic wraps, cold compresses, silicon foam padding, elastic face garments typically applied for 2–4  days, than overnight for 1–2 weeks, depending on preference. Keep head elevated overnight for 4 weeks to help edema to last quicker. The typical follow-up is 1  day, 1 week, 6 weeks, 6 months, and as needed. Protocol for external ultrasound and for light massage (Endermologie- LPG) or just lymphatic massage may be beneficial. External ultrasound 10 W for 5 min with small head twice a week for 3–4 weeks is recommended as alternative to endermologie, to soften tissue.

32.5 Discussion There has been a lot of interest in the use of ultrasonic liposuction for body contouring. Skin retraction has been reported as a result of the concomitant use of internal ultrasound from the large amount of fat removed, removal of subdermal fat, skeletonization of the superficial fascial system, and thermal effects on the subdermal surface and collagenous structures of the superficial facial system [5–8]. The theories of the cause of skin contraction include collagen constriction due to thermal injury, defatting the superficial layer results in contraction of the retained structures (skin), gentle stimulation allows contraction through controlled damage. Facial aging is due to fat and skin ptosis and not muscle or facial ptosis. Therefore, the supra-SMAS plane is ideal for the harmonic lift with ultrasonic rejuvenation of the face. The osteofacial dermal ligaments can be released or attenuated in this plane allowing

32  Face and Neck Remodeling with Ultrasound-Assisted Lipoplasty (Vaser)

direct contouring of the malar, nasolabial, jowl, and submental fat collections. Fat removed close to the under surface of intact skin results in skin retraction with permanent contour changes. Postoperative care requires careful nursing assistance, punctilious wound protection, and prolonged seclusion of elaborate makeup. Recovery time varies from 4 to 14 days. The postoperative care is limited to the use of Reston foam and elastic compression bandages that are changed by the patient. Although there are no histological examinations in this study, there have been previous reports on the results of subdermal ultrasound and liposuction [9, 10]. The long-term results have not been evaluated and are probably related to the type of skin, patient’s age and sex, and the long-term effect of ultrasound energy. Disadvantages are the cost of ultrasonic machine, increased hassle factor in the operating room, and machine dependency, but after achieving proficiency in using the machine there is no turning back because it is addicting. The conclusion, at that time, was that the harmonic lift is a safe, effective, and reproducible form of skin remodeling. It can be performed under local, regional, or general anesthesia and can be repeated with no increase in surgical difficulty or cumulative effect. Advantages include negligible blood loss and pain, short and uncomplicated recovery, and simple postoperative care. The results are comparable to those obtained with more extensive surgery that frequently involves overnight stay, higher risks, increased morbidity, and higher costs. The author has found a lot of scepticism around the utilization of ultrasound energy in the face, mainly related to the potential risks of burns. In USA, from 1995 to year 2000, a series of articles published in medical literature pointed out the increasing number of complications related to Body Contouring Procedures when ultrasound energy was involved [11]. The analysis of all these complications, though there is a difficulty in assembling all the clinical data, brought to the following results: 1. Seroma (30% of body contouring cases) 2. Delayed wound healing (18% of clinical cases) 3. Prolonged edema (15% of clinical cases) 4. Dysesthesia (12% of clinical cases) 5. Fibrosis (8% of clinical cases) 6. Asymmetries (4% of clinical cases) 7. Skin necrosis (0.3% of clinical cases) 8. Burn (0.2% of clinical cases)

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Despite the fact that burn and skin necrosis were largely the less common related complications, and represented really a rare issue, the potential risk of these two complications was overemphasized. A major issue was introduced by many authors in Literature, probably because these two related to ­procedure complications were not seen with the other technique of liposuction (superficial, traditional, power assisted). The task force established by the American Society of Aesthetic Plastic Surgery (ASAPS), by the American Society of Plastic and Reconstructive Surgery (ASPRS), by the Educational Foundation, etc., met many times in order to establish safety criteria of utilization of ultrasound energy in body contouring surgery. The first safety indication, to prevent complications such as burn and skin necrosis, was to avoid the utilization of the ultrasound probe close to the underlying skin-dermis that was really, on the contrary, the most important step of the “harmonic lift.” However, only working “superficially” with a solid ultrasound probe, the surgeon can undermine the cutaneous and subcutaneous layers, assembling a skinny but vascularized flap, more prone to retract and adapt to a reduce body volume. The great misunderstanding in those years, which lead and created confusion and mixing of clinical data, was due to the fact that all the complications-related data came through the utilization of the two most diffused ultrasound tools, in the US market: The Contour Genesis, by Mentor (Santa Barbara, California), and the Lysonics (by Inamed Corporation). These two ultrasound tools have similar technical characteristics: 1. High energy 2. Hollow probes, with simultaneous ultrasound energy administration, thus emulsification and simul­ taneous, subsequent aspiration 3. 5.0 mm large probe The SMEI sculpture tool was a less powerful tool, with solid titanium probes, with no aspiration at time of emulsification (which were, and are, two different clinical phases). In 2001, Cimino [12] published an article on power quantification and efficiency of ultrasound energy. This article was of capital importance to understand all the mistakes made by the two main American manufacturers in assembling the two most common ultrasound tools.

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Fig. 32.4  Sculpture by Smei (bottom), and infiltration peristaltic pump (top)

1. Too much energy which produced unnecessary overheating, which increased the side effects of ultrasound (seroma, mainly) without enhancing the results and the clinical outcomes. 2. Too large probes, with low efficacy in transmitting energy to the tip, and thus reducing the emulsification rate. 3. Poor design of the tip of the probe due to lack of technological research, with a reduced efficacy of the system in order to raise the rate of emulsification, the manufacturer increased the power of the tools. The two main ultrasound devices were far from a good technical standard, technologically were low developed machines, and the majority of complications came from these limits. As a matter of fact, with the sculpture Smei machine, the author has never had the complications pointed out in literature in those years, which progressively destroyed the “name” of  the ultrasound technique for fat emulsification (Fig. 32.4).

Fortunately in 2001 a new ultrasound device, called Vaser (by SST-Denver, Colorado, USA), was introduced in the US market (Fig. 32.5). This new tool has new features as: 1. New designed probes, of different caliber and shape. 2. The tip is designed (with one, two, three rings), to increase the efficiency of the emulsification, which now affects not only the tip, but also the sites of the last part of the shaft (Fig. 32.6). 3. The number of rings is related to the efficacy of the emulsion depending on the type of tissue encountered (more or less fibrotic, type of fat, more or less dense). 4. New generator of ultrasound energy, with less power, but optimization of the distribution of energy at the different frequencies and wave length. High efficiency with less energy, which means lessrelated complications due to overheat of the system. So far, in the last 5 years of the “Vaser

32  Face and Neck Remodeling with Ultrasound-Assisted Lipoplasty (Vaser)

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Fig. 32.6  Different probes with 1, 2, and 3 rings at the top of the shaft

Fig.  32.5  Vaser System-Ultrasound (top), Aspiration-Ventex (bottom) and Infiltration (top right)

Ultrasound Generation,, no report of burn or skin necrosis has been published. An insignificant percentage of seroma was reported. 5. New aspiration system, the so-called Ventex, with a new pathway expressly designed for increasing the rate of aspiration, without damaging the tissue, thus aspirating “noble” structures, as vessels nerves, elastic tissue, and impossible to be blocked by undue aspiration of wrong tissue. Skin protector, expressively designed to prevent tissue damages from friction injuries, related to the consecutive passages of the probe from the same entrance point (Fig. 32.7). 6. Reduced extension entrance scar of skin, to allow introduction of the solid titanium probes that

Fig. 32.7  Skin ports

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Fig. 32.8  The thinner the subcutaneous fat, the greater the contraction

Fig.  32.9  Layers of subcutaneous emulsification with Vaser UAL. S superficial, I intermediate, P deep

Fig. 32.10  Fat thickness varies in different body areas. Thigh and abdomen are the thickest areas. Back and face are the thinnest

A. Di Giuseppe and G. Commons

are smaller in diameter (standard probe varies from 2.2 to 3.7 mm). The facial probe is 2.2 mm large. Even the site of entrance is now compatible with the typical diameter of the standard liposuction cannulas (between 2 and 4 mm of diameter). The role of dermis, in the subcutaneous anatomical structure has been under valuated in the past. Rudolph [13] first described the importance of the dermis layer for skin retraction. In plastic surgery, it is commonly known that a split skin graft (no dermis left) is not really indicated to cover joint-areas (as elbow) for the possibility of leading to skin retraction, thus functional ­problems to the area. If a full thickness graft is utilized (with a layer of dermis but no fat) the same area is less prone to contraction and to functional problems (Fig. 32.8). This aspect has never been considered in skin contraction after ultrasound-assisted body contouring [14, 15]. Emulsifying the body fat, and thus conserving the connective, supporting structure of the subcutaneous tissue (Fig.  32.9), the skin retracts much more than in standard condition. If the surgeon can harvest a well-vascularized skin dermal flap with the auxiliary use of an instrument that helps preparing such a surgical plane, the potential of skin retraction is maximized in a safe procedure (Fig. 32.10). The surgeon using the Vaser technique for face and neck contouring can emulsify fat areas (chin, jowls, neck) or just extensively undermine the interested areas, counting on a deep, severe, intense, skin retraction, simulating the effect of a subcutaneous rhyti­ dectomy but without cutaneous scars [16] (Figs. 32.11–32.15).

32  Face and Neck Remodeling with Ultrasound-Assisted Lipoplasty (Vaser)

a

b

Fig. 32.11  (a) Preoperative 38-year-old male. (b) Postoperative following jowl, chin, and neck contouring

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a

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Fig. 32.12  (a) Preoperative 37-year-old patient. (b) Postoperative after neck, chin, and jowl contouring

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Fig. 32.13  (a) Preoperative 28-year-old male with heavy cheeks and chin retrusion. (b) One month following Vaser of cheeks and neck for contouring and intra oral chin implant

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b

Fig. 32.13  (continued)

a

Fig.  32.14  (a) Preoperative 43-year-old male with neck and chin hypertrophy. (b) Postoperative after cervical UAL and chin implant

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b

Fig. 32.14  (continued)

a

b

Fig. 32.15  (a) Preoperative 44-year-old obese female. (b) Postoperative following neck, jowl, and cheek UAL

32  Face and Neck Remodeling with Ultrasound-Assisted Lipoplasty (Vaser)

References 1. Di Giuseppe A, Menna G (2000) The harmonic lift: ultrasonic assisted skin remodelling. Int J Cosmet Surg Aesthet Dermatol 2(2):125–131 2. Klein J (2000) Tumescent technique. In: Klein J (ed) Tumescent anesthesia and microcannular liposuction. Mosby, St. Louis 3. Grotting JC, Beckestein MS (1999) The solid probe technique in ultrasound-assisted lipoplasty. Clin Plast Surg 26(2):245–254 4. Rohrich RJ, Beran SJ, Kenkel JM (1998) Ultrasound assisted liposuction. Quality Medical Publishing, St. Louis 5. Illouz YG (1990) Study of subcutaneous fat. Aesthet Plast Surg 14(3):165–177 6. Gibson T (1990) Physical properties of skin. In: McCarthy J (ed) Plastic surgery. W.B. Saunders Co, Philadelphia 7. Gibson T, Kenedi RM (1970) The structural components of the dermis. In: Montagna W, Bentley JP, Dobson L (eds) The dermis. Appleton-Century Crofts, New York 8. Southwood WF (1955) The thickness of the skin. Plast Reconstr Surg 15(5):423–429

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9. Pitman GH (1993) Liposuction and aesthetic surgery. Quality Medical Publishing, St. Louis 10. Fodor PB, Watson J (1998) Personal experience with ultrasound assisted lipoplasty: a pilot study comparing ultrasound assisted lipoplasty with traditional lipoplasty. Plast Reconstr Surg 101(4):1103–1116 11. Scheflan M, Tazi H (1996) Ultrasonically assisted body contouring. Aesthet Surg J 16:117–122 12. Cimino WW (2001) Ultrasonic surgery: power ­quantification and efficiency optimization. Aesthet Plast Surg J 21(3): 233–241 13. Rudolph R, Guber S, Suzuki M, Woodward M (1977) The life cycle of the myofibroblast. Surg Gynecol Obstet 145(3):389–394 14. Becker H (1992) Subdermal liposuction to enhance skin contraction: a preliminary report. Ann Plast Surg 28(5): 479–484 15. Gasparotti A (1992) Superficial liposuction: a new application of the technique for aged and flaccid skin. Aesthet Plast Surg 16:141–153 16. Shiffman MA, Di Giuseppe A (2006) Liposuction: principles and practice. Springer, Berlin

 

Injection/Filler Rhinoplasty

33

George John Bitar, Olalesi Osunsade, and Anuradha Devabhaktuni

33.1 Introduction Due to its low morbidity and the high patient satisfaction, non-surgical rhinoplasty (also known as a non-surgical nosejob) is a viable option for primary nasal augmentation and for correction of nasal deformities. Nonsurgical rhinoplasty, whether performed for primary nasal augmentation or post-operative revision, is increasing in popularity due to advancements in the various soft tissue fillers. There is no FDA-approved soft tissue filler specifically directed for non-surgical rhinoplasty yet; however, various soft tissue fillers have been used in off-label protocols with mixed results. Examples of such fillers include injectable silicon (a device banned by the federal government [1]), collagen, non- and crosslinked hyaluronic acid, and calcium hydroxyapatite (CaHA). These alloplasts are  regarded as minimally invasive counterparts to Fig.  33.1  Radiesse® Syringes (Used with permission of Bioform Medical, San Mateo, CA)

G.J. Bitar (*) GWU School of Medicine, Bitar Cosmetic Surgery Institute, 3023 Hamaker Court, Suite 109, Fairfax, VA 22031, USA e-mail: [email protected] O. Osunsade George Washington University School of Medicine and Health Sciences, Arlington, VA 22209, USA A. Devabhaktuni George Washington University School of Medicine and Health Sciences, Washington, DC 20037, USA

c­ artilage, fat, and other autologous grafts used in surgical nasal augmentation. In recent years, the xenograft Permacol has also been used for nasal augmentation in the UK [2]. With a non-surgical approach, it is essentially an augmentation rhinoplasty, so it has limitations compared to a surgical rhinoplasty. Various properties of the commercially available calcium hydroxyapatite media (CHM), Radiesse® (BioForm Medical, San Mateo, Calif.) will be discussed with its uses for non-surgical rhinoplasties and avoidance of pitfalls. Attention is focused on Radiesse® (Fig. 33.1) because of its longevity, ease of administration and molding, as well as its excellent safety profile.

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_33, © Springer-Verlag Berlin Heidelberg 2011

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Fig. 33.2  The dissociation equilibrium of calcium hydroxyapatite

H3PO4 pK1 = 2.1 H2PO4– pK2 = 7.2 2H2O

HPO4–2 pK3 = 12.3 Ca10(PO4)6(OH)2

10Ca+2

+

6PO4–3

+

2OH–

media, sophisticated ceramic processing techniques are utilized to prepare the CaHA particles, which are segregated into a narrow size range, maximizing the volume between the particles [3]. Particles sizes were chosen in order to minimize the possibility of migration and to allow unproblematic injection through a reasonably small needle [3].

33.3 Storage

Fig.  33.3  Radiesse® at a microscopic level. CaHA particles after implantation (Image credited to David Goldberg, MD. Used with permission of Bioform Medical, San Mateo, CA)

33.2 Biochemistry The chemical formula for calcium hydroxyapatite is Ca10(PO4)6(OH)2. In the body, hydroxyapatite is a weak base and dissociates into phosphate and hydroxyl ions (Fig.  33.2). Phosphate is capable of accepting up to three protons, but at physiological pH ranges it is only capable of existing as dihydrogen phosphate or hydrogen phosphate ions. Radiesse® is composed of a sodium carboxymethylcellulose, water, and glycerin suspension (70%) of microspheres (30%; 24–45 mM in diameter) of CaHA. In Radiesse®, the average microsphere volume is 620 cubic microns [3] (Fig. 33.3). The blend of CaHA with carrier gel is chemically referred to as CHM [4]. Before being mixed with

Radiesse® comes in 0.3, 0.8, 1.3, and 1.5  mL syringes and can be shipped and stored at room temperature for up to 2 years. It must be injected without any dilutions or alteration, immediately after opening. It should not be reused after initial use for risk of contamination. The current recommendation from the manufacturer is that the Radiesse® that is unused at the first treatment may be stored for up to 3 months for that patient before it must be discarded [5]. It is important that no visible air be present in the capped syringe to prevent premature hardening of the material [5]. The company provides three labels identifying the lot number of the Radiesse syringe in use so that the first and second procedures can be documented in the patient’s chart alongside self-adhesive labels.

33.4 Mechanism of Action Calcium hydroxyapatite media is an injectable soft tissue filler that is palpable and malleable, allowing the physician to mold it into the appropriate form. Although inorganic, it is found naturally in bones and teeth. After injection into the body, it is eventually absorbed and

33  Injection/Filler Rhinoplasty

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Fig. 33.4  Mechanism of action of Radiesse® (Used with permission of Bioform Medical, San Mateo, CA)

a

b

c

d

Fig.  33.5  Histological evidence of duration of action. Using picrosirius red staining, increased collagen deposition is seen around the CaHA microspheres at 4 (a), 16 (b), 32 (c), and 78 (d) weeks. Note the gradual changes in the appearance of the

CaHA microsphere, which can be attributed to their breakdown and resorption through normal metabolic processes (Images credited to David Goldberg, MD. Used with permission of Bioform Medical, San Mateo, CA)

metabolized into calcium and phosphate ions before being excreted through normal metabolic processes [6]. Positive long-term effects may be explained by the fact that it remains localized at injection sites. While the aqueous gel component is resorbed by 6  months

after injection [3], the CaHA microspheres remain as scaffolds for osteoblasts at the periosteum and fibroblasts in the soft tissues for a much longer period of time (Fig.  33.4). Histological evidence shows CaHA microspheres stimulate collagen production (Fig. 33.5),

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but they do not stimulate bone growth in the periosteum [7]. For this reason, Radiesse® has also been injected with harvested fibroblasts in order to study their combined effects on collagen synthesis [8]. This putative mechanism of action may explain the observation that a smaller volume of Radiesse® is needed for the same degree of correction provided by higher volumes of hyaluronic acid or collagen [7]. Hydroxyapatite cement, which is denser than the granular Radiesse®, has been used for surgical nasal implants for over two decades. This is due to its ­biocompatibility, which is associated with its osteoconductive and osseoporous properties [9]. It is nonresorpable, however, which leaves risks of infection and extrusion [10].

33.5 Duration of Action Injectable CaHA lasts longer in areas with less movement, blood supply, and lymphatic drainage because its loss is more limited in these areas [11]. Hence, injecting Radiesse® deep along the periosteum or in facial areas with less movement seems to produce greater longevity than immediately under the skin [11]. In a study involving injection into the neck of the bladder in animals, CaHA lasted for the entire 3 year length of the study [6]. For non-surgical rhinoplasty, desired results may last 1–2 years [11] (Fig. 33.5) with a single injection (approximately 1.3 mL), although additional touch-up injections may be performed around 6  months after initial treatment to maintain the desired nasal contour. Some patients report longer duration for minor improvements, such as smoothing of irregularities up to 3 years [8]. In one reported case, rhinoplasty revision surgery was performed uneventfully on a patient who received 0.6 mL of Radiesse® 14 months earlier [12]. Interestingly, no residual Radiesse® was noted during that operation [12], which is consistent with the absorption of Radiesse® gradually.

33.6 Clinical Uses 33.6.1 FDA-Approved Uses Radiesse is approved by the Food and Drug administration (FDA) as a filler to augment vocal cords, for HIV-associated facial lipoatrophy, for nasolabial folds

G.J. Bitar et al.

and smile lines, for oral and maxillofacial defects, and a radiopaque marker [13].

33.6.2 Aesthetic Off-Label Uses The only FDA-approved aesthetic use for Radiesse® is to serve as a soft tissue filler for correction of moderate to severe facial deficiencies at nasolabial folds and in HIV-associated facial lipoatrophy. The most common off-label aesthetic uses of Radiesse® are for non-surgical facial rejuvenation procedures to smooth wrinkles, fill depressions, and reduce facial asymmetry in lips (where it is sometimes associated with nodule formation), labiomandibular folds, and the pre-jowl sulcus. It is also a dependable filler for augmenting the facial boney ­contour, i.e., nose, chin, cheeks, and forehead [5]. Additionally, it has been used in spreader graft injections as a nonsurgical alternative for internal nasal valve collapse patients, minimizing obstruction and improving breathing and snoring [14]. In 2007, Stupak et al. [15] first described use of Radiesse® for correction of post-rhinoplasty contour deficiencies and asymmetries. Other off-label uses include other facial rejuvenation procedures, bladder dystrophy corrections, nipple projection after failed reconstruction surgery [16], cosmetic correction of enophthalmos [10], and restoration of orbital volume [11]. Radiesse® has received approval for many of these off-label procedures, including nonsurgical rhinoplasty, outside of the USA [13].

33.7 Safety and Efficacy Due to its inorganic nature Radiesse® is non-immunogenic, unlike collagen, so no skin testing is needed prior to injection. It has been found to be nontoxic, non-irritable, non-antigenic, and biocompatible through both in vivo and in vitro testing [17]. Should any particles become phagocytized, they are degraded in situ to calcium and phosphate ions like small fragments of bone. Furthermore, it is eventually absorbed by the body, rendering it reversible and preferable to other permanent alloplasts – such as polymethyl methacrylate (PMMA). Because it is semi-permeable, it lasts longer than collagen and hyaluronic acid-based fillers, making it more cost effective and reducing frequency of injection.

33  Injection/Filler Rhinoplasty

The major obstacle preventing formal FDA approval of Radiesse® for non-surgical rhinoplasty and other facial augmentation procedures is the lack of a large, long-term study of its safety and efficacy. There are many studies showing its effectiveness in nasal augmentation on a small scale [8, 12, 16, 17–21] thus warranting further study. A study published in 1996 following more than 200 patients during an 8-year period found the use of porous hydroxyapatite granules – similar to Radiesse® – as favorable means of augmenting the craniofacial skeleton [22]. This study, however, only included a limited number of cases involving nasal augmentation, concluding the method to be investigatory at that time [22]. Similarly, a German study followed 128 augmentations with hydroxylapatite granules filled in a Vicryl-tube in 36 patients from 1986 to 1992 [23]. Implanted in the subperiosteum, these granules proved to be well-tolerated and consistently in form in patients with facial deformities [23]. Furthermore, a Chinese study following 50 patients over 8 years found a particulate hydroxyapatite to be aesthetically stable with good long-term results for nasal augmentation [24], however, this form of hydroxyapatite differs from the granular form found in Radiesse®. In 2008, a case was reported of a 37-year-old Asian woman who experienced ptosis due to eyelid mass development secondary to receiving CaHA for nasal augmentation 3  days earlier [24]. Symptoms were relieved after surgical excision of the mass 2 months later, but this complication emphasizes the need for proper site selection, meticulous injection techniques, and avoidance of overinjection of CaHA [25].

33.8 Non-surgical Rhinoplasty Non-surgical rhinoplasty with Radiesse® (also known as a Radiesse® rhinoplasty) should be performed by a surgeon with a mastery of nasal anatomy and who is experienced in performing surgical rhinoplasties. Vari­ ous guidelines have been reported in the literature by clinicians regarding anesthesia, injection, and postoperative care related to Radiesse® rhinoplasty.

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critically assessed, as well. Past medical history should be reviewed, with an emphasis on drug use, allergies, history of cold sores, presence of autoimmune disorders, history of facial herpes virus, previous facial operations (specifically rhinoplasties or dermal filler treatments), and whether the patient is pregnant or nursing [20]. Patients should also report sinus or nasal congestion, as well as use of decongestants. Due to minor bleeding during injections, patients should not be on any blood thinners including warfarin, NSAIDs, vitamin E (including multivitamin form), certain herbs, and excessive alcohol intake. One recommendation is to cease ingesting anything that can thin the blood for 10 days prior to the procedure [6]. The authors recommend cessation of above products for 2 weeks prior to the procedure with the consent of the patient’s primary care physician. Patients should be informed of the risks and benefits of the procedure in order for them to have realistic expectations toward a satisfactory outcome. They should be informed that the results are not permanent, and may require further revision before acquiring the desired appearance. Moreover, non-surgical rhinoplasty with Radiesse® does not exclude patients from surgical rhinoplasty in the future. Patients with one or more of the following conditions may also be excluded from the procedure: acute or chronic nasal infection, existing keloid scars, history of systemic collagen diseases, severe bleeding disorders, nasal respiratory impairment, and unrealistic expectations [21]. An essential part of the informed consent is the discussion of a surgical rhinoplasty as a permanent alternative to a non-surgical rhinoplasty. It is very important for patients to know that both options, the surgical and non-surgical ones, are viable options if that is the case. Various reasons may sway the patient to have a nonsurgical rhinoplasty such as cost, lower risk, desire for a minimal change, time of recovery, and fear of surgery. Pre- and post-treatment photographs should also be taken, and patients should be given the opportunity to speak with previous patients who have undergone non-surgical rhinoplasty with Radiesse®, if possible.

33.8.2 Physical Examination 33.8.1 Initial Consult A patient’s chief complaint about his or her nose needs to be addressed. The level of nasal deformity as it relates to the magnitude of the patient’s concerns should be

Before performing a non-surgical rhinoplasty with Radiesse®, it is important to examine the nose (Fig.  33.6) thoroughly, including the skin, cartilage, boney pyramid, different relationships of the esthetic

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Nasion Dorsum

Tip Sidewall Facet Columella

Alar lobule Nostril

Fig. 33.6  Nasal anatomy

subunits, whether there is septal deviation, enlargement of inferior turbinates, difficulty breathing, prior trauma, as well as identify any possible locations of scar tissue. Also take into consideration that thickness and moisture of skin differs between ethnicities. Treatment should be delayed if any active lesions exist, with initiation of anti-viral therapy (e.g., acyclovir) for patients with a history of the facial herpes virus [6].

33.8.3 Nasal Anatomy For non-surgical rhinoplasty, good knowledge of the relations of the nasal subunits is essential. Surface anatomy is also of paramount importance. Knowledge of nerve and blood supply will allow the injecting surgeon to avoid complications. For a non-surgical rhinoplasty, Radiesse® is typically injected into depressions at the fronto-nasal angle, dorsum, nasal tip, columella, and naso-labial angle.

33.8.4 Anesthesia and Prophylaxis The most common types of anesthesia to injection sites include: lidocaine with epinephrine, topical lidocaine with tetracaine for 30 min [18], anesthetic gel [26], or topical anesthesia with BLT applied for 15–30 min prior to injection. Applying an icepack to the nose decreases sensation and provides good analgesia. A judicious

combination of the above may also be used with care not to compromise the blood supply to the nasal tip. Anesthesia can also be used as a means of loosening tissue and cartilage prior to filler injection. For this, a 25-gauge or 27-gauge needle can be used to create a space for the filler from a distal puncture site [19]. For post-rhinoplasty contour corrections, injections have been performed without anesthesia (only an alcohol pad), or in the operating room in conjunction with facial procedures [15]. In the latter, it was found that concurrent procedures do not affect injection treatment results [15]. In July 2009, the FDA approved the mixing of Radiesse® with lidocaine. This is another method of anesthesia that has been proven to improve patient comfort and satisfaction with Radiesse® injections [4]. Nerve blocks are helpful mainly when the infiltration of the anesthetic solution may cause undesirable distortion of the surgical site or require an amount of anesthetic that exceeds the maximum recommended dose [19]. For non-surgical rhinoplasty with Radiesse®, blocking the infraorbital and supratrochlear nerves, which are branches of the trigeminal nerve, has been recommended [19], although neither are used in our institute. An infraorbital nerve block specifically targets the lateral nose [19], but also anesthetizes the lower eyelid area, through the cheeks, and the upper lip [7]. Topical anesthesia may be applied to the oral mucosa prior to anesthetic injection [7]. In our institute, we administer a topical anesthesia of lidocaine 6%, tetracaine 4%, and benzocaine 20% applied for 30–45  min directly to the entire nose, along with icepack application. That application gives excellent pain control and does not distort the nasal anatomy. Prophylactic antibiotics are not used for non-surgical rhinoplasty, but there is anecdotal evidence supporting prophylactic use of Arnica montana, bromelain, and 1% vitamin K1 (phytonadione) cream to reduce bruising [7]. After anesthesia and prophylaxis are administered, patients are marked and then injected subcutaneously or into a subperiosteal plane at the desirable location of the nose. For an experienced surgeon, markings may not be necessary.

33.8.5 Needles For non-surgical rhinoplasty, Radiesse® has reportedly been injected in various ways, with any of the following needles: a 23 gauge 1.5-in. straight or angled

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spreader graft needle [14], a 25 gauge 5/8 in. needle, a 27 gauge 1.75 in. needle [5], a 27 gauge ½ in. needle [18], a 30 gauge 1.30 cm needle [15], or a 27 gauge 0.60 cm needle [15]. Our preference is a 27 gauge ½ in. needle as it is convenient to inject smoothly but does not leave a large needle hole.

33.8.6 Injection Technique The authors’ approach is to address the nose from top to bottom. First, the radix (Fig. 33.7) is assessed. Is it with appropriate height, or does it need to be augmented? Next, the dorsum is injected if necessary. If there is a dorsal hump, injection cephalad to it, or caudal to it may mask that hump (Fig. 33.7). If there is a deviated septum, the injections may be done to achieve symmetry by injecting unequal amounts to the left and right side. If there is an isolated

a

Fig. 33.7  (a) Pre-procedure Caucasian male. (b) Post-procedure following injections with Radiesse® to the dorsum and radix, resulting in increased height. (c) Pre-procedure Caucasian female. (d) Post-procedure following injections with Radiesse® at the dorsum and radix, resulting in increased height

depression, it can be addressed with a direct injection to fill it. Caution needs to be exercised if a depression is tethered to the underlying bone or cartilage, since an overly aggressive injection can create a “pin-cushion” effect, with the Radiesse® ending up surrounding the depression rather than filling it. The nasal tip skin needs to be assessed next (Fig. 33.8). If it is thick and immobile, it may be difficult to change the shape with injections, and may need to be addressed surgically. If the skin is lax, a good outcome can be expected from a nasal tip injection. The columella can also be injected if it is retracted or deficient. Because it is abundant in sebaceous glands, the nasal tip should be approached preferably from the dorsum to decrease the chance of contamination and infection. Very few times the nasal nares need to be augmented. That should be done with caution as it may narrow the internal nasal valve.

b

378 Fig. 33.7  (continued)

G.J. Bitar et al.

c

Injection is typically done into the deep dermis in a threaded fashion in doses ranging from 0.1 to 0.3 mL at any given time because higher volumes may create undue tension and cause skin necrosis. Crosshatching, linear, and fanning techniques of injection have been reported [6]. If anesthesia were not used, injections can alternatively be coupled to loosening of subcutaneous tissue. Due to its composition, Radiesse® should not be injected into the superficial or middle dermis [5]. Similarly, the thick, white texture of Radiesse® may make it visible under thin skin, which is not aesthetically pleasing. Superficial injections can lead to overcorrection and nodule formation, so it is important to finish injecting before removing the needle. Persistent nodules may be avoided with proper injection of the Radiesse® in the plane immediately deep to the dermis and proper site selection [5]. Areas of extensive scar tissue deposition may be more difficult to treat because of tissue retraction and lack of a boney base for projection. Even so, some correction can often still be achieved in such areas [8]. Care should be

d

taken not to inject into an artery, as this may cause necrosis [18].

33.8.7 Dosage Doses vary depending on individual patient characteristics, but suggested maximum doses include: 1.5 mL at the fronto-nasal angle, 0.5 mL at the dorsum, 0.5 mL at the tip, and 1.5 mL at the nasolabial angle; as maximum doses to each specific area [19]. We recommend limiting the initial total injection to 1.5  mL to avoid tension on the overlying skin as well as overcorrection. It is better to under-correct deformities, as they can be filled in or touched up during a follow-up visit in 2 weeks to 3 months.

33.8.8 Post-injection Care Ice should be applied during breaks between injec­ tions and for a period afterward to reduce edema and

33  Injection/Filler Rhinoplasty Fig. 33.8  (a) Pre-procedure Caucasian female in her early 20s. (b) Post-procedure with injections with Radiesse® to the tip, resulting in a more pointed shape. (c) Preprocedure Caucasian woman in her twenties. (d) Postprocedure after injections with Radiesse® superiorly and inferiorly around a hump on the dorsum, which masked it and resulted in the appearance of a more prominent tip

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a

b

c

d

e­ cchymosis. The procedure is typically well-tolerated, and no post-procedure pain control is typically required. Injection is followed by massaging, which molds the desired shape and ensures the absence of palpable lumps. Molding may be enhanced by micropore taping

for 24 h after injection [15, 19]. Taping may also help to reduce swelling. Splint placement for a few days after injection may prevent displacement of the filler [6]. At our institute, we do not tape or splint the nose afterward, but encourage patients to place cold compresses

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on the nose to decrease the edema for the 24 h following the non-surgical rhinoplasty. The authors have not seen the filler being displaced by this follow-up care. The most common adverse effects are local and transient. They include mild pain, erythema, ecchymoses, edema, pruritus, and hematoma [12, 17]. Other adverse effects include soreness, numbness, contour irregularities, tenderness, and irritation. Overall, Radi­ esse® rhinoplasty is typically well-tolerated and patient satisfaction for non-surgical nasal augmentation is high [8]. Removal of excess Radiesse® with an 18-g needle can lead to correction if Radiesse® is injected into the middermis [5] or in excess. Radiesse® has a 1:1 injection-to-augmentation ratio, thus it requires no additional post-treatment augmentation monitoring [27]. Additional touch-ups may be required after 2 weeks to 3 months. Patients are seen 2–3 weeks after injections to ensure that they are satisfied after most of the edema and ecchymosis has subsided.

33.8.9 Patient Satisfaction As with any aesthetic procedure, satisfaction depends not only on surgical technique, but realistic expectations from patients, as well as proper prior communi­ cation between surgeons and patients. Non-surgical rhinoplasty with Radiesse® has a high rate of patient satisfaction in the literature [8, 12, 15, 17–21], as well as at our institute. Furthermore, one study found no correlation between patient satisfaction scores and demonstration of improvement by photographic analysis [8]. In the rhinoplasty literature, the standard for measuring patient satisfaction is through patient-reported outcome measures. The most common instruments used to measure patient satisfaction after surgical rhinoplasty are the Rhinoplasty Outcomes Evaluation, the Glasgow Benefit Inventory, and the Facial Appear­ ance Sorting Test [28]. For non-surgical rhinoplasty with Radiesse®, there is a need for the use of such instruments to assess patient satisfaction.

33.9 Specific Types of Noses At the nasal radix and dorsum, Radiesse® can be used to augment height, to give a wider appearance or correct saddle deformities. By correcting retracted ­columellas,

G.J. Bitar et al.

it can give a more prominent nasal tip. Radiesse® has also been used to improve post-rhinoplasty contour defects, such as dorsal nasal defects (cartilaginous and boney), nasal sidewall depressions, overly deep supratip breaks, and alar asymmetries [15]. Typical candidates include people with ethnic noses: Asians, Middle Easterners, African–Americans, and Hispanics. This is because, in general, such people have thicker skin, lower nasal dorsums, and bulbous tips compared to Caucasian patients. When performing a rhinoplasty on any patient population it is important to take cultural issues into consideration. While such patients seek correction of nasal defects, most patients also cherish subtleties and preservation of their ethnicity. Rhinoplasty should refine facial features while maintaining ethnic identity. When they arise, also recognize language and cultural barriers.

33.9.1 Asian Augmentation rhinoplasty is a common procedure in the Asian community due to their generally lower and more caudal nasal nasion compared to Caucasian patients. A common misconception is that such rhinoplasty is done to look more “Western,” despite the fact that high, narrow bridges are aesthetically pleasing in many Asian cultures [29]. To achieve such results, surgical augmentation is performed with autogenous or alloplastic material placed into the nasal dorsum to make the nasion level higher and more cephalic. Over the years, there has been a debate over the more preferable material. To this end, it has been found that surgeons performing augmentation rhinoplasty on Asian patients have had to recognize that many are unhappy with autogenous implants and prefer alloplasts, particularly silicon, despite long-term side effects [29]. Such surgery, however, may produce conspicuous and unsatisfactory results [30], particularly due to exposure and extrusion of implants. Implant exposure can lead to scarring, which can be difficult to treat with revision surgery [31]. As inhabitants of the largest continent, Asian’s noses vary depending on different geographical reg­ ions. Northern Asian noses can have dorsal humps and high nasions extending onto the glabella [29]. Filipinos and Polynesians typically have “flat” noses which start off narrow at the bridge and gradually become wide and blunt at the tip [29]. Despite differences, the goal of rhinoplasty in Asian patients can generally be seen

33  Injection/Filler Rhinoplasty

381

as similar to the goal of Occidental rhinoplasty: a strong dorsum with a prominent origin but not competing with the tip as the leading point of the nasal profile [27]. Fig. 33.9  Asian Radiesse® rhinoplasty. (a) Pre-procedure Indian woman. (b) Postprocedure after injections with Radiesse® in the radix, dorsum, and tip. (c) Pre-procedure Chinese woman. (d) Post-procedure following injections with Radiesse® to the dorsum and radix. (e) Pre-procedure 26-year-old Philippino woman. (f) Post-procedure after injections with Radiesse® to the radix, bridge, and tip

a

Non-surgical rhinoplasty with Radiesse® in Asian patients (Fig. 33.9) can increase tip projection, create a higher dorsum, and improve tip contour [32]. Augmentation is also performed at the glabella in

b

382 Fig. 33.9  (continued)

G.J. Bitar et al.

c

d

33  Injection/Filler Rhinoplasty Fig. 33.9  (continued)

383

e

response to deficiencies there, and the columella to correct vertical deficiencies. Dorsal augmentation can also be used to create the appearance of a narrow bridge, a procedure also common in African–American noses [33]. In Asian populations, non-surgical augmentation is also frequently done as part of revision or after removal of an implant.

33.9.2 African–American A frequent complaint of African–American patients is a lack of a projection from the dorsum and the tip. In addition, African–American patients commonly complain of short columella, small nasolabial angle with

f

the upper lip too close to the nasal tip, round nostrils, and excessively broad alae [29]. Augmentation to the dorsum is as routine in ­African–American patients as hump removal is in Cau­casian  patients [29]. Approximately 50% of African–­Americans are good candidates for augmentation [29]. African–American patients with American Indian heritage frequently also have dorsal humps and high nasions that may extend on the glabella [29]. To this end, non-surgical rhinoplasty with Radiesse® in African–American patients can increase the height of the dorsum, as well as convert saddle deformities into more linear forms (Fig.  33.10). Dorsal augmentation with Radiesse® is also advantageous because the caudal end of the nose tends to be mobile, therefore rigid

384

a

G.J. Bitar et al.

b

c

Fig.  33.10  African–American Radiesse® rhinoplasty. (a) ­Pre-treatment 42-year -old African–American woman. (b) Posttreatment immediately after injections with Radiesse® to the

radix, bridge, and tip. (c) One month post-procedure after initial swelling subsided

implants are not routinely used [29]. In order to address wide-bridge appearances from frontal views, dorsal augmentation alone (without an osteotomy) can create the appearance of a narrower bridge [33]. In African–American patients, tip injections with Radiesse® can also give a more prominent appearance to an otherwise bulbous, flattened tip. The nasal tip in African–American patients has also been described as fleshy, flat, wide, depressed, pendulous, or depressed, while the aim is to create a more sculpted tip [29]. Flared nares cannot be treated with Radiesse® rhinoplasty and need surgical correction.

the cephalad aspect with the caudal aspect of the nose. Other common characteristics are insufficient anterior project of the entire nose, wide alar bases, retracted columellas, acute nasolabial angles, and depressed piriformis areas [29]. The dorsum is typically wide, and the goal is to convert it into a straight or slightly concave shape (Fig. 33.11). This is difficult to address with Radiesse®. The tip is ptotic and Radiesse® can provide a more prominent shape. Another problem site is the columella, which is often weak and found to lie above the alar rim. Radiesse® injection can increase the projection of the columella by adding structure. As with African–Americans, nostril flaring may only be corrected surgically.

33.9.3 Hispanic Nasal surgery is one of the most commonly requested aesthetic surgeries requested by Hispanic Americans. A mestiso nose typically has a narrow and deficient radix that may be augmented with Radiesse® to ­balance

33.9.4 Arabic (Middle Eastern) While generalizations should be avoided, morphologically the Middle Eastern nose falls somewhere between

33  Injection/Filler Rhinoplasty Fig. 33.11  Hispanic Radiesse® rhinoplasty. (a) Pre-operative 50-year-old Hispanic woman. (b) Post-procedure after injections with Radiesse® to the dorsum, radix, and tip

385

a

African and Caucasian noses [34]. Some of the most common features of Middle Eastern noses are: wide nasal bones, slight alar flaring, ill-defined bulbous tips, bulky infratip lobules, over-projecting radix, high and wide dorsums, and acute columellar-labial angles [34].

b

In addition, these patients commonly have thick, ­sebaceous nasal skin – especially at the tip [34]. Middle Eastern noses can also have dorsal humps and high nasions extending onto the glabella [29]. Correction with Radiesse® should proceed with caution, since this

386 Fig. 33.12  Radiesse® rhinoplasty in response to aging. (a) Sixty-two year-old male before treatment. (b) Postprocedure after Radiesse® injection above and below a dorsal hump, which masked it

G.J. Bitar et al.

a

population typically needs a “reduction” rhinoplasty as opposed to an augmentation rhinoplasty. Reduction typically involves a septorhinoplasty in response to a deviated septum, removal of a dorsum hump, correction of a crooked tip, and/or reduction of a broad base [29]. Small improvements can be offered with Radiesse® rhinoplasty such as injections to the radix to augment it if it is deficient, to the tip to offer more definition, as well as to the columella to create a more obtuse columellar-labial angle. In women, this angle should be between 95° and 105°, while in men the angle should be approximately 90° [29]. From a lateral view, the columella should lie 2–3 mm below the alar rim [29].

b

loss of elastic fibers and collagen organization, and weakening of underlying muscles [7]. In the nose, Radiesse® injection can be used to augment areas affected by the aging processes. For example, augmentation with to the base of the pyriform aperture can provide the columella with additional support. Nevertheless, it should be noted that Radiesse® can be used to smooth nasal wrinkles and depressions associated with aging in patients (Fig.  33.12). It is already used to improve aesthetic effects of aging on the forehead, cheeks, nasolabial folds, and labiomandibular lines.

33.10 Revision Rhinoplasty 33.9.5 Aging Facial aging is a complex process characterized by thinning of the epidermis, atrophy of subcutaneous fat layers, a degree of bone resorption, progressive

Contour irregularities after a rhinoplasty have to be assessed on an individual basis, and may be improved with Radiesse® injections. Because the skin may be compromised or there may be excessive scar tissue,

33  Injection/Filler Rhinoplasty

caution needs to be exercised not to compromise the blood supply to the nasal skin with an aggressive injection of Radiesse®. In this category of non-surgical rhinoplasty correction with Radiesse®, each nasal contour problem is unique and needs to be addressed on an individual basis.

33.11 Discussion The first report of using an injectable filler for nonsurgical rhinoplasty was by Han et al. [18, 35] in 2006. In that study, hyaluronic acid mixed with autologous human fibroblasts was injected subcutaneously along the nasal dorsum and immediately shaped by hand to correct flat nasal bridges. While hyaluronic acid is known not to be a long-lasting filler, when combined with fibroblasts its aesthetic results last up to approximately 1 year [35]. Drawbacks of this method of nasal augmentation are the significant preparatory time for  harvesting fibroblasts and morbidity [18]. With Radiesse®, these drawbacks are negated and results are maintained for an even longer period. Since the Han et al. [35] study and FDA approval for Radiesse® as a soft filler for nasolabial folds, which was also in 2006, there have been a plethora of studies where Radiesse® has been used for non-­ surgical nasal augmentation. Like other facial rejuvenation procedures, the most important issues for non-surgical rhinoplasty are longevity, biocompatibility of the soft tissue filler, low adverse events, and a sound cost–benefit ratio. While rhinoplasty surgery under the correct circumstances can produce astounding results, it is a very costly operation with many consequences. Some patients may prefer to spend $700–$1,000 on  Radiesse® rhinoplasty annually or biannually, as opposed to spending $6,000–$13,000 on surgical rhinoplasty. While complications were previously discussed, another possible risk is internal nasal valve collapse, although no cases have been reported [15]. There is also no evidence of granuloma formation (a problem with injectable silicon) or osteogenesis when CaHA is placed in soft tissue [7]. The problem of nodule of formation seen in the lips has also not been seen in ­non-surgical rhinoplasty with Radiesse®. Furthermore, because it is radiopaque there was concern that Radiesse® may interfere with radiological study interpretations, but this theory has been disproved [36].

387

Because non-surgical rhinoplasty with Radiesse® is a relatively new procedure, Radiesse® is injected in relatively low doses not only to avoid overcorrection, but due to concerns of safety. In the future, higher doses at more diverse locations may be attempted once longer-term analysis confirms product safety for nonsurgical rhinoplasty [19]. Furthermore, computerassisted analysis may permit even more objective measurements of nasal symmetry and contour, as seen with surgical rhinoplasty, which may lead to better injection techniques and dosages [19, 37]. Over the last 2  years the authors have performed non-surgical rhinoplasty with Radiesse® on all ethnic groups discussed previously, with patients ranging from 17 to 62 years old. Non-surgical rhinoplasty with Radiesse® has also been performed for revision after a primary surgical rhinoplasty. Approximately 30% of patients return for additional touch-ups. Overall, we have experienced no complications or adverse effects, and enjoy an over 95% satisfaction rate. Our high patient satisfaction is a result of good communication and administration of conservative dosages.

33.12 Conclusions Non-surgical rhinoplasty with Radiesse® is a feasible alternative for many patients who require nasal augmentation or correction of minor asymmetries, slight depressions, and subtle contour irregularities. A largescale, long-term study of its safety and efficacy in nonsurgical rhinoplasty may lead to Radiesse® being the first FDA-approved soft filler for this procedure, as current indications show Radiesse® is preferable. Like surgical rhinoplasty, non-surgical rhinoplasty with Radiesse® requires high-quality consultations, physical examinations, surgical knowledge of nasal anatomy, expert execution of the procedure, and ­post-injection care. Guidelines have been outlined regarding these steps, including needle specifications, dosages, and use of anesthesia and prophylaxis. Besides the actual procedural considerations, it is important to identify the potentials and limitations of non-surgical rhinoplasty with Radiesse®. Typical ­candidates for the procedure are patients in need of nasal augmentation, particularly patients with ethnic noses, as well as patients with defects related to normal nasal features, aging, or previous surgical rhinoplasty operations. While generalizations can be made

388

regarding how to approach specific ethnic and other nasal features, like surgical rhinoplasty, individual aesthetic subtleties vary between all patients. It is important to approach patients on a case-by-case basis. With a clear understanding of its background and what it entails, non-surgical rhinoplasty with Radiesse® is a high satisfaction, comparatively low-cost, and low-risk procedure aesthetic surgeons can easily incorporate into their practices as a cheaper – albeit temporary – alternative to surgical rhinoplasty.

References 1. Kontis TC, Rivkin A (2009) The history of injectable facial fillers. Facial Plast Surg 25(2):67–72 2. Pitkin L, Rimmer J, Lo S, Hosni A (2008) Aesthetic augmentation rhinoplasty with Permacol: how we do it. Clin Otolaryngol 33(6):615–618 3. Kirwan L (2009) via http://www.cosmeticplasticsurgery. uk.com/skin/radiance-cosmetic-medical-treatmentprocedure.php. Last accessed 28 July 2009 4. Busso M, Voigts R (2008) An investigation of changes in physical properties of injectable calcium hydroxylapatite in a carrier gel when mixed with lidocaine and with lidocaine/epinephrine. Dermatol Surg 34(suppl 1):S16–S23; discussion S24 5. Godin MS, Majmundar MV, Chrzanowski DS, Dodson KM (2006) Use of Radiesse® in combination with restylane for facial augmentation. Arch Facial Plast Surg 8(2):92–97 6. Jones JK (2006) Patient safety considerations regarding dermal filler injections. Plast Surg Nurs 26:156 7. Graivier MH, Bass LS, Busso M, Jasin ME, Narins RS, Tzikas TL (2007) Calcium hydroxylapatite (Radiesse® ) for correction of the mid- and lower face: consensus recommendations. Plast Reconstr Surg 120(6 suppl):55S–66S 8. Becker H (2008) Nasal augmentation with calcium hydroxylapatite in a carrier-based gel. Plast Reconstr Surg 121(6): 2142–2147 9. Maas CS, Monhian N, Shah SB (1997) Implants in rhinoplasty. Facial Plast Surg 13(4):279–290 10. Renno RZ (2007) Injectable calcium hydroxyapatite filler for minimally invasive delayed treatment of traumatic enophthalmos. Arch Facial Plast Surg 9(1):62–63 11. Vagefi MR, McMullan TF, Burroughs JR, White GL Jr, McCann JD, Anderson RL (2007) Injectable calcium hydroxylapatite for orbital volume augmentation. Arch Facial Plast Surg 9(6):439–442 12. Dayan SH, Greene RM, Chambers AA (2007) Long-lasting injectable implant for correcting cosmetic nasal deformities. Ear Nose Throat J 86(1):25–26 13. Uses and limitation on Radiesse website. http://www.radiesseusa.com/physicians/uses/. Last accessed 29 July 2009 14. Nyte CP (2006) Spreader graft injection with calcium hydroxylapatite: a nonsurgical technique for internal nasal valve collapse. Laryngoscope 116(7):1291–1292

G.J. Bitar et al. 15. Stupak HD, Moulthrop TH, Wheatley P, Tauman AV, Johnson CM Jr (2007) Calcium hydroxylapatite gel (Radiesse®) injection for the correction of post rhinoplasty contour deficiencies and asymmetries. Arch Facial Plast Surg 9(2):130–136 16. Evans KK, Rasko Y, Lenert J, Olding M (2005) The use of calcium hydroxylapatite for nipple projection after failed nipple-areolar reconstruction. Ann Plast Surg 55(1):25–29 17. Tzikas TL (2004) Evaluation of the Radiance FN soft tissue filler for facial soft tissue augmentation. Arch Facial Plast Surg 6(4):234–239 18. Rokhsar C, Ciocon DH (2008) Nonsurgical rhinoplasty: an evaluation of injectable calcium hydroxylapatite filler for nasal contouring. Dermatol Surg 34(7):944–946 19. Jacovella PF (2008) Use of calcium hydroxylapatite (Radiesse®) for facial augmentation. Clin Interv Aging 3(1):161–174 20. Siclovan HR, Jomah JA (2008) Injectable calcium hydroxylapatite for correction of nasal bridge deformities. Aesthetic Plast Surg 33(4):544–548 21. Jacovella PF (2008) Aesthetic nasal corrections with hydroxylapatite facial filler. Plast Reconstr Surg 121(5): 338e–339e 22. Gruber R, Kuang A, Kahn D (2004) Asian-American rhinoplasty. Aesthet Surg J 24(5):423–430 23. Röthler G, Waldhart E, Puelacher W, Strobl H (1994) Reconstructive procedures for improving the facial contour. Fortschr Kiefer Gesichtschir 39:114–116 [Article in German] 24. Guo X, Wu X (1997) Augmentation rhinoplasty with particulate hydroxy apatite artificial bone in 50 cases–a follow-up of 8 years. Chin J Plast Surg Burns 13(3):185–187 25. Lee MJ, Sung MS, Kim NJ, Choung HK, Khwarg SI (2008) Eyelid mass secondary to injection of calcium hydroxy­ lapatite facial filler. Ophthal Plast Reconstr Surg 24(5): 421–423 26. Braccini F, Dohan ED (2008) Medical rhinoplasty: rationale for atraumatic nasal modelling using botulinum toxin and fillers. Rev Laryngol Otol Rhinol (Bord) 129(4–5): 233–238 27. Sklar JA, White SM (2004) Radiance FN: a new soft tissue filler. Dermatol Surg 30(5):764–768 28. Kosowski TR, McCarthy C, Reavey PL, Scott AM, Wilkins EG, Cano SJ, Klassen AF, Carr N, Cordeiro PG, Pusic AL (2009) A systematic review of patient-reported outcome measures after facial cosmetic surgery and/or nonsurgical facial rejuvenation. Plast Reconstr Surg 123(6): 1819–1827 29. Matory WE (1998) Ethnic considerations in facial aesthetic surgery. Lippincott-Raven, Philadelphia 30. Lee CH, Han SK, Kim SB, Kim DW, Kim WK (2008) Augmentation rhinoplasty minimizing nasion level changes: a simple method. Plast Reconstr Surg 121(5): 334e–335e 31. Hodgkinson DJ (2007) The Eurasian nose: aesthetic principles and techniques for augmentation of the Asian nose with autogenous grafting. Aesthetic Plast Surg 31(1):28–31 32. Toriumi DM, Swartout B (2007) Asian rhinoplasty. Facial Plast Surg Clin North Am 15(3):293–307

33  Injection/Filler Rhinoplasty 33. Hubbard TJ (1998) Bridge narrowing in ethnic noses. Ann Plast Surg 40(3):214–218 34. Rohrich RJ, Ghavami A (2009) Rhinoplasty for middle Eastern noses. Plast Reconstr Surg 123(4):1343–1354 35. Han SK, Shin SH, Kang HJ, Kim WK (2006) Augmentation rhinoplasty using injectable tissue-engineered soft tissue: a pilot study. Ann Plast Surg 56(3):251–255 36. Carruthers A, Liebeskind B, Carruthers J, Forster BB (2008) Radiographic and computed tomographic studies of calcium

389 hydroxylapatite for treatment of HIV-associated facial lipoatrophy and correction of nasolabial folds. Dermatol Surg 34(suppl 1):S78–S84 37. Coghlan BA, Laitung JK, Pigott RW (1993) A computeraided method of measuring nasal symmetry in the cleft lip nose. Br J Plast Surg 46(1):13–17

 

Suture Lifting Techniques

34

Peter M. Prendergast

34.1 Introduction In the last decade, there has been a dramatic increase in the number of nonsurgical cosmetic procedures performed in the USA [1]. The rise in less invasive procedures reflects the increasing demand for facial rejuvenation that does not require prolonged recovery periods, is low risk, inexpensive, and provides results that look natural. The most commonly performed nonsurgical cosmetic procedures are chemodenervation with botulinum toxins and soft tissue augmentation with dermal fillers such as hyaluronic acid. In addition, several tissue-tightening devices using infrared light, radiofrequency, or combined technologies are available that improve skin laxity by heating the deep ­dermis [2]. None of these modalities, however, address ptosis of deeper tissues including the malar and buccal fat pads and the superficial musculoaponeurotic system (SMAS). In the author’s view, suture facelift techniques currently provide a “better alternative” to nonsurgical tissue-tightening devices and injectable procedures for patients who would benefit from lifting of mild to moderate ptosis, but they do not replace open facelift procedures for those with more severe ptosis or excessive skin laxity. Although suture lifting techniques using a variety of suture systems and designs have been widely adopted, published data on safety, efficacy, and long-term results remain scant [3].

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

They are used as adjunctive measures during ­traditional open procedures [4], as a complement to less invasive open techniques [5], or as closed procedures through minimal incisions or punctures [6]. In an office-based setting, it is most appropriate to perform closed suture lift techniques under infiltrative or regional local anesthesia. This chapter describes the techniques of coned suture lifts, barbed, and nonbarbed suture suspension of the brow, face, and neck through small hidden incisions or punctures.

34.2 Indications Several classifications for facial aging have been proposed that describe senescent changes in the upper, middle, and lower face as well as the neck [7]. Volume changes are usually involutional and occur both in the underlying bony skeleton and the soft tissues [8, 9]. Subtle changes due to volume loss and bony resorption can be addressed using soft tissue augmentation with subcutaneous or preperiosteal injections of fillers or stimulating agents such as poly-l-lactic acid. In the midface, the malar fat pad descends gradually from its normal position over the zygoma. Gravity facilitates this process by providing a vertically inferior vector for tissue that has lost elasticity, underlying structural support, or both [10]. As the fat falls away from the lid–cheek junction, the lower lid appears to lengthen and the infraorbital area above the cheek develops a crescent-shaped hollow or tear trough deformity. The nasolabial fold deepens as the malar fat pad superolateral to it drops. Further inferolateral descent of the malar fat pad accentuates the jowls and flattens the

P.M. Prendergast and M.A. Shiffman (eds.), Aesthetic Medicine, DOI 10.1007/978-3-642-20113-4_34, © Springer-Verlag Berlin Heidelberg 2011

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Fig. 34.1  The aging face. (a) The lateral brow, malar fat, jowls, and neck have become ptotic. The lower lid appears lengthened with hollowing of the tear trough and the nasolabial fold has

deepened. (b) Elevation of soft tissues using sutures improves definition of the neck and jawline, softens nasolabial folds, reduces infraorbital hollows, and lifts the eyes and lateral brow

cheek superiorly. Aging in the lower face and neck begins with accumulation of fat in the jowls and submental area, skin laxity in the neck, and prominent platysmal bands. These changes result in a loss in definition of the jawline, a rectangular-shaped face, and an increase in the cervicomental angle. The rationale for treatment using suture lifts is to reverse the early signs of aging by lifting and suspending tissues that have begun to drop. By repositioning soft tissues in this way, not only are sagging tissues lifted, but volume is also restored in important areas, such as the midface (Fig. 34.1). These techniques are not intended to correct more advanced signs of aging where significant skin laxity is present. Similarly, excessive fatty deposits in the face, submental area, and neck are not improved with suture lifting techniques alone, particularly when the overlying skin is tight. These problems require more aggressive measures such as rhytidectomy and lipoplasty. The ideal candidate for a suture lift has mild ptosis of brow, lateral canthus, malar fat pad, jowls, or neck. Even mild ptosis in these areas can produce a sad or sullen look and lifting by a few millimeters will

improve the countenance to a more pleasing one (Fig.  34.2). Skin laxity should not be excessive and facial volume should be relatively normal. If there is significant skin laxity or the face is too thin, lifting with sutures only without skin excision may lead to excessive bunching or irregularities. Most suitable candidates are 30–45  years old, although the author has successfully treated patients ranging from 27 to 66  years. Older patients requesting suture lifts are often averse to having open facelift procedures, even when it is explained that a more aggressive procedure would provide better results. Patients who previously underwent one or more open facelifts often choose a suture lift rather than repeat surgery in order to avoid general anesthesia and a prolonged recovery period. Patients should have realistic expectations and understand that suture lifting techniques do not replace conventional rhytidectomy. During the initial consultation, the procedure is explained in detail and all potential risks and ­complications are outlined. An instruction leaflet is provided (Table  34.1) and a consent form is signed (Table 34.2).

34  Suture Lifting Techniques

a

393

b

Fig. 34.2  (a) Before. (b) Immediately after suture facelift showing subtle rejuvenation and improvement in jawline definition Table 34.1  Preoperative instructions for suture face and neck lifts PREOPERATIVE INSTRUCTIONS: SUTURE LIFT   1. DO NOT SMOKE for 2 weeks prior to and 2 weeks after surgery. Smoking reduces blood circulation, slows down healing, and may increase complications   2. DO NOT TAKE ASPIRIN or products containing aspirin for 2 weeks prior to or following your scheduled surgery. Aspirin affects your blood’s ability to clot and could increase your tendency to bleed during surgery or during the postoperative period   3. DO NOT TAKE DIETARY SUPPLEMENTS for 2  weeks before and after surgery. These include vitamins, ginger, ginko biloba, garlic, ginseng and fish oils. They may increase your risk of bleeding and bruising during and following surgery   4. DO NOT DRINK ALCOHOL for 5 days prior to surgery. Alcohol may increase your risk of complications such as bruising   5. IF YOU DEVELOP A COLD, COLD SORE, FEVER, OR ANY OTHER ILLNESS PRIOR TO SURGERY PLEASE NOTIFY US   6. WASH HAIR ON THE DAY PRIOR TO SURGERY   7. LEAVE JEWELRY AND VAULABLES AT HOME. Do not wear wigs, hairpins, or hairpieces   8. AVOID WEARING MAKEUP OR FACIAL MOISTURISERS   9. SURGERY TIMES ARE ESTIMATES ONLY. You could be at the clinic longer than indicated 10. HAVE A LIGHT BREAKFAST on the morning of surgery. Your suture lift procedure will be performed under local anesthesia without sedation I HAVE READ AND FULLY UNDERSTAND THE ABOVE ITEMS 1–10 ____________________________ _________________ Patient Signature Date

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P.M. Prendergast

Table 34.2  Consent form for suture lift procedure CONSENT FOR SUTURE LIFT PROCEDURE What is a Suture Lift? A suture lift is a thread lift procedure in which a special thread (e.g. polycaproamide or polypropylene) is passed under the skin, looped around or inserted through fat or other tissue such as the superficial musculoaponeurotic system (SMAS) and retracted back to lift areas of the face or neck. It is minimally invasive, requiring a small incision or puncture, often placed behind the hairline. The procedure is performed under local anesthesia. Suitability for a Suture Lift You will be assessed thoroughly beforehand to determine if you are suitable or not. Typically, patients who are suitable have mild drooping or sagging of cheeks, jowls, neck, or brow and are otherwise in good physical and mental health. If you have more severe sagging, a suture lift might not be appropriate, and you will be advised on alternatives. Procedure A number of markings are made on the treatment area. Then a small incision is placed, usually behind the hairline where it is out of sight, and a stitch is passed under the skin in the fat or under muscle or fascia (layer above muscle). Sometimes a small patch is placed in the incision to secure the sutures. The tissues are gently retracted and the suture is tied, securing the lift. Finally, if present, the skin incision is closed. Special precautions You should not proceed with this procedure if you are pregnant or breast feeding, or if you are allergic to local anesthetic agents. If you have medical conditions or are on certain medications, such as aspirin, steroids or warfarin, treatment may be deferred, so you need to give your doctor your complete medical history. You should avoid taking vitamins and herbal supplements such as Ginko Billoba and St John’s Wort for 2 weeks before treatment. Potential risks and complications of a Suture Lift procedure A small cannula (like a needle) is passed under your skin. As such, there is always a small risk of damage to structures under the skin, including the facial nerve, other nerves and blood vessels, causing facial weakness, numbness or bleeding. Weakness, although extremely rare, may be permanent. Numbness usually resolves or improves over time You may experience some swelling, bruising, and pain following the procedure. As with any injectable or invasive procedure, you may develop an infection, though the chance is low. You will receive a course of prophylactic antibiotics for 1 week following your treatment. Benefits and outcomes of treatment It is usual to notice immediate lifting of the treatment area. You may see some “bunching” of skin near the hairline. This is normal and resolves after about 3–4 weeks. There is a small possibility that the procedure will fail if the suture cuts through the fat and tissue under the skin. Adhering to aftercare instructions will lessen this risk. Benefits of a suture lift will last a variable period of time, depending on the individual, and no guarantee of results or longevity of results is given It is usually possible to reverse or repeat the procedure if required. Alternatives to a Suture Lift procedure Alternatives to a suture Lift procedure include noninvasive skin tightening using infrared light or radiofrequency, other suture lift procedures, a surgical face lift procedure, or indeed no treatment at all. Initial: ___________________ CONSENT FOR SUTURE LIFT PROCEDURE Please answer the following questions by ticking the appropriate box Have you previously undergone a suture lift or face lift procedure? If yes, specify:________________________ Do you have any known allergies? If yes, specify:________________________ Are you currently taking any of the following medications: warfarin, aspirin, palvix, steroids? Are you pregnant or breast feeding? Have you previously completed a New Patient Data Form at Venus Medical Beauty? Please state if you have any other medical conditions, allergies, or are taking any medications not previously outlined in the New Patient Data Form:

Yes

No

Yes

No

Yes Yes Yes

No No No

34  Suture Lifting Techniques

395

Table 34.2  (continued) I have read the information on the suture lift procedure outlined on this form and fully understand the nature of treatment, all clinical implications and potential risks involved. I have had the opportunity to ask questions to my satisfaction. I understand that it is my right to withdraw consent to treatment at any time. I consent to being photographed prior to treatment and understand that this photograph will remain the property of Venus Medical Beauty and may be used for educational or academic purposes. I willingly accept and consent to treatment with the suture lift procedure. Patient signature________________

Date____________________

PRINT________________________ OFFICIAL USE ONLY I have explained to the patient the Suture Lift procedure. I have outlined the expected benefits of treatment, as well as any potential risks, complications and side-effects of treatment. I have given the patient the opportunity to read the literature pertaining to this treatment and clarified any further questions and queries where they existed. I have explained alternatives to treatment, including no treatment. Doctor signature_________________

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34.3 Suture Types and Techniques The variety of sutures and techniques available today reflects the origins of suture lifting. Suture lifts evolved not from one initial method but from a number of different techniques developed by pioneers in countries on several continents, including Russia and the USA [11]. Some of the early suture lifts used nylon or tendons to loop around tissues like a sling and suspend them in an elevated position [12, 13]. Later, polypropylene sutures with tiny projections called barbs or cogs were developed that “spear” subcutaneous fat or fascia to compress tissues, or lift them in a predetermined vector [14]. Sutures currently used for suture lifting techniques are made of nonabsorbable material such as polypropylene and polytetrafluoroethylene, or  absorbable material including polydioxanone and polycaproamide. Barbed sutures are still in widespread use today, although newer designs such as coned sutures may provide a more secure and stable lift and are more resistant to structural damage in human tissues [15]. Nonbarbed suture lifts, such as those using braided absorbable polycaproamide, may cut through tissues at the point of maximal tension unless deeper, tougher tissues such as the SMAS are lifted, and anchored to stable nonmoveable structures such as periosteum. These techniques therefore require a thorough knowledge of facial anatomy to ensure appropriate lifting without injury to underlying nerves. A classification for suture lifting techniques is presented in Table  34.3. Although a number of techniques are available, there is a lack of evidence that one technique or system is superior to the others. As such, ­personal

experience, training, and perhaps even ­marketing ­influence the decision to adopt one method over another. The author uses absorbable nonbarbed sutures for the upper and lower thirds of the face, coned sutures for the midface, absorbable barbed sutures or coned sutures for the brow, and either absorbable or coned sutures for the neck. Several hands-on workshops and preceptor courses are available internationally [16].

34.4 Barbed Sutures Sutures with tiny hook-like projections cut into their long axes are referred to as barbed sutures. The function of the barbs is to grasp tissue, distribute forces along the length of the barbed portion of the suture, and elevate or compress tissue in the direction of the barbs (Fig.  34.3). Sulamanidze invented barbed sutures for facial rejuvenation in 1998. His Aptos threads (APTOS, Moscow, Russia) are nonanchored bidirectional barbed polypropylene sutures of various lengths and sizes that are inserted subcutaneously through an 18-gauge spinal needle. Once in place, the tissues are fashioned around the sutures, creating a lifting effect perpendicular to the long axes of the sutures. The ends of the sutures are then trimmed and pushed under the skin. Happy Lift Double Needle sutures (Promoitalia International Srl, Rome, Italy) are also polypropylene sutures with bidirectional barbs, but with straight needles swaged to either end. This obviates the need for a spinal needle for placement. The barbs on these sutures are forked, presumably to improve purchase on tissues.

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Table 34.3  Classification for closed suture lifts Type Barbed suture lifts

Subtype Bidirectional barbed

Nonanchored

Anchored

Unidirectional barbed

Nonbarbed suture lifts

Subcutaneous lift

SMAS lift Coned suture lifts

Suture 1. Aptos suture (APTOS, Moscow, Russia) 2. Happy Lift Revitalizing threads (Promoitalia Int Srl, Rome, Italy) 1. Woffle’s sutures (Singapore) 2. Articulus (previously Surgical Specialties Corp., Reading, PA, USA) 3. Happy Lift Double Needle (Promoitalia Int Srl, Rome, Italy) 4. I-Lift Tensor Threads (Argentina) 1. Isse Endo Progressive Facelift suture (KMI Inc., Anaheim, CA, USA) 2. Contour Threads (previously Surgical Specialties Corp., Reading, PA, USA) 3. Happy Lift™ Ancorage (Promoitalia Int Srl, Rome, Italy) 1. Curl lift using polypropylene 2. Malar fat pad sling using ePTFEa (Gore-Tex® Inc., Flagstaff, AZ, USA) 1. Serdev technique using polycaproamide 1. Silhouette suture (Silhouette Lift, Kolster Methods Inc., Corona, CA, USA)

Expanded polytetrafluoroethylene

a

Fig.  34.3  Barbed sutures for facial rejuvenation. (a) Bidirectional convergent barbed sutures. The smooth central portion suspends the malar fat. (b) Inverted bidirectional barbed suture anchored at smooth portion in temporal fascia. (c)

Nonanchored (free-floating) barbed sutures. These sutures compress tissues to create volume and a lift that is perpendicular to the long axis of the suture

Anchored bidirectional barbed sutures have also been described that elevate soft tissues and anchor them to stable temporalis or mastoid fascia [17]. Unidirectional barbed sutures include the Isse Endo Progressive Facelift suture (KMI Inc., Anaheim, CA, USA) developed by Isse [18] and Contour Threads (Surgical Specialties

Corp., Reading, PA, USA) developed by Ruff [19]. These polypropylene sutures have unidirectional barbs that lift and suspend tissues by securing the proximal ends to the deep temporal fascia via small incisions behind the ­hairline in the temple. Although Contour Threads are no longer in distribution, they were used widely [20–22].

34  Suture Lifting Techniques

397 A C Skin { Subcutaneous fat

B A

D

Temporalis ms. B

Periosteum C G

DTF

STF

D Skull

F SMAS

H E

G

F

J Platysma

Fig.  34.4  Suture lift of SMAS (moveable) to deep fascia or periosteum (nonmoveable) through minimal incisions (red dots). The red area represents a danger area at the zygomatic arch over which the facial nerve passes (0.8–3.5 cm from external acoustic meatus). Cross sections show suture path between points. A → B under STF, A → C above STF, C → D under STF, D → B under

DTF and TM, E → F subcutaneous and catching SMAS at level of arch, E → G subcutaneous, F → G under TM, J → H subcutaneous and catching platysma at J and mastoid fascia at H. STF superficial temporal fascia, TM temporalis muscle, DTF deep temporal fascia

Happy Lift Ancorage sutures (Promoitalia International Srl, Rome, Italy) provide a similar method of lifting to Contour Threads, although there is a greater barb density on the Italian sutures and the barbs are forked. Happy Lift sutures are available in nonabsorbable polypropylene and slowly absorbable polydioxanone.

soft tissues include expanded polytetrafluoroethylene (Gore-Tex®) and polycaproamide (Polycon). For midface rejuvenation, Sasaki describes his technique using permanent CV-3 expanded polytetrafluoroethylene (Gore-Tex Inc., Flagstaff, AZ, USA) [4]. Serdev improved upon Guillemain’s original and Mendez-Florez’s revised curl lift techniques by using slowly absorbable nonbarbed semi-elastic polycaproamide sutures to lift moveable tissues and secure them to stable structures such as deep fascia or periosteum [25–27]. Using curved suture-passing needles of various lengths, the braided antimicrobial sutures are weaved through the superficial temporal fascia in the temple, the SMAS of the face, and platysma in the neck. These relatively fibrous tissues are elevated and held in place by anchoring the proximal ends of the sutures to the deep temporal fascia, periosteum, or mastoid fascia (Fig. 34.4). There are certain ­advantages of Serdev’s techniques. Unlike some less secure suture suspension lifts that elevate only subcutaneous fat, this technique requires that the SMAS is resuspended. The braided sutures also yield to movement due to their

34.5 Nonbarbed Sutures Bukkewitz described the first suture suspension lift for cosmetic enhancement in 1956 using a strip of nylon to elevate a ptotic buccolabial fold [12]. In 1970, Guillemain described the “curl lift,” a simple technique to suspend tissues using nylon or tendons inserted with a Reverdin needle [13]. Erol and Hernandez-Perez described simplified suture suspension techniques to lift the brow using nylon and polypropylene, respectively [23, 24]. Although these procedures are quick and simple, results may be short-lived since the smooth inelastic polypropylene suture tends to cut through subcutaneous fat at the point of lifting. Other nonbarbed sutures used to lift

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a

b

Fig.  34.5  Coned suture lift. (a) Dyed Silhouette sutures are also available showing poly-l-lactic acid cones and knots along its length. (b) Coned sutures pass from a temporal incision into the malar fat to lift the midface. The sutures are anchored to a

patch of polypropylene mesh sutured to the deep temporal fascia. In the neck, Silhouette sutures are passed toward the midline from a retroauricular incision

elasticity. The procedure is performed through tiny stab incisions only without the need for skin closure. Polycaproamide absorbs slowly over 2–3  years, an obvious advantage for suture lifting where subsequent procedures are likely as the aging process continues.

The rationale for using cones instead of the commonly used barbs of previous suture designs is that the biomechanics of the cone design are inherently stronger than barbs. Secondly, the tensions applied to barbs are prone to linear shredding where the barbs meet the body of the suture. Finally, the cones incite an inflammatory response around the sutures, anchoring them in place, before they absorb over 8–10  months. These coned sutures are currently marketed as the Silhouette Suture (Silhouette Lift; Kolster Methods Inc., Corona, CA, USA) and presented as a clear 3-0 polypropylene suture with eight cones along its length, held equidistant to one another by regularly spaced knots. A newer

34.6 Coned Sutures Isse developed a polypropylene suture with regularly spaced knots and cones along its length (Fig.  34.5). The cones are made of poly-l-lactic acid and are held in place along the suture by regularly spaced knots.

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399

blue dyed Silhouette suture with six cones is now available. Dyed sutures are easy to find if attempts are made to retighten the suture by opening the old incision site in the scalp. There is a 20.3  cm 20-gauge straight needle swaged to the distal end of the suture and a 26  mm half-circle needle to the proximal end. Included with Silhouette Sutures are 2.0 × 0.5 cm polypropylene mesh patches for anchorage to deep fascia in the temple. In appropriately selected patients, these sutures elevate the malar fat pad, jowls, and neck through minimal incisions under infiltrative local anesthesia and allow a quick return to normal activities. Elevating the midface, in particular, provides noticeable rejuvenation by restoring the beauty triangle

34.7 Anatomical Considerations A thorough knowledge of the anatomy of the SMAS, superficial and deep fascias, and compartments of the face as well as the motor and sensory nerves is a prerequisite for successful and safe suture lifting. The closed suture lifting techniques described here require passage of straight needles swaged to sutures or curved suturepassing needles through the tissues of the face and neck. Semi-sharp needles are passed blindly in the subcutaneous, sub-SMAS, and supraperiosteal planes in the temple, forehead, midface, and neck. Important anatomical considerations for suture lifting include the following: 1. In the temple behind the hairline, the temporalis muscle is covered with a tough shiny white deep temporal fascia (DTF). The fascia attaches to the periosteum along the superior temporal crest line. 2. The superficial temporal fascia (STF) lies loosely on the DTF and can easily be lifted from it to pass sutures in the plane between them. The STF is continuous with the SMAS in the face and the galea medial to the superior temporal crest. 3. The STF splits near the temporal hairline to envelop an intermediate temporal fat pad, temporal branches of the facial nerve, and frontal branch of the superficial temporal artery. A danger zone exists over the zygomatic arch and between the leaves of the STF toward the eyebrow (Fig.  34.6). The temporal branch of facial nerve is usually described as having a consistent course from 0.5 cm below the tragus to 1.5  cm above the lateral brow [28]. More accurately, the nerve can be found between 2.1 and 4  cm above the bony lateral canthus [29]. In this

Fig. 34.6  Facial danger zone occupied by the temporal branch of the facial nerve. This danger zone (red) extends from the inferior border of the zygomatic arch to a line above the bony lateral canthus. The zone curves anteriorly as shown from the lower line to the upper one. Within this zone, the temporal branch of the facial nerve is vulnerable to injury where it passes superficially in the superficial temporal fascia

area, needles should pass only superficially in the subcutaneous plane, or else deep to the STF just above the DTF. The facial nerve passes over the zygomatic arch between 0.8 and 3.5  cm from the external acoustic meatus. 4. Ghassemi [30] describes two variations of SMAS architecture. Type I SMAS consists of a network of small fibrous septae that traverse perpendicularly between fat lobules to the dermis and deeply to the facial muscles or periosteum. This variation exists in the forehead, parotid, zygomatic, and infraorbital areas. Type II SMAS consists of a dense mesh of collagen, elastic, and muscle fibers and is found medial to the nasolabial fold, in the upper and lower lips. Although extremely thin, type II SMAS binds the facial muscles around the mouth to the overlying skin and has an important role in transmitting complex movements during animation. Over the parotid gland, the SMAS is relatively thick and can

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P.M. Prendergast Table 34.4  Materials for coned suture lift Skin markers Sterile drapes Sterile towels Lidocaine 2% with epinephrine 1:200,000 0.9% sodium chloride 10 mL syringe Needles: 21 G, 27 G #15 blade 4-0 sutures (e.g., Miralene) Sterile gauze 10 × 10 cm

Silhouette sutures Polypropylene mesh 0.5 × 2 cm Scalpel Skin retractor Toothed forceps Artery forceps Needle holder Scissors Monopolar diathermy unit, cables, pencil, and grounding pad

34.8 Materials

Fig. 34.7  Path of the greater auricular nerve in the neck. This danger area lies 6.5 cm below the external auditory meatus, in the middle of sternocleidomastoid and parallel to the external jugular vein. The greater auricular nerve is prone to injury as it passes through this danger zone behind the border of platysma

be grasped using curved needles at the level of the zygomatic arch close to the external acoustic meatus. 5. During brow suture lifts, the needle should stay superficial to avoid the deep branch of the supraorbital nerve as it courses medial to the temporal crest line. The medial brow lies in a danger zone where the supraorbital and supratrochlear nerves exit their respective foramina or notches. 6. At a point 6.5 cm inferior to the external auditory canal, the greater auricular nerve can be found half way between the posterior and anterior borders of sternocleidomastoid [31]. Below the ear it divides into anterior and posterior branches. A danger zone can be considered as an oblong, 2  cm wide and 6 cm long, with its centre on a point 6.5 cm below the external auditory meatus oriented parallel to the external jugular vein (Fig. 34.7). Suture suspension of the platysma for neck lifting should avoid this area.

Suture lifting techniques are usually performed under infiltrative local anesthesia and can easily be performed in an office-based setting using sterile technique. The materials and instruments required depend on the technique and sutures employed. Lifting the mid and lower face using Silhouette sutures (Silhouette Lift; Kolster Methods Inc., Corona, CA, USA) requires a small incision in the temporal scalp and placement of a polypropylene anchor patch on the deep temporal fascia. Monopolar diathermy, skin retractors, and instruments for suturing and skin closure are useful for suture lifting techniques that require incisions and dissection in the scalp. A list of materials required for suture lifting using coned Silhouette sutures is provided in Table 34.4 and shown in Fig. 34.8. For techniques using nonbarbed sutures, the entire procedure can be performed through stab incisions only without the need for skin closure. The materials required for suture suspension using polycaproamide sutures are listed in Table 34.5 and shown in Fig. 34.9. Various sutures and techniques can be used to lift the brow. The method described here employs absorbable bidirectional barbed sutures to elevate the dermis of the lateral brow with anchorage under the galea at the hairline (Fig. 34.10).

34.9 Technique The suture lifting techniques described here use subcutaneously inserted coned or barbed sutures and suture suspension of the SMAS or platysma with

34  Suture Lifting Techniques

401

Fig. 34.8  Materials for lifting with Silhouette sutures

Table 34.5  Materials for nonbarbed suture suspension lift Sterile drapes

Polycaproamide sutures: USP #2&4 Lidocaine 2% with epinephrine Scalpel with #11 blade 1:200,000 0.9% sodium chloride Curved suture-passing needles 10 mL syringe Artery forceps Needles: 30G, 27G, 21G Scissors Sterile gauze 10 × 10 cm Sterile towels

absorbable braided polycaproamide sutures. For brow elevation, the author uses absorbable barbed sutures. Coned sutures placed in the thin tissues of the forehead are more likely to be visible or palpable and lifting the galea superiorly using nonbarbed sutures does not provide satisfactory elevation of the brow. Coned

suture lifts are appropriate when facial volume is normal and the malar fat pad has become ptotic. The techniques of brow lift using absorbable barbed sutures, midface, lower face, and neck lift using coned sutures, and SMAS lift for temporal, lower face, and neck lift using nonbarbed sutures will now be described.

34.10 Brow Lift with Barbed Sutures The aim of suture lifting of the brow is to provide a pleasing arch to the brow, with the highest point in line vertically with the lateral limbus or just lateral to this. To make a preoperative assessment, place the thumb 1 cm above the lateral third of the brow and lift 0.5–1.0 cm (Fig. 34.10). In older patients with dermatochalasis, manual elevation of the brow may cause unsightly creasing and “draping” of upper eyelid

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Fig. 34.9  Materials for SMAS suture suspension using polycaproamide sutures

skin. These patients may require blepharoplasty or a forehead lift. Two weeks prior to brow suture lifting, chemodenervation of lateral fibers of orbicularis oculi with botulinum toxin should be performed to alleviate the depressor action of this muscle on the lateral brow (Fig. 34.11).

A bidirectional convergent barbed polydioxanone suture (Happy Lift Revitalizing, Promoitalia, Srl, Rome, Italy) with a smooth central portion and two needles swaged to either end is used for the brow lift (Fig.  34.12). The proposed path of the suture is marked on the skin from the scalp behind the hairline

34  Suture Lifting Techniques

403

a

b

Fig.  34.10  Suture brow lift. (a) Materials for brow lift using barbed suture. (b) Close-up of convergent bidirectional barbed suture with smooth central portion (Happy Lift Revitalizing Double Needle, Promoitalia Srl, Rome, Italy). (c) Preoperative patient. The brow is elevated manually to determine the appropriate amount of lifting required. (d) Markings are made over the proposed path of the sutures from the brow to the hairline. White marker defines the superior temporal crest line. (e) Lidocaine with epinephrine is infiltrated subcutaneously along the marked areas. (f) The hydrotomy created allows easier passage of the needle in the superficial subcutaneous plane. (g) Needle punctures are made in the tail of the brow and more medially at the point where the brow should be highest. Stab incisions using a #11 blade are also made at the superior limits of the markings in the hairline. (h) One of the needles swaged to the suture is passed intradermally from the lateral to medial punc-

c

ture in the brow. (i) The needle then passes from the medial puncture, subcutaneously through the forehead to the medial incision at the hairline. The needle is pulled through so that the central smooth portion of the suture is situated in the brow between the two punctures. (j) The second needle at the other end of the suture passes from the lateral puncture in the brow to the lateral incision at the hairline. (k) The two suture ends at the hairline are gently lifted to elevate the brow to the desired height, or slightly higher to allow for minimal relaxation over the first 1–2 weeks. The barbs on the sutures grasp the subcutaneous tissues and hold the brow in an elevated position. (l) Any dimpling at the brow punctures is gently released using a needle or artery forceps to free the dermis. (m) A curved suture-passing needle is used to bring the suture end from the medial incision, under the galea (or periosteum) to the lateral incision where it is tied for anchorage

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d

e

f

g

h

i

j

k

Fig. 34.10  (continued)

34  Suture Lifting Techniques

405

l

m

Fig. 34.10  (continued) Fig. 34.12  Barbed suture used for brow lift. The suture lifts the dermis of the brow and suspends it via the anchored convergent barbs to the galea aponeurotica above the hairline

Fig.  34.11  Chemodenervation of lateral depressor fibers of orbicularis oculi. A finger placed at the correct injection site should be pulled inferiorly when the patient is asked to forcefully close the eyes, but should not rise when the patient is asked to raise the eyebrows. This avoids inadvertently denervating fibers of frontalis, which act to elevate the brow. One or more injections can be made in the orbicularis 2 weeks before a brow lift to alleviate the depressor action of this muscle

to the lateral third of the brow. About 10  mL of ­lidocaine with epinephrine (1:200,000) diluted with 10 mL of normal saline is drawn into a 20 mL syringe and infiltrated subcutaneously along the path of the marked lines and in the lateral brow. Although anesthesia of this area could be achieved with supraorbital nerve blocks, the hydrotomy achieved with infiltrative anesthesia allows easier passage of the needle in the subcutaneous tissues. In the scalp, at the proposed point of anchorage of the suture, infiltration is made deep to the galea to the level of the periosteum. Two stab incisions are made in the scalp in line with the desired vector for lifting the lateral brow. Using a 16-gauge needle, a puncture is made through the skin at the tail of the brow and in the hair of the brow at its highest point. The first needle, with suture attached, is passed from the tail of the brow, intradermally, to exit at medial puncture. The smooth central portion of the suture will come to lie in the dermis of the brow. Placement below the dermis in the subcutaneous tissue has a propensity to cut

406

through with early failure of the lift. The same needle then re-enters the medial puncture and passes subcutaneously along the marked path to exit from the incision in the scalp. The second needle passes from the tail of the brow, subcutaneously to exit the incision in the scalp. Care should be taken to stay in the superficial tissues above the lateral brow to avoid the temporal branches of the facial nerve. The needles are cut from the sutures so that two barbed suture ends exit from the scalp incisions. Since the barbs are convergent toward the smooth portion of the suture in the lateral brow, the lateral brow is lifted by gentle traction on the suture ends, and held in place by the barbs in the subcutaneous tissue. However, anchorage of the proximal cut ends of the suture under the galea further secures the lift and prevents slippage. A curved suture-passing needle is passed deep to the galea from one incision to the other and the suture ends are brought through the same incision and tied.

34.11 Temporal Lift with Nonbarbed Sutures Suture lifting in the temporal area provides a subtle but important rejuvenation in the upper face by lifting the tail of the eyebrow, the lateral canthus, and the upper cheek (Fig. 34.13). In the periorbital area, elevation of soft tissues by 2–3 mm provides noticeable rejuvenation. Markings are made at the proposed incision points. The first is along a line drawn perpendicular to the tail of the eyebrow, just behind the temporal hairline. A second point is made just behind the hairline 4–5 cm inferior to the first point. Two further points are made above the first points in line with the lifting vectors. One of these points should be along the superior temporal crest line where the deep temporal fascia attaches to periosteum. The hair is tied or retracted to expose the skin at the marked points. After skin preparation and sterile draping, local anesthesia using lidocaine 1–2% with 1:200,000 adrenaline is injected along the proposed path of the suture: subcutaneously between the lower two points, on the periosteum between the upper two points, and under the superficial temporal fascia and above the deep temporal fascia between each upper and lower point. The superficial temporal fascia is a continuation of the galea over the frontalis muscle and the SMAS of

P.M. Prendergast

the middle and lower thirds of the face. Stab incisions using a #11 blade are made at the marked points. The curved needle is passed from the upper medial incision to the lower medial incision, under the superficial temporal fascia but above the deep temporal fascia. To find this plane, lift a tuft of hair above the path of the needle and pass the needle deeply. There should be a thick layer of tissue covering the needle following passage, but it should not be so deep that the patient’s head rocks when the needle is moved. This indicates that the needle has passed under the deep temporal fascia. Once the needle tip exits the inferior point, a USP #2 polycaproamide suture is passed through the eye of the needle and the needle is withdrawn. Next, the needle is passed in the superficial subcutaneous plane from the lower lateral incision to the lower medial incision and the suture end is threaded through the needle’s eye and brought to the lower lateral incision. The suture is above the superficial temporal fascia along this line. Then the suture is brought from the lower lateral to the upper lateral incision under the superficial temporal fascia as before. Finally the needle is passed into the upper medial incision, taking a bite of periosteum and deep temporal fascia along the superior temporal fusion line, and exits from the upper lateral incision. The suture is brought from this incision to the upper medial one so that both ends exit from the same incision. The suture ends are lifted gently to elevate the superficial temporal fascia (temporal SMAS) along the hairline, and elevate the tail of the brow and upper face. The suture is tied and the incision points, if inverted or tethered down, are released using the tip of a mosquito. The incisions heal quickly by secondary intention. A small amount of bunching of skin is usual along the hairline but this contracts and disappears in 1–2 weeks. This technique provides an instant rejuvenation, particularly around the eyes.

34.12 Midface Lift with Coned Sutures The desired lifting vectors are marked out on the skin with the patient in the sitting position (Fig.  34.14). Depending on the desired effect, these can be superolateral or more vertically oriented, but always converge in the temple where the incision is made and the sutures are anchored. The inferior points mark the exit sites for

34  Suture Lifting Techniques

a

407

b

c

Fig.  34.13  Upper face (temporal) SMAS lift using slowly absorbable polycaproamide sutures. The SMAS is called the superficial temporal fascia (STF) in the temporal area and the galea aponeurotica medial to this over the forehead. (a) Four points are marked as shown and stab incisions using a #11 blade are made. One of the superior incisions (b) is made along the superior temporal crest line (red dots). (b) The curved needle is passed under the STF (above the deep temporal fascia) from point B to A. (c) A USP#2 or #4 polycaproamide suture is passed through the eye of the needle and the suture is brought back from point A to B. (d) The needle is passed from point C to A in

d

the superficial subcutaneous plane (above STF) and the suture end is threaded through. (e) The suture is brought to point D under STF as before. (f) Now both ends of the suture are exiting at the upper incisions. (g) The needle is passed deep into point B until it reaches periosteum. (h) A deep bite is taken, underneath the deep temporal fascia, and the needle receives the suture end at point D. (i) The needle is retracted so that both ends exit from point B. The sutures are gently lifted and tied. This lifts the STF, tail of the brow, and upper face. The suture is cut and buried by applying traction to the puncture site with the tip of an artery forceps

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e

f

g

h

Fig. 34.13  (continued)

34  Suture Lifting Techniques

i

Fig. 34.13  (continued)

the needles and start about 1 cm lateral to the midpoint of the nasolabial fold with 1.5 cm between each point. The points should not be made below a line drawn from the lobule of the ear to the modiolus. Sutures passing below this line could disrupt with movement of the mandible during animation and mastication. After skin preparation and draping, the marked areas are infiltrated with 2% lidocaine with 1:200,000 epinephrine. A 3 cm incision is made in the temporal area and diathermy is used for hemostasis. The superficial temporal fascia is exposed, grasped with an artery forceps, and opened to expose the white shiny deep temporal fascia. A small 1 cm × 0.5 cm patch of polypropylene mesh is placed on the deep temporal fascia and sutured in place with a 4-0 nonabsorbable suture. The first Silhouette suture is measured externally over the cheek to determine how many cones are needed to run the length of the malar area. If all of the cones are left on the suture, some of the proximal ones may be visible under the thin skin of the temple area, or they may catch on the superficial temporal fascia when the suture is retracted. The author usually cuts three to four cones from the distal end of the suture after they exit at the inferior points. If a suture with only six cones is used, most or all of them can be left on the suture. The Silhouette suture should pass in the deep subcutaneous plane above the superficial temporal fascia toward the lower exit points. If the needle penetrates the superficial temporal fascia, the facial nerve is at risk of injury

409

where it lies between the two layers of superficial temporal fascia after it splits to envelop the nerve and intermediate temporal fat pad lateral to the tail of the eyebrow. Some physicians pass the needle below the superficial temporal fascia first, and then redirect the needle to come superficially into the subcutaneous plane at the level of the temporal hairline. However, it is easier to start the needle passage in the correct plane above the superficial temporal fascia under direct vision at the temporal incision and continue into the malar fat pad in the same plane. As the needle is passed along its course, the nondominant hand gently grasps the tissues over the needle as it passes through the temple and then malar fat pad. A blunt trocar, provided by the suture company, can be used to facilitate atraumatic passage of the needle through the tissues before emerging from the skin. If the suture passes too superficially it may catch the dermis and lead to irregularities. The needle should exit the skin at the marked points perpendicularly to avoid catching the dermis and dimpling. The straight needle is pulled through until the cones begin to emerge from the skin. At this point, one or more cones can be cut from the suture as outlined above, making sure not to pull through any cones that are to remain on the suture. The suture is cut just distal to one of the knots and retracted toward the temporal incision so that the lifting effect can be assessed. If there are skin irregularities or dimples along the length of the suture, these can usually be ironed out by gentle massaging of the overlying skin from proximal to distally as the proximal end of the suture is held firmly in the other hand. The proximal half-circle needle is first passed through the superficial temporal fascia at the incision and then the deep temporal fascia and attached polypropylene mesh. The suture is not tied until all of the other Silhouette sutures have been placed. Usually four sutures are placed in the midface to lift the malar fat pad and jowls. Once all of the sutures are in place, the half-circle needles are cut from the proximal ends and the suture ends are gently lifted. Minimal tension is required to lift the soft tissues and improve the contours of the face. Each suture is tied to its neighboring suture over the mesh and the incision is closed in two layers. This suture lift rejuvenates by lifting the jowls and improving the shape of the face (Figs. 34.15 and 34.16). Although the lift alone softens the nasolabial folds and oral commissures, combining the suture lift with fillers in these areas provides synergy and improves the results further (Fig. 34.17).

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b

c

Fig. 34.14  Midface lift using Silhouette sutures. (a) The patient is marked in the sitting position. The inferior points start about 1 cm lateral to the nasolabial fold. Subsequent points are spaced 1.5 cm apart and should stay above an imaginary line from the lobule of the ear to the modiolus. (b) With the patient in the supine position, skin preparation of the face and scalp with chlorhexidine is performed and the procedure site is isolated with sterile drapes. (c, d) Local anesthetic solution is infiltrated along the marked sites in the scalp and face. (e) A 2–3 cm incision is made in the temporal area behind the hairline where the vector lines converge. Diathermy is used for hemostasis. (f) The superficial temporal fascia is grasped and opened. (g) The shiny white deep temporal fascia is exposed. (h) A 1 × 1.5 cm piece of polypropylene mesh is cut and placed in the wound on the deep temporal fascia. (i) The mesh is sutured to the deep temporal fascia using a 4-0 nonabsorbable suture. (j) The plane through which the suture needle will pass is identified by grasping the superficial temporal fascia (STF) with an artery forceps. The needle and suture pass above the STF in the subcutaneous tissue. (k) The Silhouette suture is placed over the face to measure how many cones will span the malar fat pad and midface without extending into the upper face. This determines how many cones,

if any, should be excised from the distal end of the suture after placement. (l) The straight needle swaged to the suture is passed just superficial to the superficial temporal fascia (STF) at the temporal incision, and through the substance of the cheek to exit at the first of the marked points. The STF splits into two leaves just inferior to the hairline and the temporal branch of the facial nerve travels through its layers. Staying superficial to the STF avoids inadvertent injury to the nerve. (m) The needle tip should be made to exit the skin perpendicularly to avoid dimpling when the suture is retracted. (n) Care should be taken to ensure the suture has not entered the dermis along its path from the temporal incision to the midface. This is seen as irregularities or dimpling over the needle. (o) The Silhouette suture is slowly pulled through the midface until the cones emerge from the inferior puncture. A number of cones (usually two) can be cut from the suture at this time as required. The suture is then cut distal to one of the knots. (p) The curved needle at the proximal end of the suture is passed through the STF and then the polypropylene mesh and deep temporal fascia. Each pair of neighboring suture ends are gently retracted to lift the malar fat pad and tied to one another, suspending the tissues of the midface. The incision is closed in two layers

34  Suture Lifting Techniques

411

d

e

f

g

h

i

Fig. 34.14  (continued)

412

P.M. Prendergast

j

k

l

m

o

n

Fig. 34.14  (continued)

34  Suture Lifting Techniques

p

413

34.13 Lower Face Lift with Nonbarbed Sutures (Fig. 34.17) Lower facelift using absorbable nonbarbed polycaproamide sutures improves the definition of the jawline and enhances the beauty triangle by changing the shape of the face from one that is rectangular to a more heartshaped one. This is particularly effective when soft tissue augmentation with injectable fillers is performed in the midface at the same time (Fig. 34.18). To lift the jowls, the dermal extensions of the SMAS over the zygomatic arch are grasped and suspended using an absorbable nonbarbed suture anchored to the temporalis muscle above the ear.

Fig. 34.14  (continued)

a

b

Fig. 34.15  (a–c) Before. (d–f) After suture lift with coned (Silhouette) sutures

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c

d

e

f

Fig. 34.15  (continued)

34  Suture Lifting Techniques

a

c

415

b

d

Fig. 34.16  (a–c) Before. (d–f) After Silhouette suture lift and hyaluronic acid fillers in the nasolabial folds and oral commissures

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P.M. Prendergast

e

f

Fig. 34.16  (continued)

Three points are marked: two above the ear in the hairline and one just below the zygomatic arch in front of the lobule of the ear. Between the upper two points, the temporalis muscle can be felt when the back teeth are clenched. Lidocaine with epinephrine is infiltrated below the temporalis muscle above the ear and in the subcutaneous plane between all three points. Stab incisions are made at the three points with a #11 blade. To avoid dimpling after the suture has been placed, the tip of an artery forceps is inserted into the incision below the zygomatic arch and passed through the entirety of the dermis. A curved needle is passed subcutaneously from the upper anterior incision toward the lower incision. At the level of the zygomatic arch, a deeper bite is taken to catch the SMAS extension. It is important to stay within 8  mm from the external acoustic meatus at this level to void injury to the facial nerve. The nerve always passes over the zygomatic arch at least 8 mm anterior to the external acoustic meatus, and usually 2.5 cm from it [29]. The needle immediately comes

superficial and exits through the lower incision. The suture end is passed through the eye of the needle and the needle is withdrawn to the upper anterior incision. A similar maneuver is made to pass the suture end from the lower incision to the upper lateral incision, except that the suture passage is slightly more anterior, ­creating a figure-of-eight with the first part of the suture. The needle then passes deeply from the upper lateral incision under the temporalis muscle and fascia and exits the anterior incision. In the correct position deep to the muscle, any movement of the needle should rock the patient’s head. The suture end is brought to the upper lateral incision where the two ends can be lifted gently and tied. Lifting the SMAS extension improves jowl and jawline definition and can even improve the neck. Any dimpling or inversion of skin at the puncture sites is released using the tip of an artery forceps. Some bunching of skin in front of the ear and near the hairline is normal and smoothes out over 1–2 weeks.

34  Suture Lifting Techniques

417

a

b

c

d

e

f

Fig. 34.17  Suture suspension of the SMAS for lower face lift. (a) Local anesthesia is infiltrated subcutaneously in front of the ear and under the temporalis muscle and fascia above the ear. (b) Three stab incisions are made at points E, F, and G. (c) A mosquito is used to penetrate the full thickness of the dermis at point E to prevent dimpling following suspension of the tissues. (d) The curved needle is passed in the subcutaneous plane from point F toward point E. At the lower border of the zygomatic arch a deeper bite is taken to catch the SMAS extension. (e) The needle is advanced superficially and exits from point E. A USP#2 or USP#4 polycaproamide suture is threaded through the eye of the needle. (f) The needle is

withdrawn. (g) The needle is passed subcutaneously from incision G to point E. (h) The suture end is passed through the tip of the needle. (i) The needle is withdrawn so that a sling around the SMAS is created. (j) To anchor the suture superiorly, the needle is passed under the deep temporal fascia above the ear from point G to point F. Moving the needle in the correct plane should move the patient’s whole head. (k) The suture end is passed through the tip of the needle and the needle is withdrawn. (l) Both ends exit from the incision G. Lifting the sutures lifts the patient’s jowls and even neck as the SMAS is suspended. The suture is tied. (m) The incisions are lifted with the tip of an artery forceps to bury the knot

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g

h

i

j

k

l

m

Fig. 34.17  (continued)

34  Suture Lifting Techniques

a

419

b

Fig. 34.18  (a) Before. (b) After lower face lift using nonbarbed suture suspension technique, combined with soft tissue augmentation of the cheeks with calcium hydroxylapatite (Radiesse)

a

Fig. 34.19  Nonbarbed neck lift using absorbable polycaproamide sutures. (a) Local anesthetic is infiltrated superficially along lines H to J. An incision using a #11 blade is made behind the ear (H) and over the anterior border of the sternocleidomastoid muscle (J). (b) A curved needle is passed through incision H to catch the mastoid fascia before passing subcutaneously toward J. Just before exiting at j, the needle takes a deeper bite to catch the platysma muscle (SMAS). (c) The needle exits and a USP#2 polycaproamide absorbable suture is passed through the tip. (d) The needle is retracted through point H. (e) The

b

needle is advanced again through the same puncture, taking a serpentine course through the superficial tissues, and exits at the distal incision. (f) The suture end is passed through the needle. (g) The needle is retracted again so that both suture ends exit at the retroauricular incision. (h) Traction on the sutures lifts the neck and improves the cervicomental angle. Any dimpling at the inferior incision is released with an artery forceps. (i) The sutures are tied and cut. Slight bunching along the length of the suture is normal and resolves spontaneously in 2–3 weeks

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c

d

e

f

g

h

i

Fig. 34.19  (continued)

34  Suture Lifting Techniques

a

421

b

d

c

f

e

Fig.  34.20  Coned (Silhouette) suture lift of the neck. (a) Markings are made behind the ear and along the neck under the mandible to a point about 2 cm proximal to the midline. (b) After local infiltration of lidocaine with epinephrine along the marked points, a 1 cm retroauricular incision is made. (c) The path the needle takes in the upper neck is shown. (d) The Silhouette needle is passed subcutaneously toward the midline. (e) The needle exits at the first point proximal to the midline. The needle should be made to exit perpendicular to the skin. (f) The end of the suture is

grasped and pulled through until the first knot is visible. The suture is cut just distal to the knot. (g) The half-circle needle is used to pass the proximal end through the mastoid fascia for anchorage. (h) A second suture is passed in the same way parallel to the first one. Both sutures are retracted to lift the neck, and tied to one another. (i) Some bunching of skin occurs near the incision and softens over 1–2 weeks. The retroauricular incision is closed with interrupted sutures

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P.M. Prendergast

g

Patients with excessive skin laxity usually require excisional surgery. The suture suspension technique using absorbable sutures is simple and quick (Fig. 34.19). After infiltrative local anesthesia, two skin punctures are made: one behind the ear over the mastoid and one in the upper neck over the anterior border of the sternocleidomastoid muscle. The needle is passed through the upper point, deeply at first to include the mastoid fascia or periosteum, and advanced in a sinusoidal path superficially under the skin toward the lower point. Before exiting from the lower incision, a deeper bite is taken to catch the posterior border of platysma. A USP# 2 polycaproamide suture is threaded through the needle and brought back to the retroauricular incision. Another pass is made, taking a parallel course to the first pass, and the end of the suture is passed from the lower to upper incision so that both ends of the suture exit behind the ear. The sutures are retracted enough to lift the platysma and improve the contour of the neck, and tied. If there is dimpling of the skin at the lower puncture, an artery forceps tip is passed into the incision and gently lifted until the dimple is softened. Bunching of skin along the length of the suture improves without intervention.

h

i

34.15 Neck Lift with Coned Sutures

Fig. 34.20  (continued)

34.14 Neck Lift with Nonbarbed Sutures Mild to moderate ptosis of the neck can be treated using suture lifting alone, or in combination with other procedures such as lipoplasty to remove fat under the chin, along the jawline and in the jowls. Complementary nonsurgical procedures such as botulinum toxins and infrared light tissue tightening are useful for platysmal bands and skin laxity, respectively. The author uses suture suspension of the platysma using absorbable sutures as well as subcutaneous lifting using coned sutures to improve neck ptosis.

Silhouette sutures also provide effective improvement of mild to moderate ptosis of the neck (Fig. 34.20). If submental and submandibular fatty deposits are also present, ­lipoplasty combined with suture lifting may achieve better results than either procedure alone. Botulinum toxin injections should be used for prominent platysmal bands. The Silhouette suture lift begins with markings behind the ear and along the neck under the mandible to a point just proximal to the midline. The suture is passed through a 1 cm incision over the mastoid, in the subcutaneous tissue toward the midline. If there is significant ptosis in the midline, the path of the suture can continue past the midline to a point just distal to it, so that the sutures act as a sling in the submental region. To bring the suture across the midline, the needle first exits from a point just proximal to the midline. Before the needle exits completely from the skin, with the proximal end of the needle still

34  Suture Lifting Techniques

a

423

b

Fig. 34.21  (a) Irregularities are visible in the temporal area following placement of Silhouette coned sutures. The poly-l-lactic acid cones are too superficial in the tissues. (b) After 6 months

without treatment. The cones have partially absorbed and the visible lumps have almost completely gone

under the skin, the needle is rotated so that the end of the needle with the suture attached advances toward the midline. It is passed to a point just distal to the midline where a stab incision with a #11 blade is made to allow the blunt end of the straight needle to emerge. Once the suture is seen, it is cut from the needle and the needle is removed from the site. The suture end is pulled until the most distal knot on the suture is just visible. The suture is cut just distal to the knot and the proximal end of the suture at the retroauricular incision is gently retracted. For most cases, it is sufficient to exit the skin proximal to the midline without passing underneath the chin. Usually two sutures are passed on either side of the neck. The proximal ends of the sutures are secured to the mastoid fascia using the half-circle needles and tied to one another. The incision is then closed.

taken as required. Patients are instructed to avoid excessive animation for the first week and to be gentle when handling the face for the first 4–6  weeks. Cleansing and application of make-up should be performed using gentle upward strokes, along the vectors of lift, rather than downwards against the sutures to avoid disruption. This allows fibrosis around the sutures and reduces the likelihood of cheese-wiring of the sutures through the tissues. Swelling and ecchymosis following suture lifts are usually minimal, but are ameliorated using regular cold packs and sleeping with the head elevated for the first few days. A clear instruction leaflet should be provided, including a contact telephone number should the patient have concerns following the procedure (Table  34.6). Skin sutures, if present, are removed at a follow-up appointment 1  week after the procedure.

34.16 Postoperative Care Following a suture lift, an elastic head garment should be worn for 3 days to immobilize the tissues of the face and neck. Antibiotics, such as cephalexin, are continued for 5 days. Simple analgesia is usually sufficient, although opioid-like analgesia such as Tramadol is prescribed for the first few days and

34.17 Complications Suture lifting techniques for the face and neck are well tolerated using infiltrative local anesthesia only. Sedation and general anesthesia are unnecessary and increase the risks associated with the procedure. Mild edema, ecchymosis, tenderness, and transient

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P.M. Prendergast

Table 34.6  Postoperative instructions POSTOPERATIVE INSTRUCTIONS: SUTURE LIFT IF YOU EXPERIENCE EXCESSIVE PAIN OR BLEEDING, FULLNESS OR SPREADING REDNESS IN TREATMENT AREAS, OR FEVER, PLEASE CALL US IMMEDIATELY.   1. Do not massage or rub vigorously the treatment area for at least 4 weeks; this could disrupt the sutures under the skin   2. Wear the head garment 24 h/day for 3 days and then in bed at night for a further 1 week   3. Continue to refrain from smoking for at least 2 weeks during the healing process. Smoking affects blood supply and nourishment to skin and soft tissues   4. Complete the prescribed course of antibiotics   5. Be gentle when brushing your hair until your stitches are removed   6. There may be some “bunching” of skin near the hairline following the lift. This will soften out over 1–4 weeks, depending on skin quality   7. You may experience a tighter sensation over your face where skin has been retracted. Some of this tightness will lessen over 1–2 weeks as the skin relaxes into its new position   8. You may experience some swelling, bruising or tenderness over the first week but this will subside and fade over time. If you notice increasing redness, swelling and tenderness a few days after the procedure that was not there before, call our clinic. This may be a sign of infection, which is uncommon   9. If you received skin stitches you will need to return to the clinic after 5–7 days for removal I HAVE READ AND FULLY UNDERSTAND THE ABOVE ITEMS 1–8. ____________________________ _________________ Patient Signature Date

a

b

Fig. 34.22  (a) After suture suspension of the midface. Dimpling has occurred near the nasolabial fold on the right where the suture has tethered the dermis. (b) Following subcision with a 21-gauge needle, the dimple has softened

bunching of overlying skin are common following suture lifts. Complications include infection, bleeding, palpability, visibility, skin irreg